Topic: Oxygen Transport and Hemoglobin Dynamics; Subtopic: Oxygen–Hemoglobin Dissociation Curve
Keyword Definitions:
• Oxygen–Hemoglobin Dissociation Curve: A graph showing the relationship between partial pressure of oxygen (PO₂) and hemoglobin saturation.
• Plateau Phase: The flat upper part of the curve where large changes in PO₂ cause little change in hemoglobin saturation.
• P50: The PO₂ at which hemoglobin is 50% saturated; indicates affinity for oxygen.
• Bohr Effect: The effect of pH and CO₂ concentration on hemoglobin’s oxygen affinity.
• Oxyhemoglobin: Hemoglobin bound with oxygen molecules.
Lead Question – 2014
Plateau of oxygen–hemoglobin dissociation curve signifies?
a) No oxygen is available for binding to Hb
b) No Hb molecule is available to bind with O₂
c) All oxygen is released to tissues
d) None of the above
Answer: b) No Hb molecule is available to bind with O₂
Explanation: The plateau region indicates that hemoglobin molecules are nearly fully saturated with oxygen. Even if PO₂ increases, saturation changes little, showing that most binding sites are already occupied. This provides a safety margin ensuring sufficient oxygen carriage even if alveolar PO₂ falls. Thus, option (b) is correct.
1. What causes the sigmoid shape of the oxygen–hemoglobin dissociation curve?
a) Cooperative binding of oxygen to hemoglobin
b) Linear binding of oxygen
c) Random oxygen interaction
d) pH changes only
Answer: a) Cooperative binding of oxygen to hemoglobin
Explanation: The sigmoid shape results from hemoglobin’s cooperative binding; binding of one O₂ molecule increases affinity for the next. This property allows efficient loading in lungs and unloading in tissues. The steep portion helps oxygen release with small PO₂ changes, enhancing tissue oxygen delivery efficiency under varying physiological demands.
2. Which factor shifts the oxygen–hemoglobin dissociation curve to the right?
a) Decreased temperature
b) Increased pH
c) Decreased 2,3-BPG
d) Increased CO₂ tension
Answer: d) Increased CO₂ tension
Explanation: Elevated CO₂, increased temperature, and reduced pH lower oxygen affinity, shifting the curve rightward (Bohr effect). This facilitates oxygen unloading in metabolically active tissues. Such rightward shift ensures that tissues receive more oxygen when CO₂ and acidity levels are high due to enhanced metabolism.
3. In anemia, how does the oxygen–hemoglobin curve change?
a) Shift to the right
b) Shift to the left
c) No shift, but lower oxygen content
d) Both right shift and lower oxygen content
Answer: c) No shift, but lower oxygen content
Explanation: In anemia, hemoglobin concentration decreases, so total oxygen-carrying capacity falls. However, affinity remains unchanged, so the curve shape and position are largely unaffected. The arterial oxygen content decreases, impairing tissue oxygenation despite normal saturation percentage readings, emphasizing importance of hemoglobin quantity in oxygen transport.
4. Which factor increases hemoglobin’s affinity for oxygen?
a) Increased CO₂
b) Decreased pH
c) Decreased temperature
d) Increased 2,3-BPG
Answer: c) Decreased temperature
Explanation: Lower temperature enhances hemoglobin’s affinity for oxygen, shifting the dissociation curve leftward. This occurs in lungs and cold conditions, favoring oxygen loading. Conversely, higher temperature decreases affinity, aiding oxygen release in metabolically active warm tissues. Such physiological adaptation ensures appropriate oxygen supply based on tissue metabolic activity.
5. Clinical Case: A mountain climber at 4000 m has increased 2,3-BPG. What happens to the oxygen–hemoglobin curve?
a) Shift to left
b) Shift to right
c) No change
d) Becomes linear
Answer: b) Shift to right
Explanation: At high altitude, hypoxia stimulates increased 2,3-BPG production in RBCs. This binds to deoxygenated hemoglobin, reducing affinity and shifting the curve rightward. The shift enhances oxygen release to tissues despite reduced ambient oxygen pressure, representing a key adaptation to maintain tissue oxygenation under hypoxic conditions.
6. Clinical Case: A newborn shows higher oxygen affinity than the mother. Which hemoglobin is responsible?
a) HbA
b) HbF
c) HbS
d) HbA₂
Answer: b) HbF
Explanation: Fetal hemoglobin (HbF) has greater affinity for oxygen than adult hemoglobin (HbA), facilitating oxygen transfer from maternal to fetal blood. HbF binds oxygen tightly, shifting the dissociation curve left. After birth, HbF gradually replaces HbA as the infant adapts to independent oxygenation via lungs.
7. Clinical Case: A patient with carbon monoxide poisoning has reduced oxygen delivery. Why?
a) Increased oxygen dissociation
b) CO binds to Hb decreasing available sites
c) Increased 2,3-BPG
d) Rightward shift of curve
Answer: b) CO binds to Hb decreasing available sites
Explanation: Carbon monoxide binds to hemoglobin with high affinity, blocking oxygen binding sites. It also shifts the oxygen–hemoglobin dissociation curve left, reducing oxygen release to tissues. This results in severe tissue hypoxia despite normal arterial PO₂, making prompt oxygen therapy essential for recovery.
8. What happens to P50 in case of rightward shift of the oxygen–hemoglobin dissociation curve?
a) Decreases
b) Increases
c) Remains same
d) Becomes zero
Answer: b) Increases
Explanation: A rightward shift implies decreased oxygen affinity; more oxygen tension is needed for 50% saturation, hence P50 increases. Conditions like acidosis, hyperthermia, and elevated 2,3-BPG produce this effect. This mechanism facilitates oxygen unloading at tissues, improving metabolic oxygen utilization during physiological stress.
9. Clinical Case: In septic shock, the oxygen–hemoglobin dissociation curve shifts to the right. Why?
a) Hypothermia
b) Lactic acidosis
c) Decreased CO₂
d) Hypocapnia
Answer: b) Lactic acidosis
Explanation: In septic shock, tissue hypoperfusion leads to anaerobic metabolism and lactic acid accumulation. The resulting acidosis reduces hemoglobin’s oxygen affinity, shifting the curve right. This helps release oxygen to hypoxic tissues but may not fully compensate for impaired perfusion, necessitating medical management for tissue oxygenation restoration.
10. Clinical Case: A patient with hypothermia shows altered oxygen–hemoglobin binding. Which shift occurs?
a) Rightward shift
b) Leftward shift
c) No change
d) Curve flattens
Answer: b) Leftward shift
Explanation: Hypothermia increases hemoglobin’s oxygen affinity, shifting the curve left. This reduces oxygen unloading to tissues, worsening hypoxia despite normal oxygen saturation. The leftward shift also occurs with decreased CO₂ or alkalosis. Understanding this helps guide oxygen therapy and temperature correction in critically ill hypothermic patients.
Chapter: Respiratory Physiology; Topic: Oxygen Transport; Subtopic: Myoglobin vs Hemoglobin Oxygen Dissociation Curves
Keyword Definitions:
• Oxygen Dissociation Curve: A graphical representation of the relationship between partial pressure of oxygen (PO₂) and percentage saturation of hemoglobin or myoglobin.
• Myoglobin: A monomeric protein in muscle cells that binds oxygen tightly and shows a hyperbolic dissociation curve.
• Hemoglobin: A tetrameric protein in RBCs showing cooperative binding with a sigmoid dissociation curve.
• Cooperative Binding: A phenomenon where binding of one O₂ molecule increases the affinity for subsequent O₂ molecules.
