Cardiology Practice Questions

Q: A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

Conn syndrome. The clinical presentation of a young patient with **resistant hypertension** (uncontrolled despite ≥3 drugs) and spontaneous **hypokalemia** (2.7 mEq/L) strongly suggests **Primary Hyperaldosteronism (Conn Syndrome)**. **1. Why Conn Syndrome is correct:** In Conn syndrome, an adrenal adenoma or hyperplasia produces excess aldosterone. Aldosterone acts on the principal cells of the renal collecting duct to reabsorb sodium and water (causing hypertension) and secrete potassium and hydrogen ions [1]. This leads to the classic triad seen here: * **Hypertension** (often resistant). * **Hypokalemia** (muscle weakness or asymptomatic). * **Metabolic Alkalosis** (elevated bicarbonate of 33 mg/dL). The absence of edema is due to the "Aldosterone Escape" phenomenon. **2. Why other options are incorrect:** * **Renal Vascular Hypertension:** While it causes resistant hypertension, it usually presents with an abdominal bruit or a significant rise in creatinine after starting an ACE inhibitor (Lisinopril) [3]. * **Cushing Syndrome:** Ruled out by the absence of physical findings like truncal obesity, striae, or "buffalo hump," and the normal fasting glucose (98 mg/dL). * **Carcinoid Syndrome:** Typically presents with flushing, diarrhea, and wheezing, rather than isolated resistant hypertension and hypokalemia. **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Plasma Aldosterone Concentration (PAC) to Plasma Renin Activity (PRA) ratio. A **PAC:PRA ratio > 20-30** is suggestive. * **Confirmatory Test:** Oral/Saline salt loading test (failure to suppress aldosterone) [2]. * **Management:** Surgical excision for Adenoma; Spironolactone/Eplerenone for bilateral hyperplasia [2]. * **Note:** Diuretics like Hydrochlorothiazide can worsen hypokalemia, but the severity here (2.7 mEq/L) in a young hypertensive patient should always trigger a workup for primary aldosteronism.

Q: Gibson's murmur is a feature of which cardiac condition?

Patent Ductus arteriosus. **Explanation:** **Gibson’s murmur** is the classic eponym for a **continuous machinery murmur**. It is the hallmark clinical finding of **Patent Ductus Arteriosus (PDA)** [1]. **Why Patent Ductus Arteriosus is correct:** In PDA, there is a persistent communication between the high-pressure aorta and the lower-pressure pulmonary artery [1]. Because the pressure in the aorta remains higher than in the pulmonary artery during both systole and diastole, blood flows continuously through the ductus [1]. This results in a murmur that begins in systole, peaks at the second heart sound (S2), and continues through diastole, creating the "machinery" quality. It is best heard at the **left infraclavicular area** (Gibson’s area). **Why the other options are incorrect:** * **Mitral Valve Prolapse (MVP):** Characterized by a mid-systolic click followed by a late systolic murmur. * **Pulmonary Regurgitation (PR):** Typically presents as a decrescendo diastolic murmur (Graham Steell murmur if secondary to pulmonary hypertension). * **Mitral Regurgitation (MR):** Presents as a pansystolic (holosystolic) murmur heard best at the apex, radiating to the axilla [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Best heard in the left 2nd intercostal space, just below the left clavicle. * **Differential for Continuous Murmurs:** Apart from PDA, consider Ruptured Sinus of Valsalva (RSOV), Aortopulmonary window, and Coronary AV fistula. * **Management:** Indomethacin or Ibuprofen (NSAIDs) are used for pharmacological closure in preterm neonates; surgical or device closure is indicated for persistent cases. * **Eisenmenger Syndrome:** If PDA develops right-to-left shunting, it leads to **differential cyanosis** (cyanosis and clubbing in the lower limbs, but not the upper limbs).

Q: Which of the following drugs does not reduce mortality in heart failure with reduced ejection fraction (HFrEF)?

