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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  132. SANDLER M, RUTHREN CR, WOOD C. METABOLISM OF C14-NOREPINEPHRINE AND C14-EPINEPHRINE AND THEIR TRANSMISSION ACROSS THE HUMAN PLACENTA. Int J Neuropharmacol. 1964;3:123-128. doi:10.1016/0028-3908(64)90055-3
  133. Newell J. Dopamine. CorePendium. https://www.emrap.org/corependium/drug/recZPuXuOq4bUMquk/Dopamine#h.t44uk7at4g7p. Published May 12, 2023. Accessed April 1, 2023.
  134. Alexopoulos D, Yusuf S, Johnston JA, Bostock J, Sleight P, Yacoub MH. The 24-hour heart rate behavior in long-term survivors of cardiac transplantation. Am J Cardiol. 1988;61(11):880-884. doi:10.1016/0002-9149(88)90363-3
  135. Banner NR, Patel N, Cox AP, Patton HE, Lachno DR, Yacoub MH. Altered sympathoadrenal response to dynamic exercise in cardiac transplant recipients. Cardiovasc Res. 1989;23(11):965-972. doi:10.1093/cvr/23.11.965
  136. Woo GW, Schofield RS, Pauly DF, et al. Incidence, predictors, and outcomes of cardiac pacing after cardiac transplantation: an 11-year retrospective analysis. Transplantation. 2008;85(8):1216-1218. doi:10.1097/TP.0b013e31816b677c
  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
  141. Cantillon DJ, Tarakji KG, Hu T, et al. Long-term outcomes and clinical predictors for pacemaker-requiring bradyarrhythmias after cardiac transplantation: analysis of the UNOS/OPTN cardiac transplant database. Heart Rhythm. 2010;7(11):1567-1571. doi:10.1016/j.hrthm.2010.06.026
  142. Cantillon DJ, Gorodeski EZ, Caccamo M, et al. Long-term outcomes and clinical predictors for pacing after cardiac transplantation. J Heart Lung Transplant. 2009;28(8):791-798. doi:10.1016/J.HEALUN.2009.04.034
  143. Jones DG, Mortsell DH, Rajaruthnam D, et al. Permanent pacemaker implantation early and late after heart transplantation: clinical indication, risk factors and prognostic implications. J Heart Lung Transplant. 2011;30(11):1257-1265. doi:10.1016/j.healun.2011.05.010
  144. Wellmann P, Herrmann FEM, Hagl C, Juchem G. A Single Center Study of 1,179 Heart Transplant Patients-Factors Affecting Pacemaker Implantation. Pacing Clin Electrophysiol. 2017;40(3):247-254. doi:10.1111/pace.13021

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.

Out of Proportion: Acute Leg Pain

Case Presentation

A 48-year-old male, with history of hypertension and diabetes and prior intravenous drug use (now on methadone) presents with acute onset right leg pain from his calf to the ankle, that woke him from sleep overnight. The pain has been constant, with no modifying or relieving factors. He hasn’t taken anything other than his daily dose of methadone. He hasn’t had any fevers or chills and denies any recent trauma or injuries.

Any thoughts on what else you might want to ask or know?

  • Any recent travel or prolonged immobilization?
  • Have you ever had a blood clot?
  • Are you on any blood thinners?
  • Have you used IV drugs recently?
  • Any numbness or weakness in your leg?
  • Any associated rash or color change?
  • Any back pain or abdominal pain? Any bowel or bladder incontinence?
  • Any recent antibiotics (or other medication changes)?
  • Have you ever had anything like this before?
[all of these are negative/normal]

Pause here -- what is your initial differential diagnosis looking like?

  • Deep vein thrombosis
  • Superficial vein thrombosis
  • Pyomyositis
  • Necrotizing fasciitis
  • Muscle sprain or tear
  • Arterial thromboembolism
  • Bakers cyst
  • Achilles tendonitis, Achilles tendon rupture

What are some key parts of your targeted physical exam?

