Cardiovascular System Practice Questions

Q: When recording Lead I on an ECG, the right arm is the negative electrode. Which electrode serves as the positive electrode?

Left arm. ***Left arm*** - In a standard 12-lead ECG, **Lead I** is a **bipolar limb lead** that measures the electrical potential difference between the right arm and the left arm. - The convention for Lead I dictates that the **right arm** is the **negative electrode** and the **left arm** is the **positive electrode**. *Left leg* - The **left leg** serves as the **positive electrode** for **Lead III** (with the left arm as negative) and for **aVF** (with the average of right arm and left arm as negative). - It does not serve as the positive electrode for Lead I. *Right leg* - The **right leg electrode** typically serves as a **ground electrode** in the 12-lead ECG system. - Its primary function is to minimize electrical noise and interference, not to measure potential differences for standard leads. *Right arm + left arm* - Combining the signals from the right and left arm electrodes does not result in a standard ECG lead or a designated positive electrode for Lead I. - Lead I specifically measures the potential difference *between* these two electrodes, with the left arm being positive and the right arm being negative.

Q: Cardiac hyperaemia/vasodilation is due to which mediator?

Adenosine. ***Adenosine*** - **Adenosine** is a potent endogenous vasodilator in the heart, released in response to increased myocardial oxygen demand or ischemia. - It acts on **A2A receptors** in vascular smooth muscle, leading to relaxation and increased coronary blood flow (hyperemia). *Acetylcholine* - **Acetylcholine** primarily causes vasodilation in skeletal muscle and some other vascular beds, mediated by nitric oxide release from endothelial cells. - In the heart, it mainly acts as a **negative chronotropic** and **dromotropic** agent, slowing heart rate and conduction, with variable direct effects on coronary vessels. *Adrenaline* - **Adrenaline** (epinephrine) typically causes vasoconstriction via **alpha-1 receptors** in many vascular beds, but can cause vasodilation via **beta-2 receptors** in some, such as skeletal muscle. - In the heart, its primary effect is positive chronotropy and inotropy, and it can cause **coronary vasoconstriction** or dilation depending on receptor distribution and dose. *Dopamine* - **Dopamine** has complex effects on the vasculature, depending on the dose and receptor subtypes activated. - At low doses, it can cause **renal and mesenteric vasodilation** via D1 receptors, but at higher doses, it can cause generalized vasoconstriction via alpha-adrenergic receptors.

Q: According to the Frank-Starling law of the heart, stroke volume is directly related to which parameter?

End-diastolic volume (Preload). ***End-diastolic volume (Preload)*** - The Frank-Starling law of the heart states that **stroke volume is directly proportional to end-diastolic volume (preload)**. - Increased venous return leads to greater end-diastolic volume, which stretches the cardiac muscle fibers, resulting in a more forceful contraction and increased stroke volume. - This relationship explains the intrinsic ability of the heart to adapt to varying amounts of venous return. *Cardiac output* - Cardiac output is the product of stroke volume and heart rate (CO = SV × HR). - While stroke volume affects cardiac output, the Frank-Starling law specifically describes the relationship between preload and stroke volume, not cardiac output directly. *Arterial BP* - Arterial blood pressure is influenced by cardiac output and systemic vascular resistance. - The Frank-Starling law does not directly describe the relationship between stroke volume and arterial blood pressure. *Stroke volume* - Stroke volume is the dependent variable (outcome) in the Frank-Starling relationship, not the independent variable (cause). - The law describes how preload affects stroke volume, not how stroke volume affects itself.

Q: Mean arterial pressure depends on which of the following?

Cardiac output & peripheral resistance. ***Cardiac output & peripheral resistance*** - **Mean arterial pressure (MAP)** is determined by the fundamental relationship: **MAP = Cardiac Output (CO) × Systemic Vascular Resistance (SVR)** - Both factors are **equally essential** - MAP cannot be determined by either factor alone - Changes in either CO or peripheral resistance will directly affect MAP - This represents the primary hemodynamic determinants of arterial pressure *Cardiac output alone* - While CO is a crucial component, it **does not fully determine MAP** without considering resistance - MAP can change significantly with alterations in peripheral resistance even when CO remains constant *Peripheral resistance alone* - While peripheral resistance is a key determinant, it **cannot establish MAP** without cardiac output - The volume of blood pumped (CO) must be present for resistance to generate pressure *Arterial compliance* - Arterial compliance primarily affects **pulse pressure** (systolic - diastolic), not mean arterial pressure - Reduced compliance (arterial stiffness) increases pulse pressure but has minimal direct effect on MAP - Compliance is more related to the pulsatile component rather than mean pressure

Q: Least conduction velocity is seen in which of the following?