• P50: The partial pressure of oxygen at which a pigment (Hb or Mb) is 50% saturated.
Lead Question – 2014
The oxygen dissociation curve of myoglobin & hemoglobin is different due to?
a) Hb can bind to 2 oxygen molecules
b) Cooperative binding in Hb
c) Myoglobin has little oxygen affinity
d) Hemoglobin follows a hyperbolic curve
Answer: b) Cooperative binding in Hb
Explanation: Hemoglobin exhibits cooperative binding—binding of one oxygen molecule enhances affinity for the next—producing a sigmoid curve. Myoglobin, being monomeric, binds a single O₂ molecule without cooperativity, yielding a hyperbolic curve. This allows myoglobin to store oxygen efficiently in muscles and hemoglobin to release oxygen effectively in tissues.
1. Which curve represents myoglobin’s oxygen binding property?
a) Sigmoid curve
b) Hyperbolic curve
c) Linear curve
d) Stepped curve
Answer: b) Hyperbolic curve
Explanation: Myoglobin’s oxygen dissociation curve is hyperbolic because it lacks cooperative binding. Being monomeric, it binds oxygen independently. This characteristic allows myoglobin to maintain a high affinity for oxygen, enabling it to store oxygen and supply it during muscle activity when oxygen demand is high and hemoglobin unloading occurs.
2. The sigmoid shape of the hemoglobin oxygen dissociation curve is due to?
a) Bohr effect
b) Cooperative binding
c) 2,3-BPG effect
d) Carbon monoxide binding
Answer: b) Cooperative binding
Explanation: Hemoglobin’s four subunits interact in such a way that the binding of one O₂ molecule increases the affinity of the remaining sites. This inter-subunit cooperativity creates the sigmoid shape of the oxygen dissociation curve, which is essential for efficient oxygen loading in lungs and unloading in peripheral tissues.
3. Myoglobin serves as an oxygen reservoir mainly in?
a) Brain
b) Liver
c) Skeletal and cardiac muscles
d) Lungs
Answer: c) Skeletal and cardiac muscles
Explanation: Myoglobin, located in muscle cells, acts as an oxygen reserve, especially during intense exercise or hypoxia. It binds oxygen strongly and releases it only when tissue oxygen tension is low. This ensures continuous ATP production even when blood oxygen supply from hemoglobin is temporarily reduced during muscle exertion.
4. Which protein shows a higher oxygen affinity at low PO₂?
a) Hemoglobin
b) Myoglobin
c) Both equal
d) Depends on CO₂ concentration
Answer: b) Myoglobin
Explanation: Myoglobin has a much higher oxygen affinity than hemoglobin, particularly at low PO₂ levels. This property allows it to extract oxygen from hemoglobin in capillaries and deliver it to mitochondria for oxidative metabolism, making it vital for oxygen storage in skeletal and cardiac muscle tissues.
5. Clinical Case: During strenuous exercise, myoglobin’s role is to?
a) Deliver oxygen to hemoglobin
b) Store oxygen for short-term muscle use
c) Convert CO₂ to bicarbonate
d) Facilitate hemoglobin binding
Answer: b) Store oxygen for short-term muscle use
Explanation: During intense exercise, tissue PO₂ falls, and myoglobin releases stored oxygen to sustain ATP production. This supports muscle contraction until blood flow increases. Myoglobin’s high affinity allows it to act as a rapid oxygen buffer, ensuring efficient muscle function during transient hypoxia or anaerobic transitions.
6. Clinical Case: A patient with myoglobinuria shows red urine after muscle injury. The cause is?
a) Hemoglobin leak from RBCs
b) Myoglobin release from damaged muscles
c) Porphyrin metabolism defect
d) Excess bilirubin excretion
Answer: b) Myoglobin release from damaged muscles
Explanation: Muscle trauma or rhabdomyolysis releases myoglobin into circulation. Myoglobin passes into urine, causing reddish-brown discoloration and potential renal toxicity. Early hydration and management are essential to prevent acute kidney injury. The condition reflects severe muscle breakdown rather than hemolytic causes of red urine.
7. In fetal circulation, oxygen is transferred from maternal to fetal blood because?
a) Fetal Hb has lower affinity
b) Fetal Hb has higher affinity
c) Maternal Hb binds more strongly
d) Equal affinity in both
Answer: b) Fetal Hb has higher affinity
Explanation: Fetal hemoglobin (HbF) has a higher oxygen affinity than adult hemoglobin (HbA), producing a left-shifted oxygen dissociation curve. This allows efficient transfer of oxygen from mother to fetus across the placenta even when maternal oxygen tension is relatively low, ensuring fetal tissue oxygenation during development.
8. What is the primary physiological advantage of hemoglobin’s sigmoid oxygen dissociation curve?
a) Allows constant oxygen delivery
b) Enhances unloading in tissues while maintaining loading in lungs
c) Reduces oxygen binding
d) Prevents oxygen toxicity
Answer: b) Enhances unloading in tissues while maintaining loading in lungs
Explanation: The sigmoid shape allows hemoglobin to load oxygen efficiently in lungs (high PO₂) and unload readily in tissues (low PO₂). Small drops in tissue PO₂ result in large oxygen release, optimizing tissue oxygenation without compromising oxygen loading during pulmonary circulation, ensuring balance between transport and delivery.
9. Clinical Case: A diver holds breath for long periods; which pigment supports oxygen supply in muscles?
a) Hemoglobin
b) Myoglobin
c) Cytochrome
d) Carboxyhemoglobin
Answer: b) Myoglobin
Explanation: Myoglobin acts as an oxygen reservoir during apnea or prolonged breath-holding. Its high affinity ensures oxygen availability when arterial PO₂ drops. Marine mammals like seals and whales have high myoglobin content, allowing extended underwater endurance without hypoxia. This adaptation minimizes dependence on pulmonary oxygen stores.
10. Clinical Case: In a patient with severe anemia, oxygen transport is affected because?
a) Myoglobin stores are depleted
b) Reduced hemoglobin concentration limits oxygen carriage
c) Myoglobin stops oxygen binding
d) CO₂ increases affinity for oxygen
Answer: b) Reduced hemoglobin concentration limits oxygen carriage
Explanation: In anemia, hemoglobin levels fall, lowering blood oxygen-carrying capacity. Despite normal oxygen saturation and normal myoglobin function, tissue oxygenation declines. This results in fatigue and dyspnea on exertion. The oxygen dissociation curve remains unchanged, but total oxygen content and delivery are significantly reduced.
Chapter: Cardiovascular Physiology; Topic: Blood Pressure Regulation; Subtopic: Compensatory Mechanisms in Acute Hemorrhage
Keyword Definitions:
• Acute Hemorrhage: Rapid loss of blood volume leading to decreased venous return and cardiac output.
• Baroreceptor Reflex: A rapid compensatory mechanism that maintains blood pressure during acute blood loss.
• Sympathetic Activation: Response that increases heart rate, contractility, and vasoconstriction to restore blood flow.
• Peripheral Resistance: Opposition to blood flow in vessels, increases during hemorrhage to maintain pressure.
• Cardiac Output: The amount of blood pumped by the heart per minute, determined by heart rate and stroke volume.
Lead Question – 2014
Compensatory mechanism in acute hemorrhage?
a) Decreased myocardial contractility
b) Decreased heart rate
c) Increased heart rate
d) Increased respiratory rate
Answer: c) Increased heart rate
Explanation: In acute hemorrhage, blood volume and arterial pressure fall, stimulating baroreceptors to activate the sympathetic system. This causes tachycardia, vasoconstriction, and increased contractility to maintain cardiac output and perfusion of vital organs. Simultaneously, venoconstriction enhances venous return, while renal mechanisms later restore blood volume via fluid retention.
