Cardiovascular System Practice Questions

Q: Which neurotransmitter is primarily responsible for parasympathetic effects on heart rate?

Acetylcholine. ***Acetylcholine*** - **Acetylcholine** is the primary neurotransmitter released by postganglionic parasympathetic neurons. - It acts on **muscarinic receptors** (M2 receptors) in the heart to decrease heart rate. *Norepinephrine* - **Norepinephrine** is primarily associated with the **sympathetic nervous system**, increasing heart rate and contractility. - It acts on **beta-1 adrenergic receptors** in the heart. *Dopamine* - **Dopamine** is a precursor to norepinephrine and epinephrine, and primarily functions as a neurotransmitter in the **central nervous system** and in regulating renal blood flow. - While it can have cardiac effects, it is not the primary neurotransmitter for parasympathetic actions on heart rate. *Epinephrine* - **Epinephrine** (adrenaline) is a hormone released by the adrenal medulla and a neurotransmitter in the sympathetic nervous system, causing an **increase in heart rate** and contractility. - It works through **beta-1 adrenergic receptors**, antagonistic to parasympathetic effects.

Q: The PR interval in ECG denotes?

Atrial depolarization with A - V conduction. ***Atrial depolarization with A - V conduction*** * The **PR interval** reflects the time from the beginning of **atrial depolarization** (P wave) to the beginning of **ventricular depolarization** (QRS complex). * It represents the time taken for the electrical impulse to travel through the **atria** and the **AV node** to the ventricles. *Ventricular depolarization and ventricular repolarization* * **Ventricular depolarization** is represented by the **QRS complex**, and **ventricular repolarization** is represented by the **T wave**. * The PR interval occurs before the QRS complex, not during ventricular depolarization or repolarization. *Atrial depolarization with atrial repolarization* * **Atrial depolarization** is represented by the **P wave**. * **Atrial repolarization** typically occurs simultaneously with **ventricular depolarization** (QRS complex) and is often obscured by it. The PR interval includes the P wave but extends beyond it. *Atrial depolarization only* * **Atrial depolarization** is solely represented by the **P wave**. * The PR interval is a longer duration that includes the P wave and the subsequent delay in the **AV node**.

Q: PR interval in ECG shows?

Atrial depolarization and conduction delay. ***Atrial depolarization and conduction delay*** - The **PR interval** is measured from the **beginning of the P wave** to the **beginning of the QRS complex**. - It represents the **complete time** for the electrical impulse to travel from the SA node through the atria, the AV node, the Bundle of His, and bundle branches until ventricular depolarization begins. - This includes two major components: 1. **Atrial depolarization** (represented by the P wave) 2. **Conduction delay** through the AV node and His-Purkinje system (the isoelectric segment after the P wave) - **Normal PR interval**: 0.12-0.20 seconds (120-200 ms) - The **AV nodal delay** is the longest component, allowing atrial contraction to complete before ventricular contraction begins. *Conduction through AV node* - While **AV nodal conduction** is an important component of the PR interval, this option is **incomplete**. - The PR interval begins with the **P wave** (atrial depolarization), which occurs before the impulse reaches the AV node. - Stating only "conduction through AV node" ignores the atrial depolarization component that is also part of the PR interval. *Delay in ventricular depolarization* - **Ventricular depolarization** is represented by the **QRS complex**, not the PR interval. - The PR interval *ends* when ventricular depolarization begins (start of QRS). *Delay in ventricular repolarization* - **Ventricular repolarization** is represented by the **T wave** on an ECG. - This occurs much later in the cardiac cycle and is not related to the PR interval.

Q: Cardiac event at the end of isometric relaxation phase:

Atrioventricular valves open. ***Atrioventricular valves open*** - This event marks the end of isometric relaxation, where ventricular pressure has dropped below atrial pressure, allowing the **mitral and tricuspid valves** to open and ventricular filling to begin. - During **isometric relaxation**, the ventricles relax without changing volume, causing a rapid drop in intraventricular pressure until it is overcome by atrial pressure. *Corresponds to T wave in ECG* - The **T wave** on an ECG represents **ventricular repolarization**, which occurs during the early part of ventricular diastole, *before* the end of isometric relaxation when the AV valves open. - The opening of AV valves occurs a bit later, as ventricular filling phase commences. *Atrioventricular valves close* - The closing of the **atrioventricular valves** (mitral and tricuspid) occurs at the beginning of **isovolumetric contraction (systole)**, not at the end of isometric relaxation (diastole). - This event marks the start of ventricular systole and is associated with the **first heart sound (S1)**. *Corresponds to peak of C wave in JVP* - The **C wave** in the jugular venous pressure (JVP) tracing corresponds to the bulging of the **tricuspid valve** into the right atrium during early ventricular systole, immediately after the AV valves close. - This event is distinct from the end of isometric relaxation, which occurs later in diastole, *before* atrial filling.

