Intrapulmonary Shunting during Induced Hypotension

Abstract

The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (𝑄̇s/𝑄̇t) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. 𝑄̇s/𝑄̇t significantly increased (p > 0.005) from 5.19% to 8.81%, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr (p > 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes sec/cm5 (p > 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased 𝑄̇s/𝑄̇t from 5.13% to 6.19% (p > 0.005), whereas PAP decreased from 18 to 10 torr (p > 0.005) and PVR decreased from 237 to 162.6 dynes sec/cm5 (p > 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in 𝑄̇s/𝑄̇t, PAP, or PVR. Cardiac output remained unchanged in both groups of patients. Various mechanisms to explain these results can be postulated. When hypotension is induced in patients with normal pulmonary function, PAP decreases and the effect of gravity puts more blood through dependent areas where most of the shunt units are. In patients with COPD, destructive vascular changes increase PAP, preventing vasodilators from decreasing PVR. In addition, dilation of hypoxic pulmonary vasoconstriction (if present) by SNP and TNG will occur independent of the two previously mentioned mechanisms. These results provide evidence that SNP-and TNG-induced hypotension may cause significant impairment in pulmonary gas exchange in patients with normal lung function. In patients with COPD pulmonary gas exchange is not affected after deliberate hypotension with SNP or TNG.