Cardiovascular System — MCQs

Cardiovascular System Indian Medical PG Practice Questions and MCQs

Question 851: Which of the following conditions can lead to a decrease in afterload?

A. Severe anemia (Correct Answer)
B. Hypothyroidism
C. Increased physical activity
D. None of the options

Explanation: ***Severe anemia*** - In **severe anemia**, the **blood viscosity** is reduced, and the body compensates by decreasing systemic vascular resistance to maintain tissue perfusion, thereby lowering **afterload**. - The reduced **oxygen-carrying capacity** triggers vasodilation to maximize blood flow to tissues, contributing to decreased afterload. - This represents a **chronic compensatory mechanism** that results in sustained reduction of afterload. *Hypothyroidism* - **Hypothyroidism** typically leads to an **increase in systemic vascular resistance** and thus can increase afterload. - It often results in **bradycardia** and reduced cardiac output, which can further elevate afterload to maintain pressure. *Increased physical activity* - During **physical activity**, there is **vasodilation in exercising muscles**, which acutely decreases systemic vascular resistance. - However, this is accompanied by **increased cardiac output** and **elevated blood pressure** due to sympathetic stimulation, and the afterload reduction is **transient** rather than sustained. - In the context of this question asking about conditions that lead to decreased afterload, **severe anemia** is the better answer as it represents a chronic pathological state with sustained afterload reduction, whereas exercise represents a temporary physiological response. *None of the options* - This option is incorrect because **severe anemia** is a recognized cause of decreased afterload.

Question 852: What is the mechanism by which M2 receptors mediate the inhibition of the heart by the vagus nerve?

A. Inhibition of adenylate cyclase (Correct Answer)
B. Activation of phospholipase C
C. Inhibition of cAMP breakdown
D. Opening of voltage-gated calcium channels

Explanation: ***Inhibition of adenylate cyclase*** - M2 receptors are **Gαi-protein coupled receptors**, and their activation leads to the inhibition of **adenylate cyclase**. - This inhibition reduces the intracellular concentration of **cAMP**, which in turn decreases the activity of **protein kinase A (PKA)**, leading to a decrease in heart rate and contractility. - Additionally, M2 receptors activate **inwardly rectifying potassium channels (IKACh)**, which hyperpolarizes the cell membrane and further slows heart rate. *Activation of phospholipase C* - This mechanism is characteristic of **M1 and M3 muscarinic receptors (Gq-coupled)**, which activate phospholipase C, leading to increased IP3 and DAG. - This pathway is primarily involved in smooth muscle contraction and glandular secretion, not direct cardiac inhibition by M2 receptors. *Inhibition of cAMP breakdown* - Inhibition of **cAMP breakdown** would lead to an increase in cAMP levels, which would stimulate cardiac function. - This effect is mediated by drugs like **phosphodiesterase inhibitors**, which block the enzyme responsible for cAMP degradation, and is opposite to the effect of M2 receptor activation. *Opening of voltage-gated calcium channels* - Opening of voltage-gated calcium channels would **increase** calcium influx, leading to increased contractility and heart rate. - This is the mechanism of action of **sympathetic stimulation via β1-adrenergic receptors**, not parasympathetic M2 receptor activation, which has the opposite effect.

Question 853: Inhibition of heart by vagus is mediated by which receptors?

A. M1
B. M2 (Correct Answer)
C. NN
D. NM

Explanation: ***M2*** - The **vagus nerve** primarily mediates its inhibitory effects on the heart through **muscarinic M2 receptors**. - Activation of M2 receptors by **acetylcholine** (released from the vagus nerve) decreases heart rate and contractility. *M1* - **M1 receptors** are primarily found in neuronal tissue and glands, playing a role in **gastric acid secretion** and cognitive functions. - They are not the primary muscarinic subclass responsible for vagal inhibition of the heart. *NN* - **NN receptors** are **nicotinic receptors** found on postganglionic neurons in autonomic ganglia. - They are involved in **ganglionic transmission** and are not directly responsible for efferent vagal effects on the heart. *NM* - **NM receptors** are **nicotinic receptors** found at the **neuromuscular junction** of skeletal muscles. - Their activation leads to **skeletal muscle contraction**, and they have no role in regulating heart function.

Question 854: Inotropic effect of thyroid hormone is by ?