  • VITAL SIGNS! [BP was slightly hypertensive, and he is slightly tachycardic, normothermic]
  • Neurologic exam of the affected extremity (motor and sensory)
  • Vascular exam of the affected extremity (femoral/popliteal/posterior tibialis/dorsalis pedis)
  • Musculoskeletal exam including ranging the hip, knee, ankle and palpating throughout the entire leg
  • Skin exam for signs of injury or rashes etc.
  • Consider a cardiopulmonary and abdominal exam, particularly the lower abdomen

On this patient’s exam, he was overall uncomfortable appearing and had slight tachycardia (110s, EKG shows normal sinus rhythm), normal cardiopulmonary exam, normal abdominal exam. He had a 2+ right femoral pulse and faintly palpable DP pulse that had a good biphasic waveform on doppler. His hip/knee/ankle all have painless range of motion. The compartments are soft in the upper and lower leg. He does have some diffuse calf tenderness and the medial aspect feels slightly cool compared to the contralateral side, but his foot is warm and well perfused. There isn’t any spot that is most tender. There is no rash, no crepitus, no bullae or bruising or other evidence of injury.

What diagnostic studies would you like to send?

  • CBC, BMP
  • CPK, lactate
  • DVT ultrasound?
  • Anything else?

What treatments would you like to provide?

  • Analgesia (mutli-modal)?
  • Maybe a bolus of IV fluids to help with the tachycardia?

The patient is having a lot of pain despite already getting NSAIDs, acetaminophen, and a dose of morphine. You decide to re-medicate the patient with more morphine and send him for DVT ultrasound. As soon as he gets back, he’s frustrated that you still haven’t treated his pain “at all” and he really does look uncomfortable and in a lot of pain.  You start to wonder if he’s faking it giving his history of IV drug use.

His DVT ultrasound comes back as normal. The lab work is also coming back and unrevealing. A normal CBC, metabolic panel, normal CPK, normal lactate. His pain is not really improving. You reexamine the leg, and the exam is unchanged. It really seems like his pain is out of proportion to the exam.

Pain is out of proportion to the exam should catch your attention every time. While we always need to keep malingering and less emergent causes for pain that seems to be more than expected in the back of our minds. But! Several emergent diagnoses have patients presenting in pain in a way that doesn’t fit what you can objectively identify as a cause. Diagnoses like compartment syndrome and mesenteric ischemia can be erroneously dismissed by emergency providers, and it is crucial you don’t just stop looking for the cause of pain out of proportion. In fact, it’s important you dig in deeper and rule out all potentially life and limb threatening causes.

In this case, the pain was recalcitrant to multiple doses of IV opiates and several other modes of treatment. The patient was getting so frustrated that he pulled out his IV and threatened to leave the ED. After talking with him further, he agreed to stay and a new IV was placed, more pain medication given, and a CTA with lower extremity run-off was performed, which showed the acute thrombus of the proximal popliteal artery, just below the level of the knee.

He was started on a heparin infusion and vascular surgery was consulted; the patient was admitted from the ED and taken for thrombectomy. No source of embolism was identified, and his occlusion was presumed to be thrombotic (most commonly from a ruptured atheromatous plaque leading to activation of the coagulation cascade), with particular attention to his history of diabetes and hypertension raising his risk for this. He had a fair amount of collateralization from other arteries around the occlusion, such that his foot wasn’t cold, and he had a doppler-able DP pulse. 

Remember

Go with your gut and don’t minimize pain that is out of proportion to the exam. Keep hunting for a reasonable explanation or you may miss a life or limb threatening cause of an atypical emergency presentation.

Further Reading

Deep Vein Thrombosis (DVT)

by Elif Dilek Cakal Case Presentation An 85-year-old woman, with a history of congestive heart failure, presented with right leg pain and swelling of 2

Read More »

Acute Mesenteric Ischemia

by Rabind Antony Charles Case Presentation A 75-year-old woman presents to your Emergency Department (ED) with diffuse abdominal pain for the past day, associated with

Read More »

Abdominal Pain

by Shaza Karrar Case Presentation A 39-year-old female presented to the emergency department (ED) complaining of right-lower-quadrant (RLQ) pain; pain duration was for 1-day, associated

Read More »
[cite]

Cryptic Shock – Identifying the Unseen (PART 1)

Case Presentation

A 68-year-old man presented to the Emergency Department with complaints of breathing difficulty and fever for three days. The patient is a known diabetic and hypertensive.

