Cardiovascular System Practice Questions

Q: Which of the following phases is absent in the action potential of pacemaker cells?

Phase 1. **Explanation:** The cardiac action potential differs significantly between **contractile cells** (ventricular myocytes) and **pacemaker cells** (SA and AV nodes). Pacemaker cells exhibit "slow response" action potentials characterized by automaticity and the absence of a plateau phase [1]. **Why Phase 1 is absent:** Phase 1 represents **early rapid repolarization**, which is caused by the transient outward flow of potassium ions ($I_{to}$) and the abrupt closure of fast sodium channels. In pacemaker cells, depolarization (Phase 0) is mediated by the slow influx of Calcium ($Ca^{2+}$) through L-type channels rather than fast Sodium ($Na^+$) channels [1], [2]. Because there is no rapid sodium spike or subsequent transient potassium efflux, **Phase 1 (and Phase 2/Plateau) is entirely absent.** [1] **Analysis of Incorrect Options:** * **Phase 0 (Depolarization):** Present. In pacemaker cells, this is "slow" and mediated by $Ca^{2+}$ influx (unlike the "fast" $Na^+$ influx in myocytes) [1], [2]. * **Phase 3 (Repolarization):** Present. This is caused by the efflux of $K^+$ ions through delayed rectifier potassium channels, returning the membrane to its most negative potential [1]. * **Phase 4 (Pacemaker Potential):** Present and critical. This is the spontaneous diastolic depolarization caused by the "funny current" ($I_f$) through HCN channels, $T$-type $Ca^{2+}$ channels, and reduced $K^+$ efflux [1]. This phase is responsible for **automaticity** [3]. **High-Yield NEET-PG Pearls:** * **SA Node** is the primary pacemaker because it has the steepest Phase 4 slope. * **Preload/Vagal tone** decreases the slope of Phase 4 (bradycardia), while **Sympathetic tone** increases it (tachycardia). * **Drugs:** Calcium channel blockers (Verapamil/Diltiazem) act on Phase 0 of the pacemaker cell [2], slowing the heart rate and conduction.

Q: Which peptide causes increased capillary permeability and edema?

Bradykinin. **Explanation:** **Correct Option: C (Bradykinin)** Bradykinin is a potent vasodilator and a key mediator of the inflammatory response. It acts primarily on **B2 receptors** to stimulate the release of nitric oxide and prostacyclin. Its primary effect on the microvasculature is the contraction of endothelial cells, which increases the size of intercellular junctions (pores). This leads to **increased capillary permeability**, allowing fluid and plasma proteins to leak into the interstitial space, resulting in **edema**. **Analysis of Incorrect Options:** * **A. Histamine:** While histamine also increases capillary permeability and causes edema, it is an **amine** (derived from the amino acid histidine), not a **peptide**. The question specifically asks for a peptide. * **B. Angiotensin II:** This is a potent **vasoconstrictor** peptide. It generally increases blood pressure and decreases capillary hydrostatic pressure through systemic effects, rather than increasing permeability. * **D. Renin:** Renin is an **enzyme** (protease) secreted by the juxtaglomerular cells of the kidney. It catalyzes the conversion of Angiotensinogen to Angiotensin I; it does not directly affect capillary permeability. **High-Yield Clinical Pearls for NEET-PG:** * **ACE Inhibitors & Cough:** ACE (Angiotensin-Converting Enzyme) is responsible for the breakdown of Bradykinin. ACE inhibitors lead to an accumulation of Bradykinin, which causes the classic side effects of **dry cough** and **angioedema**. * **Hereditary Angioedema:** This condition is caused by a deficiency of **C1 esterase inhibitor**, leading to overproduction of Bradykinin, resulting in episodes of severe swelling. * **Triple Response of Lewis:** Bradykinin and Histamine are both involved in the "Wheal" component of the triple response due to increased permeability.

Q: Which of these changes in fetal circulation happen immediately at birth?

