Keyword Definitions
Peripheral chemoreceptors: Carotid and aortic bodies that sense low PaO₂, high PaCO₂, and low pH.
Central chemoreceptors: Medullary neurons sensitive to H⁺ in CSF, primarily reflecting PaCO₂.
Hypoxia: Decrease in arterial oxygen tension (PaO₂), potent stimulus for carotid bodies below ~60 mmHg.
Hypocapnia: Reduced PaCO₂; depresses chemoreceptor firing and ventilation.
Acidosis: Decreased blood pH; stimulates peripheral chemoreceptors rapidly.
Low perfusion pressure: Reduced blood flow/pressure at chemoreceptors; enhances stimulus (stagnant hypoxia).
Carotid body: Peripheral chemoreceptor at carotid bifurcation; dominant O₂ sensor, CN IX afferent.
Aortic bodies: Peripheral chemoreceptors along aortic arch; CN X afferent.
PaO₂ threshold (~60 mmHg): Point where carotid body firing rises steeply.
Hypoxic drive: Ventilation driven by low PaO₂, especially in chronic hypercapnia.
Anemia/CO poisoning: Low O₂ content with normal PaO₂; weak stimulus to peripheral chemoreceptors.
Oxygen therapy in COPD: Excess O₂ may blunt hypoxic drive and worsen V/Q mismatch.
Metabolic acidosis: Low HCO₃⁻/pH; stimulates ventilation via peripheral chemoreceptors.
Hypercapnia: Elevated PaCO₂; stimulates ventilation (peripheral and central pathways).
Glossopharyngeal nerve (CN IX): Afferent from carotid body to medulla.
Vagus nerve (CN X): Afferent from aortic bodies to medulla.
Type I (glomus) cell: O₂-sensing cell in carotid body releasing neurotransmitters to afferents.
Alveolar hypoventilation: Reduced ventilation causing hypercapnia and hypoxemia.
Stagnant hypoxia: Low tissue O₂ due to poor perfusion despite normal PaO₂.
Cyanide toxicity: Blocks cellular O₂ use; PaO₂ remains normal, weak peripheral chemoreceptor stimulus.
Chapter: Respiratory Physiology Topic: Control of Breathing Subtopic: Peripheral Chemoreceptors
Lead Question – 2012
Which of the following does NOT stimulate peripheral chemoreceptors:
a) Hypoxia
b) Hypocapnia
c) Acidosis
d) Low perfusion pressure
Explanation (Answer: b) Hypocapnia)
Peripheral chemoreceptors (carotid & aortic bodies) are excited by hypoxia (especially PaO₂ < 60 mmHg), acidosis, hypercapnia, and low perfusion pressure. Hypocapnia reduces arterial CO₂ and H⁺, suppressing chemoreceptor discharge and ventilation. Therefore, among the options, hypocapnia does not stimulate peripheral chemoreceptors and is the correct exception.
1) In a 68-year-old with severe COPD and chronic hypercapnia, the major acute ventilatory drive during an exacerbation is most likely from:
a) Central chemoreceptors sensing CSF alkalosis
b) Peripheral chemoreceptors sensing hypoxemia
c) Lung stretch receptors (Hering–Breuer)
d) J-receptors in alveolar walls
Explanation (Answer: b) Peripheral chemoreceptors sensing hypoxemia)
Chronic hypercapnia blunts central chemoreceptor responsiveness. During exacerbations with low PaO₂, carotid bodies dominate the acute ventilatory drive. Correcting PaO₂ cautiously is vital, as excess oxygen can depress hypoxic drive and worsen V/Q mismatch, increasing PaCO₂. Thus, peripheral chemoreceptors sensing hypoxemia are the main stimulus here.
2) The carotid body begins a steep increase in firing when arterial PaO₂ falls below approximately:
a) 90 mmHg
b) 75 mmHg
c) 60 mmHg
d) 40 mmHg
Explanation (Answer: c) 60 mmHg)
Peripheral chemoreceptor response to oxygen tension is nonlinear. Discharge rises modestly until a threshold, then increases steeply once PaO₂ drops below about 60 mmHg. This defends against hypoxemia by increasing ventilation. Hence, 60 mmHg is the clinically important threshold for robust carotid body stimulation and reflex hyperventilation.
3) Which afferent pathway carries signals from the carotid body to the medulla?
a) Vagus nerve (CN X)
b) Glossopharyngeal nerve (CN IX)
c) Trigeminal nerve (CN V)
d) Hypoglossal nerve (CN XII)
Explanation (Answer: b) Glossopharyngeal nerve (CN IX))
The carotid body at the carotid bifurcation sends chemosensory impulses via Hering’s nerve, a branch of the glossopharyngeal nerve (CN IX), to the nucleus tractus solitarius in the medulla. Aortic bodies project through the vagus nerve (CN X). Therefore, CN IX is the correct afferent for carotid body signaling.
4) A patient with profound anemia (Hb 6 g/dL) but normal PaO₂ is least likely to show strong peripheral chemoreceptor activation because:
a) Chemoreceptors sense PaO₂, not O₂ content
b) They are inhibited by low hemoglobin
c) They respond only to pH changes
d) They are saturated by nitric oxide
Explanation (Answer: a) Chemoreceptors sense PaO₂, not O₂ content)
Peripheral chemoreceptors primarily detect arterial oxygen tension (PaO₂), carbon dioxide, and pH. In anemia, PaO₂ may remain normal despite reduced oxygen content, so chemoreceptor stimulation is limited. Clinical hypoxia occurs at the tissue level, but the carotid bodies respond weakly unless PaO₂ itself falls significantly below ~60 mmHg.
5) Following sudden administration of high-flow oxygen to a hypercapnic COPD patient, CO₂ retention may worsen mainly due to:
a) Increased dead-space from V/Q mismatch
b) Enhanced central chemoreceptor sensitivity
c) Activation of stretch receptors
d) Reduced metabolic CO₂ production
Explanation (Answer: a) Increased dead-space from V/Q mismatch)
Supplemental oxygen can reverse hypoxic pulmonary vasoconstriction, increasing perfusion to poorly ventilated alveoli and worsening V/Q mismatch. This elevates dead-space and PaCO₂. Blunting of hypoxic drive also contributes but is not the dominant mechanism. Hence, increased dead-space from V/Q mismatch explains oxygen-induced hypercapnia in susceptible COPD patients.
6) Which statement about central versus peripheral chemoreceptors is MOST accurate?
a) Central chemoreceptors detect blood pH directly
b) Peripheral chemoreceptors do not respond to pH
c) Central chemoreceptors sense CSF H⁺ driven by PaCO₂
d) Peripheral chemoreceptors are insensitive to hypoxia
Explanation (Answer: c) Central chemoreceptors sense CSF H⁺ driven by PaCO₂)
Central chemoreceptors in the medulla respond primarily to H⁺ in CSF, which reflects arterial CO₂ diffusing across the blood–brain barrier. Blood H⁺ changes without CO₂ penetrate slowly, so peripheral chemoreceptors mediate rapid pH responses. Hypoxia strongly stimulates carotid bodies. Thus, central sensing of CSF H⁺ driven by PaCO₂ is correct.
7) In cardiogenic shock with low arterial pressure, ventilation rises partly because carotid bodies are stimulated by:
a) Elevated CSF bicarbonate
b) Low perfusion pressure (stagnant hypoxia)
c) Pulmonary stretch receptor firing
d) Increased oxyhemoglobin content
Explanation (Answer: b) Low perfusion pressure (stagnant hypoxia))
Reduced blood flow through the carotid body decreases oxygen delivery despite potentially normal PaO₂, producing stagnant hypoxia. This enhances glomus-cell neurotransmission to glossopharyngeal afferents, increasing ventilatory drive. Therefore, in shock states, low perfusion pressure itself is a recognized stimulus for peripheral chemoreceptors and augments respiratory effort.
8) A young diver hyperventilates before a breath-hold. Syncope underwater occurs because hypocapnia:
a) Intensifies carotid body firing
b) Delays the urge to breathe by suppressing CO₂ stimulus
c) Increases central chemoreceptor H⁺
d) Lowers PaO₂ threshold to 80 mmHg
Explanation (Answer: b) Delays the urge to breathe by suppressing CO₂ stimulus)
Pre-dive hyperventilation lowers PaCO₂ (hypocapnia), suppressing central and peripheral chemoreceptor drive, delaying the respiratory urge. PaO₂ can fall to hypoxic levels before CO₂ rises enough to trigger breathing, causing shallow-water blackout. Thus, hypocapnia delays warning signals rather than stimulating chemoreceptors, increasing risk of syncope.
9) Which cellular element is the primary O₂-sensing unit in the carotid body?
a) Type I (glomus) cell
b) Type II sustentacular cell
c) Endothelial cell
d) Schwann cell
Explanation (Answer: a) Type I (glomus) cell)
Type I (glomus) cells detect decreases in PaO₂ and acidosis, leading to membrane depolarization, calcium influx, and neurotransmitter release onto afferent fibers of CN IX. Type II cells are supportive. Therefore, the glomus cell is the fundamental O₂-sensing unit triggering peripheral chemoreceptor signaling to the brainstem.
