Lecture 21- Respiratory failure Flashcards
define respiratory failure
impairment in gas exchange causing hypoxemia with or without hypercapnia
Type 1 respiratory failure
- paO2 <8kPa or O2 sat <90%
- pCO2 normal
- gas exchange is impaired at the level of alveolar-capillary membrane
- can progress to type 2
Type 2 respiratory failure
- paO2 <8kPA
- but high paCO2 >6.5
- reduced ventilatory effort (pump failure) or inability to overcome increased resistance to ventilation entire lung
Hypoxia vs hypoxaemia
- hypoxaemia- low pO2 in arterial blood
- hypoxia- O2 deficiency at tissue level
tissuues can be ………without ……….
- tissues can be hypoxic without hypoxaemia (e.g. anaemia, poor circulation)- however the term hypoxia is typically used to include hypoxaemia as well
normal oxygen saturations
- O2 sat 94-98%
- Tissue damage likely <90%
normal oxygen levels
- paO2 10.6-13.3 kPa
- tissue damage likely <8kPa
outline the signs and symptoms of hypoxaemia
- Impaired CNS function: confusion, irritability, agitation
- Tachypnoea
- Tachycardia
- Cardiac arrythmia and cardiac ischaemia
- Hypoxic vasoconstriction of pulmonary vessels
- Cyanosis (bluish discolouration of the skin and mucous membranes due to presence of 4-6 gm/dl of deoxyhaemoglobin (i.e. unsaturated Hb)
Central cyanosis
- Seen in oral mucosa, tongue and lips
- Indicates hypoxaemia- occurs when the level of deoxygenated haemoglobin in the arteries is below 5 g/dL with oxygen sat below 85%
- Will also have peripheral cyanosis
Peripheral cyanosis
- In fingers and toes
- Poor local circulation- more oxygen extracted by the peripheral tissues
Causes of hypoxaemia (can have more than one)
- Low inspired pO2- e.g. high altitude
- Ventilation: perfusion mismatch
- Diffusion defect- problems with the alveolar capillary membrane
- Intra-lung shunt- acute respiratory distress syndrome (ARDS)
- Hypoventilation (resp pump failure)
- Extra (outside of)- lung shunt- congenital heart defect
1) Cause of hypoxaemia: Low inspired PO2 e.g. high altitude
- PP of oxygen falls the further up we are from sea level
- Therefore pp oxygen falls in alveoli
- Therefore pp oxygen in arterial blood is low- hypoxaemia
- Fully improves with O2
what is the most common cause of hypoxaemia
Ventilation-perfusion mismatch
2) Cause of hypoxaemia: Ventilation-perfusion mismatch
- the most common cause of hypoxaemia
- optimal gas exchange when V/Q ratio is 1
- V/Q matching must happen at alveolar level
what does V:Q <1 mean
- Means that’s perfusion is higher than ventilation
- Therefore PaO2 is low
- Initially paCO2 rises until there is compensatory hyperventilation- then paCO2 will be either normal or low
- Hyperventilation (blowing off CO2) induced by peripheral chemoreceptors firing secondary to hypoxaemia
- If lung disease severe hyperventilation may not be able to compensate for V:Q <1 and CO2 remains elevated
When V:Q is >1
( e.g. the lung apices- ventilation greater than perfusion in normal human- we increase perfusion. If not healthy wont be able to perfuse)
- Ventilation is higher than perfusion
- PaO2 rises (slightly) and PaCO2 falls
- If lungs not healthy the extra air going to these parts of the lung is waste – increased dead space- alveoli ventilated but not perfused
in which conditions does V/Q mismatch occur
- Occurs in disorder where some alveoli are poorly ventilated by still perfused **i.e. main V:Q mismatch V<q></q><ul>
<li>Asthma</li>
<li>COPD</li>
<li>Pneumonia (exudate in affected alveoli)</li>
</ul></q>**
outline what physiological processes step into action when V:Q < 1
- Initially alveolar pO2 falls and PCO2 rises
- Pulmonary arterial hypoxic vasoconstriction occurs –> diverts some (but not all) blood to better ventilated areas
- If VQ ratio is still <1 –> alveolar pO2 will be low (no oxygen getting in) and pCO2 high (no CO2 getting oit
- Blood from these alveolar- low PaO2 and high PaCO2
- Mixed blood in left atrium= will have low arterial PO2 and high arterial pCO2- THEN
- Hypoxaemia stimulates peripheral chemoreceptors (aortic bodies and carotid chemoreceptors etc) –> causing hyperventilation- if there is enough functioning lung tissue CO2 levels will normalise or fall leading to final arterial blood with low PaO2 and normal or low PaCO2
V:Q mismatch in pulmonary embolism
- Embolus results in redistribution of pulmonary blood flow
- Blood is diverted to unaffected areas
- Leads to V/Q ratio <1 if hyperventilation cannot match the increased perfusion- causes hypoxaemia
- Very small minority of Pts PaO2 normal- small infarct area
- Hyperventilation sufficient to get rid of CO2 remember – 95% of people with PE tachypnoeic
- paCO2 will be low in most people if they are tachypnoeic- blowing of CO2
how does hyperventilating effect the CO2 bicarbonate buffer system
Hyperventilating will reduce amount of paCO2, therefore CO2 bicarbonate buffer system will be pushed to the left= hydrogen ions will combine with HCO3- = H+ goes down= pH goes up
name 5 causes of V/Q mismatch
Occurs in disorders where some alveoli are being poorly ventilated
e. g.
* 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 admin- but will only partially correct hypoxaemia until underlying pathology corrected
3) Cause of hypoxaemia: Diffusion defect
e.g. poor diffusion across alveolar membrane
- Issue with pO2 not pCO2
- CO2 is much more soluble, CO2 diffusion less affected than diffusion of O2
- Therefore initially Type 1 resp failure:
- pO2 low
- pCO2 normal of low
Causes of diffusion defects
- Fibrotic lung disease
- Pulmonary edema
fibrotic lung disease
thickened alveolar membrane slows gas exchange
pulmonary oedema
fluid in interstial space increases diffusion distance
restrictive pattern on spirometry caused by
- Decreased compliance
- Increased elastic recoil
FEV1:FVC = normal or higher
Acute resp distress syndrome (ARDS)
- End result of acute alveolar injury caused by different insults and probably initiated by different mechanism- inflammatory response
- Many types of injuries which lead to ultimate, common pathway i.e. damage to the alveolar capillary unit e.g. Pneumonia
- Injury produces increase vascular permeability, oedema, fibrin exudation (hyaline membranes)
- Heavy, red lungs showing congestion and oedema- alveoli contained fluid lined by hyaline membranes
- Diffuse loss of surfactant- alveolar atelectasis
- Lungs become stiff and less compliant
- Lung volume decrease and minute ventilation increases as a compensatory phenomenon
- Loss of hypoxic pulmonary vasocontraction mechanisms- possibly due to release of endogenous vasodilator prostaglandins, bradykinin and cytokines associated with the inflammatory process
- Lungs become stiff and less compliant
- Diffuse loss of surfactant- alveolar atelectasis
- Therefore a tremendous intrapulmonary shunt develops as a consequence of all of the above à no ventilation with respect to perfusion = shunt
scoliosis
is a sideway curvature of the spine
