COVID-19 (2024)

September 3, 2024November 4, 2024 ~ iEM Education Project Team ~ Leave a comment

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 (39.1^oC), 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].

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.

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.

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

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.

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.

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.

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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Reviewed By

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)

August 3, 2024September 8, 2024 ~ iEM Education Project Team ~ Leave a comment

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

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

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

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

Plain chest radiograph (CXR):
- When to do it: Mechanism suggests major polytrauma or chest trauma [9,10]; unable to exclude significant thoracic injury by NEXUS Chest Radiography Rule (Table 3) [12,13].
- Findings to look for: Pneumothorax, pneumomediastinum, subcutaneous emphysema, hemothorax, widened mediastinum, abnormal aortic contour, sternal and rib fractures, flail segments, raised hemidiaphragm, gastrointestinal herniation into thoracic cavity, foreign bodies.
- Pitfalls: Due to poor sensitivity (40% of patients with normal CXR had CT-proven thoracic injuries), normal findings do not exclude cardiac, pulmonary, aortic, or musculoskeletal injuries [9,10].

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.

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

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.

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.

Listen to the chapter

References

Lundin A, Akram SK, Berg L, Göransson KE, Enocson A. Thoracic injuries in trauma patients: Epidemiology and its influence on mortality.Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2022;30(1). doi:10.1186/s13049-022-01058-6.
Milisavljevic S, Spasic M, Arsenijevic M. Thoracic trauma. Current Concepts in General Thoracic Surgery. 2012. doi:10.5772/54139.
Chrysou K, Halat G, Hoksch B, Schmid RA, Kocher GJ. Lessons from a large trauma center: Impact of blunt chest trauma in polytrauma patients—still a relevant problem? Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2017;25(1). doi:10.1186/s13049-017-0384-y.
Eghbalzadeh K, Sabashnikov A, Zeriouh M, et al. Blunt chest trauma: A clinical chameleon. Heart. 2017;104(9):719-724. doi:10.1136/heartjnl-2017-312111.
Initial Assessment and Management. In: Advanced Trauma Life Support: Student Course Manual. Chicago, IL: American College of Surgeons; 2018:2-21.
Loseby J, Hudson A, Lyon R. Clinical handover of the trauma and medical patient: A structured approach. Journal of Paramedic Practice. 2013;5(10):563-567. doi:10.12968/jpar.2013.5.10.563.
Yamamoto L, Schroeder C, Morley D, Beliveau C. Thoracic trauma. Critical Care Nursing Quarterly. 2005;28(1):22-40. doi:10.1097/00002727-200501000-00004.
Sybrandy KC. Diagnosing cardiac contusion: Old Wisdom and new insights. Heart. 2003;89(5):485-489. doi:10.1136/heart.89.5.485.
American College of Radiology. Major blunt trauma. ACR Appropriateness Criteria Major Blunt Trauma. https://acsearch.acr.org/docs/3102405/Narrative/. Accessed April 1, 2023.
American College of Radiology. Blunt chest trauma – suspected cardiac injury. ACR Appropriateness Criteria Blunt Chest Trauma. https://acsearch.acr.org/docs/3082590/Narrative/. Accessed April 1, 2023.
Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database of Systematic Reviews. 2018. doi:10.1002/14651858.cd013031.
Rodriguez RM, Hendey GW, Mower W, et al. Derivation of a decision instrument for selective chest radiography in blunt trauma. Journal of Trauma: Injury, Infection & Critical Care. 2011;71(3):549-553. doi:10.1097/ta.0b013e3181f2ac9d.
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.
Rodriguez RM, Langdorf MI, Nishijima D, et al. Derivation and validation of two decision instruments for selective chest CT in blunt trauma: A multicenter prospective observational study (NEXUS Chest CT). PLOS Medicine. 2015;12(10). doi:10.1371/journal.pmed.1001883.
Subhani SS, Muzaffar MS, Khan MI. Comparison of outcome between low and high thoracic trauma severity score in blunt trauma chest patients. Journal of Ayub Medical College Abbottabad. 2014;26(4):474-7. PMID: 25672168.
Daurat A, Millet I, Roustan J-P, et al. Thoracic trauma severity score on admission allows to determine the risk of delayed ARDS in trauma patients with pulmonary contusion. Injury. 2016;47(1):147-153. doi:10.1016/j.injury.2015.08.031.
Chen J, Jeremitsky E, Philp F, Fry W, Smith RS. A chest trauma scoring system to predict outcomes. Surgery. 2014;156(4):988-994. doi:10.1016/j.surg.2014.06.045.
Fokin A, Wycech J, Crawford M, Puente I. Quantification of rib fractures by different scoring systems. Journal of Surgical Research. 2018;229:1-8. doi:10.1016/j.jss.2018.03.025.
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Reviewed By

Arif Alper Cevik, MD, FEMAT, FIFEM

Bradyarrhythmias (2024)

July 28, 2024November 4, 2024 ~ iEM Education Project Team ~ Leave a comment

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?

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.

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.

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).

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].

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).

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).

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].

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].

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).

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].

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

Hypotension (SBP <90 mm Hg)
Signs of shock
Altered mental status
Ischemic chest pain
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.

