Fundamentals of ACLS (2024)

by Mohammad Anzal Rehman

You have a new patient!

A 56-year-old man presents to the Emergency Department with complaints of chest pain and dizziness that began an hour ago. Upon assessment by the triage nurse, his vital signs are as follows: his heart rate is 107 beats per minute, and his respiratory rate is 22 breaths per minute. His blood pressure is  96/70 mmHg, and his oxygen saturation is at 90% on room air. His temperature is 36.8°C.

You are the student on shift when this patient arrives, and immediately, your mind begins to jump across differential diagnoses for this patient. As you rush toward the patient’s room to join your senior, you prepare to list out all the potential causes of chest pain proudly. This must be a Myocardial Infarction, or maybe even an Aortic Dissection. Perhaps it is that rare Boerhaave syndrome you read about last night!

You finally catch up to the Emergency Physician, but before you can open your mouth to wax lyrical about esophageal ruptures, the Doctor states “Let’s begin by evaluating the ABCs.”

Initial Assessment

Emergency Medicine is one of the few specialties in medicine where patient evaluation begins in the same way for every patient, regardless of the probable diagnosis. Most clinicians are wired to jump straight to the ‘mystery-solving’ component of clinical presentation, with many undergraduate curriculums based around disease recognition. Emergency Medicine, however, places an emphasis on systematic assessment of the patient, starting with ‘The Primary Survey’.

The Primary Survey – ABCDE Approach

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

Airway

A patient’s airway connects air, and therefore oxygen, from outside the body to the lungs. Airway management is a term used to evaluate and optimize the passage of oxygen in the upper airway, which may be impaired when there is a blockage or narrowing of this pathway. The most common cause of upper airway obstruction is the tongue, which may ‘close’ the oropharynx posteriorly in patients who are comatose or in cardiopulmonary arrest, for example.

Assessment of the airway typically starts by evaluating any external features that may impact the passage of air through the naso- and oro-pharynx, such as facial or neck trauma, fractures, deformities, and any masses or swelling that may disrupt the airway tract. Allergies, especially anaphylaxis, and significant burns may cause edema of the laryngeal airway and produce obstruction. Excessive secretions may also congest the oropharynx and produce airway obstruction.

A patent or ‘normal’ airway allows a responsive patient to speak in full sentences without difficulty, implying a non-obstructed air passage down the oropharynx and through the vocal cords.

Clinical signs of obstruction may include stridor, gurgling, drooling, choking, gagging, or apnea. A physician may also identify an impending airway obstruction where loss of gag reflex, intractable vomiting, or worsening laryngeal edema may inevitably compromise the passage of air to the lungs and produce a failure to oxygenate or ventilate, prompting a decision to secure the tract through intubation.

Management

In the responsive patient, allow for the patient to be seated or lying in their most comfortable position as you assess the patency of the airway.

‘Opening’ the airway involves positioning the patient’s head in the ‘sniffing position’. In this position, a slight extension of the head with flexion of the neck, keeping the external auditory meatus in line with or above the sternal notch, is used to optimally align the pharyngeal and laryngeal airway segments, preventing obstruction posteriorly by the tongue (Figure 1). This is useful in patients who are unresponsive and cannot consciously protect their airway.

Figure 1 – Use of ‘sniffing position’ to open the airway

Two maneuvers are helpful in opening an unresponsive or sedated patient’s airway, optimizing air entry to the lungs:

1. Head tilt chin lift (Figure 2A) – Using fingertips under the chin, lift the mandible anteriorly while simultaneously tilting the head back using the other hand. Do not use this if cervical spine injury is suspected!

Figure 2A – Head-tilt chin lift

2. Jaw thrust (Figure 2B) – With thenar eminences of both hands anchored over both maxillary regions of the patient’s face, use your fingers at both angles of the mandible to lift it anteriorly. This maneuver is preferable in cases of suspected cervical spine injury as it does not cause hyperextension of the neck.

In unresponsive patients with excessive secretions, use of a rigid suction device can clear fluid and particulate matter such as vomitus.

Intubation may be performed if airway assessment deems it necessary to protect or secure the airway tract in a definitive way. If intubation is required, it should be performed as early as possible to prevent the evolution of a difficult airway, which would lower the chances of a successful intubation. It may also be useful to establish the risk of an inherently difficult airway using the L-E-M-O-N airway assessment method as below:

Look externally – facial trauma, large incisors and/or tongue, hairy beard, or moustache

Evaluate the 3-3-2 rule – where optimal distance between incisors on mouth opening should be 3 finger breadths. Similarly, 3 finger breadths (patient’s fingers) should span the distance from chin to hyoid bone, while the distance from hyoid to thyroid should measure 2 finger breadths.

Mallampati score – grades the view of an open mouth, with class 3 or more predicting a difficult intubation

Obesity/obstruction – Epiglottitis or a tonsillar abscess can inhibit easy passage of an endotracheal tube.

Neck mobility – if limited, positioning is difficult and causes suboptimal views during intubation.

iEM-infographic-pearls-airway - Assessing Airway Difficulty
assessing airway difficulty

Cervical spine immobilization

When the patient arrives in the Emergency Department (ED) following a significant physical trauma, such as head injury or motor vehicle collision, it is crucial to consider the integrity of the cervical spine. If injury is present in this region, further manipulation or movement of the neck may lead to spinal cord damage. Therefore, evaluation and management of airway for these patients should go hand in hand with cervical spine immobilization.

If no specialized equipment is available, or until one is prepared for use, attempts to limit neck movement can be done using manual in-line stabilization, where the provider’s forearms or hands may be positioned at the sides of the patient’s head to prevent indirect movements that could exacerbate underlying injury (see Figure 3).

Cervical spine immobilization is then performed using a rigid cervical collar. It may be augmented with head blocks on lateral sides to limit movement further as the patient is evaluated for injury (see Figure 4). The thoracolumbar region of the spine is immobilized using a spinal backboard, which keeps the patient in a supine position with minimal external force on the spine. Frequently utilized in Emergency Medical Services (EMS) during extrication and transport, all efforts should be made to transition the patient off the spinal board in the ED as it is quite uncomfortable, with prolonged use associated with pressure ulcers and pain.

Breathing

The lungs perform the vital function of delivering oxygen from the airway to the alveoli through ventilation. Perfusion at the alveoli allows for gas exchange; therefore, effective ventilation and perfusion both play a key role in the availability and utilization of oxygen by the human body. Evaluation of the Breathing component assesses factors that would indicate a compromise in ventilation.

The chest inspection should look for respiratory rate, use of accessory muscles, position of trachea (midline versus deviated), symmetry of chest rise, and/or any visible trauma to the thorax. Auscultation evaluates breath sounds for any bilateral inequal air entry or presence of crackles, crepitus, or wheeze. Percussion, though sometimes useful, is often difficult to perform adequately in a resuscitation environment.

Let’s compare the findings in normal lungs, pleural effusion, and pneumothorax based on chest rise, trachea position, percussion, and auscultation.

Normal Lungs: Chest rise is symmetrical with the trachea in the midline position. Percussion reveals a resonant sound. Auscultation presents vesicular breath sounds peripherally and bronchovesicular sounds over the sternum, with no added sounds.

Pleural Effusion: Chest rise remains symmetrical, and the trachea is midline. Percussion is dull over the area of effusion, and auscultation shows decreased breath sounds in the region of the effusion.

Pneumothorax: Chest rise is unequal, and the trachea may be deviated in cases of tension pneumothorax. Percussion reveals a hyper-resonant sound in the area of the pneumothorax, and auscultation shows decreased breath sounds over the pneumothorax region.

Measuring oxygen saturation using pulse oximetry (spO2) provides a percentage of oxygen in circulating blood, with normal levels typically at 95% or above. However, in patients with chronic lung disease, baseline oxygen saturation levels may decrease and can be as low as 88% in many cases. For patients experiencing shortness of breath and showing signs of hypoxia, pulse oximetry readings below 94% suggest that supplemental oxygen may be necessary. This can be administered through various oxygen delivery systems, as outlined in Figure 5 and described below.

Figure 5 – Common equipment used in airway management 1- Nasal cannula, 2- Simple face mask, 3- Nebulizer,* 4- Non-rebreather mask, 5- Venturi mask valves, 6- Rigid suction tip, 7- Bag-valve mask device, 8- Oropharyngeal airway (OPA), 9- Nasopharyngeal airway (NPA), 10- Direct Laryngoscope, 11- Endotracheal tube with stylet, 12- Colorimetric end-tidal CO2 detector, 13- Bougie, 14- Laryngeal Mask Airway (LMA) *NOT an oxygen delivery device, used to administer inhaled medication such as bronchodilators and steroids CO2: Carbon dioxide

General concepts—We typically breathe in room air, which contains 21% oxygen. Each Liter per minute of supplemental oxygen provides an additional 4% inspired oxygen (FiO2) to the patient.

Nasal cannula – Administered through patient nostrils, can provide a maximum flow rate of 4-6 Liters per minute of oxygen, which equals roughly 37 – 45% FiO2

Simple face mask – Applied over the patient’s nose and mouth, can provide a maximum flow rate of 6-10 Liters per minute of oxygen, which equals roughly 40 – 60% FiO2

Venturi mask – Typically used in COPD, where over-oxygenation is avoided. Different colors deliver various flow rates to limit oxygen delivery to the required amount only; Blue (2-4L/min, FiO224%), White (4-6L/min, FiO2 28%), Yellow (8-10L/min, FiO235%), Red (10-12 L/min, FiO2 40%), Green (12-15 L/min, FiO260%)

Non-rebreather mask – Utilizes an attached bag with a reservoir of oxygenated air along with one-way valves on the mask to prevent rebreathing of expired air, optimizing oxygenation. It can provide a maximum flow rate of 15 Liters per minute of oxygen, which equals roughly 85 – 90% FiO2.

Non-invasive ventilation (CPAP/BiPAP) is a tight-fitting mask device that uses high positive pressure to keep the airway open and enhance oxygenation. It is particularly useful in conditions such as COPD exacerbation, acute pulmonary edema/heart failure, and sleep apnea.

Bag-valve mask device: A self–inflating bag attached to a reservoir delivers maximal, high-flow 100% oxygen. This method of manual ventilation is used in rescue breathing and oxygen delivery in nonresponsive or cardiopulmonary arrest patients.

Circulation

The circulation component of the Primary Survey evaluates the adequacy of perfusion by the cardiovascular system. The patient’s general appearance is assessed for signs of pallor, mottling, diaphoresis, or cyanosis, which indicate inadequate or deteriorating perfusion status. Pulses are checked centrally (e.g. carotid pulse, especially if patient with impaired breathing) and peripherally (e.g. radial) alongside hemodynamic assessment, including blood pressure and heart rate checks. Information from this segment also provides valuable insight into potential signs of shock. Extremities are palpated in order to determine any delays in capillary refill time (more than 2 seconds signifies inadequate perfusion, e.g. hypovolemia), peripheral edema in lower extremities (signs of heart failure), and skin temperature (cool or warm to touch).

In cases of trauma, systematic evaluation of circulation also seeks to ascertain areas of potential blood loss or collection, with interventions for any long-bone deformities and/or bleeding from open wounds performed as they are discovered.
Intravenous (IV) line insertion is also performed as part of the management of circulation, as any required fluid or blood products can then be administered through a large-bore IV line (16 gauge or higher). If IV insertion is difficult on multiple attempts, when volume resuscitation is urgently required, Intraosseous (IO) access should be sought to prevent delay in any needed treatment. Insertion of a peripheral venous line often occurs concomitant to blood extraction for any urgent laboratory investigations and/or point-of-care testing. Some common examples of tests performed on critically ill patients include venous blood gas, complete blood count, type and crossmatch, troponin, urea, electrolytes, and creatinine.

Finally, circulation assessment requires an evaluation of cardiac rhythm. Basic auscultation may reveal the rate and regularity of rhythm along with murmurs. However, a critically ill patient will also benefit from the immediate attachment of cardiac pads to the bare chest and connection to a cardiac monitoring device, which provides the physician with the patient’s current cardiac rhythm.

A normal sinus rhythm (Figure 6) consists of a P wave (atrial depolarization), followed by a QRS wave (ventricular depolarization – normally less than 120 ms), with a subsequent T wave (ventricular repolarization). P-R intervals typically have a duration of 120 – 200 ms. A regular rhythm, with a consistent P wave preceding QRS complexes, with a normal heart rate (between 60 – 100 beats per minute (bpm)) is required to consider a rhythm to be normal sinus on the cardiac monitor.

Figure 6 – Normal sinus rhythm

The American Heart Association’s (AHA) Advanced Cardiac Life Support (ACLS) course and guidelines outline a series of internationally recognized cardiac rhythms and their general management when encountered [2]. Some of the most important rhythms, along with the AHA bradycardia and tachycardia algorithms, are summarized below:

Figure 7.1 - Sinus bradycardia (HR < 50 bpm)

Several different conditions, including abnormal heart conduction, damage to the myocardium, metabolic disturbances, or hypoxia, can cause bradycardia. A lower heart rate can result in decreased perfusion to end-organs, such as the brain, with resultant signs and symptoms such as dizziness, confusion, shortness of breath or chest pains. Management (Figure 7.2) aims to treat the underlying cause and increase the heart rate (atropine, dopamine/epinephrine and/or cardiac pacing) if needed to restore the heart’s ability to perfuse organs adequately.

Figure 7.2 – American Heart Association’s Bradycardia Algorithm

Tachycardia (Figure 8.1) is a heart rate of more than 100 bpm that may present as several types of waveforms on the cardiac monitor. Supraventricular tachycardia (SVT) originates in the upper chambers of the heart. The rapid heart rate prevents adequate filling of the heart between contractions, causing signs and symptoms such as dizziness, palpitations, or chest pain.

Figure 8.1 - Supraventricular Tachycardia (SVT)

Management (Figure 8.2) typically involves Valsalva maneuvers, medication (e.g. adenosine), and/or synchronized cardioversion as needed to revert the rhythm back to baseline.

Figure 8.2 – American Heart Association’s Tachycardia Algorithm

SVT produces a narrow-complex tachycardia (QRS segments < 120 ms). In comparison, monomorphic Ventricular Tachycardia (Figure 8.3) originates in the lower chambers of the heart and produces a wide-complex (QRS segments > 120 ms) tachycardia on the cardiac monitor. Similarly, this rhythm may cause dizziness, shortness of breath, or chest pain and is managed with medication or synchronized cardioversion.

Figure 8.3 - Ventricular Tachycardia

ACLS algorithms often divide patients based on “stable” and “unstable” categories. This grouping aims to ascertain which individuals have a pathology severe enough to impair cardiac output to the point of causing serious inadequacies in end-organ perfusion. This ‘instability’ is manifested by altered mental status, ischemic chest pain, drastically low hemodynamic parameters (e.g. systolic BP < 90 mmHg), signs of shock, and signs of acute decompensated heart failure.

Disability

This segment evaluates the level of consciousness and responsiveness of the patient. Level of consciousness may be assessed generally using the AVPU scale (below);

Alert: fully alert patient
Verbal: some form of verbal response is present, though not necessarily coherent.
Pain: response to painful stimulus
Unresponsive: no evidence of motor, verbal or eye-opening response to pain

or more explicitly, using the Glasgow Coma Scale (GCS)

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Exposure

Complete exposure of the patient may be necessary to completely evaluate for any external signs of infection, injury, and rash. This is especially useful in trauma, where log-rolling of the patient is included to ensure the back and spine are also included in a complete assessment for any traumatic injuries. As you expose the patient, obtain consent, be mindful of their dignity, and uncover each segment of the body sequentially, covering it back to prevent any hypothermia for the patient. A core temperature reading also completes vital sign measurements for the patient.

Practical implementation of the Primary Survey

The “cursory” primary survey

It may seem surprising to consider that virtually every patient who enters the Emergency Department, despite the severity of the illness, undergoes some form of a Primary Survey by the treating physician. However, the practicality of this becomes quite obvious when you consider a simple question frequently asked at the beginning of a patient encounter:

“How are you?”

An adequate response of “I am all right” or “Well, I have had this pain in my stomach…” seems fairly standard, but it addresses most of the components detailed in the previous section. A patient who can form words without difficulty or added sounds generally has an intact or patent Airway. Their ability to form words depends on air that has been sufficiently ventilated and moving through the vocal cords, hence the Breathing is adequate. An appropriate response to the question allows us to assume that Circulation adequately perfuses the brain to allow comprehension and formulation of new words oriented to the circumstances of the encounter, hence providing insight into Circulation and, to a degree, Disability.

Synchrony in the Emergency Department

Although systematic assessment during the Primary Survey is laid out in order, it is also important to note that an Emergency Department consists of teams of healthcare professionals who often have the personnel and resources to simultaneously perform tasks to efficiently address all components of the Primary assessment, without delay between segments.
In practice, an example of how synchrony works would involve a patient who, on initial, immediate assessment, is deemed to be in significant distress and/or critically ill. The patient is immediately moved into the ED to a resuscitation area, where team members expose the chest, attach cardiac pads to connect the patient to a cardiac monitor, obtain a fresh set of vital signs, including spO2monitoring, with IV cannula insertion, blood extraction for testing as needed. At the same time, a primary survey is conducted simultaneously by another physician who moves through Airway, Breathing, Circulation, Disability and Exposure. In more advanced systems, a member may be dedicated to each component of the Primary Survey.

Adjuncts

A number of resources are accessible to the Emergency Physician that may aid in diagnosing and investigating the critically ill patient. Utilizing these alongside the initial Primary Survey provides valuable, relevant information that can further guide clinical decision-making and diagnosis during evaluation.

  1. Electrocardiogram – A 12-lead electrocardiogram provides a complete picture of the heart’s electrical activity in various vectors and segments, allowing for a more accurate evaluation for rhythm disturbances, such as in acute myocardial infarction, hyperkalemia, bundle branch blocks, and torsade de pointes. This often ties into the Circulation assessment and allows for a more comprehensive look into the heart’s electrophysiology.
  2. Portable X-rays – Particularly in trauma, urgent chest and pelvic X-ray films can often be obtained without having to transfer the patient to Radiology, hence providing more information on suspected lung pathologies (e.g. pneumothorax, effusion/hemothorax) and pelvic abnormalities (e.g. fracture, displacement).
  3. Urinary/ gastric catheters – Urinary catheters are useful to evaluate fluid status and monitor output for the patient undergoing volume resuscitation. When relevant, gastric tube insertion can assist in gastrointestinal decompression, if needed, as well as minimize the risk of aspiration in certain patients.
  4. Point-of-Care Ultrasonography (PoCUS) – A rapidly evolving and increasingly prevalent modality in the ED is the ultrasound.[3] Various probes, at different frequencies, utilize ultrasound waves to provide the physician with real-time visualization of the body’s internal structures. These images are fast and often very reliable in determining major findings that can guide decision-making in critically ill patients (e.g. presence of post-traumatic intra-abdominal free fluid, pneumothorax, cardiac tamponade). Figure outlines some examples of information that can be extracted using PoCUS.

 

HI-MAP in Shock

Reassessment

Each intervention performed in the Primary Survey should ideally be accompanied by a reassessment of vital signs and patient clinical status and a restarted Primary Survey beginning from Airway. Identifying any improvements, deteriorations, or non-responses that will be pivotal in guiding the initiation or discontinuation of further intervention as per the clinical case is crucial.

Focused History and Secondary Survey

If the patient is appropriately evaluated and stabilized following the Primary Survey, the treating physician may proceed with a focused history and secondary survey appropriate to the clinical circumstances. One example of a focused history incorporates the mnemonic SAMPLE to organize pertinent information as follows:

S – Signs/symptoms of presenting complaint

A – Allergies to any food or drugs

M – Medications (current, recent changes)

P – Pertinent past medical history

L – Last oral intake

E – Events leading to the illness or injury

A secondary survey in the Emergency Department is a more comprehensive physical examination performed systematically in a head-to-toe fashion to investigate any clinically relevant findings. In case of trauma, this also involves careful inspection for any missed injuries, deformities, or signs of underlying blood collection.

As the secondary survey is performed, relevant investigations and/or imaging may be ordered to augment the evaluation of the present clinical condition (e.g. Computerized Tomography (CT) of the brain after signs of basal skull fracture noted on inspection of the face and head). Information gathered from the survey and results of any ordered investigations, coupled with the clinical condition and/or response to therapy in the ED, if any, is used to determine patient disposition at the end of the ED encounter.

Revisiting Your Patient

You assist the Emergency Physician in performing a Primary Survey. The airway is patent, with the patient phonating in full sentences and breathing with mild tachypnea but no added sounds on auscultation. You initiate supplemental oxygen through a non-rebreather mask, with an increase in spO2 to 99%. You reassess and proceed through Airway, Breathing, and Circulation. As you discuss initiating IV fluids with your senior, the patient complains of worsening chest pain, palpitations, and dizziness.You attach the patient to the cardiac monitor and notice the rhythm below:

Cardiac pads have already been attached to the patient. Noting the presence of ischemic chest pain, you correctly identify the patient as having an unstable, narrow-complex tachycardia, most likely an SVT and prepare for synchronized cardioversion. Conscious sedation is conducted after explaining the procedure and obtaining consent from the patient. 50 joules of biphasic energy is then administered for synchronized electrical cardioversion. The rhythm changes on the monitor to the reading below:

You observe an organized rhythm but note that the patient is now unresponsive, with eyes closed and no palpable carotid pulse.

Basic Life Support

Cardiopulmonary arrest occurs when the heart suddenly stops functioning, resulting in lack of blood flow to vital organs in the body, such as the lungs and brain. Therefore, signs of arrest are manifested as a lack of breathing (apnea), lack of pulse and unresponsiveness. The most common cause of cardiac arrest is coronary artery disease.[4] Respiratory arrest refers to a cessation of lung activity, but with a present, palpable pulse and functioning heart.
The International Liaison Committee on Resuscitation (ILCOR) and the American Heart Association (AHA) are some of the key figures who have developed international guidelines on the recognition and management of cardiac arrest patients.[5] Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) courses were established to optimize the workflow and, therefore, patient outcomes in Cardiopulmonary Resuscitation (CPR).

CPR forms the cornerstone of BLS to effectively maintain the victim’s circulatory and ventilatory function until circulation either spontaneously returns or is hopefully restored through intervention. The general concepts within BLS are outlined below:

1. A person who has a witnessed collapse, lack of response or who is suspected of being unresponsive due to cardiac arrest should be approached for further assessment and management. However, it is important for the rescuer to first determine whether the scene is safe around the patient before attempting any intervention. An example of this would be a victim drowned in water, who should be removed from the body of water onto a dry surface prior to attempting life-saving chest compressions or defibrillation.

