RS Module Flashcards

1
Q

Q3. A 60-year-old male, with chronic obstructive pulmonary disease had a respiratory rate of 25 breaths/minute and bluish discoloration of the tongue on admission to the hospital.

3.1 (a) Respiratory rate of 25 breaths/minute (30 marks)

A

3.1 (a) Respiratory rate of 25 breaths/minute (30 marks)
- The patient’s respiratory rate is increased, beyond the normal range of 15-20 breaths/min.
- In Chronic Obstructive Pulmonary Disease (COPD), airways are narrowed by excess mucus accumulation and lung parenchymal destruction.
- Airway narrowing increases resistance, reducing ventilation and gas exchange.
- Damage to the alveolar capillary membrane reduces oxygenation of arterial blood.
- Air trapping in lungs leads to CO2 retention, causing a drop in blood pH.
- Hypoxia and pH drop stimulate peripheral chemoreceptors, increasing respiratory rate (tachypnea).

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1
Q

Q3. A 60-year-old male, with chronic obstructive pulmonary disease had a respiratory rate of 25 breaths/minute and bluish discoloration of the tongue on admission to the hospital.

(b) Bluish discoloration of the tongue (20 marks)

A

(b) Bluish discoloration of the tongue (20 marks)
- Central cyanosis, seen as bluish discoloration, indicates deoxygenated hemoglobin levels > 5g/dl.
- COPD increases airway resistance, reducing PAO2 levels and oxygenation of blood.
- Reduced oxygen saturation of hemoglobin leads to central cyanosis.
- Oxygen deficiency at tissue level causes extraction of more oxygen from hemoglobin, resulting in more reduced hemoglobin.
- Symptoms appear in areas like lips, tongue, nail tips, and ear lobes.

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2
Q

Explain the changes in the oxygen hemoglobin dissociation curve during cycling in a healthy adult. (26th Proper) (30 marks)

A

Explain the changes in the oxygen hemoglobin dissociation curve during cycling in a healthy adult. (26th Proper) (30 marks)
- During cycling, leg muscles demand more O2, leading to increased O2 release from hemoglobin into tissues.
- Tissue PO2 levels drop significantly due to increased O2 demand, causing lower hemoglobin saturation at low PO2 levels.
- The curve is steep below 60mmHg, indicating a large O2 supply per mmHg drop in PO2.
- Shift of O2 hemoglobin dissociation curve to the right occurs due to:
- Rise in tissue temperature, generating more heat.
- Accumulation of CO2 from increased metabolic rate.
- Drop in pH due to lactic acidosis.
- Rise in red blood cell 2,3 DPG, favoring the release of O2 into tissues.
- In exercising muscles, the P50 value increases, indicating low standard affinity for Hb.

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3
Q

Factors Affecting Gas Exchange Across the Alveolar Capillary Membrane:

A
  • Partial pressure gradient across the alveolar capillary membrane
    • Greater pressure difference results in higher diffusion rate.
    • Gases diffuse from alveoli (high O2 partial pressure) to pulmonary capillaries (low O2 partial pressure).
    • Impaired ventilation in conditions like Asthma and COPD reduces alveolar PO2 levels, decreasing the partial pressure gradient.
  • Surface area of alveolar capillary membrane
    • Larger surface area facilitates greater gas diffusion.
    • Respiratory membrane has approximately 70m² surface area.
    • Increased pulmonary capillary recruitment during exercise enhances surface area and gas exchange.
    • Conditions like COPD reduce surface area, limiting gas diffusion.
  • Thickness of the alveolar capillary membrane
    • Increased thickness slows down diffusion due to greater distance for gases to traverse.
    • Conditions such as pulmonary edema and lung fibrosis increase membrane thickness, hindering gas exchange.
  • Diffusion coefficient of the alveolar capillary membrane
    • Diffusion coefficient is proportional to solubility area/molecular weight.
    • Higher diffusion coefficient facilitates faster diffusion.
    • Small, highly soluble molecules like CO2 diffuse faster (20 times more rapidly than O2).
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4
Q

2.2 A patient was brought to the emergency unit with an acute attack of bronchial Asthma. His respiratory rate was 30 breaths/minute and O2 saturation was 85%. Patient was treated with beta 2 agonist.

