Chapter: Circulatory Biomechanics; Topic: Hemodynamics — Viscosity, Flow, and Cardiac Output; Subtopic: Effects of Hematocrit, Resistance, Compliance, and Pathophysiology on Flow
Keyword Definitions:
Blood viscosity: Internal friction of blood; depends mainly on hematocrit and temperature.
Cardiac output (CO): Volume of blood pumped by the heart per minute (CO = HR × SV).
Poiseuille’s law: Flow ∝ (pressure difference × r⁴) / (viscosity × length) — radius has greatest effect.
Resistance (R): Opposition to flow; systemic vascular resistance governs arterial pressure (ΔP = Q × R).
Compliance: ΔVolume / ΔPressure; veins are high-compliance (capacitance) vessels, arteries low-compliance.
Lead Question — 2014
In circulatory biomechanics which of the following is true?
a) Blood viscosity is increased in anemia
b) Blood viscosity is decreased in polycythemia
c) Cardiac output is increased in anemia
d) Cardiac output is decreased in Beri-Beri
Answer: c) Cardiac output is increased in anemia.
Explanation (≈100 words): In anemia the oxygen content per unit blood is reduced, so tissues demand more flow; to compensate the heart increases stroke volume and often heart rate, raising cardiac output (high-output state) to maintain oxygen delivery (DO₂ = CO × CaO₂). Blood viscosity in anemia is typically decreased (not increased) because hematocrit falls. Polycythemia increases hematocrit and therefore viscosity (option b false). Beri-beri (wet beriberi) from thiamine deficiency produces vasodilatation and high-output heart failure, so cardiac output tends to be increased, not decreased (option d false). Poiseuille’s law explains the large effect of radius on flow vs viscosity effects.
1. According to Poiseuille’s law, which change produces the largest increase in laminar flow through a vessel?
a) Doubling pressure gradient
b) Halving viscosity
c) Doubling radius
d) Halving vessel length
Answer: c) Doubling radius.
Explanation (≈100 words): Poiseuille’s law states flow ∝ r⁴, so flow is extremely sensitive to radius. Doubling radius increases flow by 2⁴ = 16-fold, far greater than doubling pressure (2×), halving viscosity (~2×), or halving length (~2×). This is why small changes in arteriolar tone (vasoconstriction/dilation) dramatically affect tissue perfusion and systemic vascular resistance. The law assumes laminar, Newtonian flow and rigid tubes; blood is non-Newtonian in small vessels, but the r⁴ dependency remains conceptually central to hemodynamics and pharmacologic control of vascular tone.
2 (clinical). A patient with polycythemia vera presents with headache and dizziness. Which hemodynamic change best explains these symptoms?
a) Decreased blood viscosity
b) Increased blood viscosity and resistance
c) Decreased cardiac output due to anemia
d) Increased capillary compliance
Answer: b) Increased blood viscosity and resistance.
Explanation (≈100 words): Polycythemia raises hematocrit, causing marked increase in blood viscosity. Elevated viscosity increases systemic vascular resistance and impairs microcirculatory flow, producing cerebral hypoperfusion symptoms like headache, dizziness, and visual disturbances. Cardiac output may initially rise to compensate but can be limited by increased afterload. Management (phlebotomy) reduces hematocrit and viscosity, improving symptoms. This clinical vignette illustrates how hematocrit-dependent viscosity changes can outweigh effects of oxygen content—despite more hemoglobin, microvascular flow suffers if viscosity becomes too high.
3. Reynolds number predicts transition to turbulent flow. Turbulence is more likely when:
a) Viscosity is high and velocity is low
b) Vessel radius is small and flow is slow
c) Velocity and vessel diameter are high
d) Hematocrit is minimal
Answer: c) Velocity and vessel diameter are high.
Explanation (≈100 words): Reynolds number (Re = ρvD/η) increases with higher velocity (v) and larger diameter (D) and falls with higher viscosity (η). Turbulent flow occurs when Re exceeds a critical value (~2000 in straight pipes). In large arteries during high flow states (exercise, aortic stenosis, or anemia with high stroke volume), turbulence causes audible murmurs and increases energy loss. High hematocrit increases viscosity, lowering Re and tending to preserve laminar flow; paradoxically, extreme anemia (low viscosity) can favor turbulence at high velocities. Clinically, carotid bruits or murmurs reflect turbulent flow conditions.
4 (clinical). A septic shock patient has warm, well-perfused extremities with low systemic vascular resistance and high cardiac output. Which mechanism explains this hemodynamic pattern?
a) Global vasoconstriction due to sympathetic surge
b) Endothelial-mediated vasodilatation and reduced afterload
c) Increased blood viscosity from leukocytosis
d) Mechanical cardiac pump failure
Answer: b) Endothelial-mediated vasodilatation and reduced afterload.
Explanation (≈100 words): Septic shock features profound systemic vasodilation driven by inflammatory mediators (NO, prostaglandins) and endothelial dysfunction, causing decreased systemic vascular resistance. To maintain perfusion, the heart often increases output (high-output state) until decompensation. Warm skin, bounding pulses, and low diastolic pressure characterize early distributive shock. This contrasts with hypovolemic or cardiogenic shock where CO is low. Management targets source control, vasopressors to restore vascular tone, and fluids to support preload. Understanding distributive physiology is crucial for targeted therapy and distinguishing shock types at the bedside.
5. Vessel compliance is highest in which category and why?
a) Large elastic arteries — because of thick smooth muscle
b) Small arterioles — because of smooth muscle tone regulation
c) Veins — because thin walls and abundant connective matrix allow high ΔV/ΔP
d) Capillaries — because of endothelium only
Answer: c) Veins — because thin walls and abundant connective matrix allow high ΔV/ΔP.
Explanation (≈100 words): Veins are capacitance vessels with large lumens, thin smooth muscle, and compliant walls, so small pressure changes produce large volume changes (high compliance). Arteries, particularly elastic ones, buffer pulsatile flow but have relatively low compliance. High venous compliance allows the body to store blood and mobilize it via sympathetic venoconstriction (e.g., during hemorrhage). Clinically, alterations in venous compliance (age, venous valves, venous disease) affect preload and cardiac output. Understanding compliance helps explain reasons for orthostatic pooling and why venous return is sensitive to posture and muscle pump activity.
6 (clinical). A patient with chronic severe anemia complains of exertional dyspnea. Hemodynamics likely show:
a) Low cardiac output and high systemic vascular resistance
b) High cardiac output, low afterload, and increased heart rate
c) Low stroke volume with bradycardia
d) Increased blood viscosity and diminished flow
Answer: b) High cardiac output, low afterload, and increased heart rate.
Explanation (≈100 words): Severe anemia reduces arterial oxygen content. The cardiovascular compensation includes increased heart rate and stroke volume, producing high cardiac output to maintain oxygen delivery. Peripheral arterioles may dilate (reduced systemic vascular resistance) to enhance flow, and blood viscosity is reduced, facilitating flow. These adaptations lead to high-output state and can cause symptoms of heart failure if prolonged. Treatment restoring hemoglobin reduces compensatory workload. This contrasts with polycythemia where viscosity increases and flow may be impaired despite higher oxygen content per unit blood.
7. Ohm’s law applied to circulation (ΔP = Q × R) implies that if cardiac output (Q) is constant, systemic arterial pressure (ΔP) can be raised by:
a) Decreasing resistance (R)
b) Increasing resistance (R)
c) Decreasing flow (Q)
d) Increasing vessel compliance only
Answer: b) Increasing resistance (R).
Explanation (≈100 words): Ohm’s law analogy shows arterial pressure is product of flow and resistance. If flow is steady, raising arteriolar tone (increasing resistance) increases arterial pressure. Clinically, vasoconstrictors (noradrenaline) raise mean arterial pressure by increasing peripheral resistance. Conversely, vasodilators lower pressure for the same CO. Altering compliance shifts pulse pressure but mean pressure depends on CO×SVR. This principle underpins antihypertensive strategies: decrease CO (β-blockers), decrease SVR (ACE inhibitors), or reduce volume (diuretics).
