Cardiology Practice Questions

Q: Which of the following is NOT a cause of Pulseless Electrical Activity (PEA)?

Hydrogen ion depletion. Pulseless Electrical Activity (PEA) is a clinical condition where an organized cardiac rhythm is visible on the monitor, but there is no palpable pulse [1]. To identify the causes of PEA, clinicians use the high-yield **"5 Hs and 5 Ts"** mnemonic [1]. **Why "Hydrogen ion depletion" is the correct answer:** The correct reversible cause of PEA is **Hydrogen ion excess (Acidosis)**, not depletion [1]. Severe metabolic or respiratory acidosis leads to myocardial depression and decreased peripheral vascular resistance, triggering PEA. Alkalosis (hydrogen ion depletion) is not a recognized primary cause of PEA in standard Advanced Cardiovascular Life Support (ACLS) protocols. **Analysis of Incorrect Options:** * **Low pO2 < 60 mm Hg (Hypoxia):** This is one of the "5 Hs." Severe hypoxia leads to myocardial ischemia and failure of the excitation-contraction coupling, resulting in PEA [1]. * **Hypokalemia:** Both Hypokalemia and Hyperkalemia are part of the "5 Hs." Electrolyte imbalances disrupt the resting membrane potential of myocytes, leading to electrical activity without mechanical output [2]. * **Hypovolemia:** This is the most common cause of PEA [1]. A lack of intravascular volume means there is insufficient preload for the heart to generate a stroke volume, even if the electrical conduction system is intact. **High-Yield Clinical Pearls for NEET-PG:** * **The 5 Hs:** Hypovolemia, Hypoxia, Hydrogen ion (Acidosis), Hypo/Hyperkalemia, Hypothermia [1]. * **The 5 Ts:** Tension pneumothorax, Tamponade (Cardiac), Toxins, Thrombosis (Pulmonary), Thrombosis (Coronary) [1]. * **Management:** PEA is a **non-shockable rhythm**. Management focuses on high-quality CPR, Epinephrine (1mg every 3–5 mins), and aggressively identifying and treating the underlying cause (the 5 Hs and 5 Ts) [1].

Q: What is the effect of beriberi on circulation?

Hyperdynamic circulation. Wet Beriberi, caused by a severe deficiency of Thiamine (Vitamin B1), leads to a classic state of high-output heart failure characterized by hyperdynamic circulation [1]. The underlying pathophysiology involves systemic peripheral vasodilation (decreased systemic vascular resistance) due to the accumulation of pyruvate and lactate, which act as local vasodilators. This results in an increased venous return to the heart, leading to an increased stroke volume and cardiac output [1]. Clinically, this manifests as a wide pulse pressure, bounding pulses [2], and warm extremities. Analysis of Incorrect Options: * B. Hypovolemic shock: Beriberi causes fluid retention and volume overload (edema) due to heart failure, the opposite of hypovolemia. * C. Bradycardia: Hyperdynamic states typically present with tachycardia to maintain the high cardiac output [1]. * D. Pulsus paradoxus: This is a sign of cardiac tamponade [3] or severe asthma/COPD, not high-output failure. High-Yield NEET-PG Pearls: * Dry Beriberi: Presents as symmetrical peripheral neuropathy (sensory and motor). * Wet Beriberi: Presents with high-output heart failure and edema. * Shoshin Beriberi: A fulminant, acute form of wet beriberi leading to rapid cardiovascular collapse and lactic acidosis. * Treatment: Immediate IV Thiamine. Always administer thiamine before glucose in malnourished patients to prevent precipitating Wernicke-Korsakoff syndrome.

Q: A 26-year-old woman complains of the abrupt onset of her chest pounding. She is diagnosed with paroxysmal atrial tachycardia. Which of the following is the most effective agent for converting paroxysmal atrial tachycardia to normal sinus rhythm?

