50 Critical Cardiology Cases & Treatment
A comprehensive emergency cardiology case bank across 10 categories — Acute Coronary Syndromes, Arrhythmias, Heart Failure/Shock, Valvular & Structural Emergencies, Vascular Emergencies, Hypertensive Emergencies, Cardiac Arrest, Electrolyte/Toxicology, Congenital/Pediatric, and Device Complications. Click each case to reveal presentation, workup, diagnosis, and treatment.
Acute Coronary Syndromes
Presentation: 60-year-old male with sudden crushing chest pain, hypotension, and clear lung fields.
History & Exam: JVD elevated, hypotensive (BP 84/56), bradycardic, no pulmonary crackles (Kussmaul’s sign present).
Investigations: ECG: ST elevation in II, III, aVF with ST elevation in V4R confirming RV infarction.
Diagnosis: Inferior STEMI with right ventricular infarction.
Treatment & Management: Primary PCI of RCA, IV fluid loading to maintain preload, avoid nitrates and diuretics, treat bradycardia/heart block with atropine or pacing.
Teaching Point: Always check right-sided leads (V4R) in inferior MI; nitrates can precipitate profound hypotension in RV infarction.
Presentation: 78-year-old with chronic kidney disease presents with two days of exertional chest discomfort and dyspnea.
History & Exam: Mild bibasilar crackles, no hemodynamic instability.
Investigations: ECG: T-wave inversion in anterolateral leads. Troponin elevated with rise-and-fall pattern.
Diagnosis: Non-ST-elevation myocardial infarction (NSTEMI).
Treatment & Management: Dual antiplatelet therapy, anticoagulation, risk stratification (GRACE score), early invasive strategy with dose-adjusted contrast precautions for renal protection.
Teaching Point: Balance early invasive strategy benefits against contrast-induced nephropathy risk in CKD patients.
Presentation: 65-year-old male, 12 hours post-anterior STEMI, develops cold extremities, confusion, and oliguria.
History & Exam: BP 78/50, HR 118, cool clammy extremities, S3 gallop, bibasilar crackles.
Investigations: Echocardiogram: LVEF 25% with anteroapical akinesis. Lactate elevated.
Diagnosis: Cardiogenic shock post-STEMI.
Treatment & Management: Emergent revascularization, inotropic/vasopressor support, consider mechanical circulatory support (IABP/Impella/ECMO) if refractory.
Teaching Point: Cardiogenic shock is the leading cause of in-hospital mortality after STEMI; early revascularization is the single most effective intervention.
Presentation: 70-year-old female, 4 days after an anterior MI treated conservatively, develops sudden dyspnea and a new murmur.
History & Exam: New harsh holosystolic murmur at the left sternal border with a palpable thrill, biventricular failure signs.
Investigations: Echocardiogram confirms a ventricular septal defect with left-to-right shunt; step-up in oxygen saturation from right atrium to right ventricle on catheterization.
Diagnosis: Post-infarction ventricular septal rupture.
Treatment & Management: Stabilize with afterload reduction, IABP as a bridge, urgent surgical or percutaneous closure.
Teaching Point: New murmur after MI should prompt immediate echocardiography to exclude mechanical complications (VSD, papillary muscle rupture, free wall rupture).
Presentation: 55-year-old male with recurrent episodes of chest pain at rest over 24 hours, each lasting 10-15 minutes.
History & Exam: Pain-free between episodes, hemodynamically stable.
Investigations: Serial ECGs show transient ST depression during pain, resolving between episodes; troponin remains negative.
Diagnosis: Unstable angina.
Treatment & Management: Dual antiplatelet therapy, anticoagulation, anti-ischemic therapy (beta-blockers, nitrates), early risk stratification and angiography.
Teaching Point: Dynamic ST changes with pain and negative troponin still warrant urgent risk stratification — unstable angina is a high-risk ACS diagnosis of exclusion.
Life-Threatening Arrhythmias
Presentation: 50-year-old male collapses suddenly at home; bystander CPR initiated.
History & Exam: Unresponsive, no pulse.
Investigations: Monitor shows coarse ventricular fibrillation.
Diagnosis: Cardiac arrest due to ventricular fibrillation.
Treatment & Management: Immediate high-quality CPR, defibrillation as soon as available, epinephrine every 3-5 minutes, amiodarone for refractory VF, treat reversible causes (H’s and T’s).
