A 65-year-old man with hypertension, type 2 diabetes, and smoking history presents with 2 brief episodes of right arm numbness, facial droop, and slurred speech lasting 5–10 minutes. He returns to baseline after each episode. MRI and echocardiography are normal. He has a severe aspirin allergy.
Which of the following describes the mechanism of action of the most appropriate medication to prevent future events?
A. blockade of the adenosine diphosphate (ADP) receptor
B. blockade of phosphodiesterase III
C. blockade of thromboxane A2
D. inhibition of factor Xa
E. inhibition of vitamin K epoxidase
A. blockade of the adenosine diphosphate (ADP) receptor ✅
Explanation:
The patient has experienced transient ischemic attacks (TIAs), which are neurologic emergencies due to high risk of stroke.
First-line prevention is antiplatelet therapy (aspirin).
Aspirin allergy → use an ADP receptor blocker (e.g., clopidogrel) instead.
Mechanism: ADP receptor antagonists prevent platelet aggregation by blocking the P2Y12 receptor.
Other options:
B: PDE III inhibitors → milrinone, for heart failure
C: Thromboxane A2 blockade → aspirin
D: Factor Xa inhibitors → anticoagulation for atrial fibrillation or VTE
E: Vitamin K epoxide inhibition → warfarin
A 65-year-old man presents with exertional chest pain for 3 months, now occurring 2–3 times per week. ECG at rest is normal. During an exercise stress test, he develops chest pain and ST-segment depression. Symptoms resolve with rest.
If two appropriate drugs are prescribed for long-term management, what are their most likely mechanisms?
A. angiotensin converting enzyme inhibition and β-blockade
B. calcium channel blockade and β-blockade
C. vasodilation and angiotensin converting enzyme inhibition
D. vasodilation and β-blockade
E. vasodilation and calcium channel blockade
D. vasodilation and β-blockade ✅
Explanation:
The patient has stable angina: exertional chest pain relieved by rest, ST depression on stress test, normal ECG at rest.
First-line therapy: combination of a β-blocker and a nitrate:
β-blocker: reduces heart rate and contractility → reduces myocardial oxygen demand
Nitrate: forms nitric oxide → activates guanylate cyclase → increases cGMP → smooth muscle relaxation → vasodilation of veins > arteries → decreases preload, modestly reduces afterload, dilates coronary arteries
Together, they reduce anginal symptoms and improve long-term outcomes.
Other options:
ACE inhibitors → helpful post-MI, heart failure, hypertension, not primary antianginal therapy
Calcium channel blockers → alternative if β-blockers contraindicated or variant angina
A 64-year-old Asian man presents with chest pain and palpitations. ECG shows a rapid, regular, narrow-complex tachycardia. Carotid sinus massage and Valsalva maneuver are unsuccessful.
Which medication is most likely effective to slow conduction through the AV node?
A. adenosine
B. dofetilide
C. epinephrine
D. lidocaine
E. nifedipine
A. adenosine ✅
Explanation:
The patient has supraventricular tachycardia (SVT), likely AV nodal reentrant tachycardia.
Adenosine is the first-line drug to acutely terminate SVT:
Increases K⁺ efflux → hyperpolarizes AV nodal cells
Shortens phase 3 of pacemaker action potential → slows AV nodal conduction
Prolongs refractory period, decreases automaticity → may terminate the arrhythmia
Other options:
Dofetilide → Class III antiarrhythmic (prolongs QT, not first-line for SVT)
Epinephrine → increases heart rate and AV conduction
Lidocaine → Class Ib antiarrhythmic, ventricular arrhythmias
Nifedipine → dihydropyridine CCB, mainly vasodilates, not used for AV nodal blockade
Key point: Adenosine has ultra-short duration (~15 sec) and is ideal for acute AV nodal-dependent SVTs.
A 75-year-old man experiences syncope and chest pain during exertion. He has mild exertional chest discomfort over the past month. Exam reveals a systolic crescendo-decrescendo murmur at the right upper sternal border radiating to the carotids.
What is the most appropriate therapy to prolong survival in this patient?
A. lisinopril
B. metoprolol
C. nitroprusside
D. percutaneous valve replacement
E. spironolactone
D. percutaneous valve replacement ✅
Explanation:
This patient has severe, symptomatic aortic stenosis (AS):
Syncope, exertional angina, systolic murmur radiating to carotids
Medical therapy does NOT prolong survival in severe AS.
