Emergency Medicine COMAT Command Center Emergency Medicine Shelf Exam Command Center

Shock is defined at the cellular level as acute circulatory failure leading to inadequate tissue perfusion, resulting in cellular hypoxia, anaerobic metabolism, and systemic lactic acidosis. Clinically, shock is categorized into four distinct pathophysiological phenotypes: hypovolemic, cardiogenic, obstructive, and distributive. In hypovolemic shock (hemorrhage, severe dehydration, third-spacing), decreased circulating plasma volume causes marked reductions in cardiac output (CO) and pulmonary capillary wedge pressure (PCWP/preload), triggering compensatory peripheral vasoconstriction that manifests as markedly elevated systemic vascular resistance (SVR). Patients present with cold, clammy extremities, collapsed jugular veins, and tachycardia.

Cardiogenic shock occurs due to primary pump failure, most frequently secondary to massive acute myocardial infarction, severe acute valvular regurgitation (e.g., papillary muscle rupture), or decompensated cardiomyopathy. Hemodynamically, cardiac contractility is profoundly impaired, leading to severely decreased cardiac output, elevated ventricular end-diastolic pressures (high PCWP), and compensatory elevated SVR. On physical exam, patients present with pulmonary edema (crackles), elevated jugular venous distention (JVD), an S3 gallop, and cool extremities. First-line medical support includes inotropes (dobutamine, milrinone) to enhance forward flow, vasopressors (norepinephrine) if mean arterial pressure (MAP) is < 65 mmHg, and prompt mechanical circulatory support (intra-aortic balloon pump [IABP] or Impella) with emergency catheterization.

Obstructive shock is characterized by physical impedance to cardiac chamber filling or right ventricular outflow. The classic etiologies include massive pulmonary embolism (RV strain, elevated CVP, low PCWP, low CO), cardiac tamponade (impaired diastolic filling of all chambers with equalization of diastolic pressures and pulsus paradoxus > 10 mmHg), and tension pneumothorax (mediastinal shift kinking the inferior vena cava). In contrast, distributive shock—predominantly septic shock, anaphylaxis, and neurogenic shock—is marked by severe pathological systemic vasodilation. Here, SVR is profoundly decreased, and in early 'warm shock', cardiac output is elevated or normal with warm, hyperemic extremities and bounding pulses. Neurogenic shock represents a unique distributive state caused by high cervical or thoracic spinal cord transection (above T6), disrupting descending sympathetic tone and resulting in the classic hemodynamic triad of hypotension, relative bradycardia, and warm dry skin without compensatory vasoconstriction.

In cardiac arrest, rhythm analysis partitions cases into shockable rhythms (Ventricular Fibrillation [VF] and Pulseless Ventricular Tachycardia [pVT]) and non-shockable rhythms (Pulseless Electrical Activity [PEA] and Asystole). For VF/pVT, immediate defibrillation (unsynchronized high-energy shock) is the single most critical determinant of survival, followed immediately by 2 minutes of uninterrupted, high-quality chest compressions (100–120 bpm, 2–2.4 inches depth, allowing complete chest recoil). Epinephrine 1 mg IV/IO is administered every 3 to 5 minutes, beginning after the second defibrillation cycle. Amiodarone (300 mg bolus, followed by a 150 mg second dose) or Lidocaine (1–1.5 mg/kg) is administered after the third shock for refractory VF/pVT.

For non-shockable rhythms (PEA/Asystole), defibrillation is strictly contraindicated. CPR and immediate administration of Epinephrine 1 mg IV/IO must occur without delay. The clinician must relentlessly search for and treat reversible underlying causes using the classic 5 H's and 5 T's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo-/Hyperkalemia, Hypothermia; Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary PE), and Thrombosis (coronary ACS). Return of spontaneous circulation (ROSC) is evidenced by an abrupt, sustained increase in end-tidal CO2 (PETCO2 ≥ 40 mmHg) or arterial pressure waveforms.

Emergency airway management in the resuscitation bay hinges upon Rapid Sequence Intubation (RSI)—the virtually simultaneous administration of a potent induction agent and a neuromuscular blocking agent to facilitate endotracheal tube placement while minimizing aspiration risk. Etomidate (0.3 mg/kg) is widely favored for its exceptional hemodynamic neutrality; however, its transient suppression of 11-beta-hydroxylase must be considered in severe septic shock. Ketamine (1.5–2 mg/kg) is ideal for hypotensive trauma and status asthmaticus due to its catecholamine-releasing sympathomimetic properties and intrinsic bronchodilation. Succinylcholine (1.5 mg/kg) is a depolarizing paralytic with rapid 45-second onset, but is strictly contraindicated in hyperkalemia, severe crush injuries > 48 hours old, extensive burns > 48 hours old, chronic denervating diseases (ALS, MS), and malignant hyperthermia susceptibility. In such settings, high-dose Rocuronium (1.2 mg/kg) is the paralytic of choice, which can be rapidly reversed with Sugammadex if needed.

