Cardiovascular System Practice Questions

Q: What is the resting pacemaker potential in cardiac tissue (in mV)?

-55 mV. **Explanation:** The resting membrane potential (RMP) of the cardiac pacemaker (SA node) is approximately **-55 to -60 mV**. Unlike ventricular myocytes, pacemaker cells lack a stable resting potential; instead, they exhibit a slow, spontaneous depolarization known as the "pacemaker potential" or Phase 4. **Why -55 mV is correct:** In the SA node, the RMP is less negative than in other cardiac tissues because the cell membranes are naturally leakier to sodium and calcium ions. This higher baseline potential is crucial because it keeps the fast sodium channels permanently inactivated, making the upstroke of the action potential dependent on slower calcium channels (L-type). **Analysis of Incorrect Options:** * **-40 mV:** This is the **threshold potential** for the SA node. Once the slow depolarization reaches this level, voltage-gated L-type calcium channels open, triggering the action potential. * **-70 mV:** This is the typical RMP for neurons or certain specialized conducting tissues like the Bundle of His, but it is too negative for the SA node. * **-90 mV:** This is the RMP for **ventricular muscle fibers** and Purkinje fibers. It is maintained by a high resting permeability to potassium ($K^+$) and is necessary for the rapid depolarization (Phase 0) mediated by fast sodium channels. **High-Yield Clinical Pearls for NEET-PG:** 1. **Funny Currents ($I_f$):** The initial phase of pacemaker depolarization is caused by $I_f$ channels, which are activated by hyperpolarization and carry sodium ions. 2. **Pre-potential:** The slope of Phase 4 determines the heart rate. Acetylcholine (vagus nerve) decreases this slope (bradycardia), while Norepinephrine increases it (tachycardia). 3. **Hierarchy:** The SA node is the primary pacemaker because it has the highest intrinsic rate of spontaneous depolarization (60-100 bpm).

Q: All of the following inflammatory mediators produce vasoconstriction except?

Bradykinin. **Explanation:** The core concept tested here is the distinction between **vasoconstrictors** and **vasodilators** released during inflammation and vascular injury. **Why Bradykinin is the correct answer:** Bradykinin is a potent **vasodilator**. It acts by stimulating the release of nitric oxide (NO) and prostacyclin ($PGI_2$) from the vascular endothelium. In the context of inflammation, Bradykinin increases capillary permeability and is a primary mediator of pain (by sensitizing nociceptors). Because it causes vasodilation rather than constriction, it is the correct "except" choice. **Analysis of Incorrect Options:** * **Endothelin-1:** This is the most potent endogenous **vasoconstrictor** known. It is produced by damaged endothelial cells and plays a significant role in maintaining vascular tone and the pathophysiology of pulmonary hypertension. * **Thromboxane A2 ($TXA_2$):** Produced by activated platelets, $TXA_2$ is a powerful **vasoconstrictor** and platelet aggregator. It works in opposition to Prostacyclin ($PGI_2$) to limit blood loss during injury. * **Platelet Activating Factor (PAF):** While PAF has complex systemic effects (including bronchoconstriction), at the local site of injury/inflammation, it can induce **vasoconstriction** and increase vascular permeability. **NEET-PG High-Yield Pearls:** * **Triple Response of Lewis:** Bradykinin and Histamine are key mediators of the "Flare" (vasodilation) component. * **ACE Inhibitors:** These drugs prevent the breakdown of Bradykinin. Elevated levels of Bradykinin are responsible for the common side effects of ACE inhibitors: **dry cough** and **angioedema**. * **Vasoconstrictor Mnemonic:** Remember **"SET"** (Serotonin, Endothelin, Thromboxane $A_2$).

Q: A 55-year-old man has been diagnosed with Stokes-Adams syndrome. Two minutes after the onset of a syncopal attack, which of the following is the pacemaker of the heart?