(a) Respiratory rate of 30 breaths per minute (40 marks)

A

(a) Respiratory rate of 30 breaths per minute (40 marks)
- Normal respiratory rate: 15-20 breaths/minute; patient’s rate is increased.
- Asthma is an obstructive respiratory disorder characterized by airway inflammation, hyperresponsiveness, mucus secretion, and bronchoconstriction.
- Airway inflammation leads to mucus secretion and bronchial wall thickening, causing airway narrowing.
- According to Poiseuille-Hagen formula, resistance (R) is inversely proportional to the 4th power of the radius (r). Even small reductions in bronchiole caliber markedly reduce airflow, impairing ventilation.
- Increased airway resistance leads to:
- Inadequate oxygenation of alveoli.
- Low alveolar oxygen partial pressure (PAO2).
- Ventilation/perfusion (V/Q) mismatch.
- Reduced O2 partial pressure gradient across the alveolar-capillary membrane.
- Hypoxic hypoxia due to inadequate tissue oxygen supply.
- Hypoxia stimulates peripheral chemoreceptors, increasing respiratory rate (tachypnea) via the medullary respiratory center and phrenic/intercostal nerves, causing shortness of breath.

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5
Q

2.2 A patient was brought to the emergency unit with an acute attack of bronchial Asthma. His respiratory rate was 30 breaths/minute and O2 saturation was 85%. Patient was treated with beta 2 agonist.

(b) Use of Beta 2 agonist in the treatment. (30 marks)

A

(b) Use of Beta 2 agonist in the treatment. (30 marks)
- Smooth muscle cells of airways contain beta 2 adrenergic receptors.
- Stimulation of beta 2 receptors by medications like Salbutamol causes bronchodilation.
- Bronchodilation reduces airway resistance (R ∝ 1/r^4), facilitating airflow.
- Reduced resistance to airflow leads to:
- Adequate oxygenation of alveoli.
- Increased PAO2.
- Enhanced O2 partial pressure gradient across the alveolar-capillary membrane.
- Adequate oxygenation of arterial blood, relieving hypoxic hypoxia.

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6
Q

Factors Affecting the Oxygen-Hemoglobin Dissociation Curve (25th Repeat) (35 marks)

A

The oxygen-hemoglobin dissociation curve represents the relationship between the partial pressure of oxygen (PO2) and the percentage saturation of hemoglobin (Hb) with oxygen. It exhibits cooperative binding of oxygen to hemoglobin.

The curve is influenced by several factors:

  • pH and Temperature:
    • An increase in temperature or a decrease in pH shifts the curve to the right.
    • This shift indicates that a higher PO2 is required for hemoglobin to bind to a given amount of oxygen.
    • Conversely, a decrease in temperature or an increase in pH shifts the curve to the left, requiring a lower PO2 for oxygen binding.
    • The decrease in O2 affinity with a decrease in blood pH (Bohr Effect) occurs due to increased CO2 content, leading to a rightward shift and a rise in P50.
  • 2,3-Diphosphoglycerate (2,3-DPG):
    • 2,3-DPG is abundant in red blood cells and is an intermediate of glycolysis.
    • When 2,3-DPG concentration increases, the equilibrium between HbO2 and Hb-2,3-DPG shifts to the right.
    • This shift favors the release of oxygen from hemoglobin, reducing its affinity for oxygen.
    • Consequently, the curve shifts to the right, indicating lower oxygen affinity.
    • The presence of 2,3-DPG facilitates the deoxygenated state of hemoglobin, promoting oxygen release.

