Pulmonary capillary pressure and tissue perfusion: clinical implications during resuscitation from shock.

During shock resuscitation, a combination of fluids, vasopressors, vasodilators, and inotropes is administered in order to achieve a cardiac output or overall oxygen delivery as per guidelines of individual clinicians. The measurement of ventricular end-diastolic pressure allows a clinician to describe a therapeutic goal of optimum cardiac output response to changes in end-diastolic pressure. This concept has formed the backbone of resuscitative strategies in many forms of shock. Ventricular end-diastolic pressure is indirectly measured as the pulmonary artery occlusion pressure (PAOP) in critically ill patients with the use of a pulmonary artery catheter. Cytokines and other mediators may injure the pulmonary capillary endothelium which will affect the rate of leakage in the pulmonary capillaries. This may have important clinical implications in the therapy of shock in inflammatory states such as sepsis and the adult respiratory distress syndrome. Therefore, the true edema-forming pressure within the pulmonary bed is of considerable importance to the intensivist at the bedside. True pulmonary capillary pressure represents the midpoint of the capillary bed and is the hydrostatic pressure which directly drives the rate of pulmonary interstitial edema formation. During shock resuscitation in disorders in which vascular integrity may be impaired, the ability to measure pulmonary capillary pressure would be of great clinical benefit. It is impossible to directly measure pulmonary capillary hydrostatic pressure in the intact lung and, therefore, only indirect measurements are clinically possible. Numerous studies have demonstrated the lack of consistent relationship between the pulmonary capillary pressure, PAOP, pulmonary artery diastolic pressure, and the severity of acute lung injury. The assumption that PAOP, and thus left atrial pressure, is a good indirect measurement of pulmonary filtration pressure within the capillary bed is erroneous, in particular in the presence of increased resistance within the pulmonary venous bed between the capillaries and the left atrium, as may exist in disorders in which there is cytokine production. It is now clear that a significant gradient between pulmonary capillary pressure and PAOP may be present in inflammatory disorders which are not present in noninflammatory states, and that pulmonary capillary pressure may be measured at the bedside of critically ill patients. Bedside measurement of pulmonary capillary pressure may allow for added precision in our therapeutic goals in resuscitation from inflammatory shock. If further studies confirm the reliability and reproducibility of bedside measurement, pulmonary capillary pressure may become an invaluable part of the hemodynamic profile in the critically ill patient in shock.