Keywords (for all questions)
Hering–Breuer reflex: Vagal afferent–mediated inflation reflex that terminates inspiration and prolongs expiration.
Pulmonary stretch receptors (PSR): Slowly adapting receptors in airway smooth muscle activated by lung inflation.
J receptors (juxtacapillary): C-fiber endings in alveolar walls; stimulated by interstitial edema; cause rapid, shallow breathing.
Deflation reflex: Lung deflation triggers increased inspiratory effort via vagal afferents.
Vagotomy: Cutting vagus abolishes Hering–Breuer reflex; tends to produce slow, deep breaths.
Apneustic center: Pontine area that promotes prolonged inspiration; normally inhibited by vagal input and pneumotaxic center.
Pneumotaxic center: Pontine center limiting inspiration, regulating rate and pattern.
Compliance: Change in lung volume per unit pressure; higher compliance augments PSR activation at a given pressure.
Tidal volume (VT): Volume of air inhaled or exhaled per normal breath (~500 mL adult).
PEEP: Positive end-expiratory pressure; affects lung volume, PSR firing, and reflexes during ventilation.
Central chemoreceptors: Sense CSF pH/PaCO₂; drive ventilation independent of PSR.
Peripheral chemoreceptors: Carotid/aortic bodies sensing PaO₂, PaCO₂, pH; mediate hypoxic drive.
Chapter: Respiratory Physiology | Topic: Neural Control of Breathing | Subtopic: Hering–Breuer Reflex
Lead Question – 2012
Herring Breuer reflex is an increase in ?
a) Duration of inspiration
b) Duration of expiration
c) Depth of inspiration
d) Depth of expiration
Explanation: The Hering–Breuer inflation reflex, mediated by slowly adapting pulmonary stretch receptors via the vagus, terminates inspiration to prevent overinflation, thereby prolonging expiratory time. This reflex is prominent at larger tidal volumes (e.g., exercise or mechanical ventilation) and is abolished by vagotomy. Answer: b) Duration of expiration.
1) In a ventilated ICU patient with high VT, activation of pulmonary stretch receptors will most likely:
a) Increase inspiratory time b) Prolong expiratory time c) Cause apnea via chemoreceptors d) Reduce vagal tone
Explanation: Large tidal volumes increase PSR firing, engaging the Hering–Breuer inflation reflex that ends inspiration and prolongs expiration, reducing respiratory rate. Chemoreceptors are not the primary mediators here; vagal afferents are. Answer: b) Prolong expiratory time.
2) Which nerve carries afferents essential for the Hering–Breuer inflation reflex?
a) Glossopharyngeal b) Vagus c) Phrenic d) Intercostal
Explanation: Slowly adapting pulmonary stretch receptors send impulses via the vagus to medullary respiratory centers. Vagotomy abolishes the reflex and leads to slower, deeper breathing patterns due to loss of inspiratory termination. Answer: b) Vagus.
3) A neonate’s breathing pattern is strongly influenced by the Hering–Breuer reflex. The primary functional benefit is:
a) Enhancing hypoxic drive b) Preventing alveolar overdistension c) Increasing dead space d) Facilitating CO₂ retention
Explanation: In neonates, the Hering–Breuer reflex is more prominent and helps terminate inspiration to avoid overdistension of compliant lungs, stabilizing VT and FRC. It does not increase dead space or promote CO₂ retention physiologically. Answer: b) Preventing alveolar overdistension.
4) Following bilateral vagotomy in an animal model, which breathing pattern is expected?
a) Rapid, shallow breathing b) Slow, deep breathing c) Cheyne–Stokes respiration d) Apneustic breathing relieved
Explanation: Loss of vagal afferents removes stretch-mediated inspiratory termination, producing slow, deep breaths. Apneustic patterns arise with pontine lesions, not isolated vagotomy. Rapid shallow breathing reflects J-receptor activity, not PSR loss. Answer: b) Slow, deep breathing.
5) In interstitial pulmonary edema, stimulation of J receptors leads to:
a) Prolonged expiration b) Rapid, shallow breathing c) Increased VT with slower rate d) Apnea followed by hyperpnea
Explanation: J (juxtacapillary) receptors are C-fiber endings sensitive to interstitial fluid; activation triggers tachypnea with low VT (rapid, shallow). This is distinct from PSR-mediated inflation reflex which prolongs expiration. Answer: b) Rapid, shallow breathing.
6) During exercise, why does the Hering–Breuer reflex become more relevant?
a) Higher PaCO₂ sensitizes PSR b) Larger VT increases PSR firing c) Airway resistance falls, silencing PSR d) Peripheral chemoreceptors inhibit PSR
Explanation: Exercise increases tidal volume; lung inflation enhances slowly adapting PSR discharge, aiding appropriate inspiratory termination and expiratory timing at high volumes. Chemoreceptor changes are parallel but not the mechanism for PSR activation. Answer: b) Larger VT increases PSR firing.
7) A patient on high PEEP shows decreased inspiratory time on the ventilator. The best explanation is:
a) Central chemoreceptor suppression b) Increased PSR activation by higher lung volume c) Haldane effect d) Reduced compliance lowering PSR firing
Explanation: PEEP elevates end-expiratory lung volume, increasing PSR activity and promoting earlier inspiratory cutoff (shorter inspiratory time), consistent with the Hering–Breuer effect. Central chemoreceptors and Haldane effect are unrelated. Answer: b) Increased PSR activation by higher lung volume.
8) Which brain region integrates vagal stretch afferents to terminate inspiration?
a) Dorsal respiratory group (DRG) b) Ventral respiratory group (VRG) c) Apneustic center alone d) Cerebellum
Explanation: DRG in the medulla receives vagal afferents from PSR and modulates inspiratory off-switch; pontine pneumotaxic influences also help, but DRG is the key medullary integrator. VRG is more active in forced breathing. Answer: a) Dorsal respiratory group (DRG).
9) In an apneustic animal (pontine lesion), intact vagal afferents would:
a) Worsen apneusis b) Partially relieve prolonged inspiration c) Cause Cheyne–Stokes pattern d) Have no effect
Explanation: Vagal stretch input can partially terminate the prolonged inspiratory “apneustic” pattern by providing an inspiratory off-switch, reducing the severity of breath-holding phases. Answer: b) Partially relieve prolonged inspiration.
10) A COPD patient shows larger VT after bronchodilator. How does this affect the Hering–Breuer reflex?
a) Diminishes reflex due to less stretch b) Augments reflex via greater stretch c) No change expected d) Converts to deflation reflex
Explanation: Improved airflow can increase VT at similar effort, raising lung stretch and PSR firing, thus enhancing the inflation reflex and earlier inspiratory termination. Answer: b) Augments reflex via greater stretch.
11) Which change most directly abolishes the Hering–Breuer inflation reflex?
a) Carotid body denervation b) Vagotomy c) Phrenic neurectomy d) Increased CSF bicarbonate
Explanation: The inflation reflex depends on vagal afferents from pulmonary stretch receptors. Cutting the vagus removes the signal to medullary centers, abolishing inspiratory off-switch. Carotid bodies and CSF buffering affect chemoreception, not PSR afferents. Answer: b) Vagotomy.
Keywords (for all questions)
Pancreatic juice volume: About 1–2 L/day in adults; classic value ≈ 1.5 L/day.
Acinar cells: Secrete enzyme-rich, proteinaceous fluid (zymogens: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase; amylase; lipase).
Ductal cells: Secrete bicarbonate-rich, watery fluid; modify Cl⁻/HCO₃⁻ via CFTR and exchangers.
Secretin (S cells): Stimulates ductal HCO₃⁻ secretion; increases volume and alkalinity.
CCK (I cells): Stimulates acinar enzyme secretion; potentiates secretin.
Vagus (ACh): Cephalic/gastric phase stimulation of both acinar and duct cells.
CFTR: Chloride channel essential for HCO₃⁻ secretion; defective in cystic fibrosis.
Enterokinase (enteropeptidase): Brush-border enzyme that activates trypsinogen to trypsin.
