Arterial pressure-flow relationship in patients undergoing cardiopulmonary bypass.

We determined the arterial pressure-flow relationship experimentally by means of step changes of blood flow in 30 adult patients undergoing cardiopulmonary bypass (CPB). Anesthesia technique was uniform. CPB was nonpulsatile; hypothermia to 25-28 degrees C, and hemodilution to 18%-25% hematocrit were used. During stable bypass, mean arterial pressure was recorded first with blood flow 2.2 L.min-1.m-2. Flow was then increased to 2.9 L.min-1.m-2 for 10 s and reverted to baseline for 1 min. Then it was decreased to 1.45 L.min-1.m-2 for 10 s, and reverted to baseline for 1 min. Subsequently, it was decreased to 0.73 L.min-1.m-2 for 10 s and then reverted to baseline. Similar sets of measurements were repeated after 0.25 mg of phenylephrine and once the patient was rewarmed. The pressure-flow function was individually determined by regression, and the critical pressure estimated by extrapolation to zero flow. All patients had zero-flow critical pressure during hypothermia, with a mean value of 21.8 +/- 6.4 mm Hg (range 8.8-38.9). It increased after 0.25 mg phenylephrine to 25.4 +/- 7.2 mm Hg (range 12.2-43.9, P < 0.001). During normothermia, critical pressure was 21.2 +/- 5 mm Hg (range 13.4-30.9), not significantly different from hypothermia. During hypothermia, the slope of the pressure-flow function (i.e., resistance) was 14.9 +/- 3.5 mm Hg.L-1.min-1.m-2 (range 7.6-22.1). It increased significantly (P < 0.001) after phenylephrine, to 19.7 +/- 6.2 mm Hg.L-1.min-1.m-2 (range 11.4-40.5), and returned to 15.4 +/- 3.4 mm Hg.L-1.min-1.m-2 (range 10.1-24.2) during normothermic bypass. Systemic vascular resistance appeared to vary reciprocally with blood flow, although this finding may represent a mathematical artifact, which can be avoided by using zero-flow critical pressure in the vascular resistance equation.

Cardiac mechanical energy and effects on the arterial tree.

Blood flow pulsatility is the result of the heart's activity as a pump unable to develop steady flow, and its interaction with the arterial tree. Thus, the heart is a cyclic energy generator whose adequate function requires the two phases of this cycle to be normal. Diastolic properties determine the degree of filling of the ventricles and the strength of the following systole. Systole, in turn, must generate enough energy to overcome forces opposing ejection. These can be divided into internal (the mechanical characteristics of the ventricle itself) and external loads (the characteristics of the arterial tree). As a result, hydraulic energy is imparted to blood (external ventricular work) that manifests itself as blood pressure and flow. Given the cyclic nature of cardiac activity, the external ventricular work has steady and pulsatile components. The steady component is energy lost during steady flow because of vascular resistance, and the pulsatile work is that lost in arterial pulsations and mainly depends on the aortic impedance. Thus, the characteristics of the arterial tree will determine the relative contribution of these two components to blood flow and the efficency of the heart. In addition, the arterial tree modifies the different waves (pressure and flow) traveling in the circulation. These modifications have important consequences for cardiac function. The ventricle and the arterial tree constitute a coupled biological system, and its overall performance is a function of the behavior of each unit at any given moment.

Thermoregulatory vasoconstriction increases the difference between femoral and radial arterial pressures.

OBJECTIVE: Thermoregulatory vasoconstriction locally increases arterial wall tension and arteriolar resistance, thereby altering physical properties of the arteries. The arterial pressure waveform is an oscillatory phenomenon related to those physical characteristics; accordingly, we studied the effects of thermoregulatory vasomotion on central and distal arterial pressures, using three hydraulic coupling systems having different dynamic responses. METHODS: We studied 7 healthy volunteers. Central arterial pressure was measured from the femoral artery and distal pressure was measured from the radial artery, using 10.8-cm long, 20-gauge catheters. Three hydraulic coupling systems were used: (1) a 10-cm-long, 2-mm internal diameter connector; (2) a 150-cm-long, 1-mm internal diameter connector (Combidyn 520-5689, B. Braun, Melsungen, Germany); (3) a 180-cm long, 2-mm internal diameter connector (Medex MX564 and MX562, Medex Inc., Hillard, OH). Brachial artery pressure was measured oscillometrically. Core temperature was measured at the tympanic membrane. The vasomotor index, defined as finger temperature minus room temperature, divided by core temperature minus room temperature, was used to estimate the degree of vasoconstriction. Constriction was considered near maximal when the index was less than 0.1, and minimal when it exceeded 0.75. Measurements were taken every 3 min. Baseline readings were obtained when subjects were warm. They then were cooled by exposure to 20 degrees C to 22 degrees C room air and a circulating-water mattress set at 4 degrees C until index was less than 0.1. They then were rewarmed by increasing water temperature to 42 degrees C and adding a forced-air warmer until the vasomotor index exceeded 0.75. Data were analyzed by ANOVA and linear regression. RESULTS: Thermoregulatory vasoconstriction was associated with marked arterial pressure waveform changes. Radial pressure showed, in lieu of a dicrotic notch, large oscillations of decreasing amplitude. Femoral pressure showed a single diastolic oscillation of smaller amplitude. The waveforms appeared different, depending on the hydraulic coupling system used, artifact being more marked with the longer connectors. On the average, radial systolic pressure exceeded femoral systolic pressure during vasoconstriction; however, during vasodilatation, femoral systolic pressure exceeded radial systolic pressure (p < 0.05). Oscillometric measurements underestimated systolic pressure, and did so more markedly during vasoconstriction. There were no differences in the values of mean and diastolic pressures. CONCLUSION: Thermoregulatory vasoconstriction alters radial arterial pressure waveform, artifactually increasing its peak systolic pressure compared with the femoral artery. Poor dynamic responses of recording systems further distort the waveforms. Consequently, radial artery pressure may be misleading in vasoconstricted patients.