10) In acute metabolic acidosis (e.g., diabetic ketoacidosis), the rapid increase in ventilation is initiated predominantly by:
a) Central chemoreceptors sensitive to CSF H⁺ immediately
b) Peripheral chemoreceptors sensing low arterial pH
c) Stretch receptors in respiratory muscles
d) Aortic baroreceptors
Explanation (Answer: b) Peripheral chemoreceptors sensing low arterial pH)
Blood H⁺ increases rapidly in metabolic acidosis. Because H⁺ crosses the blood–brain barrier slowly, medullary central chemoreceptors respond later. Carotid bodies sense the acidemia promptly and stimulate hyperventilation (Kussmaul breathing), lowering PaCO₂ to compensate. Thus, peripheral chemoreceptors mediate the early ventilatory response in metabolic acidosis.
11) A patient with suspected cyanide poisoning has normal PaO₂ and SaO₂ but tissue hypoxia. Peripheral chemoreceptor stimulation is expected to be:
a) Markedly increased due to blocked cellular respiration
b) Minimal because PaO₂ is normal
c) Driven solely by baroreceptors
d) Maximal via central chemoreceptors
Explanation (Answer: b) Minimal because PaO₂ is normal.
Cyanide prevents cellular O₂ utilization, but arterial PaO₂ and saturation remain normal. Peripheral chemoreceptors sense PaO₂ rather than cellular extraction, so their activation is limited unless hypoxemia, acidosis, or hypercapnia develops. Therefore, despite tissue hypoxia, carotid-body stimulation is relatively minimal when arterial oxygen tension is preserved.
Keyword Definitions
Peripheral chemoreceptors: Carotid/aortic bodies sensing low PaO₂, high PaCO₂, and low pH.
Central chemoreceptors: Medullary receptors sensing CSF H⁺ that reflects arterial PaCO₂.
PaO₂ (arterial oxygen tension): Partial pressure of dissolved oxygen in arterial blood.
Oxygen content (CaO₂): Total O₂ carried (mostly on Hb); may be low in anemia despite normal PaO₂.
Hypercapnia: Elevated PaCO₂; strong stimulus to ventilation (central & peripheral).
Hypocapnia: Low PaCO₂; suppresses chemoreceptor drive and ventilation.
Acidemia (low pH): Increases peripheral chemoreceptor firing; central responds after CSF equilibrates.
Low perfusion pressure: Reduced flow to carotid body causing stagnant hypoxia and stimulation.
Glomus (Type I) cell: O₂-sensing cell in carotid body that releases neurotransmitters to CN IX.
CN IX (Glossopharyngeal): Afferent from carotid body to nucleus tractus solitarius.
CN X (Vagus): Afferent from aortic bodies to medulla.
PaO₂ threshold (~60 mmHg): Level below which carotid body firing rises steeply.
Kussmaul breathing: Deep, rapid respirations in severe metabolic acidosis driven by peripheral chemoreceptors.
Hypoxic drive: Increased ventilation due to low PaO₂, prominent in chronic hypercapnia.
V/Q mismatch: Ventilation–perfusion inequality; O₂ can worsen CO₂ retention by reversing HPV.
Anemia: Reduced Hb concentration; lowers CaO₂ with typically normal PaO₂.
Cyanide poisoning: Impaired cellular O₂ use; normal PaO₂ and SaO₂, minimal chemoreceptor stimulus.
Baroreceptors: Pressure sensors; interact with respiration indirectly but are not chemoreceptors.
Alveolar hypoventilation: Inadequate ventilation causing hypercapnia and hypoxemia.
High-altitude acclimatization: Hypoxia stimulates carotid bodies leading to hyperventilation and renal compensation.
Chapter: Respiratory Physiology Topic: Control of Breathing Subtopic: Central and Peripheral Chemoreflexes
Lead Question – 2012
Peripheral and central chemoreceptors may both contribute to the increased ventilation that occurs as a result of which of the following?
a) A decrease in arterial oxygen content
b) A decrease in arterial blood pressure
c) An increase in arterial carbon dioxide tension
d) A decrease in arterial oxygen tension
Explanation (Answer: c) An increase in arterial carbon dioxide tension)
Hypercapnia raises CSF H⁺ stimulating central chemoreceptors and also activates peripheral chemoreceptors, producing robust hyperventilation. Low PaO₂ primarily stimulates peripheral receptors; low CaO₂ (anemia/CO poisoning) minimally affects them; decreased blood pressure stimulates peripheral chemoreceptors but not central ones directly. Hence both pathways are engaged by increased PaCO₂.
1) A 65-year-old with COPD and chronic hypercapnia presents somnolent. Which intervention most rapidly increases his ventilatory drive?
a) Raise FiO₂ to 1.0 immediately
b) Controlled reduction of PaCO₂ via noninvasive ventilation
c) Infuse bicarbonate
d) Administer acetazolamide acutely
Explanation (Answer: b) Controlled reduction of PaCO₂ via noninvasive ventilation)
Noninvasive ventilation lowers PaCO₂, decreasing CSF H⁺ and unloading both central and peripheral chemoreceptors toward normal responsiveness, improving ventilation. Abrupt high FiO₂ risks worsening V/Q mismatch and CO₂ retention. Bicarbonate may worsen intracellular acidosis; acetazolamide is for altitude acclimatization, not acute COPD hypercapnic encephalopathy.
2) The carotid body shows a dramatic rise in discharge when PaO₂ falls below:
a) 90 mmHg
b) 75 mmHg
c) 60 mmHg
d) 50 mmHg
Explanation (Answer: c) 60 mmHg)
Carotid body activation increases nonlinearly with hypoxemia. Below ~60 mmHg PaO₂, glomus cells depolarize strongly, driving ventilatory response. This threshold explains why modest hypoxemia provokes limited response until PaO₂ falls to clinically significant levels, as at altitude or severe lung disease, then ventilation rises steeply.
3) In severe hemorrhagic shock, tachypnea develops partly because chemoreceptors are stimulated by:
a) Elevated CSF bicarbonate
b) Low perfusion pressure at carotid bodies
c) Increased oxyhemoglobin saturation
d) Stretch of pulmonary receptors
Explanation (Answer: b) Low perfusion pressure at carotid bodies)
Reduced carotid body blood flow causes stagnant hypoxia, augmenting glomus cell activity and ventilation. Baroreflexes also interact, but primary chemoreflex stimulus is low perfusion. CSF bicarbonate elevation dampens central drive; oxyhemoglobin saturation is reduced, not increased; stretch receptors modulate tidal volume, not chemostimulation.
4) A healthy free diver hyperventilates before submersion and faints underwater. The mechanism is best explained by:
a) Hypocapnia delaying the CO₂-driven urge to breathe
b) Enhanced hypoxic sensitivity of central chemoreceptors
c) Increased PaO₂ threshold for carotid bodies
d) Reflex laryngospasm from cold water
Explanation (Answer: a) Hypocapnia delaying the CO₂-driven urge to breathe)
Pre-dive hyperventilation reduces PaCO₂, suppressing central and peripheral chemoreceptor drive. Oxygen falls to syncope-inducing levels before CO₂ rises enough to trigger breathing, causing shallow-water blackout. Central chemoreceptors are not hypoxia sensors; carotid body threshold is around 60 mmHg and is not raised by hyperventilation.
5) Which combination most powerfully stimulates ventilation through both central and peripheral pathways?
a) PaCO₂ 55 mmHg and pH 7.25
b) PaO₂ 55 mmHg with PaCO₂ 30 mmHg
c) Severe anemia with PaO₂ 95 mmHg
d) Normal PaCO₂ with metabolic alkalosis
Explanation (Answer: a) PaCO₂ 55 mmHg and pH 7.25)
Elevated PaCO₂ increases CSF H⁺ (central) and arterial H⁺ (peripheral). Concomitant acidemia further drives carotid body firing, producing strong hyperventilation. Hypocapnia (option b) suppresses drive despite hypoxemia. Anemia with normal PaO₂ weakly stimulates carotid bodies. Alkalosis blunts chemoreceptor responsiveness.
6) Which statement about anemia and chemoreception is MOST accurate?
a) Anemia strongly stimulates central chemoreceptors
b) Anemia powerfully activates carotid bodies at normal PaO₂
c) Anemia minimally activates chemoreceptors unless PaO₂ falls
d) Anemia triggers vagal J-receptors to increase ventilation
Explanation (Answer: c) Anemia minimally activates chemoreceptors unless PaO₂ falls)
Chemoreceptors sense PaO₂, PaCO₂, and pH. In isolated anemia, PaO₂ is typically normal though O₂ content is low; carotid body activation is limited. Central chemoreceptors do not detect O₂ content. J-receptors are pulmonary C fibers, not primary chemoreceptors. Hypoxemia is required for strong carotid body activation.
7) A patient with diabetic ketoacidosis exhibits deep, rapid breathing. The initial trigger for this pattern is primarily:
a) Central chemoreceptors sensing immediate CSF acidosis
b) Peripheral chemoreceptors sensing low arterial pH
c) Baroreceptors responding to hypotension
d) Stretch receptors in intercostal muscles
Explanation (Answer: b) Peripheral chemoreceptors sensing low arterial pH)
In metabolic acidosis, blood H⁺ rises quickly, which carotid bodies detect promptly, driving Kussmaul hyperventilation. CSF equilibrates more slowly; central chemoreceptors contribute later. Baroreceptors modulate cardiovascular reflexes, and muscle stretch receptors are not primary drivers of the chemoreflex ventilatory response.