Purkinje fibers. ### Explanation **Underlying Medical Concept: Ventricular Escape Rhythm** Stokes-Adams syndrome refers to sudden, transient episodes of syncope caused by a complete heart block (Third-degree AV block). When the conduction between the atria and ventricles is interrupted, the ventricles stop contracting for 5 to 30 seconds because they were previously "overdrive suppressed" by the rapid sinus rhythm. After this delay, a distal part of the conduction system—specifically the **Purkinje fibers**—begins to discharge spontaneously. This is known as **ventricular escape rhythm**, which typically occurs at a rate of 15–40 beats per minute, restoring cerebral blood flow. **Analysis of Options:** * **Purkinje fibers (Correct):** These possess intrinsic automaticity. In the event of a complete AV block, they act as the tertiary pacemaker to prevent permanent cardiac standstill. * **Sinus node (Incorrect):** While the SA node continues to fire and depolarize the atria, the electrical impulse cannot cross the AV node to reach the ventricles; thus, it cannot function as the ventricular pacemaker. * **A-V node (Incorrect):** In Stokes-Adams syndrome, the block is often located within the AV bundle (Bundle of His) or distal to it. Therefore, the AV node cannot bypass the block to pace the ventricles. * **Cardiac septum (Incorrect):** The septum is myocardial tissue. While it can conduct impulses, it does not possess the specialized rhythmic pacemaking cells required to initiate a stable escape rhythm. **NEET-PG High-Yield Pearls:** * **Overdrive Suppression:** The mechanism where a faster pacemaker (SA node) inhibits the automaticity of slower latent pacemakers. * **Intrinsic Rates:** SA node (60–100 bpm) > AV node (40–60 bpm) > Purkinje system (15–40 bpm). * **Clinical Presentation:** The "syncopal attack" occurs during the delay between the block and the onset of the Purkinje rhythm. If the delay is too long, it can be fatal.

Q: All of the following are true about cardiac muscles, EXCEPT:

10% energy is provided by anaerobic metabolism.. **Explanation:** The cardiac muscle is an **obligatory aerobic tissue**, meaning it relies almost exclusively on oxidative metabolism to function. Unlike skeletal muscle, which can sustain activity through anaerobic glycolysis during heavy exercise, the heart has a very limited anaerobic capacity. **1. Why Option C is the Correct Answer (The "Except"):** Under normal physiological conditions, **less than 1%** of the heart’s energy is derived from anaerobic metabolism. The heart is designed for endurance and continuous work; it extracts about 70-80% of oxygen from the blood even at rest. Because it cannot "pay back" an oxygen debt, it cannot rely on anaerobic pathways (which would provide 10% or more energy) without rapidly leading to muscle fatigue or ischemic injury. **2. Why the other options are incorrect (They are TRUE statements):** * **Option A (Abundant mitochondria):** This is true. Mitochondria occupy about **25-35% of the cell volume** in cardiac myocytes (compared to only 2-3% in skeletal muscle). This supports the high demand for ATP via oxidative phosphorylation. * **Option B (High myoglobin content):** This is true. Myoglobin acts as an intracellular oxygen reservoir, facilitating the rapid transport of oxygen from the sarcolemma to the mitochondria, ensuring the heart remains aerobic even during systole when coronary blood flow is restricted. **High-Yield Clinical Pearls for NEET-PG:** * **Preferred Fuel:** At rest, the heart derives 60-70% of its energy from **Fatty Acids**, followed by glucose and lactate. * **Lactate Utilization:** Unlike other tissues that produce lactate as a waste product, the heart can actually **consume lactate** and convert it to pyruvate for energy during exercise. * **Functional Syncytium:** Cardiac muscle cells are joined by **Gap Junctions** (within intercalated discs), allowing for coordinated contraction.

Q: A 65-year-old man had an ECG after a biking accident. His QRS voltage was 0.5 millivolt in lead I and 1.5 millivolts in lead III. What is the QRS voltage in lead II?