Functional closure of ductus arteriosus. **Explanation:** The transition from fetal to neonatal circulation involves immediate physiological changes and gradual anatomical changes. **Why Option C is Correct:** The **functional closure of the ductus arteriosus** occurs almost **immediately (within 10–15 hours)** after birth. This is triggered by two main factors: 1. **Increased Oxygen Tension:** As the baby takes its first breath, systemic $PaO_2$ rises, causing contraction of the smooth muscles in the ductus wall. 2. **Fall in Prostaglandin ($PGE_2$) levels:** The removal of the placenta (the primary source of $PGE_2$) and increased metabolism in the lungs lead to ductal constriction. **Why Other Options are Incorrect:** * **A & D (Obliteration of Ductus Venosus and Distal Hypogastric Arteries):** While these vessels cease to function shortly after the cord is clamped, their **obliteration** (anatomical closure) is a gradual process taking several days to weeks. * **B (Formation of Ligamentum Teres):** This is the end-stage anatomical result of the obliterated left umbilical vein. Anatomical closure of fetal remnants typically takes **2–3 months** to complete. **High-Yield NEET-PG Pearls:** * **Functional vs. Anatomical:** Functional closure (physiological) happens in hours; Anatomical closure (fibrosis) takes weeks. * **Remnants Summary:** * **Ductus Arteriosus** $\rightarrow$ Ligamentum arteriosum * **Ductus Venosus** $\rightarrow$ Ligamentum venosum * **Left Umbilical Vein** $\rightarrow$ Ligamentum teres hepatis * **Umbilical Arteries** $\rightarrow$ Medial umbilical ligaments * **Foramen Ovale** $\rightarrow$ Fossa ovalis (Functional closure is immediate due to increased left atrial pressure). * **Pharmacology:** **Indomethacin** (NSAID) is used to close a Patent Ductus Arteriosus (PDA), while **Alprostadil** ($PGE_1$) is used to keep it open in cyanotic heart diseases.

Q: A 40-year-old man presents with a resting heart rate of 180 beats/min. A pressure-volume diagram of the left ventricle is shown below. What is the cardiac output?

5.6 L/min. ***5.6 L/min*** - **Cardiac output** = **Stroke Volume** × **Heart Rate**; from the PV loop, **stroke volume** ≈ 31 mL (EDV - ESV), so CO = 31 mL × 180 bpm = 5,580 mL/min ≈ **5.6 L/min**. - The **width of the PV loop** represents stroke volume, which appears reduced due to **tachycardia** limiting ventricular filling time. *5.2 L/min* - This would correspond to a **stroke volume** of approximately 29 mL (5,200 ÷ 180), which is lower than what the PV loop demonstrates. - The calculation underestimates the actual **stroke volume** visible in the pressure-volume diagram. *4.8 L/min* - This represents a **stroke volume** of approximately 27 mL (4,800 ÷ 180), significantly lower than the loop shows. - This would indicate **severe cardiac dysfunction** with markedly reduced contractility, not consistent with the PV loop morphology. *6 L/min* - This would require a **stroke volume** of approximately 33 mL (6,000 ÷ 180), which is higher than what the PV loop indicates. - The calculation overestimates the **end-diastolic volume minus end-systolic volume** difference shown in the diagram.

Q: Which one of the following neurotransmitters functions to increase cardiac output?

Norepinephrine. **Explanation:** **Norepinephrine (Option C)** is the correct answer because it is the primary neurotransmitter of the postganglionic sympathetic nervous system. It increases cardiac output through its action on **$\beta_1$-adrenergic receptors** located in the myocardium and the sinoatrial (SA) node. This binding triggers a G-protein-mediated increase in cAMP, leading to: 1. **Positive Inotropy:** Increased force of contraction. 2. **Positive Chronotropy:** Increased heart rate. Since Cardiac Output (CO) = Stroke Volume (SV) × Heart Rate (HR), both mechanisms contribute to a significant rise in CO. **Analysis of Incorrect Options:** * **GABA (Option A):** The primary inhibitory neurotransmitter in the CNS. While it can influence central blood pressure regulation, it does not have a direct peripheral stimulatory effect on cardiac output. * **Serotonin (Option B):** Primarily involved in mood regulation and platelet aggregation. While it has complex effects on the vasculature (vasoconstriction/dilation), it is not the physiological mediator for increasing cardiac output. * **Glutamate (Option D):** The major excitatory neurotransmitter in the CNS. It is involved in synaptic plasticity and memory but does not act directly on the heart to increase output. **High-Yield Clinical Pearls for NEET-PG:** * **Receptor Specificity:** While Norepinephrine acts on $\alpha_1$ and $\beta_1$ receptors, **Epinephrine** (from the adrenal medulla) acts on $\alpha_1, \beta_1,$ and $\beta_2$. * **Parasympathetic Control:** Acetylcholine (ACh) acts on **$M_2$ receptors** to decrease heart rate (negative chronotropy), thereby decreasing cardiac output. * **Bowditch Effect:** An increase in heart rate leads to an increase in the force of contraction due to the inability of Na+/K+ ATPase to keep up, leading to higher intracellular calcium.