Figure 9 - Witness
Figure 10 - Check for responsiveness

2. Check for responsiveness. Firmly tapping both shoulders with the palms of your hands and a clear, verbal prompt, such as “Hey, are you okay?” should be incorporated to ensure that the victim is, indeed, unresponsive to an otherwise arousable stimulus.

3. You have determined that the patient is unresponsive. If you are alone, shout loudly and clearly for help and assistance. If no help is nearby, call Emergency Medical Services using your mobile phone.

Figure 11 - Call for help
Figure 12 - Open airway, palpate carotid artery, observe the chest

4. Open the patient’s airway (tilt chin upward into sniffing position). Palpate the carotid pulse by placing two fingers (index and middle finger) just lateral to the trachea on the side closest to you while simultaneously observing the chest for any spontaneous chest rise (breathing). The pulse check should take a minimum of five (5) seconds but no more than 10 seconds to avoid delay in life-saving intervention.

5. When help is available, the chain of survival begins by activating the Emergency Response System. In addition to activating the Emergency Response, ask the person who has responded to your call for help getting an Automated External Defibrillator (AED) device. An example of instruction to a bystander (out of hospital) would be to ‘call an ambulance and get an AED!’. Inside a hospital, if another healthcare provider has come to aid, you may ask them to ‘activate the Emergency Response System/’Code Blue’ and get the crash cart/AED.’

6. Begin high-quality chest compressions. Hands are placed with fingers interlaced to exert pressure using the heel of one hand at the center of the chest, over the lower half of the breastbone (sternum), in line with the nipples (in men), with shoulders directly over your hands and arms straight at a perpendicular angle to the victim’s chest. High-quality chest compression is one of the few variables which have been evidenced to improve patient survival in cardiac arrest.

Figure 13 - Chest compression

Keep the following features in mind to maintain high-quality chest compressions:

  • More than 80% of the time in resuscitation or more should be spent on compressions (Chest compression fraction of > 80%)
  • The frequency of compressions should follow a rate of 100–120 compressions per minute.
  • Compression depth in adults is at least 2 inches. In infants and children, depth should be at least one-third of the anterior-posterior diameter of the chest.
  • After each compression, the hands should be withdrawn to allow adequate chest recoil and fill the heart between compressions.
  • Minimize interruptions in chest compression
  • Avoid hyperventilation (see next point).
Figure 14 - Bag-Valve-Mask Ventilation. Two-Hand technique

7. Compressions should follow the ratio 30:2, that is, 30 compressions followed by 2 rescue breaths delivered by a mouth barrier device (pocket mask) in the sniffing position or a Bag-valve mask (BVM) device if another rescuer is present to manage the airway in hospital. The BVM’s mask should be held with a tight seal using the E-C technique over the bridge of the nose and covering the mouth. 

Breaths should be over 1 second, with enough air pushed in to observe a chest rise and no hyperventilation or excessive bagging of the BVM to avoid gastric insufflation. Two attempts at rescue breaths are performed, minimizing time to under 10 seconds and resuming chest compressions immediately after. If a definitive airway (e.g. endotracheal tube) is in place, resume compressions without pause at a rate of 100-120 compressions per minute while breaths are delivered once every 6 seconds.

8. Once an AED or cardiac monitor/defibrillator is available, place the pads on the victim’s bare chest (dry the skin if wet) in either an anterior-lateral or anterior-posterior position.When in doubt, follow the machine’s prompts and the instructions on the pads themselves to guide placement.

Figure 15 - Correct placement of transcutaneous pacing pads.jpg

9. Follow the prompts on the AED. Stop compressions when the device analyzes rhythm and stay clear of the patient (not touching any part of the patient’s body). During an in-hospital resuscitation, as per ACLS workflow, stay clear, as the team leader should analyze the initial rhythm to ascertain the presence of a shockable or non-shockable rhythm. Either way, the device or team leader should prompt whether a shock is advised. Continue compressions as the device charges, but ensure that all rescuers are clear of the patient when the shock is delivered using the AED/defibrillator device.

Figure 16 - Shock delivery.

A victim who is unresponsive but has a palpable pulse has respiratory arrest, which is managed using rescue breathing only. Breaths are delivered once every 6 seconds without chest compressions while transport to a higher level of care and/or management of any underlying cause for the condition is initiated.

Advanced Cardiac Life Support

The Advanced Cardiac Life Support algorithms were designed to deliver a higher level of resuscitative care where providers with increased training and improved resources are available. This type of augmented management is customary to the Emergency Department, where a Rapid Response Team or Code Blue team would respond when activated and initiate a more team-based approach to cardiopulmonary resuscitation.

Instead of an AED, in-hospital settings have a cardiac monitor/defibrillator, usually mounted atop a crash cart consisting of a CPR back-board (to support chest compressions by providing a firm surface to use under the patient’s chest), drawers with medication used during cardiac arrest, and various equipment for airway management and IV/IO access. Once brought to the bedside, the cardiac pads are similarly placed on the patient’s chest while BLS maneuvers (chest compressions and rescue breaths) continue. Once placed, however, compressions should be paused to assess the cardiac monitor’s cardiac rhythm. The type of rhythm should be identified asshockableornon-shockable(Figure 17s).

Figure 17.1 - NON-SHOCKABLE - Asystol
Figure 17.2 - NON-SHOCKABLE - Pulseless electrical activity – organized rhythm in the absence of palpable pulse
Figure 17.3 - SHOCKABLE - Pulseless Ventricular Tachycardia
Figure 17.4 - SHOCKABLE - Ventricular fibrillation

“Shockable” rhythms (pulseless Ventricular Tachycardia and Ventricular Fibrillation) are a product of aberrant electrical conduction of the heart. Rapid, early correction of this rhythm is the most important step in returning the body to its normal circulatory function. Early defibrillation is one of the few variables that has been evidenced to improve patient survival in cardiac arrest, the other notable one being high-quality chest compressions.[6]

Defibrillation involves using an asynchronous 200J of biphasic (360J if monophasic) energy, delivering an electric current through the cardiac pads attached to the patient’s chest to revert the heart to a rhythm that can sustain spontaneous circulation. Chest compressions should be ongoing while charging, but all persons should stay clear of the patient when shock is being delivered, and this is frequently verified with verbal feedback (‘Clear!’) before pressing the defibrillator button to deliver the shock. Immediately after the shock, chest compressions should resume to minimize interruptions between compressions.

Two minutes of chest compressions and rescue breaths make up each cycle of CPR, at the end of which a rhythm check should be performed for any changes and/or presence of pulse. Figure 18 outlines the ACLS algorithm used to manage shockable and non-shockable rhythms in cardiac arrest. Early shock in shockable rhythms is followed by a cycle of CPR, a second shock if still with a shockable rhythm, after which 1mg of IV epinephrine is given, with subsequent doses every 3 to 5 minutes. During the third cycle of CPR, after 3 shocks have been delivered for a persistent shockable rhythm, a bolus of IV Amiodarone 300mg is typically administered, with a dose of 150mg in a subsequent CPR cycle if still with a shockable rhythm.

“Non-shockable” rhythms (pulseless electrical activity (PEA) and asystole) are not typically a product of disorganized electrical activity in the heart. Instead, an underlying cause has resulted in cardiac arrest for these patients. While the majority of cardiac arrest is caused by coronary artery disease, the consideration of reversible causes by use of the H’s (hypovolemia, hypoxia, hyper-/hypokalemia, hydrogen ions (acidosis), and hypothermia) and T’s (thrombosis/embolism, toxins, tension pneumothorax, and cardiac tamponade) may help recognize and manage other possible etiologies in patients.

The management of non-shockable rhythms focuses on consistent, high-quality CPR, with regular pulse checks every 2 minutes, addressing reversible causes, and administering IV epinephrine 1mg every 3 to 5 minutes.
A palpable pulse with measurable blood pressure signals the Return of Spontaneous Circulation (ROSC).

Figure 18 - ACLS Adult Cardiac Arrest Algorithm

Resuscitation Team Dynamics

The Emergency Department is equipped with the resources and personnel to provide care beyond basic life support. Resuscitation is optimized when multiple providers work together to effectively perform tasks toward management of the patient, thereby multiplying the chances of a successful outcome for the patient. A high-performance team typically consists of members allocated to the following roles and responsibilities:

  • Airway – Opens and maintains the airway. Manages suctioning, oxygenation, and ventilation (Bag-valve mask) and assesses the need for a definitive airway if needed.
  • Medication – Inserts and maintains IV/IO access. Manages medication administration and fluids.
  • Monitor/defibrillator – Ensures attached cardiac pads and AED/cardiac monitor/defibrillator device are working appropriately to display the patient’s cardiac rhythm in clear view of the team leader. Administers shocks using the devices as needed. May alternate with the compressor every 5 cycles or 2 minutes to prevent compression fatigue
  • Compressor – Performance of high-quality chest compressions as part of CPR for the cardiac arrest patient. Focuses on quality and consistency of compressions. You may switch to another standby compressor or monitor/defibrillator every 5 cycles or 2 minutes if compressions are affected by fatigue.
  • Recorder – Documents the timing of medication, intervention (shocks, compression), and communicates these to the Team Leader, with prompts to enable timely dosing of frequent medication (e.g., ensuring epinephrine every 3 to 5 minutes is administered as per the verbalized order)
  • Team leader – A defined leader who coordinates the team’s efforts and organizes them into roles and responsibilities that are clear, well-understood, and within their individual limitations. Provides explicit instructions and direction to the resuscitation effort, focused on patient care and optimized performance from all team members. Promotes understanding and motivates members, identifying any potential deficit or depreciation of quality during resuscitation and facilitating improvement in performance as needed.

All team members are encouraged to conduct themselves with mutual respect and practice closed-loop communication, where each message or order is received with verbal confirmation of understanding, then execution of the order, centralizing all information back to the team leader. Figure 19 provides an example of the possible placement of each member during resuscitation that may optimize their workflow through the resuscitation attempt. Ideally, the team leader remains at the foot of the bed, in clear view of all members, with involvement limited to coordination of the team’s efforts and minimal direct execution of tasks.

Figure 19 - An example of optimized team placement during resuscitation

Post Arrest Care

If the patient is found to have Return of Spontaneous Circulation (ROSC), post-cardiac arrest care should be initiated to enhance the preservation of brain tissue and heart function. This involves a sequential assessment and optimization of Airway, Breathing, and Circulation in the initial stabilization phase. A definitive airway may be placed so ventilation is more appropriately controlled, with parameters set to optimize oxygen administered with ventilatory function. Figure 20 outlines the ACLS algorithm and parameters often used to help guide post-cardiac arrest care. Circulation incorporates fluids, vasopressors, and/or blood products to achieve an adequate systolic blood pressure above 90 mmHg, with Mean Arterial Pressure of at least 65 mmHg typically indicating perfusion within stable parameters.

It is imperative to obtain a 12-lead ECG early to ascertain the presence of an ST-elevation myocardial infarction (STEMI), which will require expedited transfer of the patient to a Cath Lab for definitive reperfusion therapy. The patient’s responsiveness should be reassessed, and the determination for additional investigation should be performed in conjunction with other critical care management as needed.

Of note, unresponsive patients may benefit from Targeted Temperature Management (TTM), which involves the maintenance of core body temperature at a target of 32 – 36 ℃ for 24 hours, or preferably normothermia at 36 °C to 37.5 °C with an emphasis on prevention of hyperthermia, in order to protect and optimize brain recovery post-arrest.[7]

Almost all cardiac arrest survivors will require a period of intensive care observation and management. If no immediate intervention is needed (e.g., reperfusion therapy), patients inside a hospital will need to be transitioned to an Intensive Care Unit (ICU) for further care.

Figure 20 – Post-Cardiac Arrest Care

What do you need to know?

  • Emergency Medicine, especially in critical care, emphasizes a systematic approach to the unwell patient.
  • The Primary Survey is designed to recognize and address life-threatening conditions effectively and timely.
  • The Primary Survey components are Airway (& and C-spine in trauma), Breathing, Circulation, Disability, and Exposure.
  • If an intervention is performed at any level of the survey, you must reassess the patient by commencing the Primary Survey again, starting with Airway.
  • Reassess and review your patient for changes frequently.
  • Many of the actions performed in the initial assessment of the critically ill patient may occur simultaneously when more team members are present in an Emergency Department. Do not let the chaos of the scene distract you from completing each step of the assessment.
  • The AHA has well-established guidelines for assessing and managing patients through the Primary Survey. Use the algorithms and the patient’s status as ‘stable’ or ‘unstable’ to guide the management of recognized pathologies, especially in Circulation.
  • The ED is home to a variety of adjuncts, including portable X-rays, ECG, and point-of-care ultrasound, which can provide the physician with rapid, readily accessible information to guide management.
  • Remember the SAMPLE mnemonic for a focused history in the critically ill patient.
  • An unresponsive patient should be immediately recognized, and Emergency Response Systems should be activated.
  • Performance of Basic and Advanced cardiac life support focuses on preserving blood circulation transiently to maintain the perfusion of organs, such as the brain, until the cause of the condition is reversed or managed.
  • The majority of cardiac arrest is caused due to coronary artery disease.
  • The two most important predictors of patient survival in cardiac arrest are high-quality CPR and early defibrillation (for a shockable rhythm)
  • An effective resuscitation in the ED often relies on the concerted efforts of multiple team members, led by a team leader who coordinates tasks in an organized, effective way to improve patient survival and outcomes.

Author

Picture of Mohammad Anzal Rehman

Mohammad Anzal Rehman

EM Residency Graduate from Zayed Military Hospital in Abu Dhabi, UAE. Founder/President of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Editor-in-Chief for the Emirates Society of Emergency Medicine (ESEM) Monthly Newsletter. I have a vested interest in sharing updated knowledge and developing teaching tools. As a healthcare professional, I continually strive to incorporate the newest clinical research into practice and am an active advocate for the use of Point of Care Ultrasonography (POCUS) in the ED.

Listen to the chapter

References

  1. Reynolds T. Basic Emergency Care: Approach to the Acutely Ill and Injured. World Health Organization; 2018.
  2. 2020 Advanced Cardiac Life Support (ACLS) Provider Manual. American Heart Association; 2021.
  3. Hashim A, Tahir MJ, Ullah I, Asghar MS, Siddiqi H, Yousaf Z. The utility of point of care ultrasonography (POCUS). Ann Med Surg (Lond). 2021;71:102982. Published 2021 Nov 2. doi:10.1016/j.amsu.2021.102982
  4. Cardiac Arrest Registry to Enhance Survival (CARES) 2022 Annual Report; 2022, https://mycares.net/
  5. Wyckoff MH, Singletary EM, Soar J, et al. 2021 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Neonatal Life Support; Education, Implementation, and Teams; First Aid Task Forces; and the COVID-19 Working Group. Resuscitation. 2021;169:229-311. doi:10.1016/j.resuscitation.2021.10.040
  6. Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. doi:10.1016/j.resuscitation.2021.02.010
  7. Lüsebrink E, Binzenhöfer L, Kellnar A, et al. Targeted Temperature Management in Postresuscitation Care After Incorporating Results of the TTM2 Trial. J Am Heart Assoc. 2022;11(21):e026539. doi:10.1161/JAHA.122.026539

Acknowledgements

  • Marina Margiotta – Illustrator
  • Paddy Kilian – Emergency Physician – Mediclinic City Hospital, Dubai, Director of Academic Affairs – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Rasha Buhumaid – Consultant Emergency Physician – Mediclinic Parkview Hospital, Dubai, Assistant Professor of Emergency Medicine – Mohammed Bin Rashid University Of Medicine and Health Sciences, President of the Emirates Society of Emergency Medicine (ESEM)
  • Amog Prakash – Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Fatima Al Hammadi- Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

COVID-19 (2024)

by Pei Shan Hoe, Andrew Mariotti, Prem Menon, Alexandra Digenakis

You have a new patient!

A 64-year-old male, Mr Fox, with a history of type II diabetes mellitus, hypertension, congestive heart failure, and cerebrovascular accident with chronic left-sided weakness, presented to the emergency room from a nursing home due to fever, cough, and difficulty in breathing. Per EMS, the patient’s nursing home has had an outbreak of COVID-19 infections. Mr Fox is unvaccinated against COVID-19 and has not been tested for COVID-19 before arrival. The onset of symptoms was 2 days ago, and his symptoms have progressively worsened. At the nursing home, the patient was in acute distress and was tachycardic (130 bpm), tachypneic (30 rpm), and hypoxic (82% on room air). Oxygen saturation improved to 89% on placement of a nonrebreather mask by EMS. He was borderline hypotensive (90/50 mmHg) but improved to 100/60 mmHg after 500cc of IV normal saline. On arrival, the patient appears diaphoretic and tachypneic with O2 saturation of 90% on 15L of O2 via a nonrebreather mask. Mr. Fox is alert but confused and unable to answer questions. He is febrile to 102.3F (39.1oC), remains tachycardic (132 bpm), and his blood pressure is stable at 103/67 mmHg, with delayed capillary refill (2 to 3 seconds). Mr Fox is coughing throughout the examination and has diffuse rales on auscultation of his lungs but has no obvious pitting oedema or JVD.

What do you need to know?

Importance

The COVID-19 pandemic threw the world into a tumultuous few years of fear, death, and isolation as many countries tightened borders and restricted activities. As of March 2023, there have been over 761 million confirmed cases of COVID-19 globally – including almost 7 million deaths – since the virus was first discovered in late 2019, as reported by the World Health Organisation (WHO) [1]. Healthcare institutions bore the brunt of the pandemic’s wrath as wave after wave of case surges drained resources and manpower, overwhelming hospitals and exposing healthcare workers to increased risks. Emergency departments became the frontlines of this battle against a new virus, unprecedented in its worldwide scale and extent of physical and economic disruption. This chapter lays out key information in the assessment and management of the COVID-19 infection, which are important as the virus continues to plague humankind and mutations surface.

Epidemiology

The COVID-19 virus belongs to a family of coronaviruses, which are known to produce respiratory diseases in humans. There have been three major coronavirus outbreaks in recent times, beginning with the severe acute respiratory syndrome coronavirus (SARS) in 2002, followed by the Middle East respiratory syndrome coronavirus (MERS) in 2012, and now the COVID-19 pandemic in 2019 [2].

Reports of COVID-19 cases first emerged from Wuhan, China, at the end of 2019; the virus spread rapidly to other countries worldwide, with cases reported in all continents. On March 11, 2020, WHO declared COVID-19 as a pandemic [3].

Person-to-person spread is the main mode of COVID-19 transmission. The mean or median incubation period ranges from 5 to 6 days. The duration for which a patient with COVID-19 remains infective is unclear. Viral load in the oropharyngeal secretions is highest during the early symptomatic stage of the disease. The patient can continue to shed the virus even after symptom resolution [4,5].

Pathophysiology

The virus is transmitted via respiratory droplets and aerosols from person to person. Once inside the body, the virus binds to host receptors and enters host cells through endocytosis or membrane fusion. After membrane fusion, the virus enters the lungs’ alveolar epithelial cells, and the viral contents are released. The virus undergoes replication within the host’s cells [5].

Medical History

What are the key features that should be interrogated in medical history?

Common symptoms: fever, cough and fatigue.

Other reported symptoms, typically milder and less common, are loss of taste or smell, conjunctivitis, headache, muscle aches and pains, nasal congestion, runny nose, sore throat, diarrhoea, nausea or vomiting, and different types of skin rashes.

Ask also about symptoms of pulmonary embolism, as COVID-19 can be a risk factor. These include sudden and sharp chest pain, dyspnea that worsens on exertion, and coughing that may produce bloody mucus.

There are also some people who become infected but remain asymptomatic and well [6,7,8].

What are the risk factors related to the specific disease in focus that should be picked up in medical history?

Check for any COVID-19 contact, and if the patient is vaccinated against COVID-19 Unvaccinated patients with positive contact are at higher risk of developing infection though vaccinated patients can contract COVID-19 despite vaccination.

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag symptoms that patients should monitor for include difficulty breathing or shortness of breath, confusion, loss of appetite, persistent pain or pressure in the chest [6,8].         

Physical Examination

What are the key features that should be checked during a physical examination?

Check the patient’s following systems:

  • Head, ear, nose and throat
  • Cardiovascular system
  • Respiratory system
  • Gastrointestinal system
  • Skin

What are the findings related to the specific disease in focus that should be picked up during physical examination?

Look out for signs such as [6-10]:

  • Abnormal breath sounds in lungs suggestive of pneumonia, which is the most frequent serious manifestation of infection
  • Abdominal tenderness
  • Conjunctivitis
  • Skin changes, such as maculopapular/morbilliform, urticarial, and vesicular eruptions, transient livedo reticularis, reddish-purple nodules on the distal digits similar in appearance to pernio (chilblains), also known as “COVID toes”
  • Leg swelling, erythema or tenderness on examination

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag signs include [6-10]:

  • Signs of venous thromboembolism, such as deep vein thrombosis — erythema, tenderness and swelling of the lower limbs
  • Arrhythmias
  • EncephalopathyRespiratory distress

Alternative Diagnoses

What other diseases can present with similar clinical features/conditions?

Differential diagnoses of COVID-19 include [11]:

  • Community acquired pneumonia, and other forms of pneumonia (e.g. aspiration pneumonia, pneumocystis jirovecii pneumonia)
  • Influenza
  • Middle East respiratory syndrome (MERS)
  • Avian influenza virus infection
  • Pulmonary tuberculosis

Which risk factors make COVID-19 more probable than alternative differentials?

Risk factors for COVID-19 include:

  • Close contact with COVID-19 patients
  • Lack of COVID-19 vaccinations

Acing Diagnostic Testing

Diagnosing COVID-19 infections may involve the use of multiple modes of testing and evaluation. In this section, we will discuss the role that bedside tests, lab studies, and imaging play in diagnosing and treating COVID-19.

Bedside Tests

Testing for COVID-19 that can be done at the bedside falls into one of two categories: antigen testing or nucleic acid amplification testing (NAAT), sometimes known as PCR testing due to the use of polymerase chain reaction (PCR) methods to amplify the DNA samples in question. Both have a place in testing for COVID but indications for use and the subsequent results should be approached thoughtfully.