These factors collectively modulate the oxygen-hemoglobin dissociation curve, altering the affinity of hemoglobin for oxygen and influencing oxygen transport and release in tissues.

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7
Q

Case:
A patient was brought to the emergency unit following a sudden onset of difficulty in breathing. He had experienced an extensive anterior myocardial infarction two years prior. Further examination revealed a respiratory rate of 36 breaths per minute, a blood pressure of 80/60 mmHg, and an elevated jugular venous pressure.

2.1 Respiratory rate of 36 breaths per minute. (40 marks)

A

The normal respiratory rate ranges from 15 to 20 breaths per minute. The patient’s respiratory rate is significantly elevated, indicating tachypnea.

The elevated respiratory rate in this patient can be attributed to the following factors, particularly considering the history of an extensive anterior myocardial infarction suggesting left heart failure:

  • Left Heart Failure:
    • Left ventricular pumping ability is compromised, leading to reduced cardiac output and blood pressure.
    • Back pressure from the left ventricle is transmitted through the mitral valve into the left atrium, increasing pressure in the pulmonary veins.
    • Elevated pressure in pulmonary veins results in altered Starling forces, leading to increased pressure at the venule end of pulmonary capillaries.
    • Pulmonary edema ensues due to reduced lung compliance from tissue fluid accumulation around alveoli.
    • Reduced lung compliance leads to less distension of alveoli during inspiration, impairing ventilation and reducing PAO2.
    • Increase in the thickness of the alveolar capillary membrane further slows down the diffusion rate of oxygen, impairing gas exchange.
  • Hypoxia Response:
    • Low PaO2 levels in arterial blood trigger hypoxia.
    • Hypoxia stimulates peripheral chemoreceptors at carotid and aortic bodies, increasing firing from the respiratory center.
    • Afferents via the glossopharyngeal and vagus nerves to the medullary respiratory center increase respiratory drive.
    • Efferents via the phrenic and intercostal nerves to the diaphragm and intercostal muscles increase rate and depth of breathing, leading to shortness of breath (SOB).
  • Sympathetic Activation:
    • Activation of the sympathetic nervous system also increases discharge from the respiratory center, contributing to tachypnea.

In summary, the patient’s elevated respiratory rate is likely a response to left heart failure-induced pulmonary edema, resulting in hypoxia and sympathetic activation, which collectively increase respiratory drive.

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8
Q

Variation in the Ventilation/Perfusion ratio (V/Q ratio) in the lung from apex to base in the upright position in a healthy adult. (30 marks)

A

The ventilation/perfusion (V/Q) ratio in the lungs reflects the balance between ventilation (air supply) and perfusion (blood supply) in the alveoli. In a healthy adult, this ratio varies from the apex (top) to the base (bottom) of the lung, especially in the upright position.

Ventilation:
- In the upright position, intra-pleural pressure varies due to gravity, being more negative at the apex (-10mmHg) and less negative at the base (-2.5mmHg).
- Trans-pulmonary pressure, which drives ventilation, is the difference between intra-alveolar and intra-pleural pressure.
- During inspiration, lung tissue expansion per unit pressure is less at the apex compared to the base due to differences in compliance. This is because apical alveoli are already more expanded at the onset of inspiration.
- Consequently, lung bases are better ventilated in the upright posture.

Perfusion:
- Blood flow in the lungs is greater at the bases than at the apex, primarily due to gravity.
- The relative change in blood flow from the apex to the base is greater than the relative change in ventilation.
- As a result, the V/Q ratio is higher at the lung apex and lower at the lung base in the upright posture of a healthy individual.
- At the apex, the V/Q ratio is about 3, while at the base, it is about 0.6.

Overall V/Q Ratio:
- The V/Q ratio for the entire lung at rest is approximately 0.8, calculated as the total alveolar ventilation divided by the cardiac output. This reflects a balance between ventilation and perfusion for efficient gas exchange.