8 (clinical). A patient with thiamine deficiency (wet beriberi) shows edema and bounding pulses. Hemodynamic profile most likely is:
a) Low output, high systemic resistance
b) High output with vasodilation and reduced resistance
c) Normal output with increased blood viscosity
d) Low output due to myocardial necrosis
Answer: b) High output with vasodilation and reduced resistance.
Explanation (≈100 words): Wet beriberi causes peripheral vasodilation (reduced peripheral resistance) and increased venous return; to meet metabolic demand, the heart pumps more (high-output failure). Clinical features include warm extremities, bounding pulses, wide pulse pressure, and edema. Thiamine replacement often reverses hemodynamic abnormalities. This contrasts with cardiogenic shock where CO is low and resistance high. Knowing the pattern helps differentiate causes of heart failure and guides therapy—diuretics + thiamine vs inotropes or afterload reduction depending on cause.
9. Hematocrit has a nonlinear effect on blood viscosity; small increases near normal hematocrit cause viscosity to:
a) Decrease linearly with hematocrit
b) Increase exponentially with hematocrit above normal range
c) Remain unchanged by hematocrit changes
d) Only affect viscosity in capillaries
Answer: b) Increase exponentially with hematocrit above normal range.
Explanation (≈100 words): Viscosity rises disproportionately as hematocrit increases because cell–cell interactions and aggregation dramatically increase flow resistance. At low hematocrit viscosity falls, improving flow, but beyond physiologic range viscosity increases steeply, impairing microvascular perfusion despite higher oxygen content. This explains symptoms in polycythemia and the rationale for phlebotomy. Viscosity effects are especially important in larger vessels where blood behaves more Newtonian; in very small capillaries, red cell deformability and Fåhraeus-Lindqvist effects modulate apparent viscosity.
10 (clinical). A patient with severe aortic stenosis has a low forward flow and a systolic murmur. Which statement about flow and pressure is correct?
a) Aortic valve narrowing increases flow for a given pressure gradient
b) For a fixed LV pressure, aortic stenosis reduces forward flow and raises upstream pressure (LV systolic pressure)
c) Aortic stenosis reduces LV afterload and increases stroke volume
d) Viscosity changes are the primary determinant of the murmur
Answer: b) For a fixed LV pressure, aortic stenosis reduces forward flow and raises upstream pressure (LV systolic pressure).
Explanation (≈100 words): Aortic stenosis imposes an outflow obstruction: for a given ventricular contractile pressure, less blood traverses the narrowed valve so forward stroke volume falls. To maintain flow, the LV generates higher systolic pressures, causing hypertrophy and increased LV afterload. The resulting high pressure gradient across the valve produces a systolic ejection murmur and can progress to heart failure. Flow across a stenotic orifice also depends on valve area (effective radius) per fluid dynamics; viscosity changes are minor contributors to murmur intensity compared with pressure gradients and turbulent flow past the valve.
Chapter: Cardiovascular Physiology; Topic: Hemodynamics; Subtopic: Pulmonary Capillary Wedge Pressure
Keyword Definitions:
Capillary Wedge Pressure: An indirect measure of left atrial pressure obtained by wedging a catheter into a small pulmonary arterial branch.
Hemodynamics: The study of blood flow, pressure, and resistance within the circulatory system.
Left Atrial Pressure: Reflects left ventricular end-diastolic pressure, important for assessing cardiac function.
Lead Question - 2014
Normal capillary wedge pressure ?
a) 0-2 mm Hg
b) 5-10 mm Hg
c) 15-20 mm Hg
d) 20-30 mm Hg
Answer & Explanation: (b) 5-10 mm Hg. Pulmonary capillary wedge pressure (PCWP) reflects left atrial pressure. Normal PCWP is about 6–12 mmHg in healthy adults. It is measured using a Swan-Ganz catheter. Elevated PCWP indicates left ventricular failure, mitral stenosis, or volume overload, while low values may occur in hypovolemia or septic shock.
1. An elevated pulmonary capillary wedge pressure indicates:
a) Hypovolemia
b) Left ventricular failure
c) Pulmonary embolism
d) Dehydration
Answer & Explanation: (b) Left ventricular failure. Increased PCWP occurs when left atrial pressure rises due to poor left ventricular emptying. It is a key diagnostic indicator for congestive heart failure and pulmonary edema, helping clinicians distinguish between cardiac and non-cardiac causes of respiratory distress.
2. Which of the following catheters is used to measure pulmonary capillary wedge pressure?
a) Hickman catheter
b) Swan-Ganz catheter
c) Foley catheter
d) Port-A-Cath
Answer & Explanation: (b) Swan-Ganz catheter. This balloon-tipped catheter is inserted via a central vein into the pulmonary artery. When wedged in a small arterial branch, it reflects left atrial pressure, allowing estimation of left ventricular preload and cardiac function.
3. In a patient with mitral stenosis, pulmonary capillary wedge pressure is:
a) Normal
b) Decreased
c) Increased
d) Variable
Answer & Explanation: (c) Increased. Mitral stenosis impedes blood flow from the left atrium to the left ventricle, causing an elevation of left atrial and wedge pressures. This results in pulmonary congestion and dyspnea, especially on exertion or during fluid overload states.
4. A PCWP less than 5 mmHg usually suggests:
a) Left heart failure
b) Pulmonary hypertension
c) Hypovolemia
d) Renal failure
Answer & Explanation: (c) Hypovolemia. Low wedge pressure reflects decreased left atrial filling due to volume depletion or hemorrhage. It helps guide fluid therapy in critically ill patients by indicating inadequate preload or reduced intravascular volume.
5. A patient with acute myocardial infarction presents with dyspnea. His PCWP is 22 mmHg. This suggests:
a) Pulmonary embolism
b) Left ventricular failure
c) Right heart failure
d) Dehydration
Answer & Explanation: (b) Left ventricular failure. The elevated PCWP indicates increased left atrial pressure secondary to impaired left ventricular contractility post-infarction, leading to pulmonary congestion and edema. It confirms a cardiac cause for respiratory distress.
6. Which pressure correlates most closely with left ventricular end-diastolic pressure?
a) Right atrial pressure
b) Pulmonary artery pressure
c) Pulmonary capillary wedge pressure
d) Central venous pressure
Answer & Explanation: (c) Pulmonary capillary wedge pressure. PCWP represents left atrial pressure and thus approximates left ventricular end-diastolic pressure, providing vital information about left heart filling and compliance in cardiac assessment.
7. In which condition is PCWP normal despite pulmonary edema?
a) Left heart failure
b) ARDS
c) Mitral stenosis
d) Aortic regurgitation
Answer & Explanation: (b) ARDS. In acute respiratory distress syndrome, pulmonary edema occurs due to increased capillary permeability, not elevated left atrial pressure. Hence, PCWP remains normal, helping differentiate ARDS from cardiogenic pulmonary edema.
8. During mechanical ventilation with positive end-expiratory pressure (PEEP), PCWP readings may:
a) Increase falsely
b) Decrease falsely
c) Remain unaffected
d) Reflect right atrial pressure
Answer & Explanation: (a) Increase falsely. PEEP raises intrathoracic pressure, leading to an artificial elevation of measured wedge pressure. Hence, correction or cautious interpretation is required when assessing PCWP in ventilated patients.
9. PCWP is not a reliable indicator of left atrial pressure in:
a) Mitral regurgitation
b) Left ventricular failure
c) Hypovolemia
d) Cardiogenic shock
Answer & Explanation: (a) Mitral regurgitation. In MR, pressure waves transmitted from the ventricle distort left atrial pressure readings, making PCWP less reliable. Direct left atrial measurements or echocardiography may provide more accurate assessment.
10. A patient with sepsis has PCWP of 6 mmHg and cardiac output of 8 L/min. The most likely cause is:
a) Cardiogenic shock
b) Hypovolemic shock
c) Distributive shock
d) Obstructive shock
Answer & Explanation: (c) Distributive shock. In sepsis, vasodilation and capillary leak cause low filling pressures with high cardiac output. PCWP remains normal or low despite adequate fluid resuscitation, indicating peripheral vasodilation and reduced afterload.