Digoxin. In the management of Heart Failure with reduced Ejection Fraction (HFrEF), drugs are classified into those that provide **symptomatic relief** and those that provide a **mortality benefit** (prolong life). ### **Why Digoxin is the Correct Answer** **Digoxin** is a cardiac glycoside that inhibits the Na+/K+-ATPase pump, leading to increased intracellular calcium and positive inotropy. While it effectively reduces hospitalizations and improves symptoms (hemodynamics), the **DIG Trial** conclusively showed that it has **no effect on overall mortality**. It is primarily used today for rate control in patients with co-existing Atrial Fibrillation or for refractory symptoms. ### **Explanation of Incorrect Options (Drugs that DO reduce mortality):** * **Metoprolol (Option A):** Specifically **Metoprolol succinate** (extended-release), along with Bisoprolol and Carvedilol, reduces sympathetic overactivity and remodeling, significantly decreasing mortality in stable HFrEF. * **Captopril (Option B):** As an ACE Inhibitor, it prevents the formation of Angiotensin II and the breakdown of bradykinin. ACEIs are the "gold standard" for reducing afterload and preventing cardiac remodeling, thereby improving survival. * **Potassium-sparing diuretics (Option D):** Specifically **Mineralocorticoid Receptor Antagonists (MRAs)** like Spironolactone and Eplerenone. They prevent aldosterone-mediated fibrosis and are proven to reduce mortality in NYHA Class II-IV heart failure. ### **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Mortality-Reducing Drugs:** "**B-A-S-H**" (**B**eta-blockers, **A**CEIs/ARBs/ARNIs, **S**pironolactone/MRAs, **H**ydralazine + Nitrates). * **SGLT2 Inhibitors** (e.g., Dapagliflozin) are the newest addition to the mortality-reducing "Four Pillars" of HFrEF therapy. * **Diuretics (Furosemide)** and **Digoxin** improve symptoms but **do not** improve survival.

Q: A 40-year-old woman with a history of rheumatic fever presents with shortness of breath, weight loss, fatigue, and abdominal distension. Physical examination shows rales in the lungs, hepatosplenomegaly, and 2+ pitting edema of the legs. A chest X-ray reveals only left atrial enlargement and pulmonary edema. What is the most likely cause of pulmonary edema in this patient?

Mitral stenosis. **Explanation:** The clinical presentation of a patient with a history of rheumatic fever, shortness of breath, and signs of both pulmonary congestion (rales, pulmonary edema) and systemic venous congestion (hepatosplenomegaly, pitting edema) strongly suggests **Mitral Stenosis (MS)**. **Why Mitral Stenosis is Correct:** In MS, the narrowed mitral valve orifice creates a pressure gradient between the left atrium (LA) and the left ventricle (LV). This leads to increased LA pressure, which is transmitted backward into the pulmonary veins and capillaries, causing **pulmonary edema**. Chronic elevation in pulmonary pressure eventually leads to pulmonary hypertension and **right-sided heart failure**, explaining the hepatosplenomegaly and peripheral edema. The chest X-ray finding of isolated LA enlargement without LV enlargement is a classic hallmark of MS. **Why Other Options are Incorrect:** * **Aortic Insufficiency (AI) & Aortic Stenosis (AS):** Both conditions primarily cause **Left Ventricular Hypertrophy/Dilation**. A chest X-ray in these cases would typically show a prominent left ventricular shadow (boot-shaped heart in AS or cardiomegaly in AI), which is absent here. * **Tricuspid Insufficiency (TI):** While TI causes systemic venous congestion (edema, hepatomegaly), it does **not** cause pulmonary edema. In fact, TI often occurs secondary to the pulmonary hypertension caused by MS. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of MS:** Rheumatic Heart Disease (99% of cases). * **Auscultation:** Loud S1, Opening Snap (OS), and a Mid-Diastolic Rumble at the apex. * **ECG/X-ray:** Look for "P-mitrale" (broad, notched P waves) and the "Straightening of the left heart border" on CXR due to LA enlargement. * **Management:** Percutaneous Transvenous Mitral Commissurotomy (PTMC) is the treatment of choice for symptomatic MS with favorable valve morphology.

