Nitroglycerin-induced hypoxemia does not produce myocardial ischemia.

OBJECTIVE: Nitroglycerin has been the drug of choice for relieving myocardial ischemia for more than a hundred years. Several studies have indicated that a significant reduction in arterial oxygen tension (PaO2) occurs after the administration of sublingual nitroglycerin to patients with coronary artery disease breathing room air. Because available oxygen in arterial blood is reduced, it would be reasonable to assume that oxygen delivery to the myocardium would also be impaired. The purpose of this study was to investigate whether nitroglycerin-induced arterial desaturation results in compromised oxidative metabolism of myocardium assessed by coronary sinus lactate concentration and oxygen content in patients with coronary artery disease undergoing coronary artery bypass surgery. PARTICIPANTS: Ten randomly selected patients undergoing coronary bypass surgery. SETTING: All studies were performed at Siyami Ersek Cardiovascular and Thoracic Surgery Center. METHODS: A catheter was inserted into the radial artery to measure blood gases and arterial lactate concentration. After sternotomy, and aortic and venous cannula placement, a coronary sinus catheter was introduced into the coronary sinus to measure oxygen content and lactate concentration. Control coronary sinus and arterial blood samples were obtained before nitroglycerin infusion. Nitroglycerin was then given in a dose of 2 micrograms/kg/min for a period of 5 minutes. At the end of 5 minutes, second samples were obtained from the coronary sinus and arterial catheters. MAIN RESULTS: It was found that arterial and coronary sinus oxygen tension decreased significantly. Arterial lactate concentration did not change, coronary sinus lactate concentration decreased. Despite a substantial fall in arterial oxygen tension after administration of nitroglycerin, a significant reduction in coronary sinus lactate concentration occurred. CONCLUSION: Nitroglycerin-induced hypoxia does not compromise oxidative metabolism of myocardium as can be assessed by a concomitant decrease in coronary sinus lactate concentration.

Effects of hypothermia on blood endogenous endotoxin levels during cardiopulmonary bypass.

Endotoxin activates white blood cells and complement and produces a spectrum of clinical syndromes ranging from fever to septic shock. Although production of endogenous endotoxemia during cardiopulmonary bypass (CPB) has recently been reported, the role of hypothermia on endotoxemia is not clear. In this study, we evaluated the effects of moderate (24-28 degrees C) and mild (32-34 degrees C) hypothermia on blood endotoxin levels. The study population consisted of 20 patients who underwent coronary artery bypass grafting (CABG) with CPB. Moderate systemic hypothermia was applied during aortic cross-clamping in ten patients (group 1) and mild hypothermia in the remaining ten patients (group 2). The mean rectal temperatures were 26.8 +/- 1.2 degrees C in group 1 and 33.8 +/- 0.8 degrees C in group 2. The blood samples for endotoxin level measurements were obtained before CPB, during aortic cross-clamping, immediately after the release of the cross-clamp, 20 minutes after the release of the cross-clamp, after CPB, and 2 hours postoperatively. There were no endotoxins in any of the samples before CPB, but it was detected after CPB in both groups. The endotoxin levels were significantly higher in group 1 than in group 2. The present study suggests that when hypothermia is the technique of choice, the deleterious effects of endotoxemia on patients with comorbidity must be considered.

Interaction of right and left ventricular filling pressures at the termination of cardiopulmonary bypass. Central venous pressure/pulmonary capillary wedge pressure ratio.

In 50 patients who underwent coronary bypass grafting, the interaction of left- and right-sided filling pressures were prospectively evaluated to determine whether restoration and/or maintainance of a normal central venous pressure/pulmonary capillary wedge pressure (CVP/PCWP) ratio could improve biventricular performance. In 40 patients, the CVP/PCWP ratio was normal (less than 1) and termination of cardiopulmonary bypass was uneventful. In 10 patients, during loading at the termination of extracorporeal circulation, CVP exceeded PCWP and the ratio was reversed (less than 1). Cardiac index and systolic arterial pressure were low. Restoration of normal ratio by emptying the right heart helped in the improvement of systolic arterial pressure and cardiac index. Thus, in the presence of reversed CVP/PCWP ratio at the termination of cardiopulmonary bypass, restoration of the ratio may prevent unnecessary pharmacologic and/or mechanical intervention, such as inotropic agents, balloon pumps, or assist devices.

