Cardiology — MCQs
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A patient complains of intermittent claudication, dizziness, and headache. What is the likely cardiac lesion?
Dissection of which artery is seen in pregnancy?
Which of the following is a risk factor for coronary artery disease (CAD)?
A 67-year-old man with an 18-year history of type 2 diabetes mellitus presents for a routine physical examination. His temperature is 36.9 C (98.5 F), his blood pressure is 158/98 mm Hg and his pulse is 82/minute and regular. On examination, the physician notes a non-tender, pulsatile, mass in the mid-abdomen. A plain abdominal x-ray film with the patient in the lateral position reveals spotty calcification of a markedly dilated abdominal aortic wall. Which of the following physiologic observations helps to account for the fact that 75% of the aneurysms of this patient's type are found in the abdomen and only 25% principally involve the thorax?
What is the most common cause of painful pericarditis?
A 55-year-old woman presents with recent onset of chest pain and dyspnea. Six weeks prior, the patient suffered a myocardial infarction. On physical examination, a friction rub is heard over the 5th intercostal space in the midclavicular line, along with elevated JVP. What is the most likely cause of this presentation?
A 70-year-old patient with a history of exertional chest pain for the last 4 years, which has not progressed, refuses angiography. What is the recommended management for this patient?
What is the most common form of paroxysmal supraventricular tachycardia (PSVT)?
Substernal pain is a feature of which of the following conditions?
Subacute bacterial endocarditis is caused by which organism?
Cardiology Indian Medical PG Practice Questions and MCQs
Question 1: A patient complains of intermittent claudication, dizziness, and headache. What is the likely cardiac lesion?
- A. Tetralogy of Fallot (TOF) (Correct Answer)
- B. Atrial Septal Defect (ASD)
- C. Patent Ductus Arteriosus (PDA)
- D. Coarctation of the Aorta
Explanation: ### Explanation The clinical presentation of **intermittent claudication, dizziness, and headache** in a patient with a congenital heart lesion points toward a state of **chronic hypoxia and secondary polycythemia**, which is a hallmark of **Tetralogy of Fallot (TOF)** [1]. **1. Why TOF is the Correct Answer:** TOF is the most common cyanotic congenital heart disease [1]. The right-to-left shunt leads to chronic hypoxemia. To compensate, the body increases erythropoietin production, leading to **secondary polycythemia** (elevated hematocrit). This increased blood viscosity causes: * **Hyperviscosity Syndrome:** Leading to headaches and dizziness. * **Reduced Peripheral Perfusion:** During exercise, the viscous blood and low oxygen delivery result in muscle ischemia, manifesting as **intermittent claudication**. **2. Why Other Options are Incorrect:** * **Atrial Septal Defect (ASD) & Patent Ductus Arteriosus (PDA):** These are primarily left-to-right (acyanotic) shunts [3], [4]. Unless Eisenmenger syndrome develops, they do not typically present with polycythemia-related claudication or hyperviscosity symptoms. * **Coarctation of the Aorta:** While this classically causes claudication (due to mechanical obstruction) and headaches (due to upper limb hypertension), it is an **acyanotic** lesion [2]. In the context of standard NEET-PG patterns, if the question implies a "cardiac lesion" associated with systemic cyanotic complications, TOF is the preferred answer. **3. NEET-PG High-Yield Pearls:** * **TOF Components:** VSD, Overriding of Aorta, Pulmonary Stenosis, and RV Hypertrophy [1]. * **X-ray Finding:** "Boot-shaped heart" (Coeur en sabot). * **Management of "Tet Spells":** Knee-chest position (increases systemic vascular resistance) and Morphine. * **Polycythemia Risk:** Patients are at high risk for **cerebral thrombosis** and **brain abscesses** due to the loss of pulmonary capillary filtering [2].
Question 2: Dissection of which artery is seen in pregnancy?