Definitive treatment: aortic valve replacement
Percutaneous (TAVR) preferred in older or higher-risk patients
Surgical valve replacement is an alternative in low-risk patients
Other options:
Lisinopril, metoprolol, spironolactone → symptomatic relief or comorbidity management, but do not improve survival
Nitroprusside → acute afterload reduction in hypertensive crisis, not AS
Osteopathic note: Chronic tissue texture changes (cool, dry, ropy skin) may be noted over the aortic valve area (2nd intercostal space, right sternal border).
A 61-year-old man presents with sudden crushing chest pain radiating to the left jaw after slamming his finger in a car door. Vital signs: BP 100/60, HR 111, RR 24, O₂ sat 94%.
ECG: ST elevation in V2–V6, reciprocal ST depression in II, III, aVF.
Troponin: <0.03 ng/mL (normal).
What is the most appropriate next step?
A. cancel the cardiac catheterization
B. obtain a CK-MB level
C. obtain a repeat troponin in 3 hours
D. proceed with cardiac catheterization
E. repeat the ECG
D. proceed with cardiac catheterization ✅
Explanation:
The patient has an acute ST-elevation myocardial infarction (STEMI):
Symptoms: crushing chest pain, diaphoresis
ECG: ST elevation in contiguous leads V2–V6 (anterolateral MI) with reciprocal changes
Troponin may be normal early (<30 min from symptom onset) because biomarker release takes time.
STEMI is diagnosed clinically by ECG and symptoms, not waiting for troponin.
Immediate management: emergent cardiac catheterization for reperfusion therapy (PCI), which is time-sensitive (“time is muscle”).
Other options:
A: Troponin is not required for initial STEMI management
B: CK-MB is unnecessary in the era of troponin; does not change emergent management
C: Waiting for troponin would delay life-saving treatment
E: ECG already shows STEMI; repeating is not helpful
Key point: STEMI = emergent PCI regardless of initial troponin.
88-year-old man has episodes of flushing after starting a new drug for fast heart rate due to atrial fibrillation. Pulse now 90/min. What is the drug’s mechanism?
A. Activating G-protein–coupled adrenergic receptors
B. Activating K⁺ channels
C. Binding D-ala-D-ala cell-wall precursors
D. Blocking L-type Ca²⁺ channels
E. Inhibiting β1-adrenergic stimulation
Correct Answer: D — Blocking L-type Ca²⁺ channels
Explanation:
The patient has atrial fibrillation treated with a rate-controlling calcium channel blocker (diltiazem or verapamil). Side effects include facial flushing and peripheral edema. These drugs block L-type Ca²⁺ channels in cardiac tissue and vascular smooth muscle.
63-year-old woman with history of left-sided heart failure presents with leg swelling, right upper quadrant pain, cyanosis, abdominal distension, and 3+ pitting edema. Skin around ankles is scaly and brawny.
Which finding is most specific for her condition?
A. chronic exertional dyspnea
B. jugular venous distension
C. nonproductive cough worse when lying flat
D. paroxysmal nocturnal dyspnea
E. pulmonary congestion
B. jugular venous distension ✅
Explanation:
Patient has right-sided heart failure (RHF) secondary to chronic left-sided heart failure.
RHF findings: dependent edema, hepatic congestion (RUQ pain, hepatomegaly), ascites, venous stasis (brawny skin), and jugular venous distension (JVD).
JVD is relatively specific for RHF due to elevated right atrial pressures transmitted to jugular veins.
Osteopathic note: Chapman points at right 5th–6th intercostal spaces correspond to liver viscerosomatic reflexes.
Other options:
A, C, D, E → more typical of left-sided heart failure, not specific for RHF.
56-year-old man with hypertension, hyperlipidemia, atrial fibrillation, and medications including metoprolol presents with syncope after a sudden thud, dizziness, and lightheadedness. ECG shows sporadically dropped QRS complexes (P waves not conducted).
This patient’s symptoms are most likely due to pathology in which part of the conduction system?