Scavenging of cardioplegic solution from right heart to prevent hyperkalemia.

The present study was designed to test the hypothesis that hyperkalemia can be prevented if the cardioplegic solution returning to the right heart from the coronary sinus is aspirated. In the control group (15 patients without aspiration), the potassium concentration rose from 3.5 +/- 1 (SD) mEq/L to 6.3 +/- 0.4 mEq/L (p less than 0.001) 10 minutes after the administration of cardioplegic solution and was still high before the patient was weaned from cardiopulmonary bypass (5.2 +/- 0.3 mEq/L (p less than 0.001). Electromechanical recovery time was delayed. In the second group (15 patients with aspiration), serum potassium did not change. Our data indicate that scavenging of cardioplegic solution may prevent hyperkalemia in most patients.

Bolus intravenous nitroglycerin for ST-segment depression not associated with increased myocardial oxygen demand.

Ischaemic ST-segment changes may occur in patients with coronary artery disease when myocardial oxygen consumption is increased as a result of hypertension, tachycardia or increased contractility. Ischaemia can also occur as the result of decreased coronary perfusion pressure caused by hypotension or coronary artery spasm. We report ST-segment depression in the absence of hypertension, tachycardia or hypotension. The response to bolus intravenous nitroglycerin suggested coronary artery spasm as the cause.

Arterial hypoxaemia following premedication in patients with coronary artery disease.

The effect of premedication with morphine and scopolamine, morphine alone, and scopolamine alone on arterial oxygen tension has been studied in patients with coronary artery disease undergoing bypass operations. Control arterial blood samples were obtained with the patients in the supine position breathing room air the day before operation. A second arterial blood sample was taken in the induction room with the patient breathing room air in the supine position. In the first group (scopolamine only) and second group (morphine only) cH+ (pH), PaCO2 and PaO2 did not change. In the third group (morphine and scopolamine), however, PaO2 decreased, while PaCO2 and cH+ increased (pH decreased). The changes in cH+ and PaCO2 were statistically significant, but of no clinical importance. The present study suggests that, when morphine and scopolamine premedication is used for patients with coronary artery disease, simultaneous administration of oxygen is important in helping to eliminate a possible cause of preoperative myocardial ischaemia.

Mechanism of nitroglycerin-induced hypoxemia.

We and others have previously demonstrated a consistent significant decline in arterial oxygen tension (PaO2) after sublingual nitroglycerin in premedicated and unpremedicated patients both with and without coronary artery disease and/or obstructive ventilatory disease. Thus, in our 19 patients, PaO2 fell by an average of 17% (12 mm Hg), mean systemic arterial pressure by 19% (17 mm Hg), pulmonary arterial pressure by 38% (6 mm Hg), pulmonary arterial occlusive pressure by 62% (5.3 mm Hg), and cardiac index by 16% (0.37 liter/min/m2) [P less than 0.001 for each] after nitroglycerin. Previous experimental studies suggest that the mechanism for the reduction of PaO2 may be relief of hypoxic pulmonary vasoconstriction with an increase in perfusion to poorly ventilated or nonventilated regions of the lungs. To examine this possibility, pulmonary vasodilatation was precluded by administration of a pulmonary vasoconstrictor (phenylephrine) simultaneously with nitroglycerin in nine patients with coronary artery disease. No significant change was observed in systemic or pulmonary arterial pressure, pulmonary arterial occlusive pressure, or systemic and pulmonary vascular resistance, and PaO2 did not decline. In ten other patients with coronary artery disease, the intrapulmonary right-to-left shunt fraction was determined before and after sublingual nitroglycerin; only a minimal increase in shunt fraction of 1.4% was observed, quantitatively insufficient to account for the observed decline in PaO2, thus excluding a predominant effect of nitroglycerin on nonventilated alveoli as a cause of the hypoxemia. We conclude that the reduction of PaO2 after nitroglycerin administration is attributable to pulmonary vasodilatation with a relative increase in perfusion of poorly ventilated lung units.