Medical Licensing (MD/DO) · Independent exam preparation
Emergency Medicine Written (Part I) Exam Study Guide
Practise emergency stabilization, diagnostic thresholds and safe disposition for AOBEM Written Part I with 60 focused concepts, clinical drills and recall cards.
By CertMedbry · Updated 19 October 2026
Practise recognizing instability, choosing time-critical treatment, interpreting diagnostic thresholds and making safe disposition decisions. This guide targets the Emergency Medicine Written (Part I) Exam within AOBEM primary specialty certification in Emergency Medicine. Its 60 selected concepts cover all 18 published domains with approximate weighting; the official written-exam outline defines the full examination scope. All clinical subtopic selections within the domains are editorial choices, not issuer-mandated subtopic requirements.
Try 20 free practice questionsWhat is the exam format?
Check the question types, timing and outline before planning your revision.
Which examination and certification pathway does this guide address?
The Emergency Medicine Written (Part I) Exam is a component of AOBEM primary certification in Emergency Medicine. AOBEM administers the required examinations and recommends successful candidates for certification; the AOA approves certification. The board-level listing name does not identify a separate examination.
AOBEM Written Exam · AOBEM Emergency Medicine Certification Timeline
How many questions are published, and how many are scored or pretest items?
The written-exam page describes 300 multiple-choice items organized into six sections of 50. The cited information does not specify a scored-versus-pretest breakdown, so no such split is asserted here.
How much examination time is specified?
Each of the six sections allows 60 minutes, giving six hours of section time. Section time should be distinguished from total appointment length. Consult the current candidate instructions for the applicable break schedule and administrative arrangements.
What question format is described?
The examination uses multiple-choice items, most with five possible answers. The learning questions in this guide use four options. The written examination assesses basic science, clinical knowledge, skills and emergency medicine principles.
Which blueprint and effective date apply?
This guide follows the 18 weighted areas on the live written-exam outline documented on October 10, 2026. That outline states no version or effective date. The linked handbook carries January 2020 headings and an older 20-category list; it does not replace the live weighted outline.
AOBEM Written Exam · Policies and Procedures of the American Osteopathic Board of Emergency Medicine
How does the oral examination differ?
Written and oral examinations belong to the same primary certification pathway and may be taken in either order. The oral examination assesses clinical reasoning, treatment, disposition, communication and organization through four stations, each containing two simulated emergency cases with 30 minutes allowed. Those station features do not describe the written examination.
AOBEM Emergency Medicine Certification Timeline · AOBEM Oral Exam
Does the legacy clinical examination apply to new applicants?
The clinical examination applies only to candidates approved to sit for the written examination before September 1, 2013. Initial applicants from September 1, 2013 onward do not need that component. Its separate case-category list is not the current written blueprint.
How closely do these materials reproduce the blueprint?
The 60 concepts cover every official domain with approximate weighting. The 20 questions and 20 cards each cover all 18 domains, with an additional item in each 9% domain. Small learning sets cannot reproduce every percentage exactly. All subtopic choices are editorial selections. The official written-exam outline remains the full examination scope.
These independently authored educational materials address the written component of United States osteopathic specialty board certification. They are not official examination items or a general medical licensing examination. The accompanying four-option drills support learning and do not predict examination performance.
Outline used: Undated live AOBEM Primary Certification written-exam content outline, accessed 2026-10-10. No outline version or effective date is stated. The workbook label 'American Osteopathic Board of Emergency Medicine - Certification' maps to primary certification in Emergency Medicine; these materials target its officially named Emergency Medicine Written (Part I) Exam. The assigned slug is preserved. The linked January 2020 handbook is historical supporting context, not the current weighted outline.
60 key concepts: understand, apply and avoid the traps
Work through the questions by exam domain. Explain the answer in your own words, try the example, then check the common pitfall.
Abdominal and gastrointestinal disorders9%
1.Which findings establish acute pancreatitis without immediate CT?
Acute pancreatitis is usually established by two of three findings: characteristic abdominal pain, pancreatic enzymes exceeding three times the upper limit of normal, and characteristic imaging. When typical pain and the enzyme criterion are present, CT is unnecessary merely to confirm the diagnosis. The important distinction is between establishing pancreatitis and investigating uncertainty or complications. An isolated enzyme elevation without compatible symptoms requires a broader differential.
Apply it
A patient has persistent epigastric pain radiating to the back and lipase six times the laboratory upper limit. With stable physiology and no competing diagnosis, begin treatment and assess biliary causes rather than ordering confirmatory CT.
Common pitfall: Do not require all three diagnostic features. Conversely, a modest lipase elevation alone does not establish pancreatitis or explain every episode of abdominal pain.
ACG Guideline Highlights: Acute Pancreatitis, 2024 · American College of Gastroenterology Guidelines: Management of Acute Pancreatitis - PMC
2.When does CT add value in acute pancreatitis?
Routine admission CT is discouraged when pancreatitis is already clinically established. Imaging becomes useful when the diagnosis remains uncertain or the patient fails to improve after approximately 48–72 hours of treatment. This timing helps distinguish uncomplicated early inflammation from evolving complications. Ultrasound serves a different purpose by evaluating biliary disease. Imaging should answer a specific unresolved question rather than substitute for repeated assessment of perfusion and organ function.
Apply it
A patient with established pancreatitis remains febrile, increasingly uncomfortable and unable to tolerate intake after three days of treatment. CT now addresses complications or an alternative diagnosis rather than simply confirming the original diagnosis.
Common pitfall: An early CT can provide false reassurance about complications that have not developed. Do not order it routinely solely because pancreatitis warrants admission.
3.How should early pancreatitis fluid treatment be individualized?
Pancreatitis can cause intravascular depletion through vomiting, reduced intake and inflammatory fluid shifts. Early isotonic crystalloid treatment should restore perfusion, with lactated Ringer solution generally preferred. Moderately aggressive resuscitation requires reassessment rather than an unchecked infusion. Follow blood pressure, urine output, blood urea nitrogen and signs of congestion. Cardiac or renal disease increases the importance of smaller adjustments because excess fluid can worsen pulmonary and tissue edema.
Apply it
A patient with pancreatitis, tachycardia and poor intake receives crystalloid. After blood pressure improves, new crackles and increasing oxygen needs prompt reassessment of further fluid administration instead of automatic continuation at the initial rate.
Common pitfall: Persistent tachycardia does not always mean additional fluid is beneficial. Pain, inflammation and developing respiratory complications may produce the same finding despite adequate circulating volume.
ACG Guideline Highlights: Acute Pancreatitis, 2024 · American College of Gastroenterology Guidelines: Management of Acute Pancreatitis - PMC
4.When should oral feeding resume in mild pancreatitis?
Mild acute pancreatitis does not require prolonged fasting until pancreatic enzymes normalize. Early oral feeding, generally within 24–48 hours as tolerated, supports recovery when nausea, vomiting and pain permit intake. A low-fat solid diet can be used without a mandatory clear-liquid progression. The decision depends on clinical tolerance and severity, not the persistence of an elevated lipase. Patients unable to eat require a separate nutrition assessment.
Apply it
The next morning, a patient with mild pancreatitis has improving pain, no vomiting and an appetite, although lipase remains elevated. Offer a tolerated low-fat meal rather than waiting for the laboratory value to normalize.
Common pitfall: Do not force oral intake through persistent vomiting or ileus. Early feeding means feeding when tolerated, not ignoring evidence that the gastrointestinal tract cannot manage intake.
5.How does upper gastrointestinal bleeding risk affect disposition and endoscopy?
Upper gastrointestinal bleeding requires stabilization followed by structured risk assessment. A Glasgow-Blatchford score of 0–1 can identify very-low-risk patients suitable for discharge with outpatient follow-up when the overall clinical situation supports it. Hospitalized patients generally undergo endoscopy within 24 hours of presentation. Risk scoring does not replace resuscitation, and endoscopy timing should not encourage transporting an inadequately stabilized patient directly to a procedure.
Apply it
A stable patient with a small episode of hematemesis has a calculated Glasgow-Blatchford score of zero, no ongoing bleeding and reliable follow-up. Consider outpatient management; a shocked patient requires resuscitation and hospital-based evaluation.
Common pitfall: A normal initial hemoglobin does not exclude significant acute hemorrhage. Do not let one laboratory value override hypotension, ongoing blood loss or a concerning clinical trajectory.
ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding · ACG Clinical Guideline: Upper Gastrointestinal... : American Journal of Gastroenterology
Cardiovascular disorders9%
6.When does an unstable tachyarrhythmia require synchronized cardioversion, and when is an unsynchronized shock necessary?