1. Which reflex is primarily responsible for maintaining blood pressure immediately after hemorrhage?
a) Chemoreceptor reflex
b) Baroreceptor reflex
c) Bainbridge reflex
d) Bezold-Jarisch reflex
Answer: b) Baroreceptor reflex
Explanation: The baroreceptor reflex senses reduced stretch in carotid sinus and aortic arch during blood loss, decreasing parasympathetic and increasing sympathetic activity. This elevates heart rate and peripheral resistance, rapidly restoring mean arterial pressure to maintain blood supply to critical organs like the brain and heart during acute hemorrhage.
2. During acute hemorrhage, which hormone plays a key role in long-term volume restoration?
a) Insulin
b) Vasopressin (ADH)
c) Glucagon
d) Epinephrine
Answer: b) Vasopressin (ADH)
Explanation: Vasopressin, secreted by the posterior pituitary, promotes water reabsorption from the kidneys to restore plasma volume. It also causes vasoconstriction, helping to raise arterial pressure. This long-term response complements immediate baroreceptor-mediated mechanisms that act during early stages of hemorrhage to maintain perfusion and stabilize hemodynamics.
3. Clinical Case: A trauma patient shows tachycardia and cold clammy skin. What mechanism explains this?
a) Increased parasympathetic discharge
b) Peripheral vasoconstriction due to sympathetic activation
c) Bradycardia due to vagal stimulation
d) Reduced cardiac output from vasodilation
Answer: b) Peripheral vasoconstriction due to sympathetic activation
Explanation: Following acute blood loss, sympathetic stimulation causes vasoconstriction in skin and splanchnic vessels to preserve blood flow to the brain and heart. This produces cold, pale skin and weak pulses, classic signs of hypovolemic shock. These compensatory mechanisms act to stabilize mean arterial pressure.
4. In acute hemorrhage, renal response includes?
a) Decreased renin secretion
b) Increased sodium excretion
c) Activation of RAAS
d) Inhibition of aldosterone
Answer: c) Activation of RAAS
Explanation: The renin-angiotensin-aldosterone system (RAAS) activates when renal perfusion drops. Renin release leads to angiotensin II formation, causing vasoconstriction and aldosterone secretion. Aldosterone promotes sodium and water reabsorption, increasing blood volume and pressure. This mechanism ensures long-term compensation for blood loss following hemorrhage.
5. Which of the following changes occurs during compensated hemorrhagic shock?
a) Decreased sympathetic tone
b) Increased heart rate and contractility
c) Peripheral vasodilation
d) Decreased systemic resistance
Answer: b) Increased heart rate and contractility
Explanation: In compensated hemorrhagic shock, the sympathetic system dominates, leading to tachycardia and stronger myocardial contractions. This helps sustain cardiac output despite low blood volume. Peripheral vasoconstriction increases systemic vascular resistance, maintaining perfusion pressure to vital organs like the brain and myocardium until volume replacement occurs.
6. Clinical Case: After 30% blood loss, a patient’s BP is low but heart rate is high. This is due to?
a) Increased vagal tone
b) Sympathetic compensation
c) Parasympathetic dominance
d) Myocardial depression
Answer: b) Sympathetic compensation
Explanation: Significant blood loss decreases venous return and stroke volume. The baroreceptor reflex triggers sympathetic stimulation, increasing heart rate and contractility to compensate. Although cardiac output remains reduced, this mechanism delays progression to decompensated shock and helps maintain cerebral and coronary perfusion temporarily during acute hemorrhage.
7. In the early stage of hemorrhage, which variable remains relatively constant?
a) Venous return
b) Stroke volume
c) Cardiac output
d) Arterial pressure in vital organs
Answer: d) Arterial pressure in vital organs
Explanation: Initially, compensatory vasoconstriction redistributes blood flow from nonessential organs (skin, kidneys, gut) to vital organs (brain, heart). Despite overall decreased blood volume, perfusion to these areas is maintained. This selective vasoconstriction and cardiac acceleration protect vital function during early compensated stages of hemorrhagic shock.
8. Clinical Case: In a patient with severe blood loss, which finding suggests decompensation?
a) Rapid, weak pulse
b) Normal urine output
c) Warm extremities
d) Maintained mental alertness
Answer: a) Rapid, weak pulse
Explanation: A rapid, thready pulse indicates low stroke volume and declining cardiac output, hallmarks of decompensated shock. As compensatory mechanisms fail, perfusion to critical organs drops, causing hypotension, confusion, and oliguria. Immediate fluid resuscitation and blood replacement are required to restore hemodynamic stability and prevent organ failure.
9. Following acute hemorrhage, which blood gas change is likely to occur?
a) Respiratory alkalosis
b) Metabolic acidosis
c) Respiratory acidosis
d) Metabolic alkalosis
Answer: b) Metabolic acidosis
Explanation: Decreased tissue perfusion during hemorrhage leads to anaerobic metabolism, resulting in lactic acid accumulation and metabolic acidosis. The body may initially attempt to compensate with hyperventilation (respiratory alkalosis), but persistent hypoperfusion worsens acidosis. Correction requires volume replacement and restoration of oxygen delivery to tissues.
10. Clinical Case: A post-surgical patient with blood loss shows low BP, high HR, and reduced urine output. Diagnosis?
a) Cardiogenic shock
b) Hypovolemic shock
c) Septic shock
d) Neurogenic shock
Answer: b) Hypovolemic shock
Explanation: Blood loss decreases circulating volume, leading to reduced venous return, cardiac output, and urine output. The sympathetic system increases heart rate and vasoconstriction as compensation. Without prompt volume resuscitation, hypovolemia progresses to irreversible shock. Monitoring urine output helps assess renal perfusion and effectiveness of fluid therapy.
Chapter: Cardiovascular Physiology; Topic: Jugular Venous Pulse (JVP); Subtopic: Waves of JVP and their significance
Keyword Definitions:
Jugular Venous Pulse (JVP): The oscillation of blood in the internal jugular vein that reflects right atrial pressure changes.
‘v’ wave: Represents passive filling of the right atrium during late systole when the tricuspid valve remains closed.
Tricuspid valve: Valve between the right atrium and right ventricle preventing backflow during systole.
Atrial contraction: Causes the ‘a’ wave in JVP due to blood flow into the right ventricle.
Right atrium: The upper chamber of the heart that receives deoxygenated blood from systemic circulation.
Lead Question – 2014
‘v’ Wave in JVP is due to?
a) Right atrial contraction
b) Left atrial contraction
c) Right atrial relaxation
d) Closure of tricuspid valve
Answer & Explanation: (d) Closure of tricuspid valve.
The ‘v’ wave in JVP occurs due to venous filling of the right atrium against a closed tricuspid valve during ventricular systole. As the right atrium fills, pressure rises creating the ‘v’ wave, which peaks just before the tricuspid valve opens again. It reflects atrial filling pressure and ventricular-atrial compliance.
1. In JVP tracing, the 'a' wave corresponds to:
a) Atrial filling
b) Atrial contraction
c) Ventricular relaxation
d) Atrial emptying
Answer & Explanation: (b) Atrial contraction. The 'a' wave in JVP occurs due to right atrial contraction just before ventricular systole, causing transient pressure elevation in the jugular venous system. It disappears in atrial fibrillation where atrial contraction is absent, making it a diagnostic marker for rhythm abnormalities.
