Cardiovascular System MCQ Quiz in தமிழ் - Objective Question with Answer for Cardiovascular System - இலவச PDF ஐப் பதிவிறக்கவும்

The correct answer is B and D

Concept:

• P wave: Represents atrial depolarization, which leads to atrial contraction.
• QRS complex: Represents ventricular depolarization, which leads to ventricular contraction.
• T wave: Represents ventricular repolarization, which is the recovery phase after ventricular contraction.
• QT interval: Represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization.

Explanation:

Statement B: The atrial repolarization is responsible for the T wave.

• Incorrect: The T wave represents ventricular repolarization, not atrial repolarization. Atrial repolarization is masked by the QRS complex and doesn't produce a separate wave on the ECG.

Statement D: The Q-T interval indicates plateau portion of auricular action potential.

• Incorrect: The QT interval represents the time from the start of ventricular depolarization to the end of ventricular repolarization. It doesn't correspond to atrial (auricular) action potential.

The correct answer is C and D

Concept:

• The chloride content (Cl^-) of red blood cells (RBCs) in venous blood is higher than in arterial blood due to the chloride shift, also known as the Hamburger phenomenon. This process helps to maintain ionic balance during the transport of carbon dioxide (CO₂) in the blood.
• Carbon dioxide produced by tissues diffuses into RBCs, where it is converted to bicarbonate (HCO₃^-) by the enzyme carbonic anhydrase. The bicarbonate then moves out of the RBCs into the plasma, and to maintain electrical neutrality, chloride ions move into the RBCs from the plasma.
• The pCO₂ (partial pressure of CO₂) is higher in venous blood because it has collected CO₂ from tissues, whereas arterial blood has a lower pCO₂ since it is being transported away from the lungs, where CO2 is expelled.

Explanation:

• Statement A: "The high pCO₂ in venous plasma leads to increased diffusion of CO₂ into RBC and the formation of H₂CO₃." This is correct. The high pCO₂ in venous blood causes CO₂ to diffuse into RBCs, where it is converted to carbonic acid (H₂CO₃).
• Statement B: "HCO₃- content in the RBC of venous blood becomes much greater than that in plasma." This is correct. In venous blood, RBCs convert CO₂ into bicarbonate (HCO₃-) using the enzyme carbonic anhydrase. To maintain electrochemical balance, HCO₃- is exchanged for chloride ions (Cl^-), a process known as the chloride shift or Hamburger effect. This exchange results in a higher concentration of HCO₃- in plasma as it moves out from RBCs, whereas Cl- moves into RBCs. ). This results in a higher concentration of HCO₃- in the RBC compared to plasma.
• Statement C: "The excess HCO₃^- leaves the RBC of venous blood along with Na to plasma by a Na⁺-HCO₃- symporter." This is incorrect. The HCO₃- leaves the RBCs through an anion exchanger protein (AE1), not a Na⁺-HCO₃- symporter. The exchange involves Cl^- entering the RBCs as HCO₃- leaves, without involvement of Na⁺.
• Statement D: "The increased Na⁺ in the venous plasma is transported to the RBC along with Cl^-." This is incorrect. The chloride shift mechanism does not involve Na⁺; it is strictly an exchange between Cl^- and HCO₃- to maintain ionic balance.

The correct answer is Option 1

Concept:

The Frank-Starling mechanism (also known as the Frank-Starling law of the heart) is a fundamental principle in cardiovascular physiology describing the relationship between the volume of blood filling the heart (end-diastolic volume) and the heart's ability to eject blood during systole (stroke volume). In essence, the Frank-Starling mechanism states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the venous return) up to a physiological limit. This process enables the heart to automatically adjust its pumping capacity to accommodate varying volumes of venous return, ensuring a balanced output between the right and left ventricles and maintaining an equilibrium of blood flow in the circulatory system.

Explanation:

Each graph represents the relationship between ventricular end-diastolic volume and cardiac output in a healthy adult individual at rest (solid line) and upon exercise (dotted line).