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9
Q

Q3: Physiological Basis of Clinical Findings in Bronchial Asthma

a) Respiratory rate of 32 breaths per minute (25 marks)

A

Q3: Physiological Basis of Clinical Findings in Bronchial Asthma

a) Respiratory rate of 32 breaths per minute (25 marks)

  • The patient’s elevated respiratory rate is indicative of tachypnea, which is common in acute asthma attacks.
  • Asthma is characterized by airway inflammation, mucus secretion, and bronchoconstriction, leading to increased airway resistance.
  • Increased airway resistance impairs ventilation, causing hypoxia, which stimulates respiratory drive.
  • Hyperventilation is the body’s attempt to compensate for hypoxia, resulting in a higher respiratory rate.
  • Tachypnea ensures adequate oxygen supply to tissues despite impaired gas exchange.
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10
Q

Q3: Physiological Basis of Clinical Findings in Bronchial Asthma

b) Bluish discoloration of mucous membranes in the mouth (20 marks)

A

b) Bluish discoloration of mucous membranes in the mouth (20 marks)

  • Bluish discoloration indicates central cyanosis due to decreased oxygen saturation in arterial blood.
  • In asthma, airway obstruction leads to reduced oxygenation of pulmonary capillary blood.
  • Low arterial PaO2 levels result in increased deoxygenated hemoglobin, causing cyanosis.
  • Cyanosis is commonly observed in mucous membranes, lips, and nail beds.
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11
Q

Q3: Physiological Basis of Clinical Findings in Bronchial Asthma

c) Change in Oxygen saturation in arterial blood after treatment (40 marks)

A

c) Change in Oxygen saturation in arterial blood after treatment (40 marks)

  • The initial low oxygen saturation (75%) indicates significant hypoxemia, a common feature of acute asthma exacerbations.
  • Treatment with oxygen supplementation and beta-agonists improves ventilation and oxygenation.
  • Oxygen therapy increases the fraction of inspired oxygen (FIO2), leading to higher alveolar oxygen levels.
  • Higher alveolar oxygen levels increase the partial pressure gradient for oxygen diffusion, improving oxygenation of arterial blood.
  • Consequently, arterial oxygen saturation increases to a normal range (95%) after treatment.
  • Maintaining arterial oxygen saturation within normal limits ensures adequate oxygen delivery to tissues, alleviating hypoxemia-related symptoms.
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12
Q

Q3: Physiological Basis of Clinical Findings in Bronchial Asthma

3.2 Acid-Base Imbalance in Bronchial Asthma (15 marks)

A

3.2 Acid-Base Imbalance in Bronchial Asthma (15 marks)

The patient likely exhibits respiratory alkalosis due to hyperventilation during an acute asthma attack.

  • Hyperventilation leads to excessive CO2 removal from the lungs, resulting in decreased PaCO2 levels.
  • Reduced PaCO2 levels cause a shift in the bicarbonate-carbonic acid equilibrium towards alkalosis.
  • The equation CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3- demonstrates the conversion of CO2 into carbonic acid, which dissociates into hydrogen ions (H+) and bicarbonate ions (HCO3-).
  • Decreased PaCO2 levels reduce the availability of CO2 for this reaction, resulting in decreased hydrogen ion (H+) production and increased bicarbonate ion (HCO3-) levels.
  • The net effect is an increase in blood pH, indicating respiratory alkalosis.
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13
Q

Physiological Basis of Type 2 Respiratory Failure in Myasthenia Gravis (40 marks)

A

Physiological Basis of Type 2 Respiratory Failure in Myasthenia Gravis (40 marks)

Myasthenia gravis (MG) is an autoimmune disorder affecting neuromuscular transmission, particularly involving diaphragmatic and intercostal muscles.

