Cardiovascular System — MCQs

Cardiovascular System Indian Medical PG Practice Questions and MCQs

Question 861: 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.

Question 862: Deoxygenated blood is not seen in which of the following?

A. Pulmonary artery
B. Umbilical artery
C. Pulmonary vein (Correct Answer)
D. Right atrium

Explanation: ***Pulmonary vein*** - The pulmonary veins carry **oxygenated blood** from the lungs back to the left atrium of the heart. - Their primary function is to transport blood that has undergone **gas exchange** in the lungs, making it rich in oxygen. *Pulmonary artery* - The pulmonary artery carries **deoxygenated blood** from the right ventricle of the heart to the lungs. - This is an exception to the general rule that arteries carry oxygenated blood, as its purpose is to deliver blood for **oxygenation**. *Right atrium* - The right atrium receives **deoxygenated blood** from the systemic circulation via the superior and inferior vena cava. - It acts as a collecting chamber for blood that has supplied oxygen to the body's tissues before it is pumped to the lungs. *Umbilical artery* - The umbilical arteries carry **deoxygenated blood** and waste products from the fetus to the placenta. - In fetal circulation, these arteries are responsible for removing metabolic wastes and carbon dioxide from the fetal circulation.

Question 863: All are true about baroreceptors, except?

A. Stimulated when BP decreases (Correct Answer)
B. Stimulation causes increased vagal discharge
C. Stimulate nucleus ambiguus
D. Afferents are through sino-aortic nerves

Explanation: ***Stimulated when BP decreases*** - Baroreceptors are **stretch receptors** located in the walls of the carotid sinus and aortic arch. - They are stimulated by an **increase in blood pressure (BP)**, which causes stretching of the arterial walls, not by a decrease. *Afferents are through sino-aortic nerves* - This statement is **true**. Afferent impulses from the carotid sinus baroreceptors travel via the **glossopharyngeal nerve (IX)**, and those from the aortic arch baroreceptors travel via the **vagus nerve (X)**. - These nerves collectively form the **sino-aortic nerves** that relay information to the brainstem. *Stimulation causes increased vagal discharge* - This statement is **true**. When baroreceptors are stimulated by **increased BP**, they send signals to the cardiovascular center in the medulla. - This leads to increased **parasympathetic (vagal) outflow** to the heart, causing a decrease in heart rate and contractility, and inhibition of sympathetic outflow. *Stimulate nucleus ambiguus* - This statement is **true**. The **nucleus ambiguus** is a brainstem nucleus that contains the cell bodies of preganglionic parasympathetic neurons that contribute to the vagus nerve. - Baroreceptor stimulation leads to activation of the nucleus ambiguus, thereby increasing **vagal output** to the heart.

Question 864: Which of the following is NOT an effect of Angiotensin II?

A. Stimulation of thirst
B. Aldosterone secretion
C. Increased ADH secretion
D. Vasodilation (Correct Answer)

Explanation: ***Vasodilation*** - **Angiotensin II** primarily causes **vasoconstriction** of arterioles, leading to an **increase in systemic vascular resistance** and blood pressure, rather than vasodilation. - This effect is crucial for maintaining blood pressure, especially in conditions of **hypovolemia** or **low renal perfusion**. *Stimulation of thirst* - **Angiotensin II** acts directly on the **hypothalamus** and subfornical organ to stimulate **thirst**, encouraging water intake to increase blood volume. - This helps to restore fluid balance and thereby **increase blood pressure**. *Aldosterone secretion* - **Angiotensin II** is a potent stimulator of **aldosterone secretion** from the adrenal cortex. - **Aldosterone** promotes **sodium and water reabsorption** in the kidneys, leading to increased blood volume and blood pressure. *Increased ADH secretion* - **Angiotensin II** stimulates the release of **antidiuretic hormone (ADH)**, also known as vasopressin, from the posterior pituitary gland. - **ADH** increases water reabsorption in the collecting ducts of the kidneys, contributing to higher blood volume and **blood pressure**.

Question 865: Which hormone is primarily responsible for regulating blood pressure in response to significant blood loss due to hemorrhage?

A. Vasopressin (ADH)
B. Aldosterone
C. Epinephrine (Adrenaline) (Correct Answer)
D. Atrial Natriuretic Peptide (ANP)

Explanation: ***Epinephrine (Adrenaline)*** - Released rapidly from the **adrenal medulla** within seconds of hemorrhage as part of the **sympathetic-adrenal response** - Acts as the **primary immediate hormonal response** to severe blood loss, triggering the acute stress response - **Increases heart rate and contractility** (β1 receptors), causes **vasoconstriction** in peripheral vessels (α1 receptors), and **bronchodilation** (β2 receptors) - These combined effects rapidly **maintain blood pressure** and ensure perfusion to vital organs (heart, brain) - Represents the classic **fight-or-flight hormonal response** to acute hemorrhagic stress *Vasopressin (ADH)* - Also plays a **significant role** in hemorrhagic response, with levels increasing dramatically (up to 50-100 fold) - At high concentrations during severe hemorrhage, ADH acts as a **potent vasoconstrictor** via V1 receptors on vascular smooth muscle - Additionally promotes **water reabsorption** in kidneys via V2 receptors to help restore blood volume - However, while vasopressin contributes importantly to blood pressure maintenance, **epinephrine represents the primary immediate hormonal response** in the acute phase - The combined sympathetic-adrenal (catecholamine) response is traditionally considered the first-line hormonal defense *Aldosterone* - A **mineralocorticoid** involved in **longer-term regulation** of blood pressure and volume - Promotes **sodium and water reabsorption** in the distal tubules and collecting ducts, along with **potassium excretion** - Its effects take **hours to days** to manifest, making it important for sustained volume restoration but not the primary acute response to hemorrhage - Part of the RAAS (Renin-Angiotensin-Aldosterone System) activated after hemorrhage *Atrial Natriuretic Peptide (ANP)* - Released from atrial myocytes in response to **atrial stretch** from high blood volume and pressure - Promotes **vasodilation**, **sodium and water excretion** (natriuresis and diuresis), and inhibits renin and aldosterone - Its actions are **counterproductive** during hemorrhage, as they would further lower blood pressure and volume - ANP levels typically **decrease** during hemorrhage, not increase

Question 866: In a healthy person, arterial baroreceptor activity is seen at what stage of the cardiac cycle?