Teaching Point: Early defibrillation is the single most important determinant of survival in VF arrest.
Presentation: 62-year-old male with prior MI presents with palpitations and lightheadedness.
History & Exam: HR 190, BP 92/60, mildly diaphoretic but conscious.
Investigations: ECG shows wide-complex tachycardia with AV dissociation and fusion beats, consistent with VT.
Diagnosis: Sustained monomorphic ventricular tachycardia in ischemic cardiomyopathy.
Treatment & Management: Synchronized cardioversion if unstable; IV amiodarone or procainamide if stable; evaluate for ICD implantation and catheter ablation.
Teaching Point: Any wide-complex tachycardia in a patient with structural heart disease should be treated as VT until proven otherwise.
Presentation: 74-year-old female presents with recurrent syncope and profound fatigue.
History & Exam: HR 38/min, regular, BP borderline low, no correlation between neck pulsations and heart sounds (cannon A waves).
Investigations: ECG shows complete AV dissociation with independent P waves and a slow escape rhythm.
Diagnosis: Complete (third-degree) atrioventricular block.
Treatment & Management: Temporary transcutaneous or transvenous pacing if symptomatic/unstable, followed by permanent pacemaker implantation.
Teaching Point: Complete heart block with a slow, unreliable escape rhythm is a pacemaker emergency regardless of the underlying cause.
Presentation: 68-year-old with known atrial fibrillation presents with palpitations, dyspnea, and dizziness.
History & Exam: HR 160, irregularly irregular, BP 82/54, signs of pulmonary congestion.
Investigations: ECG confirms atrial fibrillation with rapid ventricular response.
Diagnosis: Hemodynamically unstable AF with RVR.
Treatment & Management: Immediate synchronized electrical cardioversion; if stable, rate control with beta-blockers/calcium channel blockers and anticoagulation assessment.
Teaching Point: Hemodynamic instability from a tachyarrhythmia mandates emergent cardioversion rather than pharmacologic rate control.
Presentation: 45-year-old female on multiple QT-prolonging medications develops recurrent syncope.
History & Exam: Witnessed self-terminating episodes of palpitations followed by loss of consciousness.
Investigations: ECG shows a markedly prolonged QTc with polymorphic VT exhibiting a twisting morphology around the isoelectric line.
Diagnosis: Torsades de pointes secondary to acquired long QT syndrome.
Treatment & Management: IV magnesium sulfate, discontinue offending drugs, correct electrolytes (potassium, magnesium), overdrive pacing or isoproterenol if recurrent, defibrillation if degenerating to VF.
Teaching Point: IV magnesium is first-line treatment for torsades even with normal magnesium levels; always review the medication list for QT-prolonging agents.
Heart Failure & Cardiogenic Shock
Presentation: 72-year-old with known heart failure presents with acute severe dyspnea and orthopnea.
History & Exam: Respiratory rate 32, SpO2 84% on room air, bilateral crackles, JVD elevated, frothy sputum.
Investigations: Chest X-ray shows bilateral pulmonary edema; BNP markedly elevated.
Diagnosis: Acute decompensated heart failure with pulmonary edema.
Treatment & Management: Oxygen/non-invasive ventilation, IV loop diuretics, nitrates for afterload reduction if BP permits, treat precipitating cause.
Teaching Point: Non-invasive ventilation and IV diuretics with nitrates form the backbone of acute pulmonary edema management in normotensive/hypertensive patients.
Presentation: 55-year-old with known dilated cardiomyopathy presents with worsening fatigue, cold extremities, and confusion.
History & Exam: BP 80/55, cool peripheries, narrow pulse pressure, elevated JVP.
Investigations: Echocardiogram: LVEF 15%, severely reduced cardiac output; lactate elevated.
Diagnosis: Cardiogenic shock due to end-stage dilated cardiomyopathy.
Treatment & Management: Inotropic support, consideration of mechanical circulatory support, evaluation for advanced therapies (LVAD/transplant).
Teaching Point: Persistent hypoperfusion despite optimal medical therapy should trigger early referral for advanced heart failure therapies.
Presentation: 50-year-old post-surgical patient develops sudden dyspnea, syncope, and hypotension.
History & Exam: JVD elevated, right parasternal heave, hypotensive, tachycardic.
