pCO2

Abstract: Introduction Our goal was to assess the effects of titration of a norepinephrine infusion to increasing levels of mean arterial pressure (MAP) on sublingual microcirculation. Methods Twenty septic shock patients were prospectively studied in two teaching intensive care units. The patients were mechanically ventilated and required norepinephrine to maintain a mean arterial pressure (MAP) of 65 mmHg. We measured systemic hemodynamics, oxygen transport and consumption (DO 2 and VO 2 ), lactate, albumin-corrected anion gap, and gastric intramucosal-arterial PCO2 difference (ΔPCO2). Sublingual microcirculation was evaluated by sidestream darkfield (SDF) imaging. After basal measurements at a MAP of 65 mmHg, norepinephrine was titrated to reach a MAP of 75 mmHg, and then to 85 mmHg. Data were analyzed using repeated measurements ANOVA and Dunnett test. Linear trends between the different variables and increasing levels of MAP were calculated. Results Increasing doses of norepinephrine reached the target values of MAP. The cardiac index, pulmonary pressures,

Abstract: This review provides an overview of the relationship between ventilation/perfusion ratios and gas exchange in the lung, emphasising basic concepts and relating them to clinical scenarios. For each gas exchanging unit, the alveolar and effluent blood partial pressures of oxygen and carbon dioxide (PO2 and PCO2) are determined by the ratio of alveolar ventilation to blood flow (V'A/Q') for each unit. Shunt and low V'A/Q' regions are two examples of V'A/Q' mismatch and are the most frequent causes of hypoxaemia. Diffusion limitation, hypoventilation and low inspired PO2 cause hypoxaemia, even in the absence of V'A/Q' mismatch. In contrast to other causes, hypoxaemia due to shunt responds poorly to supplemental oxygen. Gas exchanging units with little or no blood flow (high V'A/Q' regions) result in alveolar dead space and increased wasted ventilation, i.e. less efficient carbon dioxide removal. Because of the respiratory drive to maintain a normal arterial PCO2, the most frequent result of wasted ventilation is increased minute ventilation and work of breathing, not hypercapnia. Calculations of alveolar-arterial oxygen tension difference, venous admixture and wasted ventilation provide quantitative estimates of the effect of V'A/Q' mismatch on gas exchange. The types of V'A/Q' mismatch causing impaired gas exchange vary characteristically with different lung diseases.

Abstract: ALTHOUGH it has long been recognized that defense of pH during acute hypercapnia is dependent on the generation of bicarbonate by body buffers,1 , 2 the quantitative aspects of the response to graded increases in carbon dioxide tension (pCO2) have not been defined in man. The characterization of such a "whole-body titration curve" § should serve the important function of providing a physiologic background against which complex acid–base disturbances in the patient with acute respiratory acidosis might be evaluated. The present study has employed a large environmental chamber to examine the acid–base response of unanesthetized man to progressive elevation of arterial . . .

Abstract: IT IS WELL established that the arterial carbon dioxide tension (Pco2) is an important factor controlling cerebral vascular resistance (CVR) and cerebral blood flow (CBF) in healthy animals and man. An acute rise in Pco2causes a decrease in CVR which increases the CBF, and a fall in Pco2has the opposite effect. However, during sustained alteration of Pco2, the CBF and absolute carbon dioxide tension often fail to correlate closely, and much recent evidence summarized by Lassen1suggests that alterations of the pH of the brain's extracellular space mediate the cerebral vascular response to carbon dioxide and that brain interstitial fluid pH is the major regulator of CBF. The pH hypothesis is physiologically attractive, but evidence against it comes from a series of experiments in several laboratories in which prolonged passive hyperventilation of animals2-5and man6producing sustained, constant arterial hypocapnia