Autonomic Drugs in Cardiovascular Disease — MCQs
Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?
A patient with hypertension on Metoprolol, Verapamil was given. This will result in?
All are effects of the parasympathetic system on the heart except?
Which of the following drugs lack vasodilatory properties but are effective in angina?
Clonidine is used as an antihypertensive agent, but if used as a fast intravenous injection, it can increase blood pressure due to:
Which class of antihypertensive drugs is known to cause erectile dysfunction?
Succinylcholine when given for endotracheal intubation causes all of the following EXCEPT –
Mechanism of action of atropine in treatment of organophosphate poisoning is?
Ocular effects that include mydriasis are characteristic of which of the following drugs?
A female has a systolic blood pressure of 130 mmHg and a diastolic blood pressure of 100 mmHg on two consecutive occasions, indicating Stage 2 hypertension. What is the best treatment?
Autonomic Drugs in Cardiovascular Disease Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following stimuli is primarily responsible for triggering the Bezold-Jarisch reflex?
- A. Parasympathetic withdrawal
- B. Decreased venous return
- C. Increased sympathetic stimulation
- D. Activation of cardiac C-fiber afferents (Correct Answer)
Explanation: ***Activation of cardiac C-fiber afferents*** - The **Bezold-Jarisch reflex** is primarily triggered by stimulation of **cardiac mechanoreceptors and chemoreceptors** located in the ventricles, particularly the inferoposterior wall of the left ventricle. - These receptors have **unmyelinated vagal C-fiber afferents** that transmit signals to the medullary cardiovascular centers. - Activation of these afferents leads to the characteristic triad: **bradycardia, hypotension, and vasodilation** via increased parasympathetic activity and withdrawal of sympathetic tone. - Common triggers include vigorous ventricular contraction with decreased filling, certain drugs (veratridine), myocardial ischemia (especially inferior wall MI), and reperfusion. *Decreased venous return* - While **decreased venous return** creates the hemodynamic context (ventricular underfilling) that can lead to vigorous contraction of a relatively empty ventricle, it is not itself the *trigger* of the reflex. - The actual trigger is the activation of the ventricular receptors sensing this abnormal contraction pattern, which then signal via C-fiber afferents. - Decreased venous return alone, without receptor activation, would not produce the reflex. *Parasympathetic withdrawal* - **Parasympathetic withdrawal** would cause tachycardia and is opposite to the Bezold-Jarisch reflex, which involves **increased parasympathetic activity**. - This is a compensatory response seen in other reflexes like the baroreceptor reflex during hypotension. *Increased sympathetic stimulation* - **Increased sympathetic stimulation** produces tachycardia, increased contractility, and vasoconstriction—effects opposite to the Bezold-Jarisch reflex. - The reflex actually causes **sympathetic withdrawal** along with parasympathetic activation.
Question 2: A patient with hypertension on Metoprolol, Verapamil was given. This will result in?
- A. Bradycardia with AV Block (Correct Answer)
- B. Atrial fibrillation
- C. Torsades de pointes
- D. Tachycardia
Explanation: ***Bradycardia with AV Block*** - Both **Metoprolol** (a beta-blocker) and **Verapamil** (a non-dihydropyridine calcium channel blocker) suppress **AV nodal conduction** and decrease heart rate. - Their combined use has an additive effect, significantly increasing the risk of profound **bradycardia**, **AV block**, and even **asystole**. *Atrial fibrillation* - This is an **arrhythmia** characterized by disorganized electrical activity in the atria, not a direct consequence of this drug combination. - While these drugs *treat* atrial fibrillation by controlling ventricular rate, they do not induce it. *Torsades de pointes* - This is a polymorphic **ventricular tachycardia** associated with **QT prolongation** from certain antiarrhythmics or other medications. - Neither Metoprolol nor Verapamil are known to cause significant QT prolongation that would lead to Torsades de pointes. *Tachycardia* - This combination of **negative chronotropic** (heart rate lowering) drugs is highly unlikely to cause tachycardia due to their direct actions on the heart's electrical system. - These drugs are specifically used to *reduce* heart rate and blood pressure.
Question 3: All are effects of the parasympathetic system on the heart except?
