Mark J. Morton

Hemodynamic changes in pregnancy

The basic mechanisms that underlie alterations in the physiology of pregnancy are virtually unknown. Basal oxygen consumption increases by some 50 mL/min in pregnant women at term. Blood volume increases gradually over gestation as does red cell mass. Cardiac output increases by some 50% by mid-third trimester. Stroke volume and heart rate increase over the course of pregnancy with heart rate increasing gradually until term. The heart of the pregnant woman remodels dramatically in the first few weeks of pregnancy; end diastolic volume increases. Stroke volume is augmented by the increase in end diastolic volume and maintenance of ejection fraction through a possible increase in contractile force. Systolic and diastolic blood pressures drop during normal pregnancy. There is evidence of blood vessel remodeling in all vessels. Venous compliance and venous blood volume are increased. Renal plasma flow increases by some 70% in pregnancy with glomerular filtration rate increasing by 50% by unknown mechanisms. The complex hormonal environment is changing throughout pregnancy. In summary, under the influence of circulating chemical mediators blood flow is redistributed to the uterus, breast, and kidney.

Aortic function during normal human pregnancy

Arterial rupture and dissection have been observed in both normal and complicated pregnancies. To understand how arterial mechanical properties might change during pregnancy, we measured aortic root diameter by M-mode echocardiography and obtained simultaneous cuff blood pressures during systole and diastole at rest and during isometric exercise. Measurements were obtained in 19 women at the end of normal gestation and again 3 to 6 months post partum. The aorta is larger and more compliant during normal human pregnancy, and these changes may not revert to prepregnant levels post partum. Increased aortic compliance, combined with decreased vascular resistance, may enhance left ventricular performance in normal pregnancy. Conversely, the presumed structural alterations leading to increased compliance may weaken diseased vessels leading to dissection or rupture during pregnancy.

Fetal lamb ventricles respond differently to filling and arterial pressures and to in utero ventilation

ABSTRACT. Right and left ventricular function were investigated in 12 fetal lambs (127-140 days gestation) instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery, and with vascular catheters. Nine fetuses were equipped with a postductal aortic occluder and the trachea was cannulated in eight. Control arterial blood values were pH 7.36 ± 0.02 (SD), PCO2 49.3 ± 2.3 torr, PO2 18.4 ± 1.7 torr, and hematoerit 37.3 ± 4.4%. Biventricular function curves relating stroke volume to mean right and left atrial pressure were generated by rapid withdrawal and reinfusion of fetal blood. Both function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Stroke volumes at the breakpoints were 0.94 ± 0.19 ml · kg-1and 0.63 ± 0.15 ml · kg-1 for right and left ventricle, respectively (p<0.001). During postductal aortic occlusion, arterial pressure increased by 19.3 ± 7.9 torr while right ventricular stroke volume decreased by ∼48% and left ventricular stroke volume decreased by ∼9%. In utero ventilation increased arterial pressure, heart rate, PO2, and oxygen content. Right atrial pressure increased from 3.9 ± 1.3 to 5.8 ± 2.9 torr (p<0.05); left atrial pressure from 3.5 ± 1.5 to 10.0 ± 4.4 torr (p<0.05). Aortic now nearly doubled (112 ± 29 to 211 ± 3 5 ml · min-1 · kg-1) (p < 0.05), and the left ventricular function curve shifted upward. The right ventricular function curve was shifted downward during ventilation. We conclude that the fetal ventricles differ significantly in their outputs, response to changes in arterial pressure, and to the onset of in utero ventilation.

Indicator amount, temperature, and intrinsic cardiac output affect thermodilution cardiac output accuracy and reproducibility