Antigen Testing

With antigen testing, a nasal or oropharyngeal swab – or even a blood sample – is used to collect mucosal secretions and saliva from the patient with a suspected COVID infection. The sample is placed in a lateral flow assay that contains antibodies to COVID antigen with a detector molecule attached. If the sample contains COVID antigen, the antibodies will bind and read as a positive test. Rapid testing can yield results in under a half-hour with 99.4% specificity and 68.4% sensitivity, is conducive for self and at-home administration, and has been an effective method for increasing access to testing [12]. Due to its high specificity, rapid testing is reliable when positive, however, one of the major drawbacks is its low sensitivity. It is important to understand that patients who test negative for COVID via an antigen test cannot be reliably ruled out for the disease until it has been verified with NAAT testing.

NAAT Testing

This form of testing – while still utilizing swabbed samples of mucosal secretions and saliva as in antigen testing – relies on a different method of disease verification using PCR and COVID specific RNA primers to amplify any viral DNA present in the sample. Results yield similar levels of specificity (98.9 – 99.2%) but have a markedly higher sensitivity of 83.2 – 84.8% making this a much more reliable testing option [13]. The major drawback to this method of testing is that it cannot be administered at home and must be done where there is a lab present that has a technician with the knowledge to perform the testing using the PCR machine.

Laboratory Tests

If both antigen and NAAT testing returns negative – or if NAAT results are pending after a negative antigen test – clinicians will often opt to send for a respiratory viral panel to determine if there is an underlying primary or comorbid infection. A respiratory viral panel uses PCR to test for a standard slate of viruses that usually includes influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus, adenovirus, rhinovirus, enterovirus, and human metapneumovirus.

While no specific set of labs is directly indicative of a COVID-19 infection, a specific constellation of lab findings has been found to be suggestive of potential COVID infection when pretest probability is high. These lab findings include lymphopenia, transaminitis – specifically elevations in AST – and an elevated c-reactive protein [14]. While not diagnostic, this constellation of laboratory results can lend support to a future diagnosis and help guide early treatment.

Imaging

Neither Magnetic Resonance Imaging (MRI), Computed Tomography (CT), nor X-ray can provide a conclusive diagnosis of COVID-19. Ground glass opacities seen on CT are a typical finding in COVID-19 infection and have been proven effective at differentiating COVID-19 and non-COVID-19 viral illnesses in certain retrospective analyses [15]. Despite this, the presence of ground glass opacities alone does not provide definitive diagnosis and would only be indicated for diagnostic purposes if COVID pre-test probability was already high due to known community presence or recent exposures [16].

Figure 1: ground glass opacities on chest CT[16]

Imaging becomes far more important when diagnosing two major sequelae of COVID-19: pneumonia and acute respiratory distress syndrome (ARDS). The prolonged, severe pulmonary inflammation of COVID-19 causes damage to capillaries and leakage of fluid into the alveoli leading to ARDS. This should be suspected in those who develop acute onset shortness of breath, hypoxemia, and/or rattling breath sounds. A chest x-ray showing a classic “white out” appearance can greatly aid in diagnosis of ARDS.

Figure 2: A chest x-ray showing classic ARDS findings[17]

Similarly, opportunistic bacterial infections can take root in damaged lung tissue secondary to COVID infection, leading to bacterial pneumonia. This should be a major consideration in patients who rapidly develop shortness of breath or pleuritic chest pain. A chest x-ray showing lung field consolidations can greatly aid in the diagnosis of pneumonia.

Figure 3: A chest x-ray showing classic consolidated findings of pneumonia[18].

Risk Stratification

When stratifying the potential risk of severity of COVID-19, the two major considerations are age and the number and type of comorbidities. Global data evaluating age in relation to COVID mortality during the early stages of the pandemic demonstrated a less than a 1.1% mortality rate in those younger than 50 years but an overall mortality rate of 12.1% among those greater than 80 years old, with each subsequent decade in between demonstrating increased mortality rates from the prior decade [19].

Furthermore, the presence of comorbid conditions increased morbidity and mortality compared to the general population, with cardiovascular disease and diabetes respectively acting as significant predictors for future intensive care requirements and lower survival rates [20]. Though individual comorbidities present a lesser risk than age alone, patients with multiple comorbidities are at greater risk of mortality than those who present with one comorbid condition. Studies have shown 10 or greater comorbidities result in a 3.8-fold increase in RR as compared to those with 1 comorbidity [21].

Risk Stratification Tools

Many tools exist to stratify patients into risk categories based on covid infection based on the setting and presentation of the patient. The notable tools with a description of their intended use are described below.

  • 4C Mortality Score – This tool was developed by the International Severe Acute Respiratory and emerging Infection Consortium (ISARIC) to predict in-hospital mortality of COVID based on age, oxygenation, renal function, and other statistical measures.
  • ACEP ED COVID-19 Management Tool – Developed by emergency physicians from around the world, this tool walks the clinician through the steps of managing a patient with COVID in an emergent setting from severity classification to treatment.
  • Pediatric COVID Risk Assessment Tool – Physicians at the University of California San Francisco created this tool to assess the risk of children with asymptomatic infection.

Management

Management options in unstable patients begin with determining the severity of disease. Mild disease presents with symptoms characteristic of upper respiratory infections such as fever, cough, malaise, and rhinorrhea. Acute, life-threatening airway, breathing and circulation concerns are absent in mild disease.

In moderate to severe disease, one of the initial signs is dyspnea. Severe disease specifically is defined by hypoxemia (oxygen saturation at or below 94% on room air) which may or may not require supplemental oxygen or even intubation. In the case of severe disease initial stabilization is followed by medical management and even certain procedures. These are described below.

Initial Stabilization

The steps to initial stabilization for severe COVID-19 infection are described below in terms of the ABCs of emergency medicine.

  • Airway – The patient should be evaluated for the ability to protect and maintain the airway. Signs that a patient may require or soon require intubation include worsening hypoxia despite maximized oxygen supplementation, increased work of breathing, and signs of distress.
  • Breathing & Circulation—Assuming patients can maintain their airway but their oxygen saturation is still below 94% on room air, they will require supplemental oxygen. Low-flow supplemental oxygen with the nasal cannula at 1-2 liters/minute can be used initially, but high-flow supplementation via non-rebreather and even non-invasive ventilation, such as a high-flow nasal cannula or BiPap, should be considered depending on patient needs.

Once the patient is stabilized per their needed oxygen and ventilation requirements, pharmaceutical and bedside management can begin with the goal of ultimately weaning the patient from their oxygen requirements.

Medical Management

The ensuing table outlines the major pharmaceutical agents used in the treatment of COVID-19. They are described based on class, indication, contraindications and adverse effects, and dosing.

Drug

Class

Indication

Contraindications (CI) &

Adverse Effects (AE)

Dosing

Nirmatrelvir/

Ritonavir (Paxlovid)

Anti-viral

Mild to moderate COVID-19 infection for patients at risk for increased severity

CI: <12 years old or eGFR <30ml/min as well as many medications interactions

AE: dysgeusia, diarrhea, hypertension, and myalgia

eGFR > 60ml/min: 300/100mg twice daily for 5 days

 

eGFR 30-60ml/min: 150/100mg twice daily for 5 days

Dexamethasone

Glucocorticoid

Severe disease in patients requiring oxygen or ventilatory support

AE: Hyperglycemia, increased secondary infection risk

6mg/day for up to 10 days

Baricitinib

JAK Inhibitor

Severe disease in patients requiring high-flow oxygen supplementation but not intubation.

CI: Already on IL-6 inhibitors, lymphopenia, neutropenia, CKD

Max 4mg/day oral

Tocilizumab

IL-6 Inhibitor

Markedly elevated inflammatory markers (D-dimer, CRP, etc.)

CI: must already be taking dexamethasone

AE: secondary infection risk

Single dose at 8mg/kg IV

Anakinra

IL-1 Inhibitor

Severe disease in patients who are at high risk of progressing to ventilatory support

AE: anaphylaxis, stomach pain, headache, nausea

100mg/day for 10 days, subcutaneous

Remdesivir

Antiviral

Severe disease in patients who are not intubated or in need of ventilatory support. Benefits uncertain in non-severe cases.

CI: under 12 years of age

AE: nausea, vomiting, fever, hyperglycemia, transaminitis

Loading dose: 200mg IV

Maintenance Dose: 100mg/day IV for up to 10 days

Monoclonal Antibodies

Antibody Based Therapy

No longer indicated due to decreased benefit from increased circulating variants

N/A

N/A

Convalescent Plasma

Antibody Based Therapy

Patients with impaired humoral immunity who have severe disease

AE: serum sickness, anaphylaxis

1 unit of high titer convalescent plasma

Ivermectin

Anthelmintic

Patients with latent Strongyloides infection undergoing glucocorticoid therapy for COVID

CI: no studies to prove efficacy against COVID-19 itself as a primary therapeutic

AE: GI upset, neurological disturbances

200ug/kg for 1-2 days

Procedures

There are few COVID specific procedures though intubation and mechanical ventilation are common requirements in severe cases. Some patients will even progress in severity to a point that extracorporeal membrane oxygenation (ECMO) will be required.

Patients who develop ARDS, independent of COVID, may benefit from proning – a technique by which the patient is rolled onto their abdomen to increase ventilation/perfusion matching of the lungs [22].  It should be noted that any procedure which must be done that involves aerosolization (bronchoscopy, intubation and extubation, suctioning, etc.) should be done under extreme caution and only after all who are present have the appropriate personal protective equipment, as these procedures increase the risk of spreading the virus to non-infected individuals. 

Complications: Long COVID

The United States Department of Health defines Long COVID as “signs, symptoms, and conditions that continue or develop after initial COVID-19 or SARS-CoV-2 infection.” These are typically present four weeks or more after the initial phase of infection and may be multisystemic [23]. Some patients may have a “relapsing-remitting pattern and progression or worsening over time, with the possibility of severe and life-threatening events even months or years after infection.”

Those who are at higher risk of developing Long COVID include patients with more severe COVID-19 illness, or with underlying health conditions, without the COVID-19 vaccine, or who experienced multisystem inflammatory syndrome (MIS) during or after COVID-19 illness.

Special Patient Groups

This chapter has already touched on the severity of this disease from the standpoint of age and comorbidities; however, this section seeks to expand on that topic by presenting special considerations for other demographics who may be infected with COVID-19.

Pediatric Populations

Pediatric populations generally have far fewer severe outcomes and are more likely to present asymptomatically when infected with COVID-19 [24]. However, it is important to be aware of a rare but potentially life-threatening complication known as multi-system inflammatory syndrome in children (MIS-C). If a patient develops MIS-C, signs and symptoms begin to present within 2-6 weeks of infection and include ongoing fever accompanied by any of the following: stomach pain, bloodshot eyes, diarrhea, lightheadedness, rash, and vomiting. If the child’s condition continues to worsen and they develop difficulties breathing, medical attention should be sought immediately. Physicians can provide supportive care as well as treatment of the underlying infection or co-occurring infections. With timely and appropriate care, MIS-C rarely leads to death or long-term complications [24].

Geriatric Populations

Geriatric populations are those defined as over the age of 65 years and represent an extremely high-risk category even in the absence of comorbidities. Because of this, geriatric patients who contract COVID-19 infections should be watched closely and receive antiviral treatments – such as Paxlovid – as soon as possible to stem the progression of disease. Other considerations for geriatric populations that may not be immediately apparent are concerns with access. Elderly patients often require assistance walking, driving, or navigating to clinic appointments due to a higher prevalence of comorbid conditions (dementia, osteoporosis, wasting, etc.) and making care more accessible to these populations is the first step in ensuring they can get the treatment they need. This position is notably called out by the World Health Organization in their considerations for caring for elderly with COVID-19.

Pregnant Populations

Individuals who are pregnant are at increased risk of complications from COVID-19 for themselves and their child. One of the best ways to help these patients is to provide timely vaccination to either prevent or reduce the severity of initial infection. Despite controversy, a myriad of clinical trials has proven that mRNA vaccines for COVID-19 are safe and without adverse outcomes for either the mother or baby during pregnancy [25]. If a mother and her unborn child do contract COVID-19 and require hospitalization, these patients should be taken care of in facilities that have the capability to monitor the status of the fetus and uterine contractions to ensure the health and safety of mom and baby. 

When To Admit This Patient

Admission criteria for COVID-19 is very specific to the individual patient and institution practices and guidelines. In general, however, admission should be considered for patients presenting with severe COVID-19 infection. This includes but is not limited to patients that are in respiratory distress, patients requiring oxygen therapy to maintain oxygen saturations >90%, or patients unable to tolerate food, fluid, or meds by mouth. Abnormal lab work can also warrant hospital admission including patients with significant electrolyte abnormalities, kidney injury, ischemic changes on EKG or elevation in cardiac markers. Persistent vital sign abnormalities could also warrant admission, including COVID-19 patients that are persistently tachycardic even after IV fluid resuscitation and fever reduction. Age can also contribute to the threshold for admission. For example, a patient over 65 with COVID-19 infection and pneumonia on X-ray could warrant admission.

Patients that are presenting with mild COVID-19 disease, have access to follow-up, have normal vital signs and with no significant abnormalities on lab and imaging studies may be safely discharged with primary care follow-up.

It is important to provide patients with COVID-19 strict return precautions should their symptoms worsen. Particularly, these patients should be told to return if they experience any worsening shortness of breath, difficulty in breathing or abnormal home oxygen saturation readings. Patients should be warned that they may lose their sense of taste and/or smell and this is a common symptom of the disease. If patients are unable to tolerate food and/or fluid, they should be instructed to return back to the emergency department. Any new altered mental status, confusion, chest pain, focal weakness or seizures should also prompt patients to return immediately to the emergency department.

Revisiting Your Patient

Let’s return to Mr. Fox, who presented to the emergency department in respiratory distress from his nursing home. The providers have high clinical suspicion for COVID-19 infection given his exposure to COVID-19 at the nursing home, and are concerned considering his risk factors for severe disease. He is placed on contact and droplet precautions and COVID-19 tests are collected. Given his severe presentation there is concern for sepsis, a lactic acid level and blood cultures to be obtained. He is started on high-flow nasal cannula oxygenation to improve his oxygen saturation, and IV fluid resuscitation is initiated to improve his hemodynamic status. He is given acetaminophen for his fever. A chest x-ray is obtained, which demonstrates bilateral patchy infiltrates. Per discussion with Mr. Fox’s nursing home, he has not been hospitalized recently or been on any antibiotic treatment. He receives cefepime and vancomycin to treat possible hospital-acquired pneumonia given he is a nursing home resident – please refer to your institution’s antibiotics guidelines – while awaiting his COVID-19 test results. Given the high concern for COVID-19 infection and Mr. Fox’s severe hypoxia, he is also started on Dexamethasone, as this has been shown to improve mortality in patients with severe COVID-19 infections.

Despite these interventions, Mr. Fox continues to have increased work of breathing and is becoming fatigued. An arterial blood gas is obtained, which demonstrates worsening respiratory acidosis. Mr. Fox is confirmed to be full code by the nursing home, and thus the decision is made to proceed with intubation. He is placed on a ventilator and started on lung-protective ventilation settings. His COVID-19 test comes back positive. He remains persistently tachycardic despite appropriate IV fluid resuscitation and correction of his fever. His providers are concerned that he may have developed a pulmonary embolism in the setting of possible hypercoagulability associated with his COVID-19 infection. A CT scan of his chest with contrast is obtained, which demonstrates multiple right-sided pulmonary emboli without evidence of right heart strain. Mr. Fox is started on a heparin drip. He is admitted to the medical intensive care unit with the diagnoses of acute hypoxic respiratory failure secondary to COVID-19 infection and right-sided pulmonary emboli.

Authors

Picture of Pei Shan Hoe

Pei Shan Hoe

Medical Officer, Ministry of Health Holdings, Singapore.

Pei Shan Hoe is a former journalist-turned junior doctor currently working at Singapore General Hospital. She studied comparative literature as an undergrad at New York University, obtained a Masters in investigative journalism from Columbia University, and then an MD from Duke-NUS Medical School. She is an ACEP/EMRA Global EM Student Leadership Program mentee (‘22-23) and co-author of published articles related to Covid-19 and ED design. Her interests lie in global health, acute care, medical education, healthcare systems and services research. She is certified for overseas disaster deployment under Singapore Red Cross and has also participated in peacetime medical missions.

Picture of Andrew Mariotti

Andrew Mariotti

Resident Physician, University of Colorado Department of Anesthesiology

Andrew Mariotti, M.H.A, has been caring for patients since 2015 as both an emergency medical technician and administrator. In 2020, Mr. Mariotti worked as an administrative fellow under the executive board of the University of Colorado Hospital where he directly aided the coordination of the hospital’s emergency response to the COVID-19 pandemic in Denver and Aurora, Colorado. He is currently a medical student at the University of Colorado, where he serves as Vice President of the student body and his research in quality improvement has led to abstract publications with the Society of Hospital Medicine and American Society of Anesthesiologists.

Picture of Prem Menon

Prem Menon

Global Emergency Medicine Fellow, Brigham and Women’s Hospital

Prem Menon is a chief resident at Emory University’s Emergency Medicine residency program in Atlanta, Georgia. Prem began his training during the height of the COVID-19 pandemic and has managed many critically ill COVID-19 patients. His interests within Emergency Medicine include Refugee, Immigrant and Asylee health and Global Emergency Medicine. During his residency training he worked to improve emergency care globally, specifically in the country of Liberia. He is originally from Austin, Texas and obtained his medical degree at the University of Texas Health San Antonio – Long School of Medicine. He will be starting fellowship in Global Emergency Medicine at Brigham and Women’s Hospital/Harvard in the Fall of 2023.

Picture of Alexandra Digenakis

Alexandra Digenakis

Clinical Assistant Professor, East Carolina University Emergency Medicine

Alexandra Digenakis, D.O., completed her undergraduate degree at Penn State University. She completed her medical school training at the Philadelphia College of Osteopathic Medicine in 2019. She completed her emergency medicine residency at the University of North Carolina in 2022. She is currently a clinical assistant professor of emergency medicine at East Carolina University. She has a strong interest in providing education, opportunities and exposure to global health to medical students and resident physicians. She has participated in the EMRA/ACEP Global Emergency Medicine Student Leadership Program as a medical student mentee, resident co-director, faculty advisor and faculty co-director.

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References

  1. WHO coronavirus (COVID-19) dashboard. World Health Organization. https://covid19.who.int/. Accessed April 13, 2023.
  2. COVID-19: Epidemiology, virology, and prevention. UpToDate. https://www.uptodate.com/contents/covid-19-epidemiology-virology-and-prevention. Accessed April 13, 2023.
  3. Dhar Chowdhury S, Oommen AM. Epidemiology of COVID-19. Journal of Digestive Endoscopy. 2020;11(1):3-7. doi:10.1055/s-0040-1712187
  4. Coronavirus disease (covid-19) faqs. United Nations. https://www.un.org/en/coronavirus/covid-19-faqs. Accessed April 13, 2023.
  5. Parasher A. COVID-19: Current understanding of its Pathophysiology, Clinical presentation and Treatment. Postgraduate Medical Journal. 2021;97(1147):312-320. doi: 1136/postgradmedj-2020-138577
  6. COVID-19: Clinical features. UpToDate. https://www.uptodate.com/contents/covid-19-clinical-features. Accessed April 14, 2023.
  7. COVID-19: Cutaneous features and issues related to dermatologic care. UpToDate. https://www.uptodate.com/contents/covid-19-cutaneous-manifestations-and-issues-related-to-dermatologic-care. Accessed April 14, 2023.
  8. Coronavirus disease 2019 (covid-19). Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/index.html. Accessed April 14, 2023.
  9. Clinical care information for covid-19. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care.html. Accessed April 14, 2023.
  10. Clinical care quick reference for covid-19. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care-quick-reference.html. Accessed April 14, 2023.
  11. Coronavirus disease 2019 (covid-19). Coronavirus disease 2019 (COVID-19) – Differentials. BMJ Best Practice US. https://bestpractice.bmj.com/topics/en-us/3000168/differentials. Accessed April 14, 2023.
  12. Jegerlehner, S., Suter-Riniker, F., Jent, P., Bittel, P., & Nagler, M. (2021). Diagnostic accuracy of a SARS-COV-2 rapid antigen test in real-life clinical settings. International Journal of Infectious Diseases, 109, 118–122. https://doi.org/10.1016/j.ijid.2021.07.010
  13. Butler-Laporte, G., Lawandi, A., Schiller, I., Yao, M., Dendukuri, N., McDonald, E. G., & Lee, T. C. (2021). Comparison of saliva and nasopharyngeal swab nucleic acid amplification testing for detection of SARS-COV-2. JAMA Internal Medicine, 181(3), 353. https://doi.org/10.1001/jamainternmed.2020.8876
  14. Brinati, D., Campagner, A., Ferrari, D., Locatelli, M., Banfi, G., & Cabitza, F. (2020). Detection of covid-19 infection from routine blood exams with Machine Learning: A feasibility study. Journal of Medical Systems, 44(8). https://doi.org/10.1007/s10916-020-01597-4
  15. Elmokadem, A. H., Bayoumi, D., Abo-Hedibah, S. A., & El-Morsy, A. (2021). Diagnostic performance of chest CT in differentiating COVID-19 from other causes of ground-glass opacities. Egyptian Journal of Radiology and Nuclear Medicine, 52(1). https://doi.org/10.1186/s43055-020-00398-6
  16. Parekh, M., Donuru, A., Balasubramanya, R., & Kapur, S. (2020). Review of the chest CT differential diagnosis of ground-glass opacities in the covid era. Radiology, 297(3). https://doi.org/10.1148/radiol.2020202504
  17. Zompatori, M., Ciccarese, F., & Fasano, L. (2014). Overview of current lung imaging in acute respiratory distress syndrome. European Respiratory Review, 23(134), 519–530. https://doi.org/10.1183/09059180.00001314
  18. De Vega Sanchez, B., Disdier Vicente, C., & Lopez Pedreira, M. R. (2017). An asymptomatic man with pathological chest radiography. Breathe, 13(4). https://doi.org/10.1183/20734735.008717
  19. Bonanad, C., García-Blas, S., Tarazona-Santabalbina, F., Sanchis, J., Bertomeu-González, V., Fácila, L., Ariza, A., Núñez, J., & Cordero, A. (2020). The effect of age on mortality in patients with COVID-19: A meta-analysis with 611,583 subjects. Journal of the American Medical Directors Association, 21(7), 915–918. https://doi.org/10.1016/j.jamda.2020.05.045
  20. Khedr, E. M., Daef, E., Mohamed-Hussein, A., Mostafa, E. F., Zein, M., Hassany, S. M., Galal, H., Hassan, S. A., Galal, I., Zarzour, A. A., Hassan, H. M., Amin, M. T., Hashem, M. K., Osama, K., & Gamea, A. (2022). Comorbidities and outcomes among patients hospitalized with covid-19 in Upper Egypt. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery, 58(1). https://doi.org/10.1186/s41983-022-00530-5
  21. Kompaniyets L, Pennington AF, Goodman AB, et al. Underlying Medical Conditions and Severe Illness Among 540,667 Adults Hospitalized With COVID-19, March 2020-March 2021. Prev Chronic Dis. Jul 1 2021;18:E66. doi:10.5888/pcd18.210123
  22. Hadaya, J., & Benharash, P. (2020). Prone positioning for acute respiratory distress syndrome (ARDS). JAMA, 324(13), 1361. https://doi.org/10.1001/jama.2020.14901
  23. Long Covid or post-covid conditions. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html. Accessed April 14, 2023.
  24. Acevedo L, Pineres-Olave BE, Nino-Serna LF, et al. Mortality and clinical characteristics of multisystem inflammatory syndrome in children (MIS-C) associated with covid-19 in critically ill patients: an observational multicenter study (MISCO study). BMC Pediatr. Nov 18 2021;21(1):516. doi:10.1186/s12887-021-02974-9
  25. Ciapponi, A., Berrueta, M., P.K. Parker, E., Bardach, A., Mazzoni, A., Anderson, S. A., Argento, F. J., Ballivian, J., Bok, K., Comandé, D., Goucher, E., Kampmann, B., Munoz, F. M., Rodriguez Cairoli, F., Santa María, V., Stergachis, A. S., Voss, G., Xiong, X., Zamora, N., … Buekens, P. M. (2023). Safety of covid-19 vaccines during pregnancy: A systematic review and meta-analysis. Vaccine, 41(25), 3688–3700. https://doi.org/10.1016/j.vaccine.2023.03.038

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Chest Trauma (2024)

CHEST TRAUMA

by Ivan Low & Jeremy Wee Choon Peng

You have a new patient!

