Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Secondary arrhythmias (electrolyte, drug-induced). These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 1: A 70-year-old man presents to his primary care physician for a general checkup. He states that he has been doing well and taking his medications as prescribed. He recently started a new diet and supplement to improve his health and has started exercising. The patient has a past medical history of diabetes, a myocardial infarction, and hypertension. He denies any shortness of breath at rest or with exertion. An ECG is performed and is within normal limits. Laboratory values are ordered as seen below.
Serum:
Na+: 139 mEq/L
Cl-: 100 mEq/L
K+: 6.7 mEq/L
HCO3-: 25 mEq/L
Glucose: 133 mg/dL
Ca2+: 10.2 mg/dL
Which of the following is the most likely cause of this patient's presentation?
- A. Medication (Correct Answer)
- B. Acute renal failure
- C. Hemolysis
- D. Dietary changes
- E. Rhabdomyolysis
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Medication***
- The patient's **hyperkalemia** (K+ 6.7 mEq/L) despite feeling well, suggests a common side effect of medications, particularly those used for his pre-existing conditions like **hypertension** (**ACE inhibitors**, **ARBs**, **spironolactone**) and **diabetes**.
- Medications are a frequent cause of asymptomatic electrolyte abnormalities, and given his complex medical history and the absence of acute symptoms, this is the most likely culprit.
*Acute renal failure*
- While acute renal failure can cause **hyperkalemia**, it typically presents with other symptoms such as **oliguria**, **fluid retention**, or other signs of organ dysfunction, which are not described.
- The patient is reported to be "doing well" without **shortness of breath** or other acute complaints, making acute renal failure less likely as the primary cause of isolated hyperkalemia.
*Hemolysis*
- **Hemolysis** can release intracellular potassium, leading to **pseudohyperkalemia**, but it would typically be suspected in cases of **blood draw errors** or conditions causing red blood cell breakdown, none of which are indicated.
- The patient's presentation does not include any signs or symptoms suggestive of red cell destruction.
*Dietary changes*
- While an extremely **high-potassium diet** or certain **supplements** could contribute to hyperkalemia, it is less common for dietary changes alone to cause such a significant elevation in a patient with normal organ function.
- Given his medical history, medication-induced hyperkalemia is a more direct and common explanation.
*Rhabdomyolysis*
- **Rhabdomyolysis** involves the breakdown of muscle tissue, releasing potassium and other intracellular contents, but it is usually associated with significant **muscle pain**, **weakness**, and elevated **creatine kinase**.
- The patient denies these symptoms and has no other indicators pointing towards severe muscle injury.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 2: A 54-year-old man comes to the emergency department because of episodic palpitations for the past 12 hours. He has no chest pain. He has coronary artery disease and type 2 diabetes mellitus. His current medications include aspirin, insulin, and atorvastatin. His pulse is 155/min and blood pressure is 116/77 mm Hg. Physical examination shows no abnormalities. An ECG shows monomorphic ventricular tachycardia. An amiodarone bolus and infusion is given, and the ventricular tachycardia converts to normal sinus rhythm. He is discharged home with oral amiodarone. Which of the following is the most likely adverse effect associated with long-term use of this medication?
- A. Angle-closure glaucoma
- B. Hepatic adenoma
- C. Shortened QT interval on ECG
- D. Progressive multifocal leukoencephalopathy
- E. Chronic interstitial pneumonitis (Correct Answer)
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Chronic interstitial pneumonitis***
- **Amiodarone** is known to cause several dose-dependent adverse effects, including **pulmonary toxicity** in the form of **interstitial pneumonitis** or fibrosis.
- This adverse effect can manifest as progressive dyspnea, cough, and infiltrates on chest imaging, requiring careful monitoring during long-term use.
*Angle-closure glaucoma*
- While some medications can cause **angle-closure glaucoma**, it is **not a classic or common adverse effect of amiodarone**.
- **Topiramate** and **sulfonamides** are more commonly associated with acute angle-closure glaucoma.
*Hepatic adenoma*
- **Hepatic adenomas** are typically associated with **oral contraceptive use** and sometimes **anabolic steroid use**, not amiodarone.
- Amiodarone can cause **hepatic toxicity** (elevated transaminases, hepatitis), but not specifically hepatic adenoma.