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/h^7,113] 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 dextrose^7,24,113 Glucagon 3-10 mg IV bolus over 3-5 min, followed by an IV infusion of 1-5 mg/h^7,96 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

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.

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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Reviewed By

Arif Alper Cevik, MD, FEMAT, FIFEM

Shock (2023)

May 8, 2023May 7, 2023 ~ iEM Education Project Team ~ Leave a comment

by Joseph Ciano

You have a new patient!

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

What do you need to know?

Importance

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

Epidemiology

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

Pathophysiology

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

Type of shock	Hemodynamics	Potential causes	Potential treatments
Hypovolemic	↓preload ↑SVR ↓CO	Dehydration, vomiting/diarrhea, burns, hemorrhage (GI bleed, traumatic wound, etc.)	IV fluids Blood products (if due to hemorrhage)
Distributive	↓preload ↓SVR ↓/↑CO	Sepsis, anaphylaxis, adrenal insufficiency, neurogenic shock	IV fluids +/- antibiotics and vasopressors. Treat underlying cause. Epinephrine (anaphylaxis) Norepinephrine (sepsis or neurogenic) Phenylephrine (neurogenic)
Cardiogenic	↑preload ↑SVR ↓CO	Heart failure, tachy/bradyarrythmias, myocardial infarction, valve failure, myocarditis, cardiomyopathy, beta-blocker overdose	Dobutamine or Epinephrine Treat underlying cause
Obstructive	↓preload ↑SVR ↓CO	Tension pneumothorax, cardiac tamponade, pulmonary embolism	IV fluids Treat underlying cause. Tension Pneumothorax– Needle decompression then tube thoracostomy Cardiac tamponade-Pericardiocentesis then pericardial window Pulmonary embolism-Anticoagulation, consider thrombolytics or surgical embolectomy

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

Medical History

Key questions to ask on history-taking

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

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

Type of shock

Presenting symptoms that may indicate shock

Key questions to ask based on cause of shock

Hypovolemic

Weakness

Syncope

Altered mental status

Vomiting/diarrhea

Hematemesis

Hematochezia/Melena

Burn injury

Trauma/fall

Dehydration

Last PO intake? Diuretic usage? Recent travel?

Vomiting/diarrhea

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

Hemorrhage (GI bleed, traumatic wound, etc.)

How much blood loss? Any anticoagulant use?

Distributive

Weakness

Syncope

Altered mental status

Fever, chills

Cough

Difficulty breathing

Dysuria

Lip/tongue swelling

Rash

Sepsis

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

Anaphylaxis

Known inciting factor or allergies? Angioedema?

Adrenal insufficiency

Steroid use? Medication changes? TB history?

Neurogenic shock

Spinal trauma? Focal weakness/numbness?

Cardiogenic

Weakness

Syncope

Altered mental status

Chest pain

Back or shoulder pain

Palpitations

Difficulty breathing Orthopnea

Peripheral edema

Heart failure, Cardiomyopathy, Valve failure

Medication changes? Chest pain? Body edema or dyspnea?

Tachy/bradyarrythmias

Syncope? Palpitations/heart fluttering?

Myocardial infarction

Chest or back pain? Diaphoresis?

Obstructive

Weakness

Syncope

Altered mental status

Difficulty breathing

Chest pain

Penetrating chest trauma

Unilateral leg pain/edema

Tension pneumothorax

Chest trauma?

Cardiac tamponade

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

Pulmonary embolism

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

Identifying “red flags”

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

Physical Examination

Key physical exam features

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

Identifying “red flags”

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

Alternative Diagnoses

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

Shock Type	Differential diagnosis ^5,6
Hypovolemic	GI losses (gastroenteritis, colitis, fistulas) Skin burns Renal losses (excess diuretic use, diabetes insipidus) Hemorrhage (e.g., GI bleed, traumatic wound, aortic aneurysmal rupture, ruptured ectopic pregnancy, coagulopathy, etc.)
Distributive	Sepsis Anaphylaxis Adrenal insufficiency (primary vs secondary causes) Thiamine deficiency (beriberi) Pancreatitis Thyroid storm Toxins (salicylates, cyanide, carbon monoxide) Neurogenic shock (trauma, spinal anesthesia)
Cardiogenic	Tachyarrhythmia or bradyarrhythmia Left ventricular failure/Cardiomyopathy Ischemic (myocardial infarction) Nonischemic (postpartum, Takotsubo, myocarditis, myocardial contusion, Ca channel/beta-blocker overdose, autoimmune) Valve dysfunction Endocarditis, post MI papillary muscle rupture, prosthetic valve problem LV outflow obstruction Hypertrophic obstructive cardiomyopathy (HOCM), aortic stenosis Device malfunction (ECMO, Ventricular assist device)
Obstructive	Tension pneumothorax Cardiac tamponade Pulmonary embolism Auto PEEP (“breath stacking”) in obstructive lung disease patient

Acing Diagnostic Testing

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

Bedside tests

Laboratory tests

Imaging tests

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

Serum lactate
CBC with differential
Serum chemistry (BUN, creatinine, electrolytes)
Hepatic function panel
Coagulation studies
Type and screen
Venous or arterial blood gas testing
Cultures (blood, urine, wound)
Pregnancy test
Urinalysis
Cortisol level