8) Signals from the carotid body reach the medulla via which pathway?
a) Vagus nerve to NTS
b) Glossopharyngeal nerve (Hering’s nerve) to NTS
c) Trigeminal nerve to spinal trigeminal nucleus
d) Hypoglossal nerve to dorsal respiratory group
Explanation (Answer: b) Glossopharyngeal nerve (Hering’s nerve) to NTS)
Carotid body afferents travel in Hering’s nerve, a branch of CN IX, projecting to the nucleus tractus solitarius. Aortic bodies project via the vagus (CN X). CN V and XII are not chemosensory pathways to the respiratory centers. Hence, glossopharyngeal afferents are correct.
9) At high altitude on day 1, a climber hyperventilates. Which change over 48–72 hours sustains ventilation despite falling CSF H⁺?
a) Renal bicarbonate retention
b) Renal bicarbonate excretion
c) Reduced carotid body sensitivity
d) Increased PaCO₂ due to hypoventilation
Explanation (Answer: b) Renal bicarbonate excretion)
Hyperventilation lowers PaCO₂ and CSF H⁺, initially limiting central drive. Kidneys excrete bicarbonate, lowering blood and CSF buffering, allowing continued central responsiveness to low PaCO₂ while hypoxia keeps carotid bodies active. Retaining bicarbonate would blunt ventilation; carotid sensitivity increases, not decreases; PaCO₂ remains low with acclimatization.
10) A 30-year-old with opioid overdose has pinpoint pupils and shallow breathing. Which immediate physiologic effect of naloxone most restores ventilation?
a) Direct stimulation of carotid glomus cells
b) Reversal of μ-receptor depression of brainstem respiratory centers
c) Rapid rise in PaO₂ stimulating central chemoreceptors
d) Activation of pulmonary stretch receptors
Explanation (Answer: b) Reversal of μ-receptor depression of brainstem respiratory centers)
Opioids suppress medullary respiratory neurons and blunt chemoreceptor responsiveness. Naloxone antagonizes μ-receptors, restoring central drive and responsiveness to PaCO₂/PaO₂. Oxygenation alone does not stimulate central chemoreceptors; stretch receptors modulate inflation reflexes. Carotid glomus cells are not directly activated by naloxone.
11) Which change most strongly depresses both central and peripheral chemoreceptor drive?
a) Acute hypercapnia
b) Hypoxemia with PaO₂ 50 mmHg
c) Iatrogenic hypocapnia from overventilation
d) Metabolic acidosis with pH 7.20
Explanation (Answer: c) Iatrogenic hypocapnia from overventilation)
Hypocapnia lowers CSF and arterial H⁺, suppressing medullary and carotid body activity, reducing ventilatory drive. Hypercapnia and acidosis stimulate chemoreceptors; hypoxemia powerfully activates carotid bodies. Thus, excessive ventilation producing low PaCO₂ is the condition that depresses both central and peripheral chemoreceptor-mediated drive.
Keyword Definitions
Transpulmonary pressure (Ptp): Difference between alveolar pressure (PA) and intrapleural pressure (Ppl).
Alveolar (intraalveolar) pressure (PA): Pressure inside alveoli; near 0 cmH2O at no flow.
Intrapleural pressure (Ppl): Pressure in pleural space; normally negative during quiet breathing.
Transairway pressure: Airway opening pressure minus alveolar pressure (Pao − PA); drives airflow.
Transrespiratory pressure: Airway opening pressure minus body surface pressure (Pao − Pbs).
Plateau pressure (Pplat): Alveolar pressure at zero flow during inspiratory hold.
Peak inspiratory pressure (PIP): Highest circuit pressure; includes resistive and elastic components.
Compliance: ΔV/ΔP; ease of lung expansion for a given pressure change.
Elastance: Reciprocal of compliance; tendency to recoil.
Hysteresis: Inflation curve differs from deflation on the pressure–volume loop.
PEEP: Positive end-expiratory pressure; maintains nonnegative end-expiratory Ptp.
CPAP: Continuous positive airway pressure; splints airways, raises end-expiratory Ptp.
Equal pressure point (EPP): Site where airway and pleural pressures are equal during forced expiration.
Dynamic airway compression: Airway narrowing beyond the EPP during forced expiration.
Auto-PEEP: Trapped gas generating intrinsic PEEP at end expiration.
Driving pressure: Pplat − PEEP; surrogate for tidal stress across the respiratory system.
Functional residual capacity (FRC): Lung volume at end-tidal expiration when forces balance.
Pneumothorax: Air in pleural space raising Ppl, reducing Ptp and collapsing lung.
Esophageal pressure: Surrogate for pleural pressure used to estimate Ptp at bedside.
Barotrauma/Volutrauma: Injury from excessive pressures/overdistension due to high Ptp.
Chapter: Respiratory Physiology Topic: Mechanics of Breathing Subtopic: Pulmonary Pressures and Pressure Gradients
Lead Question – 2012
Transpulmonary pressure is the difference between:
a) The bronchus and atmospheric pressure
b) Pressure in alveoli and intrapleural pressure
c) Atmosphere and intrapleural pressure
d) Atmosphere and intraalveolar pressure
Explanation (Answer: b) Pressure in alveoli and intrapleural pressure) Transpulmonary pressure (Ptp) equals alveolar pressure minus intrapleural pressure (P_A − P_pl). It distends alveoli, keeping them open. At functional residual capacity, Ptp balances elastic recoil. During inspiration, Ppl becomes more negative, increasing Ptp and lung volume; expiration reverses this gradient.
1) Which pressure primarily drives airflow through conducting airways during inspiration?
a) Transairway pressure
b) Transpulmonary pressure
c) Transrespiratory pressure
d) Pleural pressure
Explanation (Answer: a) Transairway pressure) Transairway pressure is mouth or airway opening pressure minus alveolar pressure (Pao − PA). It drives flow through conducting airways, unlike transpulmonary pressure, which distends alveoli. During mechanical ventilation, peak inspiratory pressure minus plateau pressure estimates resistive (transairway) component, distinguishing flow resistance from elastic recoil.
2) Which feature of the lung pressure–volume relationship reflects surfactant recruitment and opening pressures?
a) Linear compliance across volumes
b) Zero hysteresis
c) Constant elastance
d) Hysteresis on inflation/deflation
Explanation (Answer: d) Hysteresis on inflation/deflation) The pressure–volume curve shows hysteresis: at a given volume, inflation requires higher transpulmonary pressure than deflation because surfactant recruitment and alveolar opening thresholds differ. This is independent of airway resistance and reflects lung elasticity and surface tension dynamics, explaining recruitment maneuvers and PEEP effects.
3) During quiet inspiration, which immediate change increases transpulmonary pressure?
a) More positive pleural pressure
b) Increased airway resistance
c) More negative pleural pressure
d) Decreased alveolar compliance
Explanation (Answer: c) More negative pleural pressure increases Ptp) Ptp equals PA − Ppl. During inspiration, muscles make pleural pressure more negative. If alveolar pressure falls less, the difference increases, distending alveoli and drawing air inward. When pleural pressure becomes less negative or positive, Ptp drops, promoting expiration or collapse.
4) In a ventilated ARDS patient, which bedside measure most closely estimates alveolar pressure for calculating Ptp?
a) Peak inspiratory pressure
b) Plateau pressure during inspiratory hold
c) Mean airway pressure
d) End-tidal CO₂
Explanation (Answer: b) Alveolar pressure at zero flow approximates) Plateau pressure during an inspiratory hold reflects alveolar pressure at zero flow, so Ptp ≈ Pplat − Ppl (or −esophageal). Peak pressure overestimates elastic stress from resistance. Target transpulmonary pressure: limit end-inspiratory Ptp, and use PEEP to maintain nonnegative end-expiratory Ptp.
5) To minimize atelectrauma in ARDS, which end-expiratory condition is most appropriate?
a) Negative end-expiratory Ptp
b) Zero PEEP
c) Very high end-inspiratory Ptp
d) Equal or positive end-expiratory Ptp
Explanation (Answer: d) Equal or positive end-expiratory Ptp) Preventing collapse requires maintaining alveolar patency with nonnegative end-expiratory transpulmonary pressure using PEEP. Negative end-expiratory Ptp favors derecruitment and atelectrauma. Excessively high Ptp causes overdistension (volutrauma). Clinicians titrate PEEP so end-expiratory Ptp is near zero to positive, improving oxygenation while minimizing injury.
6) A tall, young man develops sudden pleuritic chest pain and dyspnea. Which process most directly abolishes transpulmonary pressure, collapsing the lung?
a) Atelectasis
b) Pleural effusion
c) Pneumothorax
d) Chest wall restriction
Explanation (Answer: c) Pneumothorax) In pneumothorax, intrapleural pressure approaches atmospheric or positive values, collapsing lung because transpulmonary pressure falls toward zero or negative. Atelectasis reduces surface area and compliance but may preserve a negative Ppl. Pleural effusion increases pleural pressure mildly; chest wall restriction reduces total compliance without nullifying Ptp.