A tachyarrhythmia causing hypotension, altered mental status, shock, ischemic chest discomfort or acute heart failure requires prompt electrical treatment. Use synchronized cardioversion when a pulse is present and the rhythm can be reliably synchronized, as with regular narrow-complex tachycardia or monomorphic ventricular tachycardia. Synchronization times the discharge to the QRS complex, avoiding the vulnerable ventricular repolarization period when a shock could provoke ventricular fibrillation. Sustained polymorphic ventricular tachycardia requires an immediate unsynchronized shock, even when a pulse is present, because its changing complexes prevent reliable synchronization. If synchronization cannot be achieved promptly during critical deterioration, deliver an unsynchronized shock rather than prolonging the delay.
Apply it
A patient with a regular narrow-complex rhythm at 190 beats/min, blood pressure 72/40 mm Hg and confusion needs immediate synchronized cardioversion when the arrhythmia explains the instability. A patient with sustained polymorphic ventricular tachycardia and a palpable pulse instead needs immediate unsynchronized shock. Sedate a conscious patient when feasible without delaying treatment.
Common pitfall: A pulse or an organized rhythm alone does not establish that synchronization is appropriate. Confirm reliable synchronization markers when synchronized cardioversion is indicated. Do not delay urgent electrical treatment for medication trials or repeated unsuccessful synchronization attempts. Establish that the arrhythmia causes the instability: sinus tachycardia from hemorrhage or sepsis requires treatment of the underlying cause.
7.Why is ventricular fibrillation treated with immediate defibrillation?
Ventricular fibrillation represents disorganized ventricular electrical activity without effective circulation. Defibrillation can terminate that activity, while high-quality compressions support coronary and cerebral perfusion between shocks. Deliver a shock promptly when a defibrillator is ready, then resume CPR immediately rather than pausing to search for a pulse. Repeated interruptions reduce perfusion and compromise the conditions needed for successful resuscitation. Medication and vascular access must not postpone defibrillation.
Apply it
A monitored patient collapses, has no pulse and displays ventricular fibrillation. With pads already attached, deliver an unsynchronized shock and immediately restart compressions rather than waiting for intravenous access or a postshock pulse check.
Common pitfall: Synchronized cardioversion requires organized complexes for timing and is inappropriate for ventricular fibrillation. Searching for synchronization can delay the shock that the patient needs.
8.How does treatment differ for pulseless electrical activity?
Pulseless electrical activity is organized electrical activity without a detectable pulse. It is a nonshockable arrest rhythm: treatment centers on high-quality CPR, epinephrine as soon as feasible and correction of reversible causes. Electrical activity alone does not establish effective mechanical contraction. Defibrillation is reserved for a shockable rhythm if one develops. Rhythm reassessment should occur within the resuscitation sequence without repeated prolonged interruptions to compressions.
Apply it
An unresponsive patient has no pulse despite an organized rhythm on the monitor. Begin CPR, give epinephrine promptly through available access and investigate causes such as hypovolemia or tension pneumothorax rather than shocking the tracing.
Common pitfall: An organized monitor rhythm is not return of spontaneous circulation. Confirm circulation clinically and with appropriate monitoring before stopping compressions or switching to post-arrest care.
9.Which findings make bradycardia an emergency?
Bradycardia requires urgent treatment when it causes poor perfusion, such as hypotension, altered consciousness, ischemic discomfort or acute heart failure. A slow rate without symptoms may not require emergency rate correction. Atropine is an initial treatment option; if ineffective, transcutaneous pacing or an appropriate chronotropic infusion can support circulation. Simultaneously investigate reversible causes, including hypoxia, ischemia, electrolyte abnormalities and medication effects. Clinical compromise matters more than the number alone.
Apply it
A patient with a heart rate of 32 beats/min is hypotensive and nearly syncopal. After initial atropine fails, initiate pacing or an appropriate infusion while evaluating the conduction disturbance and potentially reversible contributors.
Common pitfall: Do not repeatedly observe deteriorating perfusion because the patient initially remained awake. Conversely, an asymptomatic athlete with a slow pulse does not automatically need atropine.
10.When is adenosine appropriate for a regular narrow-complex tachycardia?
In a stable patient with a regular narrow-complex tachycardia, vagal maneuvers and adenosine can interrupt an atrioventricular node-dependent reentry circuit. Transient atrioventricular block may also clarify underlying atrial activity. This approach requires rhythm characterization and monitoring, not simply recognition of a fast pulse. Hemodynamic instability shifts treatment toward synchronized cardioversion. An irregular or polymorphic wide-complex rhythm falls outside the straightforward regular narrow-complex pathway.
Apply it
A comfortable patient with normal blood pressure develops an abrupt regular narrow-complex rhythm at 180 beats/min. After an appropriate vagal maneuver fails, monitored adenosine is reasonable while recording the rhythm response for diagnostic information.
Common pitfall: Do not apply an adenosine pathway indiscriminately to every tachycardia. Irregularity, a broad polymorphic appearance or instability changes the relevant risks and treatment choices.
11.How should reversible causes guide medical and traumatic arrest treatment?
Medical arrest care combines the rhythm algorithm with treatment of reversible mechanisms, including hypoxia, hypovolemia, electrolyte disorders, hypothermia, tamponade, tension pneumothorax, toxins and thrombosis. Traumatic arrest requires particular priority for hemorrhage control, oxygenation, chest decompression and relief of tamponade when indicated. Continue compressions when they do not delay or prevent correction of those causes. Compressions cannot adequately compensate for uncontrolled hemorrhage or an unrelieved mechanical obstruction to circulation.
Apply it
After penetrating chest trauma with arrest, the team prioritizes hemorrhage control, oxygenation and immediate treatment of suspected thoracic obstruction. Compressions continue when compatible with those interventions but must not postpone a necessary decompression or tamponade-relieving procedure.
Common pitfall: Do not impose a medical-arrest sequence so rigidly that it delays correction of the cause of traumatic arrest. A list of reversible causes is useful only when it leads to timely action.
2025 AHA Adult Cardiac Arrest Circular Algorithm · Special circumstances Guidelines | Resuscitation Council UK
Cutaneous disorders3%
12.Which clues demand urgent evaluation for necrotizing soft tissue infection?
Necrotizing soft tissue infection spreads along deeper tissue planes and can initially resemble cellulitis. Severe pain disproportionate to visible findings, rapid progression, systemic toxicity, bullae, skin necrosis or crepitus should raise concern. Early surgical consultation and broad antimicrobial treatment are essential because devitalized tissue requires operative source control. Imaging may help an uncertain stable presentation, but strong clinical suspicion should not wait for imaging confirmation or dramatic surface changes.
Apply it
A patient with a small erythematous thigh lesion develops rapidly worsening deep pain, hypotension and tense swelling. Arrange immediate surgical evaluation and antimicrobial treatment rather than treating the limited skin redness as uncomplicated cellulitis.
Common pitfall: Absence of gas or crepitus does not exclude necrotizing infection. Waiting for these later findings can postpone the intervention most likely to control the source.
13.Why is drainage central to treatment of a cutaneous abscess?
An abscess contains a localized collection of pus that usually requires incision and drainage for source control. Antibiotics alone may not adequately address the enclosed collection. Additional antimicrobial treatment depends on systemic illness, host defenses, treatment failure and other clinical features. Distinguish a drainable purulent focus from diffuse nonpurulent cellulitis because the primary intervention differs. Adequate drainage remains important even when an antibiotic is also indicated.
Apply it
A patient has a fluctuant, tender skin collection with surrounding erythema. Confirm that a drainable cavity is present and perform appropriate drainage; fever or significant immunocompromise would additionally influence the need for systemic antibiotics.
Common pitfall: Do not substitute a broader antibiotic for drainage of an accessible abscess. Conversely, cutting diffuse cellulitis without a collection does not provide useful source control.
Endocrine, metabolic and nutritional disorders5%
14.How is euglycemic DKA recognized and treated safely?
The 2024 adult consensus requires diabetes or glucose at least 200 mg/dL, ketosis and metabolic acidosis for DKA. Blood beta-hydroxybutyrate at least 3.0 mmol/L supports ketosis; pH below 7.3 or bicarbonate below 18 mmol/L establishes the acidosis component. Known diabetes allows diagnosis despite glucose below 200 mg/dL. SGLT2-associated urinary glucose loss can mask the glucose rise while ketogenesis continues. Stop the SGLT2 inhibitor, replace fluid and electrolytes, and delay insulin if potassium is below 3.5 mmol/L until it exceeds that threshold. Subsequent insulin treatment of euglycemic DKA requires concurrent dextrose and frequent glucose monitoring. Blood beta-hydroxybutyrate is preferable to urine ketones, which mainly detect acetoacetate and can remain positive during recovery.