The primary survey begins with Airway assessment while maintaining rigid in-line cervical spine stabilization. Any patient with a Glasgow Coma Scale (GCS) score ≤ 8, severe maxillofacial trauma, expanding neck hematoma, or severe inhalation burn requires definitive airway placement via endotracheal intubation. Breathing assessment entails immediate detection of tension pneumothorax (unilateral absent breath sounds, tracheal deviation, hemodynamic collapse), which mandates immediate needle decompression at the 2nd intercostal space midclavicular line or 4th/5th intercostal space anterior axillary line, immediately followed by tube thoracostomy (chest tube). Flail chest, defined by ≥ 2 fractures in ≥ 2 consecutive ribs, creates paradoxical chest wall motion and severe underlying pulmonary contusion; definitive therapy emphasizes early analgesia (epidural or intercostal nerve blocks) and positive pressure ventilation if respiratory failure ensues.

Circulation centers on rapid hemorrhage control and resuscitation. In hemorrhagic shock, crystalloid boluses are strictly limited to avoid hypothermia, hemodilution, and worsening trauma-induced coagulopathy ('the lethal triad': hypothermia, acidosis, and coagulopathy). The standard of care is early activation of the Massive Transfusion Protocol (MTP), delivering packed red blood cells, fresh frozen plasma, and platelets in a balanced 1:1:1 ratio. Tranexamic acid (TXA, 1 g IV over 10 minutes followed by 1 g infusion over 8 hours) must be administered within 3 hours of injury to significantly reduce all-cause mortality from trauma hemorrhage.

The Focused Assessment with Sonography for Trauma (FAST) exam rapidly screens four acoustic windows for pathological free fluid: the hepatorenal space (Morison's pouch), the splenorenal recess, the pelvis/rectovesical or rectouterine pouch, and the subxiphoid pericardial window (extended FAST adds bilateral anterior chest views for pneumothorax). In an unstable trauma patient, a positive FAST indicates hemoperitoneum and mandates immediate emergent exploratory laparotomy without waiting for CT imaging. In a hemodynamically stable patient, a positive FAST warrants contrast-enhanced abdominopelvic CT to grade solid organ injury (spleen, liver, kidney) and guide non-operative vs. interventional angiographic embolization.

Toxidromes represent clinical symptom constellations that point toward specific classes of chemical exposures. The Anticholinergic toxidrome (atropine, diphenhydramine, tricyclic antidepressants, scopolamine) is remembered by the classic medical aphorism: 'Blind as a bat (mydriasis, loss of accommodation), mad as a hatter (delirium, hallucinations), red as a beet (cutaneous flushing), hot as a hare (hyperthermia due to anhidrosis), dry as a bone (dry skin and mucous membranes), and full as a flask (urinary retention and decreased bowel sounds)'. In contrast, the Sympathomimetic toxidrome (cocaine, amphetamines, MDMA, cathinones) presents nearly identically with hyperthermia, mydriasis, hypertension, and tachycardia, but is crucially distinguished by diaphoresis (sweating) and hyperactive bowel sounds.

The Cholinergic toxidrome (organophosphate and carbamate insecticides, chemical nerve agents like sarin) inhibits acetylcholinesterase, producing massive acetylcholine accumulation at muscarinic and nicotinic receptors. Muscarinic overstimulation is remembered by DUMBELS: Defecation, Urination, Miosis, Bronchorrhea/Bradycardia/Bronchospasm (the 'killer Bs' causing asphyxiation), Emesis, Lacrimation, and Salivation. Nicotinic stimulation causes muscle fasciculations, weakness, and diaphragmatic paralysis. Immediate treatment involves high-dose Atropine (titrated to drying of respiratory secretions) and Pralidoxime (2-PAM, to regenerate active acetylcholinesterase before irreversible covalent aging occurs).