2. Absence of ‘a’ wave in JVP is seen in:
a) Atrial fibrillation
b) Tricuspid regurgitation
c) Complete heart block
d) Pulmonary hypertension
Answer & Explanation: (a) Atrial fibrillation. Since atrial contraction is absent in atrial fibrillation, the ‘a’ wave does not occur. Instead, irregular undulating waves appear. The finding is an important clue in diagnosing AF clinically by neck vein observation in cardiac patients.
3. Giant ‘v’ waves in JVP are characteristic of:
a) Tricuspid stenosis
b) Tricuspid regurgitation
c) Pulmonary stenosis
d) Mitral regurgitation
Answer & Explanation: (b) Tricuspid regurgitation. During systole, backflow of blood into the right atrium causes a large rise in atrial pressure producing giant ‘v’ waves. These waves are prominent, occur with a systolic murmur, and help distinguish tricuspid regurgitation from other valvular lesions clinically.
4. The ‘c’ wave in JVP is due to:
a) Bulging of tricuspid valve during isovolumetric contraction
b) Closure of pulmonary valve
c) Rapid ventricular filling
d) Atrial systole
Answer & Explanation: (a) Bulging of tricuspid valve during isovolumetric contraction. The ‘c’ wave occurs when right ventricular pressure rises during early systole causing the tricuspid valve to bulge into the atrium, transiently raising venous pressure seen as the ‘c’ wave in JVP tracing.
5. Prominent ‘a’ wave in JVP is seen in:
a) Atrial fibrillation
b) Pulmonary stenosis
c) Tricuspid regurgitation
d) Right ventricular failure
Answer & Explanation: (b) Pulmonary stenosis. Due to resistance to right ventricular filling, the right atrium contracts more forcefully causing a large ‘a’ wave, known as a giant ‘a’ wave. It indicates increased right atrial pressure during atrial systole and is diagnostic of outflow obstruction.
6. In complete heart block, ‘cannon’ a waves occur due to:
a) Asynchronous atrial and ventricular contractions
b) Right ventricular failure
c) Tricuspid stenosis
d) Pulmonary embolism
Answer & Explanation: (a) Asynchronous atrial and ventricular contractions. In complete heart block, the atria contract independently of ventricles, sometimes against a closed tricuspid valve, producing large ‘cannon’ a waves in the jugular venous pulse tracing, easily visible on neck examination.
7. Clinical-type: A patient with tricuspid regurgitation will show:
a) Absent ‘a’ wave
b) Prominent ‘v’ wave
c) Absent ‘c’ wave
d) Negative ‘y’ descent
Answer & Explanation: (b) Prominent ‘v’ wave. In tricuspid regurgitation, regurgitant flow from the right ventricle into the atrium during systole markedly increases the ‘v’ wave amplitude, producing a systolic pulsation of the neck veins synchronized with cardiac systole.
8. Clinical-type: A 60-year-old man with dyspnea shows elevated JVP with rapid ‘y’ descent. The likely diagnosis is:
a) Constrictive pericarditis
b) Cardiac tamponade
c) Tricuspid stenosis
d) Pulmonary embolism
Answer & Explanation: (a) Constrictive pericarditis. In this condition, the pericardium becomes rigid, limiting diastolic filling but allowing rapid early ventricular filling, causing a steep ‘y’ descent in JVP. This classical finding distinguishes it from tamponade where ‘y’ descent is blunted.
9. Clinical-type: A patient with pulsatile JVP in systole with a blowing murmur along lower sternal border likely has:
a) Pulmonary hypertension
b) Tricuspid regurgitation
c) Aortic stenosis
d) Mitral stenosis
Answer & Explanation: (b) Tricuspid regurgitation. The systolic murmur and pulsatile neck veins correspond to the regurgitant flow of blood into the right atrium during systole, causing giant ‘v’ waves, and visible venous pulsations synchronous with the cardiac cycle.
10. Clinical-type: A young patient shows elevated JVP with absent ‘y’ descent after trauma. The most probable diagnosis is:
a) Cardiac tamponade
b) Constrictive pericarditis
c) Tricuspid stenosis
d) Right heart failure
Answer & Explanation: (a) Cardiac tamponade. Fluid in the pericardial cavity restricts ventricular filling, abolishing the ‘y’ descent. The hallmark triad is hypotension, muffled heart sounds, and raised JVP with absent ‘y’ descent, known as Beck’s triad, indicating tamponade physiology.
Chapter: Cerebral Circulation and Intracranial Dynamics; Topic: Blood Supply to the Brain; Subtopic: Cerebral Blood Flow (CBF) and Regulation
Keyword Definitions:
Cerebral Blood Flow (CBF): The volume of blood passing through 100 g of brain tissue per minute, normally about 50–55 ml/100 g/min.
Autoregulation: The brain’s ability to maintain constant blood flow despite changes in mean arterial pressure between 60–160 mmHg.
Circle of Willis: Arterial circle at the brain base ensuring collateral circulation between internal carotid and vertebral arteries.
Ischemia: Inadequate blood supply leading to tissue hypoxia and neuronal injury.
CO₂ sensitivity: CBF rises by 2–4% for every 1 mmHg increase in arterial CO₂ due to vasodilation.
Lead Question – 2014
Blood supply of brain is ?
a) 1500 ml/min
b) 2000 ml/min
c) 750 ml/min
d) 250 ml/min
Answer & Explanation: (c) 750 ml/min.
Cerebral blood flow averages about 750 ml/min, constituting nearly 15% of cardiac output. This flow ensures adequate oxygen and glucose delivery to brain tissue. It is tightly regulated by autoregulatory mechanisms responding to CO₂, O₂, and mean arterial pressure. Any disruption, such as hypoxia or ischemia, can impair neuronal activity and cause irreversible damage.
1. Normal cerebral blood flow per 100 g of brain tissue is:
a) 10 ml/min
b) 25 ml/min
c) 50 ml/min
d) 100 ml/min
Answer & Explanation: (c) 50 ml/min. The brain requires a continuous blood supply of 50 ml/100 g/min to meet its metabolic demands. Gray matter receives more blood than white matter due to higher neuronal activity. A fall below 20 ml/100 g/min can impair neuronal function, while values under 10 ml/100 g/min cause irreversible neuronal death.
2. Which artery supplies the visual cortex?
a) Anterior cerebral artery
b) Middle cerebral artery
c) Posterior cerebral artery
d) Basilar artery
Answer & Explanation: (c) Posterior cerebral artery. The visual cortex, located in the occipital lobe, is supplied by the posterior cerebral artery, a branch of the basilar artery. Occlusion of this artery causes contralateral homonymous hemianopia due to loss of visual field from both eyes corresponding to the affected hemisphere.
3. The Circle of Willis is formed by all except:
a) Anterior communicating artery
b) Posterior communicating artery
c) Internal carotid artery
d) External carotid artery
Answer & Explanation: (d) External carotid artery. The Circle of Willis provides collateral circulation between anterior and posterior cerebral systems, comprising internal carotid, anterior, middle, posterior cerebral arteries, and communicating branches. The external carotid supplies extracranial structures, not intracranial circulation.
4. Increased PaCO₂ causes cerebral:
a) Vasoconstriction
b) Vasodilation
c) Ischemia
d) No change
Answer & Explanation: (b) Vasodilation. Elevated CO₂ levels increase hydrogen ion concentration in the cerebrospinal fluid, leading to relaxation of cerebral arterioles. This enhances blood flow to maintain pH homeostasis. Conversely, hyperventilation reduces CO₂, causing vasoconstriction and lowering intracranial pressure temporarily in brain edema management.