SPINK1 (trypsin inhibitor): Prevents premature trypsin activation within acinar cells.
Flow-dependent composition: Higher flow → higher HCO₃⁻, lower Cl⁻; Na⁺/K⁺ ~ plasma.
Pancreatic juice pH: Alkaline (~pH 8.0–8.3) to neutralize gastric acid in duodenum.
Somatostatin: Inhibits exocrine pancreatic secretion.
Phases of secretion: Cephalic, gastric, intestinal (intestinal predominates via CCK/secretin).
Zollinger–Ellison: Gastrinoma; secretin test paradoxically increases gastrin; high acid increases secretin release from S cells.
Bicarbonate mechanism: Carbonic anhydrase forms H⁺/HCO₃⁻; HCO₃⁻ secreted via CFTR/Cl⁻-HCO₃⁻ exchange; H⁺ returned to blood.
Chapter: Gastrointestinal Physiology | Topic: Exocrine Pancreas | Subtopic: Volume, Composition & Control of Pancreatic Secretion
Lead Question – 2012
Daily pancreatic secretion ?
a) 1.5 L
b) 2.5 L
c) 5.0 L
d) 10 L
Explanation: Normal adults secrete roughly 1–2 liters of pancreatic juice per day. Standard teaching value is ~1.5 L/day, alkaline and rich in bicarbonate to neutralize gastric acid, with enzymes from acinar cells. Larger figures are excessive for physiology. Answer: a) 1.5 L.
1) Which hormone primarily increases the bicarbonate content and volume of pancreatic juice?
a) CCK
b) Secretin
c) Gastrin
d) Motilin
Explanation: Secretin from duodenal S cells responds to acid; it stimulates ductal cells to secrete HCO₃⁻-rich, watery fluid, increasing volume and alkalinity. CCK mainly drives enzyme-rich acinar secretion and potentiates secretin’s effect but is not the primary bicarbonate stimulator. Answer: b) Secretin.
2) A patient with cystic fibrosis has recurrent steatorrhea. The pancreatic defect most responsible is:
a) Loss of amylase synthesis
b) Inactive enterokinase
c) Impaired CFTR-mediated ductal HCO₃⁻ secretion
d) Excess SPINK1
Explanation: CFTR dysfunction reduces ductal chloride cycling and bicarbonate secretion, producing viscous, acidic juice that obstructs ducts, diminishes enzyme delivery, and causes fat malabsorption (steatorrhea). Enterokinase is intestinal; SPINK1 prevents premature trypsin activation and is unrelated to CF’s ductal pathophysiology. Answer: c) Impaired CFTR-mediated ductal HCO₃⁻ secretion.
3) Which change occurs in pancreatic juice as flow rate increases?
a) Decreased HCO₃⁻ concentration
b) Increased Cl⁻ concentration
c) Increased HCO₃⁻ with reciprocal fall in Cl⁻
d) Large rise in K⁺
Explanation: At higher flow, ductal cells secrete more bicarbonate, while chloride falls reciprocally; Na⁺ and K⁺ remain near plasma levels. This optimizes neutralization of gastric acid entering the duodenum during meals. Answer: c) Increased HCO₃⁻ with reciprocal fall in Cl⁻.
4) A 45-year-old with gallstones has postprandial abdominal pain. Which mediator most strongly stimulates acinar enzyme secretion?
a) Secretin
b) CCK
c) VIP
d) Somatostatin
Explanation: CCK released from I cells in response to fatty acids and amino acids stimulates acinar cells to release enzyme-rich secretions and contracts the gallbladder. Secretin targets ductal cells. VIP is modulatory; somatostatin inhibits exocrine secretion. Answer: b) CCK.
5) In the cephalic phase of digestion, pancreatic secretion is driven mainly by:
a) Secretin from acid in duodenum
b) Vagal cholinergic activity
c) Local stretch reflex in pancreas
d) Somatostatin surge
Explanation: Sight, smell, and taste trigger vagal efferents (ACh) to acinar and duct cells, modestly increasing enzyme and fluid secretion before food reaches the duodenum. Secretin dominates the intestinal phase. Somatostatin inhibits. Answer: b) Vagal cholinergic activity.
6) Trypsinogen activation physiologically occurs in the:
a) Pancreatic acinus by trypsin
b) Duodenal brush border by enterokinase
c) Gastric lumen by pepsin
d) Blood by kallikrein
Explanation: Enterokinase (enteropeptidase) on duodenal mucosa converts trypsinogen to trypsin, which then activates other zymogens. In the pancreas, SPINK1 prevents premature activation. Gastric pepsin and kallikrein are unrelated to physiological trypsinogen activation. Answer: b) Duodenal brush border by enterokinase.
7) A secretin infusion test in suspected gastrinoma shows a paradoxical rise in serum gastrin. Secretin normally does which action on the pancreas?
a) Inhibits ductal HCO₃⁻
b) Stimulates ductal HCO₃⁻ secretion
c) Stimulates acinar protease synthesis
d) Contracts sphincter of Oddi
Explanation: Secretin physiologically stimulates pancreatic ductal bicarbonate and water secretion, increasing volume and pH of juice. It does not primarily drive enzyme synthesis or Oddi contraction. The paradoxical gastrin rise is specific to gastrinomas. Answer: b) Stimulates ductal HCO₃⁻ secretion.
8) A patient with acute pancreatitis has elevated intrapancreatic trypsin activity. Which protective factor normally limits this?
a) High luminal pH
b) SPINK1 within acinar cells
c) Secretin-mediated washout
d) Low Ca²⁺ in duct fluid
Explanation: SPINK1 (serine protease inhibitor, Kazal type 1) is a key intrapancreatic trypsin inhibitor preventing premature activation. Failure of this mechanism predisposes to autodigestion and pancreatitis. Secretin, pH, and ductal Ca²⁺ are not the principal intracellular safeguards. Answer: b) SPINK1 within acinar cells.
9) Which combination best describes typical ionic composition of high-flow pancreatic juice?
a) High Cl⁻, low HCO₃⁻
b) High HCO₃⁻, low Cl⁻
c) High K⁺, low Na⁺
d) Low Na⁺, high Ca²⁺
Explanation: With increased flow under secretin, pancreatic juice becomes rich in bicarbonate and relatively depleted of chloride; sodium and potassium remain near plasma values. This alkaline secretion neutralizes gastric acid effectively. Answer: b) High HCO₃⁻, low Cl⁻.
10) After a fatty meal, which synergism yields maximal pancreatic secretion?
a) CCK + Somatostatin
b) Secretin + CCK + Vagus
c) Secretin alone
d) Vagus alone
Explanation: Intestinal phase: secretin (ductal HCO₃⁻) and CCK (acinar enzymes) act synergistically, further potentiated by vagal cholinergic input, producing maximal volume and enzyme output. Somatostatin is inhibitory. Answer: b) Secretin + CCK + Vagus.
11) Which best explains why pancreatic juice is alkaline?
a) Acinar amylase generates OH⁻
b) Ductal carbonic anhydrase–dependent HCO₃⁻ secretion
c) Gastric mucosal diffusion
d) Hepatic bile mixing exclusively
Explanation: Ductal cells use carbonic anhydrase to generate bicarbonate and secrete it via CFTR/Cl⁻–HCO₃⁻ exchangers, producing alkaline juice (pH ~8). Bile mixing adds alkalinity but is not the core pancreatic mechanism. Enzymes do not create hydroxyl ions. Answer: b) Ductal carbonic anhydrase–dependent HCO₃⁻ secretion.
Keywords (for all questions)
Microcirculation: Network of arterioles, capillaries, venules (± metarterioles, thoroughfare channels) where exchange occurs.
Precapillary sphincter: Smooth muscle collar regulating capillary perfusion/recruitment.
Starling forces (revised): Filtration depends on hydrostatic/oncotic pressures and endothelial glycocalyx.
Glycocalyx: Endothelial surface layer modulating permeability and oncotic gradient; degraded in sepsis.