7) For a fixed transpulmonary pressure, which change yields the largest increase in lung volume on the P–V curve?
a) Increased compliance
b) Decreased compliance
c) Increased airway resistance
d) Reduced surfactant
Explanation (Answer: a) Increased compliance) For a given transpulmonary pressure, a more compliant lung exhibits greater volume change (ΔV/ΔP). Stiff lungs (low compliance) require higher Ptp to achieve the same volume. Surfactant deficiency, fibrosis, or edema decrease compliance. Emphysema increases compliance but often sacrifices elastic recoil and small-airway tethering markedly.
8) In forced expiration, which intervention moves the equal pressure point distally and reduces dynamic airway collapse?
a) Decreasing lung volume
b) Increasing lung volume with PEEP
c) Increasing airway resistance
d) Adding dead space
Explanation (Answer: b) Equal pressure point dynamics) During forced expiration, pleural pressure rises, compressing airways. Where airway pressure equals pleural pressure—the equal pressure point—dynamic compression begins. Increasing lung volume or Ptp shifts the point peripherally and splints airways via radial traction. Loss of elastic recoil (low Ptp) causes airway collapse.
9) Which expression correctly defines transrespiratory pressure?
a) PA − Ppl
b) Pao − PA
c) Pao − Pbs
d) Ppl − Pbs
Explanation (Answer: d) Transrespiratory pressure) Transrespiratory pressure equals airway opening pressure minus body surface pressure (Pao − Pbs). It represents pressure moving gas between mouth and alveoli. It partitions into transairway (resistive) plus transpulmonary (elastic) components. In spontaneous breathing, Pbs ≈ atmospheric. In mechanical ventilation, Pao is controlled by ventilator.
10) In obstructive sleep apnea, which statement about end-expiratory transpulmonary pressure and CPAP is true?
a) End-expiratory Ptp is strongly positive without CPAP
b) CPAP lowers end-expiratory Ptp below zero
c) End-expiratory Ptp can become negative; CPAP makes it nonnegative
d) CPAP reduces alveolar pressure but increases pleural pressure
Explanation (Answer: c) Negative Ptp at end expiration) Obstructive apnea with chest effort elevates intrapleural pressure negativity but may cause dynamic closure; if alveoli derecruit, end-expiratory Ptp can become negative, predisposing to atelectrauma. CPAP increases airway opening pressure, making end-expiratory Ptp less negative or positive, preventing collapse and improving oxygenation.
Keywords
Alveolar Ventilation - The amount of fresh air reaching the alveoli per minute.
Respiratory Quotient (RQ) - Ratio of CO2 produced to O2 consumed.
Dead Space - Portion of tidal volume not participating in gas exchange.
Diffusion Capacity - Ability of the lungs to transfer gas from alveoli to blood.
Oxygen Consumption (VO2) - The rate at which oxygen is used by tissues.
Carbon Dioxide Output (VCO2) - Rate at which CO2 is produced and eliminated.
Fick Principle - Relation between blood flow, O2 consumption, and arteriovenous O2 difference.
Arterial Blood Gas (ABG) - Test measuring oxygenation, ventilation, and acid-base balance.
Partial Pressure - Pressure exerted by an individual gas in a mixture.
Minute Ventilation - Total volume of air entering lungs per minute.
Alveolar Gas Equation - Formula to calculate alveolar oxygen pressure (PAO2).
Chapter: Respiratory Physiology
Topic: Pulmonary Ventilation
Subtopic: Oxygen Consumption and Carbon Dioxide Elimination
Lead Question - 2012
Difference in the amount of O2 inspired and CO2 expired?
a) 20 ml/min
b) 50 ml/min
c) 75 ml/min
d) 100 ml/min
Explanation: The average O2 consumption at rest is about 250 ml/min while CO2 output is ~200 ml/min, leaving a difference of 50 ml/min. This reflects tissue O2 utilization exceeding CO2 production. Answer: b) 50 ml/min
Q2. A patient with COPD has a resting VO2 of 300 ml/min and VCO2 of 250 ml/min. The difference between inspired O2 and expired CO2 is?
a) 30 ml/min
b) 40 ml/min
c) 50 ml/min
d) 60 ml/min
Explanation: Here, the difference is 300 - 250 = 50 ml/min. This matches normal physiology, showing metabolic balance despite disease. Answer: c) 50 ml/min
Q3. Normal oxygen consumption in an adult at rest is approximately?
a) 150 ml/min
b) 200 ml/min
c) 250 ml/min
d) 300 ml/min
Explanation: At rest, adults consume ~250 ml/min of O2. This value varies with body size, temperature, and metabolic activity. Answer: c) 250 ml/min
Q4. Carbon dioxide production in a healthy resting adult is?
a) 100 ml/min
b) 150 ml/min
c) 200 ml/min
d) 250 ml/min
Explanation: At rest, CO2 elimination averages 200 ml/min, closely linked to tissue metabolism. Answer: c) 200 ml/min
Q5. Which principle is used to calculate oxygen consumption in physiology labs?
a) Boyle’s law
b) Fick’s principle
c) Dalton’s law
d) Henry’s law
Explanation: Fick’s principle relates blood flow to O2 consumption and the arteriovenous O2 difference. Answer: b) Fick’s principle
Q6. In exercise, oxygen consumption may increase up to?
a) 500 ml/min
b) 1000 ml/min
c) 2000 ml/min
d) 4000 ml/min
Explanation: During heavy exercise, VO2 can reach 4000 ml/min or higher, reflecting increased metabolic demand. Answer: d) 4000 ml/min
Q7. A patient has O2 consumption of 270 ml/min and CO2 production of 220 ml/min. What is the respiratory quotient (RQ)?
a) 0.6
b) 0.7
c) 0.8
d) 1.0
Explanation: RQ = VCO2/VO2 = 220/270 ≈ 0.8, which is normal for a mixed diet. Answer: c) 0.8
Q8. If a patient is on pure carbohydrate diet, the expected RQ is?
a) 0.6
b) 0.7
c) 0.8
d) 1.0
Explanation: Carbohydrate metabolism yields equal O2 consumption and CO2 production, making RQ = 1.0. Answer: d) 1.0
Q9. Which factor increases oxygen consumption significantly?
a) Hypothermia
b) Sepsis
c) Sedation
d) Hypothyroidism
Explanation: Sepsis increases metabolic rate and tissue oxygen use, raising VO2. Answer: b) Sepsis
Q10. Which condition decreases carbon dioxide production?
a) Fever
b) Hyperthyroidism
c) Sedation
d) Exercise
Explanation: Sedation lowers metabolism, thereby reducing CO2 output. Answer: c) Sedation
Q11. During high-altitude hypoxia, which change occurs in VO2 and VCO2?
a) Both increase
b) Both decrease
c) VO2 same, VCO2 decreases
d) VO2 increases, VCO2 same
Explanation: At altitude, metabolism may decrease due to hypoxia, lowering both VO2 and VCO2. Answer: b) Both decrease
Keyword Definitions
Bohr effect - Rightward shift of O₂–Hb curve with increased H⁺ or CO₂, aiding O₂ unloading.
Haldane effect - Hemoglobin's reduced CO₂ affinity when oxygenated, promoting CO₂ uptake in tissues.
Oxygen affinity - How tightly haemoglobin binds O₂; influenced by pH, CO₂, temperature, 2,3-BPG.
2,3-BPG - Red cell metabolite that lowers hemoglobin O₂ affinity, shifting the curve rightward.
Right shift - Decreased O₂ affinity; facilitates O₂ release to tissues.
Left shift - Increased O₂ affinity; hemoglobin holds O₂ more tightly.
PaO₂ - Arterial O₂ partial pressure; main stimulus for peripheral chemoreceptors when low.
SaO₂ - Hemoglobin oxygen saturation.
Carboxyhemoglobin - CO bound to Hb, raises apparent SaO₂ but prevents O₂ delivery.
Pulse oximetry - Noninvasive saturation monitor; cannot distinguish dyshemoglobinemias reliably.
Chapter: Respiratory Physiology Topic: Hemoglobin & Gas Transport Subtopic: Bohr and Haldane Effects
Lead Question – 2012
Bohr effect is described as: (also September 2009)
a) Decrease in CO2 affinity of hemoglobin when the pH of blood rises
b) Decrease in CO2 affinity of hemoglobin when the pH of blood falls
c) Decrease in O2 affinity of hemoglobin when the pH of blood rises
d) Decrease in O2 affinity of hemoglobin when the pH of blood falls
Explanation: Bohr effect denotes decreased oxygen affinity of hemoglobin when blood pH falls because increased H⁺ and CO₂ stabilize deoxygenated hemoglobin, shifting the curve rightward and enhancing oxygen unloading in metabolically active tissues. Therefore, the correct choice is d) Decrease in O2 affinity of hemoglobin when the pH of blood falls.