Investigations: Echocardiogram shows RV dilation and dysfunction with McConnell’s sign; CT pulmonary angiogram confirms a large central PE.
Diagnosis: Acute right ventricular failure secondary to massive pulmonary embolism.
Treatment & Management: Systemic thrombolysis or catheter-directed thrombectomy, hemodynamic support, avoid excessive fluid loading which can worsen RV strain.
Teaching Point: In acute RV failure from PE, cautious fluid administration is key — over-resuscitation worsens RV distension and outputs.
Presentation: 28-year-old presents with rapidly progressive dyspnea and hypotension one week after a flu-like illness.
History & Exam: Tachycardic, hypotensive, signs of biventricular failure.
Investigations: Troponin elevated, echocardiogram shows global hypokinesis with reduced EF, cardiac MRI shows myocardial edema/late gadolinium enhancement.
Diagnosis: Fulminant myocarditis.
Treatment & Management: Hemodynamic support, consider mechanical circulatory support (ECMO) as a bridge to recovery, immunosuppression if indicated by biopsy findings.
Teaching Point: Fulminant myocarditis can mimic cardiogenic shock in young, previously healthy patients following a viral prodrome; early ECMO support improves survival.
Presentation: 30-year-old female presents with dyspnea and leg swelling in the last month of pregnancy.
History & Exam: Elevated JVP, bibasilar crackles, peripheral edema.
Investigations: Echocardiogram shows new-onset LV systolic dysfunction (EF 30%) with no other identifiable cause.
Diagnosis: Peripartum cardiomyopathy.
Treatment & Management: Guideline-directed heart failure therapy adjusted for pregnancy/lactation safety, bromocriptine in select cases, multidisciplinary obstetric-cardiac care.
Teaching Point: New heart failure in late pregnancy or early postpartum should prompt echocardiography to exclude peripartum cardiomyopathy.
Valvular & Structural Emergencies
Presentation: 40-year-old with fever and progressive dyspnea over one week.
History & Exam: New early diastolic murmur, wide pulse pressure, signs of acute pulmonary edema.
Investigations: Echocardiogram shows a large aortic valve vegetation with severe acute regurgitation; blood cultures positive.
Diagnosis: Acute severe aortic regurgitation secondary to infective endocarditis.
Treatment & Management: IV antibiotics targeted to organism, hemodynamic stabilization, urgent surgical valve replacement given acute decompensation.
Teaching Point: Acute severe AR is poorly tolerated by the non-dilated left ventricle and often requires emergent surgery rather than medical management alone.
Presentation: 35-year-old intravenous drug user presents with fever, malaise, and a painful swollen toe.
History & Exam: New murmur, Janeway lesions on palms, splinter hemorrhages.
Investigations: Blood cultures positive for Staphylococcus aureus; echocardiogram shows tricuspid valve vegetation.
Diagnosis: Right-sided infective endocarditis with septic pulmonary/peripheral emboli.
Treatment & Management: Prolonged targeted IV antibiotics, monitor for septic pulmonary emboli, surgery if large vegetation, recurrent emboli, or heart failure.
Teaching Point: Right-sided endocarditis is strongly associated with intravenous drug use and often presents with septic pulmonary emboli rather than systemic emboli.
Presentation: 58-year-old with a mechanical mitral valve presents with sudden dyspnea, having missed anticoagulation doses.
History & Exam: Muffled prosthetic valve sounds on auscultation, signs of pulmonary edema.
Investigations: Echocardiography/fluoroscopy shows reduced leaflet mobility with thrombus on the prosthetic valve.
Diagnosis: Obstructive prosthetic valve thrombosis.
Treatment & Management: Heparin infusion, consider thrombolysis or urgent surgical intervention depending on thrombus size and hemodynamic status.
Teaching Point: Subtherapeutic anticoagulation is the leading risk factor for prosthetic valve thrombosis; a muffled valve click is a critical clinical clue.
Presentation: 76-year-old male presents with exertional syncope and chest tightness.
History & Exam: Harsh crescendo-decrescendo systolic murmur radiating to the carotids, slow-rising pulse (pulsus parvus et tardus).
Investigations: Echocardiogram shows severe aortic stenosis with a valve area under 1.0 cm² and elevated transvalvular gradient.