Adenosine. ### Explanation **Correct Answer: D. Adenosine** **Mechanism and Rationale:** Paroxysmal Supraventricular Tachycardia (PSVT), often referred to in clinical scenarios as paroxysmal atrial tachycardia, most commonly involves a re-entry circuit involving the Atrioventricular (AV) node (e.g., AVNRT) [1], [3]. **Adenosine** is the drug of choice for the acute termination of stable PSVT [2]. It works by binding to **A1 receptors** in the AV node, causing an increase in potassium efflux and inhibition of calcium influx. This results in transient hyperpolarization and a **profound slowing of AV nodal conduction**, effectively "breaking" the re-entry circuit and allowing the SA node to regain control. It has an ultra-short half-life (<10 seconds), making it ideal for rapid conversion. **Why Other Options are Incorrect:** * **A. Digoxin:** While it slows AV conduction, its onset of action is too slow (hours) for the acute conversion of paroxysmal tachyarrhythmias [2]. * **B. Lidocaine:** This is a Class IB antiarrhythmic that acts on sodium channels in the ventricles. It is used for ventricular arrhythmias (like VT) and has no efficacy in supraventricular tachycardias [2]. * **C. Atropine:** This is an anticholinergic used to *increase* the heart rate in symptomatic bradycardia; it would worsen tachycardia. **High-Yield Clinical Pearls for NEET-PG:** * **Administration:** Adenosine must be given as a **rapid IV bolus** followed by a saline flush due to its short half-life. * **Side Effects:** Patients often experience a transient, distressing feeling of "impending doom," chest pain, or flushing. * **Contraindications:** Avoid in patients with **Asthma** (can cause bronchospasm) and high-grade heart blocks [2]. * **Drug Interactions:** The dose should be **decreased** in patients on Dipyridamole or Carbamazepine and **increased** in patients consuming high amounts of Theophylline or Caffeine (adenosine receptor antagonists) [2].

Q: Which of the following is NOT a characteristic of Prinzmetal angina?

Pain at rest and ST elevation during the attack. Prinzmetal angina (also known as variant angina) is caused by focal coronary artery vasospasm rather than atherosclerotic narrowing. This spasm leads to transient, total occlusion of a coronary artery, resulting in **transmural ischemia**. **Why Option A is the "Correct" Answer (The Exception):** In the context of this specific question format, Option A is likely intended as the "incorrect" statement because it describes the *classic* presentation of Prinzmetal angina. However, in many NEET-PG style questions, if the options are poorly phrased or overlapping, the key is to identify the statement that does not fit the "NOT" criteria. *Note: If this is a "Which is NOT" question and Option A is marked correct, it implies a technical error in the question's phrasing, as A, B, C, and D are all actually true characteristics of the disease.* **Analysis of Characteristics:** * **Option B & D:** During an acute spasm, there is **ST-segment elevation** (not depression) because the ischemia is **transmural** (involving the full thickness of the wall). This distinguishes it from stable angina, which is subendocardial. * **Option C:** A hallmark of Prinzmetal angina is that chest pain typically occurs **at rest** (often in the early morning) and the **ECG returns to normal** once the spasm resolves. **High-Yield Clinical Pearls for NEET-PG:** * **Triggers:** Smoking is a major risk factor; cocaine or triptans can precipitate attacks. * **Diagnosis:** Gold standard is coronary angiography with provocative testing (e.g., **Ergonovine or Acetylcholine**). * **Treatment:** **Calcium Channel Blockers (CCBs)** and Nitrates are first-line. [1] * **Contraindication:** **Beta-blockers** are strictly contraindicated as they can lead to unopposed alpha-adrenergic stimulation, worsening the vasospasm.

Q: Austin Flint Murmur is commonly mistaken for the murmur of which condition?

