Respo – Physio

✅ Correct Answer: High concentration of CO₂

Explanation:
Central chemoreceptors, located in the medulla oblongata, are highly sensitive to changes in arterial CO₂ levels (PaCO₂).

Here’s how the mechanism works:

• CO₂ diffuses easily across the blood–brain barrier into the cerebrospinal fluid (CSF).

• In the CSF, carbonic anhydrase converts CO₂ and H₂O into carbonic acid (H₂CO₃), which then dissociates into H⁺ and HCO₃⁻.

• The increase in H⁺ ion concentration in the CSF stimulates the central chemoreceptors, leading to an increase in ventilation to expel CO₂ and restore normal pH.

Although the receptors respond to H⁺, they are indirectly stimulated by CO₂, since H⁺ ions in the CSF come from CO₂ hydration.
Therefore, high CO₂ concentration is the most powerful and direct stimulus for central chemoreceptor activation.

❌ High concentration of bicarbonate ions
Bicarbonate levels in the CSF change slowly and do not directly stimulate central chemoreceptors.

❌ High concentration of hydrogen ions
Chemoreceptors respond to H⁺ in the CSF, but the main cause of this rise is increased CO₂, not direct entry of H⁺ from the blood (since H⁺ crosses the blood–brain barrier poorly).

❌ Low partial pressure of oxygen (PaO₂)
This primarily stimulates peripheral chemoreceptors (in the carotid and aortic bodies), not central ones.

❌ High pH in blood
Indicates alkalosis, which would actually decrease, not stimulate, respiratory drive.

Carbon dioxide (CO₂) produced by tissue metabolism diffuses into the blood and is transported to the lungs through three main forms:

1. Dissolved CO₂ in plasma (~7%)

2. Carbamino compounds (~23%), mainly with hemoglobin

3. Bicarbonate ions (HCO₃⁻) (~70%), which is the major route

Inside red blood cells, CO₂ combines with water under the action of carbonic anhydrase, forming carbonic acid (H₂CO₃), which dissociates into H⁺ and HCO₃⁻. The bicarbonate then moves out of the RBC into plasma in exchange for chloride ions (the chloride shift).

✅ Correct Option: In the form of bicarbonate ions

About 70% of CO₂ is transported as bicarbonate (HCO₃⁻) in the plasma.
This conversion is rapid and reversible, allowing efficient CO₂ transport and exhalation.

❌ Incorrect Options:

In the form of carbaminohemoglobin:
Only 20–23% of CO₂ binds directly to the globin part of hemoglobin to form carbaminohemoglobin — a minor route compared to bicarbonate.

In the form of carboxyhemoglobin:
This compound forms when CO binds to hemoglobin, not CO₂. It’s seen in carbon monoxide poisoning, not normal CO₂ transport.

By binding to plasma proteins:
CO₂ can attach weakly to plasma proteins, but this contribution is insignificant compared to hemoglobin binding or bicarbonate formation.

By dissolving in plasma:
Only a small fraction (~7%) of CO₂ remains dissolved directly in plasma — insufficient to serve as the main transport method.

✅ Correct Answer: Transpulmonary pressure

Explanation:
Transpulmonary pressure (Ptp) is defined as the difference between the alveolar pressure (Palv) and the intrapleural pressure (Pip):

This pressure represents the distending force that keeps the lungs expanded against the chest wall.

• When transpulmonary pressure increases → lungs inflate.

• When it decreases → lungs deflate.

It’s crucial in maintaining lung stability and preventing alveolar collapse.
At rest, intrapleural pressure is about –5 cm H₂O, and alveolar pressure is 0 cm H₂O (relative to atmosphere), making transpulmonary pressure +5 cm H₂O — enough to keep alveoli open.

❌ Interpulmonary pressure
Not a standard term; sometimes used interchangeably with alveolar pressure but does not describe the pressure difference.

❌ Interpleural pressure
Incorrect term — usually refers to intrapleural pressure, not the difference between pressures.

❌ Intrapleural pressure
This is the pressure within the pleural cavity, normally negative, but it is one of the components used to calculate transpulmonary pressure — not the difference itself.

❌ Atmospheric pressure
Pressure exerted by air in the environment; used as the reference point (0 cm H₂O) but not the pressure difference in question.

✅ Correct Answer: 200

Explanation:
Lung compliance refers to the ease with which the lungs expand during inspiration — it is defined as the change in lung volume per unit change in transpulmonary pressure.

Compliance (C)=ΔVΔP\text{Compliance (C)} = \frac{\Delta V}{\Delta P}Compliance (C)=ΔPΔV​

• The total (combined) compliance of both lungs in a normal healthy adult is about 200 mL/cm H₂O.

• This means that for every 1 cm H₂O increase in transpulmonary pressure, the lung volume increases by approximately 200 mL.

This property is crucial for efficient ventilation, and it depends on:

• Elastic fibers in lung tissue, and

• Surface tension within the alveoli (reduced by surfactant).

Decreased compliance occurs in conditions like pulmonary fibrosis or acute respiratory distress syndrome (ARDS), while increased compliance is seen in emphysema.

❌ 1000, 800, 600, 400
These values are much higher than the physiological range for lung compliance. Typical compliance per lung is ~100 mL/cm H₂O; for both lungs combined, it’s about 200 mL/cm H₂O.

✅ Correct Answer: Alveolar capillary pressure remains greater than alveolar air pressure

Explanation:
In the lung’s lower (basal) region — Zone 3, the pulmonary circulation pressure is highest because of gravity.
The relationship between the three pressures in this zone is:

Partery>Pvein>PalveolusP_{\text{artery}} > P_{\text{vein}} > P_{\text{alveolus}}Partery​>Pvein​>Palveolus​

This means both arterial and venous pressures in pulmonary capillaries exceed the alveolar air pressure, allowing continuous blood flow through the capillaries.

Thus, in Zone 3, alveolar capillary pressure (blood pressure) is greater than alveolar air pressure, resulting in maximal and continuous perfusion — ideal for gas exchange.

❌ Alveolar air pressure remains greater than alveolar capillary pressure
This occurs in Zone 1 (apex), where alveolar pressure > arterial pressure, causing no blood flow.

❌ It is present in the apices of lungs
Zone 3 is located at the bases of the lungs, not the apices.

❌ It receives intermittent blood flow
That describes Zone 2, where arterial pressure > alveolar pressure > venous pressure, causing intermittent (pulsatile) flow.

❌ None of these
Incorrect, since Zone 3 clearly has continuous blood flow due to high capillary pressure.

✅ Correct Answer: Without large increase in pulmonary arterial pressure

Explanation:
During strenuous exercise, cardiac output may increase four- to fivefold to meet the body’s oxygen demands. The pulmonary circulation accommodates this massive increase in blood flow without a large rise in pulmonary arterial pressure — unlike the systemic circulation, which experiences a significant pressure increase.

This is achieved through three main adaptive mechanisms:

1. Recruitment of previously closed pulmonary capillaries: New capillary pathways open up, increasing the total cross-sectional area for blood flow.

2. Distension of pulmonary vessels: Existing capillaries widen (dilate), reducing resistance.

3. Increased pulmonary compliance: The thin, elastic pulmonary vessels expand easily to handle greater volume.

Together, these mechanisms maintain low pulmonary vascular resistance, ensuring efficient gas exchange even at high cardiac output.

❌ With large increase in systemic arterial pressure
True for systemic circulation during exercise, but not for pulmonary circulation — its pressure rises only slightly.

❌ With increase in pulmonary arterial pressure
A slight increase may occur, but the key feature is that it’s not large, due to the compensatory recruitment and distension of capillaries.

❌ With decrease in pulmonary arterial pressure
Incorrect — the pressure doesn’t decrease; it stays relatively stable or slightly increases.

❌ None of these
Incorrect — pulmonary circulation clearly adapts without a large increase in pressure.

✅ Correct Answer: In the form of bicarbonate ions

Explanation:
The majority of carbon dioxide (CO₂) produced by tissue metabolism is transported in the blood as bicarbonate ions (HCO₃⁻) — this accounts for about 70% of total CO₂ transport.

Here’s how it works:

1. Inside red blood cells, CO₂ reacts with water under the influence of carbonic anhydrase:

   CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻\text{CO₂} + \text{H₂O} \leftrightarrow \text{H₂CO₃} \leftrightarrow \text{H⁺} + \text{HCO₃⁻}CO₂+H₂O↔H₂CO₃↔H⁺+HCO₃⁻

2. The generated bicarbonate ions then diffuse out of the RBCs into the plasma, exchanged with chloride ions (Cl⁻) in the chloride shift (Hamburger phenomenon).

3. In the lungs, the process reverses — bicarbonate reenters RBCs, is converted back to CO₂, and is exhaled.

❌ In the form of carbaminohemoglobin
About 20–25% of CO₂ binds to hemoglobin’s amino groups (forming carbaminohemoglobin), but this is not the main transport form.