ObjectiveTo determine the accuracy and reproducibility of four thermodilution indicators (5-mL room temperature, 10-mL room temperature, 5-mL iced, and 10-mL iced injectates) at clinically relevant flow rates. DesignQuasi-experimental study. SettingAnimal research laboratory of a health sciences university. SubjectsSix virgin western-breed ewes. InterventionsData were collected from six ewes that had ascending aorta electromagnetic flow probes and inferior vena cava occluders. Cardiac output was manipulated by inferior vena cava occlusion and isoproterenol infusion. Four thermodilution indicators were tested at high and low levels of cardiac output and compared with the electromagnetic flowmeter measurements of cardiac output. Measurements and Main ResultsThe indicator amounts were determined from both injectate volume and temperature difference between the injectate and blood. Using 5-mL room temperature injectate as a reference, 10-mL room contained 2 x, 5-mL iced 2.1 x, and 10-mL iced 4.1 x the indicator amount of 5-mL room temperature injectate. Approximately 210 simultaneous thermodilution and electromagnetic flow measurements were made for each injectate over a flow range of 1.5 to 15.7 L/min. For the entire cardiac output range, systematic error was not present. However, the r2 value (.92) for the 10-mL iced injectate group was greater (p < .05) than that value (.79) for the 5-mL iced injectate group, while r2 values were .79 for the 10-mL room temperature group and .49 for the 5-mL room temperature group. At flow rates of <4.7 L/min, r2 was not different among injectates, but reduced indicator amounts progress vely overestimated output (p < .05), reaching 21% for the 5-mL room temperature group. At flow rates of >7.7 L/min, the r2 value (.81) for the 10-mL iced group was greater (p < .05) than that value (.45) for the 5-mL iced group, while r2 values were .24 for the 10-mL room temperature group and .08 for the 5-mL room temperature group. Systematic error was not present. ConclusionsAt low cardiac output levels, reduced indicator impairs accuracy but not reproducibility, a phenomenon that is perhaps related to indicator loss. At high cardiac output rates, reduced indicator impairs reproducibility. This phenomenon is probably related to low signal-to-noise ratio. Thermodilution indicator amounts should be tailored to the output range. (Crit Care Med 1993; 21:586–597)

Abnormal exercise hemodynamics in cardiac allograft recipients 1 year after cardiac transplantation: relation to preload reserve

The well-established elevation in left ventricular filling pressures during exercise in patients after transplantation may contribute to decreased exercise tolerance. A proposed mechanism for this increase in filling pressures is an abnormal pressure-volume homeostasis of the transplanted heart. Twenty-three patients undergoing routine 1-year evaluations performed supine bicycle exercise during right heart catheterization. Within 24 hours, these patients underwent supine bicycle exercise to the identical work load during radionuclide ventriculography. For the group, resting hemodynamics and resting left and right ventricular ejection fractions were normal. With exercise, right atrial and pulmonary wedge pressure rose markedly (from 6 +/- 2 to 14 +/- 7 mm Hg, p less than 0.0001, and from 10 +/- 3 to 20 +/- 6 mm Hg, p less than 0.0001, respectively). Left ventricular ejection fraction increased appropriately with exercise (from 0.58 +/- 0.08 to 0.63 +/- 0.07, p = 0.004). End-diastolic volume also increased mildly (from 100 +/- 31 to 117 +/- 39 ml, p = 0.001), but change in end-diastolic volume was highly variable. Patients with little or no change in end-diastolic volume with exercise had the greatest resting and exercise left ventricular filling pressures resulting in significant negative correlations between filling pressures and change in end-diastolic volume (r = -0.64, p = 0.002 and r = -0.50, p = 0.025, respectively). Negative linear relations between exercise left ventricular filling pressures or resting heart rates and donor to recipient body weight ratio (r = -0.35, p = 0.10, and r = -0.37, p = 0.06, respectively) suggested that initial donor heart size influenced subsequent cardiac function.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise dynamics in late gestation: Effects of physical training

Heart rate and stroke volume were measured serially in subjects at rest in the sitting position and at the onset and end of a 6-minute period of upright bicycle exercise. Twenty-three subjects with normal pregnancy were studied in late gestation and again post partum. Rest and exercise cardiac outputs in late gestation were not different from those in the postpartum period. Heart rate was higher at rest and stroke volume lower during exercise in late gestation than post partum. At the end of exercise, stroke volume fell dramatically in late gestation but not post partum. Ten women prospectively identified as physically fit had responses that were not different from those of the nonfit cohort in late gestation. Post partum, the physically fit women had exercise responses typical of trained persons and different from those of the nonfit cohort. In late gestation, rest and exercise hemodynamics in subjects in the sitting position appeared to be dominated by factors influencing venous return, independent of physical fitness.