1) Which factor shifts the O₂–Hb dissociation curve to the right (facilitating O₂ release)?
a) Increase in pH (alkalosis)
b) Decrease in temperature
c) Increase in 2,3-BPG
d) Fetal hemoglobin presence
Explanation: Increased 2,3-BPG lowers hemoglobin O₂ affinity and shifts the curve right, promoting oxygen unloading in peripheral tissues. Clinically elevated in chronic hypoxia and anemia. Thus answer c) Increase in 2,3-BPG is correct because it decreases O₂ affinity, aiding delivery to metabolically active tissues.
2) A patient with carbon monoxide poisoning will have which effect on oxygen delivery?
a) Increased O₂ unloading to tissues
b) Left shift of O₂–Hb curve and impaired delivery
c) No change in O₂ content
d) Increased PaO₂ compensates
Explanation: Carbon monoxide binds hemoglobin tightly producing carboxyhemoglobin, causing a left shift and increased affinity of remaining sites for O₂, thereby impairing tissue delivery despite normal PaO₂. Clinically, answer b) Left shift of O₂–Hb curve and impaired delivery is correct; oxygen therapy and hyperbaric oxygen are treatments.
3) Which change best explains increased O₂ unloading during fever?
a) Decreased metabolic demand
b) Decreased temperature
c) Right shift from increased temperature
d) Lowered 2,3-BPG
Explanation: Fever raises tissue temperature which shifts the oxyhemoglobin dissociation curve to the right, decreasing O₂ affinity and enhancing unloading. Therefore c) Right shift from increased temperature is correct. Clinically during infection or exercise, this effect supports increased tissue oxygenation to meet metabolic needs.
4) The Haldane effect describes:
a) CO₂ loading when hemoglobin is oxygenated
b) Increased CO₂ carriage when hemoglobin is deoxygenated
c) O₂ binding increased by high CO₂
d) 2,3-BPG reduction with hypoxia
Explanation: The Haldane effect describes how deoxygenated hemoglobin carries more CO₂ and H⁺, facilitating CO₂ uptake in tissues and release in the lungs. Thus answer b) Increased CO₂ carriage when hemoglobin is deoxygenated is correct and explains reciprocal effects of O₂ and CO₂ carriage by hemoglobin in gas exchange physiology.
5) In chronic hypoxia (eg, COPD), which adaptation increases oxygen unloading to tissues?
a) Decreased 2,3-BPG
b) Increased 2,3-BPG
c) Elevated fetal hemoglobin
d) Reduced cardiac output
Explanation: Chronic hypoxia elevates erythrocyte 2,3-BPG levels, which lowers hemoglobin’s O₂ affinity and shifts the dissociation curve right, improving tissue oxygen delivery. Therefore b) Increased 2,3-BPG is correct. This cellular adaptation helps compensate for low arterial oxygen tensions in long-standing hypoxic states.
6) A left shift of the O₂–Hb curve occurs with:
a) Acidosis and fever
b) Increased 2,3-BPG
c) Hypothermia and decreased 2,3-BPG
d) High PCO₂
Explanation: Hypothermia and decreased 2,3-BPG raise hemoglobin affinity for O₂, shifting the curve left and reducing tissue unloading. Thus c) Hypothermia and decreased 2,3-BPG is correct. Clinically this explains reduced peripheral O₂ release in hypothermic patients and influences transfusion and oxygen strategies.
7) Which clinical condition most clearly demonstrates the Bohr effect in action?
a) Tissue hypoperfusion with alkalosis
b) Active exercising muscle with acidosis
c) Hyperventilation causing alkalosis
d) Hypothermia during surgery
Explanation: Exercising muscle produces CO₂ and H⁺ causing local acidosis that decreases Hb O₂ affinity and facilitates unloading; this is the Bohr effect. Therefore answer b) Active exercising muscle with acidosis is correct and clinically explains improved oxygen delivery to exercising tissues via rightward curve shift.
8) Which statement regarding fetal hemoglobin (HbF) is true?
a) HbF has higher 2,3-BPG binding than adult Hb
b) HbF shifts the O₂–Hb curve to the right
c) HbF has higher O₂ affinity than adult HbA
d) HbF increases CO₂ unloading in placenta
Explanation: Fetal hemoglobin binds 2,3-BPG less avidly, giving it higher O₂ affinity and a left-shifted dissociation curve relative to adult HbA, facilitating placental oxygen transfer. Thus c) HbF has higher O₂ affinity than adult HbA is correct and underlies fetal oxygen extraction from maternal blood.
9) Which lab finding would you expect with increased peripheral tissue O₂ unloading?
a) Decreased venous PCO₂
b) Increased venous O₂ saturation (SvO₂)
c) Increased arteriovenous O₂ difference
d) Decreased lactate in tissues
Explanation: Enhanced O₂ unloading lowers venous O₂ content and saturation, increasing the arteriovenous O₂ difference. Clinically a larger a-v O₂ difference (arterial minus venous O₂ content) reflects greater tissue extraction. Therefore c) Increased arteriovenous O₂ difference is the correct answer in states of high extraction.
10) A patient with sepsis is vasodilated and hypermetabolic. Which combination alters O₂ delivery and promotes Bohr effect unloading?
a) Alkalosis, hypothermia
b) Acidosis, hyperthermia
c) Decreased 2,3-BPG, left shift
d) Reduced CO₂ production
Explanation: Sepsis often produces acidosis and fever which decrease hemoglobin O₂ affinity via the Bohr effect and increased temperature, shifting the dissociation curve right and promoting tissue unloading. Thus answer b) Acidosis, hyperthermia is correct and explains increased peripheral oxygen availability despite systemic illness.
Keyword Definitions
Compliance - Change in lung volume per unit change in transpulmonary pressure (ΔV/ΔP).
Surfactant - Surface-active lipoprotein from type II pneumocytes that lowers alveolar surface tension.
Elastance - Reciprocal of compliance; tendency of lung to recoil.
Static compliance - Compliance measured with no airflow (plateau conditions).
Dynamic compliance - Compliance measured during active airflow, includes resistance effects.
FRC (Functional residual capacity) - Lung volume at end-normal expiration where elastic forces balance.
Emphysema - Destructive airspace disease increasing lung compliance and reducing elastic recoil.
Fibrosis - Interstitial scarring that reduces lung compliance and increases elastic recoil.
Esophageal pressure - Clinical surrogate for pleural pressure used to estimate transpulmonary pressure.
Surface tension - Liquid film force at air–liquid interface that reduces lung compliance if high.
Chapter: Respiratory Mechanics Topic: Lung Compliance Subtopic: Determinants and Clinical Changes
Lead Question – 2012
True statement relating to compliance of lung:
a) Increased by surfactant
b) Decreased in emphysema
c) At height of inspiration compliance is less
d) It can be measured by measuring intrapleural pressure at different lung volume
e) None
Explanation: Surfactant lowers alveolar surface tension, increasing compliance and easing inflation; hence (a) is true. Emphysema increases, not decreases, compliance. Compliance falls at high lung volumes and can be measured using intrapleural (esophageal) pressure changes—so (a) is the best single true statement. Answer: a)
1) Which condition most decreases lung compliance?
a) Pulmonary fibrosis
b) Emphysema
c) Surfactant excess
d) Increased 2,3-BPG
Explanation: Pulmonary fibrosis causes stiff, scarred lungs with reduced compliance, increasing elastic recoil and work of breathing. Fibrosis limits volume change for any transpulmonary pressure increment and causes restrictive physiology. Thus a) Pulmonary fibrosis is correct and clinically presents with low lung volumes and high elastic work during inspiration.
2) Dynamic compliance differs from static compliance because dynamic includes effects of:
a) Airway resistance during flow
b) Surface tension only
c) Blood volume changes
d) Plateaus at zero flow
Explanation: Dynamic compliance measured during active airflow incorporates airway resistance and viscous losses, unlike static compliance measured at zero flow. Increased resistance (eg, bronchospasm) lowers dynamic but not static compliance. Therefore a) Airway resistance during flow is correct; clinicians note differences when assessing ventilated patients.
3) Clinically, which bedside measurement best estimates static lung compliance in an intubated patient?
a) Tidal volume / (Plateau pressure − PEEP)
b) Peak pressure / tidal volume
c) RR × tidal volume
d) PEEP alone
Explanation: Static compliance equals tidal volume divided by (plateau pressure minus PEEP) measured during an inspiratory hold. This isolates elastic properties by eliminating flow-related resistive pressure. Thus a) is correct and commonly used to guide ventilator settings to minimize volutrauma in ARDS and other conditions.
4) In emphysema, which pattern is expected?
a) Increased compliance, reduced recoil
b) Decreased compliance, increased recoil
c) Normal compliance, increased surface tension
d) Reduced compliance, reduced dead space
Explanation: Emphysema destroys alveolar walls and elastin, increasing lung compliance and reducing elastic recoil, promoting air trapping and increased residual volume. Therefore a) Increased compliance, reduced recoil is correct and explains floppy lungs, expiratory flow limitation, and dynamic hyperinflation clinically.
5) Which factor most increases lung compliance?
a) Higher surfactant concentration
b) Interstitial fibrosis
c) Pulmonary edema
d) Atelectasis
Explanation: Surfactant lowers surface tension and increases compliance, easing alveolar expansion. Conditions like fibrosis, edema, and atelectasis increase stiffness or surface tension, reducing compliance. Thus a) Higher surfactant concentration is correct and is physiologically crucial in neonates and lung injury management.
