Cardiovascular Drugs — MCQs
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In the treatment of shock, why is Dobutamine preferred over Dopamine?
Which of the following drugs does not cause bradycardia?
A 54-year-old man with emphysema presents with a blood pressure of 157/101 mmHg. Despite treatment with angiotensin-converting enzyme inhibitors, diuretics, and calcium channel blockers, each agent had to be discontinued due to undesirable side effects. The physician then decides to prescribe a beta-antagonist. Which of the following would be most appropriate for this patient?
Sodium nitroprusside's active metabolite acts by which mechanism?
What is the dose of streptokinase to be used in myocardial infarction (MI)?
If systemic vascular resistance is twice that of normal, which of the following treatments should be initiated?
What is the antihypertensive of choice in a pregnant lady?
Which of the following drugs is used for termination as well as prophylaxis of paroxysmal supraventricular tachycardia?
What is the recommended dose of streptokinase for fibrinolysis in myocardial infarction?
What is the drug of choice for ventricular premature beats (VPC) due to digitalis toxicity?
Cardiovascular Drugs Indian Medical PG Practice Questions and MCQs
Question 671: In the treatment of shock, why is Dobutamine preferred over Dopamine?
- A. It causes fewer arrhythmias.
- B. It causes less renal vasodilation.
- C. It causes less coronary vasoconstriction.
- D. All the above. (Correct Answer)
Explanation: **Explanation:** Dobutamine is a synthetic sympathomimetic that primarily acts as a **$\beta_1$-selective agonist**, making it an ideal inotropic agent in cardiogenic shock. While both drugs increase cardiac output, Dobutamine offers several clinical advantages over Dopamine: 1. **Fewer Arrhythmias (Option A):** Dopamine triggers a significant release of endogenous norepinephrine and has a stronger effect on $\alpha$ and $\beta$ receptors at higher doses, leading to a higher incidence of tachyarrhythmias compared to Dobutamine. 2. **Renal Vasodilation (Option B):** While Dopamine at low doses ("renal dose") acts on $D_1$ receptors to cause vasodilation, this effect is often unpredictable in shock states and can lead to a "steal phenomenon." Dobutamine maintains systemic perfusion more steadily without the complex dose-dependent shifts (Dopaminergic $\rightarrow$ Beta $\rightarrow$ Alpha) seen with Dopamine. 3. **Coronary Vasoconstriction (Option C):** At the high doses often required in shock, Dopamine’s $\alpha_1$-agonist activity causes peripheral and coronary vasoconstriction, increasing afterload and myocardial oxygen demand. Dobutamine, through its mild $\beta_2$ activity, tends to decrease systemic vascular resistance (afterload), improving stroke volume without significant coronary constriction. **Clinical Pearls for NEET-PG:** * **Drug of Choice:** Dobutamine is the preferred inotrope for **Cardiogenic Shock** and is used in **Stress Echocardiography**. * **Dopamine Limitation:** It is no longer the first-line agent for shock due to the risk of arrhythmias and increased mortality in certain subsets of patients. * **Key Side Effect:** The most common side effect of Dobutamine is tachycardia. * **Vascular Effect:** Unlike Dopamine, Dobutamine is a **"Inodilator"** (Inotrope + Vasodilator).
Question 672: Which of the following drugs does not cause bradycardia?
- A. Propranolol
- B. Hydralazine (Correct Answer)
- C. Clonidine
- D. Reserpine
Explanation: The correct answer is **Hydralazine** because it is a potent direct-acting arteriolar vasodilator [1, 2]. When systemic vascular resistance drops rapidly, the body compensates via the baroreceptor reflex. This triggers a significant increase in sympathetic outflow, leading to **reflex tachycardia**, not bradycardia [3]. In clinical practice, hydralazine is often co-administered with a beta-blocker to counteract this compensatory tachycardia [3]. **Analysis of Incorrect Options:** * **Propranolol:** A non-selective beta-blocker that decreases heart rate by blocking $\beta_1$ receptors in the SA node. It is a classic cause of bradycardia [4]. * **Clonidine:** An $\alpha_2$-adrenergic agonist that acts centrally to decrease sympathetic outflow and increase vagal tone, leading to a reduction in heart rate. * **Reserpine:** An alkaloid that depletes catecholamines (norepinephrine) from peripheral sympathetic nerve endings and the CNS. The loss of sympathetic stimulation to the heart results in bradycardia. **High-Yield Clinical Pearls for NEET-PG:** * **Vasodilator Paradox:** Direct vasodilators (Hydralazine, Minoxidil, Nifedipine) typically cause reflex tachycardia [3]. In contrast, centrally acting drugs (Clonidine, Methyldopa) and sympatholytics (Reserpine, Beta-blockers) cause bradycardia. * **Hydralazine Side Effects:** Apart from tachycardia, it is famously associated with **Drug-Induced Lupus Erythematosus (DILE)**, especially in "slow acetylators." * **Clinical Use:** Hydralazine is a preferred drug for managing hypertension in pregnancy (alongside Labetalol and Methyldopa).