Diagnosis: Critical aortic stenosis with exertional syncope (a class I indication for intervention).
Treatment & Management: Avoid vasodilators/nitrates, urgent evaluation for aortic valve replacement (surgical AVR or TAVR).
Teaching Point: Exertional syncope in aortic stenosis signals critical obstruction and mandates urgent valve intervention — vasodilators can precipitate cardiovascular collapse.
Presentation: 63-year-old with myxomatous mitral valve disease develops sudden severe dyspnea.
History & Exam: New loud holosystolic murmur at the apex, acute pulmonary edema.
Investigations: Echocardiogram shows a flail mitral leaflet with severe acute mitral regurgitation and a hyperdynamic, non-dilated left ventricle.
Diagnosis: Acute severe mitral regurgitation due to spontaneous chordal rupture.
Treatment & Management: Afterload reduction, diuresis, hemodynamic stabilization (IABP if needed), urgent surgical mitral valve repair/replacement.
Teaching Point: Acute MR from chordal rupture causes rapid pulmonary edema despite a normal-sized LV; echocardiography confirms the flail segment and guides urgent surgery.
Vascular Emergencies
Presentation: 60-year-old hypertensive male with sudden severe tearing chest and back pain.
History & Exam: BP differential between arms, new diastolic murmur of aortic regurgitation, diminished femoral pulse.
Investigations: CT angiography confirms a dissection flap involving the ascending aorta.
Diagnosis: Acute Type A aortic dissection.
Treatment & Management: Emergency surgical repair, blood pressure and heart rate control (beta-blockers first) while arranging surgery.
Teaching Point: Type A dissection is a surgical emergency; medical therapy alone has high mortality due to risk of rupture or tamponade.
Presentation: 70-year-old male smoker presents with sudden severe abdominal and back pain with syncope.
History & Exam: Hypotensive, pulsatile abdominal mass, tender abdomen.
Investigations: Bedside ultrasound/CT confirms a ruptured abdominal aortic aneurysm with retroperitoneal hematoma.
Diagnosis: Ruptured abdominal aortic aneurysm.
Treatment & Management: Immediate surgical or endovascular repair, permissive hypotension during resuscitation, massive transfusion protocol activation.
Teaching Point: Triad of abdominal pain, hypotension, and a pulsatile mass should prompt immediate imaging and surgical mobilization for ruptured AAA.
Presentation: 55-year-old post-orthopedic surgery patient develops sudden collapse with hypotension and hypoxia.
History & Exam: Hypotensive, tachycardic, cyanotic, elevated JVP.
Investigations: Echocardiogram shows severe RV strain; CT pulmonary angiogram confirms bilateral massive PE.
Diagnosis: Massive (high-risk) pulmonary embolism with obstructive shock.
Treatment & Management: Systemic thrombolysis (or catheter-directed therapy/embolectomy if contraindicated), hemodynamic support, consider ECMO if refractory.
Teaching Point: Hemodynamic instability from PE defines ‘massive/high-risk’ PE and mandates immediate reperfusion therapy, not just anticoagulation.
Presentation: 34-year-old presents after a road traffic accident with chest pain and breathlessness.
History & Exam: Beck’s triad: hypotension, elevated JVP, and muffled heart sounds; pulsus paradoxus present.
Investigations: Echocardiogram shows a large pericardial effusion with right atrial/ventricular diastolic collapse.
Diagnosis: Cardiac tamponade.
Treatment & Management: Emergency pericardiocentesis or surgical drainage, IV fluids as a temporizing measure, avoid positive-pressure ventilation if possible.
Teaching Point: Beck’s triad and pulsus paradoxus are classic but not always all present; echocardiographic chamber collapse is the key confirmatory finding.
Presentation: 68-year-old with atrial fibrillation presents with sudden severe left leg pain and numbness.
History & Exam: Pale, pulseless, painful, paresthetic, and cold limb (the 5 P’s).
Investigations: Doppler ultrasound/CT angiography confirms an embolic occlusion of the femoral artery.
Diagnosis: Acute limb ischemia due to cardioembolism from atrial fibrillation.
Treatment & Management: Immediate anticoagulation, urgent embolectomy or catheter-directed thrombolysis, vascular surgery consultation.
Teaching Point: Acute limb ischemia is a limb-threatening emergency — the ‘6 P’s’ (pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia) demand urgent revascularization.
