Session 7 Flashcards
Hypoxia vs Hypoxaemia
• Hypoxaemia - low pO2 in blood • Hypoxia - O2 deficiency at tissue level Tissues can be hypoxic without hypoxaemia (eg anaemia, poor circulation) - however, the term hypoxia is typically used to include hypoxaemia as well Normal ranges • O2 saturation 94 -98% • paO2 9.3 – 13.3 kPa (UHL) When levels below LLN defined as hypoxaemia • Tissue damage most likely when – O2 saturation < 90% – pO2 < 8 kPa – These levels used to diagnose respiratory failure – the CLINICAL presentation will vary depending on whether acute respiratory failure or chronic- and an arterial blood gas may not always help to distinguish
Causes and effects of hypoxaemia?
Hypoxaemia may caused by
1. Low inspired pO2
2. Hypoventilation – (respiratory pump failure)
3. Ventilation/Perfusion mismatch
4. Diffusion defect – problems of the alveolar capillary membrane
5. Intra-lung shunt – Acute Respiratory Distress Syndrome (ARDS)
6. Right to left shunt (eg. Cyanotic heart disease) – extrapulmonary
Effects of hypoxaemia
• Impaired CNS function, confusion, irritability, agitation
• Cardiac arrhythmias & cardiac ischaemia
• Hypoxic vasoconstriction of pulmonary vessels
• Cyanosis (bluish discolouration of the skin and mucous membranes due to presence of 4 to 6 gm/dl of deoxyhaemoglobin (i.e. unsaturated Hb)
What are the types of cyanosis?
Derived from the word CYAN – meaning blue-green
Central cyanosis Seen in oral mucosa, tongue, lips Indicates hypoxaemia - occurs when the level of deoxygenated haemoglobin in the arteries is below 5 g/dL with oxygen saturation below 85%.
Peripheral cyanosis In fingers, toes Poor local circulation – more oxygen extracted by the peripheral tissues
If central cyanosis is present, peripheral cyanosis will also be present
Chronic Hypoxaemia
- Compensatory mechanisms to increase oxygen delivery and therefore decrease hypoxia – increased EPO secreted by kidney à raised Hb (Polycythemia) – Increased 2,3, DPG – shifts haemoglobin saturation curve so oxygen released more freely
- Chronic hypoxic vasoconstriction of pulmonary vessels results in • Pulmonary hypertension • Right heart failure • Cor pulmonale
Respiratory failure
Impairment in gas exchange causing hypoxaemia with or without hypercapnia
• Type 1 Respiratory failure – low pO2 < 8 kPa or O2 saturation <90% breathing room air at sea level – pCO2 normal or low – Gas exchange is impaired at the level of aveolo-capillary membrane
• Type 2 respiratory failure – low pO2 + high pCO2 > 6.5 kPa breathing room air at sea level – Respiratory pump failure
Hypoventilation
- When the entire lung is poorly ventilated
- Alveolar ventilation (minute volume) is reduced – do you remember what determines ALVEOLAR ventilation?
- Alveolar pO2 falls à arterial pO2 falls – hypoxaemia • Alveolar pCO2 rises à arterial pCO2 increases à hypercapnia
- Hypoventilation ALWAYS causes hypercapnia
- Therefore causes Type 2 respiratory failure with both hypoxaemia + hypercapnia
- Hypoxaemia secondary to hypoventilation will correct with added oxygen (does not solve hypercapnia problem though!)
Acute vs Chronic Hypoventilation
Acute Hypoventilation
• Need urgent treatment • +/- artificial ventilation
• Common causes – Opiate overdose – Head injury – Very severe acute asthma
• Need urgent treatment • +/- artificial ventilation
• Common causes – Opiate overdose – Head injury – Very severe acute asthma
Chronic Hypoventilation • Chronic hypoxaemia and chronic hypercapnia • Slow onset and progression • Time for compensation • Therefore better tolerated
• Common causes – Severe COPD – must be careful if giving oxygen!! – most common cause of chronic type 2 respiratory failure – Acute exacerbations may occur due to LRT infection
Scoliosis/ kyphosis / kyphoscoliosis
Scoliosis:is a sideways curvature of the spine
Kyphosis:is a spinal disorder in which an excessive outward curve of the spine results in an abnormal rounding of the upper back
Kyphoscoliosis: both!