• Graph 1 shows an increasing solid line and an even higher increasing dotted line. This suggests that at rest, as the ventricular end-diastolic volume increases, the cardiac output also increases. The increase is more pronounced during exercise, indicating enhanced cardiac performance with exercise, which is consistent with the Frank-Starling law. This law states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart.
• Graph 2 also shows increasing lines, but the dotted line for exercise starts to plateau. This could imply that there is a limit to how much exercise can increase cardiac output before it reaches a maximum capacity, possibly due to the heart's limited ability to increase its rate and force of contraction.
• Graph 3 indicates a slight increase in cardiac output with an increase in ventricular end-diastolic volume at rest. However, the dotted line for exercise shows a decrease beyond a certain volume. This is not typical of normal cardiac physiology and suggests a pathophysiological condition such as cardiac tamponade or heart failure where increased heart volume doesn't translate to increased output due to the heart's inability to pump effectively.
• Graph 4 depicts a constant cardiac output regardless of the ventricular end-diastolic volume both at rest and during exercise, which is not physiologically normal for a healthy individual. This could represent a scenario of severe heart dysfunction where the heart's output is fixed and cannot respond to changes in volume or the demands of exercise.

Conclusion:

The most physiologically accurate graph for a healthy individual both at rest and upon exercise is likely the first graph. It demonstrates the normal behavior of the heart under both conditions according to the Frank-Starling mechanism.

The correct answer is Option 2 i.e. B and C

Explanation:-

A. The decrease in arterial pressure after hemorrhage causes inhibition of sympathetic-vasoconstrictor system.

• Incorrect. The decrease in arterial pressure after hemorrhage would actually stimulate the sympathetic-vasoconstrictor system, leading to vasoconstriction in an attempt to increase arterial pressure and maintain perfusion of vital organs.

B. After hemorrhage, the angiotensin II level in blood is increased which causes increased re-absorption of Na⁺ in renal tubules.

• Correct. Hemorrhage leads to a reduction in blood volume and blood pressure, which can stimulate the renin-angiotensin-aldosterone system. The increased production of angiotensin II promotes renal reabsorption of Na⁺, helping to retain water (via osmosis) and increase blood volume.

C. The increased secretion of vasopressin after hemorrhage increases water reabsorption in the kidneys.

• Correct. Vasopressin (antidiuretic hormone or ADH) secretion increases in response to a decrease in blood volume or blood pressure to enhance water reabsorption in the kidneys, effectively concentrating the urine and expanding the circulating blood volume.

D. After hemorrhage, the reduced secretion of epinephrine and norepinephrine from the adrenal medulla induces decreased peripheral resistance.

• Incorrect. The opposite occurs; after hemorrhage, there's an increased secretion of epinephrine and norepinephrine from the adrenal medulla, which contributes to increasing peripheral resistance (via vasoconstriction) and cardiac output, as part of the body's compensatory response to maintain blood pressure and perfusion.

E. In hemorrhage, the central nervous system ischemic response elicits sympathetic inhibition.

• Incorrect. The central nervous system ischemic response, triggered by significantly reduced cerebral perfusion, actually results in a potent activation (not inhibition) of the sympathetic nervous system to maximize blood flow to critical organs, particularly the brain and heart, by increasing heart rate, contractility, and peripheral vasoconstriction.

Additional InformationB. Angiotensin II and Renal Reabsorption of Sodium
Following hemorrhage, the body experiences a decline in blood volume and blood pressure. This reduction is sensed by the juxtaglomerular cells of the kidneys, which respond by releasing renin into the bloodstream. Renin acts on angiotensinogen (produced by the liver) to produce angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE), primarily in the capillaries of the lungs.Angiotensin II has several crucial effects aimed at restoring blood volume and pressure:

• Vasoconstriction: It directly causes constriction of small arteries (arterioles), increasing systemic vascular resistance and blood pressure.
• Stimulation of Aldosterone Secretion: Angiotensin II stimulates the adrenal cortex to release aldosterone, a hormone that increases sodium reabsorption in the distal nephrons of the kidneys. As sodium is reabsorbed, water follows (due to osmotic forces), leading to increased retention of water, expanding blood volume, and improving circulatory status.
• Thirst Stimulation: Angiotensin II can stimulate the thirst center in the brain, prompting water intake to further aid in restoring blood volume.