Question 673: A 54-year-old man with emphysema presents with a blood pressure of 157/101 mmHg. Despite treatment with angiotensin-converting enzyme inhibitors, diuretics, and calcium channel blockers, each agent had to be discontinued due to undesirable side effects. The physician then decides to prescribe a beta-antagonist. Which of the following would be most appropriate for this patient?
- A. Metoprolol (Correct Answer)
- B. Nadolol
- C. Propranolol
- D. Sotalol
Explanation: **Explanation:** The core clinical challenge in this patient is managing hypertension in the presence of **emphysema (COPD)**. Beta-blockers are generally used with caution in patients with obstructive airway disease because blocking $\beta_2$ receptors can cause bronchoconstriction, potentially precipitating a respiratory crisis. **1. Why Metoprolol is correct:** Metoprolol is a **cardioselective ($\beta_1$-selective) antagonist**. At therapeutic doses, it preferentially blocks $\beta_1$ receptors in the heart, reducing blood pressure while having minimal effect on the $\beta_2$ receptors in the bronchial smooth muscle. This makes it the safest choice among the options for a patient with emphysema or asthma. **2. Why the other options are incorrect:** * **Propranolol:** A prototypical **non-selective** beta-blocker ($\beta_1 = \beta_2$). It significantly increases airway resistance and is strictly contraindicated in patients with asthma or symptomatic COPD. * **Nadolol:** Another **non-selective** beta-blocker with a long half-life. Like propranolol, it poses a high risk of bronchospasm. * **Sotalol:** A non-selective beta-blocker that also possesses Class III antiarrhythmic properties (potassium channel blocking). It is not used for primary hypertension and carries the same respiratory risks as propranolol. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for $\beta_1$ selective blockers:** *"A beam of Beta-1 blockers"* (**A**tenolol, **B**isoprolol, **E**smolol, **A**cebutolol, **M**etoprolol). * **Selectivity is dose-dependent:** At high doses, even cardioselective blockers lose their specificity and can block $\beta_2$ receptors. * **Drug of Choice:** While beta-blockers are not first-line for uncomplicated hypertension (per JNC-8), they are indicated in patients with compelling indications like post-MI or heart failure. * **Esmolol** is the shortest-acting beta-blocker (half-life ~9 mins), used intravenously for hypertensive emergencies or intraoperative tachycardia.
Question 674: Sodium nitroprusside's active metabolite acts by which mechanism?
- A. Inhibiting phosphokinase
- B. Stimulating guanylyl cyclase (Correct Answer)
- C. Activating phospholipase A
- D. Activating phospholipase B
Explanation: **Explanation:** **Sodium Nitroprusside (SNP)** is a potent, rapid-acting vasodilator used in hypertensive emergencies. Its mechanism of action involves the release of **Nitric Oxide (NO)**. 1. **Mechanism of the Correct Answer (B):** SNP is a prodrug that reacts with sulfhydryl groups on erythrocytes and albumin to release NO. This NO then diffuses into the vascular smooth muscle cells where it binds to and **stimulates soluble guanylyl cyclase**. This enzyme converts GTP to **cyclic GMP (cGMP)**. Increased levels of cGMP activate protein kinase G, leading to dephosphorylation of myosin light chains and sequestration of calcium, resulting in profound relaxation of both arterioles and venules (balanced vasodilator). 2. **Why Incorrect Options are Wrong:** * **Option A:** SNP does not inhibit phosphokinase; rather, it indirectly activates protein kinase G via cGMP. * **Options C & D:** Phospholipases (A and B) are involved in the metabolism of membrane phospholipids and the arachidonic acid cascade (prostaglandin synthesis). They are not the primary targets for the vasodilatory action of NO-donors. **High-Yield Clinical Pearls for NEET-PG:** * **Balanced Vasodilator:** Unlike Hydralazine (arteriolar) or Nitroglycerin (predominantly venous), SNP acts equally on **arteries and veins**, reducing both afterload and preload. * **Toxicity:** SNP contains five cyanide groups. Metabolism can lead to **Cyanide toxicity** (treated with Sodium Thiosulfate/Nitrites) and **Thiocyanate toxicity** (especially in renal failure). * **Light Sensitivity:** SNP is unstable in light; the infusion bottle must be covered with opaque foil. * **Drug of Choice:** Historically the gold standard for hypertensive emergencies, though now often replaced by Labetalol or Nicardipine due to toxicity concerns.
