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This study was designed to assess the independent effects of stroke volume and heart rate on the phases of systole and other selected hemodynamic parameters. By means of the pressure gradient technique instantaneous blood pressure and flow were recorded in the ascending aorta at fixed ventricular rates in five patients with complete heart block and in four patients with atrio-ventricular dissociation induced by ventricular pacing. Because of the variable contribution of atrial systole to ventricular filling, a wide range of stroke volumes were observed at each heart rate. The results indicate that the duration of ejection bears a close direct linear relationship to stroke volume while heart rate has only a weak but independent relation. On the other hand, the duration of total systole is related chiefly to the heart rate but stroke volume exerts an important independent effect. In a given patient, both duration of ejection and pulse pressure reflect changes of stroke volume and the product of the duration of ejection and the pulse pressure shows a good correlation with the stroke volume.

Internal carotid artery blood flow and arterial pressure were measured with a sine-wave electromagnetic flowmeter and a pressure transducer in 22 patients during control period and after the intravenous and intracarotid administration of norepinephrine, epinephrine, and angiotensin. Intravenous infusion of both norepinephrine and angiotensin was accompanied by an increase in cerebral vascular resistance. Administration of norepinephrine, epinephrine, and angiotensin into the internal carotid artery failed to alter blood flow immediately. However, when the systemic blood pressure increased, a concomitant passive rise in blood flow did not occur. Thus, at this time cerebral vascular resistance was significantly increased. It is concluded that these drugs do not have a direct action on the cerebral vessels, but that the increased cerebral vascular resistance after their administration is due to autoregulation or to a combination of autoregulation and reduced arterial carbon dioxide pressure (P(CO2)) secondary to hyperventilation. Similar studies were carried out in the external carotid artery of six patients. Within 10 sec after injection blood flow was markedly reduced, indicating a direct vasoconstricting action on this vascular bed.

Pressure-flow measurements were obtained from the vein graft of 57 patients undergoing a single aorta-to-coronary bypass procedure. The flow contour was similar to phasic left coronary artery flow in dogs except for a transient increase during systole possibly related to elongation of the graft. Flow was highest during bypass and decreased to a stable value 30 min after bypass. In 42 patients, flow at this time was 35+/-2 cm(3)/min (mean+/-sem).NO CORRELATIONS WERE DEMONSTRATED BETWEEN FLOW AND THE FOLLOWING: left vs. right grafts, presence or absence of collaterals, total vs. partial block, or the presence or absence of ventricular dyskinesis. In 32 patients, no correlation between these anatomic findings and the presence of reactive hyperemia was demonstrated. In 17 patients, occlusion of the graft for 10 sec resulted in a mean 51.5% flow debt repayment. In nine patients, injection of 0.3 mug of isoproterenol into the graft increased flow from 45+/-6 to 69+/-9 cm(3)/min within 4-7 sec without changes in rate, pressure, time derivative of left ventricular pressure (LV dp/dt), or left ventricular end diastolic pressure (LVEDP). Maximum increases to 87+/-10 cm(3)/min occurred 12-20 sec after injection with concomitant changes in these parameters. Intravenous infusion of norepinephrine did not change vascular resistance, whereas phenylephrine did. In six patients, injection of 0.2 mug of norepinephrine into the graft decreased flow from 49+/-6 to 25+/-5 cm(3)/min within 5-8 sec. Intravenous infusion of 0.15 mg of nitroglycerin decreased coronary vascular resistance from 2.7+/-0.4 to 2.3+/-0.3 mm Hg/cm(3) per min. In five patients, 0.12 mg of nitroglycerin injected into the graft increased flow from 46+/-7 to 71+/-13 cm(3)/min and lasted 20-40 sec.

The pressure-diameter relationship in the main pulmonary artery of man was estimated in 11 patients undergoing open-heart surgery. The diameter was measured with a recording caliper sutured to the vessel wall. The lateral intravascular pressure was measured with a 20-gauge needle connected directly to a Statham P23Db strain gauge. In the eight patients with normal pulmonary artery pressure the results indicate: 1) the shapes of the pressure and diameter curves are similar; 2) the mean value for the ratio of change in radius to change in pressure (ΔR/ΔP) x 103 was 8.77 cm/cm H2O (±sd 2.10); 3) the mean value for the pressure-strain elastic modulus (Ep) was 159.0 g/cm2 (±sd 26.0); and 4) the mean change in cross-sectional area during an average cardiac cycle was 22.9% of the diastolic value. In three patients with pulmonary hypertension the value of both ΔR/ΔP and the pressure-strain elastic modulus was lower.