Chapter: Renal Physiology; Topic: Osmotic Diuretics; Subtopic: Mannitol and Fluid Osmolarity
Keyword Definitions:
Mannitol: An osmotic diuretic used to reduce intracranial and intraocular pressure by increasing plasma osmolarity.
Osmolarity: The concentration of solute particles in a solution, influencing water movement across membranes.
Intracranial Pressure (ICP): The pressure within the skull; elevated levels can impair cerebral perfusion.
Osmotic Diuretic: A substance that promotes diuresis by increasing osmotic pressure in renal tubules, preventing water reabsorption.
Lead Question - 2014
Mannitol infusion causes increase in
a) Blood viscosity
b) Osmolarity
c) Intra-ocular tension
d) Intracranial tension
Answer & Explanation: (b) Osmolarity. Mannitol increases plasma osmolarity, drawing water out of brain and ocular tissues, thereby reducing intracranial and intraocular pressures. It is filtered by the glomerulus but not reabsorbed, causing osmotic diuresis. Excess use can lead to dehydration or hypernatremia if water loss exceeds sodium excretion.
1. Mannitol is primarily used in the management of:
a) Congestive heart failure
b) Acute renal failure (oliguric phase)
c) Intracranial hypertension
d) Hypertension
Answer & Explanation: (c) Intracranial hypertension. Mannitol reduces intracranial pressure by creating an osmotic gradient across the blood-brain barrier. Water moves from brain tissue into plasma, relieving cerebral edema. It is often administered intravenously in neurocritical care or post-head injury management for rapid pressure reduction.
2. Which of the following is a contraindication for mannitol use?
a) Glaucoma
b) Cerebral edema
c) Anuria due to renal failure
d) Raised intracranial pressure
Answer & Explanation: (c) Anuria due to renal failure. Mannitol requires filtration through the glomeruli for its action. In anuria, it accumulates in plasma, worsening fluid overload and leading to pulmonary edema or heart failure. Hence, renal function must be ensured before administration.
3. A 45-year-old male with head trauma is given mannitol. The drug’s primary mechanism is:
a) Decreasing cerebrospinal fluid production
b) Increasing plasma osmolarity
c) Vasodilation of cerebral vessels
d) Blocking aquaporins in the nephron
Answer & Explanation: (b) Increasing plasma osmolarity. Mannitol increases extracellular osmolarity, drawing water out of brain cells and lowering cerebral edema. It acts rapidly, improving cerebral perfusion pressure and oxygen delivery, which are crucial in head injury management.
4. Prolonged mannitol infusion may lead to:
a) Hyponatremia
b) Pulmonary edema
c) Hypokalemia
d) Hypercalcemia
Answer & Explanation: (b) Pulmonary edema. If mannitol draws excessive water into the vascular space without adequate excretion, plasma volume expansion occurs. This can precipitate pulmonary congestion, particularly in patients with heart failure or compromised renal function.
5. The major site of mannitol action in the nephron is:
a) Proximal tubule
b) Loop of Henle
c) Distal convoluted tubule
d) Collecting duct
Answer & Explanation: (a) Proximal tubule. Mannitol acts primarily in the proximal tubule and descending limb of the loop of Henle, where it inhibits water reabsorption by increasing tubular osmotic pressure. This results in increased urine output and excretion of electrolytes.
6. In acute glaucoma, mannitol reduces intraocular pressure by:
a) Stimulating aqueous humor secretion
b) Decreasing aqueous humor formation
c) Drawing fluid from the eye into plasma
d) Increasing choroidal blood flow
Answer & Explanation: (c) Drawing fluid from the eye into plasma. Mannitol increases plasma osmolarity, pulling water from ocular tissues via osmotic gradient. This reduces intraocular volume and pressure, providing rapid relief in acute glaucoma before surgical or definitive management.
7. In a patient with cerebral edema, excessive mannitol administration can lead to:
a) Rebound intracranial hypertension
b) Bradycardia
c) Hypoglycemia
d) Hypotension
Answer & Explanation: (a) Rebound intracranial hypertension. With prolonged or excessive dosing, mannitol crosses a damaged blood-brain barrier and draws water back into the brain, worsening edema. Monitoring osmolarity and using intermittent dosing helps prevent this complication in neurocritical settings.
8. Mannitol should be avoided in which of the following cardiac conditions?
a) Pericarditis
b) Heart failure
c) Myocarditis
d) Stable angina
Answer & Explanation: (b) Heart failure. Mannitol expands intravascular volume initially, which can overload the failing heart and precipitate pulmonary edema. Therefore, it must be avoided or used with extreme caution in patients with congestive cardiac failure or reduced ejection fraction.
9. A patient on mannitol therapy shows serum osmolarity of 340 mOsm/L. The infusion should be:
a) Increased
b) Continued
c) Reduced
d) Stopped immediately
Answer & Explanation: (d) Stopped immediately. Serum osmolarity beyond 320 mOsm/L increases risk of renal failure and CNS toxicity. Mannitol should be discontinued at this threshold to prevent osmotic nephrosis and electrolyte imbalances associated with hyperosmolarity.
10. Which electrolyte disturbance is commonly seen with mannitol use?
a) Hyperkalemia
b) Hyponatremia
c) Hypokalemia
d) Hypernatremia
Answer & Explanation: (d) Hypernatremia. Mannitol-induced osmotic diuresis leads to water loss exceeding sodium excretion, causing hypernatremia and dehydration. Monitoring serum sodium and osmolarity during therapy helps prevent neurologic complications and maintain proper fluid balance.
Chapter: Cardiovascular Physiology; Topic: Hemodynamics; Subtopic: Blood Flow Velocity in Circulatory System
Keyword Definitions:
Velocity of blood flow: The speed at which blood moves through a vessel, inversely related to the total cross-sectional area of that vessel type.
Aorta: The largest artery in the body carrying oxygenated blood from the left ventricle to the systemic circulation.
Vena cava: The largest vein carrying deoxygenated blood back to the heart.
Arterioles and venules: Small vessels controlling resistance and capillary exchange.
Lead Question – 2014
Correct order of velocity ?
a) Vena cava > Aorta > Vein > Artery > Venule > Arteriole
b) Aorta > Vena cava > Artery > Vein > Arteriole > Venule
c) Aorta > Artery > Vena cava > Vein > Arteriole > Venule
d) Vena cava > Vein > Aorta > Artery > Venule > Arteriole
Answer & Explanation: The correct answer is b) Aorta > Vena cava > Artery > Vein > Arteriole > Venule. Blood velocity is highest in the aorta due to its small total cross-sectional area and declines as vessels branch. Capillaries have the slowest flow allowing nutrient exchange. Venous return increases in large veins but remains slower than in arteries.
1. Velocity of blood is least in
a) Arteries
b) Arterioles
c) Capillaries
d) Veins
Answer & Explanation: The correct answer is c) Capillaries. Blood velocity is inversely proportional to the total cross-sectional area. Capillaries, having the largest total area, exhibit the slowest velocity to ensure optimal nutrient and gas exchange between blood and tissues. This slow flow also reduces shear stress on delicate capillary walls.
2. Which factor primarily determines blood flow velocity?
a) Blood viscosity
b) Vessel radius
c) Cross-sectional area
d) Pressure gradient
Answer & Explanation: The correct answer is c) Cross-sectional area. Velocity varies inversely with total cross-sectional area of vessels. In systemic circulation, capillaries collectively have the largest area, leading to slowest flow. In contrast, large arteries and veins have smaller total areas, resulting in faster velocity of blood flow.
3. A 45-year-old hypertensive patient shows decreased capillary perfusion. Which vascular change explains this?
a) Increased capillary diameter
b) Decreased arteriolar radius
c) Increased venous compliance
d) Reduced aortic compliance
Answer & Explanation: The correct answer is b) Decreased arteriolar radius. Arterioles control capillary perfusion by regulating resistance. Vasoconstriction decreases blood flow into capillaries, reducing perfusion pressure. This autoregulatory mechanism maintains systemic blood pressure but limits nutrient and oxygen delivery to tissues in hypertension.
