Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Abstract

F or decades the pulmonary circulation was not considered as important as the systemic ("greater") circulation. However, pulmonary hypertension can arise because of many diseases of the heart and lung. Therefore, increasing efforts in research have been undertaken leading to a profound increase in understanding pulmonary vascular physiology and pathophysiology. This review discusses basic physiology, clinical concepts, and treatment options for pulmonary hypertension and the related right ventricular heart failure focusing on secondary pulmonary hypertension in patients during anesthetic procedures. Physiology of Pulmonary CirculationThe pulmonary vascular bed is a high-flow, lowpressure circulation system. Pulmonary vessels have less resistance in comparison to the systemic circulation under normal conditions because of higher compliance of pulmonary precapillary arterioles with a thinner media and less smooth muscle cells (SMCs) compared with the corresponding systemic arterioles. In addition, the cross-sectional area of the pulmonary vascular bed is large and highly distensible with recruitable vessels available to accommodate increase in flow resulting in low pressure and low resistance.In contrast to the systemic arteries, pulmonary vessels constrict with hypoxia (Euler-Liljestrand reflex) and relax in the presence of hyperoxia. Furthermore, changes in cardiac output (CO), airway pressure, and gravity affect the pulmonary more than the systemic circulation. Increases in CO distend open vessels and recruit previously closed vessels. Therefore, the crosssectional area of pulmonary circulation enlarges and results in a decrease in pulmonary vascular resistance (PVR). An increase in CO has very little effect on pulmonary arterial pressure (PAP) because of the recruitment and distension of pulmonary vessels. An increased PAP or left atrial pressure (LAP) may also distend and recruit pulmonary vessels. Clinically, this means that enhanced CO caused by the administration of inotropic drugs or enlarged blood volume will passively decrease PVR.

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“…Mild hyperventilation (PaCO2 30-35 mm Hg), increasing the fraction of inspired oxygen, and correcting any acid-base derangement contribute to reducing pulmonary vascular resistance. 36 The OLT is a viable therapeutic option for patients with POPH. Swanson and coworkers demonstrated that patients with medically treated PH and OLT had a better 5-year survival (67%) than patients treated only pharmacologically without OLT (45%).…”

A Pathophysiological Approach to Understanding Pulmonary Hypertension in Cardiac Surgery

“…At functional residual capacity (FRC), PVR is minimal but increases at large or total lung capacity (TLC) and small lung volumes. Clinically, this may be observed when hyperinflation of the lungs greatly increases PVR (Fischer et al, 2003). Fig.…”

“…The differential effect on intra-and extra-alveolar vessels accounts for the U-shaped relationship of PVR and lung volume. Adapted from Fischer et al (Fischer et al, 2003).…”

Perioperative Management of Pulmonary Hypertension

“…The normal thin walls and crescent shape of the right ventricle result in a highly compliant right ventricular chamber, which is able to accommodate large increases in volume. However, the right ventricular adaptive mechanisms are not well suited to acute, large increases in pressure, (Fischer et al, 2003), as this may happen after CPB. Furthermore systemic hypotension decreases right ventricular coronary perfusion pressure and oxygen delivery.…”

“…Numerous studies (Fischer et al, 2003;Blaise et al, 2003) investigate the effect of anesthetic drugs on pulmonary vascular tone. In general, it appears that the effect of anesthetic agents on the pulmonary circulation is different from their effect on the systemic circulation, often resulting in an increase in PVR.…”