After detailed history taking, clinical examination, and radiological workup, the patient was diagnosed with right-sided lobar pneumonia (Community-acquired) and immediately started on intravenous antibiotics. In addition, necessary cultures and blood samples were taken for evaluation.

At the time of presentation, his vitals were HR – 92/min, BP – 130/70mmHg, RR – 30/min, SpO2 – 90% with RA à 96% with 2L O2. He underwent bladder catheterization.

During the 1st hour in the ER, the patient had a very low urine output, which continued for the next few hours. Lactate levels were more than 4mmol/L.

Based on the symptoms, oliguria, and hyperlactatemia, the patient was diagnosed to have sepsis and was initiated on fluid resuscitation. After 2 hours, the patient remained oliguric still, and his BP declined to 120/70mmHg.

After 6 hours, the patient’s BP became 110/60mmHg (MAP – 77). He became anuric and developed altered sensorium. Since he did not meet the criteria of septic shock, he was continued on IV fluids and antibiotics.

After 12 hours, the BP became 80/40mmHg (MAP – 63mmHg) à developed Multiorgan Dysfunction Syndrome. He was then started on vasopressors and mechanical ventilation.

By day 3, the patient further deteriorated and went into cardiac arrest. ROSC was not achieved.

Case Analysis

The treatment initiated was based on protocols like Surviving Sepsis Guidelines and Septic Shock management. So how did the process fail in order to adequately resuscitate this patient? Could something have been done more differently?

The case you read above is a very common scenario. Approximately 30% of the people coming to the ER are hypertensive, and around 10% have diabetes mellitus. They form a huge population, among whom the incidence of any other disease increases their morbidity and early mortality.

Before we delve into the pathology in these patients, let us look at the basic definitions of shock/hypotension.

  • SBP < 90mmHg
  • MAP < 65 mmHg
  • Decrease in SBP > 40mmHg
  • Organ Dysfunction
  • Hyperlactatemia
  • Shock: A state of circulatory insufficiency that creates an imbalance between tissue oxygen supply (delivery) and demand (consumption), resulting in end-organ dysfunction.
  • Septic Shock: Adult patients can be identified using the clinical criteria of hypotension requiring the use of vasopressors to maintain MAP of 65mmHg or greater and having a serum lactate level greater than 2 mmol/L persisting after adequate fluids resuscitation.
  • Cryptic Shock: Presence of hyperlactatemia (or systemic hypoperfusion) in a case of sepsis with normotension.

Based on all the information given above;

  1. what do you think was wrong with our patient?
  2. What kind of shock did he have?
  3. Could we have managed him any other way?
  4. When should we have started inotropes?
  5. Did the fact that he was hypertensive and diabetic have to do with his early deterioration? If so, how?
  6. When did the patient-first develop signs of shock?
  7. What are the different signs and symptoms of shock, and how are they recognized in the ER?

Keep your answers ready… 

Part 2 of Cryptic Shock Series – Vascular Pathology and What is considered ‘Shock’ in Hypertensive patients