Apply it
A patient with established type 2 diabetes taking dapagliflozin has vomiting, glucose 172 mg/dL, beta-hydroxybutyrate 5.2 mmol/L, bicarbonate 12 mmol/L and potassium 3.1 mmol/L. Treat euglycemic DKA, replacing potassium before insulin; once potassium permits insulin, provide dextrose concurrently and monitor glucose and electrolytes.
Common pitfall: SGLT2 inhibitor use alone does not establish diabetes because these drugs also treat heart failure and kidney disease. Neither modest glucose nor persistent urine ketones should override the relevant history, blood ketones and acid-base findings.
Hyperglycaemic Crises in Adults With Diabetes: A Consensus Report, 2024 · These highlights do not include all the information needed to use FARXIGA safely and effectively. See full prescribing information for FARXIGA. FARXIGA® (dapagliflozin) tablets, for oral useInitial U.S. Approval: 2014
15.Which four criteria establish HHS, and why must correction be controlled?
HHS requires all four criteria: plasma glucose at least 600 mg/dL; effective serum osmolality above 300 mOsm/kg or total serum osmolality above 320 mOsm/kg; beta-hydroxybutyrate below 3.0 mmol/L; and pH at least 7.3 with bicarbonate at least 15 mmol/L. Residual insulin limits ketogenesis but cannot prevent severe hyperglycemia and osmotic diuresis. Treatment requires fluid, insulin and electrolyte management with repeated reassessment. Limit the fall in osmolality to 3–8 mOsm/kg per hour. These diagnostic thresholds are also stated in [ADA Standards of Care 2026, Table 16.1](https://diabetesjournals.org/care/article/49/Supplement_1/S339/163925/16-Diabetes-Care-in-the-Hospital-Standards-of-Care).
Apply it
An older adult has confusion and dehydration with glucose 850 mg/dL, effective osmolality 335 mOsm/kg, beta-hydroxybutyrate 1.2 mmol/L, venous pH 7.36 and bicarbonate 22 mmol/L. All four HHS criteria are present. Monitor osmolality, electrolytes and cognition during controlled correction.
Common pitfall: Very high glucose alone establishes neither HHS nor an isolated hyperosmolar crisis. Significant ketonemia or acidosis requires assessment for overlapping DKA or another acid-base disorder.
Hyperglycaemic Crises in Adults With Diabetes: A Consensus Report, 2024
16.Why can combined diabetes medications increase hypoglycemia risk?
Insulin and insulin secretagogues, including sulfonylureas, can cause hypoglycemia. Dapagliflozin increases urinary glucose excretion and can increase hypoglycemia risk when combined with these treatments. Its prescribing information advises considering a lower insulin or secretagogue dose when used together. Distinguish the risk of a combination regimen from the effects of dapagliflozin alone, and use documented glucose measurements and the medication history to guide reassessment.
Apply it
A patient taking insulin and dapagliflozin reports recurrent measured low glucose after a treatment change. Review the combination and consider reducing the insulin regimen rather than assuming that every component has the same intrinsic hypoglycemia risk.
Common pitfall: Do not reduce or omit insulin indiscriminately in an SGLT2-treated patient. Under-insulinization is also a recognized precipitant of ketoacidosis, so changes require a coherent diabetes treatment plan.
Environmental disorders4%
17.Which finding distinguishes heat stroke from uncomplicated heat exhaustion?
Heat stroke is a life-threatening heat illness characterized by severe overheating with central nervous system dysfunction, such as confusion, seizures or loss of consciousness. Sweating may persist, especially in exertional heat stroke, so dry skin is not required. Heat exhaustion can cause weakness, nausea and heavy sweating without the same neurologic emergency. A concerning exposure and altered mental status should trigger immediate cooling and emergency treatment rather than observation for skin dryness.
Apply it
A runner collapses during a hot race, is confused and remains drenched in sweat. Treat the presentation as suspected exertional heat stroke and begin rapid cooling while activating emergency care and assessing other immediate threats.
Common pitfall: Sweating does not rule out heat stroke. Waiting for anhidrosis or a perfectly documented temperature can delay treatment in a neurologically impaired, overheated patient.
18.How should immediate cooling be started in suspected heat stroke?
Rapid removal of excess body heat is central to heat stroke treatment because ongoing hyperthermia can injure the brain and other organs. Move the patient from heat, remove unnecessary clothing and begin active cooling immediately. Cold-water or ice-water immersion is an effective option when feasible; other available cooling methods should begin if immersion cannot be arranged promptly. Cooling and emergency assessment proceed together rather than waiting for transport or laboratory confirmation.
Apply it
At a sports event, a confused collapsed athlete is brought to a shaded medical area. Staff activate emergency services and begin available rapid cooling immediately, arranging cold-water immersion while maintaining observation and essential airway support.
Common pitfall: Antipyretics do not correct the heat load mechanism of heat stroke. Do not delay physical cooling while attempting to treat the temperature as infectious fever.
Head, ear, nose and throat disorders5%
19.How and for how long should an anterior nosebleed be compressed?
Have the patient sit upright, lean forward and pinch all the soft lower parts of the nose against the septum. Maintain uninterrupted compression for at least five minutes before reassessment. ENT Health advises another ten minutes of compression if bleeding continues. Pressure on the bony bridge misses the usual anterior source, while repeated release disrupts clot formation. Persistent bleeding requires escalation; airway obstruction, impaired airway protection or circulatory compromise requires immediate intervention without waiting for the compression interval.
Apply it
A stable adult pinches the hard bridge and tilts backward. Demonstrate soft-nose compression while leaning forward, time five uninterrupted minutes, and repeat for another ten minutes if needed while reassessing severity.
Common pitfall: Blood disappearing from the nostrils does not prove hemostasis when the head is tilted backward. It may instead be draining into the pharynx.
20.Which clues suggest a posterior nasal bleeding source?
Posterior epistaxis originates deeper in the nasal cavity and may produce brisk bleeding into the throat, bleeding from both nostrils or failure of appropriate anterior measures. These features raise concern but do not locate the source with certainty. Assess airway protection, hemodynamics and ongoing blood loss while obtaining appropriate specialist assistance. Deep bleeding is harder to control with simple anterior compression and may require more intensive intervention and observation.
Apply it
An older patient continues to swallow blood despite correct anterior compression, and no accessible anterior focus is seen. Reassess airway and circulation and arrange specialist evaluation for a possible posterior source rather than repeating ineffective compression indefinitely.
Common pitfall: Bilateral bleeding alone does not definitively diagnose a posterior source. Use the overall bleeding pattern, examination and response to treatment to guide escalation.
21.How should acute upper-airway involvement in anaphylaxis be treated?
Rapidly developing airway compromise after a likely allergen exposure can represent anaphylaxis even without skin changes. Stop the trigger when feasible, give intramuscular epinephrine promptly and mobilize airway support. RCUK 2025 recommends 500 micrograms intramuscularly for adults, using the 1 mg/mL preparation, repeated after five minutes if improvement is inadequate. Assess breathing and circulation concurrently; give crystalloid for circulatory compromise.
Apply it
An adult develops throat swelling and difficult breathing immediately after an antibiotic. Give intramuscular epinephrine and prepare airway support even though there is no visible rash.
Common pitfall: Absence of urticaria does not exclude anaphylaxis. The intramuscular anaphylaxis regimen must not be confused with intravenous cardiac-arrest dosing.
Hematologic and immune system disorders3%
22.How are the four components of the 4Ts score assigned?
Assign 2, 1 or 0 points to each component. Platelets: 2 for a fall greater than 50% with nadir at least 20 × 10^9/L; 1 for a 30–50% fall or nadir 10–19; 0 for a fall below 30% or nadir below 10. Timing: 2 for clear onset on days 5–14 or within one day with exposure in the preceding 30 days; 1 for compatible but unclear timing, onset after day 14, or onset within one day with exposure 30–100 days earlier; 0 for onset within four days without recent exposure. Thrombosis: 2 for confirmed new thrombosis, skin necrosis, an acute systemic reaction after IV heparin or adrenal hemorrhage; 1 for progressive, recurrent or suspected thrombosis or nonnecrotizing skin lesions; 0 for none. Other causes: 2 if none apparent, 1 if possible, 0 if definite. Totals 0–3, 4–5 and 6–8 indicate low, intermediate and high probability.
Apply it
Platelets fall from 310 to 130 × 10^9/L on day seven, with new confirmed thrombosis and no alternative cause. The greater-than-50% fall with nadir above 20 earns 2; timing earns 2; thrombosis earns 2; no alternative earns 2. Total: 8, high probability.
Common pitfall: A near-normal absolute platelet count does not exclude HIT. Establish the relative fall, exposure dates and competing causes accurately.