Question 675: What is the dose of streptokinase to be used in myocardial infarction (MI)?
- A. 0.15 Million units
- B. 1.5 Million units (Correct Answer)
- C. 15 Million units
- D. 150 Million units
Explanation: **Explanation:** **1. Understanding the Correct Answer (B):** Streptokinase is a first-generation fibrinolytic agent derived from Beta-hemolytic Streptococci. In the management of ST-elevation myocardial infarction (STEMI), the standard therapeutic dose is **1.5 Million Units (MU)**. This dose is administered via intravenous infusion over 30 to 60 minutes. The goal is to activate plasminogen into plasmin, which degrades the fibrin mesh of the coronary thrombus, thereby restoring myocardial perfusion. **2. Analysis of Incorrect Options:** * **Option A (0.15 MU):** This dose is sub-therapeutic for systemic thrombolysis in MI. While lower doses may be used for catheter-directed thrombolysis in peripheral arterial occlusion, it is insufficient for coronary reperfusion. * **Options C & D (15 MU and 150 MU):** These doses are excessively high and would lead to catastrophic, life-threatening systemic hemorrhage. The therapeutic window for fibrinolytics is narrow, making precise dosing critical. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** It is a non-specific fibrinolytic (acts on both clot-bound and circulating plasminogen), leading to a "systemic lytic state." * **Antigenicity:** Because it is derived from bacteria, it is antigenic. It can cause **Type I hypersensitivity (anaphylaxis)**. * **Repeat Dosing:** It should **not** be repeated within 6 months to 1 year (or ever, ideally) due to the presence of neutralizing antibodies which render it ineffective and increase allergy risk. * **Side Effect:** Hypotension is a common side effect during infusion; if it occurs, the infusion rate should be slowed. * **Contraindication:** Previous streptococcal infection or prior streptokinase use within the last year.
Question 676: If systemic vascular resistance is twice that of normal, which of the following treatments should be initiated?
- A. Adrenaline
- B. Nor-adrenaline
- C. Sodium nitroprusside (Correct Answer)
- D. Isoprenaline
Explanation: **Explanation:** The core concept in this question is the management of **increased Systemic Vascular Resistance (SVR)**, which clinically manifests as severe hypertension or hypertensive crisis. **1. Why Sodium Nitroprusside is Correct:** Sodium nitroprusside is a potent, direct-acting **mixed vasodilator** (acting on both arterioles and venules). It works by releasing Nitric Oxide (NO), which stimulates guanylyl cyclase to increase cGMP, leading to smooth muscle relaxation. By dilating the resistance vessels (arterioles), it rapidly decreases SVR and blood pressure, making it an ideal choice for hypertensive emergencies where SVR is pathologically high. **2. Why Other Options are Incorrect:** * **Adrenaline (Epinephrine):** At high doses, it stimulates $\alpha_1$ receptors, causing vasoconstriction and further **increasing SVR**. It would worsen the condition. * **Nor-adrenaline (Norepinephrine):** This is a potent $\alpha_1$ agonist. Its primary effect is intense vasoconstriction, which significantly **increases SVR**. It is used in shock, not for high SVR states. * **Isoprenaline:** This is a pure $\beta$-agonist ($\beta_1$ and $\beta_2$). While it can decrease SVR via $\beta_2$ vasodilation, its profound positive chronotropic and inotropic effects ($\beta_1$) make it unsuitable for treating hypertensive states; it is primarily used for bradyarrhythmias. **High-Yield NEET-PG Pearls:** * **Sodium Nitroprusside Toxicity:** Prolonged infusion can lead to **Cyanide and Thiocyanate toxicity**. The antidote is Sodium Thiosulfate or Hydroxocobalamin. * **Light Sensitivity:** Nitroprusside is photosensitive; the infusion bottle must be covered with opaque foil. * **Drug of Choice:** While Nitroprusside was historically the gold standard for hypertensive emergencies, **Labetalol** or **Nicardipine** are now often preferred due to better safety profiles.