  • MG impairs neuromuscular transmission by targeting nicotinic acetylcholine receptors at the neuromuscular junction, leading to muscle weakness and fatigue.
  • Weakness of respiratory muscles, especially the diaphragm and intercostals, results in inadequate ventilation and impaired gas exchange.
  • Type 2 respiratory failure (hypercapnic respiratory failure) occurs due to decreased ventilatory effort and alveolar hypoventilation.
  • Hypercapnia (PaCO2 > 50 mmHg) ensues as a result of reduced alveolar ventilation and inadequate CO2 removal.
  • In severe cases, hypercapnia may depress the central respiratory drive, further compromising ventilation.
  • Peripheral chemoreceptors play a crucial role in stimulating respiratory effort in response to hypoxemia and hypercapnia.
  • Oxygen therapy must be carefully administered in MG patients to avoid suppressing the hypoxic drive and exacerbating hypoventilation.
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14
Q

Physiological Basis of Hypoxia in Lung Fibrosis and Surfactant Deficiency

Lung Fibrosis (20 marks)

A

Physiological Basis of Hypoxia in Lung Fibrosis and Surfactant Deficiency

Lung Fibrosis (20 marks)

  • Lung fibrosis involves the replacement of lung parenchyma with fibrous tissue, reducing lung compliance and impairing gas exchange.
  • Fibrous tissue deposition increases the thickness of the alveolar-capillary membrane, reducing gas diffusion.
  • Reduced lung compliance leads to inadequate ventilation and impaired oxygenation of arterial blood, resulting in hypoxia.
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15
Q

Physiological Basis of Hypoxia in Lung Fibrosis and Surfactant Deficiency

Surfactant Deficiency (40 marks)

A

Surfactant Deficiency (40 marks)

  • Surfactant deficiency leads to alveolar collapse during expiration due to increased surface tension.
  • Alveolar collapse reduces ventilation and causes ventilation-perfusion mismatch, lowering arterial oxygenation.
  • Without surfactant, pulmonary edema may develop due to increased alveolar surface tension, further impairing gas exchange.
  • Reduced lung compliance and increased interstitial fluid thickness contribute to inadequate oxygenation of arterial blood, leading to hypoxia.
  • Surfactant deficiency is particularly critical in premature infants, where it can lead to infant respiratory distress syndrome and severe hypoxia.
16
Q

Case:
A premature baby was found to be tachypneic & cyanosed at birth. His work of breathing was found to be increased.

2.1) List the determinants of work of breathing. (15 marks)

A
  • Compliance/Elastic Work: Work done by the stretch of elastic tissues of the lungs and chest wall (65%).
  • Work done by respiratory muscles to move inelastic tissues (7%).
  • Resistance Work: Work done by respiratory muscles to move air through respiratory passages (28%).
17
Q

Case:
A premature baby was found to be tachypneic & cyanosed at birth. His work of breathing was found to be increased.

  1. Increased Work of Breathing (40 marks):
  2. Tachypnea (25 marks):
  3. Cyanosis (20 marks):
A

2.2) Explain the physiological basis for the following in this baby:

  1. Increased Work of Breathing (40 marks):
    • The baby is likely experiencing respiratory distress syndrome (RDS) due to surfactant deficiency.
    • Surfactant, produced by type II pneumocytes, reduces alveolar surface tension, maintaining lung compliance.
    • Premature infants often lack sufficient surfactant, leading to increased alveolar surface tension, reduced compliance, and increased work of breathing.
    • The increased effort required for ventilation due to reduced compliance manifests as increased work of breathing.
  2. Tachypnea (25 marks):
    • Reduced lung compliance results in decreased ventilation and ventilation-perfusion mismatch (low V/Q ratio).
    • Pulmonary edema further impairs gas exchange, reducing arterial oxygenation and causing hypoxia.
    • Hypoxia stimulates peripheral chemoreceptors, increasing respiratory drive and resulting in tachypnea.
  3. Cyanosis (20 marks):
    • Cyanosis, a bluish discoloration of mucous membranes and tissues, occurs due to elevated levels of deoxyhemoglobin (> 5g/dL).
    • Reduced ventilation leads to decreased arterial oxygen levels, impairing oxygenation of hemoglobin.
    • Elevated levels of deoxyhemoglobin appear dark bluish, resulting in cyanosis.
    • Central cyanosis, observed in this baby, involves bluish discoloration of lips, tongue, earlobes, nail beds, and fingers.
18
Q

Case scenario 01:

(01) A premature baby was found to be tachypneic & cyanosed at birth. His work of breathing was found to be increased. A diagnosis of IRDS was made.