A. Entry site of pulmonary veins in left atrium
B. His-Purkinje system just distal to the AV node
C. Isthmus between inferior vena cava and tricuspid valve
D. Junction of crista terminalis and superior vena cava
E. Right side of interventricular septum at membranous–muscular junction
B. His-Purkinje system just distal to the AV node ✅
Explanation:
This patient has second-degree Mobitz type II AV block:
Dropped QRS complexes with nonconducted P waves, irregular rhythm
Often asymptomatic until syncope occurs
Pathophysiology: dysfunction of His-Purkinje system distal to the AV node
Causes: intrinsic conduction disease or cardioactive medications (e.g., beta-blockers, digoxin, non-dihydropyridine calcium channel blockers)
Clinical significance: higher risk of progression to complete heart block → pacemaker often required
AV node itself is usually intact; Mobitz I (Wenckebach) involves AV node, while Mobitz II involves His-Purkinje
Which part of the heart is the usual origin of atrial fibrillation, and how does its ECG differ from Mobitz type II AV block?
A. AV node; irregularly irregular rhythm with dropped QRS
B. His-Purkinje system; irregularly irregular rhythm with absent P waves
C. Entry site of pulmonary veins in left atrium; irregularly irregular rhythm with absent P waves
D. SA node; dropped QRS with progressively lengthened PR intervals
E. Ventricular myocardium; wide QRS with AV dissociation
C. Entry site of pulmonary veins in left atrium; irregularly irregular rhythm with absent P waves ✅
Explanation:
Atrial fibrillation originates from myocardial cells at the pulmonary vein entry into the left atrium.
ECG features: irregularly irregular R-R intervals, absent P waves.
Mobitz type II AV block differs: sporadically dropped QRS complexes with nonconducted P waves, regular atrial rhythm, often distal His-Purkinje pathology.
Key distinction: AF → irregular atrial rhythm, absent P waves; Mobitz II → regular atrial rhythm with intermittent conduction failure.
Where does atrial flutter usually originate, and how does its ECG differ from Mobitz type II AV block?
A. AV node; sporadically dropped QRS
B. His-Purkinje system; intermittent nonconducted P waves
C. Isthmus between inferior vena cava and tricuspid valve; sawtooth flutter waves
D. Pulmonary vein entry into left atrium; irregularly irregular rhythm
E. SA node; prolonged PR interval
C. Isthmus between inferior vena cava and tricuspid valve; sawtooth flutter waves ✅
Explanation:
Atrial flutter is caused by a macroreentrant circuit in the right atrial isthmus between the inferior vena cava and tricuspid valve.
ECG features: “sawtooth” flutter waves, atrial rate ~300 bpm.
Ventricular response can be regular (e.g., 3:1 block) or variable.
Mobitz type II AV block differs: sporadically dropped QRS complexes, regular atrial rhythm, no sawtooth waves.
Key distinction: flutter waves present in atrial flutter; absent in Mobitz II.
Where is the SA node located, and how does its block differ on ECG from Mobitz type II AV block?
A. AV node; dropped QRS with regular P waves
B. His-Purkinje system; dropped QRS without prior PR prolongation
C. Pulmonary vein entry into left atrium; irregularly irregular rhythm
D. Crista terminalis/SVC junction in right atrium; intermittent failure of atrial depolarization
E. Isthmus between IVC and tricuspid valve; sawtooth flutter waves
D. Crista terminalis/SVC junction in right atrium; intermittent failure of atrial depolarization ✅
Explanation:
The SA node is located at the junction of the crista terminalis and superior vena cava.
SA block occurs when impulses fail to leave the SA node, causing dropped P waves, sinus pauses, or sinus arrest.
ECG: intermittent absence of atrial depolarization (P waves); ventricular rhythm may continue from escape beats.
Mobitz type II AV block differs: sporadically dropped QRS complexes despite regular atrial P waves; pathology is distal His-Purkinje system.
Key distinction: SA block → P waves absent; Mobitz II → P waves present but not conducted.
A patient presents with intermittent syncope and palpitations. ECG shows regular P waves with randomly dropped QRS complexes and a constant PR interval.
Which is the most likely diagnosis and next step in management?
A. Mobitz type I AV block; observation
B. Mobitz type II AV block; pacemaker placement
C. SA node block; atropine
D. Atrial fibrillation; rate control with beta-blocker
E. Third-degree AV block; no treatment
B. Mobitz type II AV block; pacemaker placement ✅
Explanation:
ECG: Regular P waves, constant PR interval, intermittent non-conducted QRS → Mobitz II.
Clinical: Syncope, palpitations, fatigue.