ASH Pocket Guide: Diagnosis and Management of Heparin-Induced Thrombocytopenia
23.What treatment is required when HIT probability is high?
High-probability HIT requires stopping heparin exposure and starting an appropriate nonheparin anticoagulant while diagnostic testing proceeds. Simply stopping heparin leaves a substantial thrombotic risk because pathogenic platelet activation continues. Review all heparin sources, including flushes, and choose an alternative according to organ function, bleeding risk and clinical stability. Laboratory confirmation refines management, but waiting untreated for confirmatory results is inappropriate when the clinical probability is high.
Apply it
A patient develops a new deep venous thrombosis and a typical platelet fall during heparin treatment. Stop heparin, eliminate heparin flushes and initiate suitable nonheparin anticoagulation while sending the recommended immunologic and confirmatory testing.
Common pitfall: Switching from unfractionated to low-molecular-weight heparin does not solve immune HIT. Both remain heparin products and can sustain the pathogenic reaction.
ASH Pocket Guide: Diagnosis and Management of Heparin-Induced Thrombocytopenia
Systemic infectious disorders7%
24.Which vasopressor is preferred first in septic shock?
Norepinephrine is the first-line vasopressor for septic shock when circulatory support is needed. Its predominant vasoconstrictor effect helps counter infection-associated vasodilation and restore arterial pressure. Vasopressor treatment complements antimicrobial therapy, source control and individualized fluid assessment; it does not correct the infection itself. Persistent hypotension should prompt timely support rather than unlimited fluid administration, especially when additional fluid is unlikely to improve flow or is causing congestion.
Apply it
A patient with infection remains hypotensive after initial fluid treatment and develops increasing lung congestion. Start norepinephrine while reassessing perfusion and the infectious source instead of giving repeated fluid solely to normalize the blood pressure.
Common pitfall: A higher blood pressure does not prove that every tissue is adequately perfused. Continue assessing mental status, urine output, skin perfusion and the overall trajectory.
25.How should fluid responsiveness be reassessed in sepsis?
After initial resuscitation, further fluid should be guided by whether it is likely to improve circulation and whether the patient can tolerate it. Dynamic assessment, such as a passive leg raise coupled to a flow measurement, can estimate a reversible preload response. Static pressure or tachycardia alone is less informative. Reassess respiratory status and congestion alongside perfusion because a patient can remain hypotensive while additional fluid creates harm.
Apply it
A hypotensive septic patient has already received crystalloid. A monitored passive leg raise produces no meaningful increase in stroke volume, while oxygen needs rise. These findings argue against repeated empiric fluid and support reassessing circulatory treatment.
Common pitfall: Fluid responsiveness is not synonymous with a requirement for fluid. Even a measurable preload response must be weighed against congestion and the patient's current perfusion needs.
26.Why must serial lactate be interpreted with the bedside examination?
Lactate elevation can reflect impaired perfusion, stress-related metabolic changes or reduced clearance. A falling value during resuscitation may support improvement, but neither a single high value nor incomplete normalization identifies the exact remaining treatment need. Interpret the trend with blood pressure, capillary refill, urine output, mental status and respiratory findings. Repeated fluid administration aimed only at normalizing lactate can be inappropriate when perfusion has improved and congestion is developing.
Apply it
After treatment, a patient's blood pressure, urine output and alertness improve, but lactate remains mildly elevated and crackles appear. Reevaluate the cause and overall perfusion rather than automatically prescribing another fluid bolus to chase the number.
Common pitfall: A normal lactate does not independently exclude serious infection or circulatory dysfunction. Conversely, persistent elevation does not prove that intravascular volume remains inadequate.
27.How do antimicrobial treatment and source control work together in sepsis?
Antimicrobials reduce susceptible pathogens, whereas source control removes or corrects an anatomic focus that can sustain infection. An abscess, obstructed infected system or infected device may remain dangerous despite appropriate antibiotics. Identify source-control needs early and coordinate intervention while resuscitation continues. Obtain useful cultures when doing so does not meaningfully delay urgent treatment. Selection and subsequent refinement of antibiotics depend on the likely source, pathogen risks and available microbiology.
Apply it
A patient with septic shock has an obstructed infected urinary collecting system. Begin antimicrobial and hemodynamic treatment while arranging urgent drainage, because improving antibiotic coverage alone cannot reliably resolve the obstructed source.
Common pitfall: Do not interpret a temporary blood pressure improvement as proof that source control is unnecessary. An untreated focus can cause recurrent deterioration despite initial resuscitation.
Musculoskeletal disorders (nontraumatic)5%
28.When should a suspected septic native joint be aspirated?
Suspected septic arthritis requires prompt synovial fluid sampling because microbiologic identification guides treatment and the joint can sustain rapid damage. In a clinically stable patient, obtain the aspirate before starting antibiotics to preserve culture yield. This sequence changes in sepsis or septic shock, where antimicrobial treatment must not be delayed for sampling. Send fluid for bacterial identification, cell count and crystal assessment while arranging appropriate orthopedic evaluation.
Apply it
A stable patient has an atraumatic hot swollen knee and restricted motion. Arrange prompt aspiration before antibiotics. If the same patient becomes hypotensive with systemic infection, begin urgent antimicrobial treatment without waiting for the procedure.
Common pitfall: Normal peripheral blood tests cannot reliably exclude septic arthritis. Do not cancel aspiration solely because the circulating leukocyte count or inflammatory markers are unremarkable.
EBJIS Guideline for Management of Septic Arthritis in Native Joints
29.How should crystals, synovial leukocytes and Gram stain be interpreted together?
Crystal arthritis and bacterial infection can coexist. Urate or calcium pyrophosphate crystals identify an inflammatory mechanism but do not exclude infection. A synovial leukocyte count above 50,000 cells/µL increases suspicion without establishing the diagnosis; lower counts do not exclude infection, particularly in immunosuppressed patients. A positive Gram stain can rapidly support infection, but a negative result has insufficient sensitivity for exclusion. Integrate these findings with cultures and the clinical course.
Apply it
An immunosuppressed patient has fever and a hot knee. Fluid contains urate crystals, 22,000 leukocytes/µL and no organisms on Gram stain. Continue cultures and urgent infection assessment because none of these findings safely excludes concurrent septic arthritis.
Common pitfall: The 50,000-cell threshold is not a binary boundary. Crystals, negative Gram stain or temporary improvement with anti-inflammatory therapy must not override sustained clinical concern for infection.
EBJIS Guideline for Management of Septic Arthritis in Native Joints
30.When should focal muscle pain and fever suggest pyomyositis?
Pyomyositis is bacterial infection with pus within skeletal muscle, commonly caused by Staphylococcus aureus. Localized deep muscle pain, tenderness and fever may occur without superficial fluctuance. MRI best defines the muscular infection and associated collections. Obtain blood and abscess cultures, begin empiric vancomycin and drain purulent material early. Immunocompromise or open muscle trauma warrants additional enteric gram-negative coverage.
Apply it
A patient with diabetes has fever and deep thigh tenderness without a visible skin abscess. MRI identifies an intramuscular collection. Arrange drainage, cultures and intravenous antimicrobial treatment.
Common pitfall: Normal creatine kinase and absence of superficial fluctuance do not exclude a deep muscle abscess. Persistent bacteremia should prompt reassessment for undrained infection.
Nervous system disorders7%
31.Who is eligible for the Ottawa subarachnoid hemorrhage rule, and when must it not be used?
Apply the Ottawa SAH rule only to patients aged at least 16 years with GCS 15, a normal neurologic examination and a new severe nontraumatic headache reaching maximum intensity within one hour, who present within 14 days of onset. Exclusions include direct head trauma within the preceding seven days; papilledema; new focal neurologic deficits; known cerebral aneurysm, previous SAH, brain neoplasm, hydrocephalus or ventricular shunt; an established recurrent headache syndrome with at least three similar episodes over at least six months; referral with confirmed SAH; and reassessment of the same headache after investigation with both CT and lumbar puncture. In eligible patients, investigate for SAH if any criterion is present: age at least 40 years, neck pain or stiffness, witnessed loss of consciousness, onset during exertion, thunderclap headache with instantly peaking pain, or limited neck flexion on examination. A positive rule indicates investigation, not a diagnosis of SAH.
Apply it
A 46-year-old presents two hours after a first severe headache that peaked instantly during exercise. GCS is 15, the neurologic examination is normal and no exclusion applies. Age, exertional onset and thunderclap onset each independently make the rule positive. Conversely, a 30-year-old with no positive criteria who presents 16 days after onset is outside the validated population; the apparent negative result cannot justify withholding investigation.