- A. Carotid artery
- B. Aorta (Correct Answer)
- C. Coronary artery
- D. Femoral artery
Explanation: **Explanation:** **Aortic dissection** is a life-threatening cardiovascular complication significantly associated with pregnancy, particularly during the **third trimester** and the **early postpartum period** [1]. **Why Aorta is the Correct Answer:** The association between pregnancy and aortic dissection is driven by two primary factors: 1. **Hemodynamic Stress:** Pregnancy causes a significant increase in cardiac output, stroke volume, and blood pressure, which increases the shear stress on the aortic wall. 2. **Hormonal Changes:** High levels of estrogen and progesterone lead to structural remodeling of the vascular media. This includes the depletion of acid mucopolysaccharides and alterations in collagen and elastin, weakening the aortic wall (cystic medial necrosis). *Note: Over 50% of aortic dissections in women under age 40 occur during pregnancy.* **Analysis of Incorrect Options:** * **Carotid Artery:** While spontaneous carotid dissection can occur, it is much rarer than aortic involvement and is typically associated with trauma or connective tissue disorders rather than pregnancy specifically. * **Coronary Artery:** **Spontaneous Coronary Artery Dissection (SCAD)** is indeed a known cause of MI in pregnancy. However, in the context of general systemic arterial dissection and high-yield exam patterns, the **Aorta** remains the most common and classic association. * **Femoral Artery:** Dissection of peripheral arteries like the femoral is extremely rare and usually secondary to iatrogenic trauma (catheterization) rather than physiological changes of pregnancy. **NEET-PG High-Yield Pearls:** * **Most common site:** The ascending aorta (Stanford Type A) is most frequently involved [1]. * **Risk Factors:** Pre-existing **Marfan Syndrome** or Bicuspid Aortic Valve significantly increases the risk [1]. * **Clinical Presentation:** Sudden, "tearing" chest pain radiating to the back [1]. * **Management:** Type A is a surgical emergency; Type B is often managed medically with strict blood pressure control (Labetalol is the drug of choice in pregnancy).
Question 3: Which of the following is a risk factor for coronary artery disease (CAD)?
- A. High HDL
- B. Low LDL
- C. Increased homocysteine levels (Correct Answer)
- D. Decreased fibrinogen levels
Explanation: **Explanation:** Coronary Artery Disease (CAD) is driven by atherosclerosis, a process influenced by traditional and non-traditional risk factors [1]. **Why Option C is Correct:** **Increased homocysteine levels (Hyperhomocysteinemia)** is a recognized non-traditional risk factor for CAD. Elevated homocysteine promotes atherosclerosis through several mechanisms: it induces vascular endothelial injury, promotes the oxidation of LDL cholesterol, and stimulates smooth muscle cell proliferation. Furthermore, it creates a pro-thrombotic state by increasing platelet aggregation and interfering with the coagulation cascade. **Analysis of Incorrect Options:** * **Option A (High HDL):** High-Density Lipoprotein (HDL) is known as "good cholesterol." It facilitates reverse cholesterol transport (carrying cholesterol away from arteries to the liver) [3] and has antioxidant properties [4], making it **cardioprotective**, not a risk factor. * **Option B (Low LDL):** Low-Density Lipoprotein (LDL) is the primary atherogenic lipoprotein [2]. **High** levels of LDL are a major risk factor; conversely, low levels are associated with a reduced risk of plaque formation. * **Option D (Decreased fibrinogen levels):** Fibrinogen is a coagulation factor. **Increased** levels of fibrinogen (a pro-inflammatory and pro-coagulant marker) are associated with an increased risk of CAD and thrombosis. **Clinical Pearls for NEET-PG:** * **Homocysteine Metabolism:** Deficiencies in **Vitamin B12, B6, and Folic acid** can lead to hyperhomocysteinemia. * **Emerging Risk Factors:** Other high-yield non-traditional markers include **Lipoprotein(a)**, **High-sensitivity C-reactive protein (hs-CRP)**, and **Small dense LDL particles** [2]. * **Framingham Risk Score:** Remember that age, male gender, hypertension, smoking, and diabetes remain the "Big 5" traditional risk factors.