Part 3 of Cryptic Shock Series – Individualised BP management

Part 4 of Cryptic Shock Series – Latest Trends

References and Further Reading

  1. Ranzani OT, Monteiro MB, Ferreira EM, Santos SR, Machado FR, Noritomi DT; Grupo de Cuidados Críticos Amil. Reclassifying the spectrum of septic patients using lactate: severe sepsis, cryptic shock, vasoplegic shock and dysoxic shock. Rev Bras Ter Intensiva. 2013 Oct-Dec;25(4):270-8. doi: 10.5935/0103-507X.20130047.
  2. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, Bellomo R, Bernard GR, Chiche JD, Coopersmith CM, Hotchkiss RS, Levy MM, Marshall JC, Martin GS, Opal SM, Rubenfeld GD, van der Poll T, Vincent JL, Angus DC. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):801-10. doi: 10.1001/jama.2016.0287.
  3. Shankar-Hari M, Phillips GS, Levy ML, Seymour CW, Liu VX, Deutschman CS, Angus DC, Rubenfeld GD, Singer M; Sepsis Definitions Task Force. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016 Feb 23;315(8):775-87. doi: 10.1001/jama.2016.0289.
  4. Education Resources – Sepsis Trust
  5. The Research of Predicting Septic Shock – International Emergency Medicine Education Project (iem-student.org)
  6. Sepsis – International Emergency Medicine Education Project (iem-student.org)
  7. Empiric Antibiotics for Sepsis in the ED Infographics – International Emergency Medicine Education Project (iem-student.org)
  8. Sepsis – An Overview and Update – International Emergency Medicine Education Project (iem-student.org)
[cite]

Defibrillator: Clear!

Defibrillator clear

So, this is your first day at your internship rotation in the Emergency Department. You see some movement in the resuscitation room, and someone shouts: CODE!

Then, you approach the team, excited to learn and help with cardiopulmonary resuscitation (CPR). The attending physician looks at you and asks: Do you know how to use the defibrillator?

What would your answer be?

Knowing the main functions of the defibrillator is essential but not enough; you need to get used to the model in your hospital to be able to help safely with an emergency.

Defibrillators are devices used to apply electrical energy manually or automatically. Their use is indicated for electrical cardioversion, defibrillation or as a transcutaneous pacemaker.

Later that day, another patient presents with unstable atrial fibrillation (AFib).

The attending suggests cardioverting the patient. Do you know how to prepare the defibrillator?

Defibrillation versus cardioversion

Both defibrillation and cardioversion are techniques in which an electrical current is applied to the patient, through a defibrillator, to reverse a cardiac arrhythmia.

Defibrillation

Defibrillation is a non-synchronized electrical discharge applied to the chest, which aims to depolarize all myocardial muscle fibres, thus literally restarting the heart, allowing the sinoatrial node to resume the generation and control of the heart rhythm, and reversing the severe arrhythmias. It is indicated for pulseless ventricular tachycardia and ventricular fibrillation during CPR.

Electrical Cardioversion

Electrical cardioversion is the application of shock in a synchronized way to ensure the electric discharge is released in the R wave, that is, in the refractory period because accidental delivery of the shock during the vulnerable period, that is, the T wave, can trigger VF. It is reserved for severe arrhythmias in unstable patients with a pulse. It can usually be an elective procedure.

Special Situations

Digital Intoxication

Digital intoxication can present with any type of tachyarrhythmia or bradyarrhythmia. Cardioversion in this situation is a relative contraindication, as digital makes the heart sensitive to electrical stimulation. Before considering cardioversion, correct all electrolyte imbalances, otherwise, the cardioversion can degenerate the rhythm to a VF.

Pacemaker / Implantable cardioverter-defibrillator (ICD)

Cardioversion can be performed, but with care. The inadequate technique can damage the generator, the conductive system, or the heart muscle, leading to dysfunction of the device. The blades must be positioned at least 12 cm away from the generator, preferably in the anteroposterior position. The lowest possible electrical charge must be used.

Pregnancy

Cardioversion can be used safely during pregnancy. The fetal beat should be monitored throughout the procedure.

Things To Consider

Keep your devices tested!

Working in the ED is not easy. This is the place where organization and preparation should be routine. Constant checking of materials and operation of the equipment must be the rule because the smallest detail can cause a difference in saving a life.

During adversity, it is necessary to remain calm, trying to not affect the reasoning and disposition of the team. It is an arduous job, it takes practice and a lot of effort. Errors can only be corrected after they are recognized and must have the right time to be exposed. It happens.

There is no time for despair, yelling and stress when it comes to CPR.

No conductive gel, what can we do?