AV node. ***AV node*** - The **atrioventricular (AV) node** has the **slowest conduction velocity (~0.02-0.05 m/s)** in the cardiac conduction system. - This deliberate delay allows for complete **ventricular filling** before contraction, which is crucial for efficient cardiac function. - The slow conduction creates the **PR interval** on ECG, representing the AV nodal delay. *Purkinje fibres* - **Purkinje fibers** have the **fastest conduction velocity (~2-4 m/s)** in the heart, enabling rapid, synchronized ventricular depolarization. - Their extensive network ensures that both ventricles contract almost simultaneously for effective blood ejection. *Bundle of His* - The **Bundle of His** exhibits a relatively fast conduction velocity **(~1-1.5 m/s)**, transmitting the impulse from the AV node to the bundle branches. - While not as fast as Purkinje fibers, it's significantly faster than the AV node. *Ventricular myocardial fibers* - **Ventricular myocardial fibers** conduct impulses at an intermediate speed **(~0.3-1.0 m/s)**, facilitating the contractile process throughout the ventricular muscle. - Their conduction velocity is slower than the specialized conduction system but faster than the AV node.

Q: Which cell type is primarily targeted by shear stress in vascular structures?

Endothelial cells. ***Endothelial cells*** - **Endothelial cells** form the inner lining of blood vessels and are directly exposed to and sense **shear stress** and **hemodynamic forces** from blood flow. - Their response to these forces is crucial for regulating vascular tone, permeability, and angiogenesis through mechanotransduction pathways. *Fibroblasts* - **Fibroblasts** are primarily involved in synthesizing the **extracellular matrix** and are found in the adventitia, or outer layer of blood vessels. - While they contribute to vascular integrity, they are not the primary target of direct hemodynamic shear stress within the vessel lumen. *Smooth muscle cells* - **Smooth muscle cells** are located in the media, or middle layer of blood vessels, and are responsible for regulating **vascular tone** and blood pressure. - They respond primarily to circumferential stretch and various vasoactive substances, but **endothelial cells** are the initial sensors of intraluminal shear stress. *Pericytes* - **Pericytes** are contractile cells that wrap around endothelial cells of capillaries and venules, contributing to **microvascular stability** and blood flow regulation. - While they interact closely with endothelial cells, they are not the primary cells directly targeted by shear stress from blood flow within vascular structures.

Q: Which hormone is the primary regulator of short-term blood pressure changes?

Epinephrine. ***Epinephrine*** - **Epinephrine** (adrenaline) is released from the **adrenal medulla** during acute stress and acts within **seconds to minutes** to rapidly increase heart rate, cardiac contractility, and cause vasoconstriction in many vascular beds. - It is part of the **sympathetic "fight-or-flight" response** and provides the most immediate hormonal response to acute blood pressure changes. - While short-term BP regulation is primarily **neural** (baroreceptor reflex), epinephrine provides the fastest **hormonal** contribution to acute BP control. *Angiotensin II* - **Angiotensin II** is a potent vasoconstrictor that acts within minutes and is a key component of the **renin-angiotensin-aldosterone system (RAAS)**. - While it has rapid vasoconstrictor effects, it is classically considered more important for **medium-to-long-term blood pressure regulation** through sustained vasoconstriction and effects on sodium retention. - The RAAS system takes longer to activate compared to the immediate catecholamine release. *ADH (Vasopressin)* - **Antidiuretic Hormone (ADH)** primarily regulates **water reabsorption** in the kidney collecting ducts for osmotic balance. - At high concentrations, it can cause vasoconstriction (hence called "vasopressin"), but this is not its primary physiological role in short-term BP regulation. - Its main effect on BP is through **long-term fluid balance** rather than acute vascular changes. *Aldosterone* - **Aldosterone** acts on the kidneys to increase **sodium and water reabsorption** and potassium excretion, which increases blood volume over hours to days. - Its effects are the **slowest to manifest** among these options, making it primarily a **long-term blood pressure regulator** rather than contributing to immediate adjustments.

Q: Action potential conduction occurs at the fastest velocity in which part of the heart?

Purkinje fibers. ***Purkinje fibers*** - **Purkinje fibers** have a very large diameter and a high density of gap junctions, leading to the **fastest conduction velocity** (up to 4 m/s) in the heart. - This rapid conduction is crucial for the synchronized contraction of the **ventricular myocardium**. *SA node* - The **SA node** is the **primary pacemaker** and has the fastest intrinsic firing rate, but its conduction velocity within the nodal tissue is relatively slow. - It initiates the action potential, but its role is in rate generation, not rapid propagation throughout the ventricles. *AV node* - The **AV node** intentionally **slows down conduction** (0.05 m/s); this delay is critical to allow time for the atria to fully contract and fill the ventricles before ventricular contraction begins. - This delay prevents immediate propagation of atrial impulses to the ventricles. *Bundle of His* - The **Bundle of His** conducts impulses from the AV node to the bundle branches at a moderate velocity (1-2 m/s). - Its conduction speed is faster than that of the AV node but significantly slower than that of the Purkinje fibers.