Chest X-ray
CT of chest/abdomen/pelvis as supported by history + physical
Ultrasound (lung, heart, abdomen)

Bedside Tests

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

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

Laboratory Tests

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

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

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

Imaging Tests

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

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

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

Ultrasound findings in shock

Risk Stratification

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

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

Management

Initial management in unstable patients

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

Airway (“A”)

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

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

Breathing (“B”)

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

Circulation (“C”)

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

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

Medications

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

Common antibiotics used in shock

Drug name (Generic)	Potential use	Dose	Frequency	Maximum Dose	Cautions / Comments
Piperacillin-Tazobactam	Intra-abdominal, genitourinary, skin/soft tissue, pneumonia infections, febrile neutropenia	3.375-4.5g (IV)	Q6 hours	4.5gm IV	Common first line broad spectrum antibiotic in septic shock
Cefepime	Intra-abdominal, genitourinary, skin/soft tissue, meningitis, pneumonia infections, febrile neutropenia	1-2g (IV)	Q8-12 hours	2gm IV	Common first line broad spectrum antibiotic in septic shock. Similar uses as piperacillin-tazobactam
Vancomycin	Severe bacterial infections, especially MRSA, pneumonia, endocarditis, systemic anthrax, meningitis	15-20 mg/kg/ dose (IV)	Q8-12 hours	3gm IV	Common first line broad spectrum antibiotic in septic shock used in combination with cefepime or piperacillin-tazobactam
Ceftriaxone	Meningitis, pneumonia, UTI, endocarditis, typhoid fever, gonococcal infections, pelvic inflammatory disease	1-2g (IV)	Q24 hours	2gm IV	First line medication for bacterial meningitis in adults, also commonly used for UTIs and community-acquired pneumonia
Ciprofloxacin	UTI, intra-abdominal infections, prostatitis, pneumonia, bone/joint infections, typhoid fever, salmonella/shigella infections	200-400mg (IV)	Q8-12 hours	400mg IV (1000mg PO)	Can prolong QT interval and increase risk for tendon rupture
Metronidazole	Anaerobic coverage for intra-abdominal infections, Pelvic inflammatory disease, C. difficile	500mg (IV)	Q8-12 hours	500mg IV (500mg PO)	Causes disulfiram-like reaction with alcohol (avoid alcohol with this medication)
Azithromycin	Community-acquired pneumonia, chlamydial infections, COPD exacerbation, MAC treatment, pertussis	500mg then 250mg (IV)	Q24 hours	500mg IV (1000mg PO)	Can prolong QT interval Often given IV with ceftriaxone for community acquired pneumonia patients

Common vasopressors used in shock

Drug name (Generic)	Potential use	Dose	Frequency	Maximum Dose	Cautions / Comments
Norepinephrine (Noradrenaline)	First line vasopressor for most types of shock, especially if loss of vascular tone is primary problem	0.02-1 mcg/kg/min (IV)	Titrate as needed to maintain MAP >65	See dose	May cause tachyarrhythmia
Epinephrine (Adrenaline)	First line for anaphylactic shock	0.05-2 mcg/kg/min (IV) 0.3-0.5mg (SubQ or IM)	Titrate as needed to maintain MAP >65	See dose	In anaphylaxis, start with 0.3mg subQ/IM dose. This can be repeated every 10min as needed versus starting a continuous infusion. May cause tachyarrhythmia
Dobutamine	Frequently used in cardiogenic shock due to heavy beta-adrenergic receptor preference	2-20 mcg/kg/min (IV)	Titrate as needed to maintain MAP >65	See dose	May cause tachyarrhythmia
Phenylephrine	Pure alpha-adrenergic receptor agonist used as a 2^nd or 3^rd line vasopressor in shock	10-200 mcg/min (IV)	Titrate as needed to maintain MAP >65	See dose	May cause reflex bradycardia and headache Consider use when tachydysrhythmias are present
Vasopressin	Often used as a 2^nd or 3^rd line vasopressor after norepinephrine or epinephrine	0.01-0.04 units/min (IV)	Titrate as needed to maintain MAP >65	See dose	Primarily causes vasoconstriction, similar to phenylephrine

Common additional adjunctive medications used in shock

Drug name (Generic)	Potential use	Dose	Frequency	Maximum Dose	Cautions / Comments
Acetaminophen	Fever or pain	325-1000mg PO or IV	Q4-6 hours	4gm daily	Be careful with dosing this common medication to avoid overdose
Ibuprofen	Fever or pain	200-800mg PO	Q4-6 hours	3200mg daily	Can cause GI upset and increase risk for peptic ulcer disease
Morphine	Moderate-severe Pain	2.5-10mg (IV)	Q2-6 hours	n/a	Risk of respiratory depression, addiction and abuse, hypotension Use naloxone for reversal
Hydrocortisone	Adrenal crisis, vasopressor-refractory hypotension in shock	100-300mg (IV)	Q6-8 hours	1200mg daily for septic shock adjunct	Start at 100mg IV for adrenal insufficiency Taper dose over 5-7 days for septic shock adjunctive treatment
Dexamethasone	Adrenal crisis, vasopressor-refractory hypotension in shock	0.03- 0.15 mg/kg/ day	Q6-12 hours	0.15mg/kg daily for adrenal insufficiency	Alternative to hydrocortisone
Alteplase	Massive PE with obstructive shock	100mg (IV)	Single dose over 2 hours	100mg	Bleeding is main side effect

