100+ Free FC Emerg Med(SA) Part II Practice Questions

Explanation: Invasive surgical cricothyroidotomy is the definitive choice when face-to-face airway management is impossible due to massive maxillofacial trauma, active bleeding obscuring visual anatomical landmarks, and severe jaw trismus. Standard or video laryngoscopy will fail due to poor visualization and inability to open the mouth. Performing a surgical airway immediately secures oxygenation and prevents asphyxiation in a 'cannot intubate, cannot oxygenate' scenario.

Explanation: Norepinephrine infusion titrated to MAP >= 65 mmHg is recommended as the first-line vasopressor in septic shock by international Surviving Sepsis Campaign guidelines. Norepinephrine acts predominantly as a potent alpha-1 adrenergic agonist to increase systemic vascular resistance while providing modest beta-1 inotropic support. Compared to dopamine, norepinephrine demonstrates significantly lower incidence of dysrhythmias and lower overall mortality.

Explanation: Dobutamine combined with low-dose norepinephrine infusion is indicated for cardiogenic shock characterized by severe LV systolic dysfunction, elevated filling pressures, and systemic hypoperfusion. Dobutamine provides beta-1 ionotropic support to enhance cardiac output, while norepinephrine offsets dobutamine-induced vasodilation to maintain organ perfusion pressure. Nitroglycerin and fluid boluses are contraindicated in severe hypotension, and standalone high-dose loop diuretics can further worsen hypotension before perfusing organs.

Explanation: Amiodarone 300 mg IV push is indicated for refractory ventricular fibrillation or pulseless ventricular tachycardia following defibrillation attempts and vasopressor administration. Lidocaine (1 to 1.5 mg/kg) is an alternative antiarrhythmic, but amiodarone is standard first-line in ACLS algorithms for shock-refractory VF. Calcium, atropine, and sodium bicarbonate are not indicated for routine shockable arrest without specific toxicological or electrolyte etiologies.

Explanation: Titrate FiO2 downward to maintain SpO2 between 92% and 98% (or PaO2 80-100 mmHg) is critical in post-cardiac arrest care because hyperoxia (PaO2 > 200 mmHg) increases reactive oxygen species formation and neuronal apoptosis, causing brain reperfusion injury. Normoxia and normocapnia (PaCO2 35-45 mmHg) should be targeted to optimize cerebral blood flow and minimize reperfusion harm.

Explanation: Intramuscular epinephrine 0.5 mg in the anterolateral thigh is the single most critical, life-saving intervention for anaphylaxis. Epinephrine acts rapidly on alpha-1 receptors to reverse peripheral vasodilation and airway edema, and on beta-1/beta-2 receptors to produce bronchodilation and positive inotropy. Antihistamines and corticosteroids are adjunctive secondary medications and do not reverse immediate life-threatening airway collapse or distributive shock.

Explanation: Etomidate 0.3 mg/kg IV provides stable hemodynamics during induction because it lacks direct myocardial depressant effects and does not cause significant venodilation or arterial vasodilation. Ketamine (1.5 to 2 mg/kg IV) is another excellent option in shock, but etomidate remains a classic choice for maintaining blood pressure in trauma and septic shock patients undergoing emergency RSI.

Explanation: Intravenous calcium gluconate 10% (10-20 mL) is the imperative first step to stabilize the cardiac membrane potential against hyperkalemia-induced cardiotoxicity. Calcium antagonizes the membrane depolarizing effects of hyperkalemia without shifting serum potassium levels. After membrane stabilization, intracellular shifting agents (insulin/dextrose, salbutamol) and elimination methods (furosemide, hemodialysis) are administered.

Explanation: Immediate bolus of alteplase (rtPA) 50 mg IV push is indicated in cardiac arrest caused by suspected or proven massive pulmonary embolism. Following thrombolytic administration, CPR should be continued for at least 60 to 90 minutes to allow the fibrinolytic agent adequate time to lyse the pulmonary artery occlusion and restore right ventricular outflow.

Explanation: Bradycardia combined with hypotension and warm, dry peripheries is characteristic of neurogenic shock. Loss of sympathetic vascular tone below the level of the spinal cord lesion causes profound vasodilation (warm extremities) and un-opposed vagal tone (bradycardia). In contrast, hypovolemic shock features compensatory tachycardia, cool clammy skin, and elevated systemic vascular resistance.