Q: All of the following are causes of a pansystolic murmur, EXCEPT?

Atrial Septal Defect (ASD). **Explanation:** A **pansystolic (holosystolic) murmur** occurs when there is a pressure gradient between two chambers that persists throughout the entire duration of systole (from $S_1$ to $S_2$) [3]. **Why ASD is the correct answer:** In an **Atrial Septal Defect (ASD)**, the murmur is **not** caused by blood flowing across the defect itself (as the pressure gradient between the atria is too low). Instead, the increased volume in the right heart leads to increased flow across the pulmonary valve, causing a **midsystolic (ejection systolic) murmur**. Additionally, ASD is characterized by a pathognomonic **fixed, wide splitting of $S_2$**. **Why the other options are incorrect:** * **Mitral Regurgitation (MR):** High pressure in the Left Ventricle (LV) compared to the Left Atrium (LA) throughout systole causes a pansystolic murmur, loudest at the apex, radiating to the axilla [1]. * **Tricuspid Regurgitation (TR):** High pressure in the Right Ventricle (RV) compared to the Right Atrium (RA) causes a pansystolic murmur, loudest at the left lower sternal border. It characteristically increases with inspiration (**Carvallo’s sign**). * **Ventricular Septal Defect (VSD):** The significant pressure gradient between the LV and RV throughout systole produces a harsh pansystolic murmur, typically loudest at the left lower sternal border (Erb’s point) [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Small VSD (Roger’s Disease):** Produces a louder, more "mal de roussel" murmur than a large VSD [2]. 2. **Dynamic Auscultation:** MR and VSD murmurs increase with **handgrip** (increased afterload), whereas HOCM and Mitral Valve Prolapse murmurs decrease. 3. **ASD Triad:** Fixed wide $S_2$, Ejection Systolic Murmur (pulmonary area), and Mid-diastolic murmur (tricuspid area due to increased flow).

Q: On the basis of the provided ECG, what is the most probable diagnosis?

Anteroseptal MI. ***Anteroseptal MI*** - **ST elevation** and **Q waves** in leads **V1-V4** are characteristic of anteroseptal MI, indicating involvement of the **septal** and **anterior** walls of the left ventricle. - The **left anterior descending (LAD)** artery's **septal** and **diagonal branches** supply this territory, making anteroseptal MI the most likely diagnosis. *Anterolateral wall MI* - Would show **ST elevation** in leads **V1-V6** plus **lateral leads** (I, aVL, V5-V6), not just V1-V4. - Involves the **circumflex artery** territory in addition to LAD, causing a more extensive pattern than seen here. *Anterior wall MI* - Typically involves only leads **V3-V4**, sparing the **septal leads** (V1-V2) that are affected in this case. - The **mid-LAD** territory is involved, but the septal involvement seen in V1-V2 distinguishes this from pure anterior wall MI. *Extensive anterior wall MI* - Would demonstrate **ST elevation** in leads **V1-V6** and **lateral leads** (I, aVL), indicating involvement of multiple coronary territories. - Represents a **large territory** infarction involving both LAD and circumflex distributions, more extensive than the V1-V4 pattern observed.

Q: Which of the following diseases can be associated with a short QT interval on ECG?

