Hypoxemia results from two basic mechanisms: 1) alveolar hypoxia, i.e., a reduced fraction of oxygen on the alveolar side of the pulmonary units (FAO2); 2) the presence of shunt, i.e., a condition in which blood perfusing the lung parenchyma does not enter into contact with the alveolar gases. Alveolar hypoxia A low alveolar concentration of oxygen may be caused by reduced barometric pressure (e.g., high altitude) or by inhalation of gas mixtures with abnormal composition (i.e., inspired oxygen fraction, FIO2 <21%). The most common cause of alveolar hypoxia, however, is an abnormally low ventilation/perfusion ratio (VA/Q). The consequences of this condition may be quantitatively described by a rather intricate series of equations. The underlying concept, however, is rather simple. Perfusion removes from pulmonary units a given amount of oxygen, per unit time. A normal alveolar oxygen concentration is, therefore, maintained only if ventilation provides, per unit time, the same amount of oxygen as that carried away by perfusion. This condition corresponds to a VA/Q ratio close to the unit. The amount of oxygen provided by ventilation (VA) is: VO2 = (FIO2 – FEO2) • VA, where FEO2 is the expired oxygen concentration and VO2 is oxygen consumption/requirement. The amount of oxygen subtracted by perfusion is: VO2 = Δc(a-v)O2 • CO, where Δc(a-v)O2 is arterial-venous blood oxygen content difference and CO is cardiac output. It can be seen that if alveolar ventilation decreases (e.g., by 50%), with oxygen consumption remaining the same, an inverse increase in the difference between inspired and expired oxygen fractions must be observed. (i.e., it must double, in our example). If the inspired oxygen fraction is not varied, this would imply a proportional decrease in the expired oxygen concentration, which would cause, in turn, alveolar oxygen tension to decrease. It can also be seen that if cardiac output remains constant, arterial oxygen concentration (and venous oxygen concentration, as well) will decrease. Arterial oxygen content, however, usually decreases more than venous oxygen content, since cardiac output actually increases, as a compensatory response to hypoxemia. Since alveolar hypoxemia is only due to a lower-than-normal FAO2, it can simply be corrected by raising the inspired oxygen fraction. The FIO2 necessary to maintain a normal FAO2, when alveolar ventilation is progressively decreased, while cardiac output remains constant. As shown, the correction of alveolar hypoxemia is an easy task. Hypoxemia due to shunt Shunt is the fraction of cardiac output which perfuses unventilated regions of the lung. The pulmonary end-capillary blood perfusing shunt regions has the same gas tensions that those of mixed-venous blood. Shunt is the worst case alteration of the ventilation/perfusion ratio, being VA/Q =0. This implies that no gas exchange occurs in the shunt compartment, due to the absence of gas within alveolar units (e.g., micro-atelectasis, other material filling the alveoli,…). Hypoxemia due to shunt can only be partially corrected by increasing FIO2, since a greater inspired oxygen concentration will increases alveolar oxygen tension (PAO2) within ventilated compartments only, but will not affect the gasless shunt regions. With shunts of 30-35%, PaO2 can only be increased up to roughly 100 mmHg, even if breathing 100% FIO2. A great difference between correcting hypoxemia due to alveolar hypoxia or due to shunt exists. The former is an easy task; the latter, especially with consistent shunt fractions, is far more difficult, since it requires either a modification of pulmonary blood flow distribution or a modification of the anatomical status of the unventilated pulmonary units.

How can I face the refractory hypoxemia? / L. Gattinoni. ((Intervento presentato al 6. convegno Curso taller de ventilacion mecanica tenutosi a Bogotà nel 2013.

How can I face the refractory hypoxemia?

L. Gattinoni
Primo
2013

Abstract

Hypoxemia results from two basic mechanisms: 1) alveolar hypoxia, i.e., a reduced fraction of oxygen on the alveolar side of the pulmonary units (FAO2); 2) the presence of shunt, i.e., a condition in which blood perfusing the lung parenchyma does not enter into contact with the alveolar gases. Alveolar hypoxia A low alveolar concentration of oxygen may be caused by reduced barometric pressure (e.g., high altitude) or by inhalation of gas mixtures with abnormal composition (i.e., inspired oxygen fraction, FIO2 <21%). The most common cause of alveolar hypoxia, however, is an abnormally low ventilation/perfusion ratio (VA/Q). The consequences of this condition may be quantitatively described by a rather intricate series of equations. The underlying concept, however, is rather simple. Perfusion removes from pulmonary units a given amount of oxygen, per unit time. A normal alveolar oxygen concentration is, therefore, maintained only if ventilation provides, per unit time, the same amount of oxygen as that carried away by perfusion. This condition corresponds to a VA/Q ratio close to the unit. The amount of oxygen provided by ventilation (VA) is: VO2 = (FIO2 – FEO2) • VA, where FEO2 is the expired oxygen concentration and VO2 is oxygen consumption/requirement. The amount of oxygen subtracted by perfusion is: VO2 = Δc(a-v)O2 • CO, where Δc(a-v)O2 is arterial-venous blood oxygen content difference and CO is cardiac output. It can be seen that if alveolar ventilation decreases (e.g., by 50%), with oxygen consumption remaining the same, an inverse increase in the difference between inspired and expired oxygen fractions must be observed. (i.e., it must double, in our example). If the inspired oxygen fraction is not varied, this would imply a proportional decrease in the expired oxygen concentration, which would cause, in turn, alveolar oxygen tension to decrease. It can also be seen that if cardiac output remains constant, arterial oxygen concentration (and venous oxygen concentration, as well) will decrease. Arterial oxygen content, however, usually decreases more than venous oxygen content, since cardiac output actually increases, as a compensatory response to hypoxemia. Since alveolar hypoxemia is only due to a lower-than-normal FAO2, it can simply be corrected by raising the inspired oxygen fraction. The FIO2 necessary to maintain a normal FAO2, when alveolar ventilation is progressively decreased, while cardiac output remains constant. As shown, the correction of alveolar hypoxemia is an easy task. Hypoxemia due to shunt Shunt is the fraction of cardiac output which perfuses unventilated regions of the lung. The pulmonary end-capillary blood perfusing shunt regions has the same gas tensions that those of mixed-venous blood. Shunt is the worst case alteration of the ventilation/perfusion ratio, being VA/Q =0. This implies that no gas exchange occurs in the shunt compartment, due to the absence of gas within alveolar units (e.g., micro-atelectasis, other material filling the alveoli,…). Hypoxemia due to shunt can only be partially corrected by increasing FIO2, since a greater inspired oxygen concentration will increases alveolar oxygen tension (PAO2) within ventilated compartments only, but will not affect the gasless shunt regions. With shunts of 30-35%, PaO2 can only be increased up to roughly 100 mmHg, even if breathing 100% FIO2. A great difference between correcting hypoxemia due to alveolar hypoxia or due to shunt exists. The former is an easy task; the latter, especially with consistent shunt fractions, is far more difficult, since it requires either a modification of pulmonary blood flow distribution or a modification of the anatomical status of the unventilated pulmonary units.
6-lug-2013
Settore MED/41 - Anestesiologia
How can I face the refractory hypoxemia? / L. Gattinoni. ((Intervento presentato al 6. convegno Curso taller de ventilacion mecanica tenutosi a Bogotà nel 2013.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/222552
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