❌ In the form of carboxyhemoglobin
This compound results from carbon monoxide (CO) binding to hemoglobin, not CO₂.

❌ By binding to plasma proteins
CO₂ can attach to plasma proteins slightly, but this route contributes minimally to total CO₂ transport.

❌ By dissolving in plasma
Only about 5–7% of CO₂ is transported as dissolved gas directly in plasma.

✅ Correct Answer: Passive diffusion through the lipid bilayer

Explanation:
Oxygen (O₂) and carbon dioxide (CO₂) are small, nonpolar molecules, which allows them to dissolve in the lipid bilayer of the plasma membrane and move freely across it by simple (passive) diffusion.

This process:

• Requires no energy (ATP),

• Moves gases down their concentration gradients — O₂ into cells (where it’s lower) and CO₂ out of cells (where it’s higher), and

• Depends on partial pressure differences across the membrane, as described by Fick’s Law of Diffusion.

This passive movement is critical for gas exchange in the lungs and cellular respiration in tissues.

❌ Specific gas transport proteins
No carrier proteins are required for O₂ or CO₂ — both diffuse freely due to their nonpolar nature.

❌ Secondary active transport
Involves coupling one solute’s movement with another’s gradient (e.g., Na⁺–glucose cotransport), which is not how gases move.

❌ Primary active transport
Uses ATP to move ions against their gradients (e.g., Na⁺/K⁺ ATPase); gases do not require energy-dependent transport.

❌ Facilitated diffusion
Requires carrier or channel proteins (e.g., for glucose or ions); gases cross directly through the membrane, not via proteins.

✅ Correct Answer: Hypoxia

Explanation:
Hypoxia refers to a state of insufficient oxygen supply to body tissues despite adequate blood flow. It occurs when oxygen delivery or utilization is impaired.
Causes include:

• Low arterial PO₂ (as in high altitude or respiratory disease)

• Reduced hemoglobin concentration (anemia)

• Impaired blood flow (circulatory hypoxia)

• Inhibition of oxygen utilization (histotoxic hypoxia, e.g., cyanide poisoning)

If hypoxia becomes severe and prolonged, it can lead to cellular injury and death, particularly in high-demand tissues such as the brain and heart.

❌ Pulmonary embolism
It’s a cause of hypoxia, not the term for oxygen deficiency itself. It blocks pulmonary arteries, reducing oxygenation of blood.

❌ Asthma
A respiratory condition causing airway constriction and obstruction, which may lead to hypoxia, but it is not the term describing oxygen deficiency.

❌ Anemia
A condition of low hemoglobin concentration that can cause hypoxia, but it specifically refers to a blood disorder, not oxygen lack in tissues.

❌ Anoxia
Means complete absence of oxygen supply to tissues — a more extreme form of hypoxia, not the general term.

✅ Correct Answer: Carbon monoxide poisoning

Explanation:
Carbon monoxide (CO) poisoning leads to impairment of oxygen delivery to tissues because CO binds to hemoglobin with an affinity about 200–250 times higher than oxygen.

• This forms carboxyhemoglobin, which reduces the number of available binding sites for oxygen and also shifts the oxygen-hemoglobin dissociation curve to the left, meaning that the remaining oxygen is less readily released to the tissues.

• As a result, even though arterial PO₂ may appear normal, tissue hypoxia develops due to poor oxygen unloading — a state known as anemic hypoxia (due to reduced oxygen-carrying capacity).

❌ Previous history of cyanide poisoning
Cyanide affects cellular oxygen utilization by blocking cytochrome oxidase in mitochondria, causing histotoxic hypoxia, not impaired delivery of oxygen.

❌ Doing exercise early in the morning
Exercise increases oxygen demand, not its delivery impairment; in healthy individuals, oxygen transport remains efficient.

❌ Running a marathon at sea level
This increases oxygen consumption but does not impair delivery — blood oxygenation and perfusion are maintained.

❌ None of these
Incorrect, because carbon monoxide poisoning clearly impairs oxygen delivery despite normal arterial oxygen tension.

✅ Correct Answer: Downward movement of diaphragm

Explanation:
During inspiration, the diaphragm contracts and moves downward, flattening its dome shape. This action increases the vertical diameter of the thoracic cavity, allowing the lungs to expand and draw air in.

• The contraction of the diaphragm pulls its central tendon downward by about 1.5 cm during quiet breathing and up to 7 cm during deep inspiration.

• This downward movement increases the volume of the thoracic cavity and decreases intrapulmonary pressure, causing air to flow into the lungs.

❌ Upward movement of diaphragm
Occurs during expiration, not inspiration. The diaphragm relaxes and moves upward, reducing the vertical diameter of the thoracic cavity.

❌ Downward movement of ribs
Seen during forced expiration, as internal intercostal muscles pull the ribs downward and inward to reduce thoracic volume.

❌ Bucket handle movement
This refers to the lateral elevation of lower ribs (7th–10th), which increases the transverse diameter, not the vertical diameter.

❌ Pump handle movement
This involves the anterior and upward movement of upper ribs (2nd–6th), which increases the anteroposterior diameter, not the vertical diameter.

✅ Correct Answer: Histotoxic hypoxia

Explanation:
Histotoxic hypoxia occurs when cells are unable to utilize oxygen effectively, despite adequate oxygen delivery and normal arterial oxygen saturation. This typically results from toxic interference with cellular respiration, such as cyanide poisoning, which inhibits cytochrome oxidase (Complex IV) in the mitochondrial electron transport chain.

• As a result, oxygen remains in the blood (high venous O₂ content), but ATP production halts, leading to cellular energy failure and tissue death despite “normal” oxygen levels.

❌ Circulatory hypoxia
Occurs when blood flow to tissues is reduced, such as in shock or heart failure. Oxygen delivery is limited due to impaired circulation, not due to toxic inhibition of cellular metabolism.

❌ Stagnant hypoxia
A subtype of circulatory hypoxia where local blood flow is sluggish or stagnant (e.g., due to venous obstruction or low cardiac output). Oxygen utilization by cells is intact, but delivery is reduced.

❌ Hypoxic hypoxia
Results from low arterial PO₂ (e.g., in high altitude, respiratory obstruction, or hypoventilation). The oxygen content in arterial blood is decreased, unlike histotoxic hypoxia where O₂ levels are normal.

❌ Anemic hypoxia
Occurs when hemoglobin concentration or oxygen-carrying capacity of blood is reduced (e.g., in anemia or carbon monoxide poisoning). The total oxygen content is low even though arterial PO₂ may be normal.

✅ Nitrogen narcosis — Correct.
At depths greater than about 100 feet (≈30 meters), the partial pressure of nitrogen increases significantly. This causes nitrogen to dissolve into neuronal membranes, producing anesthetic-like effects such as euphoria, poor judgment, disorientation, and loss of coordination — hence the nickname “rapture of the deep.”

❌ Barotrauma — Results from unequal pressure in air-filled spaces (ears, sinuses, lungs), not from nitrogen effects.
❌ Carbon monoxide poisoning — Causes headache and cherry-red skin, unrelated to diving depth.
❌ Decompression sickness — Occurs on rapid ascent, not during descent.
❌ Oxygen toxicity — Seen when breathing high-O₂ mixtures at high pressure, causing seizures or pulmonary irritation, not euphoria.

The condition most likely described by the symptoms—joint pain, numbness, severe muscle cramps, and dizziness—following a rapid ascent from deep water is:

• Decompression sickness (DCS)

Decompression sickness (also known as “the bends” or Caisson’s disease) occurs when a diver ascends too quickly. During deep dives, compressed inert gases, primarily nitrogen, dissolve into the body’s tissues. If the pressure is reduced too rapidly, these dissolved gases come out of solution and form bubbles in the blood and tissues.

• Joint pain (the “bends”) is the most common symptom, caused by nitrogen bubbles forming in and around the joints.
• Numbness and muscle cramps (neurological/musculoskeletal DCS) are caused by bubbles affecting nerves or muscle tissue.

✅ Increased erythropoietin production — Correct.
At high altitude, low arterial PO₂ causes tissue hypoxia, which stimulates the kidneys to release erythropoietin (EPO). EPO acts on the bone marrow to increase red blood cell production, raising the hematocrit and hemoglobin concentration. This enhances the blood’s oxygen-carrying capacity, a key part of long-term acclimatization.

❌ Decreased 2,3-BPG levels — 2,3-BPG actually increases at altitude to aid oxygen unloading, not decrease.
❌ Decreased blood pH — Occurs from hyperventilation-induced respiratory alkalosis, not the cause of increased hematocrit.
❌ Increased arterial PO₂ — Altitude lowers, not raises, PO₂.
❌ Increased arterial PCO₂ — Hyperventilation reduces, not increases, PCO₂.

