Der „kranke" rechte Ventrikel

Zwißler, Bernhard

doi:10.1007/s003900170074

Cited by 3 publications

(1 citation statement)

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“…Reduction of the crosssection of the pulmonary circulation of Ͼ60%-70% decreases CO and induces RV failure (58). As previously mentioned, baseline support, IV or inhaled vasodilators should be used, keeping in mind to avoid a significant decrease in SVR.…”

Section: Specific Treatmentmentioning

confidence: 98%

Management of Pulmonary Hypertension: Physiological and Pharmacological Considerations for Anesthesiologists

Fischer¹,

Aken²,

Rkle³

2003

Anesthesia & Analgesia

171

108

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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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Section: Specific Treatmentmentioning

confidence: 98%