Common pitfall: Check eligibility before scoring the six criteria. Papilledema, known hydrocephalus or a ventricular shunt prevents use of the rule even when strength, sensation and consciousness are normal. Patients outside the validated population require assessment independent of the rule. A negative result in an eligible patient addresses SAH risk only; it does not exclude other dangerous headache causes. Returning after completed CT-plus-LP investigation also requires reassessment independent of this rule.
ACEP Clinical Policy: Acute Headache, 2019 · validation-of-sah.pdf
32.How do CT timing and residual risk determine further SAH testing?
ACEP supports a normal noncontrast head CT within six hours of symptom onset to exclude nontraumatic SAH in selected patients with a normal neurologic examination and appropriate imaging quality and interpretation. When concern persists after negative CT, use lumbar puncture or CT angiography with shared decision-making. LP assesses cerebrospinal fluid but can yield traumatic or ambiguous results; CTA adds contrast and radiation and can reveal incidental aneurysms. Analgesic improvement does not exclude hemorrhage or replace indicated investigation.
Apply it
A neurologically intact patient presents 18 hours after an instantly maximal headache. Despite negative CT and pain relief, discuss LP or CTA because the presentation does not meet the early-CT timing condition and concern persists.
Common pitfall: Measure six hours from headache onset, not arrival. An incidental aneurysm does not by itself prove hemorrhage, and a favorable response to a migraine regimen does not establish a primary headache.
33.How should suspected bacterial meningitis be evaluated and treated after a negative head CT?
A negative head CT or arterial CTA does not exclude meningitis; cerebrospinal fluid testing evaluates meningeal infection. Suspected bacterial meningitis warrants prompt empiric intravenous antibiotics regardless of whether sepsis is present. Obtain blood cultures promptly, preferably before antibiotics, without delaying treatment. Perform lumbar puncture first only when safe and without clinically significant treatment delay; never wait for CSF results before starting antibiotics. Defer lumbar puncture for a known or suspected bleeding disorder, infection overlying or near the puncture site, or hemodynamic or respiratory compromise requiring stabilization. WHO recommends cranial imaging before lumbar puncture for Glasgow Coma Score below 10, focal neurological signs, cranial nerve deficits, papilledema, new-onset seizures in adults or severe immunocompromise. These features raise concern for intracranial pathology, including a space-occupying lesion with midline shift. Give antibiotics while imaging or deferred lumbar puncture is arranged.
Apply it
An adult with fever, headache and neck stiffness has normal blood pressure and no evidence of sepsis. If lumbar puncture will be substantially delayed, obtain blood cultures promptly and start empiric intravenous antibiotics immediately. If the patient is stable, has no contraindication or imaging trigger, and lumbar puncture is immediately available, collect CSF before antibiotics. A new focal deficit instead requires imaging before lumbar puncture while treatment proceeds.
Common pitfall: A normal CT neither establishes lumbar-puncture safety nor removes the urgency of treatment. It does not resolve bleeding risk, local infection or cardiorespiratory instability. Cranial imaging is not routinely required before lumbar puncture when the specified risk features are absent. Reduced CSF culture yield after antibiotics is a diagnostic disadvantage, but preserving culture yield must never justify a clinically significant treatment delay.
ACEP Clinical Policy: Acute Headache, 2019 · Surviving Sepsis Campaign Adult Guidelines, 2026 · Meningitis · epi-win_overview-of-meningitis-guidelines_final.pdf
34.What neurologic deterioration during DKA or HHS treatment suggests cerebral edema?
New or worsening impaired consciousness during treatment of DKA or HHS requires urgent assessment for cerebral edema and other causes. Rapid osmotic shifts may contribute. Recheck glucose, reassess the neurologic examination and obtain urgent brain imaging with critical care support. The adult consensus suggests mannitol and ventilatory support for cerebral edema. Controlled correction of hyperosmolality reduces neurologic risk.
Apply it
A patient becomes newly obtunded during HHS treatment despite improving glucose. Reassess glucose and osmolality immediately and evaluate for cerebral edema rather than assuming biochemical improvement guarantees neurologic recovery.
Common pitfall: Do not attribute new obtundation automatically to sedation. Opioid respiratory depression and local anesthetic-associated seizures require the distinct treatments in the toxicology concepts.
Hyperglycaemic Crises in Adults With Diabetes: A Consensus Report, 2024
Obstetrics and gynecology disorders6%
35.Which findings suggest a ruptured ectopic pregnancy?
An ectopic pregnancy can rupture and cause major intraperitoneal hemorrhage. Pregnancy-associated abdominal pain with collapse, hypotension, shoulder-tip pain or peritoneal irritation should raise immediate concern. Visible vaginal bleeding may be limited despite substantial internal blood loss. Stabilization, blood support when indicated and urgent gynecologic surgical management take priority over prolonged outpatient-style diagnostic sequencing. A low hCG concentration does not make a clinically suspected rupture safe to observe.
Apply it
A patient with a positive pregnancy test develops unilateral abdominal pain, shoulder-tip discomfort and hypotension. Begin resuscitation and obtain emergency gynecologic intervention rather than waiting for serial hCG measurements to clarify the pregnancy's behavior.
Common pitfall: Do not estimate internal blood loss from the amount of vaginal bleeding. A patient can have severe intraperitoneal hemorrhage with little external bleeding.
36.How should pregnancy of unknown location be followed safely?
A positive pregnancy test without a pregnancy located on ultrasound is pregnancy of unknown location. Possibilities include an early intrauterine pregnancy, a resolving pregnancy and an ectopic pregnancy. Stable patients need structured serial hCG assessment and repeat ultrasound with explicit emergency precautions. A single hCG cannot establish location, and a falling value does not immediately establish resolution or eliminate rupture risk. Continue surveillance until resolution or location is established by the treating service.
Apply it
A stable patient has nondiagnostic ultrasound and later a falling hCG. Continue planned surveillance. New severe pain, syncope or shoulder-tip pain requires urgent reassessment despite the favorable laboratory trend.
Common pitfall: An empty uterus does not prove ectopic pregnancy. Present stability permits a monitored pathway; it does not guarantee that later rupture cannot occur.
37.Which findings establish medical eligibility for methotrexate treatment of ectopic pregnancy?
Methotrexate inhibits folate-dependent DNA synthesis in proliferating trophoblast. ACOG Practice Bulletin 193 supports its use for selected stable patients with an unruptured ectopic pregnancy and reliable follow-up, after reasonably excluding an intrauterine pregnancy. Assess complete blood count, renal function and hepatic function. Absolute exclusions include clinically important renal or hepatic dysfunction, significant anemia, leukopenia or thrombocytopenia, immunodeficiency, breastfeeding, active pulmonary disease, active peptic ulcer disease, methotrexate sensitivity, rupture, instability and inability to participate in follow-up. High initial hCG, embryonic cardiac activity and ectopic size greater than 4 cm predict reduced success and are relative contraindications, not universal absolute cutoffs. Serial hCG surveillance remains essential.
Apply it
A stable patient has a confirmed 2-cm unruptured tubal ectopic pregnancy, hCG 1,400 mIU/mL and no embryonic cardiac activity. Blood counts, creatinine and liver transaminases are normal; there is no immunodeficiency, breastfeeding, active pulmonary disease, active ulcer disease or methotrexate allergy. Reliable follow-up is available. These findings support discussing methotrexate alongside surgical options.
Common pitfall: A favorable hCG cannot overcome an absolute contraindication. Higher hCG increases failure risk but does not create a universal prohibition at one number. An empty uterus alone does not justify treatment.
38.When is resuscitative delivery indicated during maternal cardiac arrest?
AHA 2025 indicates resuscitative delivery when the uterine fundus is at or above the umbilicus and standard resuscitation does not achieve return of spontaneous circulation. Begin preparation at arrest recognition, aiming to complete delivery by five minutes. For in-hospital arrest, perform it at the arrest site rather than transferring to an operating room. Continue CPR with manual left uterine displacement and prioritize oxygenation. Delivery relieves aortocaval compression and improves maternal venous return and circulation. RCUK 2025 uses its own wording: relieve compression above 20 weeks, prepare early and perform resuscitative hysterotomy as soon as possible at the arrest site.
Apply it
A patient at 30 weeks arrests in the emergency department with the fundus above the umbilicus. Begin standard resuscitation, assign manual uterine displacement and prepare for delivery immediately. If ROSC is not achieved, perform resuscitative delivery at the arrest location with a goal of completion by five minutes.
Common pitfall: Five minutes is a delivery goal, not a reason to wait before preparation. The intervention supports maternal resuscitation; it must not depend on transfer to an operating room or delay essential CPR.
2025 AHA Guidelines: Special Circumstances of Resuscitation · Special circumstances Guidelines | Resuscitation Council UK
Psychobehavioral disorders4%
39.What immediate action follows current suicidal thoughts in the emergency department?