The Opioid toxidrome presents with the classic triad of central nervous system depression, miosis (pinpoint pupils), and respiratory depression (hypoventilation, respiratory acidosis). Immediate airway support and titrated Naloxone (IV, IM, or intranasal) reverses respiratory arrest without precipitating severe withdrawal agitation. Sedative-hypnotic toxicity (benzodiazepines, barbiturates) mimics opioid overdose with CNS depression and hypoventilation, but characteristically features normal pupil size and normal vitals in pure benzodiazepine ingestions; Flumazenil should generally be avoided in chronic users due to the risk of refractory withdrawal seizures.

Venous thromboembolism (VTE) presenting as acute pulmonary embolism (PE) is a major cause of preventable emergency mortality. Evaluation begins with pre-test probability scoring using the Wells Criteria. In patients with low clinical probability (Wells score < 2), the Pulmonary Embolism Rule-out Criteria (PERC: age < 50, HR < 100, SpO2 ≥ 95%, no prior DVT/PE, no recent surgery/trauma within 4 weeks, no hemoptysis, no estrogen use, no unilateral leg swelling) can rule out PE without further diagnostic testing. If any PERC criterion is positive or pretest probability is moderate, a high-sensitivity D-dimer assay is ordered. A negative D-dimer safely excludes PE; an elevated D-dimer warrants definitive diagnostic imaging with CT Pulmonary Angiography (CTPA). If renal insufficiency (GFR < 30) or severe IV contrast allergy precludes CTPA, a Ventilation-Perfusion (V/Q) scan is the gold standard alternative.

PE is classified into three clinical prognostic categories: Massive, Submassive, and Non-massive (low-risk). Massive PE is defined by sustained hypotension (systolic BP < 90 mmHg for > 15 minutes, or requiring vasopressors) due to acute right ventricular afterload mismatch and failure. Submassive PE features normal systemic blood pressure, but exhibits objective evidence of RV dysfunction (elevated troponin, elevated BNP, RV dilation or McConnell's sign on echocardiography, or RV/LV ratio > 0.9 on CTPA). Non-massive PE exhibits neither hypotension nor RV strain.

Treatment for hemodynamically stable PE involves immediate therapeutic anticoagulation with subcutaneous low-molecular-weight heparin (LMWH, Enoxaparin 1 mg/kg BID), Fondaparinux, or direct oral anticoagulants (DOACs like Apixaban or Rivaroxaban). For massive PE with refractory shock or cardiac arrest, immediate systemic thrombolysis with tissue plasminogen activator (Alteplase 100 mg IV over 2 hours) is indicated unless absolute contraindications exist (prior intracranial hemorrhage, known cerebrovascular malformation, ischemic stroke within 3 months, active internal bleeding). If thrombolysis is contraindicated or fails, emergent catheter-directed mechanical thrombectomy or surgical pulmonary embolectomy is indicated.

Acute stroke evaluation hinges upon the principle 'time is brain'. Upon arrival with focal neurologic deficits, a non-contrast head CT must be obtained and interpreted within 20 minutes to exclude intracranial hemorrhage (ICH). If the non-contrast CT is negative for blood, the patient is evaluated for intravenous thrombolysis (IV Alteplase or Tenecteplase). IV thrombolysis is indicated for disabling ischemic stroke symptoms within 4.5 hours of symptom onset (or 'last known well' time). Strict contraindications include intracranial hemorrhage, active internal bleeding, head trauma or stroke within 3 months, severe uncontrolled hypertension (BP > 185/110 mmHg refractory to IV labetalol or nicardipine), platelets < 100,000, INR > 1.7, or therapeutic DOAC use within 48 hours.

For large vessel occlusions (LVO) in the anterior circulation (internal carotid artery or proximal MCA), mechanical endovascular thrombectomy (EVT) provides dramatic morbidity reduction. EVT is recommended within 6 hours of onset, and can be extended up to 24 hours in carefully selected patients who demonstrate a favorable ischemic penumbra-to-infarct core ratio on CT perfusion or diffusion-weighted MRI (DAWN and DEFUSE-3 trials).

Spontaneous Subarachnoid Hemorrhage (SAH), most commonly from rupture of an intracranial saccular (berry) aneurysm at the anterior communicating artery, presents with the classic 'worst headache of my life' (thunderclap headache peaking within 1 second to 1 minute), accompanied by meningismus, nausea, and preretinal subhyaloid hemorrhages (Terson syndrome). If non-contrast head CT performed within 6 hours of onset is completely negative but clinical suspicion remains high, a lumbar puncture (LP) is mandatory to assess for xanthochromia (pink/yellow supernatant produced by bilirubin from lysed RBCs, confirmed by spectrophotometry) and elevated opening pressure. Nimodipine (60 mg every 4 hours) is initiated immediately to prevent delayed cerebral vasospasm and secondary ischemic infarction.