5. Decreased cerebral blood flow is caused by:
a) Hypercapnia
b) Hypocapnia
c) Acidosis
d) Increased arterial CO₂
Answer & Explanation: (b) Hypocapnia. Low arterial CO₂ due to hyperventilation induces cerebral vasoconstriction, reducing blood flow and intracranial pressure. Although this can relieve pressure temporarily in head injury, prolonged hypocapnia may reduce oxygen delivery and aggravate ischemic neuronal damage.
6. Clinical-type: A patient with head injury shows reduced cerebral perfusion despite normal systemic BP. Likely cause:
a) Cerebral vasodilation
b) Loss of autoregulation
c) Hypoxia
d) Hypercapnia
Answer & Explanation: (b) Loss of autoregulation. Brain injury impairs autoregulatory mechanisms that maintain constant flow, making CBF pressure-dependent. Even normal blood pressure may not suffice to maintain perfusion. This leads to ischemic zones, explaining why cerebral perfusion pressure is closely monitored in neurosurgical patients.
7. Clinical-type: A 50-year-old hypertensive man develops sudden weakness on the right side. Likely artery affected:
a) Anterior cerebral artery
b) Middle cerebral artery
c) Posterior cerebral artery
d) Basilar artery
Answer & Explanation: (b) Middle cerebral artery. It supplies the motor and sensory cortex for the face and upper limb. Infarction leads to contralateral hemiplegia (face and arm), aphasia if the dominant hemisphere is affected, and sensory deficits. It is the most common site of cerebral infarction.
8. Clinical-type: A patient develops coma due to global hypoxia. Which area of the brain is most vulnerable?
a) Cerebellum
b) Hippocampus
c) Medulla
d) Hypothalamus
Answer & Explanation: (b) Hippocampus. The hippocampus is highly sensitive to hypoxia and ischemia due to its high metabolic activity. Neurons here undergo early necrosis in hypoxic conditions, explaining memory impairment and altered consciousness in global cerebral ischemia.
9. Clinical-type: During carotid endarterectomy, blood flow through the ipsilateral hemisphere is maintained via:
a) Anterior communicating artery
b) Posterior communicating artery
c) External carotid branches
d) Vertebral artery
Answer & Explanation: (a) Anterior communicating artery. It connects the anterior cerebral arteries from both sides, providing collateral flow if one internal carotid is occluded. Adequate Circle of Willis integrity ensures uninterrupted perfusion during vascular surgeries like carotid endarterectomy.
10. Clinical-type: A 60-year-old with chronic COPD develops confusion and drowsiness. Cause is likely:
a) Hypercapnia causing cerebral vasoconstriction
b) Hypocapnia causing vasoconstriction
c) Hypercapnia causing vasodilation and increased ICP
d) Hypoxia causing vasoconstriction
Answer & Explanation: (c) Hypercapnia causing vasodilation and increased ICP. Chronic CO₂ retention leads to cerebral vasodilation, increasing intracranial pressure and reducing neuronal function, resulting in confusion or CO₂ narcosis. This underscores the importance of controlled oxygen therapy in COPD patients to prevent respiratory drive suppression.
Chapter: Central Nervous System; Topic: Neurotransmission in Cardiovascular Regulation; Subtopic: Nucleus Tractus Solitarius (NTS) Neurotransmitters
Keyword Definitions:
Nucleus Tractus Solitarius (NTS): A key brainstem nucleus that receives afferent signals from baroreceptors and chemoreceptors, regulating cardiovascular and respiratory reflexes.
Neurotransmitter: A chemical messenger that transmits signals between neurons across synapses.
Glutamate: The principal excitatory neurotransmitter in the central nervous system, involved in most synaptic transmission processes.
Afferent Fibers: Nerve fibers that carry sensory information from the periphery to the central nervous system.
Cardiovascular Regulation: The process by which the body maintains blood pressure and heart rate through neural and hormonal mechanisms.
Lead Question – 2014
Major neurotransmitter in afferents in nucleus tractus solitarius to regulate cardiovascular system?
a) Serotonin
b) Glutamate
c) Glycine
d) Norepinephrine
Explanation: The major neurotransmitter in afferent fibers terminating in the nucleus tractus solitarius (NTS) is Glutamate. It acts as the primary excitatory neurotransmitter, mediating baroreceptor and chemoreceptor reflexes to regulate cardiovascular functions. Activation of glutamate receptors in the NTS results in changes in heart rate and blood pressure by modulating autonomic output. Thus, the correct answer is Glutamate (b).
1) Which neurotransmitter mediates excitatory synaptic transmission in the central nervous system?
a) GABA
b) Glutamate
c) Dopamine
d) Serotonin
Explanation: The correct answer is Glutamate. It is the main excitatory neurotransmitter in the CNS, playing a major role in learning, memory, and synaptic plasticity. It acts on NMDA, AMPA, and kainate receptors to propagate excitatory signals throughout neuronal circuits, crucial for brain function and cardiovascular regulation.
2) The inhibitory neurotransmitter responsible for reducing neuronal excitability in the brain is:
a) Glycine
b) Glutamate
c) GABA
d) Dopamine
Explanation: The answer is GABA. Gamma-Aminobutyric Acid is the main inhibitory neurotransmitter in the CNS. It acts through GABA-A and GABA-B receptors to reduce neuronal excitability, counterbalancing glutamatergic excitation, thereby maintaining CNS stability and preventing overactivation.
3) A patient with baroreceptor dysfunction may have an abnormality in which brainstem nucleus?
a) Nucleus ambiguus
b) Nucleus tractus solitarius
c) Red nucleus
d) Substantia nigra
Explanation: The correct answer is Nucleus tractus solitarius (NTS). It is the main center integrating sensory input from baroreceptors and chemoreceptors, thereby maintaining arterial pressure. Damage to NTS disrupts cardiovascular reflexes, causing blood pressure instability and altered autonomic responses.
4) Which of the following neurotransmitters is excitatory and acts primarily on NMDA receptors?
a) Glutamate
b) Glycine
c) GABA
d) Serotonin
Explanation: The correct answer is Glutamate. It acts on NMDA, AMPA, and kainate receptors. NMDA receptor activation plays a vital role in learning and memory by allowing calcium influx, critical for long-term potentiation and synaptic strengthening, especially in the brainstem and cortex.
5) A lesion of the Nucleus Tractus Solitarius affects which reflex the most?
a) Corneal reflex
b) Baroreceptor reflex
c) Pupillary reflex
d) Cough reflex
Explanation: The correct answer is Baroreceptor reflex. NTS is the central termination site of baroreceptor afferents from the carotid sinus and aortic arch. Damage leads to impaired reflex control of blood pressure and heart rate, causing labile hypertension or bradycardia.
6) A patient presents with labile blood pressure and impaired vagal tone. Dysfunction of which neurotransmitter in NTS is likely?
a) Glutamate
b) Dopamine
c) Acetylcholine
d) GABA
Explanation: The answer is Glutamate. Its release in NTS is critical for initiating reflex control of heart rate and blood pressure. Disruption in glutamatergic transmission diminishes baroreflex sensitivity, resulting in unstable cardiovascular responses and reduced parasympathetic activity.
7) Which neurotransmitter is co-released with norepinephrine in sympathetic postganglionic neurons?
a) Neuropeptide Y
b) Glutamate
c) Dopamine
d) Serotonin
Explanation: The correct answer is Neuropeptide Y. It is often co-released with norepinephrine from sympathetic terminals, enhancing vasoconstriction and contributing to long-lasting effects on blood vessels, complementing rapid adrenergic action during cardiovascular stress responses.