Current suicidal thoughts require immediate safety measures and urgent mental health evaluation. The patient should not leave before appropriate assessment, and potentially dangerous items should be secured according to the care setting's procedures. Ask directly about thoughts, plan, intent, access to means and prior attempts. A calm manner or willingness to converse does not establish low risk. Medical stabilization and evaluation of intoxication or other contributors occur alongside protective observation.
Apply it
A patient says they intend to kill themselves after discharge and have access to a firearm. Maintain direct safety supervision, restrict access to dangerous items and arrange urgent psychiatric evaluation rather than completing routine discharge paperwork.
Common pitfall: A verbal promise to remain safe does not replace risk assessment or observation. Apparent cooperation can coexist with imminent intent and access to lethal means.
NIMH Adult Emergency Department Brief Suicide Safety Assessment Guide
40.How does a suicide safety plan support an appropriate discharge?
When assessment supports discharge, a collaborative safety plan specifies warning signs, coping strategies, supportive contacts, professional resources and steps to reduce access to lethal means. It turns general advice into actions the patient can use during escalating distress. Planning should include suitable follow-up and confirmation that the proposed supports are realistic. A safety plan complements a disposition decision; it cannot make an otherwise unsafe discharge appropriate or replace evaluation of imminent risk.
Apply it
After assessment finds no imminent intent, a patient identifies a sibling to call, coping activities and a crisis contact. The team also addresses medication storage and follow-up, checking that each part of the plan is feasible.
Common pitfall: A generic instruction to return if worse is not a complete safety plan. A no-suicide contract likewise does not establish safety or replace individualized planning.
NIMH Adult Emergency Department Brief Suicide Safety Assessment Guide
Renal and urogenital disorders5%
41.How should an infected obstructed urinary collecting system be treated?
Obstruction traps infected urine and creates a source that antibiotics alone may not control. Begin antimicrobials and resuscitation while arranging urgent drainage by ureteral stent or percutaneous nephrostomy. Neither method is universally superior; anatomy, stability, feasibility and available expertise determine the timely effective option. Definitive stone treatment is generally deferred until infection resolves. Drainage relieves the immediate emergency but may leave the stone requiring later treatment.
Apply it
A patient has fever, hypotension and hydronephrosis above a ureteral stone. Arrange emergency drainage while treating sepsis, then plan infection follow-up and definitive stone management after recovery.
Common pitfall: Analgesic improvement does not remove infected obstruction. Do not delay drainage while pursuing a theoretically preferred method or attempt routine outpatient stone passage in a septic patient.
42.How can SGLT2-associated volume depletion contribute to acute kidney injury?
Dapagliflozin can cause intravascular volume depletion with hypotension and acute changes in creatinine. Risk is greater in older adults, patients with impaired renal function and those taking loop diuretics. Assess volume status, blood pressure, renal function and the medication history when new kidney dysfunction develops. Distinguish this presentation from the small early fall in estimated GFR that can occur after starting therapy and then stabilize; an atypical or progressive change requires evaluation for acute kidney injury.
Apply it
An older patient taking dapagliflozin and a loop diuretic develops poor intake, hypotension and rising creatinine. Assess and correct volume depletion and review treatment rather than dismissing the change as an expected stable medication effect.
Common pitfall: Do not presume every creatinine increase is benign or caused by the drug alone. The time course and accompanying volume findings determine whether further acute kidney injury evaluation is needed.
43.How do stabilization, redistribution and removal differ in severe hyperkalemia?
Severe hyperkalemia with ECG changes requires intravenous calcium to counter cardiac toxicity. Calcium does not remove potassium. Insulin with glucose shifts potassium into cells; nebulized salbutamol can be an adjunct. Monitor glucose because insulin can cause hypoglycemia. These measures buy time while potassium is removed from the body. Refractory severe hyperkalemia, particularly with renal failure, may require dialysis. Follow potassium and ECG response rather than assuming that transient electrical improvement means the excess potassium is gone.
Apply it
A patient with renal failure has potassium 7.1 mmol/L and ECG abnormalities. Give cardiac membrane stabilization and potassium-shifting treatment while arranging definitive removal if severe hyperkalemia persists.
Common pitfall: Do not confuse a normalizing ECG after calcium with correction of the potassium concentration. Redistribution also leaves the total-body potassium burden present and can be followed by rebound.
Thoracic-respiratory disorders7%
44.Why can ventilation worsen circulation in life-threatening asthma?
Severe expiratory obstruction can trap air during successive positive-pressure breaths. Dynamic hyperinflation increases intrathoracic pressure and impairs venous return, potentially causing profound hypotension or arrest. Treat life-threatening hypoxia and assess for pneumothorax and anaphylaxis. In a ventilated patient with suspected dynamic hyperinflation, brief ventilator disconnection can permit exhalation and help relieve the pressure while ventilation is reassessed.
Apply it
An intubated patient with severe asthma develops sudden hypotension and difficult ventilation. Assess for tension pneumothorax and air trapping; suspected dynamic hyperinflation warrants brief disconnection to allow exhalation while the team corrects ventilation.
Common pitfall: Reflexively increasing ventilation can worsen trapped gas and circulatory compromise. Do not assume that deterioration after intubation is caused only by sedative medication.
45.How is an age-adjusted D-dimer threshold calculated and applied?
For patients older than 50 in an appropriate nonhigh-probability pathway, the studied age-adjusted cutoff is age multiplied by 10 ng/mL FEU when the assay's conventional cutoff is 500 ng/mL FEU. Thus, a 68-year-old has a threshold of 680 ng/mL FEU. Assess probability before interpreting the result; high-probability patients require an imaging-based pathway. Confirm assay units and compatibility because FEU thresholds cannot be transferred unchanged to DDU assays. A result above the applicable cutoff requires further evaluation and does not itself diagnose PE.
Apply it
A 68-year-old outpatient has nonhigh clinical probability and a high-sensitivity D-dimer of 640 ng/mL FEU under an age-adjusted protocol. Compare 640 with 680 rather than automatically applying the fixed 500 threshold. The same result cannot safely exclude PE in a high-probability presentation.
Common pitfall: D-dimer reflects fibrin breakdown from many causes. Neither a positive result nor correct arithmetic replaces the appropriate probability assessment and diagnostic pathway.
Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: ADJUST-PE
46.Why are rescue breaths central to drowning resuscitation?
Drowning produces respiratory impairment and hypoxia, so restoring ventilation is essential. After safe rescue, assess breathing and circulation and provide effective ventilations. RCUK 2025 specifies five initial ventilations, using 100% oxygen when available, followed by standard CPR when indicated. Use only the pressure needed for effective bag-mask breaths to reduce gastric inflation. Consider associated hypothermia and prioritize rescuer safety.
Apply it
After safe removal from water, an unresponsive person is not breathing normally. Start the drowning ventilation sequence and continue resuscitation according to breathing and pulse findings rather than providing a compression-only response to a primarily hypoxic event.
Common pitfall: Rescuer safety remains essential. Suspected spinal injury must not delay removal from the water when resuscitation is required.
47.Which persistent symptoms after pulmonary embolism require follow-up?
Follow-up after acute PE should address persistent breathlessness, exercise limitation and impaired functional recovery. These symptoms can reflect deconditioning, residual cardiopulmonary effects or chronic thromboembolic disease and deserve structured assessment rather than automatic attribution to anxiety. Review the trajectory, treatment and competing explanations, then arrange appropriate evaluation. The 2026 AHA guideline summary emphasizes continued attention to symptoms and function after the acute event, extending care beyond the initial anticoagulation decision.
Apply it
A patient treated for PE reports ongoing exertional dyspnea and cannot resume usual activities. Arrange follow-up assessment of persistent functional limitation rather than assuming that completed acute treatment means no further cardiopulmonary review is needed.
Common pitfall: Persistent dyspnea does not automatically diagnose recurrent PE or chronic thromboembolic pulmonary hypertension. It signals a need for evaluation, not a specific diagnosis by itself.
AHA: 2026 Acute Pulmonary Embolism Guideline—Top Things to Know
Toxicological disorders/clinical pharmacology5%
48.How do pulse status and recurrent depression guide opioid resuscitation?
With a definite pulse but inadequate breathing, provide immediate airway support and ventilation while administering naloxone. With no pulse, provide standard CPR, ventilation, rhythm analysis and indicated defibrillation; naloxone must not delay them. Continue monitoring after reversal because naloxone may wear off before the opioid. Recurrent respiratory depression can require renewed ventilation, repeat naloxone or an infusion. Adequate sustained breathing matters more than brief awakening.