Q: During exercise, what happens to blood flow to the brain?

Unaltered. **Explanation:** The correct answer is **Unaltered (C)**. **1. Why it is correct:** During exercise, there is a massive increase in total cardiac output to meet the metabolic demands of skeletal muscles. However, the brain requires a constant, steady supply of oxygen and glucose to maintain consciousness and neurological function. This is achieved through **Cerebral Autoregulation**. Despite fluctuations in systemic blood pressure and the redistribution of blood to muscles and skin, the cerebral blood flow (CBF) remains remarkably constant at approximately **750 mL/min (or 15% of resting cardiac output)**. While the *percentage* of total cardiac output directed to the brain decreases, the *absolute volume* of blood flow remains unchanged. **2. Why other options are incorrect:** * **A. Decreased:** The brain is a vital organ; any significant decrease in flow would lead to syncope (fainting). Autoregulation prevents this during the sympathetic surge of exercise. * **B. Increased:** While blood flow to the heart and skeletal muscles increases significantly, the rigid cranium and autoregulatory mechanisms (myogenic and metabolic) prevent hyperperfusion of the brain. * **D. Initially increased and then decreases:** There is no physiological basis for this biphasic response in a healthy individual during standard exercise. **3. NEET-PG High-Yield Pearls:** * **Most sensitive factor for CBF:** Arterial $PCO_2$. Hypercapnia causes vasodilation (increasing flow), while hypocapnia (hyperventilation) causes vasoconstriction. * **Autoregulation Range:** Cerebral blood flow remains constant between a Mean Arterial Pressure (MAP) of **60 to 140 mmHg**. * **Organ with the highest blood flow per 100g tissue:** Carotid bodies (followed by the Kidneys). * **Organ with the highest oxygen extraction ($A-V O_2$ difference):** The Heart.

Q: Which of the following causes vasoconstriction in all vascular beds?

TXA2. **Explanation** The correct answer is **TXA2 (Thromboxane A2)**. **Why TXA2 is correct:** Thromboxane A2 is a potent eicosanoid synthesized primarily by platelets via the cyclooxygenase (COX) pathway. Its primary physiological roles are **platelet aggregation** and **potent vasoconstriction**. Unlike other prostaglandins which may have varying effects depending on the tissue or receptor subtype, TXA2 acts via the TP receptor to cause generalized vasoconstriction across all vascular beds, including the renal, coronary, and pulmonary circulations. **Why the other options are incorrect:** * **PGE2 (Prostaglandin E2):** This is primarily a **vasodilator** in most vascular beds. While it can cause constriction in specific areas (like the ductus arteriosus or certain segments of the renal vasculature under specific conditions), it is generally known for its role in inflammatory vasodilation and maintaining the patency of the ductus arteriosus. * **PGF2α (Prostaglandin F2 alpha):** While PGF2α is a vasoconstrictor (especially in the pulmonary and uterine vessels), it is primarily known for its potent **smooth muscle contracting** effects on the uterus and bronchi. It does not exert a universal vasoconstrictive effect across all vascular beds as consistently as TXA2. * **PGI2 (Prostacyclin):** Produced by vascular endothelial cells, PGI2 is the functional antagonist to TXA2. It is a potent **vasodilator** and inhibitor of platelet aggregation. **High-Yield NEET-PG Pearls:** * **Aspirin's Mechanism:** Low-dose aspirin irreversibly inhibits COX-1, shifting the balance in favor of **PGI2 (vasodilator)** over **TXA2 (vasoconstrictor)**, which explains its cardioprotective effect. * **Vasoactive Mnemonic:** Remember **"I"** for **I**nhibition (PGI2 inhibits aggregation/constriction) and **"TX"** for **T**hrombus (TXA2 promotes thrombus/constriction). * **Ductus Arteriosus:** PGE2 keeps it open; NSAIDs (Indomethacin) close it by inhibiting PGE2 synthesis.

Q: Pacemaker potential occurs due to which of the following?