The main guidelines regarding the use of the conductive gel used in the defibrillator paddles are:

  • Using the proper gel for this purpose is essential. The gel is an electrically conductive material that decreases the resistance to the flow of electric current between the paddle and the chest wall. The absence of conductive material can lead to the production of an arc that causes burns in the patient and the risk of explosion if there is an oxygen source very close, among others.
  • Avoid the use of gauze soaked in saline solution, as the excess serum can cause burns on the patient’s skin, but it is a reasonable option, in an emergency
  • Do not use the ultrasound gel
  • The preference is to use adhesive paddles that already come with their own conductive gel (but this is rare in Brazil).

Location recommended by Advanced Cardiac Life Support (ACLS)

Antero-lateral

One paddle is placed on the right side of the sternum, right below the clavicle and the other laterally where the cardiac appendix would be in the anterior or medial axillary line (V5-V6).

Adhesive paddles can also be placed in an anteroposterior position: The anterior one is placed in the cardiac appendage or precordial region, and the posterior one is placed on the back in the right or left infrascapular region.

During the shock, the provider must ensure that no one is in contact with the patient. A force of approximately 8k must be used to increase the contact of the paddles with the chest. Do not allow a continuous flow of oxygen over the patient’s chest to avoid accidents with sparks.

Complications

  • Electric arc (when electricity travels through the air between the electrodes and can cause explosive noises, burns and impair current delivery)
  • Electrical injuries in spectators
  • Risk of explosion if there is a continuous flow of oxygen during the shock
  • Burning of the skin by repeated shocks
  • Myocardial injury and post-defibrillation arrhythmias and myocardial stunning
  • Skeletal muscle injury
  • Fracture of thoracic vertebrae

References and Further Reading

  1. Sunde, K., Jacobs, I., Deakin, C. D., Hazinski, M. F., Kerber, R. E., Koster, R. W., Morrison, L. J., Nolan, J. P., Sayre, M. R., & Defibrillation Chapter Collaborators (2010). Part 6: Defibrillation: 2010 international consensus on cardiopulmonary resuscitation and emergency cardiovascular care science with treatment recommendations. Resuscitation81 Suppl 1, e71–e85. https://doi.org/10.1016/j.resuscitation.2010.08.025
  2. Panchal, A. R., Bartos, J. A., Cabañas, J. G., Donnino, M. W., Drennan, I. R., Hirsch, K. G., Kudenchuk, P. J., Kurz, M. C., Lavonas, E. J., Morley, P. T., O’Neil, B. J., Peberdy, M. A., Rittenberger, J. C., Rodriguez, A. J., Sawyer, K. N., Berg, K. M., & Adult Basic and Advanced Life Support Writing Group (2020). Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation142(16_suppl_2), S366–S468. https://doi.org/10.1161/CIR.0000000000000916
  3. Ionmhain, U. N. (2020). Defibrillation Basics. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-basics/
  4. Paradis, N. A., Halperin, H. R., Kern, K. B., Wenzel, V., & Chamberlain, D. A. (Eds.). (2007). Cardiac arrest: the science and practice of resuscitation medicine. Cambridge University Press.
  5. Nickson, C. (2020). Defibrillation Pads and Paddles. Life in The Fastlane. Retrieved April 26, 2020, from https://litfl.com/defibrillation-pads-and-paddles/
[cite]

Question Of The Day #30

question of the day
qod30

Which of the following is the most appropriate next step in management for this patient?

This patient arrives to the Emergency department with the return of spontaneous circulation (ROSC) from a ventricular fibrillation cardiac arrest. His regaining of pulses was likely due to his limited downtime, prompt initiation of CPR, and prompt diagnosis and treatment of ventricular fibrillation with electrical defibrillation. Important elements of emergency post-ROSC care include avoiding hypotension, hypoxia, hyperthermia, and hypo or hyperglycemia. Maintaining proper perfusion to the brain and peripheral organs is crucial in all ROSC patients. A 12-lead EKG should always be obtained early after ROSC is achieved in order to look for signs of cardiac ischemia. Cardiac catheterization should be considered in all post-ROSC patients, but especially in patients with cardiac arrest from ventricular fibrillation or ventricular tachycardia.