C. Increased secretion of Vasopressin (Antidiuretic Hormone, ADH)
Vasopressin plays a pivotal role in the body’s response to hemorrhage. Its primary functions include:

• Water Reabsorption in the Kidneys: Vasopressin increases the permeability of the kidney's collecting ducts to water, enhancing water reabsorption back into the bloodstream, which helps to concentrate the urine and minimize water loss, thereby conserving blood volume.
• Vasoconstriction: At high concentrations, vasopressin can cause vasoconstriction, which also helps in increasing blood pressure.
• Vasopressin is released in response to increased plasma osmolality (such as would be caused by the loss of blood volume), as well as low blood pressure sensed by baroreceptors. Its secretion following hemorrhage supports the body's efforts to conserve water and reinforce blood volume, while also contributing to the restoration of vascular tone.

Conclusion:

The body's response to hemorrhagic shock involves intricate physiological mechanisms aimed at compensating for the loss of blood volume and restoring hemodynamic stability. These mechanisms include hormonal responses that reabsorb water, retain sodium, and increase vascular resistance. Angiotensin II and vasopressin are key players in these compensatory responses, orchestrating renal adjustments, stimulating thirst, and contributing to vasoconstriction to support the recovery process. Such integrated bodily responses are critical for survival in the face of acute blood loss. Therefore, the correct combination of statements regarding the recovery from hemorrhagic shock is: B and C.

Key Points

• SA nodal action potential refers to the electrical activity that happens within the Sinoatrial (SA) node, a group of cells positioned in the right atrium of the heart.
• The SA node serves as the heart's natural pacemaker, determining its rhythm. It does so by continuously generating action potentials.
• The rate at which these action potentials are generated determines the heart rate, which can be influenced by the nerves that supply the SA node.

• Phase 0:
  • This is the depolarization phase.
  • During this phase, the inside of the cell becomes positively charged, leading to an action potential.
• Phase 3:
  • This marks the repolarization phase when the membrane returns to its resting potential.
  • In this phase, voltage-gated potassium channels open, leading to an outward current of potassium ions.
  • This causes the interior of the cell to become more negatively charged again.
• Phase 4:
  • This is the phase of spontaneous depolarization, also known as the pacemaker potential.
  • During this phase, the cell spontaneously generates an action potential without any need for neural input.
  • When the membrane potential reaches the threshold between -40 and -30 mV, it triggers the next action potential
• It's important to note that, unlike other excitable cells, the SA nodal cells do not have a stable resting potential and the phases usually referred to as Phase 1 and Phase 2 in other action potentials are absent.

Explanation:

• The SA nodal cells have an unstable resting membrane potential that spontaneously depolarizes due to a pacemaker potential.
• This is caused by the “funny” Na⁺ current and a decrease in the conductance of the inward rectifier K⁺ channel.

Hence the correct answer is option 2

Key Points

Neural regulation of the cardiac cycle 

• Neural regulation of the cardiac cycle primarily involves two arms of the autonomic nervous system—the parasympathetic nervous system and the sympathetic nervous system.
• Both these systems help regulate the heart's rate and rhythm, its contractility, and the diameter of coronary vessels, thereby playing a key role in the heart's functional response to changing physiological conditions.

• The sympathetic nervous system typically increases heart rate, strengthens the force of contraction, and dilates coronary vessels to enhance blood flow through the coronary circulation.
• This can occur as a reflex response to peripheral stimuli or due to input from higher centers of the brain, an aspect referred to as "central command".

• The parasympathetic division largely via the vagus nerve, sends signals to decrease the heart rate, with negligible effects on contractility and vessel diameter.
• Specific neural structures are implicated in the direct control of cardiac function.
• Neurons of the anterior insula, anterior cingulate cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial nucleus, and several regions of the medulla influence the heart's function on a beat-to-beat basis.
• These are key regions involved in emotional responses, stress responses, and homeostatic reflexes.
• Additionally, the heart possesses its intrinsic nervous system comprising intracardiac neurons, which play a critical role in modulating the pacemaker activity of the sinoatrial and atrioventricular nodes thus further contributing to the fine-tuning of cardiac rhythm.