6) Why does compliance fall at very high lung volumes?
a) Elastic fibers reach their limit and stiffen
b) Surfactant concentration rises excessively
c) Airway resistance vanishes
d) Blood volume increases
Explanation: At high volumes, elastin and collagen fibers are stretched near their limits, requiring larger pressure changes per volume increment, so compliance falls. Thus a) Elastic fibers reach their limit and stiffen is correct. This explains the flattening of the pressure–volume curve at end-inspiration clinically.
7) Measuring compliance using intrapleural (esophageal) pressure is important because:
a) It estimates true transpulmonary pressure
b) It directly measures alveolar surface tension
c) It replaces arterial blood gas analysis
d) It determines bronchial tone
Explanation: Esophageal pressure approximates pleural pressure, allowing calculation of transpulmonary pressure (alveolar minus pleural) and thus true lung compliance. This distinction separates chest wall from lung mechanics and guides PEEP titration in ventilated patients. Therefore a) is correct and clinically useful in complex respiratory failure.
8) In acute pulmonary edema compliance usually:
a) Decreases because interstitial fluid increases stiffness
b) Increases because fluid lubricates alveoli
c) Remains unchanged
d) Is irrelevant clinically
Explanation: Interstitial and alveolar fluid increases tissue stiffness and surface tension effects, reducing lung compliance and increasing work of breathing. Therefore a) Decreases is correct. Clinicians see reduced tidal volumes and difficulty ventilating; treating edema can improve compliance rapidly.
9) Which neonatal condition has very low lung compliance?
a) Neonatal respiratory distress syndrome (surfactant deficiency)
b) Transient tachypnea of newborn
c) Meconium aspiration with hypercompliance
d) Patent ductus arteriosus
Explanation: Neonatal RDS features surfactant deficiency, high alveolar surface tension, collapse, and markedly reduced compliance. This produces stiff lungs, low volumes, and severe respiratory distress; surfactant replacement raises compliance. Thus a) is correct and is a cornerstone of neonatal respiratory management.
10) Which ventilator change increases measured static compliance if lung recruitment occurs?
a) Apply optimal PEEP to recruit alveoli
b) Increase delivered flow rate
c) Decrease inspiratory time only
d) Increase circuit resistance
Explanation: Optimal PEEP opens collapsed alveoli, increasing available volume for a given pressure and therefore raising measured static compliance. Recruitment reduces atelectasis and improves compliance; increasing flow or resistance affects dynamic measures, not static compliance. Hence a) is correct and used in ARDS ventilation strategies.
Keyword Definitions
Hematocrit - Fraction (%) of blood volume occupied by red blood cells; rises with hemoconcentration or polycythemia.
Hemoconcentration - Relative increase in red cell concentration due to reduced plasma volume (eg, dehydration).
Polycythemia - True increase in RBC mass (primary or secondary) causing high hematocrit independent of plasma volume.
Plasma electrolytes - Sodium, potassium, chloride, bicarbonate levels in plasma; reflect volume/status and acid–base balance.
Hemolysis - RBC rupture releasing intracellular K⁺ and other contents into plasma; may artifactually raise plasma K.
Hypernatremia - Increased plasma sodium concentration often from water loss causing hemoconcentration and higher hematocrit.
Metabolic alkalosis - Elevated plasma HCO₃⁻, sometimes from vomiting or diuretics; may associate with volume changes.
Chloride shift (Hamburger shift) - Movement of Cl⁻ into RBCs as HCO₃⁻ leaves during CO₂ transport in tissues.
Venous blood - Blood returning to the heart, higher CO₂, lower O₂ than arterial blood; can show concentration changes with local perfusion.
Plasma volume - Liquid component of blood; decreases in dehydration, increasing hematocrit without change in RBC mass.
Chapter: Clinical Hematology Topic: Blood Composition Subtopic: Hematocrit, Volume Status & Electrolytes
Lead Question – 2012
Venous blood with high hematocrit is seen in ?
a) RBC high chloride
b) Plasma high Na
c) Plasma high HCO3
d) RBC high K
Explanation (Answer: b) Plasma high Na) Elevated hematocrit in venous blood commonly reflects hemoconcentration from reduced plasma volume, as occurs with dehydration or water loss. This concentrates plasma solutes including sodium, so a high plasma Na (hypernatremia due to water deficit) accompanies increased hematocrit. Therefore b) is the correct choice.
1) In dehydration causing hemoconcentration, which laboratory pattern is expected?
a) ↑ Hematocrit, ↑ Plasma Na
b) ↓ Hematocrit, ↑ Plasma Na
c) ↑ Hematocrit, ↓ Plasma Na
d) ↓ Hematocrit, ↓ Plasma Na
Explanation: Dehydration reduces plasma volume leading to relative rise in hematocrit and concentration of solutes including sodium; thus both hematocrit and plasma Na increase. Clinically expect hemoconcentration with hypernatremia when water loss predominates. Answer a) is correct.
2) Which condition causes elevated hematocrit with normal plasma sodium?
a) Primary polycythemia (polycythemia vera)
b) Simple dehydration
c) Acute water intoxication
d) Diuretic-induced hypernatremia
Explanation: Primary polycythemia increases total RBC mass, raising hematocrit while plasma sodium may remain normal. Hemoconcentration from dehydration changes Na. Thus a) polycythemia vera is correct and requires distinct diagnosis (erythropoietin, JAK2 testing) compared with volume-related causes.
3) A lab sample shows high plasma K. Which preanalytical artifact could explain this with normal patient physiology?
a) Hemolysis during phlebotomy
b) Dehydration concentrating plasma
c) Diuretic-induced loss
d) Chronic kidney disease
Explanation: Hemolysis releases intracellular K⁺ into plasma, artifactually elevating measured potassium. This is a common preanalytical error and should be suspected when samples are traumatic. Thus a) hemolysis during phlebotomy explains isolated high plasma K with otherwise normal physiology.
4) Chloride shift in tissue capillaries results in which RBC change?
a) Increased RBC chloride concentration as HCO₃⁻ leaves
b) Increased RBC sodium
c) Increased RBC potassium
d) Decreased RBC chloride
Explanation: As CO₂ diffuses into erythrocytes and is converted to HCO₃⁻, HCO₃⁻ exits the cell while Cl⁻ enters to maintain electroneutrality (Hamburger shift). This increases RBC chloride concentration during CO₂ uptake in tissues. Therefore a) is correct.
5) Which scenario most likely produces low hematocrit in venous blood?
a) Acute hemorrhage with fluid resuscitation
b) Dehydration from vomiting
c) Secondary polycythemia from hypoxia
d) Erythropoietin use
Explanation: Acute hemorrhage followed by rapid crystalloid infusion dilutes remaining RBCs, lowering hematocrit (dilutional anemia). Dehydration does opposite; polycythemia and erythropoietin raise hematocrit. Thus a) is correct clinically in trauma or operative settings.
6) Metabolic alkalosis with high HCO₃⁻ is commonly associated with which volume status?
a) Contraction alkalosis with low plasma volume
b) Hypervolemia with low hematocrit
c) Euvolemia without change in hematocrit
d) Dehydration with low plasma Na
Explanation: Contraction alkalosis (eg, from diuretics or vomiting) reduces plasma volume concentrating HCO₃⁻ and electrolytes; it often accompanies hemoconcentration. So a) contraction alkalosis with low plasma volume is correct and may show relatively elevated hematocrit depending on fluid shifts.
7) Which lab pattern suggests true increased RBC mass rather than hemoconcentration?
a) ↑ Hematocrit with ↑ RBC mass on red cell mass study
b) ↑ Hematocrit with high plasma Na
c) ↑ Hematocrit that normalizes after fluid load
d) ↑ Hematocrit with low reticulocyte count only
Explanation: A red cell mass study showing increased RBC mass confirms true polycythemia rather than hemoconcentration which corrects after fluid repletion. Therefore a) is correct. Fluid-responsive hematocrit indicates volume effect; true polycythemia persists despite rehydration.
8) In diabetic ketoacidosis (DKA), initial labs often show:
a) ↑ Hematocrit due to dehydration
b) ↓ Hematocrit due to hemolysis
c) Normal hematocrit with hyperkalemia only
d) Increased plasma bicarbonate
Explanation: DKA causes osmotic diuresis and marked water loss, producing hemoconcentration and increased hematocrit. Plasma potassium may appear high due to shift from cells, though total body K is depleted. Thus, a) ↑ hematocrit due to dehydration is correct initially in DKA presentation.
9) Which chronic condition raises hematocrit via increased erythropoietin?
a) Chronic hypoxia from COPD
b) Chronic diarrheal dehydration
c) Acute sepsis with vasodilation
d) Cirrhosis with portal hypertension
Explanation: Chronic hypoxia stimulates renal erythropoietin production leading to secondary polycythemia with increased RBC mass and high hematocrit. COPD patients often exhibit this adaptation. Dehydration concentrates cells but erythropoietin-driven increases occur over weeks, so a) is correct.
