RBCs of septic patients are characterized by a more spherical shape, a decreased capacity of sphericity in hypo-osmolar solution, and a reduction in the sialic acid content of the RBC membrane. These modifications in RBC shape and membrane may contribute to the RBC rheologic abnormalities frequently described in sepsis.

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In septic shock patients, the administration of methylene blue results in a transient and reproducible increase in arterial pressure, associated with an improvement in cardiac function, but does not increase cellular oxygen availability. The significant reduction in blood lactate concentration is probably related to the reductor effect of methylene blue, rather than to an improvement in tissue oxygenation.

We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. The hypoxia-induced rise in Ppa-Ppw gradient increased from 5 to 9 mmHg in metabolic acidosis (P less than 0.001), decreased from 6 to 1 mmHg in metabolic alkalosis (P less than 0.001), remained unchanged in respiratory acidosis, and decreased from 5 to 2 mmHg in respiratory alkalosis (P less than 0.001). Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.

In 14 critically ill patients in stable cardiopulmonary status, right ventricular ejection fraction (RVEF) was measured by thermodilution technique and by radionuclear (gated first pass) technique. The pulmonary artery catheter was equipped with a fast-response thermistor and an intracardiac ECG monitor. In addition, the proximal lumen ended in a 3-hole port 21 cm from the tip of the catheter to facilitate mixing of the cold bolus above the tricuspid valve. The use of a new algorithm based on an exponential curve analysis of the thermodilution curve limited the variability of RVEF determinations to 7.6%. The correlation between RVEF measured by thermodilution and radionuclear techniques was significant (y = 12.7 +/- 0.49x, r = 0.67, p less than 0.01). However, the values obtained by thermodilution were usually lower, especially for high RVEF. Nevertheless, although some discrepancy was found, thermodilution techniques allow simple, accurate and repetitive bedside measurements of right ventricular volumes in the critically ill.

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Several reports have suggested that hypoxic pulmonary vasoconstriction (HPV) might result in deterioration of pulmonary gas exchange in severe hypoxia. We therefore investigated the effects of HPV on gas exchange in normal and diseased lungs. We incorporated a biphasic HPV stimulus-response curve observed in intact dogs (S. Brimioulle, and R. Lejeune, J.L. Vachièry, M. Delcroix, R. Hallemans, and R. Naeije, J. Appl. Physiol. 77: 476-480, 1994) into a 50-compartment lung model (J.B. West, Respir. Physiol. 7: 88-110, 1969) to control the amount of blood flow directed to each lung compartment according to the local hypoxic stimulus. The resulting model accurately reproduced the blood gas modifications caused by HPV changes in dogs with acute lung injury. In single lung units, HPV had a moderate protective effect on alveolar oxygenation, which was maximal at near-normal alveolar PO2 (75-80 Torr), mixed venous PO2 (35 Torr), and PO2 at which hemoglobin is 50% saturated (24 Torr). In simulated diseased lungs associated with 40-60 Torr arterial PO2, however, HPV increased arterial PO2 by 15-20 Torr. We conclude that HPV can improve arterial oxygenation substantially in respiratory failure.

Pulmonary hypertension associated with congestive heart failure carries a risk of right ventricular failure after cardiac transplantation. Few data, however, are available on the hemodynamic behavior of the pulmonary circulation in these patients. We therefore studied mean pulmonary artery pressure minus left atrial pressure (estimated by pulmonary artery occluded pressure) versus cardiac output relationships in 20 patients with congestive heart failure evaluated for orthotopic cardiac transplantation, and we repeated this study either within the first 3 days postoperatively (n = 10) or 1 month postoperatively (n = 11). Cardiac output was increased by physical exercise or (in the early postoperative period) by an infusion of dobutamine. Reversibility of pulmonary hypertension was tested by an infusion of prostaglandin E1. At preoperative evaluation, the extrapolated pressure intercept of pulmonary vascular pressure:flow plots was negative in 10 of the patients, suggesting active exercise-induced pulmonary vasoconstriction. In the other 10 patients, the extrapolated pressure intercept was positive, suggesting that an increased closing pressure contributed to pulmonary hypertension. However, transplantation was constantly associated with proportional decreases of pulmonary artery pressure and left atrial pressure. On the other hand, pulmonary vascular pressure:flow plots were displaced to equal or lower pressures and to higher flows by prostaglandin E1 before as well as after transplantation. We conclude that in patients with congestive heart failure evaluated for cardiac transplantation, an increased pulmonary venous pressure more than a reversible increase in closing pressure determines the severity of pulmonary hypertension.