Explanation:

• The pacemaker cells of sinoatrial node (SA node) are inhibited by the stimulation of vagus nerve (parasympathetic nervous system) as released acetyl choline signaling leads to activation of outward K causes hyperpolarization of pacemaker cells.
• Sympathetic nerves increases heart rate due to ventricles from the pulmonary trunk on the right and the aorta on the left. 

Hence the correct answer is option 4

Concept:

• Pacemaker cells in the sinoatrial (SA) node are responsible for controlling the speed and rhythm of the heartbeat.
• The vagus nerve, which is part of the parasympathetic nervous system, influences the functioning of these cells.
• When the vagus nerve is activated, it releases the neurotransmitter acetylcholine, which binds to receptors on the pacemaker cells.
• This causes potassium channels to open, leading to hyperpolarization (making the cell membrane more negative) reducing the pace of spontaneous depolarization, and therefore slowing down the heart rate.
• So, the pacemaker cells of the SA node are indeed inhibited by the activation of the vagus nerve.
• acetylcholine, upon release from parasympathetic nerves, binds to muscarinic receptors on the heart's pacemaker cells.
• This leads to the opening of G-protein-gated inwardly rectifying potassium channels (GIRKs, also known as the 'IKAch' current).
• When these channels open, they allow potassium ions to exit the cells, which hyperpolarizes the cell (makes it more negative inside), slowing the rate of depolarization and therefore reducing heart rate.
• So, the action of acetylcholine causes hyperpolarization, not depolarization, of pacemaker cells.
•  The sympathetic nervous system increases heart rate.
• This is achieved by the release of norepinephrine (or noradrenaline) from the sympathetic nerve terminals.
• Noradrenaline binds to beta-1 adrenergic receptors on the cells of the SA node.
• Upon activation, these receptors stimulate a cyclic AMP pathway, leading to an increase in the opening of T-type and L-type Ca2⁺ channels as well as funny channels (f-channels).
• An increase in these ion currents speeds up the rate of the cell's spontaneous depolarization, increasing the heart rate.
• The action potentials in the SA and AV nodes are primarily determined by changes in slow inward Ca2⁺ (via L-type calcium channels) and slow outward K⁺ currents.
• These currents create a steady pacemaker potential that slowly drives the membrane potential toward the threshold potential.
• When the threshold is reached, an action potential fires, which results in a heartbeat.
• The action potentials in these nodes do not have a steady resting potential and use calcium - instead of sodium - for the rising phase of the action potential, which distinguishes them from other cardiac tissue and makes the heart's rhythm auto-regulative

Explanation 

Statement A. This statement is incorrect. In fact, it's the opposite. The vagus nerve is part of the parasympathetic nervous system, which lowers the heart rate. It releases acetylcholine, which slows the rate of spontaneous depolarization in the sinoatrial node and therefore slows the heart rate1.

The correct answer is Option 4 i.e. D and E

Concept:

• Rhythmically discharging cells have a membrane potential  that, after each impulse, declines to the firing level. Thus, this  prepotential or pacemaker potential triggers  the next impulse.
• At the peak of each impulse, IK begins and  brings about repolarization. IK then declines, and a channel  that can pass both Na⁺ and K⁺ is activated.
• Because this channel is activated following hyperpolarization, it is referred to as  an “h” channel; however, because of its unusual (funny) activation this has also been dubbed an “f” channel.
• As Ih increases, the membrane begins to depolarize, forming the first part  of the prepotential. Ca²⁺ channels then open. These are of two  types in the heart, the T (for transient) channels and the L (for long-lasting) channels.
• When the cholinergic vagal fibers to nodal tissue are stimulated, the membrane becomes hyperpolarized and the slope of  the prepotentials is decreased because the acetylcholine released at the nerve endings increases the K⁺ conductance of nodal tissue.
• This action is mediated by M2 muscarinic receptors, which, via the βγ subunit of a G protein, open a special set of K⁺ channels.
• The resulting IKAch slows the depolarizing effect of Ih. In addition, activation of the M2 receptors decreases cyclic adenosine 3', 5'-monophosphate  (cAMP) in the cells, and this slows the opening of the Ca²⁺ channels.
• The result is a decrease in firing rate. Strong vagal stimulation may abolish spontaneous discharge for some time.
• Conversely, stimulation of the sympathetic cardiac nerves  speeds the depolarization effect of Ih, and the rate of spontaneous discharge increases.