A fifty-year-old male patient is brought into the resuscitation room following a motor vehicle accident. The patient is a motorcyclist who was hit on his left side by a lorry moving at 40mph (64.4 kph). He was flung 3 metres, and his helmet remained intact, while the motorcycle was badly damaged. Vital signs are as follows: T 36.5, BP 168/98, HR 112, RR 32, and SpO2 95% on 10L facemask. A cervical collar has been applied by paramedics on scene. On arrival, the patient appears to be in respiratory distress, using his accessory muscles of respiration.

What do you need to know?

Chest trauma occurs in approximately one-third [1] of trauma patients and causes up to 25% mortality [2] in a multiply injured patient. More than 80% of thoracic injuries were blunt [1] rather than penetrating, and 70% of blunt injuries were a result of road traffic accidents [2,3,4], with drivers and front-seat passengers being placed at highest risk [2].

Thoracic injuries can lead to clinical deterioration and death by impairing a patient’s ‘ABCs.
Airway obstruction can directly result from distortion of tracheobronchial anatomy. Breathing can be affected in two broad ways: 1) Ventilation-perfusion (V/Q) mismatch: Hypoventilation can result from mechanical chest wall or diaphragmatic disruptions, or abnormal collections of air or fluid in the pleural space limiting lung expansion. Hypoperfusion can be caused by vascular disruptions or thrombosis in a damaged lung. 2) Gas exchange abnormalities: Gas exchange can be impaired by direct damage to the alveolocapillary membrane, or dilution of the surfactant layer with blood or interstitial fluid causing alveolar collapse. Circulation can be compromised due to: hemorrhagic shock from vascular or parenchymal injuries, cardiogenic shock from cardiac injury, and obstructive shock from high intrathoracic or intrapericardial pressures (see Table 1). 
 
Table 1: Pathophysiology and patterns of injury in chest trauma

Pathophysiology

Example of injuries (non-exhaustive)

Airway

Tracheobronchial injury

Breathing

(a) V/Q mismatch

 

 

 

(b) Gas exchange abnormalities

 

Sternal or rib fractures +/– flail chest

Pneumothorax +/– hemothorax

Diaphragmatic injury

Pulmonary vascular injury or thrombosis

Pulmonary contusion or laceration

Circulation

(a) Hemorrhagic shock

(b) Cardiogenic shock

(c) Obstructive shock

 

Great vessel (e.g. aortic) disruption

Cardiac contusion or laceration

Tension pneumothorax

Cardiac tamponade

 

Medical History

The mnemonic “AMPLE” highlights several critical aspects of a patient’s history that should be gathered from all trauma patients: Allergies, Medications currently used, Past illnesses and pregnancy, Last meal, and Events related to the injury [5]. Alert patients can often provide details about the mechanism of their injury and the level of force or impact experienced. They may also report symptoms such as pain in the chest, back, or abdomen, dyspnoea, noisy breathing, hemoptysis, hematemesis, syncope or pre-syncope. Eyewitness accounts from passers-by and paramedics may be helpful in supplementing an overall picture of the scene, particularly if the patient is unable to provide a history at this point in time. The ATMIST template, which includes age, time, mechanism, injuries, signs and symptoms, and treatment, is an effective tool for guiding handovers from prehospital teams [6].

Physical Examination

A comprehensive physical examination is crucial to detect major thoracic injuries early to facilitate timely intervention. The patient’s vital signs often help identify patients who are decompensating or at higher risk of deterioration. These include abnormalities such as tachycardia, bradycardia, tachypnea, bradypnea, hypotension, and hypoxemia.

Inspection

On inspection, assess the patient for:

(a) Airway obstruction, respiratory distress, or decompensation:

  • Stridor
  • Use of accessory muscles
  • Asterixis, drowsiness, or obtundation

(b) Chest wall injuries:

  • Steering wheel or seatbelt imprints
  • Chest wall contusions, deformities, or wounds
  • Asymmetric and paradoxical chest wall movements
  • For penetrating injuries, always check for exit wounds, and assume involvement of adjacent body cavities e.g. abdomen

(c) Peripheral signs of shock or major thoracic injury:

  • Cold and clammy peripheries (most types of shock)
  • Jugular venous distension (tension pneumothorax or cardiac tamponade)

Palpation

On palpation, assess the patient for:

(a) Pneumothorax, hemothorax, or lung collapse:

  • Tracheal deviation
  • Subcutaneous emphysema

(b) Rib fractures and associated complications:

  • Bony tenderness
  • Step deformities
  • Flail segments

(c) Pulses:

  • Irregular heart rhythm (arrhythmia from cardiac injury)
  • Pulse delay or differential (aortic dissection)

Percussion

On percussion, assess the patient for:

(a) Hyperresonance: pneumothorax

(b) Dullness: hemothorax, lung collapse

Auscultation

On auscultation, assess the patient for:

(a) Stridor or wheeze: airway obstruction

(b) Reduced breath sounds: pneumothorax or hemothorax

(c) Muffled heart sounds or pericardial rub: pericardial effusion

As patients with thoracic injuries often present with concomitant abdominal and shoulder injuries, complete your examination with a thorough evaluation of the abdomen and shoulder girdles (including the clavicle and scapula).

Alternative diagnoses

The important injuries to assess all patients with chest trauma are summarised in literature as the ‘Deadly Dozen’, as listed in Table 2 [7]. The first six (‘Lethal Six’) are immediately life-threatening and ought to be detected during the primary survey, while the next six (‘Hidden Six’) may not be immediately apparent but are potentially life-threatening and should be picked up during the secondary survey.

Table 2: ‘Deadly Dozen’ in Thoracic Trauma

‘Lethal Six’

‘Hidden Six’

1. Airway obstruction

1. Thoracic aortic disruption

2. Tension pneumothorax

2. Tracheobronchial disruption

3. Cardiac tamponade

3. Myocardial contusion

4. Open pneumothorax

4. Traumatic diaphragmatic tear

5. Massive hemothorax

5. Esophageal disruption

6. Flail chest

6. Pulmonary contusion

Diagnostic testing

Apart from the ‘Lethal Six’ pathologies, early diagnostic testing can aid in the detection of life-threatening pathologies, including but not limited to the ‘Hidden Six’. A combination of point-of-care tests (POCT), chest imaging, and laboratory tests can help physicians make critical decisions in the assessment of a patient with chest trauma.

POCT

  • Arterial or venous blood gas (ABG/VBG):
    • When to do it: Signs and symptoms of respiratory distress or decompensation, or when there is a clinical suspicion of shock.
    • Findings to look for: A low PaO2:FiO2 (P/F) ratio indicates degree of respiratory failure; an elevated PaCO2level suggests hypoventilation and respiratory decompensation; an elevated serum lactate level indicates poor end-organ perfusion and shock.
  • Electrocardiogram (ECG)
    • When to do it: Mechanism suggests major chest trauma, signs and symptoms of chest wall injury, or features of active ongoing cardiac disease [8].
    • Findings to look for: Arrhythmias and ischemic changes may suggest cardiac injury; small or alternating QRS complexes may indicate pericardial effusion.
  • Point-of-care ultrasonography (POCUS):
    • When to do it: Mechanism suggests major polytrauma or chest trauma, hemodynamic instability[9,10]
    • Findings to look for: Reduced cardiac contractility or wall rupture, pericardial effusion, absence of lung sliding or presence of lung point, sternal or rib fractures [11]
    • Pitfalls: Due to poor sensitivity and operator dependence, normal findings do not exclude cardiac, pulmonary, aortic, or musculoskeletal injury [9,10]; serial assessments are recommended to improve sensitivity.

Imaging

Table 3: NEXUS Chest Radiography Rule [12]

This applies to patients 15 years or older who sustained blunt trauma within the last 24 hours. No thoracic imaging is required if none of the following criteria are met:

  • Age >60 years
  • Rapid deceleration mechanism (fall from >20ft, MVC >40mph)
  • Chest pain
  • Intoxication
  • Altered mental status
  • Distracting painful injury
  • Tenderness to chest wall palpation
  • Computer tomography of thorax or aortogram (CT Thorax / Aortogram):
    • When to do it: Mechanism suggests major polytrauma or chest trauma [9,10]; suspicion of thoracic injury based on clinical findings or CXR / POCUS; unable to exclude significant thoracic injury by NEXUS Chest CT Decision Instrument (Table 4) [14].
    • Findings to look for: Cardiac, pulmonary, aortic, or musculoskeletal injuries.
    • Pitfalls: Risk-benefit ratio needs to be assessed and possibly discussed with the patient and/or their next-of-kin in patients at risk of contrast-induced nephropathy or who are pregnant.

Table 4: NEXUS Chest CT Decision Instrument [14]

This applies to patients with stable vital signs, 15 years or older. No chest CT is required if none of the following criteria are met:

  • Chest wall, sternum, thoracic spine, or scapular tenderness
  • Abnormal chest X-ray (e.g. clavicle fracture or widened mediastinum)
  • Distracting injury
  • Rapid deceleration mechanism (fall from >20ft, MVC >40mph)

Laboratory tests

  • Cardiac enzymes:
    • When to do it: Hemodynamic instability, ECG abnormalities
    • Pitfalls: Prognostic yield remains unclear

Risk stratification

The two useful clinical tools in the emergency department are the NEXUS rules above, which both have 99% sensitivity in excluding significant thoracic injuries in the absence of all criteria, and hence may guide the judicious use of chest imaging.

There are several risk stratification tools developed to predict poorer outcomes (e.g. mortality, pneumonia, acute respiratory distress syndrome) in patients with chest trauma, including the Thoracic Trauma Severity Score (TTSS) [15,16], Chest Trauma Score (CTS)[17,18], and Rib Fracture Score (RFS)[19]. However, none are routinely used in the emergency department setting given that they do not affect clinical management in the ED and typically require advanced imaging as part of the risk stratification process.

Management

Patients with chest trauma are managed according to Advanced Trauma Life Support (ATLS) [20] principles in order to detect and address ‘ABCDE’ issues in a timely fashion.

(a) Airway

  • Establish definitive airway (intubation, front-of-neck access) if partial or complete airway obstruction is identified.

(b) Breathing

  • Administer 100% O2 if hypoxemic.
  • Apply one-way seal to open chest wounds.
  • Intubate for mechanical ventilation if there is respiratory failure (oxygenation, ventilation).
  • Finger and tube thoracostomy if there is suspicion of pneumothorax or hemothorax.

(c) Circulation

  • Administer IV crystalloids if there are signs of shock and end-organ hypoperfusion.
  • Transfuse blood products and consider activating the massive transfusion protocol if suspecting hemorrhagic shock.
  • Consider pericardiocentesis if in cardiac tamponade and no surgeon is readily available.
  • If the patient goes into traumatic circulatory arrest, there may be a role for emergency department thoracotomy (EDT), unless (1) there were no signs of life on scene, (2) the injuries are unsurvivable, or (3) prolonged downtime exceeding 15 minutes.

(d) Disability

  • Consider early intubation if the patient is drowsy (which could be a result of shock, hypercarbia, hypoxemia, or concomitant head injury).
  • Check for concomitant thoracic spine injury.

(e) Environment / Exposure

  • Assess for injuries across the chest, back, and adjacent areas such as the shoulder girdles and abdomen.
  • Keep the patient warm.

Urgent surgical consultation is often warranted in all cases of penetrating chest trauma and if there is suspicion of any of the ‘Deadly Dozen’ pathologies.

Medications

  • Analgesia is crucial for relieving pain and preventing atelectasis, but when using opioids, careful dosing is necessary to avoid hypoventilation.
  • Tranexamic acid stabilises blood clots and reduces mortality in patients with significant ongoing bleeding presenting within 3 hours of injury [21].
  • Prophylactic antibiotics and the tetanus vaccine are used to prevent infection, particularly in patients with penetrating chest trauma, significant hollow viscus injuries, or those undergoing invasive procedures. The use of these medications should follow institutional guidelines.

Special patient groups

  • Paediatric patients: Children have more compliant chest walls and hence may sustain significant intrathoracic injuries without obvious chest wall abnormalities. In addition, multiple chest wall injuries or a mechanism of injury that is incompatible with the child’s developmental milestones should raise suspicion for non-accidental injury. A careful evaluation and a high index of suspicion are required in this patient group.
  • Geriatric patients: Older adults, due to reduced pulmonary reserves, are at an increased risk of developing respiratory complications. This patient group should be counselled on the increased risks of atelectasis, pneumonia, and acute respiratory distress syndrome. Adequate analgesia and incentive spirometry may help to reduce the risk of these complications.

When to admit the patient

  • All patients with penetrating chest trauma or blunt trauma with suspicion of significant intrathoracic injury should be admitted for evaluation and monitoring.
  • Patients who remain symptomatic despite a normal initial evaluation can be observed for 8 hours, with serial physical examinations or chest radiographs scheduled.
  • Most other patients can be safely discharged with appropriate advice (to return to the ED if developing pain, dyspnoea, fever, haemoptysis, or hematemesis, which may suggest missed injuries or complications such as chest infection).

Revisiting your patient

The patient is managed according to ATLS [20] principles.

Airway: There is no stridor or obvious facial injury. The cervical spine has been immobilised.

Breathing: He is tachypnoeic and hypoxaemic. The trachea is deviated to the right. There is a left chest wall deformity with bruising, asymmetric chest wall movements, and left-sided paradoxical movements. There is no obvious penetrating injury. Crepitus and step deformities are palpated on the left chest wall. Breath sounds are reduced on the left. Tension pneumothorax and flail chest are suspected. POCUS demonstrates absent lung sliding on the left. An arterial blood gas demonstrates hypoventilation with a PaCO2 of 42 mm Hg despite the patient’s tachypnoea (PaCO2 is expected to be low). Left finger thoracostomy is performed, with a gush of air noted upon entry into the pleural cavity, and a large-bore chest tube is inserted. Intubation with manual in-line stabilisation is performed in view of impending type 2 respiratory failure.

Circulation: The patient is tachycardic and has borderline low blood pressure. His peripheries are cold and clammy. Pulses are regular and there is no pulse delay or differential. An initial FAST scan is negative for free fluid in the abdomen or pericardial sac. Heart sounds are normal. Two large-bore intravenous cannulas are inserted for crystalloid administration.

The rest of the primary survey and adjuncts: The rest of the primary survey is normal. A plain chest radiograph confirms the presence of a left pneumothorax with subcutaneous emphysema and multiple left-sided rib fractures constituting a flail segment (see example videos below). There is no obvious hemothorax, widened mediastinum, or raised hemidiaphragm. Analgesia, prophylactic antibiotics, and the tetanus vaccine are administered.

Disposition: The patient is admitted to the surgical intensive care unit and planned for further advanced imaging and operative interventions by the surgical team.

Authors

Picture of Ivan Low

Ivan Low

Ivan Low is a Resident in Emergency Medicine in Singapore's public healthcare system. He graduated from the National University of Singapore (NUS) in 2018, and is currently working as a military doctor in the Republic of Singapore Navy. He is a Designated Workplace Doctor (Compressed Air Works) and is trained in Diving and Hyperbaric Medicine. He is actively involved in medical education, particularly in the Singapore Medical Association. He has been awarded the NUS Junior Doctor Teaching Award several times in recognition of his work.

Picture of Jeremy Wee Choon Peng

Jeremy Wee Choon Peng

Dr Jeremy Wee serves as a Senior Consultant at the Department of Emergency Medicine at the Singapore General Hospital. Besides being actively involved in the care of patients at the Emergency Department, Dr Wee has a special interest in Trauma care as well as Medical Education. This led to his completion of the Masters of Science in Health Professions Education and the Masters in Trauma Sciences. He is currently the Program Director of the Singhealth Emergency Medicine Residency Program and is actively involved in undergraduate education as an Adjunct Assistant Professor Duke-NUS Graduate Medical School, Clinical Senior Lecturer with Yong Loo Lin School of Medicine.

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References

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  2. Milisavljevic S, Spasic M, Arsenijevic M. Thoracic trauma. Current Concepts in General Thoracic Surgery. 2012. doi:10.5772/54139.
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  13. Ahmadzadeh K, Abbasi M, Yousefifard M, Safari S. Value of NEXUS chest rules in assessment of traumatic chest injuries; a systematic review and a meta-analysis. The American Journal of Emergency Medicine. 2023;65:53-58. doi:10.1016/j.ajem.2022.12.038. 
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  19. Seok J, Cho HM, Kim HH, et al. Chest trauma scoring systems for predicting respiratory complications in isolated rib fracture. Journal of Surgical Research. 2019;244:84-90. doi:10.1016/j.jss.2019.06.009. 
  20. Galvagno SM, Jr., Nahmias JT, Young DA. Advanced Trauma Life Support((R)) Update 2019: Management and Applications for Adults and Special Populations. Anesthesiol Clin. 2019;37(1):13-32.
  21. Roberts I, Shakur H, Coats T, et al. The crash-2 trial: A randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, Vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013;17(10). doi:10.3310/hta17100. 
  1.  

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Bradyarrhythmias (2024)

Bradyarrhythmias

by Hassan M. Alshaqaq & Danya Khoujah

You have a new patient!

An 80-year-old male patient was brought to the emergency department (ED) by ambulance from a long-term care facility with a chief complaint of altered mental state for 2 hours. On arrival, his vitals were as follows: heart rate= 42 beats/min, blood pressure (BP)=70/50 mmHg, SpO2=95% on room air, respiratory rate=23 breaths/min, temperature=37.6°C, glucocheck= 215 mg/dL. The patient was pale, diaphoretic, alert, and disoriented. Pupils were equal and reactive to light. No neurological deficits or lateralizing signs were identified. The patient has a history of diabetes mellitus, hypertension, and ischemic heart disease. There is no history of drug ingestion or recent symptoms of infection. The patient was given 1 liter of intravenous (IV) normal saline during transport. A 12-lead electrocardiogram (ECG) was obtained (Figure 1). What are your initial assessment steps? What are the ECG features? What is the most likely diagnosis? How will you stabilize this patient?

Figure 1. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app. 
Figure 1. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app. 

Importance and Epidemiology

Bradyarrhythmias are defined as rhythms with a ventricular rate lower than 60 beats/min in adults and lower than the age-appropriate rate in pediatrics. Bradycardia may cause symptoms at a rate of <50 beats/min, which is the functional definition that most guidelines use [1]. Bradyarrhythmias are categorized into bradycardias and atrioventricular (AV) blocks [2].

Bradycardias are characterized by a slow rate of both atria and ventricles and include sinus bradycardia, junctional rhythm, idioventricular rhythm, and hyperkalemia-related sinoventricular rhythm. Bradyarrhythmias due to AV blocks are characterized by ventricular beats slower than the atria and include second- and third-degree AV blocks. Uncommonly, atrial fibrillation or flutter may present with a slow ventricular rate secondary to either significant conduction disturbance or excessive nodal-blocking medications.

Patients with bradyarrhythmias can be either stable or unstable. Patients with hemodynamically unstable bradycardia are at a high risk of cardiovascular collapse [3]. On the other hand, stable asymptomatic bradycardia could be physiological in athletes and well-conditioned individuals [4,5].

Compromising bradycardia has an incidence of 6 per 10,000 patients presenting to the ED for any reason; 20% of those require temporary pacing and 50% require a permanent pacemaker [6]. One percent of admission to the intensive care units (ICUs) from the ED are patients with compromising bradycardia, and 10% of syncope can be attributed to bradycardia [6,7]. Due to the significant potential for instability in bradycardic patients [3], emergency clinicians play a critical role in their initial stabilization, identification of underlying etiology, and treatment.

Pathophysiology

Normal cardiac electrophysiology starts with an impulse generated in the sinoatrial (SA) node, traveling into the atria via interatrial conduction pathways leading to atrial contraction, which appears as a P wave on the ECG. The impulse is then conducted down to the AV node, then from the AV node into the bundle of His and bundle branches, and finally into the Purkinje system leading to a ventricular contraction. The AV conduction appears as the PR interval, whereas the ventricular depolarization appears as the QRS complex (Figure 2). Several electrolytes, such as potassium and calcium, play a crucial role in initiating and regulating the cardiac action potential.

