Cardiovascular System — MCQs

Cardiovascular System Indian Medical PG Practice Questions and MCQs

Question 801: During which phase of the cardiac cycle does the majority of ventricular filling take place?

A. Rapid filling (Correct Answer)
B. Isovolumetric relaxation
C. Ejection
D. Isovolumetric contraction

Explanation: ***Rapid filling*** - **Ventricular filling** occurs during diastole in multiple phases, but the **rapid filling phase** (early diastole) is when approximately **75% of ventricular filling** occurs due to the maximal pressure gradient between atria and ventricles. - During this phase, the **atrioventricular (AV) valves** (mitral and tricuspid) are open, allowing blood to passively rush into the relaxing ventricles as they expand rapidly. - The remaining filling occurs during diastasis (slow filling) and atrial systole (~25%). *Isovolumetric contraction* - This phase occurs at the beginning of systole, where the ventricles contract, but all valves (AV and semilunar) are closed, resulting in a **rise in ventricular pressure** without a change in volume. - No blood enters or leaves the ventricles during isovolumetric contraction; therefore, **no ventricular filling occurs**. *Isovolumetric relaxation* - This phase occurs at the beginning of diastole, immediately after ejection, where the ventricles relax, but all valves are closed, resulting in a **fall in ventricular pressure** without a change in volume. - While it precedes ventricular filling, **no blood enters** the ventricles during this specific phase because the AV valves remain closed until ventricular pressure falls below atrial pressure. *Ejection* - The ejection phase is part of **ventricular systole**, where the semilunar valves open, and blood is actively pumped out of the ventricles into the aorta and pulmonary artery. - During ejection, the ventricles are emptying, not filling; therefore, **no ventricular filling occurs**.

Question 802: What is the primary source of calcium for cardiac muscle contraction?

A. Release from extracellular fluid
B. Release from the sarcoplasmic reticulum (Correct Answer)
C. Binding to troponin C
D. Activation of calcium-calmodulin complex

Explanation: ***Release from the sarcoplasmic reticulum*** - The influx of extracellular calcium through **L-type calcium channels** triggers the release of a much larger amount of calcium from the **sarcoplasmic reticulum** via ryanodine receptors (RyRs) in a process called **calcium-induced calcium release (CICR)**. - This massive release of calcium from the sarcoplasmic reticulum is the **primary source** of intracellular calcium responsible for initiating myocyte contraction. - Approximately **70-90%** of the calcium needed for contraction comes from the SR, making it the predominant source. *Release from extracellular fluid* - While **extracellular calcium** influx is crucial for initiating the contraction, it serves as a trigger rather than the primary source of calcium needed for the actual muscle contraction. - The amount of calcium entering from the extracellular fluid is significantly less than the amount released from the sarcoplasmic reticulum. - This extracellular calcium entry accounts for only **10-30%** of total calcium during contraction. *Binding to troponin C* - **Calcium binding to troponin C** is the primary ACTION or mechanism of calcium, not its source. - While this is crucial for the excitation-contraction coupling cascade (leading to unmasking of actin-myosin binding sites), it describes what calcium does, not where it comes from. *Activation of calcium-calmodulin complex* - The **calcium-calmodulin complex** plays a more prominent regulatory role in **smooth muscle contraction** and other cellular processes. - In cardiac muscle, while calmodulin has some functions, it is not the primary source or mechanism by which calcium triggers contraction.

Question 803: Which ion is primarily responsible for the plateau phase of the cardiac action potential?

A. Calcium (Correct Answer)
B. Sodium
C. Potassium
D. Chloride

Explanation: **✓ Calcium (Correct Answer)** - The **influx of calcium ions (Ca²⁺)** through L-type calcium channels maintains the depolarized state during the **plateau phase (Phase 2)** of the cardiac action potential. - This sustained calcium influx balances the efflux of potassium ions, prolonging depolarization and preventing premature repolarization. - The plateau phase is crucial for adequate ventricular contraction and preventing tetany. *Sodium (Incorrect)* - **Sodium influx (Na⁺)** is primarily responsible for the rapid **depolarization phase (Phase 0)** of the cardiac action potential, causing a quick rise in membrane potential. - While essential for initiation, sodium channels rapidly inactivate by the time the plateau phase begins. - Sodium plays no significant role in maintaining the plateau. *Potassium (Incorrect)* - **Potassium efflux (K⁺)** through delayed rectifier potassium channels is responsible for the **repolarization phase (Phase 3)**, returning the membrane potential to its resting state. - During the plateau phase, potassium efflux is reduced (not the primary mechanism), which contributes to maintaining the plateau, but calcium influx is the primary driver. *Chloride (Incorrect)* - Chloride ions (Cl⁻) play a relatively **minor role** in the ventricular cardiac action potential compared to sodium, potassium, and calcium. - While chloride channels exist in cardiac cells, their contribution is not significant in maintaining the plateau phase.

Question 804: A 50-year-old man presents with severe hypotension after a myocardial infarction. Which of the following compensatory mechanisms is primarily mediated by the baroreceptor reflex?