*Shortened QT interval on ECG*
- **Amiodarone** is a Class III antiarrhythmic drug that **prolongs the QT interval** by blocking potassium channels, which is its mechanism of action for suppressing arrhythmias.
- Therefore, a shortened QT interval is the **opposite of what would be expected with amiodarone use**.
*Progressive multifocal leukoencephalopathy*
- **Progressive multifocal leukoencephalopathy (PML)** is a rare, severe opportunistic infection of the brain caused by the **JC virus**, typically seen in immunocompromised individuals.
- It is **not an adverse effect of amiodarone**; drugs like natalizumab or rituximab, which affect the immune system, are associated with PML.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 3: A 72-year-old man with congestive heart failure is brought to the emergency department because of chest pain, shortness of breath, dizziness, and palpitations for 30 minutes. An ECG shows a wide complex tachycardia with a P-wave rate of 105/min, an R-wave rate of 130/min, and no apparent relation between the two. Intravenous pharmacotherapy is initiated with a drug that prolongs the QRS and QT intervals. The patient was most likely treated with which of the following drugs?
- A. Carvedilol
- B. Verapamil
- C. Flecainide
- D. Quinidine (Correct Answer)
- E. Sotalol
Secondary arrhythmias (electrolyte, drug-induced) Explanation: **Quinidine**
- Quinidine is a **Class IA antiarrhythmic** that blocks fast sodium channels, prolonging both the **QRS complex** (due to slowed conduction) and the **QT interval** (due to prolonged repolarization).
- The ECG findings of **wide-complex tachycardia** and **AV dissociation** (P-wave rate different from R-wave rate without apparent relation) are consistent with ventricular tachycardia, which Class IA drugs can treat.
*Carvedilol*
- Carvedilol is a **beta-blocker** (Class II antiarrhythmic) that primarily slows heart rate and AV nodal conduction, generally **shortening the QT interval** or having no effect, and would not widen the QRS complex.
- Beta-blockers are typically contraindicated in **decompensated heart failure** and **wide-complex tachycardia** due to their negative inotropic effects and risk of worsening decompensation.
*Verapamil*
- Verapamil is a **non-dihydropyridine calcium channel blocker** (Class IV antiarrhythmic) that mainly slows AV nodal conduction. It would not cause QRS widening and can shorten the QT interval.
- Verapamil is generally contraindicated in **wide-complex tachycardias** of unknown origin as it can precipitate cardiovascular collapse if the arrhythmia is ventricular.
*Flecainide*
- Flecainide is a **Class IC antiarrhythmic** that primarily blocks fast sodium channels, causing significant **QRS widening** but has **minimal effect on the QT interval**, which is contrary to the case description.
- Class IC agents are also generally avoided in patients with **structural heart disease** like congestive heart failure due to increased mortality risk.
*Sotalol*
- Sotalol is a **Class III antiarrhythmic** (beta-blocker with potassium channel blockade) that primarily prolongs the **QT interval** by blocking potassium channels. While it prolongs the QT, it does **not significantly widen the QRS complex**.
- Its beta-blocking effects could exacerbate **decompensated heart failure** in this patient, similar to carvedilol.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 4: A 64-year-old man presents to his physician for a scheduled follow-up visit. He has chronic left-sided heart failure with systolic dysfunction. His current regular medications include captopril and digoxin, which were started after his last episode of symptomatic heart failure approximately 3 months ago. His last episode of heart failure was accompanied by atrial fibrillation, which followed an alcohol binge over a weekend. Since then he stopped drinking. He reports that he has no current symptoms at rest and is able to perform regular physical exercise without limitation. On physical examination, mild bipedal edema is noted. The physician suggested to him that he should discontinue digoxin and continue captopril and scheduled him for the next follow-up visit. Which of the following statements best justifies the suggestion made by the physician?
- A. Long-term digoxin therapy produces significant survival benefits in patients with heart failure, but at the cost of increased heart failure-related admissions.
- B. Both captopril and digoxin are likely to improve the long-term survival of the patient with heart failure, but digoxin has more severe side effects.
- C. Captopril is likely to improve the long-term survival of the patient with heart failure, unlike digoxin.
- D. Digoxin does not benefit patients with left-sided heart failure in the absence of atrial fibrillation.