4. In which of the following vessels is blood flow velocity maximum?
a) Capillaries
b) Arterioles
c) Aorta
d) Veins
Answer & Explanation: The correct answer is c) Aorta. The aorta, having the smallest total cross-sectional area among all vessel types, shows the highest blood velocity. Despite being a single large vessel, its narrow combined area compared to capillaries leads to rapid flow directly from the left ventricle.
5. A 60-year-old with chronic heart failure has reduced venous return. Which vessel mainly contributes to this change?
a) Venules
b) Large veins
c) Arterioles
d) Capillaries
Answer & Explanation: The correct answer is b) Large veins. Veins act as capacitance vessels, storing most of the blood volume. In heart failure, reduced venous tone decreases venous return to the heart, leading to pooling in the periphery and diminished cardiac output, worsening congestion.
6. Which of the following statements about velocity of flow is true?
a) Velocity increases with total cross-sectional area
b) Velocity is constant throughout circulation
c) Velocity decreases as vessels branch
d) Velocity increases from artery to arteriole
Answer & Explanation: The correct answer is c) Velocity decreases as vessels branch. As the arterial system branches into smaller vessels, the total cross-sectional area increases, leading to decreased velocity. This ensures adequate time for diffusion and exchange in capillaries before returning to venous circulation.
7. A patient with severe dehydration exhibits increased blood viscosity. How does this affect flow velocity?
a) Increases velocity
b) Decreases velocity
c) No effect
d) Initially increases then decreases
Answer & Explanation: The correct answer is b) Decreases velocity. Increased viscosity due to hemoconcentration elevates resistance, reducing flow velocity. Poiseuille’s law states velocity is inversely proportional to viscosity when pressure and radius are constant, hence flow slows despite normal arterial pressure.
8. During exercise, which vessel type shows maximum increase in blood flow velocity?
a) Arterioles
b) Capillaries
c) Veins
d) Large arteries
Answer & Explanation: The correct answer is d) Large arteries. During exercise, sympathetic activation increases cardiac output and arterial tone. This enhances flow velocity in large arteries to meet tissue oxygen demands, while arterioles dilate to maintain capillary perfusion without excessive pressure rise.
9. In venous circulation, blood velocity increases primarily due to
a) Skeletal muscle pump
b) Capillary pressure
c) Arteriolar constriction
d) Lymphatic drainage
Answer & Explanation: The correct answer is a) Skeletal muscle pump. During movement, muscle contractions compress veins, propelling blood toward the heart and preventing pooling. Venous valves prevent backflow, enhancing velocity especially in lower limbs, which depend heavily on muscular assistance.
10. A trauma patient with hypovolemia has aortic velocity of 60 cm/s. Which of the following changes would occur next?
a) Increased capillary flow
b) Decreased venous return
c) Increased peripheral resistance
d) Decreased heart rate
Answer & Explanation: The correct answer is b) Decreased venous return. Hypovolemia reduces circulating blood volume, leading to decreased venous return and lower cardiac output. Despite compensatory vasoconstriction maintaining arterial velocity, systemic perfusion drops, resulting in tissue hypoxia and hypotension if uncorrected.
Chapter: General Physiology; Topic: Body Fluid Compartments; Subtopic: Tonicity and Osmotic Shifts
Keyword Definitions:
Hypotonic saline: A solution with lower osmolarity than plasma, causing water to move into cells by osmosis.
ICF (Intracellular Fluid): Fluid contained within the cells, comprising about two-thirds of total body water.
ECF (Extracellular Fluid): Fluid outside the cells, including plasma and interstitial fluid, comprising one-third of total body water.
Osmosis: The passive movement of water across a semipermeable membrane from a region of lower solute concentration to higher solute concentration.
Lead Question – 2014
Effect of infusion of hypotonic saline?
a) Increased ICF only
b) Increased ECF only
c) Increased in both ICF and ECF
d) Increased ICF and decreased ECF
Answer & Explanation: The correct answer is c) Increased in both ICF and ECF. When hypotonic saline is infused, water moves from the extracellular fluid (ECF) into the intracellular fluid (ICF) due to osmotic gradient. Both compartments gain water, but the ICF expands more. Plasma osmolarity decreases, cell swelling occurs, and total body water increases without change in solute amount.
1. Infusion of hypertonic saline leads to which of the following changes?
a) Increased ICF, decreased ECF
b) Decreased ICF, increased ECF
c) Increased both ICF and ECF
d) No change in ICF
Answer & Explanation: The correct answer is b) Decreased ICF, increased ECF. Hypertonic saline has higher osmolarity than plasma, drawing water out of cells into the extracellular compartment. This causes cell shrinkage, increases ECF volume, and raises plasma osmolarity, commonly used to reduce cerebral edema or hyponatremia-related brain swelling.
2. A patient receives rapid infusion of isotonic saline. What happens to ICF volume?
a) Increases
b) Decreases
c) No change
d) Initially increases then decreases
Answer & Explanation: The correct answer is c) No change. Isotonic saline has osmolarity equal to plasma, hence it distributes only in the ECF compartment without affecting ICF. It expands both plasma and interstitial fluid equally, making it ideal for replacing extracellular fluid losses due to dehydration or hemorrhage.
3. Which of the following intravenous fluids would cause cell swelling?
a) 5% Dextrose in water
b) 0.9% NaCl
c) 3% NaCl
d) 5% Albumin solution
Answer & Explanation: The correct answer is a) 5% Dextrose in water. Once infused, dextrose is metabolized to carbon dioxide and water, leaving behind free water. This free water acts as a hypotonic solution, moving into cells, increasing ICF volume, and causing cellular swelling, particularly in neurons.
4. A 50-year-old man with severe burns is given hypotonic fluid. What complication can occur if infused rapidly?
a) Hypokalemia
b) Hyponatremia
c) Hypernatremia
d) Dehydration
Answer & Explanation: The correct answer is b) Hyponatremia. Rapid infusion of hypotonic fluids dilutes plasma sodium concentration, resulting in hyponatremia. Water enters brain cells, causing cerebral edema, nausea, confusion, and even seizures if not corrected. Hence, hypotonic fluids are given cautiously in burn and trauma patients.
5. Infusion of hypotonic saline affects plasma osmolarity by
a) Increasing osmolarity
b) Decreasing osmolarity
c) No change
d) Fluctuating without pattern
Answer & Explanation: The correct answer is b) Decreasing osmolarity. Hypotonic saline has fewer solutes than plasma, lowering plasma osmolarity. This drives water movement into cells, equalizing osmotic gradients. The resultant hypo-osmolar plasma may impair neuronal function and increase risk of cerebral edema.
6. A patient presents with dehydration and hypernatremia. Which type of fluid should be administered?
a) Isotonic saline
b) Hypotonic saline
c) Hypertonic saline
d) Colloid solution
Answer & Explanation: The correct answer is b) Hypotonic saline. In hypernatremia, water deficit exceeds sodium loss. Hypotonic saline corrects cellular dehydration by shifting water into ICF, reducing sodium concentration gradually. Rapid correction can lead to cerebral edema, hence infusion rate must be carefully regulated.
7. During treatment of diabetic ketoacidosis, why is hypotonic saline preferred after initial resuscitation?
a) To increase glucose excretion
b) To prevent hypokalemia
c) To replace intracellular water loss
d) To maintain high plasma osmolarity
Answer & Explanation: The correct answer is c) To replace intracellular water loss. In diabetic ketoacidosis, hyperosmolarity causes significant cellular dehydration. After restoring circulation with isotonic saline, hypotonic saline helps rehydrate cells safely by reducing osmotic imbalance and improving metabolic recovery without causing rapid sodium shifts.