Question 677: What is the antihypertensive of choice in a pregnant lady?
- A. Methyldopa (Correct Answer)
- B. Furosemide
- C. Nitroprusside
- D. ACE inhibitors
Explanation: **Explanation:** **1. Why Methyldopa is the Correct Choice:** Methyldopa is a centrally acting alpha-2 adrenergic agonist. It has been the traditional **drug of choice** for chronic hypertension in pregnancy due to its long-standing safety profile and lack of teratogenicity. It does not affect fetal hemodynamics or uteroplacental blood flow. While **Labetalol** is increasingly used as a first-line agent in modern guidelines, Methyldopa remains the classic textbook answer for NEET-PG. **2. Why Other Options are Incorrect:** * **Furosemide (Option B):** Diuretics are generally avoided in pregnancy as they can decrease placental perfusion by reducing maternal plasma volume, potentially leading to fetal growth restriction. * **Nitroprusside (Option C):** It is contraindicated in pregnancy because its metabolism releases cyanide, which can lead to **fetal cyanide poisoning**. * **ACE Inhibitors (Option D):** These are strictly **contraindicated (Teratogenic)**. They cause "ACEI Fetopathy," characterized by fetal renal dysgenesis, oligohydramnios, skull hypoplasia, and pulmonary hypoplasia. **3. High-Yield Clinical Pearls for NEET-PG:** * **Safe Antihypertensives in Pregnancy (Mnemonic: "Better Mother Care During Hypertensive Pregnancy"):** **B**eta-blockers (Labetalol), **M**ethyldopa, **C**alcium Channel Blockers (Nifedipine), **D**ihydralazine. * **Drug of Choice for Preeclampsia/Eclampsia:** **Magnesium Sulfate (MgSO₄)** is used for seizure prophylaxis/treatment, while **Labetalol** or **Hydralazine** are used for acute blood pressure control. * **Contraindicated Drugs:** ACE inhibitors, ARBs, Direct Renin Inhibitors, Nitroprusside, and Statins.
Question 678: Which of the following drugs is used for termination as well as prophylaxis of paroxysmal supraventricular tachycardia?
- A. Digoxin
- B. Verapamil (Correct Answer)
- C. Propranolol
- D. Quinidine
Explanation: **Explanation:** **Verapamil** (a non-dihydropyridine Calcium Channel Blocker) is the correct answer because it acts primarily on the **Sinoatrial (SA) and Atrioventricular (AV) nodes**. By blocking L-type calcium channels, it slows AV conduction and prolongs the functional refractory period. This makes it highly effective for both **terminating** an acute episode of Paroxysmal Supraventricular Tachycardia (PSVT) by breaking the re-entry circuit at the AV node, and for **prophylaxis** to prevent recurrence. **Analysis of Incorrect Options:** * **Digoxin (Option A):** While it increases vagal tone and slows AV conduction, its onset of action is too slow for the acute termination of PSVT. It is primarily used for rate control in atrial fibrillation. * **Propranolol (Option C):** As a Beta-blocker, it is effective for prophylaxis and can be used for termination, but Verapamil is traditionally considered more potent for the acute termination of narrow-complex SVT in hemodynamically stable patients. * **Quinidine (Option D):** This is a Class IA antiarrhythmic. It is rarely used for PSVT and can actually worsen tachycardia by its vagolytic effect, which paradoxically increases AV conduction. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** For the **acute termination** of PSVT, **Adenosine** is the first-line drug due to its rapid onset and short half-life. * **Verapamil** is the preferred alternative if Adenosine is contraindicated (e.g., in bronchial asthma) or ineffective. * **Contraindication:** Never use Verapamil in wide-complex tachycardias of unknown origin or in WPW syndrome with atrial fibrillation, as it may precipitate ventricular fibrillation. * **Verapamil + Digoxin:** Verapamil increases digoxin levels by displacing it from tissue binding sites and reducing renal clearance.
Question 679: What is the recommended dose of streptokinase for fibrinolysis in myocardial infarction?