- E. Digoxin is useful to treat atrial fibrillation, but does not benefit patients with systolic dysfunction who are in sinus rhythm. (Correct Answer)
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Digoxin is useful to treat atrial fibrillation, but does not benefit patients with systolic dysfunction who are in sinus rhythm.***
- The patient's **atrial fibrillation** was likely triggered by the alcohol binge and has since resolved, suggesting he is now in **sinus rhythm**.
- Digoxin's primary benefit in heart failure with **systolic dysfunction** (HFrEF) is to control ventricular rate in patients with **atrial fibrillation**, but it does not offer survival benefit in HFrEF patients who are in **sinus rhythm** and well-managed with other therapies.
*Long-term digoxin therapy produces significant survival benefits in patients with heart failure, but at the cost of increased heart failure-related admissions.*
- This statement is incorrect; digoxin has been shown to **reduce hospital admissions** for heart failure, but it does **not provide a significant survival benefit** in patients with HFrEF in sinus rhythm.
- The main benefit of digoxin in HFrEF is to improve symptoms and quality of life, alongside reducing hospitalizations, but not prolonging life.
*Both captopril and digoxin are likely to improve the long-term survival of the patient with heart failure, but digoxin has more severe side effects.*
- **Captopril (an ACE inhibitor)** does improve **long-term survival** in heart failure, but **digoxin does not** demonstrably improve survival.
- While digoxin can have side effects, its lack of survival benefit for HFrEF in sinus rhythm is the primary reason for discontinuation, not just side effect severity.
*Captopril is likely to improve the long-term survival of the patient with heart failure, unlike digoxin.*
- This statement is partially correct that **captopril improves survival**, but it does not fully explain the physician's decision to discontinue digoxin.
- The key missing piece is the patient's current **sinus rhythm** and the lack of benefit of digoxin in that specific context for HFrEF.
*Digoxin does not benefit patients with left-sided heart failure in the absence of atrial fibrillation.*
- This statement is nearly correct, but "left-sided heart failure" is broad. It is specifically in patients with **systolic dysfunction (HFrEF)** who are in **sinus rhythm** that digoxin lacks significant benefit beyond symptom control, and does not provide survival benefit.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 5: An 8-year-old boy is brought to the emergency department by his parents because of vomiting, abdominal pain, and blurry vision for the past hour. The parents report that the boy developed these symptoms after he accidentally ingested 2 tablets of his grandfather’s heart failure medication. On physical examination, the child is drowsy, and his pulse is 120/min and irregular. Digoxin toxicity is suspected. A blood sample is immediately sent for analysis and shows a serum digoxin level of 4 ng/mL (therapeutic range: 0.8–2 ng/mL). Which of the following electrolyte abnormalities is most likely to be present in the boy?
- A. Hypermagnesemia
- B. Hypokalemia
- C. Hypercalcemia
- D. Hyperkalemia (Correct Answer)
- E. Hypocalcemia
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Hyperkalemia***
- **Digoxin** inhibits the **Na+/K+-ATPase pump**, leading to an increase in intracellular sodium and a decrease in intracellular potassium.
- The decreased function of the Na+/K+-ATPase pump results in reduced cellular uptake of potassium, causing **elevated extracellular potassium** levels.
*Hypermagnesemia*
- **Magnesium** is not directly affected by digoxin toxicity in a way that would lead to hypermagnesemia; in fact, hypomagnesemia can exacerbate digoxin toxicity.
- High magnesium levels are typically associated with renal failure or excessive intake of magnesium-containing antacids or laxatives.
*Hypokalemia*
- While hypokalemia can **predispose to digoxin toxicity** (by increasing digoxin binding to the Na+/K+-ATPase pump), acute digoxin overdose, as described here, often leads to **hyperkalemia** due to the direct inhibition of the pump's ability to drive potassium into cells.
- The classic association of hypokalemia with digoxin refers more to its role as a risk factor for toxicity, especially with diuretic use, rather than a direct consequence of acute overdose.
*Hypercalcemia*
- **Calcium** levels are not directly altered to hypercalcemia by digoxin toxicity.
- Digoxin's mechanism involves increasing intracellular calcium by promoting calcium influx and inhibiting its efflux via the Na+/Ca2+ exchanger, but this typically does not manifest as measurable serum hypercalcemia.
*Hypocalcemia*
- Digoxin toxicity does not directly cause hypocalcemia.