Opening of transient, rapid T-type Ca2+ channels. **Explanation:** The **Pacemaker Potential** (also known as the prepotential or Phase 4 depolarization) is the slow, spontaneous depolarization of the SA node that brings the membrane potential to the threshold, triggering an action potential. **1. Why Option A is Correct:** The pacemaker potential occurs in three sequential ionic steps: * **Initial Phase:** Triggered by the opening of **"Funny" Na+ channels ($I_f$)**, which allow sodium influx. * **Late Phase:** As the membrane depolarizes, **T-type (Transient) Ca2+ channels** open. These channels provide the final push (calcium influx) to reach the threshold potential (approx. -40 mV). * Once the threshold is reached, **L-type (Long-lasting) Ca2+ channels** open to cause the actual depolarization (Phase 0). Therefore, the opening of T-type channels is a critical component of the pacemaker potential. **2. Why Other Options are Incorrect:** * **Option B:** Opening of K+ channels causes **repolarization** (Phase 3), as K+ leaves the cell, making the interior more negative. * **Option C:** Closure of Ca2+ channels would stop depolarization; it is the *opening* of these channels that drives the potential toward the threshold. * **Option D:** The prepotential begins with the **opening** of funny Na+ channels, not their closure. **Clinical Pearls & High-Yield Facts:** * **SA Node:** The primary pacemaker because it has the steepest prepotential slope. * **Autonomic Influence:** Sympathetic stimulation increases the slope (faster heart rate), while Parasympathetic (Vagus) stimulation decreases the slope and hyperpolarizes the cell (slower heart rate). * **Ivabradine:** A clinical drug that selectively blocks the **$I_f$ (funny) channels**, used to reduce heart rate in angina and heart failure. * **Phase 0 in SA Node:** Unlike ventricular muscle (where Phase 0 is Na+ dependent), the SA node's Phase 0 is **Ca2+ dependent**.

Question 1

Which of the following phases is absent in the action potential of pacemaker cells?

Accepted Answer

Phase 1

Answer

Phase 0

Answer

Phase 3

Answer

Phase 4

Question 2

Which peptide causes increased capillary permeability and edema?

Accepted Answer

Bradykinin

Answer

Histamine

Answer

Angiotensin II

Answer

Renin

Question 3

Which of these changes in fetal circulation happen immediately at birth?

Accepted Answer

Functional closure of ductus arteriosus

Answer

Obliteration of ductus venosus

Answer

Formation of ligamentum teres

Answer

Obliteration of distal hypogastric arteries

Question 4

A patient's ECG shows Lead III with no S wave, but normal P, R, and T waves. What conclusions can be drawn about the patient's cardiac status?

Accepted Answer

No indications of cardiac abnormalities.

Answer

Abnormal activation of parts of the base of the heart.

Answer

Abnormal activation of parts of the apex of the heart.

Answer

Cardiac depression.

Question 5

What period does ventricular contraction correspond to on an ECG?

Accepted Answer

Beginning of Q wave to the end of T wave

Answer

Beginning of Q wave to end of S wave

Answer

Beginning of P wave to end of T wave

Answer

Beginning of R wave to the end of T wave, if Q wave is absent

Question 6

A 40-year-old man presents with a resting heart rate of 180 beats/min. A pressure-volume diagram of the left ventricle is shown below. What is the cardiac output?

Accepted Answer

5.6 L/min

Answer

5.2 L/min

Answer

4.8 L/min

Answer

6 L/min

Question 7

Which one of the following neurotransmitters functions to increase cardiac output?

Accepted Answer

Norepinephrine

Answer

GABA

Answer

Serotonin

Answer

Glutamate

Question 8

During exercise, what happens to blood flow to the brain?

Accepted Answer

Unaltered

Answer

Decreased

Answer

Increased

Answer

Initially increased and then decreases

Question 9

Which of the following causes vasoconstriction in all vascular beds?

Accepted Answer

TXA2

Answer

PGE2

Answer

PGF2α

Answer

PGI2

Question 10

Pacemaker potential occurs due to which of the following?

Accepted Answer

Opening of transient, rapid T-type Ca2+ channels

Answer

Opening of K+ channels

Answer

Closure of Ca2+ channels

Answer

Closure of funny Na+ channels

Cardiovascular System — MCQs

Cardiovascular System — MCQs

On this page

Practice by Chapter

Want unlimited practice?