Cardiovascular System — MCQs

The following data were obtained from a man weighing 70 kg: Aorta oxygen (O2) content is 20.0 vol%, femoral vein O2 content is 16 vol%, coronary sinus O2 content is 10 vol%, and pulmonary artery O2 content is 15 vol%. What is the cardiac output of this man, given a total body O2 consumption of 400 ml/min?

Q898

All are effects of the parasympathetic system on the heart except?

Q899

What is the primary cardiovascular compensatory mechanism in acute hemorrhage?

Q900

What characterizes the plateau (phase 2) of the ventricular myocyte action potential?

Cardiovascular System Indian Medical PG Practice Questions and MCQs

Question 891: All of the following about the Bezold-Jarisch reflex are true except

A. Bradycardia
B. Capsaicin
C. Hypertension (Correct Answer)
D. Apnea

Explanation: ***Hypertension*** - The Bezold-Jarisch reflex is characterized by a **triad of responses**: **hypotension**, bradycardia, and apnea or respiratory depression. - **Hypertension** is therefore a finding that would **not be consistent** with the activation of this reflex. - The reflex causes **hypotension** through vasodilation and decreased cardiac output mediated by vagal activation. *Bradycardia* - **Bradycardia** is a classic component of the Bezold-Jarisch reflex, resulting from increased **vagal efferent activity** to the heart. - This response helps to reduce cardiac output and myocardial oxygen demand in the face of perceived noxious stimuli, such as myocardial ischemia. *Capsaicin* - **Capsaicin**, the active component of chili peppers, is known to **activate C-fiber afferents** in the heart and lungs, which are involved in triggering the Bezold-Jarisch reflex. - Experimental administration of capsaicin can reliably induce the components of this reflex through these sensory nerve activations. *Apnea* - The Bezold-Jarisch reflex can induce changes in respiration, typically presenting as **apnea** or **respiratory depression**. - This respiratory inhibition is thought to be mediated by activation of vagal afferents from the cardiopulmonary region. - The reflex causes respiratory **inhibition**, not stimulation.

Question 892: Which of the following ECG changes is not associated with hypokalemia?

A. Prolonged QRS interval
B. Tall T wave (Correct Answer)
C. Prominent U waves
D. Depressed ST segment

Explanation: ***Tall T wave*** - **Tall, peaked T waves** are characteristic of **hyperkalemia**, reflecting rapid repolarization. - In **hypokalemia**, T waves are typically **flattened** or **inverted**, not tall. *Prolonged QRS interval* - A **prolonged QRS interval** can occur in severe hypokalemia due to slowed ventricular conduction. - This change indicates more severe electrolyte imbalance impacting the **depolarization phase** of ventricular myocytes. *Depressed ST segment* - **ST segment depression** is a common finding in hypokalemia, often associated with a reduced resting membrane potential. - This can indicate **myocardial ischemia** or simply the electrical instability caused by low potassium levels. *Prominent U waves* - **Prominent U waves** are a hallmark ECG finding in hypokalemia, often appearing as a deflection immediately following the T wave. - They are thought to represent delayed repolarization of **Purkinje fibers** or specific ventricular muscle cells.

Question 893: During the cardiac cycle, the opening of the aortic valve takes place at the:

A. Beginning of systole
B. End of isovolumetric contraction (Correct Answer)
C. End of diastole
D. End of diastasis

Explanation: ***End of isovolumetric contraction*** - The **aortic valve opens** when the pressure in the left ventricle exceeds the pressure in the aorta, marking the end of **isovolumetric contraction** and the beginning of ventricular ejection. - During **isovolumetric contraction**, the mitral and aortic valves are closed, and ventricular pressure rises rapidly without a change in volume. *Beginning of systole* - The **beginning of systole** is marked by the closure of the mitral valve, initiating **isovolumetric contraction**, not the opening of the aortic valve. - Aortic valve opening occurs later in systole, after ventricular pressure has built sufficiently. *End of diastole* - The **end of diastole** is when the ventricles are maximally filled with blood, just before contraction begins. - At this point, the mitral valve is typically still open, and the aortic valve is closed. *End of diastasis* - **Diastasis** is the period of slow passive filling of the ventricles during mid-diastole. - The **end of diastasis** is followed by atrial contraction, which occurs before systole and before the aortic valve opens.

Question 894: Which of the following normally has a slowly depolarizing "prepotential"?

