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To examine the relative roles of passive factors (flow; filling pressures of left side of heart) and active factors (acidosis; arterial unsaturation) in the genesis of pulmonary hypertension when associated with sepsis, 37 patients with sepsis and 24 patients without sepsis were examined. Pulmonary hypertension was measured by the pulmonary arterial diastolic-pulmonary wedge pressure gradient (PAd-PWP gradient) and correlated reasonably with a standard formula for calculated resistance ([PA--PWP]/CI, where PA is mean pulmonary artery pressure and CI is cardiac index). In 22 of 37 patients, sepsis was associated with a significant degree of resistance to flow in the pulmonary circulation, as measured by the PAd-PWP gradient: and the higher the PAd--PWP gradient, the greater the likelihood of early death. None of the examined passive or active factors appeared to be adequate to explain pulmonary hypertension when present. By the use of previously derived formulae to estimate the compliance of the elastic pulmonary arteries, factors affecting this part of the pulmonary microcirculation could not be held accountable for apparent pulmonary hypertension. Therefore, the presence of pulmonary hypertension in sepis appears to be an active, rather than a passive, phenomenon and unrelated to arterial oxygen saturation or acid-base imbalance. Although the exact cause is unknown, pulmonary hypertension in sepis is associated with a high mortality and may be clinically followed by measurement of the PAd-PWP gradient.
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