Management: Pacemaker placement due to high risk of progression to complete heart block.
Key point: Mobitz II is His-Purkinje system disease (distal to AV node), unlike Mobitz I which is usually AV nodal.
A patient presents with fatigue, palpitations, and syncope. ECG shows P waves and QRS complexes that are rhythmically dissociated.
What is the most likely diagnosis and recommended management?
A. Mobitz type I AV block; observation
B. Mobitz type II AV block; pacemaker placement
C. Third-degree (complete) AV block; pacemaker placement
D. SA node block; atropine
E. Atrial fibrillation; rate control with beta-blocker
C. Third-degree (complete) AV block; pacemaker placement ✅
Explanation:
ECG: Complete dissociation between atrial (P waves) and ventricular (QRS) activity.
Clinical presentation: Fatigue, lightheadedness, palpitations, syncope.
Management: Permanent pacemaker is indicated due to risk of sudden cardiac death.
Key point: In complete AV block, the His-Purkinje system or AV node fails to conduct any impulses, so atria and ventricles beat independently.
A patient presents with palpitations and irregular heartbeat. ECG shows narrow QRS complexes, absent P waves, and irregularly irregular R-R intervals.
What is the most likely diagnosis and key ECG features?
A. Atrial flutter; sawtooth flutter waves
B. Mobitz type II AV block; constant PR interval with dropped QRS
C. Atrial fibrillation; absent P waves, irregularly irregular rhythm
D. Third-degree AV block; P waves and QRS dissociated
E. SA node block; intermittent dropped P waves
C. Atrial fibrillation; absent P waves, irregularly irregular rhythm ✅
Explanation:
ECG:
Absent P waves
Irregularly irregular R-R intervals
Narrow QRS complexes
May see low-amplitude fibrillatory waves indicating continuous atrial depolarization.
Clinical: Palpitations, fatigue, possible syncope.
Key point: Most common arrhythmia; often originates in pulmonary vein myocardial tissue.
An 82-year-old woman presents with palpitations, lightheadedness, and shortness of breath. ECG shows narrow QRS complexes, irregularly irregular rhythm, and no organized P waves.
Which physiologic factor primarily determines her ventricular rate?
A. Atrial muscle depolarization rate
B. Atrioventricular (AV) node refractory period
C. Purkinje system pacemaker activity
D. Sinoatrial node discharge rate
E. Ventricular muscle refractory period
B. Atrioventricular (AV) node refractory period ✅
Explanation:
This patient has atrial fibrillation (AF): rapid, irregular atrial activity without organized P waves.
Ventricular response rate is not determined by atrial firing, sinoatrial node, or ventricular muscle directly.
The AV node filters the chaotic atrial impulses, and its refractory period largely determines how many impulses reach the ventricles, controlling ventricular rate.
Key point: In AF, AV nodal properties are the main determinant of ventricular contraction rate.
A 52-year-old man with shortness of breath, orthopnea, pitting edema, S4 gallop, hypertension, and hypokalemia (K⁺ 2.8 mEq/L) requires diuresis.
Which diuretic is most appropriate for this patient?
A. Acetazolamide
B. Ethacrynic acid
C. Furosemide
D. Hydrochlorothiazide
E. Triamterene
E. Triamterene ✅
Explanation:
This patient has heart failure with fluid overload and hypokalemia.
Potassium-sparing diuretics are preferred in patients with hypokalemia to avoid further K⁺ loss.
Epithelial sodium channel (ENaC) blockers: triamterene, amiloride
Aldosterone antagonists: spironolactone, eplerenone
Mechanism: Block Na⁺ reabsorption in the distal convoluted tubule and collecting duct, reducing K⁺ excretion → mild diuresis.
Why not loop or thiazide diuretics: They worsen hypokalemia.
Clinical features of heart failure: Orthopnea, pitting edema, fatigue, dry cough, weight gain, tachycardia, S4 gallop.
A 63-year-old woman presents with 6 hours of chest pain and dyspnea. ECG and troponin I confirm myocardial infarction.
Which intracellular change is most characteristic of ischemic cardiac myocytes?
A. Decreased K⁺ → hyperpolarization
B. Decreased K⁺ → sustained depolarization
C. Decreased Na⁺ → plateau of action potential
D. Increased K⁺ → sustained repolarization
E. Increased Na⁺ → more frequent action potentials
B. Decreased K⁺ → sustained depolarization ✅
Explanation:
Ischemia reduces ATP, impairing the Na⁺/K⁺ ATPase.
