Session 7

Question 1

1. Define hypoxia LO
2. Define hypoxaemia
3. Give an example of hypoxia withought hypoxaemia. Explain why.
4. The pO2 of the blood depends on ?
5. Difference between oxygen saturation and pO2

Answer 1

1. reduced oxygen as tissue level
2. decrease in the pO2 in the blood
3. Poor perfusion (atherosclerosis) can cause hypoxia of the affected tissue (e.g. myocardial infarction) despite normal gas exchange in the lungs and a normal arterial pO2
4. normal gas exchange in the lung
5. pO2 -> pressure oxygen would exert in atmospheric air

Oxygen saturation

Dissolved oxygen is = partial pressure x solubility coefficient

Question 2

1. State the normal ranges for O2 saturation and pO2
2. Define Type 1 Respiratory failure
3. Define type 2 respiratory failure
4. Hypoxaemia can therefore result from: (5)

Answer 2

1. O2 saturation 94-98%
   PO2 9.3-13.3 kPa
   Below these levels = hypoxaemia
   Levels used to diagnose respiratory filure
2. • low pO2 < 8 kPa or O2 saturation < 90%
   • pCO2 normal or low
3. • low pO2 + high pCO2
4. 1. Low inspired pO2 e.g. high altitude (hypoxia, and hypocapnia) (Type 1 – 2,3 -BPG)
5. Hypoventilation (low pO2 high pCO2 - Type 2 respiratory failure)
6. Ventilation/perfusion mismatch (Type 1 respiratory failure) (because hyperventilating)
7. Diffusion impairment. (Type 1 respiratory failure) (CO2 more soluble than O2)
8. Right to left shunts (e.g. Cyanotic heart disease)

Question 3

Causes of hypoventilation (4)

Answer 3

1. Respiratory centre depression: e.g. Head injury, drug overdose
2. Respiratory muscle weakness due to damage/disease of any part of nerve pathways from the respiratory centre to the muscles of respiration – ( e.g. Brain stem /spinal cord / intercostal nerves /phrenic nerve/NMJ /Muscle disease)
3. Chest wall problems (mechanical problems) e.g. Scoliosis/ kyphosis, morbid obesity, rib fractures
4. Hard to ventilate lungs due to severe lung fibrosis, or widespread severe airway obstruction (life threatening asthma, late stages of COPD),

Question 4

When give oxygen to Chronic type 2 respiratory failure: patients why might treatment of hypoxia may worsen the patients condition?

what must we do?

Answer 4

1. • Central chemoreceptors reset
     - peripheral chemoreceptors respond to change in oxygen (allowing hyperventilation)
     - O2 removes stimulus for the hypoxic respiratory drive
     - Alveolar Ventilation drops -> causes worsening hypercapnia
     - Removes pulmonary hypoxic vasoconstriction
     - increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli.

• Oxygen is life saving – it must be given, but pCO2 needs to be monitored
• Controlled oxygen therapy with a target Saturation of 88 -92%
• If oxygen therapy causes rise in pCO2 - need ventilatory support

Question 5

Explain the acute & chronic effects of hypoxia & hypercapnia LO

1. Effects of acute Hypoxia: (4)
2. Effects of acute Hypercapnia: (4)

Answer 5

1. • Impaired CNS function ( less ATP needed for Na/K pump & maybe in synapse?)
     - Central cyanosis (bluish discolouration of the mucous membranes due to presence of >50gm/litre of unsaturated Hb)
     - Cardiac arrhythmias
     - Hypoxic vasoconstriction of pulmonary vessels (cor pulmonale?)
2. • Respiratory acidosis
     - Impaired CNS function: drowsiness, confusion, coma, flapping tremors
     - Peripheral vasodilatation – warm hands, bounding pulse
     - Cerebral vasodilation - headache

Question 6

Effects of chronic hypoxia:

Answer 6

1. • Polycythaemia (Increase Hb level) due to increased EPO secretion by the kidney, increases O2 carrying capacity of blood
     - Inc in red cell 2,3, DPG levels which allows better unloading of O2
     - Hypoxia induced vasoconstriction of pulmonary arterioles which eventually leads to pulmonary hypertension
     - Right heart failure (Cor pulmonale) due to pulmonary hypertension.