Figure 2. Cardiac conduction system. Used with permission from OpenStax licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Access for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction
Figure 2. Cardiac conduction system. Used with permission from OpenStax licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Access for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction

There is an anatomical variance in the blood supply of the SA and AV nodes. The blood supply of the SA node arises from the right coronary artery in 63% and the left circumflex artery in 37% of the population [8]. The AV node is supplied by a branch of the right coronary artery in 90% and the left circumflex artery in 10% [8]. This is most relevant in acute myocardial infarction (MI), as different may arise from ischemia of the conduction system [9]. MI may also lead to ischemia through a vagal-mediated response.

Cardiac output is dependent on the heart rate and stroke volume. Initially, the reduced heart rate increases the diastolic filling leading to an augmentation in the stroke volume. This compensatory mechanism is eventually overwhelmed, leading to decreased cardiac output, hypoperfusion and potentially cardiogenic shock [2,10].

Blood pressure equals the cardiac output multiplied by the systemic vascular resistance. In patients with reduced cardiac output, endogenous sympathetic reflex leads to vasoconstriction and increased systemic vascular resistance. Therefore, patients could have hypoperfusion despite normal-appearing blood pressure.

The underlying cause of bradyarrhythmias could be either conditions affecting the automaticity of cardiac cells (i.e., their ability to generate impulses) or the conduction of impulses within the cardiac conduction system [11,12]. be intrinsic (due to an innate dysfunction of the heart) or extrinsic (Table 1). A practical mnemonic is DIE, which stands for Drugs, Ischemia, and Electrolytes. Half of the patients with compromising bradycardia have a treatable underlying etiology [6].

Table 1. Causes of bradyarrhythmias [7]

Intrinsic:

  • Myocardial ischemia/infarction
  • Cardiomyopathy
  • Congenital heart disease
  • Degenerative fibrosis (with aging)
  • Traumatic (e.g., Denervation post cardiac surgery, cardiac ablation)
  • Infectious/inflammatory (e.g., myocarditis, endocarditis, Lyme disease, syphilis, sarcoidosis, lupus)
  • Sepsis
  • Infiltrative disorders (amyloidosis, hemochromatosis)

Extrinsic:

  • Autonomic-mediated (e.g., athletes, carotid sinus hypersensitivity, situational)
  • Electrolyte disturbances (e.g., hyperkalemia, hypokalemia, hypocalcemia)
  • Hypothermia
  • Endocrinopathy (e.g., hypothyroidism)
  • Raised intracranial pressure
  • Medication overdose (e.g., β-Blockers, calcium channel blockers, digoxin, clonidine, opioids)
  • Toxicologic exposure (e.g., organophosphate)

Types of Bradycardia

Sinus Bradycardia

Sinus bradycardia is characterized by ECG findings of a P wave preceding each QRS, a fixed P-P interval equal to the R-R interval, and a ventricular rate lower than 60 beats/min (Figure. 3). Sinus bradycardia can be found in healthy individuals, particularly athletes with high resting vagal tone.

Figure 3. Sinus bradycardia. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 46 beats/min. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 3. Sinus bradycardia. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 46 beats/min. Courtesy of Dr Hassan Alshaqaq and Dr Danya Khoujah.

It could also be secondary to pathological conditions, such as acute MI (Figure 4) [9]. Patients with sinus bradycardia are usually asymptomatic and do not require any specific treatment. However, profound bradycardia causing hypoperfusion requires emergent treatment of the underlying cause. Atropine may be used, as well as cardiac pacing.

Figure 4. Sinus bradycardia with inferior STEMI. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 58 beats/min combined with ST-segment elevation in the inferior leads (Leads III and aVF), hyperacute T waves in leads III and aVF with relative loss of R wave height, early Q-wave formation in leads II, III and aVF, and reciprocal ST depression and T wave inversion in leads I and aVL. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 4. Sinus bradycardia with inferior STEMI. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 58 beats/min combined with ST-segment elevation in the inferior leads (Leads III and aVF), hyperacute T waves in leads III and aVF with relative loss of R wave height, early Q-wave formation in leads II, III and aVF, and reciprocal ST depression and T wave inversion in leads I and aVL. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Junctional Rhythm

When the SA node fails to discharge or the discharge of the SA node fails to reach the AV node, the AV node generates “junctional escape beats” at a ventricular rate ranging between 40 and 60 beats/min (Figure. 5). These QRS complexes on the ECG are not usually preceded by P waves. However, in some cases, the junctional beats conduct in retrograde into the atria, producing a P wave before or after the QRS. If present before the QRS complex, the PR interval will be abnormally short (<120 msec).

Figure 5. Junctional rhythm. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and a ventricular rate of 54 beats/min. Also, there is evidence of 2 premature ventricular contractions (PVCs). Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 5. Junctional rhythm. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and a ventricular rate of 54 beats/min. Also, there is evidence of 2 premature ventricular contractions (PVCs). Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.

Sustained junctional escape rhythm may be caused by inferior MI with right ventricle (RV) extension (Figure 6) [9], posterior MI, myocarditis, hypokalemia, and digitalis toxicity. Infrequent junctional escape beats do not require treatment. Treating the underlying etiology is the mainstay of treatment in symptomatic patients and atropine can be used as a bridge until then. Atropine enhances SA node discharge rate and AV nodal conduction, therefore suppressing slower pacemakers. In case of hemodynamic compromise, cardiac pacing might be necessary [9].

Figure 6. Junctional rhythm with inferior STEMI with posterior extension. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and ventricular rate of 43 beats/min combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF), ST elevation in lead III > II, early Q-wave formation in lead III, horizontal ST segment depression and upright T waves in leads V2-V3 (posterior MI), and reciprocal ST depression in leads V4-V6, lead I, and aVL. Courtesy of Dr. Anas Halim. Digitized using PMcardio app.
Figure 6. Junctional rhythm with inferior STEMI with posterior extension. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and ventricular rate of 43 beats/min combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF), ST elevation in lead III > II, early Q-wave formation in lead III, horizontal ST segment depression and upright T waves in leads V2-V3 (posterior MI), and reciprocal ST depression in leads V4-V6, lead I, and aVL. Courtesy of Dr. Anas Halim.

Idioventricular Rhythm

In idioventricular rhythm, beats originate from the ventricles with wide (>120 ms) and regular QRS complexes and a rate of 30-50 beats/min. In idioventricular rhythms, ECG shows no P waves (Figure 7). It is usually non-sustained; present for a short duration only. The significance of idioventricular rhythm is that it is most commonly seen in the setting of an ST-segment elevation MI (STEMI) [13].

Figure 7. Idioventricular rhythm. ECG shows regular and wide QRS complexes (>120 ms), absence of P wave, and ventricular rate of 49 beats/min. Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 7. Idioventricular rhythm. ECG shows regular and wide QRS complexes (>120 ms), absence of P wave, and ventricular rate of 49 beats/min. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Atropine may be utilized in symptomatic patients but is usually unsuccessful. If the rhythm persists and is compromising, cardiac pacing may be attempted. Antiarrhythmic agents are best avoided as these could lead to asystole by suppressing the rescue functioning pacemaker [9,14,15].

Table 2 compares ECG features of bradycardic rhythms.

Sinus bradycardia

Junctional rhythm

Idioventricular rhythm

 
  • Sinus P waves present.
  • PR interval 120-200 msec (normal).
  • Rate < 60 beats/min.
  • Absence of normal sinus P waves (may be retrograde).
  • Ventricular rate 40-60 beats/min.
  • Narrow QRS complexes.
  • Absence of P waves.
  • Ventricular rate 30-50 beats/min.
  • Regular and wide QRS complexes.
 
 
 
 

Sinus Node Dysfunction

Sinus node dysfunction is caused by the failure of the sinus node to generate or conduct appropriate cardiac potentials. It can be associated with various supraventricular rhythms, including tachycardia and bradycardia, as well as prolonged pauses (>3 secs). It is most often due to age-dependent fibrosis of the nodal tissue [16,17] or post-cardiac transplantation [18], and might also be seen in patients with myocardial ischemia [19,20], myocarditis [19], and cardiomyopathy [7, 21, 22]. On ECG, it is characterized by episodes of bradycardia and/or sinus arrest with episodes of supraventricular tachycardia (Figure 8).

Figure 8. Sinus node dysfunction. ECG shows tachycardia interspersed with long sinus pauses (absence of any electrical activity). Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 8. Sinus node dysfunction. ECG shows tachycardia interspersed with long sinus pauses (absence of any electrical activity). Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

First-Degree AV Block

First-degree AV block (more accurately described as AV delay) is characterized by delayed AV conduction of all atrial impulses to the ventricles at the level of the atria, AV node, or His-Purkinje system. There is no blocked atrial conduction. Therefore, the ECG reveals a 1:1 atrioventricular conduction (P wave for each QRS complex) and prolonged PR interval (>200 milliseconds) (Figure 9).

Figure 9. First-degree AV block. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 203 ms). Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 9. First-degree AV block. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 203 ms). Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Table 3 illustrates a comparison between ECG features of the AV block types.

 

Type of Block

 

First-degree AV block

Second-degree AV block Mobitz type I

Second-degree AV block Mobitz type II

Third-degree AV block

PQRS

 

Sinus rhythm (P wave for each QRS complex)

 

Nonconducted atrial impulse (P wave not followed by QRS complex)

Cycle repeats after a dropped beat (atrial impulse is completely blocked)

Nonconducted atrial impulse (P wave not followed by QRS complex)

PR interval remains constant after the non-conducted atrial impulse

No association between P waves and QRS complexes (complete dissociation)

Atrial rate higher than ventricular rate

 

PR interval

PR interval >200 msec

Progressively prolonged PR interval

Fixed prolonged PR interval

PR interval remains constant after the non-conducted atrial impulse

Variable PR interval

QRS

Narrow

Regular

Narrow

Narrow

Wide

Regular

First-degree AV block could be found as a normal variant or may be secondary to increased vagal tone, medication toxicity, inferior MI (Figure 10) [9], or myocarditis [15]. Those with a new-onset first-degree AV block in the setting of ACS may be at a higher risk of progression to complete heart block [9,15]. Patients with first-degree AV block usually do not require specific treatment,1 especially if asymptomatic. Symptomatic patients should have their management focused on the underlying cause. Agents with AV nodal blocking effect (Table 4) should be avoided as they would worsen the conduction delay [23].

Figure 10. First-degree AV block with inferolateral STEMI. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 205 ms) combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF) and lateral leads (V5-V6), ST depression in V1-V2 is suggestive of associated posterior infarction, and reciprocal ST depression in leads I and aVL. Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 10. First-degree AV block with inferolateral STEMI. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 205 ms) combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF) and lateral leads (V5-V6), ST depression in V1-V2 is suggestive of associated posterior infarction, and reciprocal ST depression in leads I and aVL. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Table 4. List of agents with AV nodal blocking/slowing activity [24].

Agents with potent AV nodal blocking activity:

  • Beta-blockers (e.g., Esmolol, Metoprolol)
  • Calcium channel blockers (e.g., Diltiazem, Verapamil)
  • Digoxin
  • Adenosine
  • Sotalol

Other cardiovascular agents with AV nodal blocking/slowing activity:

  • Amiodarone
  • Procainamide
  • Quinidine
  • Lidocaine
  • Flecainide
  • Propafenone
  • Disopyramide
  • Dronedarone

Second-Degree AV Block

Second-degree AV block is characterized by intermittent conduction failure, where one or more atrial impulses are not conducted; some conduction is still present. The atrial rate (P waves) is <100 bpm. The ECG shows P waves that are not followed by a ventricular contraction (QRS complex). It is classified into two types based on the pathophysiology and ECG features.

Second-Degree Mobitz Type I AV Block

Mobitz type I (also known as Wenckebach’s block) is characterized by a progressive prolongation of the AV conduction with a nonconducted atrial impulse. The ECG shows progressive prolongation of the PR interval until an atrial impulse is blocked (not followed by a QRS complex) (Figure 11). These cyclic features lead to a grouped beating in a rhythm strip.  Mobitz Type I could be identified in healthy individuals and might also be seen in patients with acute or chronic heart disease such as inferior MI [9], medication toxicity, myocarditis, or in patients after cardiac surgery. In most cases, specific treatment is not required unless hypoperfusion is present, in which case atropine is the first-line therapy [9].

Figure 11. Second-degree Mobitz type I AV Block. ECG shows progressive prolongation of PR interval with a subsequent nonconducted P wave, then the cycle repeats after the dropped beat. Courtesy of Dr. Harry Patterson, FACEM. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/. ECG digitized using PMcardio app.
Figure 11. Second-degree Mobitz type I AV Block. ECG shows progressive prolongation of PR interval with a subsequent nonconducted P wave, then the cycle repeats after the dropped beat. Courtesy of Dr. Harry Patterson, FACEM. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/.
Second-Degree Mobitz Type II AV Block

Mobitz type II block is characterized by a fixed AV conduction delay followed by a nonconducted atrial beat. ECG shows a fixed prolonged PR interval, each P wave is followed by a QRS complex until a nonconducted P wave is noted without a QRS complex (Figure 12). If 2 or more P waves are not conducted, it is called a high-grade AV block (Figure 13). Mobitz type II block represents electrical intranodal conducting system structural damage. In acute MI (most commonly anterior), it could progress into a complete heart block [9].

Figure 12. Second-degree Mobitz II AV block. The rhythm strip shows non-conducted P waves (arrows), with constant PR interval, constant P-P interval, and the RR interval surrounding the dropped beat is multiple the preceding RR interval. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 12. Second-degree Mobitz II AV block. The rhythm strip shows non-conducted P waves (arrows), with constant PR interval, constant P-P interval, and the RR interval surrounding the dropped beat is multiple the preceding RR interval. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 13. Second-degree “high-grade” AV block. ECG shows a 4:1 conduction ratio, atrial rate is approximately 140 beats/min, and ventricular rate is approximately 35 beats/min. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 13. Second-degree “high-grade” AV block. ECG shows a 4:1 conduction ratio, atrial rate is approximately 140 beats/min, and ventricular rate is approximately 35 beats/min. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/

These patients should be placed on transcutaneous pacing pads in anticipation of clinical deterioration. Although atropine is usually ineffective, it may be utilized during preparation for pacing as it is not harmful. Patients with second-degree Mobitz type II AV block and features of hypoperfusion require emergent cardiac pacing. Eventually, these patients require transvenous cardiac pacing, especially those with underlying acute MI [9].

Third-Degree AV Block

Third-degree (complete) heart block is characterized by the lack of any AV conduction between atria and ventricles, leading to AV dissociation. Atrial impulses are not conducted at all, and an escape pacemaker arises to pace the ventricles with a rate of 40-60 beats/min or lower for the intranodal level. The ECG features no association between the P waves and QRS complexes, an atrial rate higher than the ventricular rate, and wide QRS complexes (Figure 14).

Figure 14. Third-degree AV block. ECG shows complete dissociation between P waves and QRS complexes, wide QRS complexes (QRS duration=154 ms), atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, and the rhythm is maintained by a junctional escape rhythm. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app.
Figure 14. Third-degree AV block. ECG shows complete dissociation between P waves and QRS complexes, wide QRS complexes (QRS duration=154 ms), atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, and the rhythm is maintained by a junctional escape rhythm. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app.

Depending on the block’s location, it may be termed “nodal” (such as in inferior MI) or “infranodal” (such as in anterior MI) [9]. Patients with third-degree AV block are usually unstable due to the inadequate cardiac output generated by the ventricular escape pacemaker. Atropine might work in cases of nodal blockade; however, it is unlikely to be effective in infranodal blockade. If the response to atropine is inadequate, transcutaneous cardiac pacing should be started. In those patients, consider beta-adrenergic medications (epinephrine or dopamine). Eventually, transvenous pacing is necessary in the majority of cases.

Atrial Fibrillation With a Slow Ventricular Response

Patients with atrial fibrillation may present with a slow ventricular response in the setting of an overdose of nodal-blocking medications (e.g., beta-blockers, calcium channel antagonists, digoxin) or significant conduction disease [25]. A very low ventricular rate may lead to hemodynamic compromise [26]. The hallmark ECG feature in these patients is an irregularly irregular ventricular rhythm without discernible P waves, either chaotic or flat isoelectric baseline (Figure 15). Patients with an irreversible cause of slow ventricular response (such as those with intrinsic conduction system disease) may require a permanent pacemaker [27].

Figure 15. Atrial fibrillation with a slow ventricular response. ECG shows irregular rhythm with no evidence of organized atrial activity, fine fibrillatory waves, with a ventricular rate of 60 beats/min. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 15. Atrial fibrillation with a slow ventricular response. ECG shows irregular rhythm with no evidence of organized atrial activity, fine fibrillatory waves, with a ventricular rate of 60 beats/min. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Hyperkalemia-induced Bradycardia

Patients with hyperkalemia demonstrate several features on the ECG, including peaked T waves, PR prolongation, QRS widening, and sine-wave morphology [28]. Junctional rhythm is the most common bradycardic rhythm in patients with severe hyperkalemia [29], and patients may show other types of bradydysrhythmias [29]. Obtaining a serum potassium level is critical in any bradydysrhythmia, even without other ECG changes suggestive of hyperkalemia [29].

BRASH Syndrome

BRASH syndrome (Bradycardia, Renal failure, AV blockade, Shock, and Hyperkalemia) is caused by a synergistic effect of hyperkalemia and AV-blocking medications that produce dramatic bradycardia [30]. The marked bradycardia leads to poor renal perfusion, exacerbating hyperkalemia and leading to a vicious cycle, with resulting hemodynamic instability and multiorgan failure [30]. Precipitating factors identified include nephrotoxins, potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and digitalis [30].

Medical History

After stabilizing the patient, a comprehensive medical history often helps identify the underlying etiology. In patients unable to provide history (e.g., altered mentation), collateral history from family, emergency medical service (EMS) personnel, or nursing facility staff can be helpful.

Determining the stability of patients starts with their medical history. Symptoms of end-organ hypoperfusion, such as ischemic chest pain, dyspnea, altered mental state, and syncope,  may indicate hemodynamic instability [3,6]. Lack of symptoms, or only mild symptoms such as palpitations, lightheadedness, nausea, generalized fatigability, or mild anxiety [31], may indicate hemodynamic stability. It is essential to determine whether the presenting symptoms in patients with bradycardia are secondary to the bradycardia itself or whether the presence of bradycardia is coincidental.

Analyzing the characteristics of presenting symptoms is vital, including onset, progression (gradual vs. abrupt), duration, precipitating factors, preceding events, and any associated symptoms. Specific precipitating events include emotional distress, positional changes, urination, defecation, cough, prolonged standing, shaving, and head-turning [7]. Additionally, ask about symptoms of ACS, infectious diseases, and hypothyroidism.

A past medical history of rhythm disturbance, ischemic heart disease, structural heart disease, pacemaker placement, or coronary artery bypass graft (CABG) is relevant. Patients post transcatheter aortic valve replacement are at high risk for conduction system abnormalities [7]. A history of renal failure increases the risk of hyperkalemia.

Reviewing the medication list, as well as herbal substances and recreational drugs, including timing, doses, recent changes in patterns, compliance, and the possibility of overdose, is essential.

Travel history to areas endemic for infectious diseases, such as Chagas or Lyme, is relevant. Sexual history, specifically for history of or risk factor for syphilis, is relevant. Occupational history and chemical exposures (e.g., organophosphate) may offer clues for a toxicologic etiology.

Physical Examination

Physical examination of patients with rhythm disturbance primarily focuses on clues of end-organ hypoperfusion and underlying etiology. Assess the level of consciousness, and confirm adequate perfusion by examining the capillary refill, peripheral pulses, and temperature of extremities; cool extremities and delayed capillary refill (>3 sec) indicate hypoperfusion.

The cardiovascular examination includes palpating the radial pulse to determine the rate and rhythm, auscultating the heart sounds for the presence of murmurs, as well as looking for signs of heart failure (jugular venous distention, rales, edema of the extremities). Chest wall inspection for a midline sternotomy scar adds important information regarding the medical history. Palpating the skin overlying an implanted pacemaker may uncover lead abnormalities [32].

Look for signs of underlying pathology, including toxidromes (e.g., cholinergic, opioid-like), an arteriovenous fistula or dialysis catheter (indicates renal failure), head trauma, and signs of hypothyroidism. Core temperature measurement is vital in patients suspected to have hypothermia. In patients with head trauma, look for Cushing’s triad (hypertension, bradycardia, and irregular respirations). Table 5 illustrates a constellation of signs and symptoms indicating a possible underlying cause.

Table 5. Signs and symptoms suggestive of the underlying cause of bradycardia.

Possible underlying etiology

History

Physical examination

Myocardial infarction

  • Chest pain
  • Dyspnea
  • Anginal equivalent symptoms
  • Hypotension
  • Rales
  • New murmur

Myopericarditis

  • Fever
  • Dyspnea
  • Pleuritic chest pain
  • Recent respiratory or gastrointestinal infection
  • Malaise
  • Myalgias
  • Pericardial friction rub

Hyperkalemia

  • History of renal failure / dialysis
  • Arteriovenous fistula or dialysis catheter

Pacemaker malfunction

  • History of implanted cardiac device
  • History of cardiac conduction abnormality
  • Pacemaker identification card
  • Obvious device or lead abnormalities by palpation of the overlying skin

Increased ICP

  • History of head trauma
  • Headache
  • Vomiting
  • Decreased level of consciousness
  • Signs of basilar fracture
  • Depressed skull fracture
  • Focal neurologic deficit
  • Decreased level of consciousness

Beta blocker toxicity

  • Confusion
  • History of seizure
  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Depressed mental state
  • Hypoglycemia
  • Bronchospasm
  • Hypotension
  • Shock

Calcium channel blocker toxicity

  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Hyperglycemia
  • Hypotension
  • Shock

Digoxin toxicity

  • GI symptoms (abdominal pain, nausea, vomiting, anorexia)
  • Fatigue
  • Visual disturbance
  • Lethargy
  • Confusion
  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Altered mental status
  • Seizures
  • Hypotension
  • Shock

Local anesthetics toxicity

  • Perioral numbness
  • Visual disturbance
  • Confusion
  • Dizziness
  • Seizure
  • History of regional or topical anesthesia procedure
  • Altered mental status (ranging from agitation to unresponsiveness)
  • Weakness
  • Slurred speech

Clonidine overdose

  • History of drug ingestion
  • Miosis
  • Respiratory depression

Hypothyroidism

  • History of thyroid disease
  • Cold intolerance
  • Weight gain
  • Fatigability
  • Hypothermia
  • Constipation
  • Skin and hair changes
  • Thyroidectomy scar
  • Goiter
  • Pretibial myxedema
  • Coarse skin
  • Muscle hypertrophy
  • Hypothermia
  • Delayed relaxation phase of reflexes

Acing Diagnostic Testing

A 12-lead ECG is diagnostic for bradyarrhythmia. A single lead, most commonly lead II, is often adequate to make the diagnosis. ECG reading requires noting the rate, regularity, P waves, P-R interval, the relation between P waves and QRS complexes, and QRS width.