Patients who achieve ROSC can vary markedly in terms of their clinical exam. Some patients may be awake and conversive, while others are comatose and non-responsive. The neurological exam immediately post-ROSC does not predict long-term outcomes, so decisions on prognosis should not be based on these factors in the emergency department. For this reason, resuscitation efforts should not be considered medically futile in this scenario (Choice A). Vasopressors (Choice B) are medications useful in post-ROSC patients who have signs of hemodynamic collapse, such as hypotension. This patient is not hypotensive and does not meet the criteria for initiation of vasopressors. A CT scan of the head (Choice D) is a study to consider in any patient who presents to the emergency department with collapse to evaluate intracranial bleeding (i.e., subarachnoid bleeding). Although not impossible, the history of chest pain before collapse makes brain bleeding a less likely cause of death in this patient. Targeted Temperature Management (Choice C), also known as Therapeutic Hypothermia, is the best next step in this patient’s management.

Targeted Temperature Management involves a controlled lowering of the patient’s body temperature to 32-34ᵒC in the first 24 hours after cardiac arrest. This treatment has been shown to improve neurologic and survival outcomes. The theory behind this treatment is that hypothermia post-ROSC reduces free radical damage and decreases cerebral metabolism. Data behind targeted temperature management shows the greatest benefit in cardiac arrest patients due to ventricular fibrillation, but arrest from ventricular tachycardia, pulseless electrical activity, and asystole may also show benefit. Adverse effects of this treatment include coagulopathy, bradycardia, electrolyte abnormalities (i.e., hypokalemia), and shivering. Important contraindications to this treatment are an awake or alert patient (post-ROSC GCS >6), DNR or DNI status, another reason to explain comatose state (i.e., intracranial bleeding, spinal cord injury), age under 17 years old, a poor functional status prior to the cardiac arrest (i.e., nonverbal, bedbound), or an arrest caused by trauma. Correct Answer: C

References

 

[cite]

Question Of The Day #29

question of the day
qod29
842 - Wide QRS complex tachycardia

Which of the following is the most appropriate next step in management for this patient?

This patient presents to the emergency department with seven days of severe vomiting, diarrhea, tachycardia, and borderline hypotension. The clinician should be concerned about dehydration and potential electrolyte derangements induced by the vomiting and diarrhea. Certain electrolyte derangements can put a patient at risk for cardiac dysrhythmias, so ordering a 12-lead EKG is an important step in evaluating any patient with a potential electrolyte disturbance. Dangerous electrolyte disturbances that can predispose a patient to cardiac dysrhythmias include hyperkalemia, hypokalemia, hypomagnesemia, and hypocalcemia. Signs of hyperkalemia on the EKG include peaked T waves, absent or flattened P waves, widened QRS complexes, or a sine wave morphology. Low potassium, magnesium, and calcium can all prolong the QT interval and predispose the patient to polymorphic ventricular tachycardia (Torsades de Pointes). Hypokalemia on EKG may also be associated with a U wave, which is an upward wave that follows the T wave.

This patient’s 12-lead EKG shows a wide-complex tachycardia with QRS complex “twisting” around the isoelectric line and varying QRS amplitudes. These EKG signs, along with the inferred history of severe electrolyte abnormalities, support a diagnosis of Torsades de Pointes (TdP). Another risk factor for TdP is a history of congenital prolonged QT syndromes. Similar to monomorphic ventricular tachycardia, TdP should always be treated with electrical cardioversion if there are any signs of instability (i.e., altered mental status, SBP <90mmHg). A pulseless patient with TdP always necessitates unsynchronized cardioversion, also known as defibrillation. This patient may have briefly syncopized or potentially underwent cardiac arrest. Intravenous Amiodarone (Choice A) and Procainamide (Choice B) are contraindicated in TdP as both of these agents can further prolong the QT interval. These agents can be used in a stable patient with monomorphic ventricular tachycardia. Intravenous Ciprofloxacin (Choice C) is a quinolone antibiotic that is useful for treating infections from gram-negative bacteria. This may be beneficial for this patient, especially if there is a concern for bacterial gastroenteritis. However, quinolone antibiotics also can prolong the QT interval, and this medication will not acutely stabilize this patient. Intravenous Magnesium Sulfate (Choice D) shortens the QT interval and is the preferred therapy for a TdP patient with a pulse. Correct Answer: D