A. None of the options
B. Diastole
C. Systole
D. Both (Correct Answer)

Explanation: ***Both*** - Baroreceptors respond to changes in **arterial pressure**, which fluctuates throughout both systole and diastole. - The baroreflex mechanism is continuously active, monitoring and adjusting blood pressure through changes in **heart rate**, **contractility**, and **vascular resistance** during both phases of the cardiac cycle. *Systole* - While baroreceptors are active during systole due to the **rise in arterial pressure**, they are not exclusively active during this phase. - Their primary role is to detect and respond to the **peak pressure** changes that occur during **ejection**, but their activity extends beyond this. *Diastole* - Baroreceptors continue to fire during diastole, albeit at a lower rate, as blood pressure falls; however, their activity is not limited to this phase alone. - They monitor the **decline in pressure** to help regulate the overall mean arterial pressure, not just the trough. *None of the options* - This option is incorrect because arterial baroreceptors are indeed active and crucial for blood pressure regulation throughout the entire cardiac cycle, encompassing both systole and diastole. - Their continuous monitoring is essential for maintaining **hemodynamic stability**.

Question 867: 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 868: P wave is due to:

A. Atrial depolarization (Correct Answer)
B. Atrial repolarization
C. Ventricular depolarization
D. Ventricular repolarization

Explanation: **Atrial depolarization** - The **P wave** on an electrocardiogram (ECG) represents the electrical activity associated with the **depolarization of the atria**. - This depolarization leads to **atrial contraction**, pushing blood into the ventricles. *Atrial repolarization* - **Atrial repolarization** also occurs but is usually hidden within the **QRS complex** and thus not separately visible as a distinct wave on a standard ECG. - While it's an electrical event, it does not produce the P wave. *Ventricular depolarization* - **Ventricular depolarization** is represented by the **QRS complex** on an ECG. - This electrical activity leads to **ventricular contraction**, pumping blood out of the heart. *Ventricular repolarization* - **Ventricular repolarization** is represented by the **T wave** on an ECG. - This process allows the ventricles to relax and refill with blood.

Question 869: What is the blood supply of the liver in ml/min/100g?

A. 1500-2000 ml/min/100g
B. 1000-1500 ml/min/100g
C. 50-60 ml/min/100g (Correct Answer)
D. 250-300 ml/min/100g

Explanation: ***50-60 ml/min/100g*** - The liver receives a substantial blood supply, but when expressed per 100 grams of tissue, the value is around **50-60 mL/min/100g**. This demonstrates the organ's high metabolic demand. - This value represents the total blood flow from both the **hepatic artery** and the **portal vein** per unit weight of liver tissue. *1500-2000 ml/min/100g* - This value is extremely high and does not accurately represent the **blood flow per 100g of liver tissue**. Such a high flow rate would imply an unrealistic perfusion. - While the total blood flow to the liver is large, it's not at this magnitude when normalized to tissue weight. *1000-1500 ml/min/100g* - This range is closer to the **total blood flow to the entire liver** (1000-1800 ml/min), not the blood flow per 100 grams of tissue. - It's crucial to differentiate between total organ flow and flow density (per 100g). *250-300 ml/min/100g* - This value is significantly higher than the actual blood supply per 100g of liver tissue, suggesting an overestimation of the **perfusion density**. - While the liver is highly perfused, this rate is not physiologically accurate when normalized to the tissue weight.

Question 870: By what percentage can cardiac output increase in a healthy adult during intense physical activity compared to resting levels?

A. 300 - 400 % (Correct Answer)
B. 0 - 50 %
C. 50 - 100 %
D. 100 - 200 %

Explanation: ***300 - 400 %*** - In a healthy adult, **cardiac output** can increase remarkably during intense physical activity. - The heart can increase its output by **3 to 4 times** (or 300-400%) above resting levels during peak exertion. - At rest, cardiac output is approximately **5 L/min**, but during maximal exercise, it can reach **20-25 L/min** in well-conditioned individuals. - This represents the heart's **reserve capacity** to meet increased metabolic demands during exercise. *0 - 50 %* - This range represents a very **limited increase** in cardiac output and would be indicative of significant underlying cardiac impairment or **heart failure**. - A healthy individual would experience a much greater increase in cardiac output during intense activity than this small percentage. *50 - 100 %* - This range also suggests a **suboptimal cardiac response** for a healthy adult undergoing intense physical activity. - While some increase is present, it does not reflect the full capacity of a healthy cardiovascular system to adapt to extreme demands. *100 - 200 %* - While a 100-200% increase is substantial, it still **underestimates the maximal capacity** achievable in a healthy, well-conditioned individual during intense physical exertion. - The heart has a greater capacity for increasing its output to meet metabolic demands during peak exercise.

Practice by Chapter

Cardiac Electrophysiology

Practice Questions

Cardiac Cycle

Practice Questions

Cardiac Output and Its Regulation

Practice Questions

Hemodynamics and Blood Flow

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Arterial System Physiology

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Microcirculation and Lymphatics

Practice Questions

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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