Question 4: A 67-year-old man with an 18-year history of type 2 diabetes mellitus presents for a routine physical examination. His temperature is 36.9 C (98.5 F), his blood pressure is 158/98 mm Hg and his pulse is 82/minute and regular. On examination, the physician notes a non-tender, pulsatile, mass in the mid-abdomen. A plain abdominal x-ray film with the patient in the lateral position reveals spotty calcification of a markedly dilated abdominal aortic wall. Which of the following physiologic observations helps to account for the fact that 75% of the aneurysms of this patient's type are found in the abdomen and only 25% principally involve the thorax?
- A. Diastolic pressure is greater in the abdominal aorta in the supine position.
- B. Negative intrathoracic pressure reduces aortic wall tension in the thorax.
- C. The average blood flow in the abdominal aorta is greater than that in the thoracic aorta.
- D. The average blood pressure in the abdominal aorta is higher than that in the thoracic aorta. (Correct Answer)
Explanation: ### Explanation The correct answer is **D: The average blood pressure in the abdominal aorta is higher than that in the thoracic aorta.** #### **Mechanism and Pathophysiology** The distribution of aortic aneurysms is primarily dictated by hemodynamics and structural differences. According to the **Law of Laplace** ($T = P \times r$), wall tension ($T$) increases with pressure ($P$) and radius ($r$). In the arterial system, as blood moves distally from the heart, the pressure wave undergoes **peripheral amplification**. This occurs because the aorta narrows and becomes less compliant (stiffer) distally, and pressure waves reflect back from peripheral resistance vessels. Consequently, the **systolic and mean arterial pressures are higher in the abdominal aorta** compared to the thoracic aorta. This increased chronic wall stress, combined with a thinner tunica media and lack of *vasa vasorum* in the infrarenal abdominal aorta, makes it more susceptible to aneurysmal dilation. The infrarenal abdominal aorta is the most common site for non-specific aneurysm formation [1]. #### **Analysis of Incorrect Options** * **Option A:** While posture affects local pressure, the fundamental reason for the 75:25 distribution is the inherent hemodynamic profile of the arterial tree, not just the supine position. * **Option B:** Intrathoracic pressure is negative relative to atmospheric pressure, but it is the **transmural pressure** (internal minus external) that matters. The difference is physiologically negligible in the context of aneurysm formation compared to intraluminal hypertension. * **Option C:** Blood flow (volume per unit time) is actually **lower** in the abdominal aorta because several major branches (brachiocephalic, left carotid, subclavian) have already exited in the thorax. #### **NEET-PG High-Yield Pearls** * **Most common site:** The infrarenal aorta (between the renal arteries and the iliac bifurcation) [1]. Around 80% are confined to this segment [1]. * **Risk Factors:** Smoking (strongest), male gender, age >65, and atherosclerosis [1]. (Note: Diabetes is a risk factor for atherosclerosis but is paradoxically associated with a *slower* rate of AAA expansion). * **Screening:** A one-time abdominal ultrasound is recommended for men aged 65–75 who have ever smoked [1]. * **Surgical Threshold:** Repair is generally indicated if the diameter is **>5.5 cm in men** or **>5.0 cm in women**, or if it grows >0.5 cm in 6 months.
Question 5: What is the most common cause of painful pericarditis?
- A. Viral (Correct Answer)
- B. Tuberculous
- C. Uremic
- D. All of these
Explanation: **Explanation:** Acute pericarditis is characterized by the classic triad of chest pain, a pericardial friction rub, and diffuse ST-segment elevation on ECG [1]. **1. Why Viral is Correct:** Viral infections (most commonly **Coxsackievirus B** and Echovirus) are the most frequent cause of acute pericarditis in clinical practice [1]. The pain in viral pericarditis is typically sharp, pleuritic, and retrosternal, caused by the inflammation of the parietal pericardium and adjacent pleura. Because viral pericarditis involves an intense inflammatory response, it is the most common cause of **painful** pericarditis. **2. Why the other options are incorrect:** * **Tuberculous Pericarditis:** While common in developing countries like India, it usually presents as a chronic, subacute condition [2]. It often leads to pericardial effusion or constrictive pericarditis rather than acute, sharp pain [2]. * **Uremic Pericarditis:** This is a classic "high-yield" exception. Uremic pericarditis (seen in end-stage renal disease) is typically **painless** because it is a metabolic/fibrinous process rather than a purely inflammatory one. The lack of pain is due to the absence of significant inflammation of the surrounding pleura. * **All of these:** Incorrect because of the distinct clinical presentation of uremic pericarditis as painless. **Clinical Pearls for NEET-PG:** * **Positionality:** Pericarditic pain characteristically worsens when supine and is **relieved by sitting up and leaning forward**. * **ECG Findings:** Look for diffuse concave-upwards ST elevation and **PR segment depression** (the latter is highly specific for acute pericarditis) [1]. * **Treatment:** First-line treatment is NSAIDs (like Ibuprofen or Aspirin) plus **Colchicine** (to prevent recurrence) [1]. * **Dressler Syndrome:** An autoimmune form of pericarditis occurring 2–10 weeks post-Myocardial Infarction.