8) Which enzyme is essential for the synthesis of glutamate from α-ketoglutarate?
a) Glutamate dehydrogenase
b) Glutaminase
c) Glutamine synthetase
d) Monoamine oxidase
Explanation: The correct answer is Glutamate dehydrogenase. It catalyzes the reversible conversion between α-ketoglutarate and glutamate, linking amino acid metabolism with the Krebs cycle, thus maintaining neurotransmitter balance essential for neuronal excitability and synaptic transmission.
9) Clinical Case: A patient with acute brainstem ischemia develops severe bradycardia. Which neurotransmitter’s function in NTS is compromised?
a) Glutamate
b) Acetylcholine
c) GABA
d) Serotonin
Explanation: The correct answer is Glutamate. Brainstem ischemia can impair glutamatergic signaling in NTS, disrupting baroreceptor reflexes and causing autonomic imbalance. This leads to bradycardia and hypotension due to inadequate excitatory transmission to vagal efferents.
10) Clinical Case: A hypertensive patient with impaired baroreflex sensitivity shows reduced glutamate activity in NTS. Which response is expected?
a) Stable heart rate
b) Increased vagal output
c) Unstable blood pressure
d) Decreased sympathetic activity
Explanation: The correct answer is Unstable blood pressure. Reduced glutamatergic neurotransmission in NTS diminishes baroreflex control, impairing the buffering of blood pressure fluctuations. This results in autonomic instability with variable heart rate and pressure control failure, typical in chronic hypertension.
Chapter: Cardiovascular Physiology; Topic: Arterial Pulse and Pressure Waveforms; Subtopic: Dicrotic Notch and its Mechanism
Keyword Definitions:
Dicrotic Notch: A small downward deflection on the arterial pulse waveform occurring due to transient backflow of blood when the aortic valve closes.
Aortic Valve: The semilunar valve between the left ventricle and aorta that prevents backflow of blood during diastole.
Arterial Pulse: The rhythmic expansion of an artery due to the ejection of blood from the left ventricle during systole.
Systole and Diastole: Systole refers to contraction and ejection of blood; diastole refers to relaxation and filling of chambers.
Windkessel Effect: Elastic recoil of arteries that helps maintain continuous blood flow during diastole.
Lead Question – 2014
Dicrotic notch is caused by:
a) Closure of mitral valve
b) Opening of mitral valve
c) Closure of aortic valve
d) Opening of aortic valve
Explanation: The dicrotic notch on the arterial pressure waveform occurs due to the closure of the aortic valve. When ventricular pressure falls below aortic pressure, the valve closes, causing a brief retrograde flow that strikes the closed cusps, creating a notch in the pressure trace. This event marks the onset of diastole. Hence, the correct answer is Closure of aortic valve (c).
1) Which event marks the beginning of diastole in the cardiac cycle?
a) Closure of mitral valve
b) Opening of aortic valve
c) Closure of aortic valve
d) Opening of tricuspid valve
Explanation: The correct answer is Closure of the aortic valve. It signifies the end of ventricular ejection and beginning of isovolumetric relaxation. The associated dicrotic notch appears on the aortic pressure curve as a transient rise, indicating the start of diastole in the left ventricle.
2) The dicrotic notch is most prominent in which type of arterial pulse tracing?
a) Pulmonary artery
b) Aortic pressure curve
c) Right atrial pressure curve
d) Venous pulse
Explanation: The correct answer is Aortic pressure curve. The dicrotic notch results from the sudden closure of the aortic valve, which generates a brief rise in aortic pressure due to elastic recoil. This feature is typically visible in invasive arterial pressure recordings.
3) The absence of a dicrotic notch in the arterial waveform may indicate:
a) Aortic stenosis
b) Aortic regurgitation
c) Mitral stenosis
d) Mitral regurgitation
Explanation: The answer is Aortic regurgitation. In this condition, the aortic valve fails to close properly, preventing the normal rebound that produces the dicrotic notch. Consequently, the arterial waveform shows a rapid fall in diastolic pressure without a notch.
4) Clinical Case: A patient’s arterial waveform shows a deep dicrotic notch after diastolic pressure. Which physiological factor is responsible?
a) Rapid aortic valve opening
b) High arterial compliance
c) Delayed aortic valve closure
d) Increased heart rate
Explanation: The correct answer is High arterial compliance. When the arterial walls are more elastic, the rebound following aortic valve closure becomes more pronounced, deepening the dicrotic notch due to stronger retrograde pressure waves against the closed valve cusps.
5) The dicrotic notch is absent in which of the following conditions?
a) Cardiac tamponade
b) Aortic regurgitation
c) Mitral stenosis
d) Pulmonary embolism
Explanation: The correct answer is Aortic regurgitation. When the aortic valve fails to close completely, the backward flow of blood eliminates the pressure rebound responsible for the dicrotic notch, leading to its absence in arterial waveforms.
6) In which phase of the cardiac cycle does the dicrotic notch occur?
a) Isovolumetric contraction
b) Ventricular ejection
c) Isovolumetric relaxation
d) Rapid filling
Explanation: The correct answer is Isovolumetric relaxation. The dicrotic notch occurs immediately after the aortic valve closes, when ventricular pressure falls but before the mitral valve opens. This phase is characterized by no volume change but falling pressure inside the ventricle.
7) Clinical Case: A patient with low dicrotic notch amplitude may have:
a) Stiff arteries
b) Aortic stenosis
c) Bradycardia
d) Hyperdynamic circulation
Explanation: The correct answer is Stiff arteries. Reduced arterial compliance limits elastic recoil, decreasing the rebound pressure wave responsible for the dicrotic notch, which becomes less prominent or absent in elderly patients with arteriosclerosis.
8) The dicrotic notch reflects which of the following hemodynamic changes?
a) Closure of atrioventricular valves
b) Closure of semilunar valves
c) Opening of semilunar valves
d) Atrial contraction
Explanation: The answer is Closure of semilunar valves. The dicrotic notch appears due to a brief rise in aortic pressure after semilunar (aortic) valve closure, marking the transition from systole to diastole, a key event in the arterial pressure waveform.
9) Clinical Case: A patient with severe hypotension has a distinct double-peaked arterial pulse known as a “dicrotic pulse.” What does it indicate?
a) Aortic stenosis
b) Low cardiac output
c) Increased systemic resistance
d) Hypertrophic cardiomyopathy
Explanation: The correct answer is Low cardiac output. Dicrotic pulse occurs in conditions like shock or sepsis, where there’s decreased stroke volume and vascular tone. It features a noticeable secondary upstroke following the dicrotic notch in the pulse tracing.
10) Clinical Case: During intra-arterial monitoring, an intensivist observes loss of the dicrotic notch. Which technical error may cause this?
a) Overdamped transducer system
b) Loose arterial catheter
c) Air bubbles in tubing
d) All of the above
Explanation: The correct answer is All of the above. Invasive arterial monitoring systems may lose fidelity due to air bubbles, kinks, or overdamping, which attenuate waveform features, including the dicrotic notch, leading to inaccurate pressure readings and loss of diagnostic detail.
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Chapter: Cardiovascular Physiology; Topic: Regulation of Blood Flow; Subtopic: Cutaneous Circulation and Neurohumoral Control
Keyword Definitions:
Skin Blood Flow: The amount of blood supplied to the skin, regulated by sympathetic nerves to maintain temperature homeostasis.
Noradrenaline: A neurotransmitter that acts mainly on alpha-adrenergic receptors, causing vasoconstriction and reducing blood flow.