A. Increased heart rate (Correct Answer)
B. Decreased renin release
C. Vasodilation of peripheral vessels
D. Increased parasympathetic activity

Explanation: ***Increased heart rate*** - The baroreceptor reflex detects a drop in blood pressure (due to hypotension) and responds by **increasing sympathetic outflow** to the heart. - This sympathetic activation directly leads to an **increased heart rate** and contractility to restore blood pressure. *Decreased renin release* - **Renin release** is typically increased in response to hypotension, via the juxtaglomerular apparatus, to activate the **renin-angiotensin-aldosterone system** (RAAS). - A decrease in renin release would further exacerbate hypotension, which is not a compensatory mechanism. *Vasodilation of peripheral vessels* - The baroreceptor reflex, in response to hypotension, aims to **increase peripheral vascular resistance** through vasoconstriction, not vasodilation. - **Vasodilation** would further reduce blood pressure and is directly counterproductive to compensating for hypotension. *Increased parasympathetic activity* - In response to hypotension, the baroreceptor reflex primarily **decreases parasympathetic activity** and increases sympathetic activity. - Increased parasympathetic activity would lead to a **decreased heart rate**, worsening the hypotensive state.

Question 805: In a patient with hypovolemic shock, what is the expected initial compensatory mechanism?

A. Increased venous return
B. Increased sympathetic activity (Correct Answer)
C. Decreased systemic vascular resistance
D. Decreased heart rate

Explanation: ***Increased sympathetic activity*** - In **hypovolemic shock**, the body's initial response to decreased blood volume and cardiac output is to activate the **sympathetic nervous system**. - This activation leads to the release of **catecholamines** (epinephrine and norepinephrine), causing **vasoconstriction**, increased heart rate, and increased myocardial contractility to maintain blood pressure and perfusion. *Increased venous return* - **Hypovolemic shock** is characterized by a **reduction in blood volume**, leading directly to a **decreased venous return** to the heart, not an increase. - Increased venous return would typically improve cardiac output, which is the opposite of what happens in initial hypovolemic shock. *Decreased systemic vascular resistance* - **Sympathetic activation** in hypovolemic shock primarily causes **vasoconstriction**, which leads to an **increase in systemic vascular resistance (SVR)** to divert blood to vital organs and maintain blood pressure. - Decreased SVR would further lower blood pressure, exacerbating the shock state. *Decreased heart rate* - A hallmark compensatory mechanism in **hypovolemic shock** is an **increase in heart rate** (tachycardia) to compensate for the reduced stroke volume and maintain cardiac output. - A decreased heart rate would worsen cardiac output and is not an initial compensatory mechanism.

Question 806: Which of the following best describes the function of the hepatic portal vein?

A. Transports bile from the liver
B. Supplies oxygenated blood to the liver
C. Carries nutrient-rich blood from the GI tract to the liver (Correct Answer)
D. Removes toxins from the liver

Explanation: ***Carries nutrient-rich blood from the GI tract to the liver*** - The **hepatic portal vein** collects blood rich in absorbed nutrients (and toxins) from the gastrointestinal tract, spleen, and pancreas. - This **nutrient-rich blood** is then delivered to the liver for processing, metabolism, and detoxification before entering the systemic circulation. *Transports bile from the liver* - **Bile** is transported away from the liver by the **bile ducts**, which merge to form the common hepatic duct. - The hepatic portal vein carries blood *to* the liver, not bile *from* it. *Supplies oxygenated blood to the liver* - The **hepatic artery** is responsible for supplying oxygenated blood to the liver tissue, providing its metabolic needs. - The hepatic portal vein carries **deoxygenated blood** that is rich in nutrients and metabolic products. *Removes toxins from the liver* - While the liver **detoxifies** substances, the hepatic portal vein delivers these substances *to* the liver for processing. - Processed toxins and metabolic wastes are primarily excreted via **bile** or returned to the systemic circulation to be filtered by the kidneys.

Question 807: Which of the following statements about Reynolds number in physiology is MOST correct?

A. Reynolds number less than 2000 indicates laminar blood flow (Correct Answer)
B. Reynolds number greater than 3000 indicates turbulent blood flow
C. Reynolds number calculates the probability of turbulence
D. Reynolds number between 2000 and 4000 indicates transitional blood flow

Explanation: **Reynolds number less than 2000 indicates laminar blood flow** - A **Reynolds number (Re)** below 2000 in a tube context, such as blood vessels, signifies **laminar flow**, where fluid particles move smoothly in parallel layers. - In **normal, healthy arteries**, blood flow is predominantly laminar, characterized by less resistance and efficient transport. *Reynolds number greater than 3000 indicates turbulent blood flow* - While a higher Reynolds number generally indicates turbulent flow, the transition from laminar to turbulent flow typically begins around an Re of 2000, and is generally fully turbulent at Re > 4000. - Beyond **an Re of 4000**, flow is unequivocally turbulent, characterized by chaotic, irregular fluid motion. *Reynolds number between 2000 and 3000 indicates transitional blood flow* - Reynolds numbers between 2000 and 4000 indicate a **transitional flow regime**, where the flow alternates between laminar and turbulent characteristics. - This phase represents an instability where minor disturbances can trigger turbulent patterns. *Reynolds number calculates the probability of turbulence* - The Reynolds number is a **dimensionless quantity** used to predict flow patterns, specifically whether flow will be laminar or turbulent, based on fluid properties, velocity, and characteristic length. - It is a **deterministic indicator** of flow type rather than a probability calculation.