- A. 0.5 million units
- B. 1.0 million units
- C. 1.5 million units (Correct Answer)
- D. 2.0 million units
Explanation: **Explanation:** **Streptokinase** is a first-generation fibrinolytic agent derived from Beta-hemolytic Streptococci. In the management of ST-elevation myocardial infarction (STEMI), the standard recommended dose is **1.5 million units (MU)**. **Why 1.5 million units is correct:** This dose is administered via **intravenous infusion** over **30 to 60 minutes**. Clinical trials (such as GISSI-1 and ISIS-2) established that 1.5 MU provides the optimal balance between achieving coronary artery patency (reperfusion) and minimizing the risk of major systemic bleeding. It works by forming a complex with plasminogen, which then converts free plasminogen into active plasmin to degrade fibrin clots. **Why other options are incorrect:** * **0.5 and 1.0 million units:** These doses are sub-therapeutic for systemic fibrinolysis in MI and are associated with lower rates of successful reperfusion. * **2.0 million units:** Higher doses do not significantly increase the efficacy of clot lysis but drastically increase the risk of life-threatening hemorrhagic complications, such as intracranial hemorrhage. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** It is a **non-fibrin-specific** agent, meaning it causes systemic depletion of fibrinogen (unlike Alteplase). * **Antigenicity:** Because it is a bacterial protein, it is highly antigenic. It can cause **Type I hypersensitivity (anaphylaxis)**. * **Repeat Dosing:** It should **not** be repeated within 6 months to 1 year (or ever, ideally) due to the presence of neutralizing antibodies which render it ineffective and increase allergy risk. * **Side Effect:** Hypotension is a common side effect during infusion.
Question 680: What is the drug of choice for ventricular premature beats (VPC) due to digitalis toxicity?
- A. Diphenylhydantoin (Correct Answer)
- B. Quinidine
- C. Amiodarone
- D. Verapamil
Explanation: **Explanation:** Digitalis toxicity leads to an increase in intracellular calcium and delayed after-depolarizations (DADs), resulting in triggered activity and ventricular arrhythmias. **1. Why Diphenylhydantoin (Phenytoin) is the Correct Answer:** Phenytoin is the drug of choice for digitalis-induced ventricular arrhythmias because it possesses unique properties: * **Suppresses Automaticity:** It decreases the abnormal automaticity of the ventricles caused by digitalis. * **Improves AV Conduction:** Unlike most anti-arrhythmics, phenytoin actually improves AV node conduction (or has minimal depressant effect), which is beneficial since digitalis toxicity often involves AV block. * **Membrane Stabilization:** It acts as a Class IB anti-arrhythmic, shortening the action potential duration and preventing DADs. **2. Why the Other Options are Incorrect:** * **Quinidine (Option B):** It is strictly contraindicated. Quinidine reduces the renal and biliary clearance of digoxin and displaces it from tissue binding sites, doubling the plasma concentration of digoxin and worsening toxicity. * **Amiodarone (Option C):** Similar to quinidine, it can increase digoxin levels and further depress the SA and AV nodes, risking complete heart block. * **Verapamil (Option D):** It is a Calcium Channel Blocker. Since digitalis toxicity already involves intracellular calcium overload, verapamil can worsen the condition and lead to severe AV block. **3. High-Yield Clinical Pearls for NEET-PG:** * **First-line management:** For life-threatening digitalis toxicity, the definitive treatment is **Digoxin-specific antibody fragments (DigiFab/Digibind).** * **Electrolyte Correction:** Hypokalemia exacerbates digitalis toxicity; however, if the patient has hyperkalemia (common in acute overdose), potassium should not be given. * **Lidocaine:** This is an alternative to phenytoin for digitalis-induced ventricular arrhythmias if phenytoin is unavailable. * **Avoid DC Cardioversion:** It can precipitate ventricular fibrillation in a digitalis-toxic heart unless absolutely necessary (use low energy).
Practice by Chapter
Antihypertensive Agents
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Drugs for Heart Failure
Practice Questions
Antiarrhythmic Drugs
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Antianginal Agents
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Lipid-Lowering Drugs
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Anticoagulants and Antiplatelet Drugs
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Thrombolytic Agents
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Drugs Used in Pulmonary Hypertension
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Drugs Used in Shock
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Cardiovascular Effects of Non-Cardiovascular Drugs
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