✅ Increased ventilation due to hypoxia — Correct.
The primary and earliest response to high altitude is hyperventilation, triggered by peripheral chemoreceptors sensing low arterial PO₂. This increases alveolar PO₂, improving oxygen uptake. Over days, other adaptations (like increased 2,3-BPG and erythropoietin) follow, but the initial and most direct mechanism of acclimatization is increased ventilation due to hypoxia.

❌ Decreased sensitivity of chemoreceptors to low oxygen — The opposite occurs; sensitivity increases.
❌ Higher hemoglobin concentration from erythropoietin — Important but develops after several days to weeks, not immediately.
❌ Increased 2,3-BPG for oxygen unloading — Helps later but is a secondary adaptation.
❌ Increased sympathetic activity for cardiac output — Occurs but is not the main driver of acclimatization.

✅ Low cerebrospinal fluid (CSF) pH — Correct.
Central chemoreceptors in the medulla oblongata are stimulated indirectly by rising arterial CO₂. CO₂ diffuses across the blood–brain barrier and combines with water to form carbonic acid, which dissociates into H⁺ and HCO₃⁻. The resulting drop in CSF pH (increase in H⁺ concentration) is the direct stimulus for these receptors, increasing ventilation to eliminate excess CO₂.

❌ High arterial CO₂ — Triggers the response, but it’s indirect; CO₂ itself is not the direct stimulus.
❌ High arterial O₂ / Low arterial O₂ — Detected by peripheral, not central, chemoreceptors.
❌ Low arterial pH — Cannot directly affect central chemoreceptors because H⁺ ions do not cross the blood–brain barrier.

✅ Low pO₂ sensed by carotid bodies — Correct.
In obstructive sleep apnea, periods of airway obstruction cause hypoxemia. The peripheral chemoreceptors, particularly the carotid bodies, detect the low arterial pO₂ and stimulate the respiratory centers via the glossopharyngeal nerve (CN IX) to increase ventilation once airflow resumes.

❌ Baroreceptors sensing pressure — Respond to blood pressure, not oxygen levels.
❌ High CO₂ sensed by central chemoreceptors — Contributes to drive, but low O₂ sensed peripherally is the primary trigger during apnea-induced desaturation.
❌ Low pH in the bloodstream — Stimulates breathing, but this occurs secondary to CO₂ accumulation.
❌ Stretch receptors in the lungs — Limit overinflation (Hering–Breuer reflex); they do not increase ventilation during apnea.

✅ Medulla — Correct.
The medulla oblongata contains the respiratory rhythmicity centers — the dorsal respiratory group (DRG) and ventral respiratory group (VRG) — which control the basic rhythm of breathing. The DRG mainly governs inspiration, while the VRG becomes active during forced breathing. Damage to the medulla disrupts this rhythm, leading to irregular or arrested breathing.

❌ Cerebellum — Coordinates movement and balance, not respiration.
❌ Cortex — Allows voluntary control of breathing (e.g., holding your breath), but not automatic rhythm.
❌ Midbrain — Involved in reflexes and arousal, not primary respiratory control.
❌ Pons — Modifies the rhythm via pneumotaxic and apneustic centers, but the medulla generates it.

✅ Peripheral chemoreceptors — Correct.
In hypoxemia (low arterial PO₂) due to pulmonary congestion from heart failure, the peripheral chemoreceptors in the carotid and aortic bodies detect the low oxygen levels. They then send signals via the glossopharyngeal (IX) and vagus (X) nerves to the respiratory centers in the medulla, increasing respiratory rate and depth to improve oxygen uptake.

❌ Baroreceptors — Respond to blood pressure, not blood gases.
❌ Central chemoreceptors — Respond to CO₂ and pH, not directly to low O₂.
❌ Irritant receptors — Trigger cough or bronchoconstriction when the airways are irritated, not hypoxemia.
❌ Pulmonary stretch receptors — Regulate inspiratory duration (Hering–Breuer reflex), not the response to low oxygen.

✅ Decreased CO₂ — Correct.
In hyperventilation, excessive breathing causes a drop in arterial PCO₂ (hypocapnia). Low CO₂ reduces H⁺ concentration in cerebrospinal fluid (increasing pH), which inhibits central chemoreceptors in the medulla. This leads to a decrease in respiratory drive, often causing lightheadedness or dizziness due to cerebral vasoconstriction.

❌ Decreased pH — Would stimulate breathing (seen in acidosis).
❌ Increased O₂ — Has little effect on normal respiratory drive.
❌ Decreased O₂ — Stimulates breathing via peripheral chemoreceptors.
❌ Increased CO₂ — Strongly stimulates respiration, not reduces it.

✅ Central chemoreceptors — Correct.
When arterial PCO₂ rises during breath-holding, CO₂ diffuses into the cerebrospinal fluid (CSF) and forms carbonic acid, which dissociates into H⁺ and HCO₃⁻. The central chemoreceptors in the medulla oblongata sense the increased H⁺ concentration (low pH) and stimulate the respiratory center, producing the strong urge to breathe.

❌ Peripheral chemoreceptors — Respond mainly to low PO₂ and, to a lesser extent, to high CO₂ and low pH.
❌ Pulmonary stretch receptors — Regulate inspiration termination (Hering–Breuer reflex), not the urge to breathe.
❌ Mechanoreceptors — Detect movement or stretch, not gas levels.
❌ Cortical sensors — Voluntary control centers; they allow breath-holding but don’t trigger the automatic drive to breathe.

✅ Cheyne–Stokes breathing — Correct.
Cheyne–Stokes respiration is characterized by gradual increases and decreases in tidal volume (waxing and waning) followed by periods of apnea. It occurs due to delayed feedback between blood CO₂ levels and respiratory control centers, commonly seen in congestive heart failure and central nervous system disorders.

❌ Ataxic breathing — Completely irregular, with no pattern; seen in medullary damage.
❌ Biot breathing — Clusters of rapid breaths followed by apnea, seen in brainstem lesions or meningitis.
❌ Hyperpnoea — Simply deep breathing, often during exercise.
❌ Kussmaul breathing — Deep, labored breathing due to metabolic acidosis (e.g., diabetic ketoacidosis).

✅ Peripheral chemoreceptors sensing O₂ — Correct.
In chronic COPD, arterial PCO₂ is persistently elevated, causing central chemoreceptors in the medulla to become desensitized to CO₂ and pH changes. The peripheral chemoreceptors in the carotid and aortic bodies then become the primary drive to breathe, responding to low arterial PO₂ (hypoxemia). This is called the hypoxic drive.

❌ Baroreceptors — Sense blood pressure changes, not gases.
❌ Central chemoreceptors sensing CO₂ — These are blunted in chronic hypercapnia.
❌ Central chemoreceptors sensing O₂ — Central receptors do not detect O₂.
❌ Pulmonary stretch receptors — Regulate inspiration length (Hering–Breuer reflex), not the primary drive to breathe.

We use the Starling equation for net filtration pressure (NFP):

NFP = (Pc + πi) – (Pi + πc)

• Pc = capillary hydrostatic pressure = 8 mmHg

• πc = plasma colloid osmotic pressure = 28 mmHg

• πi = interstitial colloid osmotic pressure = 15 mmHg

• Pi = interstitial hydrostatic pressure = –9 mmHg

NFP = (8 + 15) – (-9 + 28)
NFP = 23 – 19
NFP = 4 mmHg

✅ Increased tissue PCO₂ — Correct.
A rise in carbon dioxide levels in tissues increases H⁺ concentration (lowers pH), promoting oxygen release from hemoglobin — this is the Bohr effect. It ensures that oxygen is unloaded where metabolism (and CO₂ production) is high.

❌ Decreased 2,3-BPG levels — Would make hemoglobin hold oxygen more tightly (shift left).
❌ Decreased temperature — Reduces oxygen release (shift left).
❌ Increased arterial PO₂ — Occurs in the lungs, favoring oxygen loading, not release.
❌ Increased blood pH — Alkalosis increases hemoglobin’s oxygen affinity (shift left), hindering oxygen delivery.

✅ Decreased hemoglobin oxygen saturation — Correct.
A reduction in alveolar PO₂ lowers the diffusion gradient driving oxygen into the pulmonary capillaries. As a result, less oxygen binds to hemoglobin, producing lower hemoglobin saturation and reduced arterial oxygen content.

❌ Decreased oxygen release at the tissues — Oxygen unloading may actually increase if tissue hypoxia stimulates a rightward shift (Bohr effect).
❌ Increased arterial oxygen content — The opposite occurs; it decreases.
❌ Increased hemoglobin affinity for CO₂ — Not directly affected by alveolar PO₂; that’s related to the Haldane effect.
❌ Increased oxygen binding to hemoglobin — Less alveolar oxygen means less binding, not more.

✅ Increased CO₂ and decreased pH enhance oxygen release — Correct.
The Bohr effect describes how increased CO₂ and lower pH (higher H⁺) reduce hemoglobin’s affinity for oxygen, causing the oxygen–hemoglobin dissociation curve to shift right. This allows more oxygen to be released to metabolically active tissues.