Q: All are true about S1 except:

heard at the end of ventricular systole. ***heard at the end of ventricular systole*** - The **S1 sound** marks the **beginning of ventricular systole**, not the end. - It occurs immediately after the atria have emptied their blood into the ventricles and before the ventricles begin to pump blood out. *better heard with diaphragm of stethoscope* - **S1** is a **high-pitched sound** produced by the closing of the **mitral and tricuspid valves**. - High-pitched sounds are best auscultated with the **diaphragm** of the stethoscope. *caused by closure of mitral valve* - **S1** is primarily caused by the simultaneous closure of the **mitral and tricuspid valves**. - The **mitral valve closure** contributes the most to the intensity and timing of S1, as it handles higher pressures. *lower frequency than s2* - **S1** has a **lower frequency** and longer duration compared to **S2**. - This is because the closure of the **AV valves** (mitral and tricuspid) produces lower-pitched sounds than the closure of the semilunar valves.

Q: A hormone involved in regulation of blood pressure is:

Angiotensin-II. ***Angiotensin- II*** - **Angiotensin II** is a potent **vasoconstrictor** that directly increases **blood pressure** by narrowing blood vessels. - It also stimulates **aldosterone** release, leading to **sodium and water retention**, further contributing to increased blood volume and blood pressure. *Serotonin* - **Serotonin** (5-hydroxytryptamine or **5-HT**) plays a role in mood, sleep, and appetite, but its direct role in systemic **blood pressure regulation** is less prominent than **Angiotensin II**. - While it can affect vascular tone locally, it is not considered a primary hormonal regulator of overall systemic BP. *Dopamine* - **Dopamine** is a neurotransmitter involved in motor control, reward, and motivation, and at low doses can cause **renal vasodilation**. - Its direct and sustained role in systemic **blood pressure regulation** is not as central as the **renin-angiotensin-aldosterone system**. *Prostaglandin* - **Prostaglandins** are lipid compounds that act as local hormones, with some (**PGE2**, **PGI2**) causing **vasodilation** and others (**PGF2α**) causing **vasoconstriction**. - They are more involved in localized inflammatory responses, blood flow to specific organs (e.g., kidneys), and pain, rather than serving as a primary systemic regulator of ongoing **blood pressure**.

Q: As a general rule, arteries carry :

Oxygenated blood. ***Oxygenated blood*** - Arteries are generally responsible for carrying **oxygenated blood** away from the heart to the rest of the body's tissues and organs. - The only exception is the **pulmonary artery**, which carries deoxygenated blood from the heart to the lungs. *Urine* - Urine is transported by the **ureters** from the kidneys to the bladder, and then by the urethra out of the body. - This is part of the **urinary system**, separate from the circulatory system. *Deoxygenated blood* - While veins primarily carry **deoxygenated blood** back to the heart, arteries generally carry oxygenated blood. - The exception is the **pulmonary artery**, which carries deoxygenated blood to the lungs for oxygenation. *Lymph fluid* - **Lymph fluid** is carried by the lymphatic system, a network of vessels and nodes that is part of the immune system. - The lymphatic system helps maintain fluid balance and fights infection, distinct from the circulatory function of arteries.

Q: Which of the following uses cGMP as a second messenger?

Atrial natriuretic peptide. ***Atrial natriuretic peptide*** - **Atrial natriuretic peptide (ANP)** primarily uses **cGMP** as its second messenger to exert its effects on the cardiovascular system and kidneys. - ANP binds to its receptor, activating **guanylate cyclase**, which then converts **GTP to cGMP**, leading to vasodilation and natriuresis. *Cortisone* - **Cortisone** is a **glucocorticoid** that primarily functions by binding to intracellular **steroid hormone receptors**, which then translocate to the nucleus to regulate gene expression. - It does not utilize cGMP as a second messenger; its signaling pathway involves direct gene transcription modulation. *GH* - **Growth hormone (GH)** typically signals through the **JAK/STAT pathway** upon binding to its receptor, leading to the phosphorylation of STAT proteins and subsequent gene transcription. - GH primarily stimulates cell growth and metabolism through tyrosine kinase-associated receptors, not via cGMP. *Thyroxine* - **Thyroxine (T4)** and its active form **triiodothyronine (T3)** are **thyroid hormones** that bind to nuclear receptors, influencing gene expression directly. - Their mechanism of action involves altering protein synthesis, and they do not use cGMP as a second messenger.