8. A 30-year-old woman develops confusion after marathon running and consuming excess water. What fluid shift occurred?
a) Water moved from ICF to ECF
b) Water moved from ECF to ICF
c) Sodium moved into cells
d) No movement
Answer & Explanation: The correct answer is b) Water moved from ECF to ICF. Overhydration decreases plasma osmolarity, leading to water entry into cells. This causes cerebral edema manifesting as confusion, headache, and sometimes seizures, a condition termed water intoxication or dilutional hyponatremia.
9. Infusion of which solution expands both ECF and ICF compartments equally?
a) 0.9% NaCl
b) 0.45% NaCl
c) 3% NaCl
d) 5% Albumin
Answer & Explanation: The correct answer is b) 0.45% NaCl. This is a hypotonic saline solution. It distributes across both ECF and ICF due to osmotic water movement. About two-thirds of the infused water enters ICF, while one-third stays in ECF, making it useful for rehydrating dehydrated cells.
10. A patient with cerebral edema should never be given
a) Hypertonic saline
b) Isotonic saline
c) Hypotonic saline
d) Mannitol
Answer & Explanation: The correct answer is c) Hypotonic saline. Hypotonic fluids worsen cerebral edema by promoting water entry into already swollen brain cells. Instead, hypertonic saline or mannitol is administered to draw water out of brain cells, reducing intracranial pressure and improving neurological outcomes.
Chapter: Cardiovascular Physiology; Topic: Electrocardiography (ECG); Subtopic: Cardiac Axis and ECG Interpretation
Keyword Definitions:
QRS axis: The average direction of ventricular depolarization recorded on the frontal plane in an ECG.
ECG leads: Electrical recordings from different viewpoints, used to determine the axis and detect abnormalities.
Depolarization: Process by which cardiac muscle cells become electrically activated before contraction.
Left axis deviation: When QRS axis is less than -30°, often seen in left ventricular hypertrophy or conduction blocks.
Lead Question – 2014
Normal QRS axis ?
a) +30 to 110°
b) -30 to +110°
c) +110° to +150°
d) -110° to -150°
Answer & Explanation: The correct answer is b) -30° to +110°. The normal QRS axis represents the direction of overall ventricular depolarization. It lies between -30° and +110° in healthy adults. Axis shifts may occur due to heart position, hypertrophy, or conduction blocks. ECG leads I and aVF are primarily used for determining the cardiac axis.
1. Left axis deviation is commonly seen in which of the following?
a) Right ventricular hypertrophy
b) Left ventricular hypertrophy
c) Dextrocardia
d) Pulmonary embolism
Answer & Explanation: The correct answer is b) Left ventricular hypertrophy. In left ventricular hypertrophy, increased muscle mass of the left ventricle alters the direction of depolarization, causing left axis deviation (axis less than -30°). It may also occur in left anterior fascicular block or inferior wall myocardial infarction.
2. Right axis deviation is most likely seen in which condition?
a) Aortic stenosis
b) Chronic lung disease
c) Left bundle branch block
d) Systemic hypertension
Answer & Explanation: The correct answer is b) Chronic lung disease. Right axis deviation (axis greater than +110°) occurs due to right ventricular hypertrophy, which often results from pulmonary hypertension or chronic obstructive pulmonary disease (COPD). It reflects increased right ventricular workload due to elevated pulmonary pressures.
3. Which ECG leads are most useful in determining the QRS axis?
a) V1 and V6
b) I and aVF
c) II and III
d) aVL and V3
Answer & Explanation: The correct answer is b) I and aVF. Leads I and aVF represent the frontal plane view of cardiac depolarization. If both show positive QRS complexes, the axis is normal. Lead I helps determine left-right orientation, and aVF helps confirm inferior-superior orientation, forming the basis of quadrant analysis.
4. A 45-year-old hypertensive man shows left axis deviation on ECG. The most probable cause is
a) Left ventricular hypertrophy
b) Right bundle branch block
c) Pulmonary embolism
d) Mitral stenosis
Answer & Explanation: The correct answer is a) Left ventricular hypertrophy. Chronic hypertension increases left ventricular workload, causing hypertrophy and shifting the mean depolarization vector toward the left. This manifests as left axis deviation on ECG, typically between -30° and -90°, often with high voltage QRS complexes.
5. Which of the following ECG findings suggests right axis deviation?
a) Positive QRS in lead I, positive in aVF
b) Negative QRS in lead I, positive in aVF
c) Positive QRS in lead I, negative in aVF
d) Negative QRS in both lead I and aVF
Answer & Explanation: The correct answer is b) Negative QRS in lead I, positive in aVF. This indicates that depolarization is directed more toward the right, consistent with right axis deviation. Common causes include pulmonary hypertension, right ventricular hypertrophy, or right bundle branch block.
6. A 65-year-old patient with COPD shows right axis deviation. What is the physiological reason?
a) Decreased right ventricular mass
b) Right ventricular hypertrophy
c) Left atrial enlargement
d) Conduction delay in left ventricle
Answer & Explanation: The correct answer is b) Right ventricular hypertrophy. Chronic lung disease causes pulmonary hypertension, increasing right ventricular workload and muscle mass. This shifts the electrical axis rightward beyond +110°, leading to right axis deviation on ECG, often seen in cor pulmonale.
7. Electrical axis can be shifted leftward physiologically in
a) Standing posture
b) Supine position
c) During exercise
d) After heavy meal
Answer & Explanation: The correct answer is b) Supine position. In the supine position, the diaphragm rises, pushing the heart to a more horizontal position. This shifts the mean QRS axis leftward. Conversely, in standing position, the diaphragm lowers, causing a rightward shift of the cardiac axis.
8. In which condition will the QRS axis appear normal but the patient has conduction defect?
a) Left anterior fascicular block
b) Right bundle branch block
c) Left posterior fascicular block
d) Complete AV block
Answer & Explanation: The correct answer is b) Right bundle branch block. In right bundle branch block (RBBB), overall QRS axis may remain within the normal range (-30° to +110°), though the right ventricle depolarizes later. ECG shows widened QRS and characteristic ‘RSR’ pattern in lead V1.
9. A 30-year-old woman presents with palpitations. ECG shows QRS axis of +150°. Which condition is most consistent?
a) Left anterior fascicular block
b) Left ventricular hypertrophy
c) Right ventricular hypertrophy
d) Left posterior fascicular block
Answer & Explanation: The correct answer is d) Left posterior fascicular block. This conduction defect delays activation of the posterior and inferior regions of the left ventricle, shifting the QRS axis markedly rightward (between +120° and +180°). It can coexist with right bundle branch block.
10. Which of the following can cause extreme axis deviation (northwest axis)?
a) Ventricular tachycardia
b) Left bundle branch block
c) Right atrial enlargement
d) Atrial flutter
Answer & Explanation: The correct answer is a) Ventricular tachycardia. In ventricular tachycardia, depolarization originates in the ventricles rather than the atria, resulting in an abnormal direction of depolarization. The QRS axis often lies between -90° and ±180°, termed an “extreme” or “northwest” axis, indicating severe conduction abnormality.
Chapter: Respiratory Physiology Topic: Neural Regulation of Respiration Subtopic: Reflex Control of Breathing
Keyword Definitions:
• Hering-Breuer Reflex: A protective reflex that prevents overinflation of the lungs during inspiration by stimulating stretch receptors in the lungs.
• Inspiration: The process of air entering the lungs due to diaphragmatic and intercostal muscle contraction.
• Expiration: The passive process of air leaving the lungs due to elastic recoil of the lungs and chest wall.
• Stretch Receptors: Mechanoreceptors located in the smooth muscle of airways sensitive to lung inflation.
• Vagus Nerve: Cranial nerve X, responsible for transmitting sensory input from lungs to the respiratory center.
Lead Question – 2014 Hering-Breuer reflex is an increase in?
a) Duration of inspiration
b) Duration of expiration
c) Depth of inspiration
d) Depth of expiration
Answer & Explanation: Answer: b) Duration of expiration
The Hering-Breuer inflation reflex inhibits inspiration when the lungs are overstretched, preventing overinflation. Pulmonary stretch receptors send signals via the vagus nerve to the medulla, stopping inspiratory impulses. This reflex lengthens expiration, allowing the lungs to deflate before the next inspiration begins. It maintains rhythmic breathing and protects alveolar structure.