Vasoconstriction: Narrowing of blood vessels due to contraction of smooth muscles in vessel walls, leading to decreased blood flow.
Thermoregulation: The physiological process that maintains body temperature through mechanisms like vasodilation and vasoconstriction.
Sympathetic Nervous System: A branch of the autonomic nervous system that regulates involuntary actions including blood vessel tone and heart rate.
Lead Question – 2014
Skin blood flow is decreased by:
a) Dopamine
b) Isoprenaline
c) Noradrenaline
d) Acetylcholine
Explanation: The correct answer is Noradrenaline. It causes vasoconstriction in cutaneous vessels by stimulating alpha-1 adrenergic receptors. This leads to reduced skin blood flow, conserving body heat and maintaining arterial pressure. In contrast, dopamine and isoprenaline cause vasodilation. Acetylcholine induces vasodilation via nitric oxide, not vasoconstriction.
1) Which adrenergic receptor subtype primarily mediates vasoconstriction in skin arterioles?
a) Beta-1
b) Alpha-1
c) Beta-2
d) Alpha-2
Explanation: The correct answer is Alpha-1. Activation of alpha-1 adrenergic receptors by noradrenaline results in smooth muscle contraction in the skin’s arterioles, producing vasoconstriction and reducing cutaneous blood flow to help conserve heat during sympathetic activation.
2) Skin blood flow increases during which of the following physiological states?
a) Cold exposure
b) Exercise
c) Shock
d) Hemorrhage
Explanation: The correct answer is Exercise. During exercise, cutaneous blood vessels dilate to dissipate excess heat produced by active muscles. This response is mediated by decreased sympathetic tone and local metabolites causing vasodilation in the skin circulation.
3) Clinical Case: A patient with high fever shows flushed skin. The cause is:
a) Sympathetic vasoconstriction
b) Parasympathetic stimulation
c) Cutaneous vasodilation
d) Capillary stasis
Explanation: The correct answer is Cutaneous vasodilation. During fever, body temperature rises, and skin blood vessels dilate to enhance heat loss via radiation and convection, producing flushed appearance and helping maintain thermal balance.
4) Dopamine causes vasodilation in the skin through which receptor type?
a) Alpha
b) Beta
c) D1 dopaminergic
d) Muscarinic
Explanation: The correct answer is D1 dopaminergic. Dopamine acts on D1 receptors in vascular smooth muscle, increasing cyclic AMP, causing relaxation and vasodilation. However, its effect is more pronounced in renal, mesenteric, and coronary vessels rather than in cutaneous circulation.
5) Which neurotransmitter causes cutaneous vasodilation during emotional blushing?
a) Noradrenaline
b) Acetylcholine
c) Serotonin
d) Dopamine
Explanation: The correct answer is Acetylcholine. Emotional blushing involves cholinergic sympathetic fibers causing vasodilation via nitric oxide release in facial skin arterioles, increasing blood flow and producing redness, especially during stress or embarrassment.
6) Clinical Case: A patient with hypovolemic shock has cold, clammy skin. The most likely cause is:
a) Increased cardiac output
b) Decreased sympathetic activity
c) Cutaneous vasoconstriction
d) Capillary leakage
Explanation: The correct answer is Cutaneous vasoconstriction. In shock, sympathetic discharge causes intense vasoconstriction in skin vessels to divert blood to vital organs like the heart and brain, resulting in pale, cold, and clammy skin.
7) Which physiological mechanism increases skin blood flow during hyperthermia?
a) Increased sympathetic tone
b) Activation of alpha-adrenergic receptors
c) Withdrawal of sympathetic vasoconstrictor activity
d) Reduced cardiac output
Explanation: The correct answer is Withdrawal of sympathetic vasoconstrictor activity. During hyperthermia, thermoregulatory centers inhibit sympathetic vasoconstrictor neurons, causing vasodilation and increased blood flow to the skin for heat dissipation.
8) Isoprenaline causes increased skin blood flow by stimulating:
a) Alpha-adrenergic receptors
b) Beta-1 receptors
c) Beta-2 receptors
d) Dopamine receptors
Explanation: The correct answer is Beta-2 receptors. Isoprenaline, a non-selective beta agonist, causes vasodilation through beta-2 receptor activation, leading to relaxation of smooth muscle in blood vessel walls and increased skin perfusion.
9) Clinical Case: A patient on norepinephrine infusion develops pallor and cool extremities. This results from:
a) Beta-2 mediated vasodilation
b) Alpha-1 mediated vasoconstriction
c) Increased cardiac preload
d) Reduced afterload
Explanation: The correct answer is Alpha-1 mediated vasoconstriction. Norepinephrine acts on alpha-1 adrenergic receptors, causing cutaneous and peripheral vasoconstriction, leading to reduced skin perfusion, pallor, and cold extremities during pressor therapy.
10) Which factor increases skin blood flow during emotional stress?
a) Activation of sympathetic cholinergic fibers
b) Activation of sympathetic adrenergic fibers
c) Increased parasympathetic tone
d) Arterial baroreceptor reflex
Explanation: The correct answer is Activation of sympathetic cholinergic fibers. Emotional stress activates specialized sympathetic cholinergic neurons that release acetylcholine, producing facial vasodilation and blushing via nitric oxide-mediated smooth muscle relaxation in cutaneous vessels.
Chapter: Cardiovascular Physiology; Topic: Heart Sounds; Subtopic: Second Heart Sound (S2)
Keyword Definitions:
Heart Sounds: Sounds produced due to closure of cardiac valves and blood flow turbulence during the cardiac cycle.
S2: The second heart sound, caused by the closure of the aortic and pulmonary valves (semilunar valves).
Semilunar Valves: Valves between ventricles and great arteries—prevent backflow of blood after ventricular contraction.
AV Valves: Atrioventricular valves (mitral and tricuspid) prevent backflow of blood from ventricles to atria.
Lead Question – 2014
S2 is associated with ?
a) Rapid ventricular filling
b) Atrial contraction
c) Closure of semilunar valves
d) Closure of AV valves
Explanation: The second heart sound (S2) occurs due to closure of the aortic and pulmonary (semilunar) valves at the end of systole. It signifies the beginning of diastole. The sound has two components—A2 (aortic) and P2 (pulmonary). Physiological splitting occurs during inspiration. Hence, the correct answer is c) Closure of semilunar valves.
1) The first heart sound (S1) corresponds to:
a) Closure of semilunar valves
b) Closure of AV valves
c) Opening of semilunar valves
d) Atrial contraction
Explanation: The first heart sound (S1) is produced by the closure of the mitral and tricuspid (AV) valves at the beginning of ventricular systole. It indicates the onset of isovolumetric contraction. The correct answer is b) Closure of AV valves.
2) Splitting of S2 during inspiration is due to:
a) Early closure of aortic valve
b) Late closure of pulmonary valve
c) Early closure of pulmonary valve
d) Late closure of aortic valve
Explanation: During inspiration, venous return to the right heart increases, delaying closure of the pulmonary valve, while left ventricular return decreases, leading to earlier closure of the aortic valve. This physiological splitting results in two distinct components (A2 and P2). The correct answer is b) Late closure of pulmonary valve.
3) Wide and fixed splitting of S2 is characteristic of:
a) Aortic stenosis
b) Atrial septal defect
c) Pulmonary hypertension
d) Left bundle branch block
Explanation: Atrial septal defect (ASD) causes continuous left-to-right shunt leading to constant increased right ventricular volume and delayed pulmonary valve closure irrespective of respiration. This produces wide and fixed splitting of S2. The correct answer is b) Atrial septal defect.