Q: The non-invasive method to measure the blood flow is:

Laser Doppler flowmetry. ***Laser Doppler flowmetry*** - This method uses **laser light** to measure blood flow in the microvasculature by detecting the **Doppler shift** caused by moving red blood cells. - It is a **non-invasive**, real-time technique used to assess blood perfusion in tissues, particularly useful for microvascular flow assessment. - Commonly applied in research and clinical settings to evaluate **skin perfusion**, **peripheral circulation**, and **microvascular function**. *Doppler ultrasound* - While **Doppler ultrasound** is also non-invasive and measures blood flow velocity using the Doppler principle, it is typically used for **larger vessels** rather than microcirculation. - It provides information about **blood flow velocity** and direction in arteries and veins, not the detailed microvascular perfusion that Laser Doppler provides. *Plethysmography* - **Plethysmography** measures volume changes in an organ or limb, which can reflect blood flow indirectly. - It is non-invasive but provides information about **total blood volume changes** rather than direct, real-time microvascular blood flow measurement. - Types include venous occlusion plethysmography and impedance plethysmography. *Fick's principle* - **Fick's principle** is used to measure cardiac output by calculating the difference in oxygen content between arterial and venous blood. - While valuable for measuring overall blood flow (cardiac output), it requires **blood sampling** or breath analysis, making it less directly non-invasive compared to Laser Doppler flowmetry for microvascular assessment.

Q: Atrial natriuretic peptide causes:

All of the options. ***All of the options*** - **Atrial natriuretic peptide (ANP)** has multiple integrated effects on the cardiovascular and renal systems, making all the listed options correct. **Vasodilation** - ANP causes **vasodilation** of both afferent and efferent renal arterioles (with greater effect on afferent), as well as systemic blood vessels - This vasodilation directly reduces systemic vascular resistance and blood pressure - Mediated through cGMP-dependent mechanisms **Promotes natriuresis by inhibiting sodium reabsorption** - ANP directly **inhibits sodium reabsorption** in the collecting duct by: - Antagonizing aldosterone effects - Inhibiting epithelial sodium channels (ENaC) - Reducing sodium transport in the distal nephron - This promotes natriuresis (sodium excretion) and diuresis (water excretion) **Increases glomerular filtration rate by acting via mesangial cells** - ANP increases **GFR** through multiple mechanisms: - Causes **relaxation of mesangial cells**, which increases glomerular capillary surface area available for filtration - Dilates afferent arteriole more than efferent, increasing glomerular capillary hydrostatic pressure - These combined effects significantly enhance glomerular filtration *Vasodilation alone* - While vasodilation is one important effect of ANP, it is not the only mechanism by which ANP regulates blood volume and pressure *Promotes natriuresis by inhibiting sodium reabsorption alone* - While natriuresis through sodium reabsorption inhibition is a key mechanism, ANP has additional important effects *Increases GFR by acting via mesangial cells alone* - While the mesangial cell relaxation and GFR increase are correct, ANP's actions are more comprehensive

Question 1

Which neurotransmitter is primarily responsible for parasympathetic effects on heart rate?

Accepted Answer

Acetylcholine

Answer

Norepinephrine

Answer

Dopamine

Answer

Epinephrine

Question 2

The PR interval in ECG denotes?

Accepted Answer

Atrial depolarization with A - V conduction

Answer

Ventricular depolarization and ventricular repolarization

Answer

Atrial depolarization with atrial repolarization

Answer

Atrial depolarization only

Question 3

PR interval in ECG shows?

Accepted Answer

Atrial depolarization and conduction delay

Answer

Conduction through AV node

Answer

Delay in ventricular depolarization

Answer

Delay in ventricular repolarization

Question 4

Cardiac event at the end of isometric relaxation phase:

Accepted Answer

Atrioventricular valves open

Answer

Corresponds to T wave in ECG

Answer

Atrioventricular valves close

Answer

Corresponds to peak of C wave in JVP

Question 5

All are true about S1 except:

Accepted Answer

heard at the end of ventricular systole

Answer

better heard with diaphragm of stethoscope

Answer

caused by closure of mitral valve

Answer

lower frequency than s2

Question 6

A hormone involved in regulation of blood pressure is:

Accepted Answer

Angiotensin-II

Answer

Serotonin

Answer

Dopamine

Answer

Prostaglandin

Question 7

As a general rule, arteries carry :

Accepted Answer

Oxygenated blood

Answer

Urine

Answer

Deoxygenated blood

Answer

Lymph fluid

Question 8

Which of the following uses cGMP as a second messenger?

Accepted Answer

Atrial natriuretic peptide

Answer

Cortisone

Answer

GH

Answer

Thyroxine

Question 9

The non-invasive method to measure the blood flow is:

Accepted Answer

Laser Doppler flowmetry

Answer

Doppler ultrasound

Answer

Plethysmography

Answer

Fick's principle

Question 10

Atrial natriuretic peptide causes:

Accepted Answer

All of the options

Answer

Vasodilation

Answer

Promotes natriuresis by inhibiting sodium reabsorption

Answer

Increases glomerular filtration rate by acting via mesangial cells

Cardiovascular System — MCQs

Cardiovascular System — MCQs

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