Management of the Patient on a Ventilator
Consider a one compartment lung model ventilated via one airway and perfused by the total pulmonary blood flow. Inspired gas having no CO2 enters the airspace perfused by mixed venous blood. In the steady state, the CO2 production (VCO2 = 250 ml/min), which was added to the arterial blood in the peripheral tissues, now moves by diffusion to equilibrate with the alveolar ventilation (VA = 41/min). Accordingly, the alveolar gas fraction is about 6%, so the alveolar PCO2(PACO2) is about 40 torr. Because PACO2 is determined by the ratio VCO2/VA, arterial CO2 retention signals alveolar hypoventilation when the CNS drive to breathe decreases (drug intoxication, head trauma), when the respiratory muscles become excessively weak (ascending polyreticulitis, myasthenia gravis, botulism), or when the load on the respiratory muscles exceeds their normal strength (status asthmaticus, acute on chronic respiratory failure). In the latter conditions, alveolar ventilation is further reduced because large amounts of the minute ventilation are wasted as dead space; increased dead space in each tidal volume (Vd/Vt) is signalled by the mixed expired CO2 becoming much less than the alveolar PCO2, because a large fraction of the tidal volume does not equilibrate with pulmonary blood flow in the alveoli (Vd/Vt) = (PACO2 - PECO2)/(PACO2). Hypercapnia is the sine qua non of hypoventilatory (Type II) respiratory failure, which is associated with arterial hypoxemia accounted for by alveolar hypoventilation (normal alveolar-arterial gradient) and correctable with supplemental oxygen [1, 2].
KeywordsChronic Obstructive Pulmonary Disease Respiratory Muscle Pulmonary Blood Flow Alveolar Ventilation Status Asthmaticus
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