❌ Decreased CO₂ increases oxygen-binding capacity — True in lungs but doesn’t define the Bohr effect (that’s part of the Haldane effect).
❌ High pH increases hemoglobin oxygen binding — Correct but represents the opposite of the Bohr effect.
❌ High temperature decreases oxygen release — Temperature rise actually increases oxygen release (right shift).
❌ Increased O₂ binding enhances CO₂ affinity — Opposite of the Haldane effect, which says increased O₂ binding reduces CO₂ affinity.

✅ Shift to the right, decreasing oxygen affinity — Correct.
In metabolic acidosis, increased H⁺ concentration (low pH) causes a rightward shift of the oxygen–hemoglobin dissociation curve (the Bohr effect). This means hemoglobin has a lower affinity for oxygen, facilitating oxygen unloading to the tissues where it’s needed most.

❌ Decrease in CO₂ binding to hemoglobin — Not directly related; CO₂ binding actually contributes to the right shift (via carbaminohemoglobin formation).
❌ Increase in oxygen binding at the tissues — The opposite occurs; oxygen is released, not held tighter.
❌ No effect on the curve — Blood pH changes significantly affect the curve.
❌ Shift to the left, increasing oxygen affinity — Would occur in alkalosis or low CO₂, not in acidosis.

✅ Increased thickness of the respiratory membrane — Correct.
In left ventricular failure, blood backs up into the pulmonary circulation, raising hydrostatic pressure in pulmonary capillaries. This causes fluid to leak into the interstitial and alveolar spaces (pulmonary edema), thereby increasing the diffusion distance and thickness of the respiratory membrane. As a result, oxygen diffusion decreases, leading to hypoxemia.

❌ Decreased alveolar partial pressure of oxygen — Alveolar PO₂ may remain near normal initially; the problem is impaired diffusion, not ventilation.
❌ Decreased nitrogen diffusion — Nitrogen is physiologically inert and not part of gas exchange.
❌ Increased diffusion capacity for oxygen — Diffusion capacity is reduced, not increased.
❌ Increased oxygen binding to hemoglobin — Oxygen binding is reduced due to less oxygen diffusing into blood.

✅ Oxygen — Correct.
In emphysema, destruction of alveolar walls leads to a reduced surface area for gas exchange. Because oxygen diffusion is less efficient than that of CO₂, it is more affected by the loss of alveolar surface area. This results in hypoxemia despite normal or near-normal CO₂ levels initially.

❌ Carbon dioxide — Diffuses 20 times faster than oxygen; its exchange is usually maintained until the disease becomes severe.
❌ Argon, Helium, Nitrogen — These are inert gases not involved in respiratory gas exchange.

✅ Increased partial pressure gradient for oxygen — Correct.
During strenuous exercise, the tissues consume more oxygen, lowering venous PO₂. This increases the alveolar–capillary PO₂ gradient, which greatly enhances the rate of oxygen diffusion across the respiratory membrane.

❌ Decreased pulmonary blood flow — The opposite occurs; blood flow increases during exercise.
❌ Decreased thickness of alveolar wall — The wall thickness doesn’t change physiologically.
❌ Increased ventilation–perfusion ratio — Both ventilation and perfusion rise, but the ratio stays near normal; it’s not the main factor for diffusion rate.
❌ Increased alveolar surface area for oxygen — Slightly increases as more capillaries open, but the pressure gradient is the primary factor boosting diffusion.

✅ Internal intercostal and abdominal muscles contract — Correct.
During forced expiration, such as blowing up a balloon, the internal intercostal muscles pull the ribs down and inward, while the abdominal muscles push the diaphragm upward by increasing intra-abdominal pressure. Together, they decrease thoracic volume and expel air forcefully.

❌ Diaphragm contracts & external intercostal relaxes — Diaphragm contracts during inspiration, not expiration.
❌ Diaphragm contracts & internal intercostal relaxes — Opposite of what happens; internal intercostals contract in forced expiration.
❌ External intercostal contracts and diaphragm relaxes — External intercostals elevate ribs for inspiration, not expiration.
❌ No muscle will contract — Wrong; quiet expiration is passive, but forced expiration (like blowing) is active.

✅ Decreased alveolar surface area — Correct.
In emphysema, destruction of alveolar walls leads to a loss of surface area available for gas exchange. According to Fick’s law of diffusion, the rate of diffusion is directly proportional to surface area — so when alveolar walls are destroyed, oxygen diffusion decreases.

❌ Increased diffusion distance — Seen in fibrosis, not emphysema.
❌ Decreased lung compliance — Emphysema actually causes increased compliance due to loss of elastic tissue.
❌ Increased hemoglobin concentration — Would improve, not impair, oxygen transport.
❌ Increased oxygen concentration — Increases diffusion gradient, not decrease it.

✅ Bronchoconstriction via muscarinic receptor activation — Correct.
Parasympathetic stimulation (via the vagus nerve) releases acetylcholine, which binds to muscarinic M3 receptors on bronchial smooth muscle, causing bronchoconstriction and increased mucus secretion.

❌ Bronchoconstriction via alpha-1 receptor activation — Alpha-1 receptors are sympathetic, not parasympathetic, and mainly cause vasoconstriction, not bronchoconstriction.
❌ Bronchoconstriction via nicotinic receptor activation — Nicotinic receptors are at autonomic ganglia, not directly on airway smooth muscle.
❌ Bronchodilation via beta-2 receptor activation — This is a sympathetic effect (mediated by epinephrine), not parasympathetic.
❌ Bronchodilation due to acetylcholine receptor activation — Acetylcholine causes the opposite — bronchoconstriction, not dilation.

✅ Correct Answer: To increase airway pressure during expiration to reduce air trapping

Explanation:

• Emphysema is characterized by destruction of alveolar walls and loss of elastic recoil, leading to air trapping and hyperinflation.
• Pursed-lip breathing creates a small back pressure in the airways during exhalation, which prevents premature airway collapse and allows more complete emptying of the lungs.
• This technique helps reduce dyspnea, improve ventilation, and maintain oxygenation.

Why the other options are incorrect:

• To regulate filling of lungs that have increased compliance: ❌
  → While emphysematous lungs are more compliant, pursed-lip breathing primarily affects expiration, not inspiration.
• To avoid chest discomfort during inspiration: ❌
  → The maneuver mainly assists expiration, not the relief of inspiratory discomfort.
• Reflex response to severe breathlessness: ❌
  → It is a voluntary, learned technique, not an automatic reflex.
• To prevent cyanosis and hypoperfusion: ❌
  → Pursed-lip breathing improves ventilation indirectly, but its main mechanism is reducing airway collapse, not directly preventing cyanosis.

Explanation:

• The pH is 7.1 → acidemia.
• HCO₃⁻ is 5 mmol/L → markedly low, indicating primary metabolic acidosis.
• pCO₂ is 16.1 mmHg → low, reflecting respiratory compensation through hyperventilation.
• The observed pCO₂ matches the expected compensation according to Winter’s formula, confirming primary metabolic acidosis with respiratory compensation.

Why the other options are incorrect:

• Respiratory acidosis with partial compensation: ❌
  → Would have high pCO₂, not low.
• Respiratory alkalosis: ❌
  → Low pCO₂, but the primary issue is low HCO₃⁻ and acidemia, not high pH.
• Respiratory acidosis: ❌
  → Would present with high pCO₂ and acidemia.
• Metabolic alkalosis: ❌
  → Would present with high HCO₃⁻ and elevated pH.

Correct Answer: Constriction of blood vessel adjacent to alveoli

Explanation:

• Mechanism:
  • This is known as hypoxic pulmonary vasoconstriction (HPV).
  • When alveolar PO₂ falls below ~70–73 mmHg, the small pulmonary arterioles constrict.
  • Purpose: redirect blood flow from poorly ventilated alveoli to well-ventilated alveoli, optimizing ventilation-perfusion (V/Q) matching and improving oxygenation.
• Clinical relevance:
  • Chronic hypoxia (as in COPD or high altitude) can lead to pulmonary hypertension due to sustained vasoconstriction.

Why the other options are incorrect:

• Decreased physiological shunt: ❌
  → Shunt refers to blood that bypasses ventilated alveoli. Hypoxic vasoconstriction reduces shunt, but “decreased shunt” is not the primary event; the mechanism is vasoconstriction itself.
• Damage to type I pneumocytes: ❌
  → Occurs due to severe injury or ARDS, not mild hypoxia.
• Increase in nitrogen content: ❌
  → Nitrogen content in alveoli is relatively stable; partial pressure changes of oxygen don’t increase nitrogen.
• Expansion of alveoli: ❌
  → Low PO₂ does not cause alveolar expansion; it may reduce perfusion, but not volume.