Functional hyperemia: ↑Flow to active tissues via metabolites (adenosine, CO₂, H⁺, K⁺).
Reactive hyperemia: Transient ↑Flow after occlusion due to vasodilator washout and myogenic response.
Autoregulation: Local maintenance of flow vs pressure via myogenic/metabolic mechanisms.
Poiseuille’s law: Resistance ∝ viscosity × length / radius⁴; small radius changes drastically alter flow.
Fåhræus–Lindqvist effect: Apparent blood viscosity falls in small vessels (down to ~10–300 μm).
Diffusion distance: Capillaries keep cells within ~100 μm for adequate O₂ exchange.
Capillary types: Continuous (muscle, brain), fenestrated (kidney, intestine), sinusoidal (liver, spleen).
NO/Endothelin: Endothelial vasodilator (NO) and vasoconstrictor (endothelin-1) balancing tone.
Capillary hydrostatic pressure (Pc): ~15–35 mmHg; higher at arteriolar end.
Lymphatics: Return filtered fluid/proteins; failure → edema.
Sepsis microvascular dysfunction: Glycocalyx loss, shunting, ↑permeability → lactate rise.
Chapter: Cardiovascular Physiology | Topic: Microcirculation | Subtopic: Structure and Function
Lead Question – 2012
Microcirculation consists of ?
a) Capillaries
b) Capillaries venules and arterioles
c) Aorta
d) Arteries and veins
Explanation: Microcirculation refers to the smallest vessels involved in exchange and resistance control—terminal arterioles, capillaries, and venules (often including metarterioles/thoroughfare channels). Large arteries, veins, and the aorta are macrocirculatory. Exchange and Starling flux occur at this level. Answer: b) Capillaries venules and arterioles.
1) A runner’s active skeletal muscle shows increased flow. The predominant cause at the microvascular level is:
a) Sympathetic α1 vasoconstriction
b) Local metabolic vasodilation
c) Increased venous pressure
d) Baroreceptor unloading
Explanation: Functional hyperemia is driven by local metabolites (adenosine, CO₂, K⁺, H⁺) opening precapillary sphincters and dilating arterioles, recruiting capillaries and boosting exchange. Sympathetic activity is overridden locally during exercise. Venous pressure/baroreflex are not primary drivers here. Answer: b) Local metabolic vasodilation.
2) Which structure directly regulates the entry of blood into true capillaries?
a) Postcapillary venule
b) Precapillary sphincter
c) Vasa vasorum
d) Sinusoid
Explanation: Precapillary sphincters are smooth muscle cuffs at capillary origins from metarterioles/arterioles. Their tone modulates capillary recruitment and surface area for exchange according to local metabolic demand. Postcapillary venules mainly handle leukocyte trafficking and fluid reabsorption. Answer: b) Precapillary sphincter.
3) A patient with sepsis develops edema despite normal hydrostatic pressures. The best explanation is:
a) Increased plasma oncotic pressure
b) Endothelial glycocalyx degradation
c) Reduced interstitial compliance
d) Lymphatic hyperactivity
Explanation: Sepsis damages the glycocalyx, increasing permeability and altering the effective oncotic gradient in Starling forces, promoting filtration and interstitial edema even with modest pressures. Plasma oncotic rises would oppose, not favor, edema. Lymphatics may be overwhelmed, not “hyperactive.” Answer: b) Endothelial glycocalyx degradation.
4) In which capillary type is bulk protein passage physiologically greatest?
a) Continuous (brain)
b) Fenestrated (glomerulus)
c) Sinusoidal (liver)
d) Continuous (muscle)
Explanation: Liver sinusoids have discontinuous endothelium and incomplete basement membrane, allowing protein exchange between plasma and space of Disse; this supports albumin synthesis. Brain continuous capillaries with tight junctions severely restrict proteins. Fenestrated glomeruli filter little protein due to charge/size selectivity. Answer: c) Sinusoidal (liver).
5) A 65-year-old with uncontrolled hypertension has reduced tissue perfusion in toes. According to Poiseuille’s law, which change most powerfully improves flow?
a) 10% decrease in viscosity
b) 10% increase in vessel radius
c) 10% decrease in vessel length
d) 10% increase in pressure
Explanation: Resistance varies inversely with radius⁴, so small increases in arteriolar radius markedly reduce resistance and enhance flow, dominating effects of viscosity, length, or pressure in microvessels. Thus vasodilation is the most potent intervention. Answer: b) 10% increase in vessel radius.
6) At the arteriolar end of a typical systemic capillary, which relationship favors filtration?
a) Pc < πc
b) Pc > πc
c) Pi > Pc
d) πi > πc
Explanation: Higher capillary hydrostatic pressure (Pc) at the arteriolar end exceeds capillary oncotic pressure (πc), favoring filtration; toward the venular end, πc dominates, favoring reabsorption (modulated by glycocalyx). Interstitial pressure typically remains low/slightly negative. Answer: b) Pc > πc.
7) A limb is occluded for two minutes and then released. The marked flushing is due to:
a) Decreased tissue PCO₂
b) Accumulated vasodilators and myogenic relaxation
c) Increased sympathetic tone
d) Venoconstriction
Explanation: Reactive hyperemia follows brief ischemia: metabolites (adenosine, CO₂, H⁺, K⁺) and myogenic relaxation dilate arterioles; upon release, flow overshoots until vasodilators wash out and tone normalizes. Sympathetic activity is not the primary determinant. Answer: b) Accumulated vasodilators and myogenic relaxation.
8) Which venule segment is the principal site of leukocyte adhesion and increased permeability in inflammation?
a) Terminal arteriole
b) Postcapillary venule
c) Muscular venule
d) Collecting vein
Explanation: Postcapillary venules express adhesion molecules (e.g., selectins, ICAM) and exhibit gap formation with inflammatory mediators, promoting leukocyte transmigration and fluid extravasation—key microcirculatory responses in acute inflammation. Answer: b) Postcapillary venule.
9) In severe anemia, tissue oxygen delivery is maintained partly by microvascular changes including:
a) Increased viscosity raising resistance
b) Fåhræus–Lindqvist effect lowering apparent viscosity
c) Decreased capillary recruitment
d) Diffusion distance increase
Explanation: In small vessels, apparent viscosity falls (Fåhræus–Lindqvist effect), reducing resistance and improving microvascular flow. Capillary recruitment and increased cardiac output also sustain delivery; diffusion distance tends to decrease with recruitment, aiding exchange. Answer: b) Fåhræus–Lindqvist effect lowering apparent viscosity.
10) A patient with nephrotic syndrome develops pitting edema. The most proximate microcirculatory cause is:
a) Increased plasma oncotic pressure
b) Decreased plasma oncotic pressure
c) Decreased capillary hydrostatic pressure
d) Increased lymphatic pumping
Explanation: Hypoalbuminemia lowers capillary oncotic pressure, tipping Starling balance toward filtration across systemic microvessels; lymphatics initially compensate but are overwhelmed, producing interstitial fluid accumulation and pitting edema. Answer: b) Decreased plasma oncotic pressure.
11) Nitric oxide infusion into a limb primarily causes which microvascular change?
a) Arteriolar dilation and capillary recruitment
b) Venular constriction with reduced filtration
c) Precapillary sphincter constriction
d) Increased blood viscosity
Explanation: NO relaxes arteriolar smooth muscle, lowering resistance and opening precapillary sphincters; more capillaries are perfused (recruitment), enlarging surface area for exchange and improving oxygen delivery. Venules are less responsive; viscosity is unaffected. Answer: a) Arteriolar dilation and capillary recruitment.
Keywords (for all questions)
Diffusion: Movement of gas down partial pressure gradients across thin membranes.
Partial pressure (P): Driving force for gas transfer; P_O₂ and P_CO₂ determine direction and rate.
Capillary: Thin-walled microvessel providing maximal surface area for gas exchange.
Transit time: Time blood spends in capillary; affects equilibration of gases.