1.1 List the determinants of work of breathing (WOB). (10 marks)

A

Case scenario 01:

(01) A premature baby was found to be tachypneic & cyanosed at birth. His work of breathing was found to be increased. A diagnosis of IRDS was made.

1.1 List the determinants of work of breathing (WOB). (10 marks)

  • Compliance
  • Airway resistance
19
Q

(01) A premature baby was found to be tachypneic & cyanosed at birth. His work of breathing was found to be increased. A diagnosis of IRDS was made.

1.2 Explain the Physiological basis for the following:
A. Increased WOB (35 marks):
B. Tachypnea (35 marks):
C. Cyanosis (20 marks):

A

1.2 Explain the Physiological basis for the following:

A. Increased WOB (35 marks):
- IRDS results from surfactant deficiency due to underdeveloped type 2 pneumocytes.
- Surfactant normally reduces surface tension at the air-gas interface, but in IRDS, surface tension is increased, leading to reduced compliance.
- Negative interstitial fluid pressure and pulmonary edema further decrease compliance, resulting in increased work of breathing.

B. Tachypnea (35 marks):
- Reduced compliance and pulmonary edema contribute to ventilation-perfusion mismatch, reducing arterial oxygen levels.
- Hypoxia stimulates peripheral chemoreceptors, leading to increased respiratory rate and depth (tachypnea).

C. Cyanosis (20 marks):
- Reduced ventilation results in decreased alveolar oxygen levels and oxygenation of hemoglobin, leading to increased concentration of reduced hemoglobin and central cyanosis.

20
Q

02) Describe the factors that affect the oxygen-hemoglobin dissociation curve. (35 marks)

A
  • pH, temperature, 2,3-diphosphoglycerate (2,3-DPG), and PCO2 affect the oxygen-hemoglobin dissociation curve.
  • A rise in temperature or a fall in pH shifts the curve to the right, requiring a higher PO2 for hemoglobin to bind to oxygen.
  • Conversely, a fall in temperature or a rise in pH shifts the curve to the left, requiring a lower PO2.
  • Increased 2,3-DPG levels reduce hemoglobin’s affinity for oxygen, shifting the curve to the right.
21
Q

Case scenario 02:

A 70-year-old man with long-standing pulmonary fibrosis (idiopathic pulmonary fibrosis) presented to a respiratory clinic with progressively worsening shortness of breath.

Explain the physiological basis for PaO2- 50mmHg (35 marks):

A

Case scenario 02:

A 70-year-old man with long-standing pulmonary fibrosis (idiopathic pulmonary fibrosis) presented to a respiratory clinic with progressively worsening shortness of breath.

Explain the physiological basis for PaO2- 50mmHg (35 marks):
- Pulmonary fibrosis causes fibrosis and distortion of lung parenchyma, leading to reduced compliance, ventilation, and PAO2, as well as increased thickness of the alveolar capillary membrane, constriction of lung parenchyma, and reduced surface area for diffusion, resulting in reduced PaO2.

State whether the management is correct or not and give the basis for your answer. (30 marks):
- The management is correct because providing oxygen at FiO2 of 35% increases the partial pressure gradient of oxygen across the alveolar-capillary membrane, leading to increased diffusion and improved PaO2. Since the patient has Type 1 respiratory failure (hypoxia without hypercapnia), oxygen therapy is appropriate until SpO2 exceeds 96%.