References

[cite]

Question Of The Day #28

question of the day
qod28

EKG#1

710 - hyperkalemia

EKG#2

855 - bradycardia

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

This patient presents to the emergency department with vague and nonspecific symptoms of nausea, fatigue, and palpitations. The initial EKG (EKG #1) demonstrates a wide-complex tachycardia (QRS >120msec) with a regular rhythm. The differential diagnosis for wide-complex tachyarrhythmias include ventricular tachycardia (monomorphic ventricular tachycardia), torsades de pointes (polymorphic ventricular tachycardia), coarse ventricular fibrillation, supraventricular tachycardias with aberrancy (i.e. underlying Wolf Parkinson White Syndrome or Ventricular Bundle Branch Block), electrolyte abnormalities (i.e., Hyperkalemia), and from medications (i.e., Na channel blocking agents). If the history is unclear or the patient shows signs of instability, Ventricular tachycardia should always be the assumed tachyarrhythmia. This is managed with electrical cardioversion or with medications (i.e., amiodarone, procainamide, lidocaine), depending on the patient’s symptoms and hemodynamic stability.

The prior EKG for the patient (EKG #2) is helpful in showing that the patient does not have a wide QRS complex at baseline. There also are no EKG signs of Wolf Parkinson White Syndrome (Choice B) on EKG #2, making this choice incorrect. Signs of this cardiac pre-excitation syndrome on EKG include a shortened PR interval and a delta wave (slurred upstroke at the beginning of the QRS complex). Anxiety (Choice D) can cause sinus tachycardia and be a symptom associated with any arrhythmia, but it is not the underlying cause for this patient’s bizarre wide-complex tachydysrhythmia. On a closer look, the patient’s EKG (EKG #1) demonstrates tall, peaked T waves in the precordial leads. This supports a diagnosis of hyperkalemia. Other signs of hyperkalemia on EKG include flattened or absent P waves, widened QRS complexes, or a sine wave morphology. A common underlying cause of hyperkalemia is renal disease (Choice C). Ischemic heart disease (Choice A) is a common underlying cause for ventricular tachycardia. Ventricular tachycardia is less likely in this case given the presence of peaked T waves and the lack of fusion beats, capture beats, or signs of AV dissociation on the 12-lead EKG. Correct Answer: C 

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Ventricular Tachycardia – Monomorphic VT. Life in The Fast Lane. Retrieved from https://litfl.com/ventricular-tachycardia-monomorphic-ecg-library/

[cite]

Question Of The Day #27

question of the day
qod27
756.1 - palpitation - SOB

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient has a narrow-complex, regular tachycardia that is causing the sensation of palpitations. The clinical history, rapid heart rate, and 12-lead EKG provide enough information to diagnose this patient with supraventricular tachycardia, also known as “SVT.” Supraventricular tachycardias refer to a broad range of arrhythmias, including sinus tachycardia, atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and AV nodal re-entry tachycardia. This scenario specifically depicts an AV nodal re-entry tachycardia (AVNRT). AVNRT is a common type of SVT that can occur spontaneously or is triggered by sympathomimetic agents (i.e., cocaine, amphetamines), caffeine, alcohol, exercise, or beta-2 agonists using in asthma treatment (i.e., albuterol, salbutamol). AVNRTs are narrow-complex tachycardias with rates that range from 120-280bpm. P waves are typically absent in AVNRTs, but rarely they may be present as retrograde inverted P waves located immediately before or after the QRS complex. Symptoms experienced by the AVNRT patient may include pre-syncope, syncope, dizziness, palpitations, anxiety, or mild shortness of breath. Patients with AVNRTs are more likely to be young and female over male.