Fick’s law: Rate ∝ (diffusion coefficient × area × ΔP) / thickness.
Diffusion coefficient: Depends on gas solubility and molecular weight (CO₂ diffuses faster than O₂).
Diffusion distance: Separation between blood and tissue; increased by edema or fibrosis.
Capillary recruitment: More capillaries perfused increases exchange surface area (important in exercise).
Oxygen content vs PO₂: Content depends on hemoglobin concentration and saturation; PO₂ measures dissolved gas.
Diffusion limitation vs perfusion limitation: Diffusion-limited when membrane thickening limits equilibration; perfusion-limited when transit time limits uptake.
Clinical examples: Pulmonary fibrosis → diffusion limitation; anemia → low O₂ content; pulmonary edema → increased diffusion distance.
Chapter: Respiratory Physiology | Topic: Gas Exchange | Subtopic: Tissue Gas Exchange
Lead Question – 2012
Gas exchange in tissues takes place at ?
a) Artery
b) Capillary
c) Vein
d) Venules
Explanation: Gas exchange in tissues occurs across capillary walls where oxygen diffuses from blood to cells and carbon dioxide diffuses back into plasma. Capillaries provide thin endothelium and large surface area for diffusion; arterioles/venules serve as conduits. Thus exchange primarily occurs in capillaries. Answer: b) Capillary.
1) Which law best describes the rate of gas transfer across the capillary membrane?
a) Fick's law
b) Boyle's law
c) Henry's law
d) Charles's law
Explanation: Fick’s law quantifies net gas transfer across membranes: rate = (diffusion coefficient × area × partial pressure difference)/thickness. Increasing surface area or partial pressure gradient or diffusion coefficient, or decreasing membrane thickness, augments exchange. Clinically, emphysema reduces area, pulmonary fibrosis increases thickness, reducing oxygen transfer markedly. Answer: a) Fick’s law.
2) During strenuous exercise capillary transit time falls. What is the usual effect on O₂ uptake?
a) O₂ uptake falls drastically
b) Minimal effect due to compensation
c) Equilibration impossible
d) O₂ uptake becomes zero
Explanation: During exercise capillary transit time shortens due to increased cardiac output; despite reduced transit, elevated perfusion and larger partial pressure gradients maintain oxygen uptake by increased diffusion and recruitment of capillaries. In severe pathology, very short transit may limit saturation. Answer: b) Minimal effect due to compensation in healthy individuals.
3) Interstitial edema increases diffusion distance. What happens to tissue oxygenation?
a) No change
b) Increased oxygenation
c) Decreased tissue oxygenation
d) Only CO₂ affected
Explanation: Interstitial edema increases diffusion distance between capillary and cells, reducing oxygen delivery and impairing CO₂ removal; tissues may become hypoxic despite normal arterial oxygen content. Severe edema in lungs causes impaired gas exchange and hypoxemia. Clinically, pulmonary edema reduces arterial PO₂. Answer: c) Decreased tissue oxygenation, especially during exertion episodes.
4) Which gas diffuses faster across biological membranes?
a) Carbon dioxide
b) Oxygen
c) Nitrogen
d) Helium
Explanation: Carbon dioxide diffuses approximately 20 times faster than oxygen across biological membranes because of higher solubility despite lower gradient; CO₂'s greater diffusion coefficient allows rapid removal from tissues though O₂ transport remains diffusion-limited. Clinically, CO₂ clearance often preserved when oxygenation fails. Answer: a) Carbon dioxide in many disease states too.
5) Typical systemic arterial PO₂ that provides driving force for tissue diffusion is approximately?
a) 40 mmHg
b) 100 mmHg
c) 250 mmHg
d) 760 mmHg
Explanation: Normal systemic arterial PO₂ is about 100 mmHg, creating a substantial gradient versus tissue PO₂ (~40 mmHg) that drives diffusion. Lowered arterial PO₂ reduces this gradient and compromises oxygen delivery, leading to tissue hypoxia if severe. Answer: b) Arterial PO₂ ≈ 100 mmHg, commonly measured by arterial blood gas analysis.
6) In anemia, how is tissue oxygen delivery affected despite normal PaO₂?
a) Unchanged oxygen content
b) Increased oxygen content
c) Reduced oxygen content despite normal PaO₂
d) PaO₂ falls dramatically
Explanation: In anemia arterial oxygen content falls due to reduced hemoglobin concentration despite normal saturation and PO₂; tissues compensate by increasing cardiac output and extracting more oxygen, but severe anemia produces tissue hypoxia even with normal gas exchange. Transfusion raises oxygen content. Answer: c) Reduced oxygen content despite normal PaO₂ levels.
7) Which pathology is classically diffusion-limited for O₂ transfer?
a) Pulmonary fibrosis
b) Right-to-left shunt
c) Hypoventilation
d) Anemia
Explanation: Pulmonary fibrosis thickens alveolar-capillary membrane, increasing diffusion distance and causing diffusion limitation especially during exercise when transit time shortens; oxygen uptake is impaired causing hypoxemia and widened A–a gradient. Right-to-left shunt causes hypoxemia but not diffusion limitation mechanism. Answer: a) Pulmonary fibrosis treatment may include oxygen therapy and antifibrotic agents.
8) Exercise increases oxygen exchange by which microvascular change?
a) Decreased diffusion capacity
b) Increased diffusion capacity due to recruitment
c) Reduced capillary surface area
d) Increased diffusion distance
Explanation: During exercise pulmonary and systemic capillary recruitment and increased perfusion elevate overall diffusion capacity for oxygen (DL_O₂), shortening transit time but increasing surface area and partial pressure gradients, thereby enhancing gas exchange. Diffusion capacity measurements rise with workload. Answer: b) Increased diffusion capacity due to recruitment and higher cardiac output.
9) Diffusion hypoxia is a clinical phenomenon seen when?
a) Nitrous oxide is discontinued
b) Patient breathes 100% oxygen for prolonged period
c) During carbon monoxide poisoning
d) With severe anemia only
Explanation: Diffusion hypoxia occurs when nitrous oxide is discontinued; rapid efflux of N₂O from blood into alveoli dilutes alveolar oxygen and may transiently lower its partial pressure, causing hypoxia if supplemental oxygen not provided. This is a clinical example of diffusion phenomenon. Answer: a) After nitrous oxide discontinuation during emergence recovery.
10) Why are venules not primary sites for gas exchange?
a) They have maximal exchange
b) They have thin walls like capillaries
c) They are upstream of capillaries
d) Venules are not primary exchange sites
Explanation: Venules and veins have thicker walls, lower surface area, and are located downstream where diffusion gradients are reduced; primary gas exchange occurs across capillary endothelium with minimal exchange at venules. Venules specialize in fluid and leukocyte trafficking rather than gas diffusion. Answer: d) Venules are not primary exchange sites clinically.
Chapter: Cardiovascular Examination | Topic: Heart Sounds & Murmurs | Subtopic: Third Heart Sound (S3)
Lead Question – 2012
All of the following statements about third Heart sound (S3) are true, except:
a) Occurs due to rapid filling of the ventricles during atrial systole
b) Seen in Constrictive Pericarditis
c) Seen in Atrial Septal Defect (ASD)
d) Seen in Ventricular Septal Defect (VSD)
Explanation: S3 is an early diastolic sound from rapid passive ventricular filling (not atrial systole). It appears in volume-overload states (VSD, ASD) and systolic dysfunction. Constrictive pericarditis typically produces a pericardial knock (early diastolic) rather than a true S3, but S3 can occasionally be heard. Answer: a) Occurs due to rapid filling of the ventricles during atrial systole.
1) The classical timing of S3 is:
a) Late diastole (presystolic)
b) Early diastole (rapid filling)
c) Mid-systole
d) Continuous through systole and diastole
Explanation: S3 occurs in early diastole during the rapid filling phase soon after S2. It is not presystolic (that is S4). S3 reflects ventricular wall vibrations from brisk inflow; clinically significant when new in older adults and associated with heart failure or volume overload. Answer: b) Early diastole (rapid filling).