Procedures

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

Indication or Problem	Procedure
Tension pneumothorax	Needle thoracostomy (Followed by tube thoracostomy)
Cardiac tamponade	Pericardiocentesis (Followed by pericardiotomy)
Persistent hypotension despite intravenous fluids with need for prolonged vasopressor administration Inability to establish IV access in hemodynamically unstable patient	Central venous line placement (Triple lumen catheter)
Inability to establish IV access in hemodynamically unstable patient	Intraosseous line placement (or central venous line)
Respiratory failure or inability to protect airway	Endotracheal tube placement (Intubation)
Empyema, hemothorax, or after needle decompression of tension pneumothorax	Tube thoracostomy (Chest tube placement)

Patient reassessment

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

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

Special Patient Groups

Pediatrics

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

Geriatrics

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

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

Pregnant patients

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

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

Other patient groups

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

When to admit shock patients

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

Revisiting your patient

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

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

Author

Joseph CIANO

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

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Cite This Article

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

[cite]

2018 version of this topic – https://iem-student.org/shock/

References

Nicks BA, Gaillard JP. Approach to Nontraumatic Shock. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed January 31, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=218079826

Gitz Holler J, Bech CM, Henriksen DP, et al. Nontraumatic hypotension and shock in the emergency department and the prehospital setting, prevalence, etiology, and mortality: A systematic review. PLoS One. 2015;10(3): e0119331. doi: 10.1371/journal.pone.0119331.

Gitz Holler J, Jensen HK, Henriksen DP, et al. Etiology of Shock in the Emergency Department: A 12-Year Population-Based Cohort Study. Shock. 2019;51(1):60-67. doi:10.1097/SHK.0000000000000816

Bloom JE, Andrew E, Dawson LP, et al. Incidence and outcomes of nontraumatic shock in adults using emergency medical services in Victoria, Australia. JAMA Netw Open. 2022;5(1): e2145179. doi:10.1001/jamanetworkopen.2021.45179

Farkas J. Approach to shock. EMCrit Project. https://emcrit.org/ibcc/shock/ . Published November 29, 2021. Accessed January 31, 2023.

Doerschug KC, Schmidt GA. Shock: Diagnosis and Management. In: Oropello JM, Pastores SM, Kvetan V. eds. Critical Care. McGraw Hill. Accessed February 07, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=1944&sectionid=143516997

Weingart SD, Duque D, Nelson B. The RUSH exam: Rapid ultrasound for shock and hypotension. EMCrit Project. https://emcrit.org/rush-exam/. Accessed February 8, 2023.

Puskarich MA, Jones AE. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 08, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=220292051

Shock index. MDCalc. https://www.mdcalc.com/calc/1316/shock-index. Accessed February 8, 2023.

Orsborn J, Braund C. Emergencies & Injuries. In: Bunik M, Hay WW, Levin MJ, Abzug MJ. Current Diagnosis & Treatment: Pediatrics, 26e. McGraw Hill; 2022. Accessed February 22, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=3163&sectionid=266216337

Levine M. Geriatric trauma and medical illness: Pearls and pitfalls. emDocs. http://www.emdocs.net/geriatric-trauma-medical-illness-pearls-pitfalls/ Published August 21, 2016. Accessed February 22, 2023.

Fleischman RJ, Ma O. Trauma in the Elderly. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 22, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=221180950

Clifford KM, Dy-Boarman EA, Haase KK, Maxvill K, Pass SE, Alvarez CA. Challenges with Diagnosing and Managing Sepsis in Older Adults. Expert Rev Anti Infect Ther. 2016;14(2):231-241. doi:10.1586/14787210.2016.1135052

Burns BD, Fisher ES. Resuscitation in Pregnancy. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw Hill; 2020. Accessed February 23, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=206322334

Acknowledgement

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

Reviewed By

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Question Of The Day #100

August 12, 2022July 16, 2022 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

This patient arrives to the Emergency department with 1 week of melena and fatigue. His medication list includes an antiplatelet and an anticoagulant medication. There is tachycardia and melena noted on examination. This patient likely has an upper GI bleed based on his signs and symptoms with peptic ulcer disease as the most common cause. The patient’s anticoagulation serves as a risk factor for GI bleeding and is an important contributing factor in this scenario. Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

Gastroenterology consultation for emergent endoscopy (Choice B) is not necessary as the patient is not acutely unstable. He may need a diagnostic and therapeutic endoscopy during an inpatient admission, but the GI consultants do not need to be called emergently for this procedure. An acutely unstable upper GI bleed patient, such as a patient with hemodynamic instability, requiring intubation for airway protection, receiving multiple blood product transfusions, or with brisk (rapid) bleeding on exam should prompt GI consultation for an emergent endoscopy for source control. Surgery consultation for gastrectomy (Choice C) is not a first-line treatment for upper GI bleeding. Gastroenterology should first perform a diagnostic and therapeutic endoscopy for most upper GI bleed patients. Surgical esophageal transection, gastrectomy, colectomy, and other surgical procedures are last resort measures to control GI bleeding. Administration of IV Ceftriaxone (Choice D) is not needed in this scenario and should not be given routinely in upper GI bleeds. This patient has no infectious signs or symptoms. Antibiotics, such as Ceftriaxone or quinolones, should be given to upper GI bleed patients with chronic liver disease (i.e., cirrhosis), or presumed gastroesophageal variceal bleeds. Antibiotics have been found to have a mortality benefit in this patient population with GI bleeds.

