Intrapulmonary shunt and O2 Tx
Last updated: 03/03/2015
Blood passing through areas of absolute shunt receives no oxygen (V/Q = 0), therefore, arterial hypoxemia resulting from intrapulmonary shunt is minimally responsive to supplement oxygen. Shunt effect (venous admixture or low V/Q) is the more common clinical scenario in which areas of lung have poor alveolar ventilation compared to the degree of alveolar perfusion ( 0 < V/Q < 1). Because these areas still participate in gas exchange, albeit small, arterial hypoxemia improves with supplemental oxygen. Normally, a small percentage of venous blood from the pleural, bronchiolar and thebesian veins bypasses the right ventricle and empty into the left atrium; this represents a true anatomic shunt, which is 2-5% of cardiac output. The arterial hypoxemia that arises from hepatopulmonary syndrome also represents an intrapulmonary anatomic shunt secondary to pulmonary AV malformations. Other disease states that represent an absolute shunt include acute lobar atelectasis, ARDS, advanced pulmonary edema and consolidated pneumonia. Disease states that create venous admixture or low V/Q states include mild pulmonary edema, post-op atelectasis, and COPD. All these disease states are normally mitigated by hypoxic pulmonary vasoconstriction, which refers to the attempt of normal lungs to optimally match ventilation and perfusion. This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood flow to well-ventilated alveoli. Distinguishing between true shunt and reduced V/Q can also be performed noninvasively by simultaneously plotting SaO2 versus FiO2. A true shunt shifts the curve downward, whereas venous admixture (low V/Q) shifts the curve rightward.
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