Mitral stenosis. ### Explanation **1. Why Mitral Stenosis is the correct answer:** The **Austin Flint murmur** is a low-pitched, mid-diastolic rumbling murmur heard at the apex in patients with **severe chronic Aortic Regurgitation (AR)**. It occurs because the regurgitant jet from the aorta strikes the anterior leaflet of the mitral valve, causing it to partially close (functional narrowing) and vibrate [2]. This creates a "functional" mitral stenosis. Because both the Austin Flint murmur and true **Mitral Stenosis (MS)** are mid-diastolic rumbles heard best at the apex, they are frequently confused [3]. **2. Why other options are incorrect:** * **Mitral Regurgitation (A):** This is a pansystolic murmur radiating to the axilla, whereas Austin Flint is diastolic [1]. * **Pulmonary Regurgitation (B):** This causes an early diastolic murmur (Graham Steell murmur) heard at the left upper sternal border, not a mid-diastolic rumble at the apex. * **Tricuspid Stenosis (C):** While this is a mid-diastolic rumble, it is heard best at the left lower sternal border and increases with inspiration (Carvallo’s sign), unlike the Austin Flint murmur [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Differentiation:** To distinguish Austin Flint from true MS, look for the **Opening Snap (OS)** and **Loud S1**. These are present in MS but **absent** in Austin Flint [4]. * **Amyl Nitrite Test:** Inhalation of amyl nitrite decreases peripheral resistance, increasing the Austin Flint murmur (due to increased AR) but decreasing the murmur of true MS. * **Eponyms to remember:** * *Graham Steell Murmur:* Pulmonary regurgitation secondary to pulmonary hypertension. * *Carey Coombs Murmur:* Mid-diastolic murmur in acute Rheumatic Fever (due to mitral valvulitis).

Q: A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

Pulsus tardus. **Explanation:** The clinical presentation of syncope, exertional fatigue, and a systolic ejection murmur radiating to the carotids is classic for **Aortic Stenosis (AS)**. In severe AS, the narrowed valve orifice creates a mechanical obstruction to left ventricular outflow, leading to a characteristic arterial pulse known as **Pulsus parvus et tardus**. [1] * **Pulsus tardus** refers to a delayed upstroke (slow-rising pulse), while **pulsus parvus** refers to a small/low amplitude. This occurs because the blood is ejected slowly through the stenotic valve, prolonging the time to reach peak pressure. [1] **Analysis of Incorrect Options:** * **Pulsus paradoxus:** Defined as an exaggerated drop in systolic BP (>10 mmHg) during inspiration. It is characteristic of **Cardiac Tamponade**, severe asthma, or COPD, not valvular stenosis. * **Hyperkinetic pulse (Water-hammer pulse):** A rapid, forceful upstroke with sudden collapse. This is seen in **Aortic Regurgitation** or high-output states (e.g., thyrotoxicosis, anemia). [3] * **Bisferiens pulse:** A "double-peaked" systolic pulse. It is typically found in **AR combined with AS** or in **Hypertrophic Obstructive Cardiomyopathy (HOCM)**. **High-Yield Clinical Pearls for NEET-PG:** 1. **Gallavardin Phenomenon:** In AS, the murmur may sound musical and be heard best at the apex, mimicking mitral regurgitation. [1] 2. **S2 Changes:** A paradoxical splitting of S2 or a soft/absent A2 component is a sign of severe AS. [1] 3. **The "SAD" Triad:** Symptoms of AS include **S**yncope, **A**ngina, and **D**yspnea (Heart Failure). [2] Once symptoms appear, the prognosis without valve replacement is poor.

Q: Hyperdynamic circulation is seen in all EXCEPT:

Cor pulmonale. **Explanation:** **Hyperdynamic circulation** is a state of increased cardiac output (CO) and decreased systemic vascular resistance (SVR). It is characterized by a "bounding pulse" and increased stroke volume [2]. **Why Cor Pulmonale is the Correct Answer:** Cor pulmonale refers to right ventricular hypertrophy and failure resulting from chronic pulmonary hypertension (usually due to lung disease like COPD) [3]. In this condition, there is **increased pulmonary vascular resistance**, which leads to a **low-output state** rather than a high-output state [1]. The heart struggles to pump blood through the lungs, eventually leading to decreased systemic cardiac output. **Analysis of Incorrect Options:** * **Anemia:** Reduced hemoglobin leads to tissue hypoxia, triggering compensatory vasodilation and increased stroke volume to maintain oxygen delivery. * **Beriberi (Wet):** Thiamine (Vitamin B1) deficiency causes systemic vasodilation and high-output heart failure due to impaired aerobic metabolism. * **AV Fistula:** An abnormal connection between an artery and a vein bypasses the high-resistance capillary bed, significantly reducing SVR and forcing the heart to increase CO to maintain systemic pressure. **NEET-PG High-Yield Pearls:** * **Common causes of Hyperdynamic Circulation:** Pregnancy, Thyrotoxicosis, Fever, Paget’s disease of the bone, Liver Cirrhosis, and Sepsis (early phase). * **Clinical Signs:** Water-hammer pulse (Corrigan’s pulse), wide pulse pressure, and a mid-systolic flow murmur [2]. * **Mnemonic:** Remember **"ABCD P"** for High Output: **A**nemia, **B**eriberi/BMR (Thyrotoxicosis), **C**irrhosis, **D**-AV fistula, **P**regnancy/Paget's.

Question 1

Which of the following is NOT a cause of Pulseless Electrical Activity (PEA)?

Accepted Answer

Hydrogen ion depletion

Answer

Low pO2 < 60 mm Hg

Answer

Hypokalemia

Answer

Hypovolemia

Question 2

What is the effect of beriberi on circulation?

Accepted Answer

Hyperdynamic circulation

Answer

Hypovolemic shock

Answer

Bradycardia

Answer

Pulsus paradoxus

Question 3

A 26-year-old woman complains of the abrupt onset of her chest pounding. She is diagnosed with paroxysmal atrial tachycardia. Which of the following is the most effective agent for converting paroxysmal atrial tachycardia to normal sinus rhythm?

Accepted Answer

Adenosine

Answer

Digoxin

Answer

Lidocaine

Answer

Atropine

Question 4

Which of the following is NOT a characteristic of Prinzmetal angina?

Accepted Answer

Pain at rest and ST elevation during the attack

Answer

ST elevation during the attack

Answer

Pain at rest and a normal ECG without pain

Answer

Pain at rest and represents transmural ischemia

Question 5

Austin Flint Murmur is commonly mistaken for the murmur of which condition?

Accepted Answer

Mitral stenosis

Answer

Mitral regurgitation

Answer

Pulmonary regurgitation

Answer

Tricuspid stenosis

Question 6

What is the most common complication of cardiac catheterization?

Accepted Answer

Vascular bleeding

Answer

Arrhythmia

Answer

Hypertension

Answer

Contrast reaction

Question 7

A 76-year-old woman presents with new-onset syncope and has noticed early fatigue on exertion for the past year. On examination, there is a systolic ejection murmur at the right sternal border that radiates to the carotids. What is the characteristic arterial pulse finding in this patient with suspected aortic stenosis?

Accepted Answer

Pulsus tardus

Answer

Pulsus paradoxus

Answer

Hyperkinetic pulse

Answer

Bisferiens pulse

Question 8

A 56-year-old woman presents with dyspnea, blurry vision, and headaches that began this morning and are worsening. Her past medical history includes hypertension and osteoarthritis. She discontinued her anti-hypertensive medications three months ago due to side effects. On examination, her blood pressure is 210/130 mm Hg, heart rate is 100 beats/min, and oxygen saturation is 95%. Fundoscopy reveals retinal hemorrhages and papilledema. Heart sounds are normal except for an S4, and lung auscultation reveals lower lobe crackles. Which of the following is the most appropriate agent to reduce her blood pressure?

Accepted Answer

IV nitroprusside

Answer

IV hydralazine

Answer

IV labetalol

Answer

Oral methyldopa

Question 9

Hyperdynamic circulation is seen in all EXCEPT:

Accepted Answer

Cor pulmonale

Answer

Anemia

Answer

Beriberi

Answer

AV fistula

Question 10

Which of the following dietary interventions has shown to reduce mortality in patients with coronary heart disease?

Accepted Answer

Omega 3 polyunsaturated fatty acids

Answer

High Fibre diet

Answer

Stanol Esters

Answer

Potassium supplements

Cardiology — MCQs

Cardiology — MCQs

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