The best next step in management is to treat the patient’s tachycardia with normal saline (Choice A) for volume resuscitation. This patient may eventually need blood products, but crystalloid IV fluids are okay to start until the Complete Blood Count results return. This patient is not in overt hemorrhagic shock, so blood products can be held until there is evidence that the hemoglobin is below 7g/dL. Reversal of the patient’s anticoagulation with Vitamin K and fresh frozen plasma may also be needed depending on the INR level. Reversal can wait until coagulation studies are complete since the patient is not acutely unstable. An unstable patient should have their anticoagulant reversed immediately. Correct Answer: A

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Farkas J. (2019). Anticoagulant reversal. EMCRIT: The Internet Book of Critical Care. https://emcrit.org/ibcc/reverse/
Thomas L & Thompson L. (2019). GI bleed. Society of Academic Emergency Medicine. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-approach-to/gi-bleed
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

[cite]

Question Of The Day #99

August 5, 2022July 16, 2022 ~ Joseph Ciano, USA ~ Leave a comment

Complete Blood Count	Result	(Reference Range)
BUN	36.2	5 -18 mg/dL
Creatinine	1.1	0.7 – 1.2 mg/dL
Hemoglobin	9.2	13.0 – 18.0 g/dL
Hematocrit	27.6	39.0 – 54.0 %

Which of the following is the most appropriate advice for this patient’s condition?

Explanation

This patient arrives to the Emergency department after a single hematemesis episode. On exam he has a borderline low blood pressure and tachycardia. The laboratory results demonstrate an elevated BUN and a low hemoglobin and hematocrit. The patient’s vital signs in combination with the laboratory values point towards a diagnosis of an upper GI bleed with early signs of hemorrhagic shock. The history of alcohol abuse also should raise concern for possible gastro-esophageal variceal bleeding as the cause of the GI bleed.

Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

Although this patient is not acutely unstable, his vital signs are abnormal and he should receive volume resuscitation and close observation in the Emergency department. After initial resuscitation and treatment, it is sometimes difficult to know the best disposition for the patient (admit versus discharge). The Glasgow-Blatchford Score isa validated risk satisfaction tool used to assist in determining the disposition of patients with an upper GI bleed. The scoring criteria and instructions on how to use the score are below.

Glasgow-Blatchford Score

A validated risk stratification tool for patients with upper GIB

Scoring Criteria

Numerical Score

BUN (mg/dL)

<18.2

18.2-22.3

22.4-28

28-70

>70

Hemoglobin (g/dL) for men

>13

12-13

10-12

<10

Hemoglobin (g/dL) for women

>12

10-12

<10

Systolic blood pressure (mmHg)

>110

100-109

90-99

<90

Other criteria

Pulse >100 beats/min

Melena present

Syncope

Liver disease history

Cardiac failure history

Instructions:

Low risk= Score of 0. Any score higher than 0 is high risk for needing intervention: transfusion, endoscopy, or surgery. Consider admission for any score over 0.

This patient has a Glasgow-Blatchford score of 15, and should not be discharged home. A plan to discharge with gastroenterology follow up in 1 week (Choice A) or discharge with instructions to return if there are repeat hematemesis episodes (Choice B) should not be followed. This patient may have future hematemesis episodes in the Emergency department, be at risk for aspiration, require endotracheal intubation, and become more hypotensive. A Sengstaken-Blakemore tube (Choice C) is a specialized oro-gastric tube with a gastric and esophageal balloon. Placement of this tube is considered an invasive procedure that is only used after a patient has been endotracheally intubated to prevent aspiration. Once placed correctly, the balloons in the tube can be inflated to tamponade any bleeding variceal vessels in the distal esophagus or stomach. This tube is used as a last resort measure prior to endoscopic treatment for presumed gastro-esophageal variceal bleeds.

The best advice for this patient would be to admit the patient for monitoring and endoscopy (Choice D).

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
MDcalc. Glasgow-Blatchford bleeding score (GBS). https://www.mdcalc.com/glasgow-blatchford-bleeding-score-gbs
Thomas L & Thompson L. (2019). GI bleed. Society of Academic Emergency Medicine. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-approach-to/gi-bleed
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

[cite]

Question Of The Day #98

July 29, 2022July 16, 2022 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

This man presents to the Emergency department with epigastric pain and hematemesis. His exam shows hypotension, tachycardia, pale conjunctiva, and a tender epigastrium and left upper quadrant. This patient likely has an upper GI bleed based on his signs and symptoms.

Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

Risk factors for GI bleeds include alcohol use, anticoagulant use, NSAID (non-steroidal anti-inflammatory drug) use (i.e., ibuprofen, aspirin, naproxen), recent gastrointestinal surgery or procedures, prior GI bleeds, and a history of conditions that are associated with GI bleeds (i.e., gastritis, peptic ulcers, H. Pylori infection, ulcerative colitis, Chron’s disease, hemorrhoids, diverticulosis, or GI tract cancers). Fatty meals (Choice A) can trigger gastroesophageal reflux disorder (GERD) symptoms or biliary colic symptoms from cholelithiasis. However, fatty meals do not increase the risk for GI bleeding. Physiological stress, such as sepsis or bacteremia (Choice B), can increase the risk for GI bleeding. This patient does not have any infectious exam signs or symptoms that would support the presence of bacteremia. Acetaminophen use (Choice D) can cause liver failure if taken in excess, but acetaminophen does not cause GI bleeding. NSAIDs, unlike Tylenol, are associated with GI bleeding.

Systemic steroid use (Choice C) can increase the risk for GI bleeding and is the likely cause of this patient’s upper GI bleed. Correct Answer: C

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Thomas L & Thompson L. (2019). GI bleed. Society of Academic Emergency Medicine. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-approach-to/gi-bleed
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

[cite]

Question Of The Day #97

July 22, 2022July 16, 2022 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

This patient arrives to the Emergency department after multiple episodes of hematemesis. Her exam shows tachycardia, borderline hypotension, and mild tachypnea. While in the Emergency department the patient decompensates after more hematemesis episodes and develops altered mental status. This patient has an upper GI bleed most likely from a gastroesophageal variceal bleed. Gastro-esophageal (GE) varices are dilated blood vessels at the GE junction that result from portal hypertension. Variceal bleeding can be catastrophic and cause hemorrhagic shock and problems with airway patency as seen in this scenario. The management of GE variceal bleeding, like other GI bleeds, begins with management of the “ABCs” (Airway, Breathing, and Circulation). Unlike in other causes of upper GI bleeds, IV antibiotics and IV octreotide are used in GE variceal bleeds. IV antibiotics have a mortality benefit when used in this setting. Early gastroenterology consultation is another important component of GE variceal bleed management for definitive diagnosis and treatment with variceal banding or ligation. Please see the chart below for further details on general GI bleed causes, signs and symptoms, and ED management.

This patient with a depressed mental status needs to have a definitive airway established to prevent aspiration with bloody vomitus. IV Pantoprazole (Choice B) is used in upper GI bleeds from peptic ulcers but has no role in this acutely ill variceal bleed patient. The airway should be established prior to medications, such as pantoprazole are considered. A cricothyrotomy (Choice D) would establish an airway, but this is an invasive approach to airway management and not the best approach in this patient. A cricothyrotomy involves piercing a needle or scalpel in the anterior neck (cricothyroid membrane) to establish an airway surgically. This procedure is performed in special situations where a patient cannot be intubated through the trachea (i.e., angioedema of the lips and tongue, facial mass, facial trauma) and cannot ventilate independently (i.e., depressed mental status). This patient does not meet the criteria for this invasive procedure. Endotracheal intubation should be attempted first on this patient. A Sengstaken-Blakemore tube (Choice A) is a specialized oro-gastric tube with a gastric and esophageal balloon. Once placed correctly, the balloons on the tube can be inflated to tamponade any bleeding variceal vessels in the distal esophagus or stomach. This tube should be placed only after intubating a patient and is used as a last resort measure prior to endoscopic treatment. The best next step in management of this patient is to perform endotracheal intubation (Choice C) for airway protection. Correct Answer: C

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Long B. (2018). EM@3AM: Gastroesophageal varices. emDocs. http://www.emdocs.net/em3am-gastroesophageal-varices/
Nickson C. (2020). Sengstaken-Blakemore and Minnesota tubes. Life in the Fast Lane. https://litfl.com/sengstaken-blakemore-and-minnesota-tubes/
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

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Question Of The Day #96

July 8, 2022July 1, 2022 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

This patient arrives to the Emergency department with upper abdominal pain and hematemesis. The exam demonstrated hypotension, tachycardia, pale conjunctiva, and abdominal ascites. The patient decompensates during the exam requiring endotracheal intubation for airway protection. This patient has an upper GI bleed most likely from gastro-esophageal varices given her history of liver cirrhosis and stigmata of chronic liver disease. Gastro-esophageal (GE) varices are dilated blood vessels at the GE junction that result from portal hypertension. Variceal bleeding can be catastrophic and cause hemorrhagic shock and problems with airway patency as seen in this scenario. The management of GE variceal bleeding, like other GI bleeds, begins with management of the “ABCs” (Airway, Breathing, and Circulation). Unlike in other causes of upper GI bleeds, IV antibiotics and IV octreotide are used in GE variceal bleeds. IV antibiotics have a mortality benefit when used in this setting. First line antibiotics are IV ceftriaxone or IV ciprofloxacin. Early gastroenterology consultation is another important component of GE variceal bleed management for definitive diagnosis and treatment with variceal banding or ligation.