2) Best method to auscultate an S3 is:
a) Diaphragm at left sternal border
b) Bell at apex with patient in left lateral decubitus
c) Bell at right midclavicular line
d) Diaphragm over epigastrium
Explanation: S3 is a low-frequency sound best detected using the bell at the cardiac apex with the patient lying in the left lateral decubitus position, which brings the left ventricle closer to the chest wall. Diaphragm and other positions are less sensitive for low-frequency S3. Answer: b) Bell at apex with patient in left lateral decubitus.
3) A newly developed S3 in an elderly patient most likely indicates:
a) Normal aging
b) Reduced left ventricular systolic function
c) Atrial fibrillation only
d) Isolated hypertension without dysfunction
Explanation: A new S3 in an older adult commonly signifies impaired left ventricular systolic function and increased filling pressures, often preceding overt congestive heart failure. In contrast, physiologic S3 is typical in young people; atrial fibrillation or hypertension alone do not typically produce an isolated new S3. Answer: b) Reduced left ventricular systolic function.
4) S3 is most commonly heard in which of the following conditions?
a) Hypertrophic cardiomyopathy
b) Dilated cardiomyopathy
c) Aortic stenosis without regurgitation
d) Isolated pericarditis without effusion
Explanation: Dilated cardiomyopathy features increased chamber volumes and reduced systolic function, predisposing to an S3 from vigorous early filling and wall vibration. Hypertrophic cardiomyopathy more often has S4; aortic stenosis and simple pericarditis without volume overload do not classically produce S3. Answer: b) Dilated cardiomyopathy.
5) Which physiologic state can produce a benign S3?
a) Elderly sedentary adult
b) Healthy young athlete
c) Chronic heart failure
d) Acute myocardial infarction
Explanation: In young healthy individuals and well-trained athletes, increased cardiac output and compliant ventricles can produce a physiologic S3 without pathology. In contrast, elderly persons, heart failure, or recent MI with new S3 usually indicate pathology and require evaluation. Answer: b) Healthy young athlete.
6) Which auscultatory feature helps distinguish S3 from a pericardial knock?
a) S3 is high-pitched
b) Pericardial knock occurs earlier in diastole than S3
c) S3 is louder with expiration
d) Pericardial knock is only audible at the apex
Explanation: A pericardial knock typically occurs earlier in diastole, soon after S2, due to abrupt cessation of ventricular filling from a rigid pericardium; S3 follows slightly later in the rapid filling phase. Pitch and positional changes help differentiate them clinically. Answer: b) Pericardial knock occurs earlier in diastole than S3.
7) In mitral regurgitation, S3 occurs because of:
a) Decreased left atrial pressure
b) Volume overload of left ventricle
c) Increased ventricular stiffness only
d) Mitral valve prolapse exclusively
Explanation: Chronic mitral regurgitation causes volume overload of the left ventricle with increased early diastolic filling, producing an S3. Ventricular stiffness relates more to S4; mitral valve prolapse can have varied sounds but is not the exclusive cause of S3. Answer: b) Volume overload of left ventricle.
8) Which statement about S3 frequency and auscultation tool is correct?
a) High-frequency sound heard with diaphragm
b) Low-frequency sound best heard with bell
c) Audible only with electronic stethoscopes
d) Best heard over carotids
Explanation: S3 is a low-frequency vibration best detected using the bell of the stethoscope, placed lightly over the apex in left lateral decubitus. The diaphragm is less sensitive to low-frequency sounds; carotid auscultation is for bruits and systolic murmurs, not S3. Answer: b) Low-frequency sound best heard with bell.
9) A VSD produces an S3 because it causes:
a) Left ventricular outflow obstruction
b) Increased pulmonary venous pressure only
c) Increased volume flow and early diastolic filling
d) Isolated right atrial enlargement
Explanation: A ventricular septal defect increases left-to-right shunt and volume load on ventricles, causing brisk early diastolic filling and vibrations that produce an S3. It is not due to outflow obstruction or isolated atrial changes. Clinical assessment includes murmur plus possible S3. Answer: c) Increased volume flow and early diastolic filling.
10) Which maneuver increases the intensity of a pathologic S3?
a) Valsalva strain phase
b) Leg elevation to increase venous return
c) Standing from supine
d) Deep inspiration only
Explanation: Increasing venous return (leg raise or supine positioning) augments early diastolic filling and may increase S3 intensity in volume-overloaded ventricles. Valsalva and standing decrease venous return and generally lessen S3; deep inspiration has minor effects on left-sided S3. Answer: b) Leg elevation to increase venous return.
11) How does S3 prognosis differ with age?
a) Always ominous regardless of age
b) Benign if young, pathologic if new in older adults
c) Indicative of pulmonary embolism only
d) Only related to valvular calcification
Explanation: An S3 in children or young adults is often physiologic and benign. In older adults, a newly detected S3 usually indicates increased ventricular filling pressures and systolic dysfunction, carrying worse prognosis; it warrants evaluation for heart failure or volume overload causes. Answer: b) Benign if young, pathologic if new in older adults.
Keywords (for all questions)
Second heart sound (S2): Produced by closure of aortic (A2) and pulmonary (P2) valves; its timing and components reflect great-vessel and ventricular ejection dynamics.
Components A2 and P2: A2 corresponds to aortic valve closure, P2 to pulmonary valve closure; normal respiratory variation alters their relative timing.
Physiologic split: Normal inspiratory widening of S2 due to increased right-sided ejection time and delayed P2.
Fixed split: Unchanged by respiration; classically seen in atrial septal defect (ASD).
Paradoxical split: Split that narrows or reverses on inspiration; occurs with delayed A2 (e.g., LBBB, severe AS).
Pericardial knock: Early diastolic sound in constrictive pericarditis, occurring earlier than S3 and differing in timing and pitch.
Auscultation tips: Use the diaphragm at the base for higher frequency components and the bell at the apex for low-frequency diastolic sounds when appropriate.
Phonocardiography: Instrumental method to record and measure sound timing and duration precisely.
Clinical relevance: Changes in S2 duration, splitting, or intensity help diagnose valvular disease, conduction defects, and hemodynamic abnormalities.
Chapter: Cardiovascular Examination | Topic: Heart Sounds & Murmurs | Subtopic: Second Heart Sound (S2) Duration
Lead Question – 2012
Duration of 2" heart sound is ?
a) 0.15 sec
b) 0.12 sec
c) 0.08 sec
d) 0.1 sec
Explanation: The normal second heart sound (S2) is brief, representing aortic and pulmonary valve closure. Typical duration is about 0.08 seconds due to rapid valve deceleration. Prolongation suggests pathology. Answer: c) 0.08 sec. It is best heard at the cardiac base with the diaphragm during quiet respiration in most healthy adults.
1) S2 components consist of:
a) A2 only
b) A2 & P2
c) P2 only
d) M1 & T1
Explanation: S2 comprises two nearly simultaneous components: A2 from aortic valve closure and P2 from pulmonary valve closure. Their timing varies with respiration. The split widens on inspiration due to increased venous return and delayed P2. Clinically, S2 components reflect great vessel dynamics. Answer: b) A2 & P2 in normal subjects.
2) Physiologic splitting of S2 varies with respiration because:
a) Decreased systemic vascular resistance
b) Increased venous return delays P2
c) Left atrial contraction delays A2
d) Pulmonary embolism accelerates P2
Explanation: Physiologic splitting of S2 widens during inspiration because increased venous return prolongs right ventricular ejection, delaying pulmonary valve closure (P2). Simultaneously, reduced left ventricular filling slightly shortens A2. These dynamic changes produce normal respiratory variation in S2 that distinguishes physiologic from fixed splits. Answer: b) Increased venous return delays P2.