- Digoxin actually leads to **increased intracellular calcium**, which is responsible for its positive inotropic effect, but this change is primarily intracellular and does not result in systemic hypocalcemia.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 6: A 52-year-old man comes to the physician because of a 3-day history of intermittent chest tightness that worsens with exercise. He has chronic atrial fibrillation treated with a drug that prolongs the QT interval. During cardiac stress testing, an ECG shows progressive shortening of the QT interval as the heart rate increases. Which of the following drugs is this patient most likely taking?
- A. Lidocaine
- B. Flecainide
- C. Carvedilol
- D. Dofetilide (Correct Answer)
- E. Diltiazem
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Dofetilide***
- **Dofetilide** is a **Class III antiarrhythmic** that blocks potassium channels (IKr) and **prolongs the QT interval**, making it the drug described in the stem.
- It is **FDA-approved for conversion and maintenance of sinus rhythm in atrial fibrillation**, matching this patient's treatment history.
- The QT shortening observed during stress testing is **normal physiologic behavior** seen with all drugs—the QT interval naturally decreases as heart rate increases (the corrected QT, or QTc, accounts for this).
- Dofetilide carries a significant **risk of torsades de pointes**, especially with QT prolongation, which is why the stem emphasizes QT monitoring.
*Lidocaine*
- **Lidocaine** is a **Class IB antiarrhythmic** that primarily shortens or has minimal effect on the QT interval.
- It is used for **ventricular arrhythmias** (especially in acute MI), **not for atrial fibrillation**.
- Does not match the described QT-prolonging treatment.
*Flecainide*
- **Flecainide** is a **Class IC antiarrhythmic** that primarily slows conduction by blocking sodium channels.
- It **does not significantly prolong the QT interval**—it may widen the QRS complex but doesn't affect ventricular repolarization substantially.
- While it can be used for atrial fibrillation, it doesn't match the QT-prolonging drug described.
*Carvedilol*
- **Carvedilol** is a **non-selective beta-blocker** with alpha-1 blocking properties used for rate control in atrial fibrillation and heart failure.
- Beta-blockers **do not prolong the QT interval**; they may slightly shorten it or have no effect.
- Does not match the stem description.
*Diltiazem*
- **Diltiazem** is a **non-dihydropyridine calcium channel blocker** used for rate control in atrial fibrillation.
- It **does not prolong the QT interval**—calcium channel blockers affect AV nodal conduction but not ventricular repolarization.
- Does not match the drug described in the stem.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 7: A 25-year-old woman is brought to the emergency department 12 hours after ingesting 30 tablets of an unknown drug in a suicide attempt. The tablets belonged to her father, who has a chronic heart condition. She has had nausea and vomiting. She also reports blurring and yellowing of her vision. Her temperature is 36.7°C (98°F), pulse is 51/min, and blood pressure is 108/71 mm Hg. Abdominal examination shows diffuse tenderness with no guarding or rebound. Bowel sounds are normal. An ECG shows prolonged PR-intervals and flattened T-waves. Further evaluation is most likely to show which of the following electrolyte abnormalities?
- A. Increased serum K+ (Correct Answer)
- B. Decreased serum K+
- C. Decreased serum Na+
- D. Increased serum Na+
- E. Increased serum Ca2+
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Increased serum K+***
- The patient presents with classic symptoms of **digoxin toxicity**, including **nausea, vomiting, blurry and yellow vision, bradycardia**, and ECG changes like **prolonged PR interval** and **flattened T-waves**.
- **Digoxin inhibits the Na+/K+-ATPase pump**, leading to an increase in extracellular potassium as potassium cannot enter the cells.
*Decreased serum K+*
- While hypokalemia can exacerbate digoxin toxicity by increasing digoxin binding to the Na+/K+-ATPase, digoxin overdose itself typically causes **hyperkalemia** due to its direct effect on the pump.
- ECG changes like **flattened T-waves** can be seen in hypokalemia, but the overall clinical picture, especially the history of overdose and bradycardia, points more strongly to digoxin toxicity with hyperkalemia.
*Decreased serum Na+*
- **Hyponatremia** is not a characteristic feature of acute digoxin overdose.
- Digoxin primarily affects potassium and calcium channels, with less direct impact on sodium levels, unless related to fluid status changes which are not indicated here.
*Increased serum Na+*
- **Hypernatremia** is not typically associated with digoxin toxicity.
- Digoxin's mechanism of action does not directly lead to increased serum sodium; rather, it primarily inhibits the Na+/K+-ATPase.
