Respiratory Failure
Monday, 20 September 2021 5:02 PM
Causes
- Ventilatory failure
o A defect along the respiratory control pathway from the medulla through the
respiratory muscles
§ Depressed central respiratory drive
• Morphine and barbiturate
§ Defect in nerves to respiratory muscles
• Decrease excitability of brain cells
• Cannot produce AP
§ Neuromuscular disease
• Production in auto antibody that attacks acetylcholine receptors at
neuromuscular junction
o Blocks neuromuscular transmission
o Muscle weakness = no contraction – reduced force
• In severe conditions patient needs a ventilatory pump
o A defect in the ventilatory apparatus
§ Thoracic cage disorder
• Decreases the compliance of the chest due to abnormal curvature of
the spine that deforms the chest cage and limits the movement of the
chest during breathing
• Excessive fatty tissue pushes the diaphragm into the thoracic cage
§ Respiratory muscle weakness
• E.g. due to trauma
• Injury to chest wall or respiratory muscles
§ Limitation in lung expansion
• Decrease in lung compliance
• Interstitial lung diseases which increase scarring of the lung that
increases elasticity and limits lung expansion
o Lower ventilation
§ Obstruction of airway
• Emphysema / chronic bronchitis
• Contribute to airway resistance – chronic obstruction
- Gas exchange failure
o Defective alveolocapillary membrane
§ Too thick / lower surface area
§ ARDS
• Acute respiratory distress syndrome
• significant fluid buildup in alveoli
o V/Q mismatching
§ Ventilation and perfusion mismatching
§ Common in COPD
, § Too thick / lower surface area
§ ARDS
• Acute respiratory distress syndrome
• significant fluid buildup in alveoli
o V/Q mismatching
§ Ventilation and perfusion mismatching
§ Common in COPD
§ Increases RAW = lower ventilation
§ Pulmonary fibrosis = decrease ventilation = decrease in V/Q ratio
§ Vascular decreases
• Decreases pulmonary perfusion = affects Q
• Output lowers = increases ratio
• Pulmonary embolism
- Curve
o 100mmhg
§ CO2 about 40mmg
• Use alveolar oxygen equation using respiratory coefficient = R
o Dashed line shows cutoff of respiratory failure at 60mmhg
§ or co2 above 50mmhg
o hypoventilation – type II
§ low ventilation
• inadequate alveolar ventilation
§ low blood oxygen levels = below 60mmhg = hypoxemia
§ co2 blood levels increase to 80mmhg = hypercapnia
• caused CO2 retention
• lack of ventilation means CO2 accumulate
§ no ventilatory compensation
• blocked by the defects
§ causes
• defect in central respiratory control / ventilatory apparatus
o Chronic obstructive airway diseases – type II
§ V/Q mismatching
§ Hypoxemia = low oxygen level
• More severe than hypoventilation
§ high CO2 level = hypercapnia
• Less severe than hypoventilation
§ Ventilatory compensation limited by high RAW
• Not completely blocked so some compensation occurs
• So slightly lowers CO2 level therefore CO2 retention not as severe
o Interstitial lung disease – type I
§ Hypoxemia
§ CO2 remains normal
• No hypercapnia
§ V/Q mismatching
• Diffusion impairment
§ Ventilatory compensation in effect
• Normalizes CO2 retention – diffusion of CO2 much faster across blood
gas barrier
o Therefore doesn’t affect CO2 equilibrium
• But decreases O2
o Adult respiratory distress syndrome – type I
Monday, 20 September 2021 5:02 PM
Causes
- Ventilatory failure
o A defect along the respiratory control pathway from the medulla through the
respiratory muscles
§ Depressed central respiratory drive
• Morphine and barbiturate
§ Defect in nerves to respiratory muscles
• Decrease excitability of brain cells
• Cannot produce AP
§ Neuromuscular disease
• Production in auto antibody that attacks acetylcholine receptors at
neuromuscular junction
o Blocks neuromuscular transmission
o Muscle weakness = no contraction – reduced force
• In severe conditions patient needs a ventilatory pump
o A defect in the ventilatory apparatus
§ Thoracic cage disorder
• Decreases the compliance of the chest due to abnormal curvature of
the spine that deforms the chest cage and limits the movement of the
chest during breathing
• Excessive fatty tissue pushes the diaphragm into the thoracic cage
§ Respiratory muscle weakness
• E.g. due to trauma
• Injury to chest wall or respiratory muscles
§ Limitation in lung expansion
• Decrease in lung compliance
• Interstitial lung diseases which increase scarring of the lung that
increases elasticity and limits lung expansion
o Lower ventilation
§ Obstruction of airway
• Emphysema / chronic bronchitis
• Contribute to airway resistance – chronic obstruction
- Gas exchange failure
o Defective alveolocapillary membrane
§ Too thick / lower surface area
§ ARDS
• Acute respiratory distress syndrome
• significant fluid buildup in alveoli
o V/Q mismatching
§ Ventilation and perfusion mismatching
§ Common in COPD
, § Too thick / lower surface area
§ ARDS
• Acute respiratory distress syndrome
• significant fluid buildup in alveoli
o V/Q mismatching
§ Ventilation and perfusion mismatching
§ Common in COPD
§ Increases RAW = lower ventilation
§ Pulmonary fibrosis = decrease ventilation = decrease in V/Q ratio
§ Vascular decreases
• Decreases pulmonary perfusion = affects Q
• Output lowers = increases ratio
• Pulmonary embolism
- Curve
o 100mmhg
§ CO2 about 40mmg
• Use alveolar oxygen equation using respiratory coefficient = R
o Dashed line shows cutoff of respiratory failure at 60mmhg
§ or co2 above 50mmhg
o hypoventilation – type II
§ low ventilation
• inadequate alveolar ventilation
§ low blood oxygen levels = below 60mmhg = hypoxemia
§ co2 blood levels increase to 80mmhg = hypercapnia
• caused CO2 retention
• lack of ventilation means CO2 accumulate
§ no ventilatory compensation
• blocked by the defects
§ causes
• defect in central respiratory control / ventilatory apparatus
o Chronic obstructive airway diseases – type II
§ V/Q mismatching
§ Hypoxemia = low oxygen level
• More severe than hypoventilation
§ high CO2 level = hypercapnia
• Less severe than hypoventilation
§ Ventilatory compensation limited by high RAW
• Not completely blocked so some compensation occurs
• So slightly lowers CO2 level therefore CO2 retention not as severe
o Interstitial lung disease – type I
§ Hypoxemia
§ CO2 remains normal
• No hypercapnia
§ V/Q mismatching
• Diffusion impairment
§ Ventilatory compensation in effect
• Normalizes CO2 retention – diffusion of CO2 much faster across blood
gas barrier
o Therefore doesn’t affect CO2 equilibrium
• But decreases O2
o Adult respiratory distress syndrome – type I