Hypertensive Emergencies
Presentation: 65-year-old presents with severe dyspnea and BP 220/130 mmHg.
History & Exam: Bilateral crackles, JVP elevated, severe respiratory distress.
Investigations: Chest X-ray shows pulmonary edema; end-organ assessment (renal function, troponin) performed.
Diagnosis: Hypertensive emergency with acute pulmonary edema (end-organ damage).
Treatment & Management: IV antihypertensives (nitroglycerin, nitroprusside), diuretics, controlled BP reduction (avoid overly rapid drops), oxygen/non-invasive ventilation.
Teaching Point: Hypertensive emergency requires acute end-organ damage, not blood pressure number alone, to define the diagnosis and urgency of IV therapy.
Presentation: 58-year-old presents with severe headache, confusion, and BP 230/140 mmHg.
History & Exam: Altered mental status, no focal neurological deficits.
Investigations: MRI brain shows posterior reversible encephalopathy syndrome (PRES) changes; no hemorrhage or infarct.
Diagnosis: Hypertensive encephalopathy.
Treatment & Management: Controlled IV antihypertensive therapy (target ~25% MAP reduction in the first hour), close neurological monitoring.
Teaching Point: Reduce blood pressure gradually in hypertensive encephalopathy to avoid cerebral hypoperfusion — overly aggressive lowering can cause ischemic stroke.
Presentation: 50-year-old with poorly controlled hypertension presents with blurred vision and reduced urine output.
History & Exam: BP 210/125, papilledema and flame hemorrhages on fundoscopy.
Investigations: Renal function acutely worsened; urinalysis shows proteinuria and hematuria.
Diagnosis: Malignant hypertension with grade IV retinopathy and acute kidney injury.
Treatment & Management: IV antihypertensive therapy with gradual BP reduction, nephrology involvement, treat underlying cause.
Teaching Point: Fundoscopic examination (papilledema, hemorrhages) is essential in suspected malignant hypertension and confirms acute end-organ involvement.
Presentation: 42-year-old presents with episodic severe headache, palpitations, sweating, and BP spikes to 240/140 mmHg.
History & Exam: Pallor during episodes, tremor, tachycardia.
Investigations: Elevated plasma free metanephrines; imaging reveals an adrenal mass.
Diagnosis: Hypertensive crisis due to pheochromocytoma.
Treatment & Management: Alpha-blockade (phenoxybenzamine) before beta-blockade, IV phentolamine for acute crisis, surgical resection once stabilized.
Teaching Point: Never give beta-blockers first in suspected pheochromocytoma — unopposed alpha stimulation can cause a severe hypertensive crisis.
Presentation: 27-year-old, 34 weeks pregnant, presents with severe headache, visual disturbance, and a witnessed seizure.
History & Exam: BP 190/120, hyperreflexia, peripheral edema.
Investigations: Proteinuria present; liver enzymes and platelet count checked to exclude HELLP syndrome.
Diagnosis: Eclampsia with severe hypertension.
Treatment & Management: IV magnesium sulfate for seizure prophylaxis/treatment, IV labetalol or hydralazine for BP control, urgent obstetric delivery planning.
Teaching Point: Magnesium sulfate is first-line for seizure control in eclampsia — it is a neuroprotective and anticonvulsant, not simply an antihypertensive.
Cardiac Arrest & Post-Resuscitation Care
Presentation: 55-year-old achieves return of spontaneous circulation after a witnessed VF arrest with prompt defibrillation.
History & Exam: Remains comatose post-ROSC, hemodynamically labile.
Investigations: ECG shows ST elevation suggesting the precipitating cause; lactate elevated.
Diagnosis: Post-cardiac arrest syndrome.
Treatment & Management: Targeted temperature management (32-36°C), hemodynamic optimization, urgent coronary angiography if ischemic cause suspected, neuroprognostication after 72 hours.
Teaching Point: Post-cardiac arrest care bundles (targeted temperature management, hemodynamic optimization, early angiography) significantly improve neurological outcomes.
Presentation: 48-year-old collapses in hospital; monitor shows organized rhythm but no palpable pulse.
History & Exam: No pulse despite an organized rhythm on the monitor.
Investigations: Bedside ultrasound performed during pulse check reveals a large pericardial effusion.