10) A venous sample shows high hematocrit and high sodium. Best immediate clinical step is:
a) Assess volume status and consider rehydration if hypovolemic
b) Start phlebotomy for polycythemia vera immediately
c) Ignore as lab artifact always
d) Give bicarbonate to correct sodium
Explanation: High hematocrit with hypernatremia suggests hemoconcentration from volume loss; assess clinical volume status and treat dehydration with appropriate fluids. Phlebotomy is for true polycythemia after confirmation. Therefore a) is correct as a pragmatic immediate step in management.
Keyword Definitions
2,3-DPG - Red cell metabolite that binds deoxygenated hemoglobin and lowers O₂ affinity.
O₂–Hb dissociation curve - Relationship between PaO₂ and hemoglobin saturation; shifts indicate affinity changes.
Right shift - Reduced Hb O₂ affinity; facilitates O₂ release to tissues (favored by ↑2,3-DPG, ↑CO₂, ↑H⁺, ↑T).
Left shift - Increased Hb O₂ affinity; impairs O₂ unloading (favored by ↓2,3-DPG, ↓CO₂, ↓H⁺, ↓T, fetal Hb).
PaO₂ - Partial pressure of oxygen in arterial blood; primary determinant of SaO₂ at physiologic range.
SaO₂ / SvO₂ - Arterial and venous hemoglobin oxygen saturations; reflect oxygen loading/unloading balance.
Hypoxia - Reduced tissue oxygen delivery; stimulates adaptive increases in 2,3-DPG over days.
Anemia - Reduced O₂ content that can trigger higher 2,3-DPG to improve tissue O₂ delivery.
Acidosis - Increased H⁺ promotes right shift (Bohr effect), complementing 2,3-DPG effects.
Transfusion storage - Stored RBCs lose 2,3-DPG; transfused blood may transiently impair O₂ unloading until levels recover.
Chapter: Respiratory Physiology Topic: Hemoglobin & Gas Transport Subtopic: 2,3-DPG and O₂–Hb Affinity
Lead Question – 2012
Which of the following is/are effect of increased 2,3-DPG on oxygen-hemoglobin dissociation curve?
a) ↑ ed affinity of heamoglobin to oxygen
b) ↓ ed affinity of haemoglobin to oxygen
c) Left shift of oxygen-hemoglobin dissociation curve
d) Right shift of oxygen-hemoglobin dissociation curve
e) No change in oxygen-hemoglobin dissociation curve
Explanation: Increased 2,3-DPG binds deoxygenated hemoglobin, reducing O₂ affinity and causing a rightward shift of the O₂–Hb curve; this facilitates oxygen unloading to tissues (eg, chronic hypoxia, anemia). Therefore options b) (decreased affinity) and d) (right shift) are correct together, not a, c, or e.
1) In chronic hypoxemia, rise in erythrocyte 2,3-DPG primarily serves to:
a) Increase arterial PaO₂
b) Enhance tissue O₂ unloading
c) Increase Hb affinity for O₂
d) Promote left shift of O₂–Hb curve
Explanation: Chronic hypoxemia stimulates red cell 2,3-DPG synthesis, lowering hemoglobin O₂ affinity and shifting the curve right. This adaptation increases tissue oxygen delivery despite low PaO₂. Clinically seen in high altitude and chronic lung disease. Answer: b) Enhance tissue O₂ unloading.
2) Stored packed red blood cells may impair immediate O₂ delivery because:
a) They have elevated 2,3-DPG
b) They have reduced 2,3-DPG
c) They shift O₂–Hb curve right
d) They carry more CO₂
Explanation: During storage, RBCs lose 2,3-DPG, increasing hemoglobin O₂ affinity (left shift) and temporarily reducing tissue unloading after transfusion. 2,3-DPG regenerates over 24–72 hours in recipient cells. Therefore answer: b) They have reduced 2,3-DPG.
3) Which combination most strongly produces a right shift similar to ↑2,3-DPG?
a) Alkalosis, hypothermia
b) Acidosis, hypercapnia
c) High fetal hemoglobin, low 2,3-DPG
d) Low CO₂, low temperature
Explanation: Acidosis and hypercapnia increase H⁺ and CO₂, promoting a right shift (Bohr effect) that, like 2,3-DPG, reduces O₂ affinity and enhances unloading in tissues. Clinically present during exercise or sepsis. Answer: b) Acidosis, hypercapnia.
4) A patient with anemia adapts by increasing 2,3-DPG. Expected change in venous O₂ saturation (SvO₂) is:
a) Increased SvO₂
b) Decreased SvO₂
c) No change in SvO₂
d) SvO₂ equals SaO₂
Explanation: Increased 2,3-DPG lowers Hb O₂ affinity causing greater peripheral extraction and lower SvO₂ (larger a–v O₂ difference). Although arterial saturation may be preserved, venous saturation falls, reflecting enhanced unloading in tissues. Answer: b) Decreased SvO₂.
5) Which clinical state would most likely show elevated 2,3-DPG?
a) Recent blood transfusion with old stored blood
b) High-altitude acclimatization over days
c) Acute carbon monoxide poisoning
d) Hypothermia during surgery
Explanation: High-altitude acclimatization stimulates erythrocyte glycolysis and 2,3-DPG production over days to weeks, enhancing tissue O₂ delivery despite low PaO₂. Acute transfusion of stored blood lowers 2,3-DPG transiently; CO poisoning and hypothermia reduce delivery. Answer: b) High-altitude acclimatization.
6) Which hemoglobin variant interaction contrasts with 2,3-DPG effects?
a) Adult HbA has lower O₂ affinity when 2,3-DPG high
b) Fetal Hb (HbF) binds 2,3-DPG more avidly than HbA
c) HbF has higher O₂ affinity and binds less 2,3-DPG than HbA
d) HbS increases 2,3-DPG binding dramatically
Explanation: Fetal hemoglobin (HbF) has reduced binding to 2,3-DPG, giving it increased O₂ affinity (left shift) compared with adult HbA. This facilitates placental O₂ transfer opposite to effects of ↑2,3-DPG. Answer: c) HbF has higher O₂ affinity and binds less 2,3-DPG than HbA.
7) In sepsis with high metabolic demand and tissue hypoxia, what happens to 2,3-DPG and oxygen unloading?
a) 2,3-DPG falls and unloading decreases
b) 2,3-DPG rises and unloading increases
c) 2,3-DPG unchanged
d) 2,3-DPG rises but unloading decreases
Explanation: Tissue hypoxia and increased glycolytic flux in sepsis can elevate 2,3-DPG, diminishing Hb O₂ affinity and enhancing peripheral oxygen unloading. Combined with local acidosis and temperature rise, this improves oxygen delivery to metabolically active tissues. Answer: b) 2,3-DPG rises and unloading increases.
8) Which therapeutic action would counteract a right shift caused by elevated 2,3-DPG?
a) Administer warmed fluids to raise temperature
b) Give 100% oxygen to raise PaO₂ and promote left shift
c) Induce mild acidosis
d) Give transfusion of fresh stored RBCs low in 2,3-DPG
Explanation: Transfusion of fresh (or stored) RBCs low in 2,3-DPG can transiently increase Hb O₂ affinity (left shift), countering right shift effects. High inspired O₂ raises PaO₂ but does not directly reverse biochemical 2,3-DPG effects on Hb binding; answer: d) Give transfusion of fresh stored RBCs low in 2,3-DPG.
9) Which lab feature indirectly suggests increased 2,3-DPG activity clinically?
a) Increased arterial O₂ content with low extraction
b) Normal SaO₂ with low SvO₂ and increased a–v O₂ difference
c) Elevated PaO₂ with increased SaO₂
d) High carboxyhemoglobin
Explanation: Increased 2,3-DPG enhances tissue extraction causing lower venous saturation and a larger a–v O₂ difference while arterial saturation may appear unchanged. Thus b) Normal SaO₂ with low SvO₂ and increased a–v O₂ difference is indicative of enhanced peripheral unloading consistent with elevated 2,3-DPG.
10) Which statement about 2,3-DPG kinetics after transfusion of stored blood is correct?
a) Recipient’s RBCs restore 2,3-DPG in donor cells immediately
b) 2,3-DPG levels in transfused RBCs regenerate over 24–72 hours
c) 2,3-DPG never recovers in stored RBCs after transfusion
d) Storage increases 2,3-DPG so regeneration is unnecessary
Explanation: Stored RBCs have depleted 2,3-DPG that regenerates after transfusion in the recipient’s circulation over 24–72 hours as glycolytic metabolism resumes, restoring normal O₂ unloading capacity. Clinically this transient left shift may modestly impair immediate tissue oxygenation. Answer: b) 2,3-DPG levels regenerate over 24–72 hours.
Chapter: Respiratory System
Topic: Pulmonary Physiology
Subtopic: Alveolar Stability
Keyword Definitions:
Alveoli - Tiny air sacs in lungs where gas exchange occurs.
Surfactant - Substance secreted by type II pneumocytes that reduces surface tension in alveoli.
Residual Volume - Amount of air left in lungs after maximal expiration.
Lung Compliance - Measure of lung’s ability to expand.
Intrapleural Pressure - Negative pressure within pleural cavity that prevents lung collapse.
Surface Tension - Force at the liquid-air interface tending to collapse alveoli.
Type II Pneumocytes - Alveolar cells producing surfactant.