Apply it
A patient with a pulse and occasional ineffective breaths receives assisted ventilation and naloxone. Later somnolence with slow breathing requires renewed support and reversal assessment, not reassurance from the earlier response.
Common pitfall: Do not wait for naloxone before supporting breathing. In unexplained coma, empiric flumazenil can provoke withdrawal seizures in benzodiazepine dependence or remove seizure suppression in mixed poisoning; reserve it for appropriately selected exposures.
49.What treatments address life-threatening beta-blocker poisoning?
Use vasopressors for hypotension from life-threatening beta-blocker poisoning. If hypotension remains refractory, administer high-dose insulin with euglycemia support and close metabolic monitoring. Glucagon bolus followed by infusion is another reasonable treatment for symptomatic bradycardia or hypotension. Refractory cardiogenic shock may require extracorporeal circulatory support. Treatment must address inadequate circulation rather than focusing only on whether the pulse rate increases.
Apply it
After a beta-blocker overdose, profound hypotension persists despite vasopressors. Begin high-dose insulin with glucose support, follow blood glucose and electrolytes closely, and reassess perfusion while escalating circulatory care.
Common pitfall: High-dose insulin therapy requires active glucose management and repeated monitoring; it is not an unmonitored insulin bolus. A transient improvement in heart rate does not establish recovery from shock.
50.How does cardiovascular collapse from local anesthetic toxicity alter resuscitation?
Stop local anesthetic administration and provide oxygenation, ventilation and resuscitation support. RCUK 2025 guidance recommends 20% intravenous lipid emulsion, initially 1.5 mL/kg as a bolus followed by 15 mL/kg per hour, with further adjustment according to response and the protocol. It also recommends reduced epinephrine dosing, at most 1 microgram/kg per dose rather than the usual 1-mg arrest bolus. Treat seizures with benzodiazepines and consider prolonged resuscitation or extracorporeal support when needed.
Apply it
A patient develops a seizure followed by cardiovascular collapse during local anesthetic administration. Initiate systemic-toxicity treatment, including lipid emulsion, and use the modified resuscitation approach rather than treating the event as an ordinary isolated arrhythmia.
Common pitfall: Distinguish micrograms from milligrams when applying the reduced epinephrine recommendation. A seizure may precede cardiovascular collapse, so stopping the seizure does not complete treatment or justify resuming the anesthetic.
Traumatic disorders8%
51.When should tension pneumothorax be decompressed without imaging?
Tension pneumothorax traps pleural air under pressure, impairing ventilation and venous return. In a severely unstable trauma patient, compatible findings such as unilateral markedly reduced breath sounds, respiratory compromise and shock justify immediate decompression without waiting for imaging. Tracheal deviation may be late or absent. The decision rests on the physiologic emergency and clinical context, followed by reassessment of response and continued evaluation for other causes of shock.
Apply it
After chest trauma, a patient becomes hypotensive and severely dyspneic with almost absent breath sounds on one side. Perform immediate emergency decompression while resuscitation continues rather than transporting the unstable patient for confirmatory CT.
Common pitfall: Do not require every classic sign before acting. Waiting for tracheal deviation or a radiograph can permit preventable cardiovascular collapse in a compatible unstable presentation.
52.Why is definitive pleural drainage needed after emergency decompression?
Emergency decompression rapidly releases pressure but may not provide durable control of an ongoing pleural air leak. Definitive tube drainage is generally required after decompression of traumatic tension pneumothorax. Reassess ventilation and circulation immediately, because inadequate access, catheter obstruction, recurrent tension or another injury can explain persistent instability. A brief improvement is useful evidence of response, but it does not complete treatment or eliminate the need for monitoring and definitive pleural management.
Apply it
Needle decompression improves a trauma patient's blood pressure and breathing. Arrange definitive chest drainage and continued reassessment rather than regarding the temporary catheter and initial physiologic improvement as sufficient treatment for the remainder of care.
Common pitfall: A decompression device can kink, obstruct or fail to reach the pleural space. Persistent deterioration requires prompt reassessment instead of assuming tension has been permanently excluded.
53.How does rib-fracture analgesia protect respiratory function?
Pain from rib fractures can cause splinting, shallow breathing and ineffective coughing, increasing the risk of atelectasis and pulmonary complications. Adequate analgesia supports ventilation, secretion clearance and participation in respiratory care. Use an individualized multimodal approach and consider regional techniques where appropriate. Reassess both pain relief and respiratory status because sedating medication can itself impair breathing. Effective treatment aims at useful respiratory function rather than a pain score in isolation.
Apply it
An older patient with multiple rib fractures takes shallow breaths and cannot cough because of pain. Improve analgesia and reassess inspiratory effort and oxygenation rather than accepting immobility and splinting as unavoidable consequences of the fractures.
Common pitfall: Escalating systemic sedation until the patient is sleepy may worsen ventilation. The relevant outcome is improved breathing and coughing with an acceptable level of alertness.
54.What named framework permits observation of a small traumatic pneumothorax?
The WSES-AAST 2025 guideline permits conservative management of a traumatic pneumothorax measuring 2 cm or less in a stable patient with at least 24 hours of observation. This is a linear imaging size category, not a percentage of lung collapse. Document the imaging modality and measurement site; the guideline separately describes an apical air rim up to 3.5 cm, so differing measurement descriptions should not be treated as interchangeable. Positive-pressure ventilation, respiratory impairment or hemodynamic compromise strongly favors drainage. Reassess symptoms, oxygenation and imaging during observation.
Apply it
A spontaneously breathing, stable patient has a traumatic pneumothorax reported as 1.5 cm under the trauma service's documented measurement method. Consider at least 24 hours of monitored observation; impending positive-pressure ventilation or deterioration changes the drainage decision.
Common pitfall: The WSES-AAST criterion is not a universal cutoff across trauma protocols. Do not transfer a measurement from one imaging method or anatomic site into another rule without checking its framework.
55.How does a traumatic hemothorax contribute to shock?
A hemothorax collects blood in the pleural space, reducing circulating volume and potentially compromising ventilation. In a shocked trauma patient, diminished breath sounds may reflect blood rather than air, and both injuries can coexist. Management combines hemorrhage resuscitation, pleural drainage when indicated and urgent assessment for ongoing bleeding requiring operative control. Drain output and physiology help guide escalation, but waiting for an arbitrary volume is inappropriate when the patient remains unstable.
Apply it
A patient with penetrating chest trauma is hypotensive, and bedside assessment shows a large pleural fluid collection. Treat hemorrhagic shock, arrange chest drainage and involve the surgical team promptly to assess ongoing intrathoracic bleeding and the need for operative control.
Common pitfall: Do not assume every unilateral reduction in breath sounds represents pneumothorax. Pleural blood requires attention to blood loss and definitive hemorrhage control as well as breathing.
EMS, disaster medicine and administrative aspects of emergency medicine2%
56.How does SALT sorting prioritize assessment and lifesaving interventions?
SALT begins with global sorting: assess those who are still or have obvious life threats first, those making purposeful movements next and walking patients later. This initial ordering is not the final triage category. Individual assessment includes rapid lifesaving interventions that can be performed within the algorithm, available resources and provider capability, such as major hemorrhage control or airway opening. The objective is efficient prioritization across many casualties rather than completing comprehensive treatment for one patient.
Apply it
At a mass casualty scene, walking patients gather in a designated area while responders first assess motionless casualties. A rapidly controlled major hemorrhage is addressed during individual triage before the responder moves on to assess others.
Common pitfall: Walking status does not guarantee a final minimal category. Global sorting determines assessment order; individual findings and response to rapid interventions determine subsequent triage decisions.
Procedures/skills6%
57.Which method best confirms endotracheal tube placement during resuscitation?
Continuous waveform capnography, used with clinical assessment, is the most reliable method for confirming and monitoring endotracheal tube placement during cardiac arrest. Repeated detection of exhaled carbon dioxide supports tracheal placement and provides ongoing information unavailable from a single auscultation. Chest rise and breath sounds alone can be misleading. Low pulmonary blood flow during arrest may reduce carbon dioxide values, so interpret the waveform and the entire resuscitation context together.
Apply it
After intubation during CPR, the team sees chest movement but has not documented exhaled carbon dioxide. Attach waveform capnography immediately and evaluate placement rather than accepting chest rise and a single breath-sound check as sufficient confirmation.
Common pitfall: Condensation in a tube is not reliable proof of tracheal placement. Likewise, a low numeric carbon dioxide reading during arrest requires contextual interpretation rather than automatic reassurance.
58.What does sudden loss of a capnography waveform require?
