BACKGROUND AND HYPOTHESIS: Carbon dioxide is currently used as an arterial and venous contrast agent; however, little is known of its effects on left ventricular function. This study was undertaken to investigate those effects. METHODS: Ascending doses of 5, 10, and 20 ml of carbon dioxide were administered into the left main coronary artery of domestic swine with and without a continuous infusion of intravenous nitroglycerin (50 micrograms/min). RESULTS: Carbon dioxide had an immediate and profound depressant effect on both systolic and diastolic left ventricular function associated with ischemic electrocardiographic changes. Compared with controls (% change), ascending doses of carbon dioxide decreased systolic pressure by -35 +/- 7, -48 +/- 8, and -53 +/- 4 in the absence of nitroglycerin, and by -32 +/- 9, -50 +/- 9, and -60 +/- 9 in the presence of nitroglycerin. Peak+dP/dt decreased by -54 +/- 7, -61 +/- 11, and -64 +/- 3 in the absence of nitroglycerin, and by -36 +/- 13, -55 +/- 11, and -65 +/- 11 in the presence of nitroglycerin. Minimum -dP/dt increased by 65 +/- 8,71 +/- 8, and 77 +/- 3 in the absence of nitroglycerin, and by 63 +/- 7,71 +/- 8, and 78 +/- 7 in the presence of nitroglycerin. No significant changes in heart rate were observed; however, widespread ST-segment elevation was observed in all animals. Coronary angiography following carbon dioxide injection revealed a marked decrease in coronary flow velocity until the gas was cleared from the microcirculation. This was also documented by direct measurement of flow velocity using a Doppler catheter in an additional animal. Left ventriculography demonstrated immediate global dilation and depression of systolic function. CONCLUSIONS: In the swine model, relatively small doses of intracoronary carbon dioxide cause profound yet reversible global left ventricular dysfunction which appears to be ischemic in origin.
BACKGROUND AND HYPOTHESIS: Carbon dioxide is currently used as an arterial and venous contrast agent; however, little is known of its effects on left ventricular function. This study was undertaken to investigate those effects. METHODS: Ascending doses of 5, 10, and 20 ml of carbon dioxide were administered into the left main coronary artery of domestic swine with and without a continuous infusion of intravenous nitroglycerin (50 micrograms/min). RESULTS:Carbon dioxide had an immediate and profound depressant effect on both systolic and diastolic left ventricular function associated with ischemic electrocardiographic changes. Compared with controls (% change), ascending doses of carbon dioxide decreased systolic pressure by -35 +/- 7, -48 +/- 8, and -53 +/- 4 in the absence of nitroglycerin, and by -32 +/- 9, -50 +/- 9, and -60 +/- 9 in the presence of nitroglycerin. Peak+dP/dt decreased by -54 +/- 7, -61 +/- 11, and -64 +/- 3 in the absence of nitroglycerin, and by -36 +/- 13, -55 +/- 11, and -65 +/- 11 in the presence of nitroglycerin. Minimum -dP/dt increased by 65 +/- 8,71 +/- 8, and 77 +/- 3 in the absence of nitroglycerin, and by 63 +/- 7,71 +/- 8, and 78 +/- 7 in the presence of nitroglycerin. No significant changes in heart rate were observed; however, widespread ST-segment elevation was observed in all animals. Coronary angiography following carbon dioxide injection revealed a marked decrease in coronary flow velocity until the gas was cleared from the microcirculation. This was also documented by direct measurement of flow velocity using a Doppler catheter in an additional animal. Left ventriculography demonstrated immediate global dilation and depression of systolic function. CONCLUSIONS: In the swine model, relatively small doses of intracoronary carbon dioxide cause profound yet reversible global left ventricular dysfunction which appears to be ischemic in origin.