1) Which nerve mediates the Hering-Breuer reflex?
a) Glossopharyngeal nerve
b) Vagus nerve
c) Phrenic nerve
d) Intercostal nerve
Answer & Explanation: Answer: b) Vagus nerve
The vagus nerve carries afferent impulses from stretch receptors in lung tissue to the medullary respiratory center. It plays a vital role in terminating inspiration and initiating expiration during the Hering-Breuer reflex, thereby preventing excessive lung inflation and maintaining normal tidal volume rhythmically.
2) In which condition is the Hering-Breuer reflex more prominent?
a) During quiet breathing
b) During deep breathing
c) During sleep
d) During apnea
Answer & Explanation: Answer: b) During deep breathing
The reflex becomes more active during deep or forceful inspiration, as lung inflation stretches the alveoli more significantly. The activation of pulmonary stretch receptors at high lung volumes triggers the vagus nerve, halting inspiration and allowing expiration. In quiet breathing, its role is minimal.
3) The Hering-Breuer reflex mainly functions to:
a) Increase respiratory rate
b) Prevent alveolar collapse
c) Prevent overinflation of lungs
d) Stimulate chemoreceptors
Answer & Explanation: Answer: c) Prevent overinflation of lungs
The reflex serves as a protective mechanism to prevent alveolar damage caused by overdistension. It achieves this by terminating inspiration through vagal feedback to the medullary centers, ensuring controlled tidal volume and maintaining pulmonary elasticity.
4) Which receptors are involved in the Hering-Breuer reflex?
a) Irritant receptors
b) Chemoreceptors
c) Stretch receptors
d) J receptors
Answer & Explanation: Answer: c) Stretch receptors
Stretch receptors, located in smooth muscles of the bronchi and bronchioles, detect lung inflation. Their activation stimulates afferent vagal fibers that inhibit inspiratory neurons, ending inspiration and extending expiration. They play a crucial role in maintaining ventilatory control under high tidal volumes.
5) Which part of the brain integrates the Hering-Breuer reflex?
a) Pons
b) Medulla oblongata
c) Midbrain
d) Cerebellum
Answer & Explanation: Answer: b) Medulla oblongata
The medulla houses the dorsal respiratory group (DRG) that integrates vagal input from pulmonary stretch receptors. This feedback inhibits inspiratory signals, ensuring expiration follows after sufficient inflation. Thus, medullary centers orchestrate the rhythmic pattern of breathing via reflex feedback.
6) A patient on mechanical ventilation exhibits prolonged expiration; this is due to activation of:
a) J receptors
b) Pulmonary stretch receptors
c) Carotid body receptors
d) Central chemoreceptors
Answer & Explanation: Answer: b) Pulmonary stretch receptors
During mechanical ventilation, the lungs are inflated more than normal, activating pulmonary stretch receptors. These receptors send inhibitory impulses via the vagus nerve to suppress inspiration, causing prolonged expiration as part of the Hering-Breuer inflation reflex.
7) In which situation would the Hering-Breuer reflex be suppressed?
a) Bilateral vagotomy
b) Increased tidal volume
c) Hypercapnia
d) Pulmonary edema
Answer & Explanation: Answer: a) Bilateral vagotomy
The reflex depends on intact vagal afferent fibers. Bilateral vagotomy disrupts vagal transmission from lung stretch receptors, eliminating the reflex, resulting in prolonged inspiration and irregular breathing patterns. It highlights the crucial role of vagal feedback in breathing regulation.
8) Which receptor type mediates the opposite reflex — promoting inspiration after deflation?
a) Stretch receptors
b) Deflation receptors
c) J receptors
d) Baroreceptors
Answer & Explanation: Answer: b) Deflation receptors
Deflation receptors are stimulated during lung collapse, sending excitatory impulses to promote inspiration. This reflex ensures that breathing resumes after expiration, maintaining cyclic ventilation. It complements the Hering-Breuer reflex by balancing inflation and deflation cycles.
9) In neonates, the Hering-Breuer reflex:
a) Is absent
b) Helps establish rhythmic breathing
c) Causes apnea
d) Inhibits expiratory neurons
Answer & Explanation: Answer: b) Helps establish rhythmic breathing
In newborns, the reflex plays a vital role in stabilizing breathing patterns by regulating the depth and duration of inspiration. It prevents overexpansion of immature alveoli and supports the development of rhythmic ventilation cycles crucial for survival.
10) A patient with COPD shows diminished Hering-Breuer reflex due to:
a) Decreased lung compliance
b) Increased stretch receptor sensitivity
c) Increased vagal tone
d) Enhanced elastic recoil
Answer & Explanation: Answer: a) Decreased lung compliance
In COPD, chronic airway obstruction and loss of elastic recoil reduce lung compliance. As a result, pulmonary stretch receptors are less stimulated, weakening the Hering-Breuer reflex. This contributes to abnormal respiratory rhythm and inefficient ventilation observed in chronic obstructive diseases.
Chapter: Respiratory Physiology Topic: Regulation of Respiration Subtopic: Chemoreceptor Control of Breathing
Keyword Definitions:
• Carotid Bodies: Small chemoreceptive structures located at the bifurcation of the common carotid arteries that detect changes in blood oxygen, carbon dioxide, and pH.
• Aortic Bodies: Chemoreceptors located along the aortic arch that sense changes in arterial oxygen levels.
• Hypoxia: A condition in which tissue oxygen levels fall below normal.
• Peripheral Chemoreceptors: Receptors sensitive mainly to changes in PaO₂ and slightly to pH and PaCO₂.
• PaO₂: Partial pressure of oxygen in arterial blood, normally around 100 mmHg.
Lead Question – 2014
Carotid and aortic bodies are stimulated when?
a) Oxygen saturation decreases below 90%
b) Oxygen saturation decreases below 80%
c) Oxygen saturation decreases below 70%
d) Oxygen saturation decreases below 60%
Answer & Explanation:
Answer: d) Oxygen saturation decreases below 60%
Peripheral chemoreceptors in the carotid and aortic bodies respond vigorously when arterial oxygen tension (PaO₂) drops below 60 mmHg, corresponding to roughly 90% oxygen saturation. This triggers increased afferent activity via glossopharyngeal and vagus nerves to the medulla, stimulating ventilation. The reflex enhances oxygen intake during hypoxemia or altitude exposure.
1) Which nerve carries impulses from carotid bodies to the medulla?
a) Vagus nerve
b) Glossopharyngeal nerve
c) Phrenic nerve
d) Hypoglossal nerve
Answer & Explanation:
Answer: b) Glossopharyngeal nerve
The carotid bodies send afferent signals through the glossopharyngeal nerve (cranial nerve IX) to the dorsal respiratory group in the medulla. When oxygen levels fall, the increased firing rate stimulates respiratory centers, enhancing both respiratory rate and depth to restore arterial oxygen tension.
2) The aortic bodies send impulses to the respiratory center via:
a) Glossopharyngeal nerve
b) Vagus nerve
c) Phrenic nerve
d) Trigeminal nerve
Answer & Explanation:
Answer: b) Vagus nerve
Aortic bodies, situated along the aortic arch, detect arterial oxygen tension and communicate through afferent fibers of the vagus nerve to the medullary respiratory center. Their activation under hypoxic conditions contributes to the reflex increase in ventilation to maintain oxygenation.
3) Which of the following primarily stimulates peripheral chemoreceptors?
a) Increased PaCO₂
b) Decreased PaO₂
c) Increased pH
d) Increased PaO₂
Answer & Explanation:
Answer: b) Decreased PaO₂
Peripheral chemoreceptors are highly sensitive to decreases in arterial oxygen tension (PaO₂), especially when it falls below 60 mmHg. While they can respond modestly to increased PaCO₂ and decreased pH, hypoxemia remains their main stimulant for triggering reflex hyperventilation.