An abdominal paracentesis (Choice A) is not the best next step in this unstable cirrhotic patient. Antibiotics are routinely given in gastro-esophageal variceal bleeds due to their mortality benefit, so there is no need for an emergent paracentesis to evaluate for spontaneous bacterial peritonitis (SBP) with an ascitic fluid sample. IV Tranexamic acid (Choice C) is an anti-fibrinolytic agent with pro-coagulative effects. Its use is recommended in post-partum hemorrhage and traumatic hemorrhages, but it has no utility in the setting of GI bleed. Early gastroenterology consultation for endoscopy is preferred over general surgery consultation (Choice D). Surgery consultants can assist in a TIPS procedure (Transjugular intrahepatic portosystemic shunt) to reduce portal hypertension, esophageal resection, or gastrectomy, but less invasive endoscopic therapies with GI specialists are preferred over these procedures.

IV Ceftriaxone (Choice B) is the best next step in this scenario due to the mortality benefit of antibiotics in chronic liver disease patients with variceal bleeds.

Please see the chart below for further details on general GI bleed causes, signs and symptoms, and ED management.

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Long B. (2018). EM@3AM: Gastroesophageal varices. emDocs. http://www.emdocs.net/em3am-gastroesophageal-varices/
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

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Question Of The Day #95

July 1, 2022May 26, 2022 ~ Joseph Ciano, USA ~ Leave a comment

Complete Blood Count	Result	(Reference Range)
WBC Count	16.2	4.0 – 10.5 X 10³/mL
Hemoglobin	10.8	13.0 – 18.0 g/dL
Hematocrit	32.4	39.0 – 54.0 %
Platelets	220	140 – 415 x 10³/mL

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

Explanation

This patient arrives to the Emergency department with bright red bloody stools and lower abdominal pain. The exam shows fever, tachycardia, and left-sided abdominal tenderness. The laboratory results provided show leukocytosis and anemia. This patient likely has a lower GI bleed based on her signs and symptoms. Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

All choices provided are causes of lower GI bleeding and are possible in this patient. However, that patient’s signs, symptoms, and risk profile make certain diagnoses less likely than others. Diverticulosis (Choice A) is the most common cause of lower GI bleeding. Diverticulosis often occurs in older patients and should not be associated with pain or fever, which support a diagnosis of an inflammatory or infectious etiology (i.e., diverticulitis, Shigellosis, ulcerative colitis, chron’s disease, etc.). This patient is young and has fever and leukocytosis, making diverticulosis less likely. Colon malignancy (Choice B) is also possible but is less likely given the patient’s young age, the presence of fever, and the acute onset of symptoms over 2 days. Colon malignancy tends to cause slow GI bleeding over a longer period of time, rather than acutely over 2 days. Ischemic colitis (Choice C), such as mesenteric ischemia, is less likely in a young patient without any cardiac risk factors or recent abdominal surgeries.

Ulcerative colitis (Choice D) is the most likely diagnosis in this scenario. Peak incidence for ulcerative colitis occurs in the second and third decades of life, and women are more likely than men to have this diagnosis. Definitive diagnosis requires a biopsy and colonoscopy, but a CT scan of the abdomen and pelvis can show findings consistent with ulcerative colitis for a new diagnosis. Treatment of an ulcerative colitis flare includes general supportive care, IV steroids, and IV antibiotics if there is concern for a concurrent infectious process. Intestinal perforation and toxic megacolon also should be evaluated for with CT imaging.

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Trueblood W & Simon E. ()2016). Inflammatory bowel disease in the Emergency department. EMDocs. http://www.emdocs.net/inflammatory-bowel-disease-emergency-department/

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Question Of The Day #94

June 24, 2022May 26, 2022 ~ Joseph Ciano, USA ~ Leave a comment

Complete Blood Count	Result	(Reference Range)
WBC Count	4.5	4.0 – 10.5 X 10³/mL
Hemoglobin	5.3	13.0 – 18.0 g/dL
Hematocrit	15.9	39.0 – 54.0 %
Platelets	138	140 – 415 x 10³/mL

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

Explanation

This patient arrives to the Emergency Department with bright red bloody stools in the setting of warfarin use. His exam shows hypotension and tachycardia. The laboratory results show a low hemoglobin and hematocrit, but no INR or other coagulation studies are provided. This patient is in hemorrhagic shock due to a lower gastrointestinal bleed. This patient’s condition may be due to coagulopathy from his warfarin (i.e., supratherapeutic INR), diverticulosis, or other conditions. Initial management of this unstable patient should include management of the airway, breathing, and circulation (“ABCs”). This includes aggressive and prompt treatment of the patient’s hypotension and tachycardia and reversal of the patient’s anticoagulation. Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

This patient’s platelet level is just below the lower limit of normal, so administration of a platelet transfusion (Choice A) would not be the next best step. Platelet administration should be considered if the platelet count is below 50,000-100,000, or if a massive transfusion protocol is initiated to prevent coagulopathy. No INR value is provided in the question stem, but prompt reversal of warfarin should not be delayed for an INR level (Choice D). Reversal of warfarin should be promptly initiated when a patient is unstable (i.e., hypotensive GI bleed, traumatic wound hemorrhage, intracranial bleed, etc.). Medication reversal in these settings includes both IV Vitamin K 10mg and IV Fresh Frozen Plasma 10-20cc/kg. IV Vitamin K helps reverse the Vitamin K antagonistic effect of Warfarin, but it does not acutely provide new Vitamin K-dependent coagulation factors (Factors X, V, II, VII). IV Vitamin K gives the liver the ‘materials’ needed to regenerate these coagulation factors, but this process takes time. Fresh frozen plasma contains ‘ready-to-use’ coagulation factors that will help control the hemorrhage acutely. For this reason, both Vitamin K and FFP are given together in an unstable patient. An alternative to fresh frozen plasma (FFP) is prothrombin complex concentrate (PCC), which is a concentrated version of coagulation factors. PCC is not broadly available in all countries, and is generally more expensive than FFP.