✅ Correct Answer: Passive diffusion through the lipid bilayer

Explanation:

• Mechanism:
  • Oxygen (O₂) and carbon dioxide (CO₂) are small, nonpolar gases, allowing them to freely diffuse across the alveolar and capillary membranes.
  • This process follows Fick’s law of diffusion, where the rate of gas transfer depends on:
    • Surface area of the membrane
    • Thickness of the membrane
    • Partial pressure gradient of the gas
• Clinical relevance:
  • Any condition that thickens the alveolar-capillary membrane (e.g., pulmonary fibrosis) reduces gas exchange.
  • Hypoxia in such conditions is due to impaired diffusion, not defective transporters.

Why the other options are incorrect:

• Specific gas transport proteins: ❌
  → Hemoglobin carries oxygen in blood, but gases cross the membrane by diffusion, not via proteins.
• Secondary active transport: ❌
  → Requires energy indirectly via ion gradients, not used for O₂ or CO₂ transport.
• Primary active transport: ❌
  → Requires ATP to move molecules against a gradient, irrelevant for gases.
• Facilitated diffusion: ❌
  → Needs carrier proteins for polar or large molecules; oxygen and CO₂ are nonpolar and diffuse freely.

✅ Correct answer: Increased carbon dioxide in blood

Explanation:

• In healthy individuals, arterial CO₂ levels (hypercapnia) are the primary driver of respiration.
• Mechanism:
  • CO₂ diffuses into the cerebrospinal fluid (CSF) and forms carbonic acid, which dissociates into H⁺ ions.
  • Central chemoreceptors in the medulla oblongata detect this increase in H⁺ concentration and stimulate the respiratory center to increase ventilation.
• This leads to faster and deeper breathing, helping to eliminate CO₂ and restore normal blood pH.

Key point: While low oxygen (hypoxia) can stimulate breathing, in healthy individuals, CO₂ levels are more sensitive and dominant in controlling ventilation.

Why the other options are incorrect:

• High pH and high carbon dioxide: ❌
  → High pH (alkalosis) would inhibit respiration, even if CO₂ is elevated.
• Loss of oxygen in tissue: ❌
  → Hypoxia only becomes a strong respiratory stimulus when oxygen saturation drops significantly (PaO₂ < 60 mmHg), which is less sensitive than CO₂ changes.
• Increase in pH of blood: ❌
  → Alkalosis actually reduces respiratory drive.
• Decrease in pH of blood: ❌
  → While acidosis can stimulate breathing, the primary and most powerful stimulus in healthy individuals is CO₂, not systemic pH changes alone.

✅ Correct answer: Acclimatization

Explanation:

Acclimatization refers to the physiological adjustments that occur over days to weeks in response to changes in the environment, such as reduced oxygen availability at high altitude.

• Mechanism in high altitude:
  • Increased ventilation: Deeper and faster breathing to increase oxygen uptake.
  • Enhanced red blood cell production: More hemoglobin to carry oxygen.
  • Metabolic adjustments: Tissue oxygen utilization becomes more efficient.
  • Renal compensation: Adjusts bicarbonate to stabilize pH.
• These adaptations improve oxygen delivery and allow climbers to tolerate lower atmospheric oxygen levels than would be possible without gradual acclimatization.

Key point: Acclimatization requires time; immediate exposure triggers symptoms like acute mountain sickness.

Why the other options are incorrect:

• Familiarization: ❌
  → Refers to getting used to a task or environment behaviorally, not physiological adaptation.
• Accommodation: ❌
  → Usually refers to eye lens adjustment or general short-term physiological adjustments, not long-term altitude adaptation.
• Modification: ❌
  → A vague term; does not specifically describe adaptive physiological responses.
• Alteration: ❌
  → Non-specific term; does not indicate systematic physiological changes to environmental stress.

✅ Correct answer: Pneumotaxic center

Explanation:

The pneumotaxic center, located in the pons, plays a key role in regulating the rate and pattern of breathing. Its primary function is to:

• Inhibit the inspiratory neurons of the medullary dorsal respiratory group
• Limit the duration of inspiration (inspiratory time, T_I)
• As a result, increase the respiratory rate

By sending inhibitory signals, the pneumotaxic center prevents over-inflation of the lungs and helps coordinate a smooth rhythm of breathing.

Why the other options are incorrect:

• Ventral respiratory group of neurons: ❌
  → Mainly responsible for active expiration and forced inspiration; does not limit inspiratory duration.
• Dorsal respiratory group of neurons: ❌
  → Integrates sensory input from chemoreceptors and mechanoreceptors to control basic inspiration; does not limit inspiration.
• Chemotaxic center: ❌
  → This is not a standard respiratory center; likely a distractor.
• Apneustic center: ❌
  → Located in the lower pons, it promotes prolonged inspiration, the opposite of what limits inspiration.

✅ Correct answer: Respiratory acidosis

Step-by-step explanation:

Let’s interpret the ABG values one by one 👇

• pH = 7.3 → ↓ (Normal = 7.35–7.45) → Acidosis is present.
• pCO₂ = 55 mmHg → ↑ (Normal = 35–45 mmHg) → High CO₂ → Respiratory cause.
• HCO₃⁻ = 28 mEq/L → Slightly ↑ (Normal = 22–26 mEq/L) → Renal compensation (kidneys retaining bicarbonate to buffer acid).

Interpretation

➡ pH ↓ (acidosis)

➡ pCO₂ ↑ (retained CO₂)

➡ HCO₃⁻ ↑ (compensation)

This combination fits perfectly with compensated respiratory acidosis.

Why the others are incorrect:

• Respiratory alkalosis → pCO₂ would be low, not high.
• Metabolic alkalosis → pH would be high, not low.
• Metabolic acidosis → pH low, but pCO₂ low (compensatory hyperventilation).
• None of these → Incorrect because values clearly show respiratory acidosis.

✅ Increased tidal volume — Correct.
Alveolar ventilation (VA) = (Tidal volume – Dead space) × Respiratory rate.
By increasing tidal volume, a larger fraction of each breath reaches the alveoli (since dead space volume remains constant). This leads to a significant increase in effective gas exchange.

❌ Decreased lung compliance — Makes the lungs harder to expand, reducing tidal volume and thus alveolar ventilation.
❌ Increased pulmonary blood flow — Affects perfusion, not ventilation.
❌ Increased dead space — Increases wasted ventilation and reduces alveolar ventilation.
❌ Increased respiratory rate with shallow breaths — Causes most of each breath to stay in the dead space, lowering alveolar ventilation.

✅ Increased alveolar dead space — Correct.
In pulmonary embolism, a clot blocks blood flow (perfusion) to part of the lung. Although the alveoli are still ventilated, there is no perfusion, meaning no gas exchange occurs in that region. This increases the alveolar dead space and raises the V/Q ratio (approaching infinity).

❌ Decreased alveolar ventilation — Ventilation is usually normal or even increased; the problem is lack of blood flow, not airflow.
❌ Increased carbon dioxide exchange — CO₂ removal decreases, since there’s no blood to carry it away.
❌ Increased oxygen uptake — Oxygen cannot enter blood without perfusion.
❌ Increased perfusion — Perfusion is actually absent or reduced due to the embolism.

✅ Increased airway resistance — Correct.
In COPD, chronic inflammation and loss of elastic recoil cause airway narrowing, mucus accumulation, and destruction of alveolar walls. These changes lead to increased airway resistance, making it harder to exhale. As a result:

• Residual volume increases due to air trapping.

• FEV₁/FVC ratio decreases because forced expiratory volume drops more than vital capacity.

❌ Decreased airway resistance — Opposite of what happens; resistance actually rises.
❌ Decreased functional residual capacity — FRC is increased due to air trapping.
❌ Decreased lung compliance — In fibrosis, not COPD. COPD shows increased compliance.
❌ Increased alveolar surface tension — Would occur if surfactant were deficient (as in RDS), not in COPD.

✅ 75% — Correct.
At a PO₂ of about 40 mmHg (the average partial pressure in systemic tissues), hemoglobin is roughly 75% saturated with oxygen. This means it releases about 25% of its oxygen to the tissues under resting conditions — an efficient balance between oxygen loading in the lungs and unloading in peripheral tissues.

❌ 20%, 25%, 40%, 50% — These values are far below normal saturation at tissue level and would indicate severe hypoxia rather than normal physiology.

✅ Hering–Breuer reflex — Correct.
This reflex protects the lungs from over-inflation during deep inspiration. When the pulmonary stretch receptors in the smooth muscles of bronchi and bronchioles are activated by excessive lung expansion, they send inhibitory signals via the vagus nerve to the respiratory center in the medulla, causing inhibition of inspiration.

❌ Carotid body chemoreceptors — Respond to low oxygen (hypoxia), not lung stretch.
❌ Central chemoreceptors — Respond to raised CO₂ or H⁺ levels in the cerebrospinal fluid.
❌ Cough reflex — Clears the airway, triggered by irritants, not over-inflation.
❌ Stretch receptors in diaphragm — Not involved in this reflex; the diaphragm lacks the sensory stretch receptors responsible for limiting inspiration

✅ Correct answer: Pneumotaxic centre

Explanation:

• The pneumotaxic centre is located in the upper pons.
• It inhibits inspiration by sending inhibitory signals to the dorsal respiratory group (DRG) in the medulla.
• This limits the duration of inspiration → thus reducing tidal volume.
• As a result, respiration becomes faster and shallower (↑ respiratory rate).