Furthermore, ECG may identify the underlying cause, such as acute ischemic changes (e.g., hyperacute T waves, ST-segment elevation/depression, T waves inversions, Q-waves), hyperkalemic changes (e.g., peaked T waves, P wave flattening, PR prolongation, wide QRS), cerebral T-waves (i.e., deep, symmetric, inverted T waves) in elevated intracranial pressure (ICP), downsloping ST depression in digoxin toxicity, and Osborn wave (i.e., positive deflection at the J point) in severe hypothermia (<32˚C). In patients with a malfunctioning implanted pacemaker, the ECG may show pacing spikes not followed by a QRS complex (electrical non-capture).

Given the intermittent nature of some bradyarrhythmia, a normal ECG does not exclude the diagnosis, especially in asymptomatic patients. Moreover, bradyarrhythmia may evolve; therefore, serial ECGs are advisable [2]. 

Point-of-care ultrasound (POCUS) helps in the assessment of volume status (inferior vena cava [IVC] assessment) and pulmonary edema (B-lines: vertical comet tail artifact).

Laboratory work-up to uncover the underlying etiology should be tailored to the clinical assessment. It may include the following:

  • Cardiac biomarkers (e.g., troponin) for identifying acute MI.
  • Electrolytes profile for identifying electrolyte abnormalities (particularly potassium and calcium).
  • Creatinine and blood urea nitrogen (BUN) can help diagnose acute and chronic renal failure.
  • Brain natriuretic peptide (BNP) elevation may indicate fluid overload and heart failure in the appropriate context.
  • Infectious work-up: 3 sets of peripheral cultures for infective endocarditis, serologic testing for syphilis, Lyme serology for Lyme disease, and thick and thin blood smear for Chagas disease.
  • Thyroid function test (TSH and free T4) for suspected hypothyroidism or myxedema coma.
  • Drug levels such as digoxin.

As for imaging, a chest X-ray may show evidence of pulmonary edema in patients with heart failure. In patients with pacemakers, it can identify lead fracture and migration.

Transthoracic echocardiography is essential in evaluating patients with newly identified Mobitz type II or third-degree AV block for cardiac wall motion abnormalities (indicative of an MI), valvular abnormalities, and structural heart disease. However, in patients with asymptomatic bradycardia or first-degree AV block, routine echocardiography is usually not indicated [7].

In patients with signs of a head injury and suspected increased ICP, obtain a head computed tomography (CT) scan.

Risk Stratification

Stability of Patient

Determining the hemodynamic stability of patients with bradyarrhythmia critical to management. Unstable patients require immediate treatment. Instability indicators include hypotension (defined as systolic BP [SBP] of <90 mm Hg), signs of shock (cold and moist skin, pale skin, delayed capillary refill time), ischemic chest pain, altered mental state, and dyspnea secondary to pulmonary edema (Table 6). Patients’ condition may change during treatment or ED stay, necessitating frequent reassessment to recognize impending clinical deterioration.

Table 6. Indicators of instability in patients with bradydysrhythmias

  1. Hypotension (SBP <90 mm Hg)
  2. Signs of shock
  3. Altered mental status
  4. Ischemic chest pain
  5. Dyspnea secondary to pulmonary edema

Symptomatic versus Asymptomatic

The presence of symptoms guides management. Generally, asymptomatic patients do not require treatment and may need monitoring only. In symptomatic patients, it is important to determine whether symptoms are caused by bradycardia or if the bradycardia is incidental to the actual cause of the presenting complaint.

Management

Pre-hospital care considerations

Stabilization might be started by EMS personnel, such as administration of atropine, epinephrine/dopamine infusion, and transcutaneous cardiac pacing [11,33-37], depending on their capabilities and local protocols. Transportation to a PCI-capable center is optimal for patients suspected to have an underlying ischemic pathology.

Initial Stabilization

Initial stabilization must start with a rapid assessment of the circulation, airway, and breathing “the CABs”), as well as the vital signs and signs of instability (Table 6). Patients with symptomatic bradyarrhythmia require a monitored bed with flat positioning [7]. Perform fingerstick glucose, establish two large-bore IVs, attach the patient to a continuous cardiac rhythm monitor, obtain a 12-lead ECG, and prepare for drug and electrical therapy simultaneously. If IV access cannot be obtained, attempt intraosseous (IO) access or a central line. Patients with significant symptomatic bradyarrhythmia, those with advanced heart block, and those predicted to deteriorate should be placed on pacer pads, irrespective of stability.

Although electrical cardiac pacing is immediately indicated in unstable patients, medical management may be more immediately available, making it reasonable to administer both while simultaneously identifying and treating the underlying cause [1,11]. However, atropine administration should never delay the initiation of transcutaneous pacing in unstable patients.1

A resuscitation cart, transvenous pacer kit, and airway equipment should be available at the bedside in anticipation of deterioration of critically ill patients with bradyarrhythmia. Oxygen is indicated to target SpO2 ≥94%. In select patients with hypotension (SBP < 90 mmHg), crystalloid fluids may improve blood pressure; caution must be taken in patients with decompensated heart failure. Hypotension refractory to fluid resuscitation may require inotropic and/or vasopressor support (e.g., epinephrine).

For unstable Mobitz Type II or third-degree AV block, initiate transcutaneous pacing, as well as atropine, if immediately available.  If ineffective, administer epinephrine 2-10 µg/min IV infusion. Although atropine is considered the first line of medical therapy, epinephrine may be preferred in critically unstable patients [38,39], and may be administered short-term through a peripheral IV access [40].

In patients with a wide QRS complex, atropine is unlikely to be effective due to a block at the distal conduction system; therefore, proceed immediately to epinephrine and transcutaneous pacing [1,41].

Patients with symptomatic bradycardia, or second- or third-degree AV block should be placed on continuous ECG monitoring (Class I recommendation) [42].

Figure 16 illustrates emergency approach and management of acute bradyarrhythmia in the ED.

Figure 16. Emergency management approach of patients with bradydysrhythmia. *Atropine should not be given to patients after heart transplantation. Abbreviations: BP, blood pressure; ECG, electrocardiogram; HR, heart rate; ICP, intracranial pressure; IV, intravenous; kg, kilogram; mA, milliampere; mg, milligram; mcg, microgram; MI, myocardial infarction; PCI, percutaneous coronary intervention; RR, respiratory rate; SpO2, oxygen saturation.
Figure 16. Emergency management approach of patients with bradydyarrhythmia. *Atropine should not be given to patients after heart transplantation. Abbreviations: BP, blood pressure; ECG, electrocardiogram; HR, heart rate; ICP, intracranial pressure; IV, intravenous; kg, kilogram; mA, milliampere; mg, milligram; mcg, microgram; MI, myocardial infarction; PCI, percutaneous coronary intervention; RR, respiratory rate; SpO2, oxygen saturation. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Treatment Considerations

The anatomical location causing the bradycardia may predict the management and outcomes of bradyarrhythmia. Narrow QRS complex bradycardia indicates dysfunction at the level of the SA or AV node, usually requires minimal intervention, and is rarely life-threatening. On the other hand, wide QRS complex bradycardia indicates dysfunction at the level of distal His-Purkinje, usually requires aggressive management, is unlikely to respond to atropine, may require electrical pacing, and is associated with an elevated mortality rate [3].

Medications

Atropine

Atropine is the first-line treatment to increase the heart rate in patients with symptomatic bradycardia [1,2]. Atropine is an antimuscarinic medication with direct vagolytic activity, increasing the SA node’s automaticity and potentiating the AV node’s conduction. Atropine is most effective in sinus bradycardia and junctional rhythm. It is usually not useful in infranodal blocks presenting with wide QRS bradyarrhythmia. Atropine should be used cautiously in the setting of ACS due to the potential risk of exacerbating ischemia and infarct size from the resulting tachycardia [43-48]. Additionally, atropine should not be used in patients who have undergone heart transplants due to the lack of vagal innervation, as atropine may cause paradoxical AV block and asystole [1,7,49,50]. The dose of atropine is 0.5-1 mg IV every 3-5 min until resolution or maximum dose is reached (3 mg) [1,7].

Epinephrine

Epinephrine is an alternative medical therapy for bradyarrhythmia, and is the preferred adjunct medical management to electrical therapy in unstable patients, particularly those with Mobitz Type II and third-degree AV block [7]. Epinephrine acts on β1- and β2-receptors, working on the entire myocardium to increase the heart rate (inotropic and chronotropic effects), as well as enhancing the AV nodal conduction [51-52]. The dose of epinephrine is 2-10 mcg/min IV infusion, titrated to desired heart rate [7].

In peri-arrest bradycardia, some experts recommend a temporizing bolus dose of 20-50 mcg of epinephrine as an IV push, followed by infusion and electrical pacing [38,39,53,54], despite the lack of supporting data [53,54].

Dopamine

Dopamine may be used in bradyarrhythmia refractory to atropine (Class IIb) [7]. It acts on dopaminergic α1-, β1-, and β2-receptors. Higher doses (>10 mcg/kg/min) have a vasoconstrictive effect, while lower doses (1-2 mcg/kg/min) have a selective inotropic effect on the heart rate [1]. The dose of dopamine is 2 to 20 mcg/kg/min IV infusion titrated by 5 mcg/kg/min every 2 minutes to the desired heart rate [7,33], monitoring peripheral perfusion to avoid profound vasoconstriction [7].

Dobutamine

Dobutamine is a β-agonist agent with a weak α-adrenergic activity that may be used in symptomatic bradycardia; its predominant effect is inotropic via stimulation of β1-receptors [55]. Dobutamine can lead to vasodilation (via β2-receptors) and hypotension, thus, it should not be used in hypotensive patients. It can be used in cases of bradycardia resistant to standard therapy with normal or elevated blood pressure [7,38]. Dobutamine is administered as a 2-20 µg/kg/min IV infusion, titrated to desired heart rate.

Isoproterenol

Isoproterenol infusion is indicated in post-heart transplant patients with unstable bradycardia [7]. It can also be used in refractory bradyarrhythmia and AV blocks not responding to epinephrine [38]. It is a non-selective β-agonist stimulating β1– and β2-receptors, speeding up the SA and AV nodes and enhancing cardiac contractility (chronotropic and inotropic) [56]. It does not have any vasopressor effects.  Isoproterenol is given as a 2-10 mcg/min IV infusion, titrated to effect, or can be administered as an IV bolus of 1-2 mcg [1]. Isoproterenol is contraindicated in patients with angina/active ischemia due to concerns about increasing myocardial oxygen demand (β1 effect) and decreasing coronary perfusion (β2 effect), as well as in digoxin toxicity [7,57-60].

Aminophylline and Theophylline

Aminophylline and theophylline are methylxanthines, which exert positive chronotropic effects on the myocardium, likely by inhibiting the suppression effect of the adenosine on the SA node [7]. Both are reasonable to use if clinically indicated in symptomatic post-cardiac transplant patients [7,61-63] and sinus node dysfunction secondary to spinal cord injury, based on a limited case series [7,64-67].

In addition, aminophylline (250 mg IV bolus) has been used in treating second- and third-degree AV block associated with acute inferior MI, despite the limited direct evidence [7,68-70]. Aminophylline is administered with a dose of 6 mg/kg over 20-30 minutes, followed by an infusion of 0.3-0.5 mg/kg/hour [7]. Theophylline is administered as a bolus dose of 300 mg IV, followed by an oral dose of 5–10 mg/kg/day titrated to effect [7]. Although recommended by the guidelines, evidence for the use of methylxanthines is limited [7].

Table 7. Present bradyarrhythmia medications’ mechanism of action, dosing, pharmacokinetics, contraindications, and adverse events. 

Table created by authors

Electrical Cardiac Pacing

Electrical cardiac pacing is a procedure that aims to stimulate effective cardiac depolarization. Cardiac pacing is the mainstay management of acutely symptomatic patients with bradyarrhythmia, particularly unstable bradyarrhythmia or stable symptomatic bradyarrhythmia refractory to medical therapy, including type II second-degree and third-degree AV blocks [7]. It is of little value in toxin-induced bradyarrhythmia [32]. Cardiac pacing is performed using either a transcutaneous or transvenous approach. Transcutaneous cardiac pacing is a temporary bridging treatment until transvenous pacing or resolution of symptoms [7,32,38,39]. Transvenous pacing is also temporary until the resolution of the underlying cause or placement of a permanent pacemaker [7]. 

In crashing bradycardia, transcutaneous pacing should be started immediately. It is minimally invasive, instituted rapidly, and effectively treats hemodynamically unstable bradydysrhythmia [32]. The pacing pads are placed on the patient’s chest using one of two positions, an anterolateral or anteroposterior (Figure 17); positioning placement is selected based on the patient’s habitus and clinician’s preference [32]. Sedation and analgesia should be initiated as soon as possible utilizing hemodynamically stable agents such as low-dose fentanyl and/or ketamine, keeping in mind that most patients requiring electrical pacing are hemodynamically unstable.

Figure 17. Correct placement of transcutaneous pacing pads. A, anterolateral position; the anterior adhesive pad is placed inferior to the right clavicle, and the lateral adhesive pad is placed on the left fifth intercostal space at the anterior axillary line. B, anteroposterior position; the anterior adhesive pad is placed on the sternum, and the posterior adhesive pad is placed on the left infrascapular area. “Illustration by Malak Alraygi / re-designed Arif Alper Cevik”
Figure 17. Correct placement of transcutaneous pacing pads. A, anterolateral position; the anterior adhesive pad is placed inferior to the right clavicle, and the lateral adhesive pad is placed on the left fifth intercostal space at the anterior axillary line. B, anteroposterior position; the anterior adhesive pad is placed on the sternum, and the posterior adhesive pad is placed on the left infrascapular area. “Illustration by Malak Alraygi / re-designed by Arif Alper Cevik”

Adjust the pacing setting targeting a rate of 80-100 beats/min (start at 80 mA and reduce to the lowest energy) [2,39]. If the pacing is successful, the ECG will show electrical capture, which are pacing spikes followed by wide QRS complexes. Mechanical capture is demonstrated by a palpable pulse corresponding to each paced QRS complex on the cardiac monitor, preferably the femoral pulse to avoid the muscular contractions triggered by the pacer near the carotid artery, which may be confused with a pulse [32]. POCUS may be used to confirm myocardial contractions corresponding to each pacing spike and in confirming femoral pulse. In cases of cardiac arrest during transcutaneous pacing, chest compressions can be safely performed over the pacing pads [32].

Transvenous pacing has a high success rate (>95%) and is preserved for unstable bradyarrhythmias refractory to medications and transcutaneous pacing [6]. Transvenous pacing is contraindicated in patients with severe hypothermia [32]. Transvenous pacing is performed by introducing a transvenous pacing catheter into the right ventricle through a central venous catheterization (either right internal jugular or left subclavian central line). Pacemaker wire may be advanced into the endocardial wall of the right ventricle either blindly, or under the guidance of ECG or ultrasound (four-chamber view) [32]. Observe the cardiac monitor during the advancement of the wire [32]. Capture is confirmed by pacer spikes followed by QRS and ST-segment elevation, which indicates proper positioning [32]. Set the pacer generator on full-demand mode, with an output of 5 mA and a rate of 80 beats/min or at least 10 beats/min faster than the underlying ventricular rhythm [32]. Afterward, confirm electrical and mechanical capture. Continuous electrocardiographic monitoring is recommended for all patients on pacing (both transcutaneous and transvenous) until pacing is discontinued (class I) [42].

Patients with structural or electrophysiological conduction abnormalities often require definitive management with permanent pacemaker implantation. Class I recommendations have been issued for the implantation of permanent pacemakers in patients with acquired Mobitz type II AV block, high-grade AV block, and third-degree AV block not caused by reversible or physiologic causes, irrelevant of the presence of symptoms, due to the high risk of decompensation [7]. The decision to place a permanent pacemaker in patients with symptomatic sinus node dysfunction, persistent and symptomatic sinus bradycardia, and atrial fibrillation with symptomatic bradycardia in the absence of nodal blocking medications is dependent on the presence of symptoms and its correlation with the block itself [7].

Treatment of underlying etiology

Ischemia-related bradycardia

Patients with symptomatic bradyarrhythmia secondary to acute MI require stabilization and immediate reperfusion therapy, either PCI or thrombolysis, depending on feasibility.

Toxicity-related bradycardia

Patients with toxic or metabolic causes of bradycardia respond poorly to atropine and electrical pacing, and those patients require immediate treatment of the underlying cause, by eliminating the offending agent, utilizing supportive care, and administering an agent-specific antidote, if available [7]. Consulting toxicology and/or the local poison center early is paramount. Table 8 presents specific treatment strategies for toxicities related to bradycardia. In cardiac arrest secondary to an overdose, extracorporeal membrane oxygenation (ECMO) might be indicated to maintain perfusion until the underlying agent level is reduced or eliminated [6].

Table 8. Management of toxicologic causes of bradycardia.

Toxicity

Treatment

Beta-blocker toxicity

  • High-dose insulin 1 unit/kg IV bolus, followed by an infusion of 0.5 units/kg/h co-administered with dextrose 7,24,111
  • Glucagon 3-10 mg IV bolus over 3-5 min, followed by an IV infusion of 1-5 mg/h 7,96
  • Intravenous lipid emulsion112

Calcium channel blockers toxicity

  • 10% Calcium chloride 1-2 g IV bolus every 10-20 min or an infusion of 0.2-0.4 mL/kg/h7,113]
  • 10% calcium gluconate 3-6 g IV every 10-20 min or an infusion at 0.6-1.2 mL/kg/h7
  • High-dose insulin 1 unit/kg bolus, followed by an infusion of 0.5 units/kg/h co-administered with dextrose7,24,113
  • Glucagon 3-10 mg IV bolus over 3-5 min, followed by an IV infusion of 1-5 mg/h7,96
  • Intravenous lipid emulsion113

Digoxin toxicity

  • Digoxin-specific antibody fragments (dosage is dependent on amount of ingestion or serum level and whether acute or chronic toxicity)7. It is indicated in unstable bradydysrhythmias or K+ >5.0.

Organophosphate poisoning

  • Decontamination.
  • Atropine 1-3 mg IV every 5 min (0.01-0.04 mg/kg IV in children) with doubling the dose each time, followed by IV maintenance of 0.4-4 mg/hr.
  • Pralidoxime 1-2 g IM (20-40 mg/kg in children) with normal saline infused over 5-10 min followed by IV infusion of 500 mg/h (5-10 mg/kg/h in children).

Local anesthetic systemic toxicity

  • Intravenous lipid emulsion, initial bolus of 100 mL IV over 2–3 min, followed by an infusion of 200–250 mL IV over 15–20 min (for those <70 kg, the bolus dose is 1.5 mL/kg IV over 2–3 min, followed by 0.25 mL/kg/min IV infusion)114,115

Opioids toxicity

  • Naloxone 0.4-2 mg IV/IM/SC bolus repeated every 3 min (pediatrics: 0.1 mg/kg IV/IO/ET75).

Abbreviations: ET, endotracheal; ; g, gram; h, hour; IM, intramuscular; IO, intraosseous;  IV, intravenous; kg, kilogram; mg, milligram; min, minutes; mL, milliliter; mcg, microgram; SC, subcutaneous.

Hyperkalemia-related bradycardia treatment
Hyperkalemia may lead to profound bradycardia and mimic AV blocks [116]. Treatment should include the administration of 2 g calcium gluconate IV or 1 g calcium chloride IV to stabilize the cardiac membrane, in addition to treatments that shift the potassium across the cellular membrane and enhance its elimination.
BRASH syndrome treatment

Treating patients with BRASH syndrome involves a simultaneous approach that targets all associated conditions. The treatment strategy includes usual care of bradycardia (medications [such as epinephrine infusion] and/or pacing), hyperkalemia therapy (IV calcium, IV insulin and dextrose, and/or emergent dialysis), and fluid resuscitation [30]. In addition, it may include further advanced therapies in refractory cases or patients with AV-nodal blocking medication toxicity (e.g., lipid emulsion, glucagon, high-dose insulin, and digoxin-specific antibody) [30].

Hypothermia-related bradycardia treatment

In hypothermia, the first management line is rewarming, even before pacing. Due to the arrhythmogenic effect of hypothermia, pacing severely hypothermic patients has not been recommended due to concerns of precipitating ventricular fibrillation [23, 117]; however, case reports of successful pacing have been reported [118]. ECMO might be considered for severe hypothermia (<32 °C) and cardiac instability [119,120].

Myxedema coma-related bradycardia treatment

Patients with bradycardia secondary to myxedema coma require emergent thyroid hormone replacement (Levothyroxine [T4] 200-400 mcg IV, lower dose in geriatric patients) [121,122]. Adjunctive therapy includes hydrocortisone (100 mg IV), correction of hypoglycemia and electrolyte abnormalities (such as hyponatremia) and supportive care [121,122]. Moreover, identify and treat triggers causing decompensated hypothyroidism (e.g., infection, medications, MI, heart failure, and GI bleeding) [121]. 

Elevated ICP-related bradycardia treatment
For patients with bradycardia secondary to head trauma and increased ICP, treatment should be directed to lower the ICP, such as head elevation, hyperventilation, and mannitol or hypertonic saline.

Special Patient Groups

Considerations of bradycardia in pediatrics

The initial assessment of children is unique. The Pediatric Assessment Triangle is a rapid assessment tool to identify patients with respiratory or circulatory compromise who require immediate stabilization, and stands for appearance, breathing, and circulatory status [123, 124]. This is followed by a primary assessment using the ABCDE approach, similar to adults.

Clinically significant bradycardia in pediatric patients is defined as a heart rate less than the age-appropriate rate with impaired systemic perfusion [125]. The heart rate definition of pediatrics differs based on age, and in infants, an asleep heart rate has a different cut-off than an awake heart rate [126].

In pediatrics, always consider bradycardia as secondary to a reversible cause until proven otherwise. Bradycardia in the pediatric age group is usually associated with hypoxia (the most common cause), hypotension, acidosis, hypothermia, and medications, whereas primarily cardiac causes are rare [74,126].