3) Fixed wide splitting of S2 is characteristic of:
a) Ventricular septal defect
b) Left bundle branch block
c) Atrial septal defect (ASD)
d) Mitral stenosis
Explanation: Fixed wide splitting of S2, unchanged by respiration, is characteristic of atrial septal defect due to persistent right ventricular volume overload causing consistently delayed P2. Unlike physiologic splitting, fixed splitting persists during inspiration and expiration, aiding diagnosis. Other causes are rare. Answer: c) Atrial Septal Defect (ASD) on auscultation commonly.
4) Paradoxical splitting of S2 is typically due to:
a) Right bundle branch block
b) Left bundle branch block (LBBB)
c) Atrial septal defect
d) Pulmonary embolism
Explanation: Paradoxical splitting occurs when A2 is delayed, causing the split to narrow or reverse with inspiration; typical causes include left bundle branch block or severe aortic stenosis. The delayed aortic valve closure makes P2 precede A2, producing paradoxical timing that increases with expiration. Answer: b) Left bundle branch block (LBBB).
5) A pericardial knock is most characteristic of:
a) Dilated cardiomyopathy
b) Constrictive pericarditis
c) Mitral regurgitation
d) Atrial fibrillation
Explanation: A pericardial knock is an early diastolic high-amplitude sound occurring in constrictive pericarditis due to sudden cessation of ventricular filling when rigid pericardium limits expansion. It occurs earlier than S3 and is distinguished by timing, high intensity, and association with signs of constriction. Answer: b) Constrictive pericarditis on cardiac auscultation commonly.
6) Inspiration typically causes which change in S2?
a) Split narrows on inspiration
b) Split widens on inspiration
c) S2 disappears on inspiration
d) S2 becomes continuous
Explanation: Inspiration increases venous return to the right heart, prolonging right ventricular ejection and delaying pulmonary valve closure, widening the physiologic split of S2. Simultaneously, reduced left ventricular filling may slightly advance A2. These respiratory mechanics explain normal variation in S2, useful clinically. Answer: b) Split widens on inspiration in healthy.
7) A single (unsplit) S2 is commonly seen in:
a) Aortic stenosis
b) Atrial septal defect
c) Pulmonary hypertension only
d) Mitral stenosis only
Explanation: A single S2 occurs when A2 and P2 are closely synchronous or one component is inaudible. Severe aortic stenosis often produces a single loud A2 because P2 may be soft; alternatively, pulmonary hypertension can accentuate P2. In either case components merge, producing a solitary second sound. Answer: a) Aortic stenosis commonly.
8) Compared to S1, the duration of S2 is generally:
a) Shorter than S1
b) Longer than S1
c) Identical to S1
d) Variable only in children
Explanation: S2 is usually shorter than S1 because semilunar valve closure produces a brisk, brief vibration. S1 arises from mitral and tricuspid valve closure with greater myocardial involvement, yielding longer duration. Thus S2’s brevity reflects rapid valve recoil and minimal sustained tissue vibration. Answer: a) Shorter than S1 in most adults.
9) Prolongation of S2 duration is most suggestive of:
a) Aortic stenosis
b) Mitral stenosis
c) Pericarditis only
d) Tricuspid atresia
Explanation: Prolongation of the second heart sound indicates delayed semilunar valve closure often from prolonged ejection time. Severe aortic stenosis prolongs left ventricular ejection, delaying A2 and lengthening overall S2 duration. Clinical correlation with murmurs and ECG (e.g., LBBB) helps differentiate causes. Answer: a) Aortic stenosis commonly.
10) The best method to measure precise S2 duration is:
a) Phonocardiography
b) Handheld stethoscope
c) Standard ECG
d) Chest X-ray
Explanation: Phonocardiography provides objective visual and temporal measurement of heart sound durations including S2 by converting acoustic signals into tracings, allowing precise measurement in seconds and detection of subtle splitting or knocks. Auscultation is subjective; echocardiography assesses structure not sound timing directly. Answer: a) Phonocardiography is preferred for exact duration measurement.
Keywords (for all questions)
Volume (low-pressure) receptors: Mechanosensitive afferents in atria and pulmonary veins sensing central blood volume and atrial distension.
Afferents: Travel mainly in the vagus (cranial nerve X) to medullary and hypothalamic centers; carotid sinus uses glossopharyngeal (IX).
Physiologic effects: Modulate thirst, vasopressin (ADH) secretion, renal sympathetic tone, natriuresis, and diuresis according to central volume status.
Distension signal: Increased atrial stretch → increased firing; decreased stretch → reduced firing and activation of compensatory neurohormonal responses.
Interaction with hormones: Work with angiotensin II, ANP and osmoreceptors to regulate fluid balance and blood pressure.
Clinical relevance: Dysfunction or resetting in heart failure and sepsis alters ADH, RAAS, and thirst responses, contributing to fluid retention or inappropriate diuresis.
Chapter: Cardiovascular & Endocrine Integration | Topic: Volume Receptors & Fluid Homeostasis | Subtopic: Physiology of Low-Pressure Baroreceptors
Lead Question – 2012
True about volume receptors are all, EXCEPT:
a) They are low pressure receptors
b) They provide afferents for thirst control
c) They are located in carotid sinus
d) They mediate vasopressin release
Explanation: Volume receptors are low-pressure mechanoreceptors in atria/pulmonary vessels signaling central blood volume to hypothalamus; they influence thirst and vasopressin release. They are not located in the carotid sinus (a high-pressure arterial baroreceptor site). Answer: c) They are located in carotid sinus which is incorrect here.
1) Where are the primary volume receptors located?
a) Atria
b) Carotid sinus
c) Kidneys
d) Aorta
Explanation: Cardiac volume receptors are low-pressure receptors residing primarily in the atria and pulmonary veins; they detect central venous pressure and blood volume changes. Activation modifies autonomic outflow, thirst, and vasopressin release. They are distinct from high-pressure arterial baroreceptors in carotid sinus and aortic arch. Answer: a) Atria for volume sensing purposes.
2) Which nerve carries afferents from cardiac volume receptors?
a) Vagus nerve (X)
b) Glossopharyngeal nerve (IX)
c) Phrenic nerve
d) Sympathetic cardiac nerves
Explanation: Low-pressure volume receptor afferents travel primarily via the vagus (cranial nerve X) to medullary and hypothalamic centers, conveying central blood volume information. These signals alter sympathetic tone, thirst, and vasopressin secretion. Glossopharyngeal nerves convey high-pressure carotid baroreceptor input, not volume receptor input. Answer: a) Vagus nerve for reflex regulation.
3) Volume receptors respond to which mechanical change?
a) Increase firing with atrial distension
b) Decrease firing with atrial distension
c) Respond only to chemical stimuli
d) Respond only to arterial pressure
Explanation: Volume receptors are mechanosensitive nerve endings that increase firing when atrial and pulmonary venous walls are stretched by increased blood volume or central venous pressure. Elevated afferent activity suppresses vasopressin and stimulates diuresis and natriuresis; reduced firing during hypovolemia promotes thirst and vasopressin release mechanism. Answer: a) Increase with distension.
4) Activation of volume receptors causes which effect on vasopressin (ADH)?
a) Decrease vasopressin secretion
b) Increase vasopressin secretion
c) No effect on vasopressin
d) Variable effect unrelated to volume
Explanation: Atrial volume receptor activation with increased central blood volume inhibits vasopressin secretion from the posterior pituitary via hypothalamic pathways, promoting water excretion. Conversely, reduced receptor firing during hypovolemia removes inhibition, causing vasopressin release. Thus volume receptors indirectly regulate plasma osmolality and volume through antidiuretic hormone modulation. Answer: b) Decrease vasopressin.
5) Do volume receptors contribute afferents for thirst control?
a) Yes
b) No
c) Only in dehydration
d) Only in overhydration
Explanation: Low-pressure volume receptor signals influence hypothalamic osmoregulatory centers and contribute to thirst modulation: decreased atrial filling reduces afferent firing, triggering thirst and drinking behavior, while increased filling suppresses thirst. They act alongside osmoreceptors and angiotensin II to control fluid intake, integrating volume and osmotic signals. Answer: a) Yes they do.