QRS complexes in AVNRTs are often narrow (<120msec), however, wide QRS complexes may be present in AVNRTs if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AVNRTs are often stable and do not require electric cardioversion. Signs that indicate instability and necessitate cardioversion are hypotension (SBP <90mmHg), altered mental status, or ischemic chest pain (more common if known history of ischemic heart disease). This patient lacks all of these signs and symptoms.

Treatment of AVNRT focuses on restoring the patient to normal sinus rhythm, which leads to resolution of symptoms. First-line medications for AVNRTs are short-acting AV nodal blocking agents, like adenosine (Choice A). Beta-blockers or calcium channel blockers act as second-line agents for patients who do not respond to adenosine. Metoprolol is a beta-blocker (Choice C) and Diltiazem is a calcium channel clocker (Choice D). Prior to any medications, vagal maneuvers should always be attempted first in a stable patient with AVNRT. The Valsalva maneuver (Choice B), or “bearing down,” is a commonly used vagal maneuver in the termination of AVNRTs. Other vagal maneuvers include the carotid massage or the Diving reflex (place bag of ice and water on face). Correct Answer: B

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020). Supraventricular Tachycardia (SVT). Life in the Fast Lane. Retrieved from https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

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Question Of The Day #26

question of the day
qod26
38 - atrial fibrillation

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient presents to the emergency department with palpitations, a narrow complex tachycardia (<120msec), and an irregularly irregular rhythm. A close look at this patient’s EKG reveals the absence of discrete P waves and QRS complexes that are spaced at varying distances from each other (most apparent in lead V6). These signs support a diagnosis of Atrial Fibrillation, or “AFib.” Atrial Fibrillation is an arrhythmia characterized by an irregularly irregular rhythm, the absence of P waves with a flat or undulating baseline, and narrow QRS complexes. Wide-QRS complexes may be present in AFib if there is a concurrent bundle branch block or Wolff-Parkinson White Syndrome. AFib is caused by the electric firing of multiple ectopic foci in the atria of the heart. This condition is triggered by a multitude of causes, including ischemic heart disease, valvular heart disease, dilated or hypertrophic cardiomyopathies (likely related to this patient’s congestive heart failure history), sepsis, hyperthyroidism, excess caffeine or alcohol intake, pulmonary embolism, and electrolyte abnormalities.

The main risk in AFib is the creation of thrombi in the atria as they fibrillate, resulting in emboli that travel to the brain and cause a stroke. The CHA2DS2VASc scoring system is used to risk stratify patients and determine if they require anticoagulation to prevent against thrombo-embolic phenomenon (i.e. stroke). This patient has a high CHA2DS2VASc score, so she would require anticoagulation. In addition to anticoagulation, A fib is treated with rate control (i.e. beta blockers or calcium channel blockers), rhythm control (i.e. anti-arrhythmic agents), or electrical cardioversion. Electrical cardioversion (choice A) is typically avoided when symptoms occur greater than 48 hours, since the risk of thrombo-emboli formation is higher in this scenario. An exception to this would be a patient with “unstable” AFib. Signs of instability in any tachyarrhythmia are hypotension, altered mental status, or ischemic chest pain. This patient lacks all of these signs and symptoms. Although this patient lacks signs of instability, this patient’s marked tachycardia should be addressed with medical treatment. General observation (Choice C) is not the best choice for this reason. Intravenous adenosine (Choice D) is the best choice for a patient with supraventricular tachycardia (SVT). This is a narrow-complex AV nodal re-entry tachycardia with rates that range from 120-280bpm. SVT also lacks discrete P waves. A key factor that differentiates A fib from SVT is that SVT has a regular rhythm, while AFib has an irregular rhythm. Intravenous metoprolol (Choice B) is the best treatment option listed in order to decrease the patient’s heart rate.

References

  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218687685
  • Burns, E. (2020) Atrial Fibrillation. Life in The Fast Lane. Retrieved from https://litfl.com/atrial-fibrillation-ecg-library/

 

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