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Hepatorenal syndrome (HRS) is defined as the development of renal insufficiency in chronic liver disease with portal hypertension when other causes of functional renal failure are excluded. Incidence in patients with refractory ascites is 8%, with an overall incidence of renal failure in end stage liver disease being 75%. HRS is predictive for the prognosis of end stage liver failure but its pathogenesis is complex and currently not fully understood. [ABSTRACT FROM AUTHOR]

Blood gas analysis provides valuable information about both the extracellular acid-base status and gas exchange. A blood gas analyzer measures pH, partial pressure of oxygen(pO(2)), partial pressure of carbon dioxide (pCO(2)), O(2) saturation, and hemoglobin concentration. A number of calculated parameters can be derived from these direct measurements such as bicarbonate concentration, base excess, oxygen content, etc. This contribution introduces the basic technical aspects of a blood gas analyzer and then describes some of the parameters that facilitate evaluation of the acid-base status and the oxygenation status of the blood. Finally, proper sampling and handling of blood gas samples is addressed. [ABSTRACT FROM AUTHOR]

Background: This study investigates whether long-term treatment with an angiotensin converting enzyme inhibitor (ACEI) impairs the hemodynamic regulation during the early phase of spinal anaesthesia.Methods: Forty-two patients undergoing minor surgery were studied. Twenty-one patients were long-term treated (ACEI group), while the other patients served as controls (nonACEI group). All patients received a balanced electrolyte solution (6 ml kg(-1)) 20 min before spinal anaesthesia.Results: Mean arterial blood pressure decreased 19% in both groups within 20 min after spinal anaesthesia. Heart rate did not change in either group. Plasma renin concentration increased from 7.3 +/- 2.1 to 12.8 +/- 4 pg ml(-1) during spinal anaesthesia in nonACEI patients (P < 0.05), whereas an elevated plasma renin level remained unchanged in the nonACEI group. The angiotensin II concentration increased in both groups during spinal anaesthesia (P < 0.05). The vasopressin concentration did not change during spinal anaesthesia in the ACEI group, but increased from 1.2 +/- 0.3 to 2.2 +/- 0.5 pg ml(-1) in patients with ACEI treatment (P < 0.05). The norepinephrine concentration increased transiently 5 min after spinal anaesthesia in both groups, and returned to baseline levels within 15 min.Conclusion: Long-term ACEI treatment does not further exaggerate the blood pressure decrease in the early phase of spinal anaesthesia. The increase in vasopressin concentrations in ACEI treated patients seems to be sufficient to compensate for the inhibited renin-angiotensin system. In addition, the transient increase in plasma norepinephrine, which occurs independent of preoperative ACEI treatment, seems to be involved in blood pressure regulation during spinal anaesthesia. [ABSTRACT FROM AUTHOR]

Objectives: To study the effects of an inhaled endothelin A (ET(A)) receptor antagonist on hemodynamics and pulmonary gas exchange in experimental acute lung injury (ALI).Design and Setting: Prospective, randomized, and controlled study in a university laboratory.Participants and Interventions: Sixteen pigs were ventilated in a volume controlled mode during general anesthesia. ALI was induced by surfactant depletion using repetitive lung lavages until the PaO2/FIO2 ratio was below 100 mmHg. The animals were then randomly assigned to receive either a nebulized ET(A) receptor antagonist (LU-135252, 3 mg/kg, inhaled over 1 h; LU group) or nebulization of saline (5-10 ml inhaled over 1 h) with no further intervention (controls).Measurements and Results: Parameters of hemodynamics and gas exchange were measured for 6 h after induction of ALI. In the LU group intrapulmonary right-left shunting (QS/QT) decreased from 58 +/- 8% at the onset of ALI to 27 +/- 12% 3 h and 24 +/- 9% 6 h after ALI (p < 0.05); PaO2 increased from 55 +/- 12 to 257 +/- 148 mmHg 3 h and 270 +/- 136 mmHg 6 h after ALI. (p < 0.05), whereas in controls QS/QT and PaO2 did not improve over the 6 h after onset of ALI. In the LU group mean pulmonary artery pressure was stable for 6 h after ALI (26-29 mmHg), while in controls it increased from 28 +/- 2 to 41 +/- 2 mmHg (p < 0.05). Inhaled LU-135252 reduced cardiac output by 31 +/- 11% (p < 0.05) and increased systemic vascular resistance by 60 +/- 29 % (p < 0.05), while these parameters remained stable in controls.Conclusion: In this porcine model of ALI the inhalation of an ET(A) receptor antagonist improved arterial oxygenation and maintained a stable pulmonary artery pressure without inducing systemic vasodilatation. [ABSTRACT FROM AUTHOR]