Bradyarrhythmia in pediatrics is commonly a pre-arrest rhythm125; therefore, an early aggressive approach in children with bradycardia with poor perfusion has been recommended [127]. Immediate evaluation of adequate oxygenation and ventilation is necessary. In patients with a persistent heart rate of <60 and poor perfusion despite adequate oxygenation and ventilation, start chest compressions and follow the pediatric advanced life support (PALS) bradycardia algorithm [74,127], even if there is a detectable pulse.

Considerations for bradycardia in geriatrics

Older adults have a relatively high incidence of symptomatic bradycardia (6%), admission rate for symptomatic bradycardia (39%), rate of unstable bradycardia (16%), and mortality (5%) [128]. In older adults, ischemia tends to present atypically; thus, clinicians should have a high index of suspicion for an underlying ischemic cause. Moreover, polypharmacy is more common in older adults, thereby increasing the risk of drug-induced bradycardia and drug interactions.

Considerations of bradycardia in pregnancy

In critically ill pregnant patients, no medication should be withheld due to concerns of fetal teratogenicity [129,130]. Atropine crosses the placenta and risks and benefits of its use in stable patients should carefully weighed [131]. In unstable patients, atropine or epinephrine may be administered [132]. Epinephrine is preferred over dopamine in pregnancy [133].

Pregnant patients with symptomatic bradycardia necessitating atropine or vasoactive agents (e.g., epinephrine or dopamine) or those with advanced heart block require a multidisciplinary team, including obstetricians and neonatologists for maternal–fetal intensive monitoring [129], which may require transfer.

Bradycardia in patients with a heart transplant

Resting heart rate in heart transplant recipients ranges from 80-110 beats/min [134,135]. Therefore, bradycardia in these patients is defined as a heart rate persistently <70-80 beats/min [7,18,136]. Post-transplant bradycardia could be attributed to several mechanisms, including sympathetic denervation, SA ischemic injury, graft ischemia, and drug-induced [137-139].

Atropine is contraindicated due to the potential risk of paradoxical AV block and asystole [7,49]. Medications used to increase the heart rate include isoproterenol, aminophylline, and theophylline [7,61,140]. Target heart rate for temporary pacing, if indicated, is over 90 beats/min [140].

Following stabilization, those patients may require transport to an advanced heart transplant center for monitoring. It is recommended (Class I) to treat sinus node dysfunction medically in the postoperative period (1-6 weeks) and observe for resolution before attempting pacemaker implantation [21], which is eventually required in 7-24% of patients [136,141,144].

Disposition

All patients with symptomatic bradyarrhythmias require cardiology consultation [23]. Patients presenting with unstable or symptomatic bradyarrhythmias, particularly Mobitz type II or third-degree heart block, require admission to a cardiac ICU for monitoring.  Patients with secondary bradycardia often require admission for definitive treatment of the underlying etiology, either to the ICU or an intermediate care unit (i.e., stepdown). On the other hand, asymptomatic patients with benign ECG features and a normal ED work-up may be followed by cardiology on an outpatient basis; ambulatory electrocardiography monitoring and/or electrophysiology studies may be considered.

Revisiting your patient

The patient was rushed into a monitored bed. IV lines were established. The patient was placed on pacer pads. Atropine 1 mg IV was given with no response. ECG confirmed evidence of third-degree heart block (complete dissociation between P waves and QRS complexes, wide QRS complexes [QRS=154 ms], atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, rhythm is maintained by a junctional escape rhythm). Epinephrine and transcutaneous pacing were initiated. Electrical capture was demonstrated on the ECG. The pacing rate was 85 beats/min.

The patient returned to his baseline mental state. Capillary refill improved, extremities became warm, the peripheral pulse became strong, and lactate clearance was appropriate.  Central line access was obtained to transition the patient into transvenous pacing. Cardiac biomarkers resulted, revealing a significantly elevated troponin level at seven times the upper limit of normal. The patient was diagnosed with non-ST elevation occlusive MI. Cardiology was consulted, and they admitted the patient to the cardiac ICU. The patient was taken to the cardiac catheterization laboratory for PCI the following day.

Authors

Picture of Hassan M. Alshaqaq, MBBS

Hassan M. Alshaqaq, MBBS

Hassan Alshaqaq is an Emergency Medicine PGY1 Resident at King Saud University Medical City. He is passionate about EM, research, medical education, resuscitation, and critical care. His research work has appeared in various medical journals and has been awarded by EM and critical care societies. He has been involved with several medical societies in different leadership and educational roles. He is interested in developing clinical practice guidelines and has contributed to the Saudi Critical Care Society guidelines. He is the student club president of the Saudi Society of EM. He is an enthusiast in contributing to EM education, particularly FOAMed.

Picture of Danya Khoujah, MBBS, MEHP

Danya Khoujah, MBBS, MEHP

Dr. Danya Khoujah is an American board-certified Emergency Physician with a keen interest in medical education. She completed her emergency medicine residency and faculty development fellowship at the University of Maryland in Baltimore and a Master of Education in Health Professions from Johns Hopkins University. She has developed over 120 lectures, 75 podcasts, and 50 publications on various emergency medicine and medical education topics that have been well received. She is most passionate about simplifying the science to allow healthcare practitioners to better care for their patients, whether seasoned physicians, resident physicians-in-training, medical students, or allied health professionals.

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  137. Thajudeen A, Stecker EC, Shehata M, et al. Arrhythmias after heart transplantation: mechanisms and management. J Am Heart Assoc. 2012;1(2):e001461. doi:10.1161/JAHA.112.001461
  138. Jacquet L, Ziady G, Stein K, et al. Cardiac rhythm disturbances early after orthotopic heart transplantation: prevalence and clinical importance of the observed abnormalities. J Am Coll Cardiol. 1990;16(4):832-837. doi:10.1016/s0735-1097(10)80330-4
  139. DiBiase A, Tse TM, Schnittger I, Wexler L, Stinson EB, Valantine HA. Frequency and mechanism of bradycardia in cardiac transplant recipients and need for pacemakers. Am J Cardiol. 1991;67(16):1385-1389. doi:10.1016/0002-9149(91)90469-2
  140. Costanzo MR, Dipchand A, Starling R, et al. The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients. J Heart Lung Transplant. 2010;29(8):914-956. doi:10.1016/j.healun.2010.05.034
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Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Shock (2023)

Shock

by Joseph Ciano

You have a new patient!

A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.

What do you need to know?

Importance

Shock is a true emergency. Shock has a wide array of clinical causes (e.g., sepsis, hemorrhage, pulmonary embolism), categories, and different hemodynamic physiologies. The mortality rate of untreated shock is high, but it varies depending on the specific cause and type of shock. For example, the mortality rate of septic shock is 26% and is almost 50% for cardiogenic shock [1]. This means that rapid identification and treatment of shock matters in order to improve outcomes.

Epidemiology

Because shock has many different causes and no single accepted test for diagnosis, it is difficult to measure its prevalence accurately. The different causes of shock may also vary across different country contexts. A systematic review defining shock as a systolic blood pressure under 90 mmHg estimated 0.4-1.3% of patients arrive at the Emergency Department in shock [2]. Other studies have shown variable rates among the different shock categories, but the obstructive shock is typically the least common type of shock [3,4].

Pathophysiology

Shock is a state of circulatory collapse where the body is unable to adequately perfuse tissues to meet the body’s metabolic demands. Shock is characterized by global hypoperfusion and hypoxia. The four major categories of shock are hypovolemic, distributive, cardiogenic, and obstructive shock. Each category of shock has differences in hemodynamics, causes, and treatments. If left untreated, shock will lead to multiorgan system dysfunction and failure.  Shock is often associated with hypotension (systolic blood pressure under 90 mmHg), but shock can occur with a “normal blood pressure”. For example, a systolic blood pressure of 100-120 mmHg in conjunction with other signs and symptoms could be considered a relative hypotensive state and indicate shock in a chronically hypertensive patient. The chart below summarizes the different types of shock.

Type of shock

Hemodynamics

Potential causes

Potential treatments

Hypovolemic

↓preload

↑SVR

↓CO

Dehydration, vomiting/diarrhea, burns, hemorrhage (GI bleed, traumatic wound, etc.)

IV fluids

Blood products (if due to hemorrhage)

Distributive

↓preload

↓SVR

↓/↑CO

Sepsis, anaphylaxis, adrenal insufficiency, neurogenic shock

IV fluids +/- antibiotics and vasopressors.

Treat underlying cause.

Epinephrine (anaphylaxis)

Norepinephrine (sepsis or neurogenic)

Phenylephrine (neurogenic)

Cardiogenic

↑preload

↑SVR

↓CO

Heart failure, tachy/bradyarrythmias, myocardial infarction, valve failure, myocarditis, cardiomyopathy,

beta-blocker overdose

Dobutamine or Epinephrine

Treat underlying cause

Obstructive

↓preload

↑SVR

↓CO

Tension pneumothorax, cardiac tamponade, pulmonary embolism

IV fluids

Treat underlying cause.

Tension Pneumothorax

Needle decompression then tube thoracostomy

Cardiac tamponade-Pericardiocentesis then pericardial window

Pulmonary embolism-Anticoagulation, consider thrombolytics or surgical embolectomy

(CO= Cardiac Output; SVR= Systemic Vascular Resistance)

Medical History

Key questions to ask on history-taking

Since shock has a multitude of causes, the patient’s history helps us identify shock and guides us in determining the underlying cause. Certain nonspecific presenting symptoms, such as generalized weakness, syncope, or altered mental status, can be seen in all types of shock as these symptoms indicate hypoperfusion. History-taking should be symptom based and also include review of the past medical history, past surgical history, medications, allergies, and drug or alcohol use. The mnemonic “OPQRST” (Onset of symptoms, Provoking/Palliating factors, Quality, Radiation, Severity, Timing) can be used to assist in gathering symptom-based information from the patient.

Being able to narrow down the potential causes will help decide which laboratory and imaging investigations to order and what initial treatments are indicated. Suggestions for key questions to ask are illustrated in the table below. 

Type of shock

Presenting symptoms that may indicate shock

Key questions to ask based on cause of shock

Hypovolemic

Weakness

Syncope

Altered mental status

Vomiting/diarrhea

Hematemesis

Hematochezia/Melena

Burn injury

Trauma/fall

Dehydration

  • Last PO intake? Diuretic usage? Recent travel?

 

Vomiting/diarrhea

  • How many times? Presence of blood? Recent travel? Fevers?

 

Hemorrhage (GI bleed, traumatic wound, etc.)

  • How much blood loss? Any anticoagulant use?

 

Distributive

Weakness

Syncope

Altered mental status

Fever, chills

Cough

Difficulty breathing

Dysuria

Lip/tongue swelling

Rash

Sepsis

  • Fevers, cough, dyspnea, dysuria, skin changes, headaches, neck stiffness, chest or abdominal pain?

 

Anaphylaxis

  • Known inciting factor or allergies? Angioedema?

 

Adrenal insufficiency

  • Steroid use? Medication changes? TB history?

 

Neurogenic shock

  • Spinal trauma? Focal weakness/numbness?

 

Cardiogenic

Weakness

Syncope

Altered mental status

Chest pain

Back or shoulder pain

Palpitations

Difficulty breathing Orthopnea

Peripheral edema

Heart failure, Cardiomyopathy, Valve failure

  • Medication changes? Chest pain? Body edema or dyspnea?

 

Tachy/bradyarrythmias

  • Syncope? Palpitations/heart fluttering?

 

Myocardial infarction

  • Chest or back pain? Diaphoresis?

 

Obstructive

Weakness

Syncope

Altered mental status

Difficulty breathing

Chest pain

Penetrating chest trauma

Unilateral leg pain/edema

Tension pneumothorax

  • Chest trauma?

 

Cardiac tamponade

  • Chest trauma? History of renal disease, HIV, or cancer history?

 

Pulmonary embolism

  • Sudden onset dyspnea or chest pain? Leg pain or swelling? Use of hormones? Recent travel, hospitalizations, or surgeries? Cancer history?

 

Identifying “red flags”

Shock can sometimes be subtle without marked hypotension or tachycardia, so it is important to be vigilant for red flags detected on history-taking to aid in early identification.  Some red flags include altered mental status or confusion, syncope, or chest pain. These symptoms may indicate hypoperfusion of the brain or heart and can point towards shock. Belonging to a special patient group, such as an elderly or neonatal patient, an immunosuppressed patient, or a pregnant patient, may be associated with a more atypical presentation of shock or less favorable patient outcomes.  

Physical Examination

Key physical exam features

Shock is a state of global hypoperfusion, so many physical exam features will reflect this (e.g., delirium, comatose state, tachypnea, etc.). However, shock exists along a continuum of severity and is impacted by patient age, medications, comorbidities, the cause of shock, and other factors. Hypotension and tachycardia are often regarded as key findings of shock, but these vital sign changes may not be present on initial examination depending on where the patient is in the timeline of their shock, as well as other factors described above. For this reason, it is important to look at the combination of the patient’s physical exam findings, rather than a single finding to assist in the diagnosis of shock [1]. Refer to the chart below for physical exam findings seen in shock.

shock - physical exam findings chart

Identifying “red flags”

Similar to patient history-taking, it is important to identify “red flags” during physical examination to aid in the early identification and treatment of shock. Some red flags on physical examination include hypotension with a MAP below 65mmHg, severe bradycardia, low urine output, delirium or altered mental status, and angioedema of lips or tongue [5]. A MAP below 65mmHg indicates severe hypoperfusion that requires prompt aggressive intravenous fluid or vasopressor administration. Bradycardia below 45bpm in shock may indicate poor cardiac output and a lack of physiologic ability to increase cardiac output properly in a shock state. Low urine output and altered mental status are signs of renal and cerebral hypoperfusion, respectively. Angioedema can occur in anaphylactic shock and can pose an acute airway emergency.

Alternative Diagnoses

Shock can have a variety of causes and clinical presentations that can range from the subtle to the severe. Determining the patient’s type of shock and specific diagnosis responsible for the shock state is dependent on details from the patient history, physical exam, and diagnostic testing (discussed more in next section). See the chart below for a list of differential diagnoses for the different categories of shock. Use this table in conjunction with the tables provided in the previous sections to assist in differentiating shock types and causes.

Shock Type

Differential diagnosis 5,6

Hypovolemic

  • GI losses (gastroenteritis, colitis, fistulas)
  • Skin burns
  • Renal losses (excess diuretic use, diabetes insipidus)
  • Hemorrhage (e.g., GI bleed, traumatic wound, aortic aneurysmal rupture, ruptured ectopic pregnancy, coagulopathy, etc.)

Distributive

  • Sepsis
  • Anaphylaxis
  • Adrenal insufficiency (primary vs secondary causes)
  • Thiamine deficiency (beriberi)
  • Pancreatitis
  • Thyroid storm
  • Toxins (salicylates, cyanide, carbon monoxide)
  • Neurogenic shock (trauma, spinal anesthesia)

Cardiogenic

  • Tachyarrhythmia or bradyarrhythmia
  • Left ventricular failure/Cardiomyopathy
    • Ischemic (myocardial infarction)
    • Nonischemic (postpartum, Takotsubo, myocarditis, myocardial contusion,
  • Ca channel/beta-blocker overdose, autoimmune)
  • Valve dysfunction
    • Endocarditis, post MI papillary muscle rupture, prosthetic valve problem
  • LV outflow obstruction
    • Hypertrophic obstructive cardiomyopathy (HOCM), aortic stenosis
  • Device malfunction (ECMO, Ventricular assist device)

Obstructive

  • Tension pneumothorax
  • Cardiac tamponade
  • Pulmonary embolism
  • Auto PEEP (“breath stacking”) in obstructive lung disease patient

Acing Diagnostic Testing

There is no single diagnostic test to rule in or rule out shock. The diagnosis of shock is based on a constellation of diagnostic test results in combination with the history and physical exam of the patient. Whenever possible, diagnostic testing should be based on the presumed cause of shock (e.g., CT pulmonary angiogram for pulmonary embolism, EKG for myocardial infarction, etc.). The table below summarizes different bedside tests, laboratory tests, and imaging tests to consider ordering in patients with shock.  Rational and use behind these tests is discussed in more detail in sections that follow the table.

Bedside tests

Laboratory tests

Imaging tests

  • EKG
  • Point of care testing, if available (pregnancy, glucose, arterial or venous blood gas testing)

 

  • Serum lactate
  • CBC with differential
  • Serum chemistry (BUN, creatinine, electrolytes)
  • Hepatic function panel
  • Coagulation studies
  • Type and screen
  • Venous or arterial blood gas testing
  • Cultures (blood, urine, wound)
  • Pregnancy test
  • Urinalysis
  • Cortisol level
  • Chest X-ray
  • CT of chest/abdomen/pelvis as supported by history + physical
  • Ultrasound (lung, heart, abdomen)

 

Bedside Tests

The EKG is a basic screening test helpful in all shock patients to assess for cardiac dysrhythmias, myocardial infarction, or EKG interval disturbances from medication overdoses. The EKG is clearly valuable in potential cardiogenic shock patients, but it is also helpful in obstructive shock (e.g., low voltage QRS in cardiac tamponade, EKG changes in pulmonary embolism).

Point of care pregnancy testing can help rule out a ruptured ectopic pregnancy.  Glucose testing screens for hypoglycemia which can be seen in septic shock, GI losses with decreased oral intake, and adrenal insufficiency. Point of care blood gas testing can aid in the assessment of the patient’s acid-base and blood gas status which can assist in immediate therapeutic decisions at the bedside. 

Laboratory Tests

Lactate is a common test ordered and trended in shock.  Lactate is a nonspecific marker for poor perfusion and anaerobic metabolism. An elevated lactate >2mmol/L can occur in all types of shock as it indicates poor perfusion, but it does not necessarily mean the patient has a diagnosis of shock. Increasing lactate levels have been associated with increased mortality in many shock types [1].

CBC and type and screen testing are helpful in hemorrhagic shock to measure hemoglobin and prepare for the need for blood product transfusion. The CBC can assess the white blood count which can be helpful in septic shock, especially when trended overtime. Serum chemistry, a hepatic function panel, and coagulation studies screen for signs of end-organ damage (e.g., acute kidney injury, transaminitis (“shock liver”), coagulopathy, etc.).

Blood gas testing is valuable as a screening test in any type of shock to evaluate acid-base and blood gas balance. Urinalysis testing and cultures, blood cultures, and wound cultures do not change management in the emergency department, but they are helpful in identifying sources of infection in septic shock which can be utilized to make antibiotic therapy more targeted as part of the patient’s larger plan of care. Cortisol testing can be beneficial in making the diagnosis of adrenal insufficiency.

Imaging Tests

The chest X-ray is another basic screening test that can be performed as a portable test in the unstable shock patient.  The chest X-ray screens for pneumonia (septic shock), cardiomegaly (cardiogenic and obstructive shock), tension pneumothorax (diagnosis should be made clinically prior to X-ray), pulmonary edema (cardiogenic shock), hemothorax (hemorrhagic shock), amongst other relevant findings.

CT imaging can be used to identify the source of infection or bleeding in septic and hemorrhagic shock, respectively.  However, it should be used after reviewing the risks and benefits in an unstable shock patient.  For example, CT imaging may involve the patient travelling to a less monitored setting outside of the emergency department with less resources and tools for resuscitation.  Contrast-induced nephropathy is another risk to consider when ordering CT imaging with IV contrast in shock patients who likely have hypo-perfused kidneys.  Conversely, CT imaging can lead to a definitive diagnosis (e.g., acute appendicitis, retroperitoneal bleed, ruptured spleen, etc.) that can direct management [1].

Ultrasound is an incredibly valuable bedside diagnostic modality in shock.  Ultrasound can be used to determine the patient’s type of shock through a physiologic assessment of the heart, lungs, and abdomen.  Specific diagnostic information that can be gathered by ultrasound includes the cardiac ejection fraction, presence of a large pericardial effusion with right ventricular compression (cardiac tamponade),  right ventricular dilation (may indicate pulmonary embolism), Inferior vena cava (IVC) dilation or collapse, presence of abdominal free fluid in trauma (hemoperitoneum), abdominal aortic aneurysm presence, absence of bilateral lung sliding (pneumothorax), pulmonary edema (cardiogenic shock if diffuse, infectious if localized), and pleural effusions (infectious or hemothorax depending on the historical context). Organized ultrasound protocols exist that aim to assess these body systems in an algorithmic manner.  One example is the RUSH protocol (Rapid Ultrasound for Shock and Hypotension) [1,5]. This protocol can be executed using the curvilinear (abdominal) or phase-array (cardiac) probe.  Operator competency is needed to obtain meaningful diagnostic data from bedside ultrasound, but with practice and education, proficiency can be achieved.  See the images below for a visual representation of the RUSH protocol and a summary of ultrasound findings in the different types of shock [5,7].

Ultrasound findings in shock

Risk Stratification

Since shock has many potential causes and clinical presentations, there is no single risk stratification tool that is broadly applicable to all types of shock.  There are some tools available to assist in early diagnosis of sepsis by identifying risk factors, like the SIRS criteria (Systemic inflammatory response syndrome criteria) and qSOFA score (Quick sequential organ failure assessment score) [8]. These scores are not specific and can be “positive” in conditions other than sepsis, like diabetic ketoacidosis or severe anxiety.  The shock index measurement is another tool that takes into account heart rate and systolic blood pressure to identify occult shock, especially in trauma or acute hemorrhage. A shock index above 0.5-0.7 may point towards occult shock in the presence of normal vital signs [9].   

Shock is ultimately a clinical diagnosis, so clinical assessment of the patient with the history, physical exam, and diagnostic test results are often used in combination with the clinical picture to predict risk.  Clinical factors that may be associated with poorer outcomes are high serum lactate levels not responsive to fluid resuscitation, severe acidosis, low MAP, elderly and neonatal patient populations, and immunosuppressed patients [1,5,8]. 

Management

Initial management in unstable patients

Management of the shock patient starts with the primary survey, or the “ABCs” (Airway, Breathing, Circulation).  The primary survey is an algorithmic approach used for ill patients to help organize patient assessment, identify life-threatening conditions quickly, and treat time sensitive conditions. 