*Increased serum Ca2+*
- Digoxin **increases intracellular calcium** by inhibiting the Na+/K+-ATPase, which indirectly leads to increased Na+/Ca2+ exchanger activity.
- However, this primarily affects intracellular levels and **does not typically result in increased serum calcium**.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 8: A 40-year-old woman comes to the physician for a 6-month history of recurrent episodes of chest pain, racing pulse, dizziness, and difficulty breathing. The episodes last up to several minutes. She also reports urinary urgency and two episodes of loss of consciousness followed by spontaneous recovery. There is no personal or family history of serious illness. She does not smoke or drink alcohol. Vitals signs are within normal limits. Cardiopulmonary examination shows no abnormalities. Holter monitoring is performed. ECG recordings during episodes of tachycardia show a QRS duration of 100 ms, regular RR-interval, and absent P waves. Which of the following is the most likely underlying cause of this patient's condition?
- A. AV node with slow and fast pathway (Correct Answer)
- B. Pre-excitation of the ventricles
- C. Mutations in genes that code for myocyte ion channels
- D. Macroreentrant rhythm in the right atria through cavotricuspid isthmus
- E. Fibrosis of the sinoatrial node and surrounding myocardium
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***AV node with slow and fast pathway***
- This describes **AV nodal reentrant tachycardia (AVNRT)**, a common cause of **paroxysmal supraventricular tachycardia (PSVT)**. The ECG findings of **narrow QRS (100 ms)**, regular RR-interval, and **absent P waves** (often hidden within the QRS complex) are characteristic of AVNRT.
- The patient's symptoms of recurrent chest pain, racing pulse, dizziness, and spontaneous recovery from loss of consciousness fit the episodic nature of **AVNRT**. The presence of two pathways (slow and fast) within the AV node facilitates the reentrant circuit.
*Pre-excitation of the ventricles*
- **Pre-excitation syndromes** (e.g., Wolff-Parkinson-White syndrome) involve an accessory pathway that bypasses the AV node, leading to a **delta wave** and **short PR interval** on the baseline ECG.
- While they can cause SVT, the ECG during tachycardia would typically show a **wide QRS complex** if the accessory pathway is part of the reentrant circuit (antidromic), or a narrow QRS with a visible P wave if orthodromic and the accessory pathway is used for retrograde conduction, which doesn't fully align with the absent P waves and typically *normal* QRS during tachycardia as described.
*Mutations in genes that code for myocyte ion channels*
- This refers to **channelopathies** (e.g., long QT syndrome, Brugada syndrome), which predispose to **ventricular arrhythmias** like **polymorphic ventricular tachycardia** and **ventricular fibrillation**.
- These conditions typically cause **wide QRS tachycardias** and have distinct ECG patterns (e.g., prolonged QT interval, Brugada pattern) not described here. The narrow QRS and regular rhythm point away from primary ventricular channelopathies as the cause of this specific tachycardia.
*Macroreentrant rhythm in the right atria through cavotricuspid isthmus*
- This describes **atrial flutter**, which typically presents with characteristic **"sawtooth" F waves** on ECG, representing atrial activity.
- While atrial flutter can cause recurrent episodes of rapid heart rate, the ECG description of **absent P waves** and a **narrow QRS complex** without F waves makes atrial flutter less likely.
*Fibrosis of the sinoatrial node and surrounding myocardium*
- **Sinoatrial node dysfunction (sick sinus syndrome)** can lead to bradycardia, sinus pauses, or alternating bradycardia and tachycardia (tachy-brady syndrome).
- It does not primarily cause the described paroxysmal narrow-complex tachycardia with absent P waves. The patient's symptoms are more consistent with an abrupt-onset, regular supraventricular tachycardia.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 9: A 45-year-old man comes to the physician for a routine health maintenance examination. He feels well. He underwent appendectomy at the age of 25 years. He has a history of hypercholesterolemia that is well controlled with atorvastatin. He is an avid marathon runner and runs 8 miles per day four times a week. His father died of myocardial infarction at the age of 42 years. The patient does not smoke or drink alcohol. His vital signs are within normal limits. Cardiopulmonary examination shows no abnormalities. His abdomen is soft and nontender with a surgical scar in the right lower quadrant. Laboratory studies are within normal limits. An ECG is shown. Which of the following is the most likely diagnosis?