The management of stable patients with a supratherapeutic INR includes holding warfarin doses and sometimes providing PO Vitamin K, depending on the INR level. Administration of IV Vitamin K only (Choice C) is not the correct treatment in this scenario. IV Vitamin K and IV Fresh Frozen Plasma (Choice B) is the best next step to reverse this patient’s anticoagulant.

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Farkas J. (2019). Anticoagulant reversal. EMCRIT: The Internet Book of Critical Care. https://emcrit.org/ibcc/reverse/
Thomas L & Thompson L. (2019). GI bleed. Society of Academic Emergency Medicine. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-approach-to/gi-bleed
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

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Question Of The Day #93

June 17, 2022May 26, 2022 ~ Joseph Ciano, USA ~ Leave a comment

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

Explanation

This patient arrives to the Emergency Department with bright red bloody stools and generalized abdominal pain. His exam shows hypotension, tachycardia, a diffusely tender abdomen, and pale conjunctiva. He also takes warfarin daily for anticoagulation. This patient is in hemorrhagic shock due to a lower gastrointestinal bleed. This patient’s condition may be due to coagulopathy from his warfarin (i.e., supratherapeutic INR), diverticulosis, ischemic colitis (i.e., mesenteric ischemia), and other conditions. Initial management of this unstable patient should include management of the airway, breathing, and circulation (“ABCs”). This includes aggressive and prompt treatment of the patient’s hypotension and tachycardia. Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.

A CT Angiogram of the abdomen and pelvis (Choice A) may be helpful in clarifying the etiology and site of the patient’s bleeding, but this is not the best next step in management. The patient’s shock state first should be managed prior to any imaging studies. Gastroenterology consultation for colonoscopy (Choice B) may be important later in this patient’s management, but it is not the best next step in management. His shock state should be treated prior to calling any consultants. An IV Pantoprazole infusion (Choice C) is helpful in upper GI bleeds due to peptic ulcer disease. Proton pump inhibitor medications, like pantoprazole, help reduce findings of ulcer bleeding during endoscopy. Proton pump inhibitor use has been controversial in upper GI bleeds as there is no evidence that their use decreases mortality, decreases blood product requirements, or ulcer rebleeding, but these medications are often given due to their generally small risk profile.

The best next step for this patient in hemorrhagic shock is administration of packed red blood cells (Choice D). He also should have reversal of his warfarin with IV Vitamin K and fresh frozen plasma to prevent continued bleeding.

References

Carrol M, Mudan G, & Bentley S. Gastrointestinal bleeding. International Emergency Medicine Education Project. https://iem-student.org/gi-bleeding/
Department of Emergency Medicine. (2015). Proton pump inhibitors in upper GI bleeds. Washington University School of Medicine in St. Louis. https://emergencymedicine.wustl.edu/items/proton-pump-inhibitors-in-upper-gi-bleeds/
Thomas L & Thompson L. (2019). GI bleed. Society of Academic Emergency Medicine. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-approach-to/gi-bleed
White K (2017). EM@3AM: GI bleed. emDocs. http://www.emdocs.net/em3am-gi-bleed/

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You have a new patient!

What do you need to know?

Importance

Epidemiology

Pathophysiology

Medical History

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

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

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

Physical Examination

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

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

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

Alternative Diagnoses

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

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

Acing Diagnostic Testing

Bedside Tests

Antigen Testing

NAAT Testing

Laboratory Tests

Imaging

Risk Stratification

Risk Stratification Tools

Management

Initial Stabilization

Medical Management

Procedures

Complications: Long COVID

Special Patient Groups

Pediatric Populations

Geriatric Populations

Pregnant Populations

When To Admit This Patient

Revisiting Your Patient

Authors

Pei Shan Hoe

Andrew Mariotti

Prem Menon

Alexandra Digenakis

Listen to the chapter

References

Reviewed By

Arif Alper Cevik, MD, FEMAT, FIFEM

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Like this:

You have a new patient!

What do you need to know?

Medical History

Physical Examination

Inspection

Palpation

Percussion

Auscultation

Alternative diagnoses

Diagnostic testing

POCT

Imaging

Laboratory tests

Risk stratification

Management

Medications

Special patient groups

When to admit the patient

Revisiting your patient

Authors

Ivan Low

Jeremy Wee Choon Peng

Listen to the chapter

References

Reviewed By

Arif Alper Cevik, MD, FEMAT, FIFEM

Sharing is caring

Like this:

You have a new patient!

Importance and Epidemiology

Pathophysiology

Types of Bradycardia

Sinus Bradycardia

Junctional Rhythm