Why others are incorrect:

• Ventral respiratory group (VRG) → ❌ Mainly active during forced breathing (both inspiration & expiration). It increases tidal volume rather than limiting it.
• Dorsal respiratory group (DRG) → ❌ Controls normal inspiration by sending impulses to the diaphragm; it is the target, not the limiter.
• Central chemoreceptors → ❌ Respond to ↑ CO₂ or ↓ pH in cerebrospinal fluid; they adjust breathing rate but not by directly limiting tidal volume.
• Apneustic centre → ❌ Located in the lower pons; it prolongs inspiration, causing deep breaths (opposite effect of the pneumotaxic centre).

✅ Correct answer: Type II alveolar epithelial cells

Explanation:

• Type II alveolar cells (pneumocytes) are cuboidal cells found in the alveoli.
• They secrete pulmonary surfactant, a phospholipid-rich substance (mainly dipalmitoyl phosphatidylcholine) that:
  • Reduces surface tension inside alveoli
  • Prevents alveolar collapse (atelectasis)
  • Increases lung compliance

Why others are incorrect:

• Squamous epithelial cells of trachea → ❌ Form part of the airway lining, not involved in gas exchange or surfactant production.
• Type I alveolar epithelial cells → ❌ Cover ~95% of alveolar surface, responsible for gas exchange, not secretion.
• Endothelial cells → ❌ Line pulmonary capillaries; involved in gas diffusion barrier but not surfactant secretion.
• Secretory cells (Clara/Club cells) → ❌ Found in bronchioles; secrete detoxifying enzymes and non-surfactant proteins, not the true alveolar surfactant.

✅ The volume of air that lingers in the lungs after a regular exhalation. — Correct.
Functional Residual Capacity (FRC) represents the volume of air remaining in the lungs after a normal (tidal) expiration. It includes:

• Expiratory reserve volume (ERV) + Residual volume (RV).
  A decrease in FRC suggests reduced lung compliance or lung collapse, as in pneumothorax, pleural effusion, or restrictive lung injury after trauma.

❌ Sum of inspiratory reserve and tidal volume — That’s inspiratory capacity (IC).
❌ Volume of air expelled after a standard exhalation — That’s expiratory reserve volume (ERV).
❌ Volume of air inhaled and exhaled during a typical breath — That’s tidal volume (TV).
❌ Volume of air that stays in the lungs after complete exhalation — That’s residual volume (RV).

✅ Correct Answer: Bronchoconstriction via muscarinic receptors

Explanation:

Parasympathetic stimulation of the respiratory system occurs through the vagus nerve, which releases acetylcholine (ACh).

ACh acts on M3 (muscarinic) receptors located on bronchial smooth muscle, causing:

• Contraction of smooth muscle → Bronchoconstriction
• Increased mucus secretion from submucosal glands

This response helps conserve energy and protect the lungs by limiting airflow when full ventilation isn’t needed.

Why the Other Options Are Incorrect:

• Bronchodilation due to acetylcholine receptor activation:
  ❌ ACh causes bronchoconstriction, not dilation.
• Bronchoconstriction via nicotinic receptors:
  ❌ Nicotinic receptors are found at autonomic ganglia and neuromuscular junctions, not on airway smooth muscle.
• Bronchoconstriction via alpha 1 receptors:
  ❌ Alpha-1 receptors are sympathetic adrenergic receptors; they affect blood vessels, not bronchioles.
• Bronchodilation via beta 2 receptors:
  ❌ This is caused by sympathetic stimulation (e.g., epinephrine or β₂ agonists like salbutamol), not parasympathetic.

Restrictive lung disease is characterized by reduced lung compliance, meaning the lungs cannot expand fully. This limitation affects the volumes of air that can be inhaled and exhaled, especially the larger lung volumes.

Vital capacity (VC) is the maximum volume of air a person can exhale after a maximal inhalation.

In restrictive disease:

• Inspiratory reserve volume (IRV) decreases due to limited expansion.

• Expiratory reserve volume (ERV) decreases slightly.

• Tidal volume (TV) may decrease minimally.

• Residual volume (RV) is often normal or slightly reduced because the lungs empty more completely due to increased elastic recoil.

The most significantly reduced parameter is VC, making it the key indicator of restrictive lung disease on pulmonary function tests.

❌ Why the Other Options Are Incorrect

• Inspiratory reserve volume: Reduced, but not as drastically as VC.

• Expiratory reserve volume: Slightly reduced; contributes to VC reduction but is not the main measure.

• Residual volume: Usually normal or slightly decreased; not the primary feature of restriction.

• Tidal volume: Decreases minimally; not the main affected parameter.

Functional residual capacity (FRC) is defined as the volume of air remaining in the lungs after a normal, passive exhalation.

FRC=Expiratory Reserve Volume (ERV)+Residual Volume (RV)

FRC represents the balance point between the outward recoil of the chest wall and the inward elastic recoil of the lungs.

• Reduction in FRC can occur in conditions such as atelectasis, pulmonary edema, obesity, or trauma, where lung expansion is impaired.

• A lower FRC means less air remains in the lungs between breaths, reducing oxygen reserve and increasing the risk of hypoxemia.

❌ Why the Other Options Are Incorrect

• The volume of air that stays in the lung after a complete exhalation: This describes residual volume, not FRC.

• The volume of air inhaled and exhaled during a typical breath: This is tidal volume, not FRC.

• The volume of air expelled after a standard exhalation: This is expiratory reserve volume (ERV), a component of FRC, not the entire FRC.

• The sum of inspiratory reserve volume and tidal volume: This is the inspiratory capacity, unrelated to FRC.

Alveolar ventilation rate is the volume of air reaching the alveoli per minute and participating in gas exchange. It is calculated using the formula:

Alveolar ventilation rate= (Tidal volume – Dead space volume) × Respiratory rate

Anatomical dead space ≈ 150 ml in adults

1. Subtract dead space from tidal volume:

      200−150=50 ml

2. Multiply by respiratory rate:

     50×40=2000 ml/min

So the alveolar ventilation rate is 2000 ml/min.

❌ Why the Other Options Are Incorrect

• 4600 ml/min / 6000 ml/min: These values overestimate alveolar ventilation.

• 400 ml/min / 200 ml/min: These values underestimate alveolar ventilation and do not account correctly for the number of breaths per minute and dead space.

During intense exercise, muscles may switch to anaerobic metabolism due to insufficient oxygen supply. This leads to the formation of lactic acid from pyruvate. After exercise, the body needs to repay the oxygen debt, primarily to provide the oxygen necessary for the Cori cycle, in which lactic acid is transported to the liver and converted back into glucose.

This process restores normal blood glucose levels and prevents lactic acidosis, allowing muscles to recover and prepare for subsequent activity. Additional oxygen is also used to restore ATP and phosphocreatine stores, but the major component of oxygen debt is related to lactic acid metabolism.

❌ Why the Other Options Are Incorrect

• Reconvert phosphocreatine to creatinine and phosphate: Phosphocreatine is replenished back to creatine and phosphate, but this uses only a small fraction of the oxygen debt.

• Oxygen bound with myoglobin only: Myoglobin stores oxygen, but restoring its oxygen content contributes minimally to overall oxygen debt.

• Reconvert ATP and ADP to AMP: ATP is resynthesized from ADP and Pi, not to AMP; this is part of general energy restoration, not the main driver of oxygen debt.

• Elevate body temperature: Increased temperature occurs during exercise but is not the primary reason for post-exercise oxygen consumption.

Obstructive sleep apnea (OSA) occurs when there is recurrent collapse of the upper airway during sleep. In obese individuals, excess fat deposits around the pharynx can narrow the airway. During sleep, especially in the REM stage, the pharyngeal muscles relax, reducing the airway diameter. This causes intermittent obstruction, leading to apnea (cessation of airflow) or hypopnea (reduced airflow).

The body responds to these episodes with brief arousals, increasing muscle tone and restoring airway patency. Over time, this leads to fragmented sleep, hypoxia, hypercapnia, and increased cardiovascular risk.

❌ Why the Other Options Are Incorrect

• A decrease in carbon dioxide levels: This is not the cause; in fact, PaCO₂ rises during apnea episodes.

• An increase in blood oxygen levels: Blood oxygen actually falls during apneic episodes; elevated oxygen would reduce the drive for breathing, not cause obstruction.

• A decrease in lung compliance: Lung stiffness is unrelated to airway collapse in OSA.

• Overactive diaphragm muscles: The diaphragm continues to attempt ventilation during apnea; overactivity is not the cause.