​Explanation:

Statement A: Incorrect

• When the cholinergic vagal fibers to nodal tissue are stimulated, the membrane becomes hyperpolarized.

Statement B: Incorrect

• The slope of the pacemaker potential is decreased.

Statement C: Incorrect

• Acetylcholine released at the nerve endings increases the K⁺ conductance of nodal tissue.

Statement D: Correct

• By M2 muscarinic receptors, which, via the βγ subunit of a G protein, open a special set of K⁺ channels. The resulting IKAch slows the depolarizing effect of Ih.

Statement E: Correct

• Activation of the M2 receptors decreases cyclic adenosine 3',5'-monophosphate  (cAMP) in the cells, and this slows the opening of the Ca²⁺  channels. The result is a decrease in firing rate. 

Hence statement D and E is correct.

Additional Information

• Norepinephrine secreted by the sympathetic endings binds to β1 receptors, and the resulting increase in intracellular cAMP facilitates the opening of L channels, increasing ICa and the rapidity of the  depolarization phase of the impulse.
• The rate of discharge of the SA node and other nodal tissue is influenced by temperature and by drugs.
• The discharge frequency is increased when the temperature rises, and this may contribute to the tachycardia associated with fever.
• Digitalis depresses nodal tissue and exerts an effect like that of vagal stimulation, particularly on the AV node.

Concept

• Atrial natriuretic peptide (ANP) is the first hormone isolated from the heart as a potent natriuretic, diuretic, and hypotensive factor.
• ANP has an intramolecular ring structure connected by two cysteine residues, and N-terminal and C-terminal extensions from it.
• ANP is present in mammals, amphibians, and bony fish, but absent in birds, reptiles, cartilaginous fish, and cyclostomes.
• ANP induces profound natriuresis, diuresis, hypotension, and the inhibition of aldosterone secretion in mammals and amphibians.

Explanation:

Fig 1: Atrial natriuretic peptide effects

• Atrial natriuretic peptide (ANP) is a small peptide secreted by the heart upon atrial stretch and high systemic blood pressure.
• The acute effects of this potent, short-lived peptide include increased glomerular filtration and increased renal excretion of sodium and water.
• These changes may serve to decrease blood volume and subsequently lower blood pressure.
• Given its unique pleiotropic functions in promoting natriuresis, diuresis and vasodilation and inhibiting aldosterone and renin secretion, ANP represents a promising drug candidate for cardiovascular disease such as heart failure.

Correct option: 3) It acts to increase blood pressure

Concept:

• The autonomic nervous system (ANS) is the component of the peripheral nervous system that controls cardiac muscle contraction, visceral activities, and glandular functions of the body.
• The sympathetic nervous system releases noradrenaline while the parasympathetic nervous system releases acetylcholine (ACh). Sympathetic stimulation increases heart rate and myocardial contractility.

​Explanation:

Fig 1: Sympathetic nerves and cardiac myocyte

• The whole mammalian heart is innervated by Sympathetic nerves (SNs), which enter the heart from the epicardium and extend their processes throughout the myocardial interstitium, running parallel to capillary vessels.
• In Sympathetic neurotransmission, the arrival of an action potential in the synaptic nerve terminal leads to Ca2+ entry via voltage-gated Ca2+ channels.
• This triggers exocytosis of noradrenaline into the synaptic clefts, which acts on the β1 adrenoreceptor, altering myocyte behavior by opening L-calcium channels and signaling cascade in the myocyte.

​

​hence the correct answer is option 4