After a tracheal tube has been confirmed, sudden loss of the carbon dioxide waveform requires immediate assessment of the patient, airway and ventilation equipment. Possibilities include tube displacement, obstruction, circuit disconnection or a major fall in pulmonary blood flow. Capnography is therefore ongoing safety monitoring, not merely a one-time placement test. Check ventilation and circulation directly while identifying the cause, rather than assuming the monitor alone has malfunctioned or automatically removing a correctly placed tube.
Apply it
During transport of an intubated patient, the waveform abruptly disappears. Assess chest movement, circulation, tube position and circuit connections immediately, supporting ventilation while determining whether the problem is displacement, obstruction, equipment failure or circulatory collapse.
Common pitfall: Do not silence the alarm without evaluating the patient. Conversely, waveform loss has several causes and does not justify blind tube removal without assessment.
59.When should intraosseous access replace unsuccessful intravenous attempts?
During adult cardiac arrest, intravenous access is the preferred initial route for medication delivery. Intraosseous access is reasonable when intravenous access is unsuccessful or not feasible. The practical objective is timely usable access without distracting from compressions and defibrillation. Repeated peripheral attempts should not indefinitely postpone indicated drugs. Access placement is a parallel task, and neither intravenous nor intraosseous procedures should create avoidable interruptions in the core resuscitation sequence.
Apply it
During cardiac arrest, prompt peripheral intravenous attempts fail while compressions and rhythm treatment continue. Move to intraosseous access rather than repeatedly searching for a difficult vein and delaying indicated medication delivery through a usable route.
Common pitfall: Obtaining access is not a prerequisite for defibrillating ventricular fibrillation. Do not let a technically difficult procedure displace the rhythm-specific intervention with immediate survival value.
60.How can ultrasound be used during arrest without compromising CPR?
Point-of-care ultrasound may help skilled clinicians identify reversible causes during arrest, but its use must not prolong pauses in chest compressions. Plan image acquisition around an already scheduled brief interruption, then interpret the saved image while CPR resumes. An ultrasound finding should be integrated with clinical evidence rather than used in isolation. The diagnostic benefit is lost if image acquisition repeatedly reduces perfusion through extended hands-off time during active resuscitation.
Apply it
A clinician prepares the probe before a scheduled rhythm check, obtains a brief view and reviews the recorded image after compressions restart. The team avoids extending the pause simply to obtain a more aesthetically complete examination.
Common pitfall: Do not stop compressions for a leisurely diagnostic scan. Ultrasound is an adjunct to resuscitation and should not independently determine termination from one isolated image.
What to focus on during revision
The following are CertMedbry study suggestions. Use the official outline to check the full scope of your examination.
- Abdominal and gastrointestinal disorders — 9%: pancreatitis diagnosis, selective imaging, feeding and bleeding disposition.
- Cardiovascular disorders — 9%: instability, rhythm-specific treatment and reversible causes, including traumatic-arrest priorities.
- Cutaneous disorders — 3%: recognize deep infection and choose effective source control.
- Endocrine, metabolic and nutritional disorders — 5%: euglycemic DKA, all four HHS criteria and medication-associated hypoglycemia.
- Environmental disorders — 4%: identify heat-related neurologic dysfunction and initiate rapid cooling.
- Head, ear, nose and throat disorders — 5%: effective epistaxis treatment, posterior bleeding clues and anaphylactic upper-airway compromise.
- Hematologic and immune system disorders — 3%: score each 4Ts component and address HIT's thrombotic mechanism.
- Systemic infectious disorders — 7%: individualize fluids, vasopressors, perfusion reassessment and source control.
- Musculoskeletal disorders (nontraumatic) — 5%: septic-joint sampling, imperfect synovial tests and deep muscle infection.
- Nervous system disorders — 7%: Ottawa eligibility, time-dependent SAH testing, meningitis and acute cerebral edema.
- Obstetrics and gynecology disorders — 6%: ectopic rupture, unresolved pregnancy location, methotrexate exclusions and timed maternal resuscitative delivery.
- Psychobehavioral disorders — 4%: protect immediate safety and construct an actionable discharge safety plan.
- Renal and urogenital disorders — 5%: infected obstruction, volume-associated acute kidney injury and severe hyperkalemia.
- Thoracic-respiratory disorders — 7%: asthma-related air trapping, probability-dependent PE testing, drowning ventilation and post-PE follow-up.
- Toxicological disorders/clinical pharmacology — 5%: opioid ventilation, beta-blocker shock and local anesthetic systemic toxicity.
- Traumatic disorders — 8%: tension physiology, defined observation criteria, hemorrhage and pain-related respiratory compromise.
- EMS, disaster medicine and administrative aspects of emergency medicine — 2%: distinguish SALT sorting from final individual triage.
- Procedures/skills — 6%: confirm and monitor airways, establish timely access and protect compression time.
A practical preparation plan
1. Map the complete written outline
Use the official 18-domain outline as your coverage map. Start with the two 9% domains and traumatic disorders at 8%, then distribute study time across the remaining weights. Add topics beyond this selective guide so that familiar examples do not become an artificial syllabus boundary. All subtopics selected here are editorial choices.
2. Practise identifying the decisive cue
For each case, state the immediate physiologic threat, the finding that changes management and the tempting alternative that the finding defeats. Contrast synchronized cardioversion with defibrillation, stable joint aspiration with septic shock treatment, and uncomplicated colic with infected obstruction.
3. Rehearse thresholds with their conditions
Write DKA and HHS criteria, potassium precautions, all four 4Ts component scores and age-adjusted D-dimer calculations from memory. Attach the population, units and limitations to every threshold. Rehearse methotrexate absolute exclusions separately from reduced-success predictors, and state the indication and five-minute completion goal for AHA resuscitative delivery.
4. Use timed sections and analyze reasoning
Build toward the published pace of 50 questions in 60 minutes using a broader question resource. Use these 20 drills to identify reasoning errors, then record whether each error involved recognition, sequencing, interpretation or disposition. Reattempt the underlying decision rather than memorizing an option position.
5. Connect intervention to reassessment
After selecting treatment, specify what response you expect and what failure would mean. Revisit perfusion after fluids, breathing after naloxone, physiology after pleural decompression and tube safety after intubation. Distinguish new neurologic deterioration from expected metabolic recovery. Use the recall cards to explain these mechanisms aloud before returning to mixed cases.
Use your sample score as a starting point
The free set contains 20 original practice questions. It is a small learning sample, not an official examination or a validated pass prediction. Review each explanation and its source before moving to another topic.
Start the free sampleOfficial sources and updates
- AOBEM Written Exam
- AOBEM Emergency Medicine Certification Timeline
- AOBEM Oral Exam
- AOBEM Clinical Exam
- Policies and Procedures of the American Osteopathic Board of Emergency Medicine
- ACG Guideline Highlights: Acute Pancreatitis, 2024
- ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding
- 2025 AHA Guidelines: Adult Advanced Life Support
- 2025 AHA Adult Cardiac Arrest Circular Algorithm
- IDSA Guidelines for Skin and Soft Tissue Infections
- Hyperglycaemic Crises in Adults With Diabetes: A Consensus Report, 2024
- CDC: Heat-related Illnesses
- AAO-HNS ENT Health: Nosebleeds
- ASH Pocket Guide: Diagnosis and Management of Heparin-Induced Thrombocytopenia
- Surviving Sepsis Campaign Adult Guidelines, 2026
- EBJIS Guideline for Management of Septic Arthritis in Native Joints
- ACEP Clinical Policy: Acute Headache, 2019
- RCOG: Ectopic Pregnancy
- NIMH Adult Emergency Department Brief Suicide Safety Assessment Guide
- EAU Guidelines on Urolithiasis
- Age-Adjusted D-Dimer Cutoff Levels to Rule Out Pulmonary Embolism: ADJUST-PE
- AHA: 2026 Acute Pulmonary Embolism Guideline—Top Things to Know
- 2025 AHA Guidelines: Special Circumstances of Resuscitation
- Thoracic Trauma WSES-AAST Guidelines, 2025
- HHS CHEMM: SALT Mass Casualty Triage Algorithm
- American College of Gastroenterology Guidelines: Management of Acute Pancreatitis - PMC
- ACG Clinical Guideline: Upper Gastrointestinal... : American Journal of Gastroenterology
- Special circumstances Guidelines | Resuscitation Council UK
- These highlights do not include all the information needed to use FARXIGA safely and effectively. See full prescribing information for FARXIGA. FARXIGA® (dapagliflozin) tablets, for oral useInitial U.S. Approval: 2014
- Ectopic-Pregnancy-ACOG.pdf
- Meningitis
- epi-win_overview-of-meningitis-guidelines_final.pdf
- validation-of-sah.pdf
Confirm current eligibility, fees, scheduling and policies directly with the examination provider. CertMedbry is independent and is not endorsed by these organisations. How we handle content and corrections.