Central chemoreceptors, located in the medulla oblongata near the ventrolateral surface of the medulla, play a key role in the automatic regulation of breathing. They are highly sensitive to changes in PaCO₂.

CO₂ in arterial blood diffuses into the cerebrospinal fluid (CSF) and reacts with water to form carbonic acid, which dissociates into H⁺ ions and bicarbonate. The increase in H⁺ concentration in CSF stimulates central chemoreceptors, which then signal the respiratory centers in the medulla to increase ventilation, thus reducing PaCO₂ back toward normal.

This mechanism is the primary drive for ventilation under normal, healthy conditions, whereas oxygen levels play a secondary role.

❌ Why the Other Options Are Incorrect

• Input from irritant receptors: These trigger coughing or bronchoconstriction, not baseline ventilation regulation.

• Input from stretch receptors: These mediate the Hering-Breuer reflex, preventing overinflation of lungs, not chemical regulation.

• Arterial pH: While pH does influence ventilation, central chemoreceptors primarily respond to PaCO₂, which indirectly changes pH. Peripheral chemoreceptors are more sensitive to arterial pH changes.

• PaO₂: Low oxygen levels mainly stimulate peripheral chemoreceptors in the carotid and aortic bodies, not central chemoreceptors.

At high altitudes, atmospheric oxygen pressure decreases, leading to hypoxemia (low arterial oxygen tension). The peripheral chemoreceptors, located mainly in the carotid bodies (and to a lesser extent in the aortic bodies), are highly sensitive to decreases in PaO₂.

When PaO₂ falls below ~60 mmHg, these chemoreceptors are activated and send impulses via the glossopharyngeal (CN IX) and vagus (CN X) nerves to the respiratory centers in the medulla oblongata. This stimulation increases both the rate and depth of breathing (hyperventilation) to enhance oxygen uptake and restore arterial oxygen levels.

❌ Why the Other Options Are Incorrect

• Central chemoreceptors in the medulla oblongata: These respond primarily to changes in CO₂ and pH (H⁺ concentration), not directly to oxygen. They are less important during the initial response to hypoxia.

• The stretch receptors in the lungs: These mediate the Hering-Breuer reflex, which prevents lung overinflation — they are not involved in altitude-induced respiratory adjustments.

• The somatic nervous system: It controls voluntary respiration (e.g., holding your breath), not the automatic, hypoxia-driven changes in breathing rate.

• The Hering-Breuer reflex: This reflex limits inspiration during deep breathing but doesn’t regulate respiration in response to low oxygen tension.

The parasympathetic nervous system, through the vagus nerve, releases acetylcholine (ACh), which binds to muscarinic (M3) receptors on the smooth muscle of the bronchi and bronchioles. Activation of these receptors increases intracellular calcium levels in the smooth muscle, leading to bronchoconstriction and increased airway resistance. This response helps limit airflow during restful states, conserving energy and moisture in the airways.

Conversely, sympathetic stimulation causes bronchodilation via β₂ receptors, enhancing airflow during stress or physical activity.

❌ Why the Other Options Are Incorrect

• Bronchodilation due to acetylcholine receptor activation: Acetylcholine causes bronchoconstriction, not dilation, via muscarinic receptors.

• Bronchoconstriction via nicotinic receptors: Nicotinic receptors are found in autonomic ganglia and neuromuscular junctions, not in airway smooth muscle.

• Bronchoconstriction via alpha 1 receptors: Alpha 1 receptors primarily mediate vasoconstriction in blood vessels, not bronchial smooth muscle constriction.

• Bronchodilation via beta 2 receptors: This occurs with sympathetic stimulation (not parasympathetic), using epinephrine/norepinephrine, not acetylcholine.

Muscles Involved in Inspiration

1. Diaphragm

• The principal muscle of inspiration.

• When it contracts, it descends, increasing the vertical dimension of the thoracic cavity.

• This action also compresses abdominal viscera, pushing them downward and outward.

• Accounts for about 75% of the air entering the lungs during quiet inspiration.

2. External Intercostal Muscles

• Run obliquely downward and forward from the lower border of one rib to the upper border of the rib below.

• On contraction, they elevate the ribs, increasing both the anteroposterior and transverse diameters of the thorax.

• Facilitate bucket-handle and pump-handle movements of the ribs.

• Major contributors during quiet inspiration, along with the diaphragm.

3. Accessory Muscles (during deep or labored breathing)

• Scalenes, sternocleidomastoids, pectoralis minor, and serratus anterior may assist when more forceful inspiration is needed.

• They elevate the upper ribs and sternum.

❌ Why the Other Options Are Incorrect:

• Diaphragm and internal intercostal muscles:
  Internal intercostals are mainly expiratory, not inspiratory.

• Rectus abdominis and internal intercostals:
  Both are expiratory muscles; they aid in forced expiration, not inhalation.

• Internal and external intercostal muscles:
  External intercostals assist inspiration, but internal intercostals assist expiration — they act in opposite directions.

• Scalenes and internal intercostals:
  Scalenes are accessory inspiratory muscles, but internal intercostals oppose inspiration.

The oxygen–hemoglobin dissociation curve illustrates how readily hemoglobin binds to and releases oxygen at varying partial pressures of O₂ (PO₂).
A rightward shift of this curve indicates reduced affinity of hemoglobin for oxygen — meaning oxygen is released more easily to tissues.

🔹 Effect of Increased PCO₂:

When PCO₂ increases, as in airway obstruction or hypoventilation, the following occurs:

1. CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻

   • Increased CO₂ drives this reaction to the right → ↑ H⁺ → ↓ pH (acidosis).

2. Bohr Effect:

   • Increased H⁺ and CO₂ reduce hemoglobin’s affinity for O₂.

   • This causes more O₂ to be released from hemoglobin to the tissues.

   • The oxygen dissociation curve therefore shifts to the right.

3. Physiological Significance:

   • In metabolically active tissues (where CO₂ is high), this ensures that oxygen is more easily unloaded where it’s needed most.

🔹 Factors Affecting the O₂–Hb Dissociation Curve:

❌ Why the Other Options Are Incorrect:

• Remain the same:

  • Would occur only if CO₂ and pH levels remained normal.

  • Here, increased PCO₂ definitely alters the equilibrium, shifting the curve.

• Shift to left:

  • Occurs with low PCO₂, alkalosis, low temperature, or low 2,3-BPG — the opposite of this case.

  • Left shift = increased affinity = less O₂ released to tissues.

• Shift down:

  • Not a standard description in physiology.

  • The curve shifts rightward or leftward, not vertically, when affinity changes.

• Shift up:

  • “Upward” would indicate higher oxygen saturation at the same PO₂, which occurs in a left shift, not with elevated CO₂.

Arterial partial pressure of oxygen (PaO₂) reflects the amount of oxygen dissolved in arterial blood.

• Normal PaO₂ in healthy adults: ~ 95 mmHg (range: 80–100 mmHg)

• Lower values: indicate hypoxemia

  • 70–75 mmHg → mild hypoxemia

  • 55 mmHg → moderate hypoxemia

  • 20 mmHg → severe, life-threatening hypoxemia

During quiet (normal) inspiration, only the diaphragm and external intercostals are primarily involved:

• Diaphragm contraction → increases vertical thoracic diameter

• External intercostals → elevate ribs 1–2 slightly

During forced inspiration, accessory muscles contribute:

• Scalenes, sternocleidomastoid, and external intercostals of 2–7 ribs

• This significantly increases the anterior-posterior and transverse thoracic diameter

Other options:

• Contraction of diaphragm / external intercostals → occur in quiet inspiration

• Elevation of first rib → occurs in both quiet and forced inspiration

• Relaxation of internal intercostals → mainly during passive expiration

Lung compliance measures the ease with which the lungs expand:

Compliance = (Change in lung volume) / (Change in transpulmonary pressure)

• Normal total lung compliance (both lungs): ~ 200 mL/cm H₂O

• High compliance: lungs expand too easily (e.g., emphysema)

• Low compliance: lungs stiff and resist expansion (e.g., fibrosis, ARDS)

Other options:

• 50–110 mL/cm H₂O → abnormally low

• 400–600 mL/cm H₂O → abnormally high

During inspiration, the diaphragm contracts and moves downward, and the external intercostal muscles elevate the ribs, expanding the thoracic cavity.

This expansion increases thoracic volume and thereby decreases intrapleural pressure (pressure within the pleural cavity) — making it more negative than its resting level.

• At rest (end of expiration): Intrapleural pressure ≈ –2 to –4 mm Hg relative to atmospheric pressure.

• During inspiration: It becomes even more negative (≈ –6 to –8 mm Hg), helping draw air into the lungs as alveolar pressure briefly falls below atmospheric pressure.

This negative pressure is essential for lung expansion and airflow into alveoli.

❌ Why the Other Options Are Incorrect

• More negative than +2 mm Hg:
  ❌ Incorrect — a positive intrapleural pressure never occurs during normal inspiration; it would indicate airway obstruction or forced expiration.