2.0 millivolts. ### Explanation **1. The Underlying Concept: Einthoven’s Law** The correct answer is **2.0 millivolts** based on **Einthoven’s Law**. In electrocardiography, the standard limb leads (I, II, and III) form a mathematical relationship known as Einthoven’s Triangle. The law states that the electrical potential of any complex in Lead II is equal to the sum of the potentials in Lead I and Lead III. **Formula:** Lead II = Lead I + Lead III **Calculation:** 0.5 mV (Lead I) + 1.5 mV (Lead III) = **2.0 mV** **2. Analysis of Incorrect Options** * **Option A (0.5 mV):** This simply repeats the value of Lead I. * **Option B (1.0 mV):** This represents the difference between Lead III and Lead I, which is mathematically incorrect for calculating Lead II. * **Option C (1.5 mV):** This repeats the value of Lead III. **3. Clinical Pearls & High-Yield Facts for NEET-PG** * **Einthoven’s Triangle:** An equilateral triangle with the heart at the center. The vertices represent the right arm (RA), left arm (LA), and left leg (LL). * **Lead Polarities:** * Lead I: RA (-) to LA (+) * Lead II: RA (-) to LL (+) * Lead III: LA (-) to LL (+) * **Goldberger’s Equation:** Relates augmented limb leads to standard leads (e.g., aVF = [LII + LIII] / 2). * **Low Voltage ECG:** Defined as QRS amplitude <0.5 mV in all limb leads or <1.0 mV in all precordial leads. Common causes include pericardial effusion, obesity, and emphysema.

Q: All are true about nitric oxide except?

Acts through cGMP. **Explanation:** Nitric Oxide (NO), formerly known as Endothelium-Derived Relaxing Factor (EDRF), is a potent vasodilator synthesized from **L-arginine** by the enzyme Nitric Oxide Synthase (NOS). **1. Why Option A is the "Except" (Correct Answer):** The question asks for the false statement. Option A is actually a **true** statement regarding NO's mechanism of action. NO diffuses into vascular smooth muscle cells and activates **soluble Guanylyl Cyclase**, which increases intracellular **cGMP**. This leads to protein kinase G activation, resulting in dephosphorylation of myosin light chains and subsequent vasodilation. Since the statement is true, it is the correct choice in an "except" format. **2. Analysis of Other Options:** * **Option B (True):** NO is the primary regulator of basal vascular tone. Constant release of NO maintains a state of vasodilation; inhibition of NO leads to significant hypertension. * **Option C (True):** NO is the principal mediator of penile erection. It is released from parasympathetic non-adrenergic non-cholinergic (NANC) nerves in the corpora cavernosa. (Clinical link: Sildenafil works by inhibiting PDE-5, preventing the breakdown of cGMP). * **Option D (True):** Cigarette smoke contains high levels of free radicals that deactivate NO and impair endothelial NOS function. Consequently, chronic smokers have **reduced bioavailability** of NO, contributing to endothelial dysfunction and atherosclerosis. **High-Yield Clinical Pearls for NEET-PG:** * **Precursor:** L-Arginine. * **Enzymes:** eNOS (Endothelial), nNOS (Neuronal), and iNOS (Inducible - seen in septic shock). * **Inhaled NO:** Used in the treatment of Persistent Pulmonary Hypertension of the Newborn (PPHN). * **Nitroglycerin:** Acts as a prodrug that is converted into NO to relieve angina.