22
Q

Case scenario 02:

A 70-year-old man with long-standing pulmonary fibrosis (idiopathic pulmonary fibrosis) presented to a respiratory clinic with progressively worsening shortness of breath.

State whether the management is correct or not and give the basis for your answer. (30 marks):

A
  • The management is correct because providing oxygen at FiO2 of 35% increases the partial pressure gradient of oxygen across the alveolar-capillary membrane, leading to increased diffusion and improved PaO2. Since the patient has Type 1 respiratory failure (hypoxia without hypercapnia), oxygen therapy is appropriate until SpO2 exceeds 96%.
23
Q
  1. List the main methods of oxygen and CO2 transport in the blood.
A
  • Oxygen transport:
    • 99% bound with hemoglobin (OxyHb)
    • Remainder dissolved in plasma
    • CO2 transport:
      • 94.5% of CO2 in the combined form – mainly as HCO3–
      • Less amount as carbamino compounds (mainly carbamino-Hb)
      • Remainder in dissolved form
24
Q
  1. Explain the role of the Oxygen Hemoglobin Dissociation Curve in facilitating O2 release at tissues and O2 binding at the lung level
A
  • Sigmoid shape of the O-Hb DC is due to the Tense–Relaxed form interconversion.
    • At high PO2 levels at the alveoli, Hb in pulmonary capillaries are nearly 100% saturated.
    • In systemic arteries, despite lower PO2 levels, % saturation of Hb remains high due to the flattening of the curve.
    • In tissues with low PO2, there’s a large drop in % saturation facilitating increased oxygen release from Hb.
25
Q
  1. Explain the physiological basis of the following:
    • c) The shift of the Oxygen Hemoglobin Dissociation Curve in exercise
A
  • Shift to the right due to:
    - Increased 2,3-diphosphoglycerate (2,3-DPG) levels
    - Temperature rise in active tissues
    - Accumulation of CO2 and metabolites, lowering the pH
26
Q
  • a) PCV (Haematocrit) in venous blood is higher than in arterial blood
A
  • Due to increased osmolality in RBC in venous blood, causing RBCs to take up water and increase size.
    • The chloride shift mechanism plays a role in this process.
27
Q
  1. Explain the role of “Haldane effect” on CO2 transport
A
  • DeoxyHb binds more CO2 than OxyHb and forms carbamino compounds more readily, facilitating CO2 transport.
    • Venous blood carries more CO2 than arterial blood due to the Haldane effect.
28
Q
  1. Physiological basis for the differences in the oxygen dissociation curves for fetal haemoglobin and adult hemoglobin
A
  • HbF exhibits a left shift compared to HbA due to less binding to 2,3 DPG, which binds to the beta haemoglobin chain not present in HbF.
29
Q
  1. Explain the physiological basis for the changes seen in the oxygen haemoglobin dissociation curve due to
    • a. Carbon monoxide poisoning
    • b. Anaemia
A
  • a. Carbon monoxide poisoning
    • Curve shifts to the left and O2 content is reduced due to increased affinity for CO over O2.
    • b. Anaemia
      • Sigmoid shape remains, but total oxygen content bound to Hb is reduced due to low Hb concentration.
30
Q
  1. What is meant by Ventilation-Perfusion ratio?
A
  • Ratio of ventilation to blood flow at the level of a single alveolus or the whole lung.
    • VA/Q is calculated as alveolar ventilation per min (VA) divided by capillary blood flow (Qc).
    • VA/Q = 0.8 for the whole lung at rest.
31
Q
  1. Give the physiological basis for the V/Q abnormality seen in -
    • i. Collapse of a lung lobe
    • ii. Pulmonary embolism
A
  • i. Collapse of a lung lobe
    • No ventilation but perfusion occurs, leading to low V/Q.
    • ii. Pulmonary embolism
      • Reduced perfusion with intact ventilation leads to high V/Q.