Acute appendicitis is the most common emergency surgical condition. Obstruction of the appendiceal lumen by a fecalith or lymphoid hyperplasia leads to luminal distention, visceral pain in the periumbilical region (T10 dermatome), followed by transmural inflammation and localized parietal peritoneal irritation in the right lower quadrant (McBurney's point). Hallmark exam signs include Rovsing's sign (RLQ pain on LLQ palpation), Psoas sign (pain on passive right hip extension), and Obturator sign (pain on passive internal rotation of the flexed right hip). In non-pregnant adults, contrast-enhanced CT of the abdomen/pelvis is the diagnostic gold standard; in children and pregnant patients, graded compression ultrasonography or pelvic MRI is preferred to avoid ionizing radiation.

Acute Mesenteric Ischemia is a critical vascular emergency classically characterized by 'pain out of proportion to physical examination' in an elderly patient with underlying atrial fibrillation, peripheral vascular disease, or recent myocardial infarction. The most common etiology (50%) is acute embolism from the left atrium to the superior mesenteric artery (SMA). Initial abdominal exam is deceptively benign without peritoneal signs; however, progression to transmural bowel infarction produces peritoneal signs, hematochezia, severe lactic acidosis, and sepsis. CT mesenteric angiography is the diagnostic test of choice (revealing arterial occlusion, bowel wall thickening, or pneumatosis intestinalis). Emergent surgical embolectomy, revascularization, and resection of necrotic bowel are life-saving.

Acute Upper Gastrointestinal Bleeding (UGIB) originates proximal to the ligament of Treitz, presenting as hematemesis ('coffee-ground' or bright red) or melena. Resuscitation requires two large-bore IVs (16-gauge or 18-gauge), rapid crystalloid boluses, and restrictive blood transfusion targeting hemoglobin ≥ 7 g/dL (or ≥ 8 g/dL in coronary artery disease). In suspected variceal bleeding (cirrhosis, stigmata of chronic liver disease), IV Octreotide (50 mcg bolus followed by 50 mcg/hr infusion) reduces portal venous pressure, and prophylactic Ceftriaxone (1 g IV daily) significantly decreases bacterial peritonitis, rebleeding, and mortality. Emergent upper endoscopy (EGD) within 24 hours provides definitive diagnosis and endoscopic band ligation.

Accidental hypothermia is defined as an involuntary drop in core body temperature < 35°C (95°F). It is stratified into Mild (32–35°C: vigorous shivering, ataxia, dysarthria), Moderate (28–32°C: cessation of shivering, hypoventilation, altered mental status, J-waves / Osborn waves on ECG), and Severe (< 28°C: comatose, extreme bradycardia or ventricular fibrillation, apparent rigor mortis). In severe hypothermia, the myocardium is exceedingly irritable; rough handling or unnecessary movement can trigger refractory ventricular fibrillation. If VF occurs, defibrillation and ACLS medications are typically ineffective until the patient is rewarmed > 30°C. Active internal rewarming methods include warmed humidified O2, warmed IV crystalloids (40–42°C), thoracic or peritoneal lavage with warmed fluids, and extracorporeal membrane oxygenation (ECMO). A key board dictum: 'a patient is not dead until warm and dead' (core temp > 32°C with absent vitals).

Heat emergencies exist on a spectrum from Heat Exhaustion (core body temp < 40°C, intact mental status, profuse sweating, headache, nausea) to Heat Stroke (core body temp > 40°C [104°F] accompanied by profound central nervous system dysfunction: encephalopathy, delirium, seizures, or coma). Heat stroke is a medical emergency with high mortality from multiorgan failure and rhabdomyolysis. Immediate, aggressive evaporative or ice water immersion cooling is the treatment of choice, aiming to rapidly lower core temperature to < 39°C. Antipyretics (acetaminophen, aspirin) have NO role because hypothalamic temperature set-point is normal.

Thermal burns are quantified using the Rule of Nines: Head (9%), Entire Anterior Trunk (18%), Entire Posterior Trunk (18%), Each Upper Extremity (9%), Each Lower Extremity (18%), Perineum (1%). Fluid resuscitation for 2nd and 3rd degree burns > 20% Total Body Surface Area (TBSA) is calculated using the Parkland Formula: 4 mL × body weight (kg) × % TBSA burned, administering half of the total volume over the first 8 hours from the time of burn, and the remaining half over the subsequent 16 hours. Resuscitation is titrated to maintain a target urine output of 0.5–1.0 mL/kg/hr in adults.