Diagnosis: Pulseless electrical activity due to cardiac tamponade.
Treatment & Management: High-quality CPR, immediate treatment of the reversible cause (emergency pericardiocentesis), epinephrine per ACLS protocol.
Teaching Point: PEA arrest survival depends entirely on rapidly identifying and treating the reversible cause — point-of-care ultrasound during pulse checks is invaluable.
Presentation: 60-year-old remains unresponsive after successful resuscitation from an out-of-hospital cardiac arrest.
History & Exam: Comatose, no purposeful movement, preserved brainstem reflexes.
Investigations: EEG monitoring initiated; core temperature managed and monitored closely.
Diagnosis: Post-anoxic coma requiring targeted temperature management.
Treatment & Management: Maintain target temperature (32-36°C) for at least 24 hours, avoid fever, sedation/paralysis as needed, delayed neuroprognostication.
Teaching Point: Avoid early prognostication — clinical exam, EEG, and biomarkers are unreliable before 72 hours post-arrest, especially with sedation on board.
Presentation: 65-year-old with end-stage renal disease who missed dialysis presents in cardiac arrest.
History & Exam: History of missed dialysis sessions, known hyperkalemia risk.
Investigations: Prior ECG showed peaked T waves and a widened QRS; potassium markedly elevated.
Diagnosis: Cardiac arrest secondary to severe hyperkalemia.
Treatment & Management: IV calcium gluconate to stabilize the myocardium, insulin-glucose and beta-agonists to shift potassium intracellularly, emergent dialysis, continue CPR per ACLS.
Teaching Point: Suspect hyperkalemia as a reversible cause in dialysis patients presenting in arrest — IV calcium should be given immediately to stabilize the cardiac membrane.
Presentation: 8-year-old child pulled unresponsive from a pool, found in cardiac arrest.
History & Exam: Hypothermic, no spontaneous breathing or pulse.
Investigations: Core temperature markedly low; initial rhythm asystole.
Diagnosis: Cardiac arrest secondary to drowning with hypothermia.
Treatment & Management: Continue high-quality CPR, active rewarming, do not withhold resuscitation based on hypothermia alone (“not dead until warm and dead”), standard ACLS with temperature-adjusted drug intervals.
Teaching Point: Hypothermic cardiac arrest may warrant prolonged resuscitation efforts, as hypothermia can be neuroprotective and mimic irreversible arrest.
Electrolyte & Toxicology-Related Emergencies
Presentation: 72-year-old on ACE inhibitors and potassium-sparing diuretics presents with weakness and palpitations.
History & Exam: Muscle weakness, irregular pulse.
Investigations: ECG shows peaked T waves and widened QRS; potassium 7.2 mmol/L.
Diagnosis: Severe hyperkalemia with ECG changes.
Treatment & Management: IV calcium gluconate for membrane stabilization, insulin-dextrose infusion, nebulized salbutamol, remove offending drugs, consider dialysis if refractory.
Teaching Point: Treat ECG changes of hyperkalemia as an emergency regardless of the exact potassium level — calcium first to protect the myocardium, then measures to shift and eliminate potassium.
Presentation: 80-year-old on digoxin for atrial fibrillation presents with nausea, visual disturbances (yellow-green halos), and palpitations.
History & Exam: Irregular pulse with occasional pauses.
Investigations: ECG shows atrial tachycardia with block; digoxin level elevated; potassium may be elevated in acute toxicity.
Diagnosis: Digoxin toxicity.
Treatment & Management: Discontinue digoxin, correct electrolytes, digoxin-specific antibody fragments (Fab) for severe toxicity/arrhythmia, avoid calcium administration.
Teaching Point: Atrial tachycardia with AV block is a classic arrhythmia of digoxin toxicity; digoxin immune Fab is definitive treatment in life-threatening cases.
Presentation: 25-year-old presents after an intentional tricyclic antidepressant overdose with altered mental status.
History & Exam: Drowsy, dry mouth, dilated pupils, hypotensive.
Investigations: ECG shows a widened QRS (>100 ms) and a terminal R wave in aVR.
Diagnosis: Tricyclic antidepressant toxicity with cardiotoxicity.
Treatment & Management: IV sodium bicarbonate to narrow QRS and counter cardiotoxicity, airway protection, avoid Class Ia/Ic antiarrhythmics.