Question 6: A 55-year-old woman presents with recent onset of chest pain and dyspnea. Six weeks prior, the patient suffered a myocardial infarction. On physical examination, a friction rub is heard over the 5th intercostal space in the midclavicular line, along with elevated JVP. What is the most likely cause of this presentation?
- A. Cardiac rupture syndrome
- B. Thromboembolism
- C. Dressler syndrome (Correct Answer)
- D. Ventricular aneurysm
Explanation: ### Explanation **Dressler Syndrome (Post-Myocardial Infarction Syndrome)** The correct answer is **Dressler syndrome**. This is an immune-mediated (Type III hypersensitivity) pericarditis that typically occurs **2 to 10 weeks** after a myocardial infarction (MI). The clinical triad includes fever, pleuritic chest pain, and a pericardial friction rub. The presence of elevated JVP and a friction rub 6 weeks post-MI strongly points toward this delayed inflammatory response. **Analysis of Incorrect Options:** * **Cardiac Rupture Syndrome:** This is a catastrophic early complication, usually occurring within the **first 3–7 days** post-MI. It presents with sudden cardiac tamponade and electromechanical dissociation, not a subacute presentation at 6 weeks. * **Thromboembolism:** While common post-MI due to mural thrombi, it typically presents with focal neurological deficits (stroke) or acute limb ischemia, rather than a pericardial friction rub and JVP elevation. * **Ventricular Aneurysm:** This late complication (weeks to months) usually presents with heart failure, persistent ST-segment elevation on ECG, or ventricular arrhythmias. While it can cause elevated JVP due to heart failure, it does not typically cause a friction rub unless associated with Dressler syndrome. **NEET-PG High-Yield Pearls:** * **Timeline is Key:** * *Fibrinous Pericarditis:* 1–3 days post-MI (localized inflammation). * *Dressler Syndrome:* 2–10 weeks post-MI (autoimmune). * **Pathophysiology:** Formation of antibodies against myocardial antigens released during necrosis. * **Treatment:** High-dose Aspirin or NSAIDs; Colchicine is often added [1]. Corticosteroids are reserved for refractory cases [1]. * **Classic Sign:** Pericardial friction rub is best heard with the patient leaning forward during expiration.
Question 7: A 70-year-old patient with a history of exertional chest pain for the last 4 years, which has not progressed, refuses angiography. What is the recommended management for this patient?
- A. Administer low-dose aspirin. (Correct Answer)
- B. Prescribe sublingual nitroglycerin before exertion.
- C. Advise to continue exercise even after experiencing chest pain.
- D. Advise to stop exercising if chest pain occurs.