A. Sinoatrial node (Correct Answer)
B. Atrial muscle cells
C. Bundle of His
D. Purkinje fibers

Explanation: ***Sinoatrial node*** - The **sinoatrial (SA) node** is the **normal primary pacemaker** of the heart, with cells that exhibit characteristic **slow depolarization** during phase 4 of their action potential, known as the **prepotential** or pacemaker potential. - This prepotential is primarily due to the **funny current (If)**, T-type Ca²⁺ channels, and decreasing K⁺ efflux, which gradually brings the membrane potential to threshold. - The SA node has the **fastest intrinsic rate** (60-100 bpm), which is why it normally dominates cardiac rhythm. *Atrial muscle cells* - Atrial muscle cells are **contractile cells** and do not spontaneously depolarize; they require an external stimulus from the SA node or other pacemaker cells. - Their action potential phase 4 maintains a **stable resting membrane potential** of about -90 mV, without prepotential. *Bundle of His* - The Bundle of His does possess **latent pacemaker activity** with a slowly depolarizing prepotential, but with a much slower intrinsic rate (40-60 bpm) than the SA node. - Under **normal conditions**, the SA node fires first and suppresses the Bundle of His through **overdrive suppression**, so it does not normally initiate the heartbeat. - It only becomes the dominant pacemaker if both the SA and AV nodes fail. *Purkinje fibers* - **Purkinje fibers** also have intrinsic pacemaker activity with a slowly depolarizing prepotential, but with the slowest rate (20-40 bpm) among cardiac pacemaker tissues. - Like the Bundle of His, they are **subsidiary pacemakers** that are normally suppressed by faster upstream pacemakers through overdrive suppression. - They only initiate rhythm in pathological conditions when higher pacemakers fail.

Question 895: The largest component of the total peripheral resistance is due to:

A. Venules
B. Arterioles (Correct Answer)
C. Capillaries
D. Precapillary sphincters

Explanation: ***Arterioles*** - **Arterioles** are the primary site of **resistance** in the cardiovascular system due to their relatively small diameter and the significant ability of their **smooth muscle** walls to constrict or dilate. - This resistance plays a crucial role in regulating **blood flow** to various organs and contributes to **mean arterial pressure**. *Venules* - **Venules** are primarily involved in collecting blood from capillaries and have relatively low resistance compared to arteries and arterioles. - While they contribute to capacitance, their impact on **total peripheral resistance** is minimal. *Capillaries* - Although **capillaries** have very small diameters, their sheer number in parallel reduces the overall resistance of the capillary bed. - The primary function of capillaries is **exchange** of nutrients and waste, not primarily resistance. *Precapillary sphincters* - **Precapillary sphincters** control blood flow *into* capillaries from arterioles, acting as gates. - While they regulate flow to specific capillary beds, they are not the largest *component* of total systemic resistance; the **arterioles themselves** are.

Question 896: Which of the following is the main factor for the ductus arteriosus closure postnatally?

A. Increase in partial pressure of oxygen (PaO2) (Correct Answer)
B. Elevated levels of circulating prostaglandins
C. Reduction in pulmonary vascular resistance
D. Postnatal increase in systemic vascular resistance

Explanation: ***Increase in partial pressure of oxygen (PaO2)*** - The **increase in PaO2** after birth causes a profound relaxation of the **pulmonary arterioles** and constriction of the **ductus arteriosus**. - This is the most crucial physiological change, leading to the **functional closure** of the ductus within hours of birth. *Postnatal increase in systemic vascular resistance* - While systemic vascular resistance (SVR) does increase postnatally as the **placental circulation** ceases, it is not the primary direct cause of ductus arteriosus closure. - An increased SVR contributes to the **pressure gradient** changes in the heart, but the oxygen-mediated constriction is more direct and powerful for the ductus itself. *Elevated levels of circulating prostaglandins* - **Prostaglandins**, particularly PGE2, are responsible for **maintaining the patency** of the ductus arteriosus *in utero*. - After birth, the **decrease in prostaglandin levels** (due to lung metabolism and removal of the placenta) is essential for closure, but elevated levels would actually keep it open. *Reduction in pulmonary vascular resistance* - A reduction in **pulmonary vascular resistance (PVR)** is indeed a significant postnatal change, allowing for increased pulmonary blood flow. - While this change alters blood flow dynamics, the direct cause of ductus arteriosus constriction is the **increased PaO2**, not solely the fall in PVR.

Question 897: The following data were obtained from a man weighing 70 kg: Aorta oxygen (O2) content is 20.0 vol%, femoral vein O2 content is 16 vol%, coronary sinus O2 content is 10 vol%, and pulmonary artery O2 content is 15 vol%. What is the cardiac output of this man, given a total body O2 consumption of 400 ml/min?