A. Membrane receptors
B. cAMP
C. cGMP
D. Enhancement of Catecholamines (Correct Answer)

Explanation: ***Enhancement of Catecholamines*** - Thyroid hormones **potentiate the effects of catecholamines** (like adrenaline and noradrenaline) on the heart, leading to increased heart rate and contractility, which is an **inotropic effect**. - This occurs by increasing the number and sensitivity of **beta-adrenergic receptors** on cardiac muscle cells. *Membrane receptors* - While thyroid hormones do have some rapid, non-genomic effects that may involve **membrane receptors**, their primary and well-established inotropic effect is mediated indirectly through catecholamine sensitivity. - The classic action of thyroid hormones is via intracellular receptors that modulate gene expression, not direct membrane receptor signaling for inotropic effects. *cAMP* - **cAMP** is a common second messenger for many hormones, particularly those acting via G protein-coupled receptors. - While catecholamines themselves act through cAMP to exert their cardiac effects, thyroid hormones *enhance the action* of catecholamines rather than directly using cAMP as their primary inotropic mechanism. *cGMP* - **cGMP** is a second messenger often associated with nitric oxide signaling and vasodilation, contributing to cGMP-dependent protein kinases. - It is not the primary mediator for the *positive inotropic effect* of thyroid hormones on the heart.

Question 855: The ST Segment of an ECG corresponds to which phase of the action potential?

A. Rapid repolarization
B. Final repolarization
C. Plateau phase (Correct Answer)
D. Rapid depolarization

Explanation: ***Plateau phase*** - The **ST segment** of the ECG represents the period when the ventricles are completely depolarized and corresponds to the **plateau phase (phase 2)** of the ventricular myocardial action potential. - During this phase, there is a balance between **calcium influx** and **potassium efflux**, maintaining the depolarized state and contributing to the sustained contraction of the ventricles. *Rapid depolarization* - This phase, represented by the **QRS complex** on the ECG, signifies the rapid influx of sodium ions into the ventricular cells. - It corresponds to **phase 0** of the action potential, where there is a sharp upstroke. *Rapid repolarization* - This corresponds to **phase 3** of the ventricular action potential, where potassium ions rapidly exit the cell, leading to repolarization. - On the ECG, this phase is represented by the **T wave**. *Final repolarization* - This is **not a standard electrophysiological term** in cardiac action potential nomenclature. - The complete repolarization process is represented by the **T wave** (phase 3), which returns the ventricle to its resting potential (phase 4). - The term may cause confusion as it doesn't correspond to a specific phase or ECG component.

Question 856: Aortic valve closure occurs in which part of cardiac cycle?

A. Beginning of isovolumetric contraction
B. During rapid ventricular filling
C. Beginning of ventricular ejection
D. Beginning of isovolumetric relaxation (Correct Answer)

Explanation: ***Beginning of isovolumetric relaxation*** - Aortic valve closure marks the end of **ventricular systole** and the start of **isovolumetric relaxation**, as blood ceases to be ejected and the ventricle begins to relax while remaining closed. - This event corresponds to the **second heart sound (S2)** and signifies the beginning of a period where ventricular volume remains constant, but pressure drops. *Beginning of isovolumetric contraction* - This phase begins with the closure of the **mitral and tricuspid valves** (first heart sound, S1), as ventricular pressure rises but volume remains constant before ejection. - The aortic valve is still closed at this point, as ventricular pressure is not yet high enough to open it. *Beginning of ventricular ejection* - This phase begins when the **aortic valve opens** as ventricular pressure exceeds aortic pressure, allowing blood to be ejected from the left ventricle. - Aortic valve closure occurs *after* ejection, not at its beginning. *During rapid ventricular filling* - Rapid ventricular filling occurs when the **mitral valve opens** (following isovolumetric relaxation), allowing blood to flow from the atria into the ventricles. - During this phase, the aortic valve is closed, but its closure happened earlier, at the beginning of isovolumetric relaxation.

Question 857: Which of the following factors is most commonly targeted therapeutically for blood pressure control?

A. Heart rate
B. Peripheral resistance (Correct Answer)
C. Cardiac output
D. Stroke volume

Explanation: ***Peripheral resistance*** - **Peripheral resistance** is primarily determined by the **arteriolar tone**, which can be effectively modulated by various antihypertensive medications. - Medications like **ACE inhibitors**, **ARBs**, **calcium channel blockers**, and **diuretics** all influence peripheral resistance to lower blood pressure. *Heart rate* - While heart rate contributes to **cardiac output** and thus blood pressure, it is not the most common primary target for hypertension management. - **Beta-blockers** reduce heart rate, but they are often used for specific indications beyond essential hypertension, such as angina or post-MI. *Cardiac output* - **Cardiac output** is a product of **heart rate** and **stroke volume**, and while it directly impacts blood pressure, directly targeting cardiac output as a whole is less common than modulating its individual components or peripheral resistance. - Many antihypertensive drugs reduce cardiac output as a secondary effect of reducing blood volume or heart rate, but directly reducing cardiac output is not the primary mechanism for the most common medications. *Stroke volume* - **Stroke volume** is influenced by **preload**, **afterload**, and **contractility**, and while it impacts cardiac output, it is generally less accessible for direct pharmacological manipulation in hypertension management compared to peripheral resistance. - **Diuretics** can indirectly reduce stroke volume by decreasing preload, but this is often considered a mechanism related to volume status rather than a direct myocardial effect.