Explanation: The patient presents with symptoms consistent with **Stable Ischemic Heart Disease (SIHD)**, characterized by exertional chest pain that has remained unchanged for four years [2]. In patients with stable angina, the primary goals of management are to reduce the risk of major adverse cardiovascular events (MACE) and improve quality of life. **1. Why Option A is Correct:** Low-dose aspirin (75–150 mg daily) is the cornerstone of pharmacological management in SIHD [1]. It acts as an antiplatelet agent, reducing the risk of myocardial infarction and death by preventing thrombus formation over atherosclerotic plaques. Since the patient refuses invasive procedures (angiography), aggressive medical management with aspirin and statins is mandatory to improve survival [1]. **2. Why Incorrect Options are Wrong:** * **Option B:** While sublingual nitroglycerin is used for acute relief of anginal symptoms, it is a **symptomatic treatment** and does not improve the prognosis or reduce mortality [1]. * **Option C:** Continuing exercise after the onset of chest pain is dangerous. It increases myocardial oxygen demand in the face of fixed supply, potentially leading to acute ischemia, arrhythmias, or infarction. Standard advice is to exercise up to, but not beyond, the point of chest discomfort [1]. * **Option D:** While stopping exercise when pain occurs is a standard safety instruction, it is a **behavioral modification**, not a definitive pharmacological management strategy for a 70-year-old with established CAD. ### High-Yield Clinical Pearls for NEET-PG: * **First-line for Symptom Control:** Beta-blockers (e.g., Metoprolol, Atenolol) are the first-line drugs to reduce the frequency of anginal episodes [3]. * **Mortality Benefit in SIHD:** Only Aspirin, Statins, and Beta-blockers (especially post-MI) have proven mortality benefits. * **Refusal of Angiography:** If a patient is stable and refuses invasive intervention, "Optimal Medical Therapy" (OMT) is the standard of care. * **Nitrates:** These are contraindicated in patients taking Sildenafil (PDE-5 inhibitors) or those with Right Ventricular Infarction.
Question 8: What is the most common form of paroxysmal supraventricular tachycardia (PSVT)?
- A. Tachycardia originating from the atrium
- B. AV nodal reentrant tachycardia (Correct Answer)
- C. Wolff-Parkinson-White (WPW) syndrome
- D. Focal atrial tachycardia
Explanation: **AV nodal reentrant tachycardia (AVNRT)** is the most common form of paroxysmal supraventricular tachycardia (PSVT), accounting for approximately **60% of cases**. It is caused by a functional reentrant circuit within the AV node itself, facilitated by the presence of dual pathways: a **fast pathway** (long refractory period) and a **slow pathway** (short refractory period) [1]. During an episode, an atrial premature beat typically triggers the circuit, leading to a rapid, regular heart rate (usually 150–250 bpm) with P-waves often buried within or immediately following the QRS complex [1]. **Analysis of Options:** * **Option A & D:** Tachycardias originating from the atrium (like focal atrial tachycardia) are less common than reentrant types [2]. Focal atrial tachycardia usually arises from a specific site (e.g., crista terminalis) and accounts for only about 5-10% of PSVTs. * **Option C:** Wolff-Parkinson-White (WPW) syndrome involves an anatomical accessory pathway (Bundle of Kent) leading to **AV reentrant tachycardia (AVRT)** [3]. While it is the second most common cause of PSVT (approx. 30%), it is less frequent than AVNRT. **High-Yield Clinical Pearls for NEET-PG:** 1. **First-line Management:** Vagal maneuvers (Valsalva or Carotid sinus massage). 2. **Drug of Choice (Acute):** Adenosine (6mg IV rapid bolus). It works by transiently blocking the AV node. 3. **Definitive Treatment:** Radiofrequency ablation (RFA) of the **slow pathway** [2]. 4. **ECG Hallmark:** "Pseudo-S" wave in lead II or "Pseudo-R'" in V1 (representing the retrograde P-wave).
Question 9: Substernal pain is a feature of which of the following conditions?