A. 10 L/min
B. 8 L/min (Correct Answer)
C. 6 L/min
D. 5 L/min

Explanation: ***8 L/min*** - The cardiac output is calculated using the **Fick principle**: CO = Total body O2 consumption / (Arterial O2 content - Mixed venous O2 content). - In this case, **Arterial O2 content is 20 vol%** and **Mixed venous O2 content (pulmonary artery) is 15 vol%**. So, CO = 400 ml/min / (20 vol% - 15 vol%) = 400 ml/min / 5 ml O2/100 ml blood = 400 / 0.05 = 8000 ml/min = **8 L/min**. *10 L/min* - This result would be obtained if the arteriovenous oxygen difference was smaller, specifically 4 vol% (400 / 0.04 = 10000 ml/min). - This calculation does not correctly use the given **mixed venous O2 content** from the pulmonary artery. *6 L/min* - This result would be obtained if the arteriovenous oxygen difference was larger, specifically 6.67 vol% (400 / 0.0667 ≈ 6000 ml/min). - This calculation misrepresents the **actual O2 extraction** from the arterial blood. *5 L/min* - This result would be obtained if the arteriovenous oxygen difference was 8 vol% (400 / 0.08 = 5000 ml/min). - This choice indicates an incorrect application of the **Fick principle** or misidentification of the relevant oxygen content values.

Question 898: 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 899: What is the primary cardiovascular compensatory mechanism in acute hemorrhage?

A. Decreased myocardial contractility
B. Increased respiratory rate
C. Decreased heart rate
D. Increased heart rate (Correct Answer)

Explanation: ***Increased heart rate*** - In acute hemorrhage, the body senses a decrease in **blood volume** and **blood pressure**, triggering the **baroreceptor reflex**. - This reflex leads to increased sympathetic nervous system activity, causing an immediate compensatory **increase in heart rate** to maintain **cardiac output** and tissue perfusion. *Decreased myocardial contractility* - A decrease in myocardial contractility would worsen the situation in hemorrhage by further reducing **cardiac output** and is not a primary compensatory mechanism. - While prolonged severe hemorrhage can lead to myocardial depression due to ischemia, it is a pathological consequence, not a compensatory response. *Decreased heart rate* - A decrease in heart rate would reduce **cardiac output** and further compromise blood flow to vital organs during hemorrhage, which is precisely the opposite of what the body needs. - This response is usually seen with vagal stimulation, not in response to hypovolemic shock. *Increased respiratory rate* - An **increased respiratory rate** is a compensatory mechanism for conditions like **metabolic acidosis** (which can occur in severe shock due to lactic acid accumulation) or to improve oxygenation, but it is not the primary cardiovascular compensatory mechanism for maintaining blood pressure and cardiac output in acute hemorrhage. - While it often accompanies hemorrhage, it acts to regulate oxygen and CO2 levels, not directly blood volume or pressure.

Question 900: What characterizes the plateau (phase 2) of the ventricular myocyte action potential?

A. Describes when Ca2+ influx is predominant but K+ efflux is also significant.
B. Describes when Ca2+ influx is balanced by K+ efflux.
C. Describes when Ca2+ influx is balanced by K+ efflux, with Na+ channels inactivated. (Correct Answer)
D. Can be influenced by sympathetic nerve stimulation.

Explanation: ***Describes when Ca2+ influx is balanced by K+ efflux, with Na+ channels inactivated.*** - During phase 2, the **influx of calcium ions** through L-type Ca2+ channels (maintaining depolarization) is roughly balanced by the **efflux of potassium ions** through delayed rectifier K+ channels. - The **inactivation of Na+ channels** after phase 0 prevents further Na+ influx and contributes to the plateau's stability, prolonging the action potential and allowing complete ventricular contraction. *Describes when Ca2+ influx is predominant but K+ efflux is also significant.* - While **Ca2+ influx is key** during phase 2, the unique characteristic is the **balance** between Ca2+ influx and K+ efflux, not the clear predominance of one over the other. - If Ca2+ influx were solely predominant, the membrane potential would continue to depolarize, not maintain a plateau. *Describes when Ca2+ influx is balanced by K+ efflux.* - This statement accurately describes a key aspect of phase 2 but is incomplete as it **omits the crucial role of inactivated Na+ channels**. - The inactivation of **fast Na+ channels** is fundamental to preventing premature repolarization and establishing the sustained plateau. *Can be influenced by sympathetic nerve stimulation.* - While sympathetic stimulation (via **catecholamines**) *can modulate* the duration and amplitude of the action potential, including the plateau, it is **not a *characterizing feature*** of the plateau phase itself. - Rather, it's an external regulatory mechanism that affects ion channel activity, not a fundamental description of the ion fluxes defining phase 2.

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