4) Which condition most effectively activates the carotid body?
a) Metabolic alkalosis
b) Hypoxia
c) Hyperoxia
d) Anemia
Answer & Explanation:
Answer: b) Hypoxia
Carotid body activation occurs primarily due to decreased oxygen partial pressure (PaO₂). Although anemia reduces oxygen content, it does not significantly alter PaO₂, so it does not strongly stimulate chemoreceptors. Hypoxia directly triggers glomus cell depolarization and neurotransmitter release to enhance ventilation.
5) Which ion channel plays a major role in carotid body oxygen sensing?
a) Sodium channel
b) Potassium channel
c) Calcium channel
d) Chloride channel
Answer & Explanation:
Answer: b) Potassium channel
Under hypoxia, inhibition of oxygen-sensitive potassium channels in glomus cells causes depolarization, opening calcium channels and releasing neurotransmitters such as dopamine. This neurotransmitter release stimulates afferent nerves to signal low oxygen, promoting increased respiratory drive.
6) A patient with COPD experiences chronic hypoxia. Which chemoreceptors primarily drive respiration?
a) Central chemoreceptors
b) Peripheral chemoreceptors
c) J receptors
d) Baroreceptors
Answer & Explanation:
Answer: b) Peripheral chemoreceptors
In chronic hypercapnia, central chemoreceptors become desensitized to CO₂. Hence, the hypoxic drive mediated by carotid and aortic bodies becomes the dominant stimulus for respiration. Administration of excessive oxygen can suppress this drive, leading to hypoventilation in such patients.
7) Which gas most strongly stimulates central chemoreceptors?
a) Oxygen
b) Carbon dioxide
c) Nitrogen
d) Helium
Answer & Explanation:
Answer: b) Carbon dioxide
Central chemoreceptors located in the medulla respond to changes in the hydrogen ion concentration produced by CO₂ diffusion across the blood-brain barrier. Increased CO₂ elevates [H⁺] in cerebrospinal fluid, stimulating ventilation to restore acid-base balance. Peripheral receptors, in contrast, sense oxygen changes.
8) A mountain climber at high altitude experiences increased ventilation due to:
a) Central chemoreceptor activation
b) Peripheral chemoreceptor activation
c) Baroreceptor stimulation
d) Decreased metabolic rate
Answer & Explanation:
Answer: b) Peripheral chemoreceptor activation
At high altitude, low atmospheric oxygen reduces arterial PaO₂, activating peripheral chemoreceptors. The reflex response increases ventilation to raise oxygen delivery to tissues, counteracting hypoxemia. This is part of acclimatization to high-altitude environments.
9) A patient develops hypoventilation following a brainstem stroke. Which receptors are most affected?
a) Peripheral chemoreceptors
b) Central chemoreceptors
c) Baroreceptors
d) Stretch receptors
Answer & Explanation:
Answer: b) Central chemoreceptors
Central chemoreceptors are located on the ventrolateral surface of the medulla. Damage from a brainstem stroke disrupts CO₂-sensitive neurons, impairing the feedback mechanism that regulates respiratory rate and pH. This results in hypoventilation and carbon dioxide retention.
10) A 60-year-old smoker with chronic bronchitis shows increased respiratory drive after oxygen therapy. Why?
a) Increased CO₂ sensitivity
b) Reduced hypoxic drive inhibition
c) Stimulation of baroreceptors
d) Activation of J receptors
Answer & Explanation:
Answer: b) Reduced hypoxic drive inhibition
In chronic CO₂ retainers, hypoxia acts as the main ventilatory drive via peripheral chemoreceptors. Supplemental oxygen suppresses this hypoxic stimulus, reducing ventilation and leading to hypercapnia. Hence, oxygen therapy in COPD must be cautiously administered to avoid hypoventilation.
Chapter: Cardiovascular Physiology
Topic: Regulation of Blood Pressure
Subtopic: Baroreceptor Reflex Mechanism
Keyword Definitions:
• Baroreceptors: Stretch-sensitive mechanoreceptors located in the carotid sinus and aortic arch that detect changes in arterial pressure.
• Carotid Sinus: Dilated area at the bifurcation of the common carotid artery that senses blood pressure changes.
• Aortic Arch: The curved portion of the aorta where baroreceptors monitor systemic arterial pressure.
• Glossopharyngeal Nerve: Cranial nerve IX carrying afferent signals from the carotid sinus to the medulla.
• Vagus Nerve: Cranial nerve X transmitting signals from aortic baroreceptors to the brainstem.
Lead Question – 2014
Baroreceptor are?
a) Carotid body
b) Carotid sinus
c) Aortic body
d) None
Answer & Explanation:
Answer: b) Carotid sinus
Baroreceptors are stretch-sensitive receptors primarily found in the carotid sinus and aortic arch. They sense changes in arterial wall tension due to blood pressure fluctuations. Increased pressure stretches the vessel wall, stimulating afferent nerves (glossopharyngeal and vagus), which signal the medullary cardiovascular center to reduce heart rate and vasodilation, maintaining homeostasis.
1) Which nerve carries impulses from carotid sinus baroreceptors?
a) Vagus nerve
b) Glossopharyngeal nerve
c) Phrenic nerve
d) Trigeminal nerve
Answer & Explanation:
Answer: b) Glossopharyngeal nerve
The carotid sinus baroreceptors transmit afferent signals to the nucleus tractus solitarius in the medulla via the glossopharyngeal nerve (cranial nerve IX). These signals help regulate arterial blood pressure by influencing heart rate and peripheral resistance, forming part of the baroreceptor reflex arc.
2) Which of the following nerves transmits signals from aortic arch baroreceptors?
a) Glossopharyngeal nerve
b) Vagus nerve
c) Accessory nerve
d) Hypoglossal nerve
Answer & Explanation:
Answer: b) Vagus nerve
Aortic baroreceptors send afferent impulses through the vagus nerve (cranial nerve X) to the medullary cardiovascular centers. This reflex decreases sympathetic outflow and increases parasympathetic activity to lower blood pressure during hypertension.
3) Baroreceptors respond primarily to which stimulus?
a) Change in blood CO₂
b) Change in blood pH
c) Change in vessel wall stretch
d) Change in oxygen concentration
Answer & Explanation:
Answer: c) Change in vessel wall stretch
Baroreceptors are mechanoreceptors activated by arterial wall stretching. When blood pressure increases, vessel stretch enhances baroreceptor firing, leading to reflex bradycardia and vasodilation. Reduced stretch (hypotension) decreases firing, increasing sympathetic tone to restore pressure.
4) Which center integrates baroreceptor input in the brain?
a) Hypothalamus
b) Nucleus tractus solitarius
c) Cerebellum
d) Basal ganglia
Answer & Explanation:
Answer: b) Nucleus tractus solitarius
The nucleus tractus solitarius (NTS) in the medulla receives afferent input from baroreceptors and adjusts autonomic output. Increased NTS activity enhances vagal tone and inhibits sympathetic outflow, reducing blood pressure and heart rate through coordinated cardiovascular control.
5) Sudden standing from a lying position causes baroreceptor-mediated:
a) Vasodilation
b) Bradycardia
c) Increased sympathetic discharge
d) Reduced cardiac output
Answer & Explanation:
Answer: c) Increased sympathetic discharge
On standing, venous pooling reduces venous return and arterial pressure. Decreased baroreceptor firing triggers reflex sympathetic activation, increasing heart rate, contractility, and vasoconstriction, preventing orthostatic hypotension and maintaining cerebral perfusion.
6) In baroreceptor denervation, the immediate effect is:
a) Persistent hypertension
b) Persistent hypotension
c) Marked blood pressure fluctuations
d) Bradycardia
Answer & Explanation:
Answer: c) Marked blood pressure fluctuations
Loss of baroreceptor input removes rapid reflex control over blood pressure, causing large moment-to-moment fluctuations. Over time, the mean arterial pressure normalizes due to renal and hormonal compensatory mechanisms, but beat-to-beat stability remains impaired.