Atelectasis - Collapse of alveoli due to lack of surfactant or obstruction.
Lead Question - 2012
Stability of alveoli is maintained by?
a) Lung compliance
b) Negative intrapleural pressure
c) Increase in alveolar surface area by the surfactant
d) Residual air in alveoli
Explanation: Alveolar stability is primarily maintained by surfactant, which reduces surface tension, preventing collapse of smaller alveoli into larger ones. Compliance and intrapleural pressure support lung expansion, but surfactant directly stabilizes alveoli. Thus, the correct answer is c) Increase in alveolar surface area by the surfactant.
Guessed Question 1
Newborn with respiratory distress likely has deficiency of?
a) Type I pneumocytes
b) Type II pneumocytes
c) Macrophages
d) Ciliated cells
Explanation: Neonatal respiratory distress syndrome is due to deficiency of surfactant, secreted by type II pneumocytes. This leads to alveolar collapse and hypoxemia. Hence the correct answer is b) Type II pneumocytes.
Guessed Question 2
A 45-year-old smoker develops recurrent alveolar collapse. Which factor is most impaired?
a) Residual volume
b) Surfactant secretion
c) Intrapleural pressure
d) Lung compliance
Explanation: Smoking reduces surfactant production and damages alveolar walls. Lack of surfactant increases surface tension, leading to alveolar instability. The correct answer is b) Surfactant secretion.
Guessed Question 3
In premature infants, alveolar collapse is due to?
a) Increased intrapleural pressure
b) Surfactant deficiency
c) Increased lung compliance
d) Increased residual volume
Explanation: Premature infants (b) Surfactant deficiency.
Guessed Question 4
Which law explains tendency of alveoli to collapse without surfactant?
a) Poiseuille’s law
b) Boyle’s law
c) Laplace’s law
d) Dalton’s law
Explanation: Laplace’s law states pressure within alveoli is directly proportional to surface tension and inversely proportional to radius. Without surfactant, small alveoli collapse. Correct answer: c) Laplace’s law.
Guessed Question 5
Which condition leads to increased surfactant production?
a) Prolonged bed rest
b) Glucocorticoid administration
c) Hypercapnia
d) Hypothermia
Explanation: Corticosteroids stimulate surfactant production, hence are given antenatally to mothers at risk of preterm delivery. Correct answer: b) Glucocorticoid administration.
Guessed Question 6
Surfactant secretion starts at which fetal week?
a) 12 weeks
b) 20 weeks
c) 24 weeks
d) 34 weeks
Explanation: Surfactant production begins at 24 weeks and reaches sufficient levels for alveolar stability by 34–36 weeks of gestation. Correct answer: c) 24 weeks.
Guessed Question 7
A patient with ARDS develops alveolar collapse. Mechanism?
a) Increased compliance
b) Loss of surfactant
c) Increased intrapleural negativity
d) Increased residual air
Explanation: ARDS leads to diffuse alveolar damage and surfactant dysfunction, causing alveolar collapse and impaired gas exchange. Correct answer: b) Loss of surfactant.
Guessed Question 8
Which component of surfactant is most important?
a) Sphingomyelin
b) Lecithin (Dipalmitoylphosphatidylcholine)
c) Cholesterol
d) Glycolipids
Explanation: The major active component of surfactant is lecithin (DPPC), which lowers alveolar surface tension and maintains alveolar stability. Correct answer: b) Lecithin (DPPC).
Guessed Question 9
Which test estimates fetal lung maturity?
a) Lecithin-sphingomyelin ratio
b) Amniotic fluid bilirubin
c) Amniotic fluid creatinine
d) Fetal hemoglobin
Explanation: Lecithin-sphingomyelin (L/S) ratio in amniotic fluid indicates fetal lung maturity. Ratio ≥2 suggests adequate surfactant and alveolar stability. Correct answer: a) Lecithin-sphingomyelin ratio.
Guessed Question 10
Which alveolar cell is responsible for surfactant recycling?
a) Type I pneumocyte
b) Type II pneumocyte
c) Macrophage
d) Endothelial cell
Explanation: Type II pneumocytes both secrete and recycle surfactant, ensuring continuous maintenance of alveolar stability. Correct answer: b) Type II pneumocyte.
Chapter: Respiratory System
Topic: Pulmonary Volumes and Capacities
Subtopic: Vital Capacity
Keyword Definitions:
Tidal Volume (TV) - Air inspired or expired during normal breathing.
Inspiratory Reserve Volume (IRV) - Extra volume of air inhaled after normal inspiration.
Expiratory Reserve Volume (ERV) - Extra air exhaled after normal expiration.
Residual Volume (RV) - Air remaining in lungs after maximal expiration.
Vital Capacity (VC) - Maximum air exhaled after maximum inspiration.
Total Lung Capacity (TLC) - Sum of all lung volumes.
Functional Residual Capacity (FRC) - Air left after normal expiration.
Spirometry - Test to measure lung volumes and capacities (except RV).
Restrictive Lung Disease - Condition with reduced VC due to decreased lung expansion.
Obstructive Lung Disease - Condition with increased RV due to airflow limitation.
Lead Question - 2012
Which of the following defines vital capacity?
a) Air in lung after normal expiration
b) Maximum air that can be expirated after normal inspiration
c) Maximum air that can be expirated after maximum inspiration
d) Maximum air in lung after end of maximal inspiration
Explanation: Vital capacity is defined as the maximum volume of air a person can exhale after a maximal inspiration. It includes tidal volume, inspiratory reserve volume, and expiratory reserve volume but excludes residual volume. The correct answer is c) Maximum air that can be expirated after maximum inspiration.
Guessed Question 1
A 50-year-old smoker undergoes spirometry. His vital capacity is reduced. Likely cause?
a) Emphysema
b) Pulmonary fibrosis
c) Asthma
d) Chronic bronchitis
Explanation: Pulmonary fibrosis restricts lung expansion, lowering vital capacity. In obstructive diseases like asthma and emphysema, VC is relatively preserved, though residual volume increases. Thus, the correct answer is b) Pulmonary fibrosis.
Guessed Question 2
Which lung volume cannot be measured by spirometry?
a) Tidal volume
b) Vital capacity
c) Residual volume
d) Inspiratory reserve volume
Explanation: Spirometry measures all volumes except residual volume, functional residual capacity, and total lung capacity. Residual volume cannot be exhaled and requires helium dilution or body plethysmography. Correct answer: c) Residual volume.
Guessed Question 3
A patient with kyphoscoliosis has reduced vital capacity. The mechanism is?
a) Increased compliance
b) Reduced chest wall expansion
c) Increased residual volume
d) Airway obstruction
Explanation: In kyphoscoliosis, chest wall restriction prevents full lung expansion, reducing vital capacity. It is a restrictive pattern. Correct answer: b) Reduced chest wall expansion.
Guessed Question 4
Which combination of volumes constitutes vital capacity?
a) TV + IRV + ERV
b) TV + IRV + RV
c) IRV + ERV + RV
d) TV + ERV + RV
Explanation: Vital capacity is the sum of tidal volume, inspiratory reserve volume, and expiratory reserve volume. It does not include residual volume. Correct answer: a) TV + IRV + ERV.
Guessed Question 5
Vital capacity is maximum in which position?
a) Supine
b) Standing
c) Sitting
d) Prone
Explanation: Vital capacity is maximum in standing position due to reduced abdominal pressure on diaphragm and maximum lung expansion. It decreases in supine due to abdominal viscera pushing the diaphragm upwards. Correct answer: b) Standing.
Guessed Question 6
A patient with severe COPD shows increased total lung capacity but decreased vital capacity. Cause?
a) Increased IRV
b) Increased RV
c) Reduced TV
d) Reduced ERV
Explanation: In COPD, air trapping leads to increased residual volume, which decreases vital capacity despite increased TLC. Correct answer: b) Increased RV.
Guessed Question 7
A medical student performs spirometry. FVC = 3L, FEV1 = 2.7L. Interpretation?
a) Normal lung function
b) Obstructive disease
c) Restrictive disease
d) Mixed disorder
Explanation: FEV1/FVC ratio = 2.7/3 = 90% (normal >80%), with reduced FVC. This suggests restrictive lung disease where vital capacity is reduced. Correct answer: c) Restrictive disease.
Guessed Question 8
In an athlete, which factor contributes to increased vital capacity?
a) Decreased residual volume
b) Stronger respiratory muscles
c) Reduced total lung capacity
d) Decreased tidal volume
Explanation: Athletes have stronger respiratory muscles and better lung expansion, leading to increased vital capacity. Correct answer: b) Stronger respiratory muscles.
Guessed Question 9
A patient has TLC = 6L, RV = 2L. What is the vital capacity?
a) 2L
b) 4L
c) 6L
d) 8L
Explanation: Vital capacity = TLC – RV = 6 – 2 = 4L. Correct answer: b) 4L.
Guessed Question 10
A 70-year-old man shows age-related changes in lung volumes. Which is true?
a) VC increases
b) RV decreases
c) VC decreases
d) TLC decreases
Explanation: With aging, lung compliance increases, residual volume increases, and vital capacity decreases due to weaker respiratory muscles. Total lung capacity remains nearly constant. Correct answer: c) VC decreases.