Emergency Medicine Flashcards

A 52-year-old presents in cardiogenic shock after intentional verapamil overdose. Despite calcium gluconate (3 g IV), atropine (3 mg total), norepinephrine (0.5 mcg/kg/min), and vasopressin, MAP remains 45 mmHg and HR 38 bpm. Which intervention has the strongest evidence for improving myocardial function by restoring cardiomyocyte glucose uptake in this setting?

Answer: High-dose insulin euglycemia therapy (HIET): 1 unit/kg IV bolus followed by 0.5–1 unit/kg/hr infusion with concurrent dextrose

High-dose insulin euglycemia therapy (HIET) is the preferred rescue intervention in severe calcium channel blocker (CCB) toxicity refractory to standard measures. CCB toxicity impairs glucose uptake in cardiomyocytes, which rely on glucose during metabolic stress. Insulin bypasses this block via non-receptor-mediated mechanisms, restoring oxidative metabolism and improving inotropy. Glucagon is often ineffective in severe CCB poisoning (unlike beta-blocker toxicity) because it relies on cAMP pathways already depressed by the high drug burden. ILE is more established for lipophilic drug toxicity (especially local anesthetics). Sodium bicarbonate addresses sodium channel blockade (e.g., tricyclics), not calcium channel pathophysiology.

A 29-year-old is retrieved from a frozen lake in cardiac arrest with a core temperature of 23°C. CPR has been ongoing for 50 minutes in the field and ED. Three defibrillation attempts and cumulative amiodarone 450 mg IV have been given; ventricular fibrillation persists. Which is the most appropriate next step according to current ERC/ESICM guidelines?

Answer: Transfer urgently to an ECMO-capable centre for extracorporeal CPR and active internal rewarming

In severe accidental hypothermia (<28°C), the myocardium is refractory to defibrillation and antiarrhythmics until rewarmed. The principle 'not dead until warm and dead' applies: standard defibrillation attempts beyond three should be deferred until the core temperature exceeds 30°C. Extracorporeal CPR (ECPR) with venoarterial ECMO simultaneously maintains perfusion and achieves rapid internal rewarming — the only modality proven to reliably reverse hypothermic cardiac arrest. ERC 2021 guidelines specifically recommend transport to an ECMO-capable centre if there are no clear signs of futility (e.g., non-asphyxia aetiology, serum potassium <12 mmol/L). Continued field defibrillation without rewarming has no additional benefit.

A 26-year-old woman at 30 weeks gestation presents to the ED with headache and dizziness after a house fire. She is alert and GCS 15. Carboxyhemoglobin (COHb) is 18%. SpO2 by pulse oximetry reads 97%. Regarding hyperbaric oxygen (HBO) therapy, which statement is most accurate?

Answer: The COHb threshold for HBO in pregnant patients is lower than in non-pregnant adults, and fetal haemoglobin has a higher affinity for CO, prolonging fetal exposure

Both components of option B are correct and clinically critical. Fetal haemoglobin (HbF) has a higher affinity for carbon monoxide than adult haemoglobin (HbA), producing carboxyfoetal haemoglobin that dissociates far more slowly — the fetal half-life of CO-HbF is approximately 7 hours vs. ~5 hours for maternal COHb on 100% O2. This means the fetus suffers disproportionate and prolonged exposure even after maternal levels normalise. For this reason, HBO thresholds in pregnancy are set lower: most guidelines recommend HBO for any pregnant patient with COHb >15–20% or any neurological symptoms, regardless of gestational age. Pulse oximetry cannot distinguish COHb from oxyhaemoglobin, making SpO2 readings falsely reassuring in CO poisoning — co-oximetry is required.

A 61-year-old with Child-Pugh C liver cirrhosis is admitted in generalised convulsive status epilepticus. IV lorazepam 4 mg has been given twice without effect (refractory status). IV valproate is relatively contraindicated due to hepatotoxicity risk. Which third-line agent is pharmacokinetically most appropriate?

Answer: Levetiracetam 60 mg/kg IV (max 4500 mg) — renally excreted with minimal hepatic metabolism

Levetiracetam (LEV) is the preferred third-line agent in severe hepatic impairment. It is excreted predominantly unchanged by the kidneys (~66% renal), undergoes minimal hepatic metabolism (hydrolysis in blood), and has no significant protein binding interactions. Phenytoin is heavily protein-bound and hepatically hydroxylated — in cirrhosis, hypoalbuminaemia increases free drug, creating unpredictable toxicity. Phenobarbital is hepatically metabolised and accumulates in liver failure while also worsening encephalopathy. Lacosamide undergoes approximately 40% hepatic metabolism and the drug insert recommends dose reduction in severe hepatic impairment. LEV's renal clearance profile makes it uniquely safe in this context, and it has established IV bioequivalence.

During labour epidural placement, a parturient develops sudden tonic-clonic seizures then pulseless electrical activity (PEA). The anaesthetic team suspects local anaesthetic systemic toxicity (LAST). CPR is initiated. After 4 minutes of resuscitation including a standard 1 mg epinephrine dose, ROSC has not occurred. Which statement about ongoing management is most accurate?

Answer: Administer 20% intravenous lipid emulsion (ILE) 1.5 mL/kg bolus IV and limit epinephrine to small doses (≤1 mcg/kg) to avoid worsening the arrhythmia

Intravenous lipid emulsion (ILE) is the cornerstone pharmacological rescue in LAST. The 'lipid sink' mechanism sequesters lipophilic local anaesthetics (e.g., bupivacaine, ropivacaine) away from cardiac sodium channels. Critically, high-dose epinephrine (≥1 mg) is associated with worse outcomes in animal LAST models — it precipitates VF and impairs post-resuscitation myocardial function. The AAGBI/ASRA guidelines recommend small incremental epinephrine doses (≤1 mcg/kg) during LAST resuscitation. Amiodarone is relatively contraindicated: it also blocks sodium and potassium channels, compounding the local anaesthetic-mediated sodium channel blockade. Perimortem caesarean section (at 4 minutes of arrest in a term pregnancy) should be performed to improve venous return and CPR effectiveness, but simultaneous ILE administration is essential, not deferred.

A 68-year-old on long-term carvedilol (beta-1/beta-2/alpha-1 blocker) for heart failure develops severe anaphylaxis following IV contrast administration. He receives three doses of IM epinephrine 0.5 mg without haemodynamic improvement (BP 55/30 mmHg). Inhaled salbutamol has not relieved bronchospasm. IV fluid resuscitation is ongoing. Which intervention most specifically addresses the mechanism of epinephrine resistance in this patient?

Answer: IV glucagon 1–2 mg bolus, followed by infusion, acting via non-adrenergic adenylate cyclase activation

Beta-blocker therapy causes epinephrine resistance in anaphylaxis because carvedilol competitively occupies beta-1 and beta-2 receptors — the primary targets of epinephrine's life-saving bronchodilatory and inotropic effects. Glucagon is the specific antidote: it activates myocardial adenylate cyclase and increases intracellular cAMP via glucagon receptors, entirely bypassing adrenergic receptors. This restores inotropy and chronotropy independent of beta-receptor occupancy. While vasopressin addresses hypotension via V1 receptors, it does not reverse bronchospasm and is not specific to beta-blocker-mediated resistance. High-dose epinephrine in a patient on a non-selective blocker risks paradoxical alpha-1-mediated hypertension and reflex bradycardia while bronchospasm persists. Corticosteroids act over hours and are not rescue therapy. Glucagon 1–2 mg IV bolus (repeated if necessary) followed by infusion is the guideline-recommended intervention in this scenario.