Effects of estrogen and progestin on aortic size and compliance in postmenopausal women

OBJECTIVE Our purpose was to determine whether sex steroids alter aortic size and compliance in postmenopausal women. STUDY DESIGN Twenty-six postmenopausal women were randomized to receive either conjugated estrogens 0.625 mg per day (group 1) or conjugated estrogens 0.625 mg per day and medroxyprogesterone 2.5 mg per day (group 2). Aortic cross-sectional area was measured by magnetic resonance imaging before and after 3 months of hormone therapy. RESULTS Estradiol levels increased in both group 1 and group 2 (p < 0.0001). Ascending aortic cross-sectional area increased from 439 +/- 7 mm2 to 466 +/- 7 mm2 in group 1 (p < 0.008) but was unchanged in group 2. Within the range of aortic pressures studied, no change in aortic compliance could be detected. CONCLUSION Estrogen therapy in postmenopausal women was associated with an increase in aortic size; but this effect was not detectable with the addition of progestin. The potential antagonistic effect of progestin on estrogen-induced aortic enlargement suggests that the favorable cardiovascular effects of postmenopausal estrogen therapy cannot be automatically extended to the combination estrogen-progestin.

Arteriovenous fistula: A rare complication of arterial puncture for cardiac catheterization

Abstract Arteriovenous (A-V) fistula is a rare complication of cardiac catheterization, 1–5 occurring in 0.01 to 0.02% of cases. 2,3 This report reviews the course of 5 patients who developed A-V fistulas.

Mild pressure loading alters right ventricular function in fetal sheep.

Right ventricular function before and during 10 days of mild pressure loading (10 mm Hg increase in mean pulmonary arterial pressure) was compared with right ventricular function in unloaded near-term fetal sheep. Pressure loading did not alter fetal arterial blood gases or vascular pressures. The right ventricular function curve (stroke volume versus mean right atrial pressure) was not significantly altered by loading. However, the relation between right ventricular stroke volume and increased arterial pressure was dramatically shifted upward, indicating improved ventricular function after the 10-day loading period. Normalized free wall of the loaded right ventricles became thicker (1.2 +/- 0.2 versus 0.9 +/- 0.2 mm/kg, p less than 0.01) and heavier (2.7 +/- 0.4 g/kg versus 2.2 +/- 0.4 g/kg, p less than 0.05) than control, and the ratio of the equatorial radius of curvature to wall thickness decreased (3.2 +/- 0.5 versus 4.5 +/- 0.9, p less than 0.005). Left ventricular free wall and septal weights and thicknesses were not significantly changed. The in vitro diastolic pressure-volume curves of both ventricular chambers of loaded hearts shifted to the left, indicating smaller ventricles than controls at physiological filling pressures. These data suggest the transduction of right ventricular loading effects to the left ventricle. Improved right ventricular function after loading is predicted by the law of Laplace based on the decreased radius of curvature-to-wall thickness ratio.

Cardiac size and function in pregnancy-induced hypertension.

The physiologic cardiac enlargement characteristic of normal pregnancy could result in important left ventricular dysfunction in the presence of elevated blood pressure. Using M-mode echocardiography, we measured left ventricular dimensions, fractional shortening, and radius-to-wall thickness ratio in 23 patients who had a diagnosis of pregnancy-induced hypertension at rest and during isometric exercise. Seventeen subjects with normal pregnancies were similarly studied and served as controls. The average gestation of patients with pregnancy-induced hypertension was 38 +/- 2 weeks, and that of control subjects was 37 +/- 1 weeks. The average age was 25 +/- 5 years for patients with pregnancy-induced hypertension, and that for control subjects was 29 +/- 4 years. The patients with pregnancy-induced hypertension did not show the normal eccentric cardiac enlargement observed during pregnancy; the average radius-to-wall thickness ratio was reduced in patients with pregnancy-induced hypertension. Fractional shortening, a reflection of ventricular performance, was maintained both at rest and during exercise in the hypertensive group. One patient, who did not show a reduced radius-to-wall thickness ratio, had marked reduction of left ventricular performance in the presence of severe pregnancy-induced hypertension. Left ventricular performance in most subjects with pregnancy-induced hypertension is normal. Preservation of left ventricular performance despite increased arterial pressure may be related to the absence of eccentric gestational cardiac enlargement.