Q: Which of the following is NOT a positive wave in the jugular venous pressure (JVP) tracing?

x descent (atrial relaxation). ***x descent (atrial relaxation)*** - The **x descent** represents the **atrial relaxation** and the downward movement of the tricuspid annulus during ventricular systole, causing a drop in right atrial pressure, making it a **negative deflection**. - In JVP terminology, **waves** are positive deflections (a, c, v), while **descents** are negative deflections (x, y). - All other options describe positive waves in the JVP tracing. *a wave (right atrial contraction)* - The **a wave** is a **positive deflection** occurring late in diastole and represents the increase in right atrial pressure due to **atrial contraction**. - It precedes the first heart sound (S1) and is typically the most prominent positive wave. *c wave (tricuspid valve bulging)* - The **c wave** is a **positive deflection** occurring early in systole and is caused by the **bulging of the tricuspid valve** into the right atrium during isovolumic contraction of the right ventricle. - It coincides with the carotid pulse. *v wave (venous return increase during systole)* - The **v wave** is a **positive deflection** occurring in late systole and reflects the **passive filling of the right atrium** while the tricuspid valve is closed, causing an increase in pressure due to venous return. - It occurs after the second heart sound (S2) and immediately precedes the opening of the tricuspid valve.

Q: The vasodilator involved in autoregulation of the coronary blood flow is:

Adenosine. ***Adenosine*** - **Adenosine** is a potent local vasodilator produced by cardiac myocytes in response to increased metabolic activity or oxygen demand. - It acts to match **coronary blood flow** to myocardial oxygen consumption, particularly in conditions of increased cardiac work or reduced oxygen supply. *Acetylcholine (ACh)* - **Acetylcholine** primarily mediates vasodilation through endothelial-dependent mechanisms, stimulating **nitric oxide (NO)** release; however, it is not the primary mediator of metabolic autoregulation in the coronary circulation. - While it can cause vasodilation, it's more involved in **parasympathetic regulation** rather than local metabolic control of coronary flow. *CO2* - **Carbon dioxide (CO2)** is a potent vasodilator in the **cerebral circulation** and to some extent in other vascular beds, but its primary role in coronary autoregulation is less dominant compared to adenosine. - Increased CO2 levels typically reflect overall metabolic activity, but **adenosine** is a more direct and specific regulator for coronary blood flow in response to myocardial oxygen demand. *Nitric Oxide (NO)* - **Nitric oxide (NO)** is a crucial vasodilator in the coronary circulation, produced by endothelial cells, and plays a role in endothelium-dependent vasodilation. - While important for maintaining basal tone and mediating the effects of other vasodilators like acetylcholine, NO is not considered the primary local metabolic autoregulatory substance in response to myocardial oxygen demand; that role largely falls to **adenosine**.

Question 1

When recording Lead I on an ECG, the right arm is the negative electrode. Which electrode serves as the positive electrode?

Accepted Answer

Left arm

Answer

Right arm + left arm

Answer

Left leg

Answer

Right leg

Question 2

Cardiac hyperaemia/vasodilation is due to which mediator?

Accepted Answer

Adenosine

Answer

Acetylcholine

Answer

Adrenaline

Answer

Dopamine

Question 3

According to the Frank-Starling law of the heart, stroke volume is directly related to which parameter?

Accepted Answer

End-diastolic volume (Preload)

Answer

Cardiac output

Answer

Stroke volume

Answer

Arterial BP

Question 4

Mean arterial pressure depends on which of the following?

Accepted Answer

Cardiac output & peripheral resistance

Answer

Cardiac output

Answer

Peripheral resistance

Answer

Arterial compliance

Question 5

Least conduction velocity is seen in which of the following?

Accepted Answer

AV node

Answer

Purkinje fibres

Answer

Bundle of His

Answer

Ventricular myocardial fibers

Question 6

Which cell type is primarily targeted by shear stress in vascular structures?

Accepted Answer

Endothelial cells

Answer

Fibroblasts

Answer

Smooth muscle cells

Answer

Pericytes

Question 7

Which hormone is the primary regulator of short-term blood pressure changes?

Accepted Answer

Epinephrine

Answer

Aldosterone

Answer

Angiotensin II

Answer

ADH

Question 8

Action potential conduction occurs at the fastest velocity in which part of the heart?

Accepted Answer

Purkinje fibers

Answer

SA node

Answer

AV node

Answer

Bundle of His

Question 9

Which of the following is NOT a positive wave in the jugular venous pressure (JVP) tracing?

Accepted Answer

x descent (atrial relaxation)

Answer

a wave (right atrial contraction)

Answer

c wave (tricuspid valve bulging)

Answer

v wave (venous return increase during systole)

Question 10

The vasodilator involved in autoregulation of the coronary blood flow is:

Accepted Answer

Adenosine

Answer

CO2

Answer

Acetylcholine (ACh)

Answer

Nitric Oxide (NO)

Cardiovascular System — MCQs

Cardiovascular System — MCQs

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