6) Which statement correctly classifies volume receptors?
a) Low-pressure baroreceptors
b) High-pressure arterial baroreceptors
c) Osmoreceptors
d) Chemoreceptors
Explanation: Volume receptors are low-pressure baroreceptors located in the atria and pulmonary veins; they directly sense venous return and central blood volume rather than arterial pressure. High-pressure baroreceptors in carotid sinus and aortic arch monitor arterial pressure. Renal afferents provide signals related to tubular flow and renin release. Answer: a) Atria.
7) Activation of volume receptors promotes which renal effect?
a) Natriuresis and diuresis
b) Antinatriuresis
c) No renal effect
d) Direct renin inhibition only
Explanation: Atrial volume receptor activation during increased central blood volume initiates reflex pathways promoting natriuresis and diuresis by decreasing sympathetic renal tone and facilitating atrial natriuretic peptide release. These responses lower blood volume and pressure to restore homeostasis. Dysfunction in heart failure impairs these reflexes, contributing to fluid retention. Answer: a) True.
8) Volume receptors sense primarily which parameter?
a) Volume/atrial stretch
b) Arterial pressure
c) Plasma osmolarity
d) Blood oxygen tension
Explanation: Volume receptors respond to changes in intravascular volume and atrial distension (stretch), not directly to osmolarity or oxygen tension. They transduce mechanical deformation into neural signals modulating thirst, vasopressin, sympathetic tone, and renal handling. Their sensitivity integrates with hormonal signals like angiotensin II for coordinated volume regulation. Answer: b) Volume/stretch.
9) Which afferent transmits carotid sinus baroreceptor signals?
a) Glossopharyngeal nerve (IX)
b) Vagus nerve (X)
c) Phrenic nerve
d) Sympathetic chain
Explanation: High-pressure baroreceptors in the carotid sinus transmit afferent signals via the glossopharyngeal nerve (cranial nerve IX) to the nucleus tractus solitarius, regulating sympathetic outflow and heart rate. These sensors monitor arterial pressure rapidly, complementing low-pressure volume receptors that monitor venous return and blood volume. Answer: b) Glossopharyngeal nerve (IX) clinically.
10) Reduced firing of volume receptors triggers which hormonal cascade?
a) Renin-angiotensin-aldosterone activation
b) Immediate ANP surge only
c) Direct insulin release
d) Increase in pulmonary surfactant
Explanation: When central volume receptors sense reduced atrial filling they decrease afferent firing, triggering compensatory neurohumoral responses including sympathetic activation and renin release from kidneys, which increases angiotensin II and aldosterone. This conserves sodium and water to restore effective circulating volume. Clinically contributes to fluid retention in hypovolemia. Answer: a) True.
Chapter: Cardiovascular Physiology
Topic: Coronary Circulation
Subtopic: Regulation of Coronary Blood Flow
Keywords:
• Coronary Blood Flow – blood supply to myocardium through coronary arteries
• Perfusion Pressure – pressure gradient driving blood flow through tissues
• Vascular Resistance – opposition offered by vessels to blood flow
• Autoregulation – intrinsic ability of tissue to maintain constant flow despite pressure changes
• Oxygen Demand – myocardial requirement driving blood flow regulation
Lead Question - 2012
Which one of the following is the CORRECT statement regarding coronary blood flow?
a) Coronary blood flow is directly related to perfusion pressure and inversely related to resistance
b) Coronary blood flow is inversely related to perfusion pressure and directly related to resistance
c) Coronary blood flow is directly related to perfusion pressure and also to resistance
d) Coronary blood flow is inversely related to both pressure and resistance
Explanation: Coronary blood flow is directly proportional to perfusion pressure and inversely proportional to coronary vascular resistance. The myocardium relies on autoregulation and oxygen demand to control flow. Hence, option (a) is correct.
Guessed Question 1
In coronary circulation, maximum blood flow occurs during:
a) Systole
b) Early diastole
c) Mid-diastole
d) Late systole
Explanation: Coronary perfusion predominantly occurs during diastole due to compression of intramyocardial vessels in systole. Peak flow is in early diastole. Correct answer: (b).
Guessed Question 2
Which factor is the most important regulator of coronary blood flow?
a) Perfusion pressure
b) Myocardial oxygen demand
c) Autonomic nervous system
d) Endothelial factors
Explanation: The primary determinant of coronary blood flow is myocardial oxygen demand. Metabolites like adenosine mediate vasodilation. Hence, option (b) is correct.
Guessed Question 3
In left ventricular coronary circulation, systolic flow is reduced because:
a) Aortic valve closure
b) High intramyocardial pressure
c) Reduced perfusion pressure
d) Increased venous return
Explanation: High intramyocardial pressure during systole compresses coronary vessels, especially in the left ventricle, reducing flow. Correct answer: (b).
Guessed Question 4
Coronary flow reserve is:
a) The difference between basal and maximal coronary blood flow
b) Maximum coronary blood flow
c) Flow at rest
d) Myocardial venous return
Explanation: Coronary flow reserve is the ability of coronary circulation to increase flow above basal level in response to demand. Correct answer: (a).
Guessed Question 5
Coronary steal phenomenon occurs due to:
a) Vasodilation in stenosed vessels
b) Preferential blood flow to non-stenosed vessels
c) Coronary spasm
d) Increased venous drainage
Explanation: In stenosed vessels, distal arterioles are already maximally dilated. Vasodilators divert blood to normal vessels, reducing flow to ischemic zones—coronary steal. Correct answer: (b).
Guessed Question 6
Which substance is the most potent coronary vasodilator?
a) Adenosine
b) Nitric oxide
c) Carbon dioxide
d) Prostacyclin
Explanation: Adenosine, generated during hypoxia, is the most powerful coronary vasodilator, matching supply to oxygen demand. Correct answer: (a).
Guessed Question 7
In coronary circulation, autoregulation maintains flow between pressures of:
a) 30–60 mmHg
b) 60–140 mmHg
c) 80–180 mmHg
d) 40–100 mmHg
Explanation: Coronary autoregulation works effectively between mean arterial pressures of 60–140 mmHg, maintaining constant flow despite fluctuations. Correct answer: (b).
Guessed Question 8
Which vessel supplies blood to the sinoatrial (SA) node in most individuals?
a) Right coronary artery
b) Left coronary artery
c) Circumflex artery
d) Anterior interventricular artery
Explanation: In ~60% of cases, the SA node is supplied by the right coronary artery; in others, the circumflex. Correct answer: (a).
Guessed Question 9
A patient develops chest pain at rest due to coronary vasospasm. This condition is termed:
a) Stable angina
b) Unstable angina
c) Prinzmetal’s angina
d) Silent ischemia
Explanation: Prinzmetal’s (variant) angina occurs due to transient coronary vasospasm at rest, often with ST elevation. Correct answer: (c).
Guessed Question 10
The major site of resistance in coronary circulation is:
a) Epicardial arteries
b) Arterioles
c) Capillaries
d) Venules
Explanation: Coronary arterioles are the main resistance vessels controlling coronary flow. Correct answer: (b).
Chapter: Cardiovascular Physiology
Topic: Electrocardiography
Subtopic: Einthoven’s Law
Keywords:
• Einthoven’s Triangle – imaginary equilateral triangle around the heart formed by limb leads
• Bipolar Limb Leads – leads I, II, III measuring potential difference between limb electrodes
• Augmented Leads – unipolar limb leads (aVR, aVL, aVF)
• Vector – direction and magnitude of electrical activity of the heart
• Lead Axis – orientation of a lead in the frontal plane
Lead Question - 2012
Einthoven’s law -
a) I + III = II
b) I - III = II
c) I + II + III = 0
d) I + III = avL
Explanation: Einthoven’s law states that in a standard ECG, the potential of lead II is equal to the sum of the potentials of leads I and III (II = I + III). This relationship helps in verifying lead placement and ECG recording accuracy. Correct answer: (a).
