Gas exchange and pulmonary hypertension following acute pulmonary thromboembolism: has the emperor got some new clothes yet?

Patients present with a wide range of hypoxemia after acute pulmonary thromboembolism (APTE). Recent studies using fluorescent microspheres demonstrated that the scattering of regional blood flows after APTE, created by the embolic obstruction unique in each patient, significantly worsened regional ventilation/perfusion (V/Q) heterogeneity and explained the variability in gas exchange. Furthermore, earlier investigators suggested the roles of released vasoactive mediators in affecting pulmonary hypertension after APTE, but their quantification remained challenging.

Estimation of endothelin-mediated vasoconstriction in acute pulmonary thromboembolism.

We aimed to investigate the role of endothelin-mediated vasoconstriction following acute pulmonary thromboembolism (APTE). Thirteen anesthetized piglets (~25 kg) were ventilated with 0 PEEP. Cardiac output (Qt) and wedge pressure (Pw) were measured by a Swan Ganz catheter, along with arterial and venous blood gases.

The DNR Order: What Does it Mean?

As medical science continues to advance, patients nowadays with progressive cardiopulmonary diseases live to older ages. However, they too will eventually reach their unsustainable physiological limit and many die in poor health and discomfort prior to their demise. Regrettably many physicians have not kept pace in dealing with the inevitable end-of- life issues, along with modern technological developments.

Regional CO2 tension quantitatively mediates homeostatic redistribution of ventilation following acute pulmonary thromboembolism in pigs.

Previous studies reported that regional CO(2) tension might affect regional ventilation (V) following acute pulmonary thromboembolism (APTE). We investigated the pathophysiology and magnitude of these changes. Eight anesthetized and ventilated piglets received autologous clots at time = 0 min until mean pulmonary artery pressure was 2.

Endothelin receptor blockade does not improve hypoxemia following acute pulmonary thromboembolism.

We studied the roles of endothelins in determining ventilation (Va) and perfusion (Q) mismatch in a porcine model of acute pulmonary thromboembolism (APTE), using a nonspecific endothelin antagonist, tezosentan. Nine anesthetized piglets (approximately 23 kg) received autologous clots (approximately 20 g) via a central venous catheter at time = 0 min. The distribution of Va and Q at five different time points (-30, -5, 30, 60, 120 min) was mapped by fluorescent microspheres of 10 different colors.

Spatial pattern of ventilation-perfusion mismatch following acute pulmonary thromboembolism in pigs.

We studied the spatial distribution of the abnormal ventilation-perfusion (Va/Q) units in a porcine model of acute pulmonary thromboembolism (APTE), using the fluorescent microsphere (FMS) technique. Four piglets ( approximately 22 kg) were anesthetized and ventilated with room air in the prone position. Each received approximately 20 g of preformed blood clots at time t = 0 min via a large-bore central venous catheter, until the mean pulmonary arterial pressure reached 2.