Session 7 Flashcards
- Define hypoxia LO
- Define hypoxaemia
- Give an example of hypoxia withought hypoxaemia. Explain why.
- The pO2 of the blood depends on ?
- Difference between oxygen saturation and pO2
- reduced oxygen as tissue level
- decrease in the pO2 in the blood
- 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
- normal gas exchange in the lung
- pO2 -> pressure oxygen would exert in atmospheric air
Oxygen saturation
Dissolved oxygen is = partial pressure x solubility coefficient
- State the normal ranges for O2 saturation and pO2
- Define Type 1 Respiratory failure
- Define type 2 respiratory failure
- Hypoxaemia can therefore result from: (5)
- O2 saturation 94-98%
PO2 9.3-13.3 kPa
Below these levels = hypoxaemia
Levels used to diagnose respiratory filure - • low pO2 < 8 kPa or O2 saturation < 90%
• pCO2 normal or low - • low pO2 + high pCO2
- Low inspired pO2 e.g. high altitude (hypoxia, and hypocapnia) (Type 1 – 2,3 -BPG)
- Hypoventilation (low pO2 high pCO2 - Type 2 respiratory failure)
- Ventilation/perfusion mismatch (Type 1 respiratory failure) (because hyperventilating)
- Diffusion impairment. (Type 1 respiratory failure) (CO2 more soluble than O2)
- Right to left shunts (e.g. Cyanotic heart disease)
Causes of hypoventilation (4)
- Respiratory centre depression: e.g. Head injury, drug overdose
- 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)
- Chest wall problems (mechanical problems) e.g. Scoliosis/ kyphosis, morbid obesity, rib fractures
- Hard to ventilate lungs due to severe lung fibrosis, or widespread severe airway obstruction (life threatening asthma, late stages of COPD),
When give oxygen to Chronic type 2 respiratory failure: patients why might treatment of hypoxia may worsen the patients condition?
what must we do?
- 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.
- Central chemoreceptors reset
- 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
Explain the acute & chronic effects of hypoxia & hypercapnia LO
- Effects of acute Hypoxia: (4)
- Effects of acute Hypercapnia: (4)
- 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?)
- Impaired CNS function ( less ATP needed for Na/K pump & maybe in synapse?)
- Respiratory acidosis
- Impaired CNS function: drowsiness, confusion, coma, flapping tremors
- Peripheral vasodilatation – warm hands, bounding pulse
- Cerebral vasodilation - headache
- Respiratory acidosis
Effects of chronic hypoxia:
-
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.
-
Polycythaemia (Increase Hb level) due to increased EPO secretion by the kidney, increases O2 carrying capacity of blood
- What is polycythaemia?
- Causes of polycythemia?
- Polycythemia vs erythrocytosis
- State how chronic hypercapnia resets the central chemoreceptors
- hematocrit (the volume percentage of red blood cells in the blood) is >55%
- Increase in the no. of red blood cells = absolute polycythemia
Decrease in the volume of plasma = relative polycythemia
- Polycythemia -> increase in RBC
Erythrocytosis = increase of red cell mass - • 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)
Explain what cyanosis is & the difference between central & peripheral cyanosis LO
- Cyanosis is defined as ?
- 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
- V/Q mismatch is the most common cause of ?
- Ventilation-perfusion mismatch can occur in two ways: causes of each?
- Present when >50gm/L of de-saturated Hb in blood -> bluish discolouration of the skin or mucous membranes
- Central cyanosis: oral mucosa, tongue, lips Indicates hypoxaemia
Peripheral cyanosis: fingers, toes poor local circulation - hypoxaemia
- 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
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?
- What happens to the V/Q ration in the alveoli in Pulmonary embolism?
- mixed blood in left atrium
* *Central and peripheral chemoreceptors are stimulated** –> causing hyperventilation
Affected alveoli V/Q <1
Unaffected segments V/Q > 1
- 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
- What is a restrictive disease?
2 what causes pulmonary fibrosis?
- How will the flow volume curve look like for a patient with fibrosis? Why?
- Restrictive disease:
problem in expanding lungs (Reduced compliance) → less air inhaled → less available to exhale
(Vital Capacity is reduced in both)
- • Idiopathic Fibrosing alveolitis
• Asbestosis
• Extrinsic allergic alveolitis
• Pneumoconiosis
iPEA P PULMONARY
How will the graph change in hyperventilation
What is restrictive lung disease?
What respiratory failure is pulmonary fibrosis
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
Work out the V/Q ratio