- A. Tachycardia
- B. Emphysema
- C. Angina pectoris (Correct Answer)
- D. Thrombi and emboli
Explanation: Explanation: Angina pectoris is the correct answer because it is the clinical manifestation of myocardial ischemia, typically caused by an imbalance between myocardial oxygen supply and demand [1]. The classic presentation is substernal chest pain or pressure, often described as "heaviness" or "tightness." This occurs because the visceral afferent nerves supplying the heart enter the spinal cord at the T1-T5 levels, leading to poorly localized, midline (substernal) discomfort that may radiate to the left arm, neck, or jaw [1]. Analysis of Incorrect Options: * Tachycardia: While severe tachycardia can trigger angina by increasing oxygen demand, tachycardia itself is a clinical sign (increased heart rate) rather than a primary cause of substernal pain [1]. * Emphysema: This is a form of Chronic Obstructive Pulmonary Disease (COPD). Patients typically present with progressive dyspnea and a "barrel chest" rather than acute substernal pain. If pain occurs, it is usually pleuritic (lateralized) due to complications like pneumothorax. * Thrombi and emboli: While a pulmonary embolism can cause chest pain, it is typically pleuritic (sharp and worsening with inspiration) and lateralized, rather than classic substernal pressure. Coronary thrombosis leads to Myocardial Infarction, which presents with substernal pain, but "Angina Pectoris" is the more specific clinical term for the pain itself. High-Yield Clinical Pearls for NEET-PG: * Levine’s Sign: A patient pressing a clenched fist against the sternum to describe anginal pain—highly suggestive of myocardial ischemia [1]. * Stable vs. Unstable Angina: Stable angina is provoked by exertion and relieved by rest/nitroglycerin; Unstable angina occurs at rest or with increasing frequency [1]. * Differential Diagnosis: Always rule out other "Big 5" causes of chest pain: MI, Aortic Dissection, Pulmonary Embolism, Tension Pneumothorax, and Esophageal Rupture.
Question 10: Subacute bacterial endocarditis is caused by which organism?
- A. Streptococcus viridans (Correct Answer)
- B. Hemolytic streptococci
- C. Staphylococcus aureus
- D. Neisseria
Explanation: ### Explanation **Correct Answer: A. Streptococcus viridans** Infective endocarditis (IE) is clinically classified into two types based on the severity and progression of the disease: **Acute** and **Subacute**. **1. Why Streptococcus viridans is correct:** *Streptococcus viridans* (a group of commensals found in the oropharynx) is the most common cause of **Subacute Bacterial Endocarditis (SBE)** [1]. It typically affects individuals with **pre-existing structural heart disease** (e.g., rheumatic heart disease, bicuspid aortic valve, or mitral valve prolapse). The organism has low virulence, leading to a gradual, indolent clinical course characterized by low-grade fever, night sweats, and weight loss over weeks to months. **2. Why the other options are incorrect:** * **Staphylococcus aureus (Option C):** This is the most common cause of **Acute Bacterial Endocarditis** [1]. It is highly virulent and can attack previously **normal heart valves**, leading to rapid valvular destruction and embolic complications. It is also the leading cause of IE in intravenous drug users (IVDU) [1]. * **Hemolytic streptococci (Option B):** Specifically Group A Strep (*S. pyogenes*), these are more commonly associated with Acute Rheumatic Fever rather than subacute endocarditis [1]. * **Neisseria (Option D):** These are rare causes of endocarditis and typically present as an acute, fulminant infection rather than a subacute one. **3. High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of IE overall:** *Staphylococcus aureus* [1]. * **Most common cause of IE in damaged/prosthetic valves (late):** *Streptococcus viridans*. * **Early Prosthetic Valve Endocarditis (<60 days):** *Staphylococcus epidermidis*. * **IE in IV Drug Users:** *S. aureus* (most common site: **Tricuspid valve**). * **Culture-negative IE:** Most commonly due to prior antibiotic use or **HACEK** group organisms. * **Streptococcus bovis IE:** Strongly associated with **Colorectal carcinoma** [1].
Practice by Chapter
Coronary Artery Disease and Angina
Practice Questions
Acute Coronary Syndromes
Practice Questions
Heart Failure
Practice Questions
Cardiac Arrhythmias
Practice Questions
Valvular Heart Diseases
Practice Questions
Cardiomyopathies
Practice Questions
Pericardial Diseases
Practice Questions
Congenital Heart Disease in Adults
Practice Questions
Hypertension and Hypertensive Emergencies
Practice Questions
Pulmonary Hypertension
Practice Questions
Non-invasive Cardiac Diagnostics
Practice Questions
Preventive Cardiology
Practice Questions
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