Causes of ventilatory failure
slide 7 lec 1
Effects of hypercapnia
• Respiratory acidosis • Impaired CNS function: drowsiness, confusion, coma, flapping tremors, patients may become obtunded - carbon dioxide narcosis • Peripheral vasodilatation –warm hands, bounding pulse • Cerebral vasodilation – headache
Chronic hypercapnia • Respiratory acidosis compensated by retention of HCO3- by kidney • Acclimation to CNS effects • Vasodilation mild but may still be present – “pink” puffers
Chronic CO2 retention –effect on central chemoreceptors
– CO2 diffuses in to CSF à CSF pH drops à stimulates central chemoreceptors – Persistently CSF acidity harmful to neurons – low CSF pH corrected by choroid plexus cells which secrete [HCO3-] in to CSF – 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
– Therefore persistent hypoxia stimulates peripheral chemoreceptors – Respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)
Chronic type 2 respiratory failure:
Why treatment of hypoxia may worsen hypercapnia (2 possible mechanisms) 1. Treatment with O2 improves pO2 level; BUT removes stimulus for the hypoxic respiratory drive Resp. rate & depth reduces àAlveolar Ventilation drops à causes worsening hypercapnia
2. Correction of hypoxia removes pulmonary hypoxic vasoconstriction leads to increased perfusion of poorly ventilated alveoli, diverting blood away from better ventilated alveoli. Increasing CO2 retention may happen gradually over 24-48 hours –only sign may be rising blood bicarb….
WATCH OUT FOR IT!
So, what should we do? Oxygen is life saving – it must be given, but pCO2 needs to be monitored
• Give controlled oxygen therapy with a target Saturation of 88 -92%
• If oxygen therapy causes rise in pCO2 - need ventilatory support
Ventilation-perfusion mismatching and V/Q ratio
• Ventilation - Perfusion Ratio – optimal gas exchange when V/Q ratio is 1 V/Q matching must happen at alveolar level
• When V/Q ratio is <1 the Alveolar pO2 falls and pCO2 rises
• When V/Q ratio is > 1 the (e.g. hyperventilation due to anxiety) pO2 rises and pCO2 falls
V/Q mismatch -1 Occurs in disorders where some alveoli are being poorly ventilated E.g. Asthma (variable airway narrowing ) Pneumonia (exudate in affected alveoli) • V/Q ratio is < 1 in these alveoli
• Alveolar pO2 falls and pCO2 rises – hypoxic vasoconstriction occurs àthis diverts some (but not all) blood to better ventilated areas • If V/Q ratio is still <1 à Alveolar pO2 will be low and pCO2 high – Blood from these alveoli have a low arterial pO2 and high arterial pCO2
– Mixed blood in left atrium = will have a low arterial pO2 and high arterial pCO2
• Central and peripheral chemoreceptors are stimulated –> causing hyperventilation
V/Q Mismatch -2 Hyperventilation occurs due to stimulation of chemoreceptors by hypoxia and/or hypercapnia (depending on chronicity) – Affected alveoli still poorly ventilated due to pathology ( asthma etc.) V/Q <1 – Unaffected segments have increased ventilation V/Q > 1 – pO2 rises and pCO2 falls • Rise in pO2 à increases dissolved oxygen (very small amount) • But Hb is fully saturated when pO2 above 10 kPa • Further increases in pO2 has no effect on Hb • O2 content not significantly increased (only tiny amount of extra dissolved O2) • Insufficient to compensate for low pO2 from segments with V/Q <1 • Drop in pCO2 accompanied by reduction in total CO2 content in blood • Sufficient to compensate for CO2 retention from segments with V/Q <1 Final result: low pO2 with normal (or low) pCO2 - Type 1 respiratory failure
V/Q mismatch causes
Occurs in disorders where some alveoli are being poorly ventilated
Example: –Asthma (variable airway narrowing ) –Pneumonia (exudate in affected alveoli) –RDS in newborn (some alveoli not expanded) –Pulmonary oedema ( fluid in alveoli) –Pulmonary embolism Will improve with oxygen administration – but will only partially correct hypoxaemia until underlying pathology corrected
Pulmonary embolism
- 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
- Causes hypoxaemia. • Hyperventilation sufficient to get rid of CO2