Teaching Point: QRS widening on ECG is the key marker of TCA cardiotoxicity; sodium bicarbonate is the cornerstone treatment, working via sodium loading and alkalinization.
Presentation: 45-year-old presents after ingesting a large quantity of propranolol, with bradycardia and hypotension.
History & Exam: HR 40, BP 78/50, altered mental status, possible seizures (lipophilic beta-blockers).
Investigations: ECG shows sinus bradycardia; glucose may be low.
Diagnosis: Beta-blocker overdose with cardiogenic shock.
Treatment & Management: High-dose glucagon, IV calcium, high-dose insulin-euglycemia therapy, atropine/pacing for bradycardia, vasopressors, consider lipid emulsion for lipophilic agents.
Teaching Point: High-dose insulin-euglycemia therapy is increasingly favored over glucagon alone for refractory beta-blocker toxicity.
Presentation: 50-year-old presents after amlodipine overdose with profound hypotension and bradycardia.
History & Exam: BP 70/40, HR 45, cool extremities, altered sensorium.
Investigations: ECG shows bradycardia with varying degrees of AV block; glucose often elevated (unlike beta-blocker toxicity).
Diagnosis: Calcium channel blocker overdose with cardiogenic/vasodilatory shock.
Treatment & Management: IV calcium (often high-dose/repeated), high-dose insulin-euglycemia therapy, vasopressors, consider lipid emulsion therapy and mechanical circulatory support if refractory.
Teaching Point: High-dose insulin-euglycemia therapy is a key treatment for CCB overdose, improving myocardial glucose utilization and inotropy independent of calcium channels.
Congenital & Pediatric Cardiac Emergencies
Presentation: 3-day-old neonate presents with cyanosis and poor feeding, worsening as the ductus arteriosus closes.
History & Exam: Central cyanosis unresponsive to oxygen, weak femoral pulses.
Investigations: Echocardiogram confirms transposition of the great arteries (or other duct-dependent lesion).
Diagnosis: Duct-dependent congenital heart disease (e.g., transposition of the great arteries).
Treatment & Management: IV prostaglandin E1 infusion to maintain ductal patency, urgent pediatric cardiology/cardiac surgery referral (e.g., balloon atrial septostomy, arterial switch operation).
Teaching Point: Any neonate with cyanosis unresponsive to oxygen and collapsing femoral pulses should receive prostaglandin E1 promptly while awaiting definitive diagnosis.
Presentation: 18-month-old known case of Tetralogy of Fallot becomes acutely more cyanotic and irritable during crying.
History & Exam: Increased cyanosis, tachypnea, decreased intensity of the murmur during the spell.
Investigations: Known right ventricular outflow tract obstruction on prior echocardiogram.
Diagnosis: Hypercyanotic (Tet) spell.
Treatment & Management: Knee-to-chest positioning, oxygen, morphine, IV fluids, phenylephrine to increase systemic vascular resistance, beta-blockers to relieve infundibular spasm.
Teaching Point: Knee-to-chest positioning increases systemic vascular resistance, reducing right-to-left shunting and improving pulmonary blood flow during a Tet spell.
Presentation: 2-month-old infant presents with poor feeding, irritability, and rapid breathing.
History & Exam: HR 260/min, difficult to palpate individual beats, signs of poor perfusion.
Investigations: ECG shows a narrow-complex tachycardia with no visible P waves.
Diagnosis: Supraventricular tachycardia (SVT) in infancy.
Treatment & Management: Vagal maneuvers (ice to face), IV adenosine as first-line, synchronized cardioversion if hemodynamically unstable.
Teaching Point: Infants with SVT often present with nonspecific feeding difficulty and irritability rather than palpitations; ice-to-face is the preferred vagal maneuver in infants.
Presentation: 3-year-old presents with 6 days of persistent fever, rash, conjunctival injection, and cracked lips.
History & Exam: Bilateral non-purulent conjunctivitis, strawberry tongue, cervical lymphadenopathy, extremity changes.
Investigations: Echocardiogram reveals coronary artery dilation/aneurysm formation.
Diagnosis: Kawasaki disease with coronary artery involvement.
Treatment & Management: IV immunoglobulin (IVIG) and high-dose aspirin, close echocardiographic follow-up for aneurysm progression, long-term antiplatelet/anticoagulant therapy for large aneurysms.