- A. Negative chronotropic
- B. Negative dromotropic
- C. All are seen
- D. Negative inotropic (Correct Answer)
Explanation: ***Negative inotropic*** - While the parasympathetic system (via the **vagus nerve**) primarily affects the **sinoatrial (SA) and atrioventricular (AV) nodes** to decrease heart rate and conduction velocity, it has a **minimal direct effect on ventricular contractility** (inotropy) in humans. - The ventricles are less densely innervated by parasympathetic fibers compared to the atria, so acetylcholine's direct negative inotropic effect is **clinically insignificant** in a healthy heart. - This is the **EXCEPTION** - not a significant parasympathetic effect on the heart. *Negative chronotropic* - The parasympathetic system, primarily through **acetylcholine** acting on **muscarinic receptors** in the SA node, decreases the heart rate (chronotropy). - This slows the rate of spontaneous depolarization of pacemaker cells. - This **IS** a major parasympathetic effect. *Negative dromotropic* - Parasympathetic stimulation also slows the conduction velocity through the **AV node** (dromotropy). - This increases the PR interval on an ECG and can lead to various degrees of AV block in extreme cases. - This **IS** a major parasympathetic effect. *All are seen* - This option is incorrect because the **negative inotropic effect** is NOT a significant parasympathetic effect on the heart. - While negative chronotropic and negative dromotropic effects are prominent features of parasympathetic activity, the direct influence on ventricular contractility is minimal.
Question 4: Which of the following drugs lack vasodilatory properties but are effective in angina?
- A. Metoprolol (Correct Answer)
- B. Isosorbide dinitrate
- C. Nifedipine
- D. Verapamil
Explanation: ***Metoprolol*** - **Metoprolol** is a beta-blocker that reduces myocardial oxygen demand by decreasing heart rate, contractility, and blood pressure, without direct vasodilatory effects. - Its efficacy in angina is primarily due to these **cardiac depressant actions**, which relieve myocardial ischemia. *Isosorbide dinitrate* - **Isosorbide dinitrate** is a nitrate that works by releasing nitric oxide, leading to **venodilation** and **arterial dilation**, particularly reducing preload and improving coronary blood flow. - Its anti-anginal effect is directly linked to its **vasodilatory properties**. *Nifedipine* - **Nifedipine** is a dihydropyridine calcium channel blocker that produces potent **vasodilation** of both coronary and peripheral arteries. - Its primary mechanism of action in angina involves **reducing afterload** and improving coronary blood flow through vasodilation. *Verapamil* - **Verapamil** is a non-dihydropyridine calcium channel blocker that causes **coronary and peripheral vasodilation**, reducing afterload and improving myocardial perfusion. - While it also reduces heart rate and contractility, its direct **vasodilatory effects** contribute significantly to its anti-anginal action.
Question 5: Clonidine is used as an antihypertensive agent, but if used as a fast intravenous injection, it can increase blood pressure due to:
- A. Agonistic action on vascular Alpha 2 adrenergic receptors (Correct Answer)
- B. Cardiac stimulation
- C. Stimulation of the vasomotor center leading to increased sympathetic output
- D. Release of noradrenaline from adrenergic nerve endings
Explanation: ***Agonistic action on vascular Alpha 2 adrenergic receptors*** - When administered rapidly intravenously, clonidine initially acts as an agonist on **postsynaptic α2-adrenergic receptors** in the vascular smooth muscle. - This direct peripheral vasoconstrictive effect occurs before central effects dominate, leading to a transient increase in blood pressure. *Stimulation of the vasomotor center leading to increased sympathetic output* - Clonidine's primary antihypertensive effect is through **central α2-receptor agonism**, which *decreases* sympathetic outflow from the vasomotor center. - It would not stimulate the vasomotor center to *increase* sympathetic output, as this contradicts its fundamental mechanism of action. *Cardiac stimulation* - Clonidine is known for its **cardiac depressant effects** due to reduced sympathetic outflow, leading to decreased heart rate and contractility. - It does not directly stimulate the heart, and any initial blood pressure rise is due to vascular effects, not increased cardiac output. *Release of noradrenaline from adrenergic nerve endings* - Clonidine is an **α2-adrenergic agonist**, and activation of presynaptic α2-receptors typically *inhibits* the release of noradrenaline. - It does not cause a direct release of noradrenaline but rather modulates its release in the opposite direction.
Question 6: Which class of antihypertensive drugs is known to cause erectile dysfunction?
- A. Calcium channel blocker
- B. ACE inhibitors
- C. AT1 receptor antagonists
- D. Beta-blockers (Correct Answer)
Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients
Question 7: Succinylcholine when given for endotracheal intubation causes all of the following EXCEPT –
- A. Prolonged apnea
- B. Hypokalemia in paraplegic patient (Correct Answer)
- C. Raised intraocular pressure
- D. Bradycardia
Explanation: ***Hypokalemia in paraplegic patient*** - Succinylcholine is a **depolarizing neuromuscular blocker** that can cause a significant efflux of **potassium from cells**, leading to **transient hyperkalemia**, particularly in patients with muscle denervation (e.g., paraplegia, burns, crush injuries). - Therefore, it causes **hyperkalemia**, not hypokalemia, in predisposed patients. *Prolonged apnea* - **Prolonged apnea** can occur if a patient has atypical pseudocholinesterase, leading to a delayed metabolism of succinylcholine. - This enzyme deficiency causes **succinylcholine to remain active** for a longer duration, resulting in extended paralysis and respiratory depression. *Raised intraocular pressure* - Succinylcholine causes **contraction of extraocular muscles**, leading to an increase in **intraocular pressure**. - This effect is a concern in patients with **open globe injuries** or acute **narrow-angle glaucoma**. *Bradycardia* - Succinylcholine can stimulate **muscarinic receptors** at the sinoatrial node, leading to a **decrease in heart rate** (bradycardia). - This effect is more common with **repeated doses** or in **pediatric patients**.