Question 858: In an ECG the cardiac event corresponding to the ST segment is:

A. Atrial depolarisation
B. Ventricular depolarisation
C. Atrial repolarisation
D. Ventricular repolarisation (Correct Answer)

Explanation: ***Ventricular repolarisation*** - The **ST segment** represents the **early phase of ventricular repolarization**, corresponding to the **plateau phase (Phase 2)** of the ventricular action potential. - During this phase, the ventricles are completely depolarized and calcium influx balances potassium efflux, creating an isoelectric (flat) segment on the ECG. - The ST segment extends from the **end of the QRS complex (J point)** to the **beginning of the T wave**, after which rapid repolarization occurs. - Together, the **ST segment and T wave** represent the complete process of ventricular repolarization. *Atrial depolarisation* - **Atrial depolarization** is represented by the **P wave** on the ECG, not the ST segment. - This occurs first in the cardiac cycle, triggering atrial contraction and filling of the ventricles. *Ventricular depolarisation* - **Ventricular depolarization** is represented by the **QRS complex**, which immediately **precedes** the ST segment. - This event triggers ventricular contraction (systole) and occurs before the plateau phase. *Atrial repolarisation* - **Atrial repolarization** occurs during the QRS complex and is **obscured** by the much larger electrical signal from ventricular depolarization. - It is not visible as a separate deflection on the standard ECG.

Question 859: Coronary steal phenomenon caused due to

A. Preferential vasodilation of normal coronary vessels over stenotic vessels (Correct Answer)
B. Dilation of large coronary arteries
C. Dilation of epicardial coronary vessels
D. Dilation of capacitance vessels

Explanation: ***Preferential vasodilation of normal coronary vessels over stenotic vessels*** - In a coronary steal phenomenon, **vasodilator drugs** or agents cause **normal coronary arteries** to dilate significantly. - This increased flow in normal areas *diverts blood away* from areas supplied by **stenotic vessels**, leading to **ischemia** in the compromised regions. *Dilation of large coronary arteries* - While large coronary arteries can dilate, this alone does not fully explain the steal phenomenon. The critical factor is the *unbalanced dilation* between healthy and stenotic regions. - Most pharmacological agents used to induce steal, like **dipyridamole** or **adenosine**, primarily affect the **resistance arterioles**. *Dilation of epicardial coronary vessels* - **Epicardial coronary vessels** are the larger conductive arteries, and their dilation does not directly cause the steal phenomenon. - The steal occurs at the level of the **microvasculature**, where resistance is regulated and blood flow away from ischemic areas is diverted. *Dilation of capacitance vessels* - **Capacitance vessels** (mainly veins) store blood but do not play a significant direct role in regulating coronary blood flow or causing the coronary steal phenomenon. - The phenomenon is driven by changes in **arteriolar resistance** and distribution of flow.

Question 860: What is the role of gap junctions in cardiac muscle function?

A. Are not found in cardiac muscles
B. Are not found in smooth muscles
C. Have no significant role in cardiac muscle function
D. Facilitate impulse transmission between cardiac myocytes (Correct Answer)

Explanation: ***Facilitate impulse transmission between cardiac myocytes*** - **Gap junctions** are specialized channels between adjacent cells that allow for direct communication and rapid movement of **ions** and small molecules. - In cardiac muscle, they form an essential part of **intercalated discs**, enabling the heart to function as a **syncytium** by allowing electrical impulses to spread quickly from one myocyte to another. *Are not found in cardiac muscles* - This statement is incorrect; **gap junctions** are a defining feature of **cardiac muscle** and are crucial for its coordinated contraction. - They are located within the **intercalated discs** that connect individual cardiac muscle cells. *Are not found in smooth muscles* - This statement is incorrect; **gap junctions** are indeed found in **smooth muscle**, particularly in single-unit smooth muscle, where they contribute to synchronized contractions, such as in the **gastrointestinal tract**. - They allow for the rapid propagation of electrical signals, leading to coordinated muscle activity. *Have no significant role in cardiac muscle function* - This statement is incorrect; **gap junctions** play a critically significant role in cardiac muscle function by ensuring the **rapid and synchronized spread of electrical impulses**. - Without functional gap junctions, the heart would not be able to contract efficiently or effectively as a pump.

Practice by Chapter

Cardiac Electrophysiology

Practice Questions

Cardiac Cycle

Practice Questions

Cardiac Output and Its Regulation

Practice Questions

Hemodynamics and Blood Flow

Practice Questions

Arterial System Physiology

Practice Questions

Microcirculation and Lymphatics

Practice Questions

Venous Return and Central Venous Pressure

Practice Questions

Cardiovascular Reflexes

Practice Questions

Regional Circulations

Practice Questions

Cardiovascular Responses to Exercise and Stress

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free