Intrapulmonary Shunting during Induced Hypotension

Abstract

lntrapulmonary shunting during induced hypotension. Anesth Analg 1982;61:231-5.The effect of sodium nitroprusside (SNP) and nitroglycerin (TNG) on pulmonary shunting (Qs/Qt) in 14 consenting adults [nine with normal lung function and five with chronic obstructive pulmonary disease (COPD)] was studied under general anesthesia. Qs/Qt significantly increased ( p < 0.005) from 5.1 9% to 8.81 %, whereas pulmonary arterial pressure (PAP) decreased from 18.5 to 8 torr ( p c 0.005) and pulmonary vascular resistance (PVR) decreased from 235 to 147.75 dynes.sec/cm5 ( p c 0.025) when SNP was administered to patients with normal lung function. Nitroglycerin increased Qs/Qt from 5.13% to 6.19% ( p < 0.005), whereas PAP decreased from 18 to 10 torr ( p c 0.005) and PVR decreased from 237 to 162.6 dynessec/cm5 ( p c 0.025) in these patients. In patients with COPD, SNP and TNG produced no significant changes in Qs/Qt, 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 SNPand 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.

Photoacoustic imaging of in vivo hemodynamic responses to sodium nitroprusside

“…The above dynamics are mirrored in our observation in most animals (five out of seven): SNP first causes a decrease in arterial sO 2 due to pulmonary shunting, as well as a much larger decrease in venous sO 2 due to oxygen extraction. Our data therefore support the hypothesis in earlier studies that SNP increases the intrapulmonary shunting [33,40]. Since this is a highly variable parameter that depends on the animal size and age, quality of ventilation, as well as the presence of atelectasis, it could explain the inter-animal variability reported in our study.…”

“…As reported in previous studies [33,38,39], cerebral tissue oxygen (PtO 2 ) decreased in response to SNP administration, which was attributed to increased arteriovenous shunting and hypotension-induced inadequate capillary perfusion, resulting in relative tissue hypoxia [33,39]. It was further hypothesized that increased intrapulmonary shunts could contribute to this observation [33,40]. Previous studies however did not have the ability to assess vessel-by-vessel sO 2 as reported in our study using PAM, and thus could not distinguish sO 2 levels in veins and arteries.…”

Cardiac output affects the response to pulsed inhaled nitric oxide in mechanically ventilated anesthetized ponies determined by CT angiography of the lung

“…and Vd/Vt increase due to vasodilation of pulmonary vessels in dependent lung regions and a fall in PVR. 34,35 It is possible that this effect of hypotension during anesthesia may counteract the response to PiNO. However, when hypotension is induced with isoflurane, gas exchange is not affected significantly, suggesting that nitroprusside itself, may have an effect on pulmonary gas exchange rather than hypotension per se.…”