4) Paradoxical splitting of S2 occurs in:
a) Right bundle branch block
b) Aortic stenosis
c) Pulmonary stenosis
d) ASD
Explanation: In paradoxical splitting, P2 occurs before A2. This happens when A2 is delayed due to left ventricular conduction delay or aortic stenosis. During inspiration, the splitting narrows instead of widening. Hence, the correct answer is b) Aortic stenosis.
5) A loud S2 is heard in which condition?
a) Aortic stenosis
b) Pulmonary hypertension
c) Mitral regurgitation
d) Tricuspid stenosis
Explanation: In pulmonary hypertension, elevated pulmonary arterial pressure causes forceful closure of the pulmonary valve, producing a loud P2 component, making S2 accentuated. Hence, the correct answer is b) Pulmonary hypertension.
6) A patient with pulmonary stenosis will have:
a) Loud A2
b) Soft P2
c) Wide fixed split S2
d) Paradoxical split S2
Explanation: Pulmonary stenosis leads to delayed and reduced closure of the pulmonary valve, resulting in a soft or absent P2 and a widened split of S2. The correct answer is b) Soft P2.
7) In severe aortic stenosis, which heart sound is affected?
a) S1 diminished
b) S2 absent or soft
c) S3 increased
d) S4 increased
Explanation: In severe aortic stenosis, the aortic valve becomes calcified and immobile. This causes S2 to be soft or absent due to reduced movement of the aortic valve cusps. The correct answer is b) S2 absent or soft.
8) A third heart sound (S3) is heard in:
a) Early diastole
b) Late systole
c) End diastole
d) Early systole
Explanation: The third heart sound (S3) occurs in early diastole during rapid ventricular filling. It is caused by the sudden deceleration of blood flow into the ventricle. It may be physiological in young individuals but pathological in heart failure. The correct answer is a) Early diastole.
9) A 50-year-old hypertensive male presents with a loud S4. What does it indicate?
a) Normal diastolic relaxation
b) Increased ventricular compliance
c) Decreased ventricular compliance
d) Aortic regurgitation
Explanation: The fourth heart sound (S4) occurs due to atrial contraction against a stiff, noncompliant ventricle, commonly seen in hypertensive heart disease or aortic stenosis. It indicates reduced ventricular compliance. Hence, the correct answer is c) Decreased ventricular compliance.
10) In a young athlete, an S3 heart sound is detected. This finding is:
a) Always pathological
b) Physiological
c) Indicates mitral stenosis
d) Suggests heart failure
Explanation: In young individuals and athletes, an S3 may be physiological due to enhanced ventricular filling and high cardiac output. It is usually harmless unless accompanied by symptoms of heart disease. Hence, the correct answer is b) Physiological.
Chapter: Cardiovascular Physiology; Topic: Vascular System; Subtopic: Capacitance Vessels
Keyword Definitions:
Capacitance Vessels: Veins that store most of the blood at rest; high compliance vessels.
Elastic Tissue: Connective tissue fibers that provide stretch and recoil to vessels.
Muscle Tissue in Vessels: Smooth muscle that regulates vessel diameter and vascular tone.
Vascular Compliance: Ability of a vessel to expand and store blood volume with minimal pressure change.
Veins: Blood vessels carrying blood toward the heart, functioning as capacitance vessels.
Lead Question – 2014
Capacitance vessels have in their wall ?
a) More elastic tissue and less muscle
b) Less elastic tissue and more muscle
c) More elastic tissue and more muscle
d) Less elastic tissue and less muscle
Explanation: Capacitance vessels, mainly veins, are designed to store blood at low pressure. Their walls contain more elastic tissue to allow stretch and less smooth muscle compared to arteries. This composition allows veins to accommodate large volumes without significant rise in pressure. They act as blood reservoirs, contributing up to 70% of blood volume at rest. Therefore, the correct answer is a) More elastic tissue and less muscle.
1) Arteries are called resistance vessels because:
a) They have high compliance
b) They have thick muscular walls
c) They store large blood volume
d) They have low pressure
Explanation: Arteries have thick smooth muscle and elastic fibers, allowing them to withstand and regulate high blood pressure. They resist flow changes and determine systemic vascular resistance. Therefore, arteries are termed resistance vessels. Correct answer is b) They have thick muscular walls.
2) Compliance of veins compared to arteries is:
a) Lower
b) Higher
c) Same
d) Negligible
Explanation: Veins have thin walls with more elastic tissue and less smooth muscle, making them highly distensible. They accommodate large blood volumes with minimal pressure increase, giving them higher compliance compared to arteries. Correct answer is b) Higher.
3) Venous return is increased by:
a) Sympathetic stimulation causing venoconstriction
b) Parasympathetic stimulation
c) Decreased muscle tone
d) High venous compliance
Explanation: Sympathetic stimulation reduces venous compliance by constricting veins, pushing blood toward the heart and increasing venous return. This compensates for reduced blood volume or increased demand. Correct answer is a) Sympathetic stimulation causing venoconstriction.
4) Clinical condition associated with decreased venous capacitance is:
a) Heart failure
b) Varicose veins
c) Aortic stenosis
d) Arteriovenous fistula
Explanation: In heart failure, increased sympathetic tone and venoconstriction reduce venous capacitance, contributing to elevated venous pressures and congestion. Veins become less compliant, pushing blood toward central circulation. Correct answer is a) Heart failure.
5) Splanchnic veins act as:
a) Resistance vessels
b) Capacitance vessels
c) Exchange vessels
d) Lymphatic vessels
Explanation: Splanchnic veins contain high compliance and large capacity, storing up to 20-25% of blood volume. They serve as blood reservoirs and can mobilize blood during hypovolemia. Hence, they are classic capacitance vessels. Correct answer is b) Capacitance vessels.
6) Venous valves function to:
a) Increase compliance
b) Prevent backflow
c) Regulate arterial pressure
d) Store oxygen
Explanation: Venous valves prevent retrograde flow of blood, ensuring unidirectional movement toward the heart. They are crucial in lower limbs to counter gravity, particularly during standing. Correct answer is b) Prevent backflow.
7) Exercise increases venous return primarily due to:
a) Increased arterial compliance
b) Skeletal muscle pump action
c) Decreased heart rate
d) Reduced blood volume
Explanation: Skeletal muscle contractions compress veins, propelling blood toward the heart. Venous valves prevent backflow. This skeletal muscle pump is a major mechanism for increasing venous return during exercise. Correct answer is b) Skeletal muscle pump action.
8) Varicose veins result from:
a) Excessive arterial pressure
b) Venous valve incompetence
c) Reduced capillary permeability
d) Increased venous smooth muscle
Explanation: Incompetent venous valves lead to retrograde blood flow, pooling, and vein dilation. This chronic venous hypertension results in varicosities, mainly in superficial veins. Correct answer is b) Venous valve incompetence.
9) During hemorrhage, venous capacitance vessels:
a) Relax to store more blood
b) Constrict to maintain venous return
c) Remain unchanged
d) Cause hypotension
Explanation: Sympathetic stimulation during hemorrhage causes venoconstriction, reducing capacitance, mobilizing stored blood toward the heart to preserve preload and cardiac output. Correct answer is b) Constrict to maintain venous return.
10) Compared to veins, arteries have:
a) Higher compliance
b) Lower resistance
c) Lower compliance
d) Higher capacitance
Explanation: Arteries have thick muscular walls and relatively stiff elastic tissue, giving them low compliance but high resistance to blood flow. They cannot store large blood volumes. Correct answer is c) Lower compliance.