Multiple myeloma. The correct answer is **Multiple Myeloma**. The underlying medical concept linking Multiple Myeloma to a short QT interval is **Hypercalcemia**. 1. **Why Multiple Myeloma is correct:** Multiple myeloma is a plasma cell dyscrasia characterized by extensive osteolytic bone lesions [1]. These lesions release calcium into the bloodstream, leading to hypercalcemia. On an ECG, hypercalcemia causes a shortening of the ST segment, which results in a **shortened QT interval**. This occurs because high extracellular calcium levels accelerate phase 2 (plateau phase) of the cardiac action potential, leading to faster repolarization. 2. **Why the other options are incorrect:** * **Chronic Myeloid Leukemia (CML), Chronic Lymphocytic Leukemia (CLL), and Hodgkin’s Disease:** While these are hematological malignancies, they are not classically associated with the profound, bone-resorption-driven hypercalcemia seen in Multiple Myeloma. While any advanced malignancy can cause hypercalcemia of malignancy (usually via PTHrP), Multiple Myeloma is the "textbook" association for this electrolyte abnormality in the context of ECG changes. **High-Yield Facts for NEET-PG:** * **Short QT Interval Causes:** Hypercalcemia, Hyperkalemia [2], Digoxin toxicity, and Congenital Short QT Syndrome. * **Long QT Interval Causes:** Hypocalcemia, Hypokalemia [2], Hypomagnesemia, and drugs (Class IA and III antiarrhythmics, Macrolides, TCAs). * **Formula:** The QT interval must be corrected for heart rate using **Bazett’s Formula** ($QTc = QT / \sqrt{RR}$). * **Clinical Pearl:** In hypercalcemia, the "shortening" specifically involves the ST segment; the T-wave duration usually remains normal.

Q: Blood pressure is difficult to measure in a patient with which of the following conditions?

Atrial fibrillation. The correct answer is Atrial Fibrillation (AF). In Atrial Fibrillation, the heart rhythm is "irregularly irregular" due to disorganized electrical activity in the atria. This leads to varying ventricular filling times (variable diastole) and inconsistent stroke volumes from beat to beat [1]. Consequently, the systolic blood pressure fluctuates significantly with every pulse. When using a sphygmomanometer, the Korotkoff sounds appear and disappear at different pressure levels, making it technically difficult to pinpoint a single, accurate systolic or diastolic value. In clinical practice, an average of multiple readings is often required. Analysis of Incorrect Options: * Mitral Stenosis (A): While it may lead to a low pulse pressure or trigger AF as a complication, the rhythm itself remains regular unless AF develops. BP measurement is generally straightforward. * Aortic Stenosis (B): This condition typically presents with a "pulsus parvus et tardus" (small and slow rise pulse) and a narrow pulse pressure, but the rhythm remains regular, allowing for consistent BP measurement [2]. * Complete Heart Block (C): Although the heart rate is slow (bradycardia), the ventricular rhythm is usually regular (driven by a stable escape rhythm). This results in a consistent, often wide pulse pressure that is easy to measure. High-Yield Clinical Pearls for NEET-PG: * Pulse Deficit: In AF, the difference between the apical heart rate and the radial pulse rate is called the pulse deficit (usually >10 bpm), occurring because some beats have insufficient stroke volume to open the aortic valve or reach the periphery. * Auscultatory Gap: This is a period of silence between systolic and diastolic pressures often seen in hypertensive patients; it can lead to underestimation of systolic BP. * Gold Standard: For patients with highly irregular rhythms like AF, invasive intra-arterial blood pressure monitoring remains the most accurate method.

Q: Plethoric, non-collapsible IVC on echocardiography denotes?

Right heart failure. **Explanation:** The Inferior Vena Cava (IVC) serves as a reliable surrogate for measuring **Central Venous Pressure (CVP)** and right-sided heart function. In a healthy individual, the IVC diameter decreases by >50% during inspiration (the "sniff test") due to the negative intrathoracic pressure drawing blood into the right atrium. **Why Right Heart Failure is correct:** In **Right Heart Failure**, the heart cannot effectively pump blood forward, leading to a "backlog" of pressure in the venous system. This results in a **plethoric** (dilated, usually >2.1 cm) and **non-collapsible** IVC (collapse <50%). This lack of respiratory variation indicates high CVP and fluid overload. **Analysis of Incorrect Options:** * **Budd-Chiari Syndrome:** This involves obstruction of hepatic venous outflow. While it may cause IVC narrowing or membranes, it typically leads to hepatomegaly and ascites rather than generalized IVC plethora unless the obstruction is at the level of the suprahepatic IVC. * **Hepatic Venous Malformation:** These are localized vascular anomalies and do not typically cause systemic venous congestion or alter IVC respiratory dynamics. * **IVC Thrombosis:** While a thrombus can distend the vessel locally, it usually presents with intraluminal echoes (the clot itself) and distal venous engorgement, rather than the classic "plethoric" appearance associated with systemic heart failure. **High-Yield Clinical Pearls for NEET-PG:** * **IVC Index:** (Max diameter - Min diameter) / Max diameter. An index ** 10-15 mmHg). * **Shock Assessment:** A small, hyper-collapsible IVC ("kissing walls") is a hallmark of **hypovolemic shock**. * **Point-of-Care Ultrasound (POCUS):** The IVC is best visualized in the subxiphoid long-axis view.

