Effect of Cigarette Smoking and Breathing Carbon Monoxide on Cardiovascular Hemodynamics in Anginal Patients

Open Access
Publisher Website
Google Scholar
Abstract
Smoking high-nicotine cigarettes caused a significant increase in systolic and diastolic arterial pressure, heart rate, left ventricular end-diastolic pressure, and coronary sinus, arterial, and venous CO levels, no significant change in left ventricular dp/dt, aortic systolic ejection period, and cardiac index, and a significant decrease in stroke index and coronary sinus, arterial, and venous PO2 levels in eight anginal patients with documented coronary disease. One week later, these patients inhaled 150 ppm of carbon monoxide until their increase in coronary sinus CO was similar to that produced after smoking their third cigarette. Inhaling carbon monoxide caused a significant increase in left ventricular end-diastolic pressure and coronary sinus, arterial, and venous CO levels, no significant change in systolic and diastolic arterial pressure, heart rate, and systolic ejection period, and a significant decrease in left ventricular dp/dt, stroke index, cardiac index, and coronary sinus, arterial, and venous PO2 levels. Nicotine caused the increased systolic and diastolic arterial pressure and heart rate after smoking. Carbon monoxide caused the negative inotropic effect which increased the left ventricular end-diastolic pressure and decreased the stroke index after smoking.