Question 8: Mechanism of action of atropine in treatment of organophosphate poisoning is?
- A. It inhibits secretion of acetylcholine
- B. It has antimuscarinic activity (Correct Answer)
- C. It is reactivator of acetylcholine esterase enzyme
- D. It is agonist of acetylcholine receptors
Explanation: ***It has antimuscarinic activity*** - **Organophosphate poisoning** leads to **excessive acetylcholine** at muscarinic receptors, causing symptoms like miosis, bradycardia, and increased secretions. - **Atropine** is a **competitive antagonist** at these muscarinic receptors, thereby blocking the effects of excess acetylcholine. *It inhibits secretion of acetylcholine* - Atropine does not directly inhibit the secretion of **acetylcholine** from nerve terminals. - Its action is postsynaptic, specifically at the **receptor level**. *It is reactivator of acetylcholine esterase enzyme* - **Pralidoxime (2-PAM)** and other **oximes** are the drugs that reactivate **acetylcholinesterase**. - Atropine does not reactivate the enzyme; it only blocks the effects of acetylcholine. *It is agonist of acetylcholine receptors* - An **agonist** would mimic the effects of acetylcholine, which would worsen the symptoms of organophosphate poisoning. - Atropine is an **antagonist**, meaning it blocks the receptors.
Question 9: Ocular effects that include mydriasis are characteristic of which of the following drugs?
- A. phenylephrine (alpha agonist) (Correct Answer)
- B. neostigmine (cholinesterase inhibitor)
- C. phentolamine (alpha blocker)
- D. mecamylamine (ganglionic blocker)
Explanation: ***phenylephrine (alpha agonist)*** - **Phenylephrine** is a direct-acting **alpha-1 adrenergic agonist** that causes contraction of the **pupillary dilator muscle**, leading to **mydriasis** (pupil dilation). [1] - It is frequently used clinically to dilate pupils for **ophthalmologic examinations** due to its selective action on alpha-1 receptors in the eye. [2] *neostigmine (cholinesterase inhibitor)* - **Neostigmine** inhibits acetylcholinesterase, increasing acetylcholine at the neuromuscular junction and muscarinic receptors. This leads to **miosis** (pupil constriction), not mydriasis. - Its ophthalmic use is primarily for treating **glaucoma** by improving aqueous humor outflow through cholinergic effects on the ciliary muscle. *phentolamine (alpha blocker)* - **Phentolamine** is a **non-selective alpha-adrenergic antagonist** that blocks both alpha-1 and alpha-2 receptors. - Alpha-1 receptor blockade in the eye would relax the pupillary dilator muscle, leading to **miosis** or prevention of mydriasis, not its induction. *mecamylamine (ganglionic blocker)* - **Mecamylamine** is a **ganglionic blocker** that antagonizes nicotinic receptors in both sympathetic and parasympathetic ganglia. - Blocking parasympathetic ganglia can cause some mydriasis, but ganglionic blockers have widespread, non-selective autonomic effects and are not primarily used for isolated mydriasis.
Question 10: A female has a systolic blood pressure of 130 mmHg and a diastolic blood pressure of 100 mmHg on two consecutive occasions, indicating Stage 2 hypertension. What is the best treatment?
- A. Rest
- B. Sedative
- C. Error in BP Machine
- D. Anti-hypertensive drugs (Correct Answer)
Explanation: ***Anti-hypertensive drugs*** - A blood pressure of 130/100 mmHg on two consecutive occasions confirms **Stage 2 hypertension**, necessitating pharmacological intervention. [1] - Due to the elevated **diastolic blood pressure**, medication is required to prevent target organ damage and cardiovascular events. [1] *Rest* - While rest can temporarily lower blood pressure, it is insufficient to manage **chronic hypertension** at this stage. [1] - It does not address the underlying physiological dysregulation causing the sustained elevated pressure. *Sedative* - Sedatives might acutely lower blood pressure by reducing anxiety but are not a primary treatment for **hypertension**. - They do not provide long-term control and can have significant side effects. *Error in BP Machine* - While a machine error is always a possibility, repeating the measurement on **two separate occasions** makes a systemic error less likely. - Relying solely on the possibility of an error without further investigation and management of the presented values is irresponsible.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free