ABSTRACT
OBJECTIVE: Clinical and experimental data indicate that when there is lung disease, wedging the pulmonary artery catheter (PAC) could cause decreases in cardiac output and systemic arterial blood pressure and an increase in mean pulmonary artery pressure (PAP). The authors studied whether wedging would alter mean left atrial pressure (LAP), and report perforations with PACs in their unit since 1975. DESIGN: Observational study. SETTING: University hospital operating room and intensive care unit. PARTICIPANTS: Ten adult patients undergoing cardiac surgery. INTERVENTIONS: Placement of epidural catheters in the left atrium and pulmonary artery, and a PAC. MEASUREMENTS AND MAIN RESULTS: After weaning from cardiopulmonary bypass, mean LAP, mean PAP, and cardiac output were measured before and during wedging with the chest open and closed. Mean LAP decreased during wedging, from 13.5 +/- 2.8 (SD) mmHg to 13.0 +/- 3.0 mmHg (open chest) and from 15.8 +/- 3.2 mmHg to 15.3 +/- 3.1 mmHg (closed chest; p < 0.001), and mean PAP increased, from 18.8 +/- 3.5 mmHg to 19.7 +/- 3.5 mmHg (open chest) and from 21.3 +/- 4.3 mmHg to 21.9 +/- 4.2 mmHg (closed chest; p < 0.001). Mean PAP-mean LAP increased by 20% to 25%. Wedge pressure did not differ from mean LAP. Cardiac output and systemic arterial pressure did not change. Four perforations due to PACs occurred since 1975. CONCLUSIONS: In adult patients undergoing cardiac surgery, wedging of a PAC resulted in a small decrease in mean LAP and a small increase in mean PAP. The wedging maneuver carries a small risk. How wedging is performed could influence the risk for perforation.
Subject(s)
Blood Pressure , Catheterization, Swan-Ganz/adverse effects , Pulmonary Artery/injuries , Adult , Aged , Atrial Function, Left , Catheterization, Swan-Ganz/methods , Female , Humans , Male , Middle Aged , Pulmonary Artery/physiologyABSTRACT
OBJECTIVES: Pulmonary endothelium-dependent vasodilation is impaired after cardiopulmonary bypass. One explanation might be the generation of reactive oxygen species during the period without flow in the pulmonary artery. The aim of the current study was to investigate if treatment with antioxidants could improve pulmonary endothelial function after cardiopulmonary bypass and influence the blood oxidative status. DESIGN: A prospective, randomized, double-blind study. SETTING: The operating room, intensive care unit, and the biochemistry laboratory in University Hospitals. PARTICIPANTS: Patients scheduled for cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: Treatment with vitamin E, vitamin C, allopurinol, and acetylcysteine (n = 12) or placebo (n = 10). MEASUREMENTS AND MAIN RESULTS: The pulmonary reactivity to an infusion of acetylcholine and markers of oxidative stress in blood were measured before and after cardiopulmonary bypass. Sixteen control patients received saline instead of acetylcholine. Before surgery the pulmonary vascular resistance index decreased during infusion of acetylcholine by 24% and 21% in the treatment and placebo groups. After surgery the decrease was 20% and 8%, respectively, (p = 0.422 and p = 0.026) compared with preoperative response. Pulmonary vasodilation induced by acetylcholine was better maintained in the group treated with antioxidants (p = 0.048). In the treatment group, the blood concentrations of early intermediates of lipid peroxidation were higher, but not that of the end products. Glutathione and oxidized glutathione increased after cardiopulmonary bypass in the treatment group. CONCLUSION: The better maintained endothelium-dependent vasodilation after cardiopulmonary bypass in the treatment group indicated that antioxidant therapy reduced endothelial dysfunction.
Subject(s)
Antioxidants/therapeutic use , Cardiopulmonary Bypass , Endothelium, Vascular/drug effects , Endothelium, Vascular/physiopathology , Lung/blood supply , Lung/physiopathology , Acetylcholine/therapeutic use , Aged , Aged, 80 and over , Double-Blind Method , Female , Glutathione Disulfide/blood , Humans , Infusions, Intra-Arterial , Lipid Peroxidation/drug effects , Male , Middle Aged , Prospective Studies , Pulmonary Artery/drug effects , Pulmonary Artery/physiopathology , Pulmonary Circulation/drug effects , Pulmonary Wedge Pressure/drug effects , Treatment Outcome , Vascular Resistance/drug effects , Vasodilation/drug effects , Vasodilator Agents/therapeutic useABSTRACT
Direct measurements of endogenous nitric oxide (NO) release is of great interest but difficult to perform in vivo. We hypothesized that endogenous NO release from vasoactive substances would be detectable in exhaled air. Exhaled NO was measured after intravenous injections of various endothelium-dependent and endothelium-independent vasoactive drugs, in anesthetized pigs and humans. In pigs, a dose-dependent release of exhaled NO was observed for acetylcholine (ACh), bradykinin, substance P, endothelin (ET)-1, and nitroglycerine. Each compound had an individual and highly reproducible release pattern. Bradykinin-induced NO release was enhanced by angiotensin converting enzyme inhibition. ET receptor antagonism markedly reduced the response in exhaled NO to ET-1, whereas atropin abolished the NO response to ACh. NO synthase inhibition abolished basal levels of exhaled NO as well as the responses in exhaled NO to all compounds except nitroglycerine. In humans, ACh evoked a dose-dependent increase of NO levels in exhaled air. NO release by endogenous vasoactive agonists can be measured online in the exhaled air of pigs and humans. These novel findings may be useful when characterizing NO release from compounds that interfere with NO synthesis or drugs that act as donors of NO. Moreover, the possibility of using exhaled NO as an indicator of pulmonary endothelial dysfunction merits further studies.