Question 808: During which phase of the cardiac cycle does the majority of coronary blood flow to the myocardium take place?

A. Systole
B. Early diastole (Correct Answer)
C. Late diastole
D. Isovolumetric contraction

Explanation: ***Early diastole*** - During **early diastole**, immediately after **aortic valve closure**, the **left ventricle** relaxes, and intramyocardial pressure drops significantly, allowing the **coronary arteries** to be perfused readily. - The combination of **low myocardial compression** and a still relatively high **aortic diastolic pressure** creates an optimal pressure gradient for blood flow into the coronary circulation. - Approximately **70-80% of left coronary blood flow** occurs during diastole, with the peak flow in the early phase. *Systole* - During **systole**, the contraction of the **ventricular myocardium** compresses the intramural coronary arteries, significantly impeding blood flow, especially in the **left ventricle**. - **Aortic pressure** is highest during systole, but the mechanical compression outweighs this, reducing myocardial perfusion. *Late diastole* - While there is some **coronary flow** during late diastole, it is less than in early diastole because **venous return** and **ventricular filling** increase intraventricular pressure. - The **aortic pressure** also gradually declines towards the end of diastole, reducing the driving force for coronary perfusion compared to early diastole. *Isovolumetric contraction* - During **isovolumetric contraction**, the **ventricular muscle** tenses but does not yet eject blood, leading to a rapid increase in **intraventricular pressure**. - This high intramyocardial pressure severely **compresses the coronary vessels**, virtually stopping blood flow to the **myocardium** during this brief phase.

Question 809: The immediate response of the body to acute hypervolemia is mediated by which receptors?

A. Chemoreceptors
B. Nociceptors
C. Thermoreceptors
D. Baroreceptors (Correct Answer)

Explanation: ***Correct: Baroreceptors*** - Baroreceptors are **stretch-sensitive mechanoreceptors** located in the carotid sinuses and aortic arch that detect changes in blood pressure and blood volume. - In acute hypervolemia, the increased blood volume leads to **increased central venous pressure and arterial pressure**, which stimulates these baroreceptors. - This triggers an **immediate compensatory response** including decreased sympathetic activity, increased parasympathetic activity, and decreased vasopressin release to reduce blood volume and pressure. *Incorrect: Chemoreceptors* - Chemoreceptors primarily detect changes in **blood pH, oxygen (pO2), and carbon dioxide (pCO2)** levels. - While they play a role in regulating respiration and can influence cardiovascular function, they are **not the primary immediate sensors for changes in blood volume**. *Incorrect: Nociceptors* - Nociceptors are **pain receptors** that respond to noxious stimuli, signaling potential tissue damage. - They are completely unrelated to the physiological regulation of blood volume or pressure in the context of hypervolemia. *Incorrect: Thermoreceptors* - Thermoreceptors detect changes in **temperature**, both internal and external. - They are involved in maintaining body temperature homeostasis and do not play any direct role in the immediate response to acute hypervolemia.

Question 810: How does moderate hyperkalemia primarily affect the resting membrane potential and excitability of cardiac muscle cells?

A. Increased excitability due to increased membrane potential
B. Decreased excitability due to decreased membrane potential (Correct Answer)
C. Increased excitability due to decreased membrane potential
D. Decreased excitability due to increased membrane potential

Explanation: ***Decreased excitability due to decreased membrane potential*** - Moderate hyperkalemia causes a **decrease (depolarization)** of the **resting membrane potential**, making it less negative. - While initially this might seem to increase excitability, the sustained depolarization inactivates **voltage-gated sodium channels**, thereby *decreasing overall excitability* and slowing conduction velocity. *Increased excitability due to decreased membrane potential* - Although moderate hyperkalemia does cause a **decreased resting membrane potential (depolarization)**, this initial effect does not lead to *increased excitability* in the long term for cardiac muscle. - The sustained depolarization leads to the *inactivation of fast sodium channels*, preventing further action potentials from firing efficiently. *Increased excitability due to increased membrane potential* - This option is incorrect because hyperkalemia causes a *decrease* (depolarization), not an increase, in the **resting membrane potential**. - Additionally, sustained depolarization reduces, rather than increases, excitability in cardiac cells by inactivating sodium channels. *Decreased excitability due to increased membrane potential* - This is incorrect because hyperkalemia results in a *decrease* in the **resting membrane potential** (makes it less negative), not an increase. - While it correctly states decreased excitability, the reasoning for the membrane potential change is flawed.

Practice by Chapter

Cardiac Electrophysiology

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Cardiac Cycle

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Cardiac Output and Its Regulation

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Hemodynamics and Blood Flow

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Arterial System Physiology

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Microcirculation and Lymphatics

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Venous Return and Central Venous Pressure

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Cardiovascular Reflexes

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Regional Circulations

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Cardiovascular Responses to Exercise and Stress

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