This decreases K⁺ transport into the cell and Na⁺/Ca²⁺ transport out.
Result: decreased intracellular K⁺ → membrane remains depolarized, inactivating fast Na⁺ channels.
Consequences: slow phase 0 upstroke, reduced excitability, and impaired contraction.
Other options:
A: Hyperpolarization occurs with increased, not decreased, K⁺ gradient.
C: Plateau is Ca²⁺-driven; ischemia reduces Ca²⁺ influx, not Na⁺ depletion.
D: Intracellular K⁺ decreases, not increases, in ischemia.
E: Increased Na⁺ occurs, but action potentials cannot fire more frequently because the membrane is depolarized and Na⁺ channels are inactivated.
Key point: Ischemic myocytes are partially depolarized due to K⁺ loss, impairing normal action potential generation.
A 72-year-old woman with hypertension on verapamil presents for a routine checkup. She is asymptomatic, vital signs are normal, and the ECG shows a slowed conduction through the AV node.
Question: What is the most likely cause of this patient’s electrical rhythm?
A. Mild myocardial infarction
B. Recent stressful episode
C. Sinus tachycardia
D. Tick bite
E. Verapamil therapy
E. Verapamil therapy ✅
Explanation:
Verapamil is a non-dihydropyridine calcium channel blocker.
It slows conduction through the AV node by inhibiting L-type Ca²⁺ channels, which may prolong PR interval or produce first-degree AV block on ECG.
This effect is expected and usually asymptomatic in patients without structural heart disease.
Additional notes:
Other choices:
Mild MI: usually shows ST changes or Q waves.
Stress: typically increases heart rate (sinus tachycardia), not slows AV conduction.
Tick bite: may cause Lyme carditis, but usually associated with higher-degree AV block and symptomatic bradycardia.
Sinus tachycardia: heart rate >100/min; patient’s HR is normal.
A 40-year-old man with schizophrenia is brought in agitated and confused. He is treated with IV haloperidol and lorazepam. One hour later, he develops palpitations, BP 108/72 mmHg, and ECG shows prolonged QT interval with polymorphic ventricular tachycardia (Torsades de Pointes).
Question: What is the most appropriate treatment?
A. Amiodarone
B. Calcium gluconate
C. Cyproheptadine
D. Dantrolene
E. Magnesium sulfate
E. Magnesium sulfate ✅
Explanation:
Torsades de Pointes (TdP) is a polymorphic ventricular tachycardia associated with prolonged QT interval.
Common causes:
Medications: haloperidol, other antipsychotics, antiarrhythmics
Electrolyte abnormalities: hypomagnesemia, hypokalemia
Treatment:
IV magnesium sulfate is first-line, even if serum magnesium is normal.
Correct underlying electrolyte abnormalities.
Stop offending medications.
Temporary pacing or isoproterenol may be used in refractory cases.
Other options:
Amiodarone: not recommended, can further prolong QT.
Calcium gluconate: used in hyperkalemia or calcium channel blocker overdose.
Cyproheptadine: for serotonin syndrome.
Dantrolene: for malignant hyperthermia or neuroleptic malignant syndrome.
Key point: Antipsychotics like haloperidol can prolong the QT interval, predisposing to TdP, especially in acutely agitated patients receiving IV doses.
A 43-year-old male coal miner is rescued after a shaft collapse, with crush injuries to multiple extremities. He is hypotensive and tachycardic. ECG shows peaked T waves. Laboratory tests are pending.
Question: What is the most appropriate immediate management?
A. β-adrenergic antagonist
B. Calcium gluconate
C. Glucagon
D. Normal saline with KCl
E. Spironolactone
Answer: B. Calcium gluconate ✅
Calcium gluconate is the first-line treatment for hyperkalemia with ECG changes, as it is cardioprotective and prevents progression to fatal arrhythmias.
Explanation:
Crush injury → rhabdomyolysis → hyperkalemia from massive potassium release from damaged muscle.
ECG changes: Peaked T waves, widening QRS, sine-wave pattern → risk of ventricular arrhythmia.
Immediate treatment:
Calcium gluconate: Stabilizes cardiac myocytes, preventing fatal arrhythmias. Does not lower K+, only cardioprotective.