• More negative than 0.4 mm Hg:
  ❌ Incorrect — this value is far too small; intrapleural pressure is much lower (around –4 mm Hg) even at rest.

• More positive than +4 mm Hg:
  ❌ Incorrect — intrapleural pressure never becomes positive during inspiration; positive pressures appear only during forced expiration or Valsalva maneuver.

• More negative than –4 mm Hg:
  ❌ Incorrect — while this can occur in deep or forced inspiration, normal quiet inspiration typically reaches around –6 mm Hg, not beyond that physiologically in quiet breathing.

The oxygen-hemoglobin dissociation curve shows the relationship between PO₂ and hemoglobin saturation.

• Right shift → hemoglobin releases oxygen more easily to tissues

• Causes of right shift (factors that decrease Hb affinity for O₂):

  • Increased 2,3-DPG

  • High CO₂ (Bohr effect)

  • Low pH (acidosis)

  • High temperature → occurs during strenuous exercise

• Left shift → hemoglobin holds oxygen more tightly

  • Low 2,3-DPG, fetal hemoglobin, low temperature, high pH

Other options:

• Low 2,3-DPG / fetal Hb / low temperature / high pH → shift left, increasing oxygen affinity

This phenomenon is called hypoxic pulmonary vasoconstriction (HPV):

• Mechanism: When alveolar PO₂ falls below ~70 mmHg, pulmonary arterioles constrict.

• Purpose: Redirects blood flow from poorly ventilated alveoli to better-ventilated alveoli, improving ventilation-perfusion (V/Q) matching.

• Other options:

  • Decreased physiological shunt → actually V/Q mismatch can increase shunt

  • Damage to type-1 pneumocytes → not an immediate response to low PO₂

  • Nitrogen content increases → irrelevant to this mechanism

In infants, the thoracic cage is highly compliant due to cartilaginous ribs and underdeveloped musculature:

• Increased elasticity of chest wall → thoracic movements contribute less to tidal volume

• Diaphragm becomes the primary muscle of respiration → abdominal (diaphragmatic) breathing is observed

• Ribs are more horizontal, limiting expansion, but the main reason is soft, elastic chest wall

Other options:

• Accessory cervical ribs → rare congenital anomaly, not normal

• Bucket handle / obliquity of ribs → relate to adult-type rib movement, not infant breathing

Lung compliance refers to how easily the lungs can expand in response to pressure changes — it’s a measure of their distensibility.

🔹 Normal Values:

• Compliance of one lung: ≈ 100 ml/cm H₂O

• Therefore, total lung compliance (both lungs) = 200 ml/cm H₂O

This means that for every 1 cm H₂O increase in transpulmonary pressure, the total lung volume increases by 200 ml in a healthy adult.

🔹 Determinants of Compliance:

1. Elastic tissue content (elastin and collagen)
2. Alveolar surface tension (regulated by surfactant)
3. Lung volume — compliance is lower at extremes of inflation

❌ Why the Other Options Are Incorrect:

• 250 ml of air/cm H₂O:
  Too high — normal total lung compliance does not reach this level even in emphysema; this value would overestimate lung distensibility.

• 100 ml of air/cm H₂O:
  This represents the compliance of one lung, not both. Total lung compliance doubles because both lungs contribute.

• 400 ml of air/cm H₂O:
  Far above physiological range — lungs this compliant would not maintain proper elastic recoil, severely impairing expiration.

• 300 ml of air/cm H₂O:
  Still higher than normal; might theoretically occur in advanced emphysema, but not in healthy lungs.

The lungs have an inherent elastic recoil, meaning they naturally tend to collapse inward due to their elastic fibers and surface tension within the alveoli. The transpulmonary pressure (P_tp) is the pressure that counteracts this recoil — it represents the distending pressure keeping the lungs inflated.

🔹 Definition:

Transpulmonary pressure (P_tp) = Alveolar pressure (P_A) – Pleural pressure (P_pl)

• Alveolar pressure (P_A): Pressure inside the alveoli.

• Pleural pressure (P_pl): Pressure within the pleural cavity, typically negative relative to atmospheric pressure.

🔹 Physiological Role:

• The transpulmonary pressure acts as the force opposing lung collapse.

• It determines the degree of lung inflation — the greater the transpulmonary pressure, the more the lungs expand.

• When the pleural pressure becomes less negative (e.g., in pneumothorax), the transpulmonary pressure decreases, and the lung collapses.

❌ Why the Other Options Are Incorrect:

• Transthoracic pressure:
  This is the pressure difference between the pleural pressure and atmospheric pressure. It represents the elastic recoil of the chest wall, not the lungs.

• Alveolar pressure:
  Pressure inside the alveoli — it fluctuates slightly above or below atmospheric pressure during breathing but does not represent elastic recoil.

• Pleural pressure:
  The pressure within the pleural space — typically negative during quiet breathing — but it’s a component used to calculate transpulmonary pressure, not a measure of lung recoil itself.

• Lung pressure:
  This term is nonspecific; it doesn’t correspond to any defined physiological pressure difference in respiratory mechanics.

🩺 Clinical Correlates:

1. Pneumothorax:
   When air enters the pleural space, pleural pressure becomes equal to atmospheric pressure — the transpulmonary pressure drops to zero, and the lung collapses due to its elastic recoil.
2. Emphysema:
   Destruction of elastic fibers reduces lung recoil; thus, for a given transpulmonary pressure, the lungs become overly compliant and hyperinflated.

According to Fick’s law of diffusion, the rate of gas diffusion across a membrane is:

Rate ∝ (A × ΔP × S) / (T × sqrt(MW))

Where:

• A = Surface area

• ΔP = Partial pressure difference

• S = Solubility

• T = Thickness

• MW = Molecular weight

• Increasing surface area (e.g., healthy alveoli) enhances diffusion, even if partial pressure is normal.

• Other factors: membrane thickness, solubility, and molecular weight also influence diffusion.

Other options:

• Decreased surface area → lowers diffusion (seen in emphysema)

• Decreased solubility / velocity → reduces diffusion

• Solubility of gas → affects diffusion, but “increased surface area” is the key factor in the question

In emphysema, alveolar walls are destroyed, reducing surface area for gas exchange. This leads to CO₂ retention (hypercapnia).

• Hypoventilation (respiratory rate 8/min) worsens CO₂ buildup.

• Increased PCO₂ → lowers blood pH, causing respiratory acidosis.

• The kidneys may compensate over time by retaining bicarbonate, but the primary disturbance is respiratory.

Other options:

• Respiratory alkalosis → caused by hyperventilation, not hypoventilation.

• Metabolic acidosis / alkalosis → disturbances in HCO₃⁻ or metabolic acids, not primarily due to emphysema.

The majority of CO₂ in the blood (~70%) is transported as bicarbonate (HCO₃⁻) in plasma. The rest is carried as:

• Carbaminohemoglobin (CO₂ bound to hemoglobin) → ~23%

• Dissolved CO₂ in plasma → ~7%

This conversion occurs via carbonic anhydrase in red blood cells and is critical for CO₂ transport from tissues to lungs.

CO₂ Transport in Blood

1. Total CO₂ content in arterial blood:
   Normal total CO₂ in 100 ml of arterial blood is about 48 ml.

2. Forms of CO₂ in blood:

   • Bicarbonate (HCO₃⁻) → ~70% of total CO₂

   • Carbaminohemoglobin (CO₂ bound to Hb) → ~23%

   • Dissolved CO₂ in plasma → ~7%

3. Dissolved CO₂ alone:
   If someone quotes ~4 ml, they are probably referring only to the dissolved CO₂ fraction, not the total CO₂ content.

Conclusion:

• 48 ml/100 ml blood → total CO₂ content transferred from tissues to lungs

• 4 ml/100 ml → only dissolved CO₂, insufficient to represent the total transfer.

Thromboxane A₂ (TXA₂) is a potent vasoconstrictor and platelet aggregator. It is synthesized primarily by activated platelets via the cyclooxygenase (COX) pathway from arachidonic acid.
It plays a crucial role in hemostasis and thrombosis.

Other options:

• Respiratory/olfactory epithelium → involved in lining and sensory functions, not TXA₂ production

• Neutrophils → produce leukotrienes, not TXA₂

• Mast cells → release histamine and leukotrienes, not TXA₂

The radial artery is the most common site for arterial puncture when obtaining arterial blood gases (ABG) — especially in conditions like respiratory distress syndrome (RDS).
It’s preferred because:

• It’s superficial and easily palpable.

• Has good collateral circulation via the ulnar artery and palmar arches.

• Minimizes complications if thrombosis occurs.

Other options:

• Ulnar artery → not preferred; used only if radial access is unavailable.

• Carotid artery → risky; close to vital structures.

• Popliteal artery → deep, difficult, and uncomfortable.

• Tibial artery → small and not ideal for ABG.