7) A patient with carotid sinus hypersensitivity experiences syncope due to:
a) Excessive sympathetic discharge
b) Reflex bradycardia and vasodilation
c) Increased cardiac output
d) Elevated arterial resistance
Answer & Explanation:
Answer: b) Reflex bradycardia and vasodilation
Carotid sinus hypersensitivity causes exaggerated vagal activation in response to mild pressure (e.g., tight collars), leading to sudden bradycardia, vasodilation, and transient cerebral hypoperfusion, manifesting as syncope.
8) Which receptor type responds to long-term blood pressure regulation?
a) Baroreceptors
b) Chemoreceptors
c) Renal volume receptors
d) Pulmonary stretch receptors
Answer & Explanation:
Answer: c) Renal volume receptors
Baroreceptors mediate short-term blood pressure control, while renal volume and juxtaglomerular receptors regulate long-term control via renin release and sodium-water balance, maintaining stable mean arterial pressure.
9) A patient with aortic arch baroreceptor damage shows:
a) Tachycardia and hypertension
b) Bradycardia and hypotension
c) Tachypnea
d) Decreased cardiac contractility
Answer & Explanation:
Answer: a) Tachycardia and hypertension
Loss of baroreceptor-mediated inhibitory feedback results in unchecked sympathetic activity, producing tachycardia, vasoconstriction, and elevated blood pressure due to reduced afferent inhibitory signaling to medullary centers.
10) During carotid massage, what physiological change occurs?
a) Increased heart rate
b) Increased sympathetic discharge
c) Reflex bradycardia and vasodilation
d) Reflex tachycardia
Answer & Explanation:
Answer: c) Reflex bradycardia and vasodilation
Carotid sinus massage mimics elevated blood pressure, increasing baroreceptor firing. The reflex response involves enhanced parasympathetic activity via the vagus nerve and suppression of sympathetic tone, resulting in reduced heart rate and vasodilation. This maneuver is used therapeutically to terminate supraventricular tachycardia.
Chapter: Cardiovascular Physiology
Topic: Regulation of Blood Pressure
Subtopic: Baroreceptor Reflex Mechanism
Keyword Definitions:
• Baroreceptors: Stretch-sensitive mechanoreceptors located in the carotid sinus and aortic arch that detect changes in arterial pressure.
• Carotid Sinus: Dilated area at the bifurcation of the common carotid artery that senses blood pressure changes.
• Aortic Arch: The curved portion of the aorta where baroreceptors monitor systemic arterial pressure.
• Glossopharyngeal Nerve: Cranial nerve IX carrying afferent signals from the carotid sinus to the medulla.
• Vagus Nerve: Cranial nerve X transmitting signals from aortic baroreceptors to the brainstem.
Lead Question – 2014
Baroreceptor are?
a) Carotid body
b) Carotid sinus
c) Aortic body
d) None
Answer & Explanation:
Answer: b) Carotid sinus
Baroreceptors are stretch-sensitive receptors primarily found in the carotid sinus and aortic arch. They sense changes in arterial wall tension due to blood pressure fluctuations. Increased pressure stretches the vessel wall, stimulating afferent nerves (glossopharyngeal and vagus), which signal the medullary cardiovascular center to reduce heart rate and vasodilation, maintaining homeostasis.
1) Which nerve carries impulses from carotid sinus baroreceptors?
a) Vagus nerve
b) Glossopharyngeal nerve
c) Phrenic nerve
d) Trigeminal nerve
Answer & Explanation:
Answer: b) Glossopharyngeal nerve
The carotid sinus baroreceptors transmit afferent signals to the nucleus tractus solitarius in the medulla via the glossopharyngeal nerve (cranial nerve IX). These signals help regulate arterial blood pressure by influencing heart rate and peripheral resistance, forming part of the baroreceptor reflex arc.
2) Which of the following nerves transmits signals from aortic arch baroreceptors?
a) Glossopharyngeal nerve
b) Vagus nerve
c) Accessory nerve
d) Hypoglossal nerve
Answer & Explanation:
Answer: b) Vagus nerve
Aortic baroreceptors send afferent impulses through the vagus nerve (cranial nerve X) to the medullary cardiovascular centers. This reflex decreases sympathetic outflow and increases parasympathetic activity to lower blood pressure during hypertension.
3) Baroreceptors respond primarily to which stimulus?
a) Change in blood CO₂
b) Change in blood pH
c) Change in vessel wall stretch
d) Change in oxygen concentration
Answer & Explanation:
Answer: c) Change in vessel wall stretch
Baroreceptors are mechanoreceptors activated by arterial wall stretching. When blood pressure increases, vessel stretch enhances baroreceptor firing, leading to reflex bradycardia and vasodilation. Reduced stretch (hypotension) decreases firing, increasing sympathetic tone to restore pressure.
4) Which center integrates baroreceptor input in the brain?
a) Hypothalamus
b) Nucleus tractus solitarius
c) Cerebellum
d) Basal ganglia
Answer & Explanation:
Answer: b) Nucleus tractus solitarius
The nucleus tractus solitarius (NTS) in the medulla receives afferent input from baroreceptors and adjusts autonomic output. Increased NTS activity enhances vagal tone and inhibits sympathetic outflow, reducing blood pressure and heart rate through coordinated cardiovascular control.
5) Sudden standing from a lying position causes baroreceptor-mediated:
a) Vasodilation
b) Bradycardia
c) Increased sympathetic discharge
d) Reduced cardiac output
Answer & Explanation:
Answer: c) Increased sympathetic discharge
On standing, venous pooling reduces venous return and arterial pressure. Decreased baroreceptor firing triggers reflex sympathetic activation, increasing heart rate, contractility, and vasoconstriction, preventing orthostatic hypotension and maintaining cerebral perfusion.
6) In baroreceptor denervation, the immediate effect is:
a) Persistent hypertension
b) Persistent hypotension
c) Marked blood pressure fluctuations
d) Bradycardia
Answer & Explanation:
Answer: c) Marked blood pressure fluctuations
Loss of baroreceptor input removes rapid reflex control over blood pressure, causing large moment-to-moment fluctuations. Over time, the mean arterial pressure normalizes due to renal and hormonal compensatory mechanisms, but beat-to-beat stability remains impaired.
7) A patient with carotid sinus hypersensitivity experiences syncope due to:
a) Excessive sympathetic discharge
b) Reflex bradycardia and vasodilation
c) Increased cardiac output
d) Elevated arterial resistance
Answer & Explanation:
Answer: b) Reflex bradycardia and vasodilation
Carotid sinus hypersensitivity causes exaggerated vagal activation in response to mild pressure (e.g., tight collars), leading to sudden bradycardia, vasodilation, and transient cerebral hypoperfusion, manifesting as syncope.
8) Which receptor type responds to long-term blood pressure regulation?
a) Baroreceptors
b) Chemoreceptors
c) Renal volume receptors
d) Pulmonary stretch receptors
Answer & Explanation:
Answer: c) Renal volume receptors
Baroreceptors mediate short-term blood pressure control, while renal volume and juxtaglomerular receptors regulate long-term control via renin release and sodium-water balance, maintaining stable mean arterial pressure.
9) A patient with aortic arch baroreceptor damage shows:
a) Tachycardia and hypertension
b) Bradycardia and hypotension
c) Tachypnea
d) Decreased cardiac contractility
Answer & Explanation:
Answer: a) Tachycardia and hypertension
Loss of baroreceptor-mediated inhibitory feedback results in unchecked sympathetic activity, producing tachycardia, vasoconstriction, and elevated blood pressure due to reduced afferent inhibitory signaling to medullary centers.
10) During carotid massage, what physiological change occurs?
a) Increased heart rate
b) Increased sympathetic discharge
c) Reflex bradycardia and vasodilation
d) Reflex tachycardia
Answer & Explanation:
Answer: c) Reflex bradycardia and vasodilation
Carotid sinus massage mimics elevated blood pressure, increasing baroreceptor firing. The reflex response involves enhanced parasympathetic activity via the vagus nerve and suppression of sympathetic tone, resulting in reduced heart rate and vasodilation. This maneuver is used therapeutically to terminate supraventricular tachycardia.