Q: For cardiac muscle, Vmax can be used as a measure of:

Contractility. **Explanation:** **1. Why Contractility is Correct:** In cardiac physiology, **Vmax** (maximal velocity of shortening) represents the intrinsic ability of the myocardial fibers to contract at zero load. According to the **Force-Velocity relationship**, as the load (afterload) on a muscle fiber decreases, the velocity of shortening increases. When the load is extrapolated to zero, the resulting Vmax is independent of initial fiber length (preload) but is highly sensitive to the **inotropic state** of the heart. Therefore, Vmax serves as a reliable index of **myocardial contractility**. An increase in contractility (e.g., via sympathetic stimulation) shifts the force-velocity curve upward and to the right, increasing Vmax. **2. Why Other Options are Incorrect:** * **Excitability (Bathmotropy):** This refers to the ability of cardiac cells to respond to a stimulus by generating an action potential. It is determined by the resting membrane potential and threshold potential, not the velocity of muscle shortening. * **Rhythmicity (Chronotropy):** This refers to the heart's ability to generate its own periodic impulses (pacemaker activity), primarily governed by the SA node. * **Conductivity (Dromotropy):** This refers to the speed at which electrical impulses spread through the heart's conduction system (e.g., AV node delay). **3. High-Yield Clinical Pearls for NEET-PG:** * **Frank-Starling Law:** States that within physiological limits, the force of contraction is proportional to the initial length of the muscle fiber (preload). Note that while preload increases the *force*, it does **not** change Vmax. * **Inotropic Agents:** Digitalis and Catecholamines increase contractility, thereby increasing Vmax. * **Lusitropy:** Refers to the rate of myocardial relaxation (an active process requiring ATP for calcium reuptake via SERCA).

Question 1

What is the resting pacemaker potential in cardiac tissue (in mV)?

Accepted Answer

-55 mV

Answer

-40 mV

Answer

-70 mV

Answer

-90 mV

Question 2

All of the following inflammatory mediators produce vasoconstriction except?

Accepted Answer

Bradykinin

Answer

Endothelin-1

Answer

Thromboxane A2

Answer

Platelet activating factor

Question 3

A 55-year-old man has been diagnosed with Stokes-Adams syndrome. Two minutes after the onset of a syncopal attack, which of the following is the pacemaker of the heart?

Accepted Answer

Purkinje fibers

Answer

Sinus node

Answer

A-V node

Answer

Cardiac septum

Question 4

The chemoreceptor reflex primarily causes which of the following physiological responses?

Accepted Answer

Bradycardia and vasoconstriction

Answer

Mild tachycardia and vasodilation

Answer

Mild tachycardia and vasoconstriction

Answer

Bradycardia and vasodilation

Question 5

Which of the following statements regarding cardiac conduction functions are TRUE/FALSE?

Accepted Answer

a,c,e-True & b,d-False

Answer

a,b,c,d,e-True & None-False

Answer

a,e-True & b,c,d-False

Answer

b,c,d-True & a,e-False

Question 6

All of the following are true about cardiac muscles, EXCEPT:

Accepted Answer

10% energy is provided by anaerobic metabolism.

Answer

Abundant mitochondria are present.

Answer

Has high content of myoglobin.

Answer

None of the above.

Question 7

A 65-year-old man had an ECG after a biking accident. His QRS voltage was 0.5 millivolt in lead I and 1.5 millivolts in lead III. What is the QRS voltage in lead II?

Accepted Answer

2.0 millivolts

Answer

0.5 millivolt

Answer

1.0 millivolt

Answer

1.5 millivolts

Question 8

All are true about nitric oxide except?

Accepted Answer

Acts through cGMP

Answer

Helps to regulate vascular tone

Answer

Important role in penile erection

Answer

Present in low concentration in cigarette smokers

Question 9

Signal from baroreceptors is transmitted to which of the following medullary areas?

Accepted Answer

Rostral ventrolateral medulla

Answer

Caudal ventrolateral medulla

Answer

Nucleus of the tractus solitarius

Answer

None of the above

Question 10

For cardiac muscle, Vmax can be used as a measure of:

Accepted Answer

Contractility

Answer

Excitability

Answer

Rhythmicity

Answer

Conductivity

Cardiovascular System — MCQs

Cardiovascular System — MCQs

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