Guessed Question 1
A 60-year-old male presents with chest pain. His ECG shows ST elevation in leads II, III, and aVF. Which coronary artery is most likely involved?
a) Left anterior descending artery
b) Left circumflex artery
c) Right coronary artery
d) Left main coronary artery
Explanation: ST elevation in leads II, III, and aVF indicates inferior wall myocardial infarction, most commonly due to right coronary artery occlusion. Correct answer: (c).
Guessed Question 2
Lead aVR normally shows:
a) Upright P wave and QRS
b) Negative deflection of P, QRS, and T waves
c) Positive ST segment
d) No consistent wave pattern
Explanation: Lead aVR usually records negative deflections for P, QRS, and T waves because it views the heart from the right shoulder, opposite to the main vector. Correct answer: (b).
Guessed Question 3
PR interval on ECG represents:
a) Atrial depolarization
b) Conduction time from atria to ventricles
c) Ventricular depolarization
d) Atrial repolarization
Explanation: The PR interval corresponds to the time taken for impulse conduction from atria through AV node to ventricles, normally 0.12–0.20 seconds. Correct answer: (b).
Guessed Question 4
In complete heart block, the ECG shows:
a) Prolonged PR interval
b) Progressive PR prolongation
c) Dissociation between P waves and QRS complexes
d) Absent P waves
Explanation: In complete heart block, atrial and ventricular activities are independent, with P waves not related to QRS complexes. Correct answer: (c).
Guessed Question 5
QT interval on ECG corresponds to:
a) Ventricular depolarization
b) Atrial depolarization
c) Ventricular depolarization and repolarization
d) Atrial repolarization
Explanation: The QT interval represents the total duration of ventricular depolarization and repolarization. It is rate-dependent and prolongation predisposes to arrhythmias. Correct answer: (c).
Guessed Question 6
In a patient with hyperkalemia, which ECG change is most characteristic?
a) Flattened T waves
b) Tall peaked T waves
c) Short PR interval
d) Prolonged QT interval
Explanation: Hyperkalemia classically produces tall, peaked T waves due to accelerated repolarization. Severe hyperkalemia can lead to conduction block and cardiac arrest. Correct answer: (b).
Guessed Question 7
Which ECG lead best represents atrial activity?
a) Lead I
b) Lead II
c) Lead III
d) Lead aVL
Explanation: Lead II best shows atrial activity (P waves) because its axis is parallel to the atrial depolarization vector. Correct answer: (b).
Guessed Question 8
A 25-year-old male experiences sudden syncope during exercise. His ECG shows prolonged QT interval. The likely diagnosis is:
a) Brugada syndrome
b) Long QT syndrome
c) WPW syndrome
d) AV nodal reentrant tachycardia
Explanation: Long QT syndrome, congenital or acquired, predisposes to torsades de pointes and sudden death during exertion. Correct answer: (b).
Guessed Question 9
Which component of the ECG corresponds to ventricular depolarization?
a) P wave
b) QRS complex
c) T wave
d) U wave
Explanation: The QRS complex corresponds to ventricular depolarization. Normally < 120 ms, its widening indicates conduction delay or bundle branch block. Correct answer: (b).
Guessed Question 10
A 50-year-old hypertensive patient has left ventricular hypertrophy. Which ECG finding is most consistent?
a) Tall R waves in V1
b) Tall R waves in left chest leads (V5, V6)
c) Deep S waves in V5, V6
d) Low voltage QRS
Explanation: Left ventricular hypertrophy produces tall R waves in left-sided chest leads (V5, V6) and deep S waves in V1, V2 due to increased left ventricular mass. Correct answer: (b).
Chapter: Cardiovascular Physiology
Topic: Cardiac Electrophysiology
Subtopic: Parasympathetic Regulation of Heart Rate
Keywords:
• Acetylcholine – parasympathetic neurotransmitter acting on muscarinic receptors
• SA Node – pacemaker of the heart controlling heart rate
• Diastolic Depolarization – slow rise of membrane potential in pacemaker cells
• Vagal Stimulation – reduces firing rate of SA node
• Chronotropy – effect on heart rate
Lead Question - 2012
Mechanism by which Ach decreases heart rate is by:
a) Delayed diastolic depolarization
b) Increase in plateau
c) Decrease preload
d) Increase afterload
Explanation: Acetylcholine (ACh) released by vagus nerve activates M2 muscarinic receptors in the SA node, increasing K⁺ efflux and reducing slope of diastolic depolarization. This slows pacemaker activity, lowering heart rate. Correct answer: (a).
Guessed Question 1
A 25-year-old athlete presents with episodes of dizziness and bradycardia. Increased vagal tone is suspected. What is the direct ionic mechanism?
a) Increased Ca²⁺ influx
b) Increased K⁺ efflux
c) Decreased Na⁺ influx
d) Increased Cl⁻ influx
Explanation: Vagal stimulation releases ACh, which increases K⁺ efflux via muscarinic K⁺ channels, hyperpolarizing SA node cells and slowing pacemaker firing. Correct answer: (b).
Guessed Question 2
Parasympathetic stimulation primarily affects which cardiac region?
a) Ventricular myocardium
b) SA node and AV node
c) Purkinje fibers
d) Papillary muscles
Explanation: Parasympathetic fibers mainly innervate the SA and AV nodes, altering conduction and rate. Ventricles have minimal vagal innervation. Correct answer: (b).
Guessed Question 3
Increased vagal activity during sleep results in:
a) Tachycardia
b) Bradycardia
c) Increased stroke volume
d) Hypertension
Explanation: During sleep, parasympathetic tone predominates, reducing heart rate and producing physiologic bradycardia without compromising cardiac output. Correct answer: (b).
Guessed Question 4
A patient receives atropine. Which of the following changes is expected?
a) Decreased heart rate
b) Increased heart rate
c) AV nodal delay
d) Enhanced vagal tone
Explanation: Atropine blocks muscarinic receptors, thereby inhibiting vagal effects and increasing heart rate. Correct answer: (b).
Guessed Question 5
Carotid sinus massage produces reflex bradycardia primarily by:
a) Increased vagal discharge
b) Increased sympathetic discharge
c) Reduced baroreceptor firing
d) Decreased preload
Explanation: Carotid massage stretches baroreceptors, enhancing vagal discharge and slowing SA node activity, producing bradycardia. Correct answer: (a).
Guessed Question 6
A 40-year-old man develops AV block due to excessive vagal stimulation. Which interval is prolonged on ECG?
a) PR interval
b) QRS duration
c) QT interval
d) ST segment
Explanation: Excessive vagal stimulation slows AV nodal conduction, prolonging the PR interval. Correct answer: (a).
Guessed Question 7
Which neurotransmitter is responsible for parasympathetic slowing of heart rate?
a) Noradrenaline
b) Dopamine
c) Acetylcholine
d) Adrenaline
Explanation: Acetylcholine released by vagal nerve endings binds muscarinic receptors, slowing the SA node pacemaker. Correct answer: (c).
Guessed Question 8
During vasovagal syncope, the patient faints due to:
a) Sympathetic overactivity
b) Combined bradycardia and vasodilation
c) Hypertension and tachycardia
d) Coronary spasm
Explanation: Vasovagal syncope results from sudden vagal discharge causing bradycardia and systemic vasodilation, leading to transient cerebral hypoperfusion. Correct answer: (b).
Guessed Question 9
Which drug enhances vagal effect on the heart and is contraindicated in bradyarrhythmias?
a) Digoxin
b) Atropine
c) Dobutamine
d) Isoprenaline
Explanation: Digoxin enhances vagal tone, slowing AV nodal conduction, beneficial in supraventricular tachyarrhythmias but contraindicated in bradycardia. Correct answer: (a).
Guessed Question 10
A 32-year-old patient with acute inferior wall MI develops sinus bradycardia. This is most likely due to:
a) Increased sympathetic tone
b) Vagal hyperactivity
c) AV node ischemia
d) Loss of pacemaker cells
Explanation: Inferior wall MI often involves the right coronary artery supplying SA node, leading to vagal hyperactivity and sinus bradycardia. Correct answer: (b).