Teaching Point: Early IVIG administration (within 10 days of fever onset) significantly reduces the risk of coronary artery aneurysm in Kawasaki disease.
Presentation: 2-week-old neonate presents with poor feeding, irritability, and signs of heart failure.
History & Exam: Weak or absent femoral pulses with strong brachial pulses, differential blood pressure between upper and lower limbs.
Investigations: Echocardiogram confirms coarctation of the aorta.
Diagnosis: Coarctation of the aorta presenting in infancy with heart failure.
Treatment & Management: Prostaglandin E1 to reopen the ductus arteriosus and bypass the coarctation, stabilize heart failure, surgical or balloon repair.
Teaching Point: Absent or weak femoral pulses relative to brachial pulses in an infant should always raise suspicion for coarctation of the aorta.
Device & Post-Procedural Complications
Presentation: 80-year-old pacemaker-dependent patient presents with dizziness and near-syncope.
History & Exam: Bradycardic, symptomatic.
Investigations: ECG shows pacing spikes without subsequent QRS complexes (failure to capture).
Diagnosis: Pacemaker malfunction — failure to capture.
Treatment & Management: Increase pacing output/threshold testing, evaluate lead position and battery status, temporary pacing if hemodynamically unstable, device/lead revision.
Teaching Point: Failure to capture in a pacemaker-dependent patient is an emergency; assess lead integrity, battery status, and pacing thresholds promptly.
Presentation: 65-year-old with an implantable cardioverter-defibrillator (ICD) receives multiple shocks within an hour.
History & Exam: Anxious, distressed following repeated shocks, hemodynamically variable between episodes.
Investigations: Device interrogation confirms recurrent appropriate shocks for sustained ventricular arrhythmias.
Diagnosis: ICD electrical storm (≥3 appropriate shocks within 24 hours).
Treatment & Management: IV amiodarone/beta-blockade, sedation, treat reversible triggers (ischemia, electrolyte imbalance), consider emergent catheter ablation, deep sedation if refractory.
Teaching Point: Electrical storm requires urgent antiarrhythmic therapy and evaluation for a reversible trigger — repeated shocks alone do not treat the underlying arrhythmic substrate.
Presentation: 68-year-old develops sudden hypotension and chest pain during a percutaneous coronary intervention.
History & Exam: Acute hypotension intra-procedurally, muffled heart sounds.
Investigations: Angiography shows contrast extravasation consistent with coronary perforation; echocardiogram confirms a new pericardial effusion with tamponade physiology.
Diagnosis: Coronary artery perforation with cardiac tamponade during PCI.
Treatment & Management: Immediate balloon occlusion to control bleeding, pericardiocentesis, covered stent placement or surgical repair as needed, reverse anticoagulation.
Teaching Point: Sudden hypotension during PCI should prompt immediate consideration of coronary perforation and tamponade — rapid pericardial drainage and bleeding control are lifesaving.
Presentation: 60-year-old, 12 hours after coronary artery bypass surgery, develops falling blood pressure and reduced chest tube output.
History & Exam: Hypotensive, elevated JVP, sudden cessation of previously brisk chest tube drainage.
Investigations: Echocardiogram shows a localized pericardial/mediastinal hematoma causing tamponade physiology.
Diagnosis: Post-cardiac surgery tamponade.
Treatment & Management: Emergency re-exploration/surgical evacuation of the hematoma, hemodynamic support in the interim.
Teaching Point: Sudden cessation of chest tube drainage after cardiac surgery, especially with hemodynamic deterioration, suggests tube occlusion by clot and localized tamponade — a surgical emergency.
Presentation: 82-year-old develops bradycardia and dizziness one day after TAVR.
History & Exam: Bradycardic, otherwise stable hemodynamics.
Investigations: ECG shows new complete heart block, a recognized conduction complication of TAVR given proximity to the conduction system.
Diagnosis: New complete heart block post-TAVR.
Treatment & Management: Temporary pacing, monitor for resolution over 24-48 hours, permanent pacemaker implantation if heart block persists.
Teaching Point: New conduction abnormalities are among the most common complications post-TAVR due to the proximity of the aortic annulus to the AV conduction system; a period of monitoring guides the need for permanent pacing.