Airway (“A”)

Establishing a definitive airway may be needed to prevent aspiration or as the precursor to mechanical ventilation for respiratory failure.  Listen for any gurgling sounds or poor effort in phonation that may indicate a risk for aspiration.  Since shock is a state of hypoperfusion, many patients may have poor cerebral perfusion, somnolence, and require an invasive airway.  Positive pressure ventilation and many pre-intubation sedation medications can cause hypotension, so strongly consider initiating volume resuscitation or vasopressors to improve hemodynamics prior to performing intubation [1]. 

Assess for any obvious external swelling of the face, lips, or tongue, which may occur in anaphylaxic shock.  Although this angioedema should improve with prompt epinephrine administration, airway management is sometimes needed.  Look for tracheal deviation which can occur in tension pneumothorax.  Be sure to consider cervical spinal fracture and provide a rigid cervical collar for spinal immobilization in the presence of trauma.

Breathing (“B”)

Assistance in respiration is sometimes needed in the shock patient due a primary pulmonary cause of shock (e.g., septic shock due to pneumonia), respiratory compensation for lactic acidosis, or respiratory changes due to toxic overdoses causing shock (e.g., distributive shock from salicylate overdose).  Noninvasive positive pressure ventilation, such as BIPAP or CPAP, or invasive mechanical ventilation with intubation may be required to manage work of breathing and respiratory failure.

Circulation (“C”)

Shock is a state of systemic hypoperfusion, so a key part of treatment often involves some type of volume resuscitation.  Most commonly this involves administration of crystalloid fluids (e.g., normal saline, lactated ringers solution) or blood products.  If the specific type or cause of shock is unclear after assessment of the patient, start with administration of small volume boluses of fluids with frequent reassessments.  A 250-500mL crystalloid fluid bolus is a reasonable initial intervention in the undifferentiated shock patient.  Fluid should be administered rapidly over 5-20minutes to a total of 20-30mL/kg, depending on the cause of shock [1]. Balanced isotonic crystalloid fluids, like lactated ringers solution, may provide a small mortality benefit over normal saline, especially if large volumes of fluid administration are expected [1]. Large volume administration of normal saline can also cause hyperchloremic metabolic acidosis.   For this reason, if lactated ringers solution is readily available and a cost-effective alternative to normal saline, it may be a worthwhile alternative.  Blood products, rather than crystalloid fluids, should be prioritized if hemorrhagic shock is the assumed cause of shock.

Although volume resuscitation is a crucial component of treatment, caution should be taken in aggressive fluid administration in the presence of cardiogenic shock as this may lead to pulmonary edema.  If the patient remains hypotensive after fluid administration with a MAP below 65mmHg, vasopressors should be initiated [1,5].

Medications

Intravenous crystalloid fluids and blood products are common treatments in shock, but depending on the cause of shock, additional medications may be needed.  Some examples are broad spectrum antibiotics in septic shock, steroids in adrenal insufficiency, or thrombolytics in massive pulmonary embolism with obstructive shock.  See the charts below for a list of adjunctive medications along with their doses and uses.   

Common antibiotics used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Piperacillin-Tazobactam

Intra-abdominal, genitourinary, skin/soft tissue, pneumonia infections, febrile neutropenia

3.375-4.5g

(IV)

Q6 hours

4.5gm IV

Common first line broad spectrum antibiotic in septic shock

Cefepime

Intra-abdominal, genitourinary, skin/soft tissue, meningitis, pneumonia infections, febrile neutropenia

1-2g

(IV)

Q8-12 hours

2gm IV

Common first line broad spectrum antibiotic in septic shock.

 

Similar uses as piperacillin-tazobactam

Vancomycin

Severe bacterial infections, especially MRSA, pneumonia, endocarditis, systemic anthrax, meningitis

15-20 mg/kg/

dose (IV)

Q8-12 hours

3gm IV

Common first line broad spectrum antibiotic in septic shock used in combination with cefepime or piperacillin-tazobactam

Ceftriaxone

Meningitis, pneumonia, UTI, endocarditis, typhoid fever, gonococcal infections, pelvic inflammatory disease

1-2g (IV)

Q24 hours

2gm IV

First line medication for bacterial meningitis in adults, also commonly used for UTIs and community-acquired pneumonia

Ciprofloxacin

UTI, intra-abdominal infections, prostatitis, pneumonia, bone/joint infections, typhoid fever, salmonella/shigella infections

200-400mg

(IV)

Q8-12 hours

400mg IV (1000mg PO)

Can prolong QT interval and increase risk for tendon rupture

Metronidazole

Anaerobic coverage for intra-abdominal infections, Pelvic inflammatory disease, C. difficile

500mg (IV)

Q8-12 hours

500mg IV

(500mg PO)

Causes disulfiram-like reaction with alcohol (avoid alcohol with this medication)

Azithromycin

Community-acquired pneumonia, chlamydial infections, COPD exacerbation, MAC treatment, pertussis

500mg then 250mg

(IV)

Q24 hours

500mg IV (1000mg PO)

Can prolong QT interval

Often given IV with ceftriaxone for community acquired pneumonia patients

Common vasopressors used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Norepinephrine (Noradrenaline)

First line vasopressor for most types of shock, especially if loss of vascular tone is primary problem

0.02-1 mcg/kg/min

(IV)

Titrate as needed to maintain MAP >65

See dose

May cause tachyarrhythmia

Epinephrine (Adrenaline)

First line for anaphylactic shock

0.05-2 mcg/kg/min (IV)

0.3-0.5mg (SubQ or IM)

Titrate as needed to maintain MAP >65

See dose

In anaphylaxis, start with 0.3mg subQ/IM dose. This can be repeated every 10min as needed versus starting a continuous infusion.

May cause tachyarrhythmia

Dobutamine

Frequently used in cardiogenic shock due to heavy beta-adrenergic receptor preference

2-20

 mcg/kg/min (IV)

Titrate as needed to maintain MAP >65

See dose

May cause tachyarrhythmia

Phenylephrine

Pure alpha-adrenergic receptor agonist used as a 2nd or 3rd line vasopressor in shock

10-200 mcg/min (IV)

Titrate as needed to maintain MAP >65

See dose

May cause reflex bradycardia and headache

Consider use when tachydysrhythmias are present

Vasopressin

Often used as a 2nd or 3rd line vasopressor after norepinephrine or epinephrine

0.01-0.04 units/min (IV)

Titrate as needed to maintain MAP >65

See dose

Primarily causes vasoconstriction, similar to phenylephrine

Common additional adjunctive medications used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Acetaminophen

Fever or pain

325-1000mg PO or IV

Q4-6 hours

4gm daily

Be careful with dosing this common medication to avoid overdose

Ibuprofen

Fever or pain

200-800mg PO

Q4-6 hours

3200mg daily

Can cause GI upset and increase risk for peptic ulcer disease

Morphine

Moderate-severe Pain

2.5-10mg (IV)

Q2-6 hours

n/a

Risk of respiratory depression, addiction and abuse, hypotension

 

Use naloxone for reversal

Hydrocortisone

Adrenal crisis, vasopressor-refractory hypotension in shock

100-300mg (IV)

Q6-8 hours

1200mg daily for septic shock adjunct

Start at 100mg IV for adrenal insufficiency

 

Taper dose over 5-7 days for septic shock adjunctive treatment

Dexamethasone

Adrenal crisis, vasopressor-refractory hypotension in shock

0.03- 0.15 mg/kg/

day

Q6-12 hours

0.15mg/kg

daily for adrenal insufficiency

Alternative to hydrocortisone

Alteplase

Massive PE with obstructive shock

100mg (IV)

Single dose over 2 hours

100mg

Bleeding is main side effect

Procedures

Some patients in shock may need emergent procedures as part of their treatment plan.  The chart below summarizes relevant procedures that may be encountered in the care of the shock patient.

Indication or Problem

Procedure

Tension pneumothorax

Needle thoracostomy (Followed by tube thoracostomy)

Cardiac tamponade

Pericardiocentesis (Followed by pericardiotomy)

Persistent hypotension despite intravenous fluids with need for prolonged vasopressor administration

Inability to establish IV access in hemodynamically unstable patient

 

Central venous line placement (Triple lumen catheter)

 

 

Inability to establish IV access in hemodynamically unstable patient

 

Intraosseous line placement (or central venous line)

Respiratory failure or inability to protect airway

Endotracheal tube placement (Intubation)

Empyema, hemothorax, or after needle decompression of tension pneumothorax

Tube thoracostomy (Chest tube placement)

Patient reassessment

Reassessment is an important part of management.  The primary survey (“ABCs”) is conducted on initial evaluation of the patient to guide management, but it can be repeated after therapies have started as clinical changes can occur. Fluid administration too rapidly in a patient with cardiac or renal comorbidities may result in pulmonary edema, requiring fluid administration to be halted.  Patients may develop worsening mental status or hypoxemia overtime due to respiratory muscle fatigue, requiring supplemental oxygen or more aggressive airway management.  Complications can develop after procedures, such pneumothorax after internal jugular central venous line placement or re-expansion pulmonary edema after chest tube placement.  These changes in clinical course are only identified if the patient is reassessed after treatment is initiated. 

Bedside ultrasound can also assist in patient reassessment.  A RUSH exam can be repeated or used as a framework to guide sonographic reassessments.  Some examples of pertinent findings on reassessment include pulmonary B-lines after IV fluid administration (alveolar fluid present), the absence of lung sliding (may indicate pneumothorax), or changes in the IVC size after IV fluid administration (a flat IVC may indicate fluid responsiveness) [5,7].  

Special Patient Groups

Pediatrics

Pediatric patients in shock are often well compensated physiologically and may not have hypotension on initial presentation.  For this reason, unexplained tachycardia in the pediatric patient should always raise concern for possible occult or early shock [10]. Hypovolemic shock is the most common type of shock in the pediatric patient population, while obstructive shock is the least common type of shock.  Volume status in infants can be assessed through evaluation of the fontanelles (flat or sunken), the presence or absence of tears, and changes in urine output estimated by the number of wet diapers per day (e.g., less than baseline or baseline) [10]. Similar to adults, shock should be managed aggressively with volume resuscitation with the exception of cardiogenic shock where fluids should be used judiciously and vasopressors used early (e.g., epinephrine).  Septic shock is the most common type of distributive shock in pediatric patients, and volume resuscitation should be aggressive with up to three 20mL/kg fluid boluses given (60mL/kg total) [10]. This should be contrasted with the recommendation of a 20-30mL/kg fluid bolus in adults for most types of shock [1].

Geriatrics

The diagnosis and treatment of shock in geriatric patients may be more challenging due to unique factors associated with this population.  Unlike pediatric patients, elderly patients often do not have a robust physiologic reserve to compensate in a shock state.  Elderly patients often have more comorbidities and take more medications than adults and children which may blunt the tachycardia response or lead to an atypical clinical presentation [11,12]. For example, beta blockers and calcium channel blockers may prevent a tachycardic response in a hypoperfusion state.  Blood pressure may also be “normal” in elderly patients in shock who are chronically hypertensive [11]. For example, blunt trauma patients over 65 years-old with systolic blood pressures below 110mmHg and heart rates above 90 beats/min have an association with an increase in mortality [12]. Elderly patients with sepsis are also less likely to have a fever or leukocytosis than younger adult patients [13]. Do not rely only on vital signs or abnormal investigations to diagnose shock in the elderly patient.

Management of shock in the elderly patient should involve more gentle volume resuscitation with small fluid boluses (e.g., 250-500mL) and frequent reassessments for response or a change in clinical status (e.g., pulmonary edema).  Have a low threshold to start blood products in elderly hemorrhagic shock patients to avoid excess crystalloid fluid administration and volume overload [12]. Consider drug-drug interactions and the impact of baseline comorbidities (e.g., chronic renal insufficiency) when prescribing antibiotics or other therapies for the elderly patient in shock [13].     

Pregnant patients

Pregnant patients have physiologic and hormonal changes that make certain causes of shock more likely than others.  Some common causes of shock to consider in the pregnant patient include pulmonary embolism, hyperemesis gravidarum, peripartum or postpartum hemorrhage, pyelonephritis, and peripartum cardiomyopathy amongst other causes.  

Other pregnancy-related factors include a higher circulating plasma and blood volume in pregnancy, hypercoagulability due to hormonal changes, and risk of vena caval compression by the growing uterus [14]. Volume resuscitation in pregnancy should accommodate for the pregnant patient’s increase in blood and plasma volume. It is recommended that a 50% additional volume of fluids be given to the pregnant patient in shock to account for this [14]. Standard vasopressors administered in shock, like norepinephrine (noradrenaline), dopamine, and vasopressin, may decrease uterine blood flow from vasoconstriction but have limited data on use in pregnancy.  However, these medications are typically given in pregnant shock patients as the benefit of restoring normal maternal perfusion and hemodynamics outweighs any potential risk to the fetus [14]. Treatment of the pregnant shock patient should also incorporate positioning the patient in the left lateral decubitus position.  This avoids compression of the inferior vena cava by the gravid uterus which could reduce cardiac preload [14].

Other patient groups

Other patient groups that may have more nonspecific or atypical findings in shock are immunosuppressed patients, such as those on chemotherapy for malignancies, post-splenectomy patients, post-transplant patients on immunomodulators, or patients on chronic steroid therapy [5,8]. Diagnosing shock in these special patient groups starts with identifying risk factors and keeping occult shock on the differential diagnosis list.  These patient groups should, similar to typical adult patients, receive aggressive and early volume resuscitation, vasopressors when needed, and adjunctive therapies as appropriate (e.g., broad spectrum antibiotics for septic shock). 

When to admit shock patients

All patients with a diagnosis of shock should be admitted due to the high morbidity and mortality associated with shock [1]. Many patients may need to go to a hospital ward with a high level of monitoring, such as an intensive care unit, due to risk of hemodynamic decompensation [1].  Although some causes of shock are “reversible”, such as tube thoracostomy for tension pneumothorax, these patients should be admitted for further monitoring and treatment due to high risk for poor outcomes.

Revisiting your patient

A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.

You identify that your patient is hypotensive, tachycardic, tachypneic, and appears to be in a shock state. You quickly perform a primary survey and note that the airway is patent, lungs are clear bilaterally, and distal extremities are cool with bounding pulses. Two large bore peripheral IV lines are placed, comprehensive laboratory investigations are drawn and sent, supplemental oxygen is applied, and 2 liters of normal saline are administered rapidly. 

A 12-lead EKG demonstrates sinus tachycardia without acute ischemic abnormalities. A bedside ultrasound exam shows diffuse pulmonary A lines (no alveolar fluid) with good lung sliding bilaterally, no pericardial effusion, and a dilated inferior vena cava.  The right ventricle appears dilated and hypokinetic. You diagnose the patient with obstructive shock, likely due to massive pulmonary embolism. You rule out tension pneumothorax and cardiac tamponade as alternative diagnoses with your physical exam and bedside ultrasound findings.  Thrombolytics are promptly administered. The patient’s vital signs slowly stabilize, and he is admitted to the medical intensive care unit for continued monitoring and care.

Author

Picture of Joseph CIANO

Joseph CIANO

Dr Ciano is an Emergency Medicine Physician from New York, USA. He completed his Emergency Medicine Residency in Brooklyn, NY and a Fellowship in Global Emergency Medicine in the Northwell-LIJ Health System. He is interested in building the educational infrastructure of EM in countries where Emergency Medicine is not yet recognized as a field and in countries that are in the early stages of this process. He has partnered with international NGOs in Emergency Medicine educational projects and works as a visiting Emergency Medicine faculty member in West Bengal, India. He is excited to collaborate with the other authors of the iEM Education Project to contribute to the world of FOAM-ed.

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Please replace “iEM Education Project Team” below with the author(s) surname and initials.

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2018 version of this topichttps://iem-student.org/shock/

References

  1. Nicks BA, Gaillard JP. Approach to Nontraumatic Shock. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed January 31, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218079826
  1. Gitz Holler J, Bech CM, Henriksen DP, et al. Nontraumatic hypotension and shock in the emergency department and the prehospital setting, prevalence, etiology, and mortality: A systematic review. PLoS One. 2015;10(3): e0119331. doi: 10.1371/journal.pone.0119331.
  1. Gitz Holler J, Jensen HK, Henriksen DP, et al. Etiology of Shock in the Emergency Department: A 12-Year Population-Based Cohort Study. Shock. 2019;51(1):60-67. doi:10.1097/SHK.0000000000000816
  1. Bloom JE, Andrew E, Dawson LP, et al. Incidence and outcomes of nontraumatic shock in adults using emergency medical services in Victoria, Australia. JAMA Netw Open. 2022;5(1): e2145179. doi:10.1001/jamanetworkopen.2021.45179
  1. Farkas J. Approach to shock. EMCrit Project. https://emcrit.org/ibcc/shock/ . Published November 29, 2021. Accessed January 31, 2023.
  1. Doerschug KC, Schmidt GA. Shock: Diagnosis and Management. In: Oropello JM, Pastores SM, Kvetan V. eds. Critical Care. McGraw Hill. Accessed February 07, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=1944&sectionid=143516997
  1. Weingart SD, Duque D, Nelson B. The RUSH exam: Rapid ultrasound for shock and hypotension. EMCrit Project. https://emcrit.org/rush-exam/. Accessed February 8, 2023.
  1. Puskarich MA, Jones AE. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 08, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=220292051
  1. Shock index. MDCalc. https://www.mdcalc.com/calc/1316/shock-index. Accessed February 8, 2023.
  1. Orsborn J, Braund C. Emergencies & Injuries. In: Bunik M, Hay WW, Levin MJ, Abzug MJ. Current Diagnosis & Treatment: Pediatrics, 26e. McGraw Hill; 2022. Accessed February 22, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=3163&sectionid=266216337
  1. Levine M. Geriatric trauma and medical illness: Pearls and pitfalls. emDocs. http://www.emdocs.net/geriatric-trauma-medical-illness-pearls-pitfalls/ Published August 21, 2016. Accessed February 22, 2023.
  1. Fleischman RJ, Ma O. Trauma in the Elderly. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 22, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=221180950
  1. Clifford KM, Dy-Boarman EA, Haase KK, Maxvill K, Pass SE, Alvarez CA. Challenges with Diagnosing and Managing Sepsis in Older Adults. Expert Rev Anti Infect Ther. 2016;14(2):231-241. doi:10.1586/14787210.2016.1135052
  1. Burns BD, Fisher ES. Resuscitation in Pregnancy. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 23, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=206322334

Acknowledgement

The patient image was created with the assistance of DALL·E 2 by iEM editorial team.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Question Of The Day #60

question of the day
Which of the following is the most likely cause for this patient’s condition? 

This first-trimester pregnant patient presents with generalized weakness, nausea, and vomiting.  She is hypotensive and tachycardic with no sign of urinary infection on the urinalysis.  The many ketones in the urine indicate the patient has inadequate oral nutrition and is breaking down muscle and adipose tissue for energy.  This is likely related to the persistent vomiting the patient is experiencing.  This patient has hyperemesis, a common condition in the first trimester of pregnancy that is caused by rising levels of beta-human chorionic gonadotropin (BHCG).  Treatment for this patient should include IV hydration and antiemetics.  Admission criteria for these patients includes intractable vomiting despite antiemetic administration, over 10% maternal weight loss, persistent ketone or electrolyte abnormalities despite rehydration, or uncertainty in the diagnosis. 

The fluid losses caused by vomiting in this condition result in hypovolemic shock (Choice B).  Distributive shock (Choice C) is caused by other conditions, like sepsis, anaphylaxis, and neurogenic shock.  A ureteral stone (Choice D) is unlikely as the patient does not report any abdominal, back, or flank pain.  The urinalysis also does not show any hematuria, which is a common sign of a ureteral stone.  Pyelonephritis (Choice A) can cause vomiting and septic shock which can result in hypotension and tachycardia.  However, there is no sign of infection in the urinalysis provided, no fever, and no back or flank pain.  The best answer is choice B.  

References

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Question Of The Day #59

question of the day
38 - atrial fibrillation

Which of the following is the most likely cause for this patient’s respiratory condition?

This patient presents to the Emergency Department with palpitations, generalized weakness, and shortness of breath after discontinuing all her home medications.  She has hypotension, marked tachycardia, and pulmonary edema (crackles on lung auscultation).  The 12-lead EKG demonstrates atrial fibrillation with a rapid ventricular rate.  This patient is in a state of cardiogenic shock and requires prompt oxygen support, blood pressure support, and heart rate control. 

Pulmonary embolism (Choice A) can sometimes manifest as new atrial fibrillation with shortness of breath and tachycardia, but pulmonary embolism initially causes obstructive shock.  If a pulmonary embolism goes untreated, it can progress to right ventricular failure, pulmonary edema, and cardiogenic shock.  This patient has known atrial fibrillation and stopped all her home medications.  The abrupt medication change is a more likely cause of the patient’s cardiogenic shock.  Dehydration (Choice D) and systemic infection (Choice D) are less likely given the above history of abruptly stopping home maintenance medications.  Untreated cardiac arrythmia (Choice B) is the most likely cause for this patient’s pulmonary edema and cardiogenic shock. 

The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

References

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Question Of The Day #57

question of the day

Which of the following is the most likely cause for this patient’s condition?  

This young female presents with dizziness, fatigue, nausea, generalized abdominal pain, hypotension, tachycardia, and a positive urine pregnancy test.  The anechoic (black) areas on the bedside ultrasound indicate free fluid (blood) in the peritoneal space.  See the image below for clarification. Yellow arrows indicates free fluids.

This patient is in a state of physiologic shock.  Shock is an emergency medical state characterized by cardiovascular or circulatory failure.  Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure.  Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic.  The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap.  The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam.  Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. 

This patient’s condition is caused by a presumed ruptured ectopic pregnancy and intraperitoneal bleeding.  This is considered hypovolemic/hemorrhagic shock (Choice A). The other types of shock in Choices B, C, and D are less likely given the clinical and diagnostic information in the case.  The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

References

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Question Of The Day #56

question of the day

Which of the following is the most likely cause of this patient’s condition?

This trauma patient arrives with hypotension, tachycardia, absent unilateral lung sounds, and distended neck veins. This should raise high concern for tension pneumothorax, which is a type of obstructive shock (Choice C). This diagnosis should be made clinically without X-ray imaging. Bedside ultrasound can assist in making the diagnosis by looking for bilateral lung sliding, if available. Treatment of tension pneumothorax should be prompt and includes needle decompression followed by tube thoracostomy. Other types of shock outlined in Choices A, B, and D do not fit the clinical scenario with information that is given.

Recall that shock is an emergency medical state characterized by cardiovascular or circulatory failure. Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure. Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic. The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap. The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam. Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.

 

References

[cite]