Question 1

A 27-year-old male has had hard-to-control hypertension for 2 years. He is taking clonidine, hydrochlorothiazide, verapamil, and lisinopril. His blood pressure is 170/105 mmHg, pulse 90 beats/min, and respirations 16/min. The cardiopulmonary exam is normal. Pedal pulses are intact and there is no edema or misdistribution of fat. Laboratories show potassium of 2.7 mEq/L, BUN 20 mg/dL, creatinine 1.2 mg/dL, bicarbonate 33 mg/dL, and fasting glucose 98 mg/dL. What is the most likely diagnosis?

Accepted Answer

Conn syndrome

Answer

Renal vascular hypertension

Answer

Cushing syndrome

Answer

Carcinoid syndrome

Question 2

Gibson's murmur is a feature of which cardiac condition?

Accepted Answer

Patent Ductus arteriosus

Answer

Mitral Valve prolapse

Answer

Pulmonary regurgitation

Answer

Mitral regurgitation

Question 3

Which of the following drugs does not reduce mortality in heart failure with reduced ejection fraction (HFrEF)?

Accepted Answer

Digoxin

Answer

Metoprolol

Answer

Captopril

Answer

Potassium-sparing diuretics

Question 4

A 40-year-old woman with a history of rheumatic fever presents with shortness of breath, weight loss, fatigue, and abdominal distension. Physical examination shows rales in the lungs, hepatosplenomegaly, and 2+ pitting edema of the legs. A chest X-ray reveals only left atrial enlargement and pulmonary edema. What is the most likely cause of pulmonary edema in this patient?

Accepted Answer

Mitral stenosis

Answer

Aortic insufficiency

Answer

Aortic stenosis

Answer

Tricuspid insufficiency

Question 5

All of the following are causes of a pansystolic murmur, EXCEPT?

Accepted Answer

Atrial Septal Defect (ASD)

Answer

Ventricular Septal Defect (VSD)

Answer

Tricuspid Regurgitation (TR)

Answer

Mitral Regurgitation (MR)

Question 6

On the basis of the provided ECG, what is the most probable diagnosis?

Accepted Answer

Anteroseptal MI

Answer

Anterolateral wall MI

Answer

Anterior wall MI

Answer

Extensive anterior wall MI

Question 7

Which of the following diseases can be associated with a short QT interval on ECG?

Accepted Answer

Multiple myeloma

Answer

Chronic myeloid leukemia

Answer

Chronic lymphocytic leukemia

Answer

Hodgkin's disease

Question 8

Blood pressure is difficult to measure in a patient with which of the following conditions?

Accepted Answer

Atrial fibrillation

Answer

Mitral stenosis

Answer

Aortic stenosis

Answer

Complete heart block

Question 9

A patient with heart failure developed ventricular arrhythmia. What is/are the appropriate treatment(s)?

Accepted Answer

Flecainide

Answer

Encainide

Answer

Intracardiac Defibrillation

Answer

Beta-blockers

Question 10

Plethoric, non-collapsible IVC on echocardiography denotes?

Accepted Answer

Right heart failure

Answer

Budd-Chiari syndrome

Answer

Hepatic venous malformation

Answer

IVC thrombosis

Cardiology — MCQs

Cardiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?