A patient is diagnosed with atrial flutter. Which class of medications is typically first-line for ventricular rate control?
A. Class I antiarrhythmics
B. β-blockers and calcium channel blockers
C. Digoxin and amiodarone only
D. ACE inhibitors and ARBs
E. Nitrates
B. β-blockers and calcium channel blockers ✅
Explanation:
Atrial flutter is a macro-reentrant atrial tachycardia, usually with atrial rates of ~250–350 bpm.
Ventricular response is often regular but fast (commonly 2:1 AV conduction → ~150 bpm).
Rate control:
β-blockers: Reduce sympathetic stimulation → slow AV node conduction.
Non-dihydropyridine calcium channel blockers (verapamil, diltiazem): Slow AV node conduction directly.
Other considerations:
Digoxin can be used in patients with heart failure or when other agents are contraindicated.
Rhythm control (e.g., cardioversion or antiarrhythmics like ibutilide) may be needed for symptom relief or in cases of rapid ventricular rates despite rate control.
Goal: Control ventricular rate and reduce risk of thromboembolism (anticoagulation as indicated).
A 55-year-old woman with diastolic heart failure takes an extra dose of furosemide and develops lightheadedness, hypotension, and signs of dehydration. Which additional lab or physiologic finding is most likely?
A. Bradycardia
B. Elevated renin
C. Hyperkalemia
D. Metabolic acidosis
E. Vasodilation of renal efferent arterioles
B. Elevated renin ✅
Explanation:
Mechanism: Diuretic-induced hypovolemia → decreased renal perfusion pressure → activation of the renin-angiotensin-aldosterone system (RAAS).
Result:
↑ Renin → ↑ Angiotensin II → ↑ Aldosterone
Sodium and water retention to restore blood pressure and volume
Potential hypokalemia and metabolic alkalosis (not acidosis)
Clinical clue: Orthostatic hypotension, dry mucous membranes, poor skin turgor.
Key point: Any hypovolemic state triggers RAAS activation, making elevated renin a hallmark early finding.
A 63-year-old woman with atrial fibrillation on warfarin presents for routine labs. Her INR is 4.1 (therapeutic goal 2–3). She recently started a new medication. Which drug is most likely responsible for the supratherapeutic INR?
A. Aspirin
B. Cholestyramine
C. Metoprolol succinate
D. Trimethoprim/sulfamethoxazole
E. Vitamin K
D. Trimethoprim/sulfamethoxazole (TMP/SMX) ✅
Explanation:
TMP/SMX increases warfarin activity by:
Inhibiting CYP2C9, slowing warfarin metabolism
Displacing warfarin from plasma proteins, increasing free warfarin
Result: ↑ Warfarin effect → prolonged PT and supratherapeutic INR
Other options:
Aspirin: ↑ bleeding risk but does not affect INR
Cholestyramine: ↓ warfarin absorption → lowers INR
Metoprolol: no significant interaction with warfarin
Vitamin K: reverses warfarin, lowers INR
Key point: Always check for antibiotics, especially TMP/SMX, metronidazole, or fluoroquinolones, when INR is supratherapeutic in a patient on warfarin.
A 72-year-old man presents with inferior STEMI (ST elevation in II, III, aVF) and is given sublingual nitroglycerin. Thirty minutes later, he develops severe dyspnea, hypotension (75/50 mmHg), cold clammy skin, but clear lungs. What is the most likely cause of his decompensation?
A. Decreased left ventricular ejection fraction
B. Decreased left ventricular end-diastolic volume
C. Increased pulmonary artery systolic pressure
D. Increased pulmonary capillary wedge pressure
E. Increased systemic vascular resistance
B. Decreased left ventricular end-diastolic volume ✅
Explanation:
This patient likely has a right ventricular (RV) infarction, as suggested by inferior STEMI.
RV infarctions make patients preload-dependent, meaning cardiac output depends on adequate venous return (LVEDV).
Nitrates (venodilators) reduce preload → LVEDV decreases → precipitous hypotension and shock.
Key features:
Clear lungs (not pulmonary edema)
Hypotension
Cold, clammy skin
Inferior STEMI pattern on ECG
High-yield point:
Avoid nitrates and aggressive diuresis in suspected RV infarction.
Treat with IV fluids to maintain preload and support RV output.