Question 7

1. What is polycythaemia?
2. Causes of polycythemia?
3. Polycythemia vs erythrocytosis
4. State how chronic hypercapnia resets the central chemoreceptors

Answer 7

1. hematocrit (the volume percentage of red blood cells in the blood) is >55%
2. Increase in the no. of red blood cells = absolute polycythemia

Decrease in the volume of plasma = relative polycythemia

3. Polycythemia -> increase in RBC
   Erythrocytosis = increase of red cell mass
4. • CO2 diffuses in to the CSF -> CSF pH drops -> stimulates central chemoreceptors

• acidity harmful to neurons
• choroid plexus cells which secrete [HCO3-]
• The CSF pH returns to normal; central chemoreceptors no longer stimulated
• pCO2 in the blood is still high but central chemoreceptors now unresponsive to this pCO2
• i.e. Central chemoreceptors have reset to a new higher CO2 level
• The persistent hypoxia stimulates peripheral chemoreceptors
• Respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)

Question 8

Explain what cyanosis is & the difference between central & peripheral cyanosis LO

1. Cyanosis is defined as ?
2. How can cyanosis be classed? What are the features of each? Which on is more serious?

Outline the important causes of ventilation/perfusion mismatch & explain why ventilation/perfusion mismatch causes Type 1 respiratory failure LO

3. V/Q mismatch is the most common cause of ?
4. Ventilation-perfusion mismatch can occur in two ways: causes of each?

Answer 8

1. Present when >50gm/L of de-saturated Hb in blood -> bluish discolouration of the skin or mucous membranes
2. Central cyanosis: oral mucosa, tongue, lips Indicates hypoxaemia
   Peripheral cyanosis: fingers, toes poor local circulation
3. hypoxaemia
4. Ventilation reduced:

Asthma (early stages), COPD (early stages), pneumonia (EXUDATE),

Respiratory distress syndrome of new-born (alveoli are not expanded -> less surfactant)

Perfusion is reduced:

PE (obstruction -> blood is diverted to unaffected parts of the pulmonary circulation -> If this extra blood flow (increased perfusion Q) cannot be not matched by the ventilation (V) of these alveoli, the reduced V/Q ratio causes a drop in paO2

note in late COPD -> DIFFUSE vascular constriction -> PA inc -> RV hypertrophy -> cor pulmonale

Question 9

Q. If V/Q ratio is still <1 -> Alveolar pO2 will be low and pCO2 high
Blood from these alveoli have a low arterial pO2 and high arterial pCO2
What does this result in?

2. What happens to the V/Q ration in the alveoli in Pulmonary embolism?

Answer 9

1. mixed blood in left atrium
   * *Central and peripheral chemoreceptors are stimulated** –> causing hyperventilation

Affected alveoli V/Q <1
Unaffected segments V/Q > 1

2. A. • The embolus results in redistribution of pulmonary blood flow
   • The blood is diverted to unaffected areas of the pulmonary circulation
   • Leads to V/Q ratio < 1 if hyperventilation cannot match the increased perfusion
   • hypoxaemia
   • Hyperventilation sufficient to get rid of CO2

Question 10

1. What is a restrictive disease?

2 what causes pulmonary fibrosis?

3. How will the flow volume curve look like for a patient with fibrosis? Why?

Answer 10

1. Restrictive disease:

problem in expanding lungs (Reduced compliance) → less air inhaled → less available to exhale

(Vital Capacity is reduced in both)

2. • Idiopathic Fibrosing alveolitis
   • Asbestosis
   • Extrinsic allergic alveolitis
   • Pneumoconiosis

iPEA P PULMONARY

Question 11

Answer 11

Question 12

How will the graph change in hyperventilation

Answer 12

Question 13

What is restrictive lung disease?

Answer 13

Question 14

What respiratory failure is pulmonary fibrosis

Answer 14

Q. • More than 1 mechanism may be responsible for respiratory failure
seen in disease states give examples.
A. Lung fibrosis -> diffusion defect, but if severe hypoventilation will also be present
pulmonary oedema -> diffusion defect, and V/Q mismatch

Question 15

Work out the V/Q ratio

Answer 15