- A. Mobitz type II AV block
- B. First-degree AV block
- C. Mobitz type I AV block (Correct Answer)
- D. Third-degree AV block
- E. Atrial fibrillation
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Mobitz type I AV block***
- The ECG shows progressive prolongation of the **PR interval** followed by a dropped QRS complex, which is characteristic of a **Mobitz type I (Wenckebach) AV block**.
- This rhythm disturbance is often benign, especially in athletes with high **vagal tone**, and does not usually require treatment.
*Mobitz type II AV block*
- **Mobitz type II AV block** is characterized by a constant PR interval before the dropped QRS complex.
- This type of block is generally more serious and indicative of a conduction disturbance below the AV node, often requiring a **pacemaker**.
*First-degree AV block*
- A **first-degree AV block** presents with a consistently prolonged PR interval (greater than 0.20 seconds) on every beat, without any dropped beats.
- In this patient's ECG, there is a dropped QRS complex after progressive PR prolongation.
*Third-degree AV block*
- **Third-degree (complete) AV block** is characterized by complete dissociation between the P waves and QRS complexes.
- There is no relationship between atrial and ventricular activity, and the ventricular rate is typically very slow and escape rhythms are observed.
*Atrial fibrillation*
- **Atrial fibrillation** is an irregularly irregular rhythm with no discernible P waves and varying R-R intervals.
- The ECG provided shows clear P waves and a regular, albeit interrupted, rhythm pattern.
Secondary arrhythmias (electrolyte, drug-induced) US Medical PG Question 10: A 55-year-old man with a past medical history of obesity and hyperlipidemia suddenly develops left-sided chest pain and shortness of breath while at work. He relays to coworkers that the pain is intense and has spread to his upper left arm over the past 10 minutes. He reports it feels a lot like the “heart attack” he had a year ago. He suddenly collapses and is unresponsive. Coworkers perform cardiopulmonary resuscitation for 18 minutes until emergency medical services arrives. Paramedics pronounce him dead at the scene. Which of the following is the most likely cause of death in this man?
- A. Pericarditis
- B. Aortic dissection
- C. Atrial fibrillation
- D. Ventricular tachycardia (Correct Answer)
- E. Free wall rupture
Secondary arrhythmias (electrolyte, drug-induced) Explanation: ***Ventricular tachycardia***
- The patient's history of MI **1 year ago** creates a substrate of **scarred myocardium** that predisposes to life-threatening ventricular arrhythmias.
- The current presentation of sudden chest pain radiating to the arm suggests **acute re-infarction**, which triggers electrical instability in already compromised myocardium.
- **Ventricular tachycardia (VT)** degenerating to **ventricular fibrillation (VF)** is the **most common cause of sudden cardiac death** in patients with prior MI, especially during acute ischemic events.
- The rapid collapse and death within minutes, despite CPR, is classic for fatal ventricular arrhythmia.
*Free wall rupture*
- Free wall rupture is a **mechanical complication** that occurs **3-14 days** (typically days 3-7) after an **acute MI**, not 1 year later.
- By 1 year post-MI, the ventricular wall has either healed with fibrous scar tissue or formed a chronic ventricular aneurysm.
- While this would cause sudden death via cardiac tamponade, the **timing makes this unlikely** in this scenario.
*Pericarditis*
- Pericarditis causes **pleuritic chest pain** that is sharp, positional, and typically relieved by leaning forward.
- It is **not an immediate cause of sudden cardiac death** and would not explain the rapid collapse and unresponsiveness.
- While post-MI (Dressler) pericarditis can occur weeks after MI, it doesn't cause this presentation.
*Aortic dissection*
- Aortic dissection presents with **sudden, severe, tearing chest pain** often radiating to the back.
- While potentially fatal, the patient's description of pain "a lot like the heart attack he had a year ago" and his cardiac risk factors make **recurrent MI with fatal arrhythmia more likely**.
- No mention of blood pressure differential or pulse deficits that would suggest dissection.
*Atrial fibrillation*
- Atrial fibrillation is a **supraventricular arrhythmia** that causes palpitations, dyspnea, and irregular pulse.
- It is **not typically immediately fatal** in isolation and does not cause sudden collapse and death within minutes.
- While AF can lead to stroke or heart failure over time, it doesn't explain this acute sudden cardiac death.
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