Little Change In Stroke Volume Research Articles

Role of cardiac sympathetic nerves in preventing orthostatic hypotension in Parkinson's disease

PurposeCardiac sympathetic denervation is associated with orthostatic hypotension (OH) in Parkinson's disease (PD); however, the physiological role of cardiac sympathetic nerves has yet to be elucidated. To clarify the role of the heart in orthostatic stress, we evaluated whether cardiac sympathetic nerves can alter cardiac activity and systolic blood pressure (BP) in association with elevations or depressions of total peripheral resistance during the head-up tilt test. MethodsNinety-five PD patients and 17 normal controls were enrolled. Using impedance cardiography, we measured total peripheral resistance, stroke volume, heart rate, and systolic BP during the head-up tilt test. Cardiac denervation was defined as a heart-to-mediastinum ratio <1.7 for cardiac 123I-metaiodobenzylguanidine uptake on delayed images. ResultsAt 60° tilt, total peripheral resistance decreased from the initial value in 49 PD patients. Among these, 36 patients exhibited cardiac denervation with severe reductions in systolic BP but little change in stroke volume; among these patients 22 had OH. The remaining 13 patients without cardiac denervation exhibited significant increases in stroke volume and well-preserved systolic BP with no OH. On the other hand, 46 patients had elevations in total peripheral resistance and reduced stroke volume, but little change in systolic BP, regardless of the presence or absence of cardiac denervation. Only one of these patients experienced OH. ConclusionUnder orthostatic stress, cardiac sympathetic denervation with failure to increase total peripheral resistance leads to large reductions in systolic BP. However, patients without cardiac denervation exhibited a positive inotropic response against vasodilatation, which may prevent OH.

Stroke Volume Dynamics During Progressive Exercise in Healthy Adolescents

Understanding cardiac responses to exercise in healthy subjects is important in the evaluation of youth with heart disease. This review article incorporates previously published original research from the authors' laboratory to examine changes in stroke volume during progressive exercise which are consistent with a model in which circulatory responses are controlled by alterations in the systemic vascular resistance. Stroke volume dynamics and cardiovascular responses to a progressive upright cycle test were examined in three groups of healthy, untrained adolescent subjects. These indicated a) a progressive decease in systemic vascular resistance, b) little change in stroke volume after an initial rise related to orthostatic changes in ventricular refilling, c) evidence of a constant or slightly declining left ventricular end diastolic filling pressure, d) and increases in markers of ventricular contractility. These observations are consistent with peripheral (vascular resistance) rather than central (cardiac) control of circulation with exercise. Changes in stroke volume during exercise need to be interpreted in respect to alterations in heart rate and myocardial functional capacity.

Theoretical analysis of the relationship between the ratio of ventricular systolic elastance to diastolic stiffness and stroke volume.

The maintenance of adequate blood circulation requires a sufficient ventricular contractility; in addition, to eject blood, the ventricles must first receive a sufficient volume, requiring a low diastolic stiffness. A simplified cardiovascular model was used to derive formulae for stroke volume (SV) as a function of atrial pressure and the ratio of ventricular end-systolic elastance to end-diastolic stiffness. A more complex cardiovascular model was used to assess the ability of the expressions to predict stroke volume under various steady-state conditions. The predicted SV correlated linearly with the model SV over a wide range of diastolic stiffnesses and systolic elastance. The formulae predict that with fixed right atrial pressure the SV is proportional to the ratio of end-systolic elastance to end-diastolic stiffness (GR) for the right ventricle, but relatively insensitive to the ratio (GL) for the left ventricle provided that GL is greater than GR. Model simulations confirmed this. When the right atrial pressure was not fixed increases in GR with fixed GL reduced the right atrial pressure with little change in SV. Similarly, varying GL with fixed GR produced little change in SV. The ratios highlight the importance of diastole to cardiac function.

Pulmonary blood volume: analysis during exercise in patients with left ventricular dysfunction.

Recent reports have demonstrated substantial increases in pulmonary activity during radionuclide stress exercise studies in patients with coronary heart disease. These studies have shown that the degree of the increase reflected the severity of the underlying disease. We studied the effects of supine exercise on systolic function and pulmonary activity in ten normal control subjects and 20 patients with congestive cardiomyopathy (12 ischemic and 8 idiopathic). Ejection fraction rose in the normals (P less than 0.001), end-diastolic volume increased slightly but significantly (P less than 0.05), and pulmonary activity rose by less than 16%, (mean 10%) while cardiac output increased by 162%. On the other hand, the myopathy patients demonstrated a small increase in cardiac output, (+49%) with a more substantial increase in pulmonary activity (+25%, P less than 0.05 vs normals). In these patients, ejection fraction did not change during exercise, while end-diastolic and end-systolic volumes rose. In the myopathy patients, the cause for an increase in cardiac output was a rise in heart rate, with little change in stroke volume. We conclude that pulmonary activity rises in myopathy patients to a greater extent than in normal controls. This probably reflects the greater elevation in filling pressures these patients need to maintain forward cardiac output.

Effect of sublingual nitroglycerin on left ventricular function at rest and during spontaneous angina pectoris: Assessment with a radionuclide approach

Left ventricular function and size were assessed with equilibrium radionuclide angiography at rest and after administration of 0.6 mg of sublingual nitroglycerin in 12 patients with a history of previous myocardial infarction. Spontaneous angina developed in five patients and seven patients had no pain at the time of study. Sequential ejection fractions and end-diastolic and end-systolic volumes were developed by summing multiple R-R intervals to produce a composite time-activity curve. Volumes were calculated with a nongeometric method that utilizes counts at end-diastole and end-systole and is corrected for total heartbeats and plasma radioactivity. In the patients without acute ischemia, peak increase in ejection fraction occurred 6 to 8 minutes after ingestion of nitroglycerin and was associated with an equal decrease in end-diastolic and end-systolic volumes with no change in stroke volume. End-diastolic and end-systolic volumes, stroke volume, heart rate and systolic blood pressure all returned to baseline levels by 1 hour after nitroglycerin. In the patients with spontaneous angina, ejection fraction and stroke volume decreased before pain occurred. End-diastolic volume increased slightly (7 percent), but end-systolic volume increased markedly (38 percent), thus explaining the decrease in stroke volume. After nitroglycerin, end-diastolic volume and end-systolic volume and systolic blood pressure decreased and stroke volume and ejection fraction increased. Improvement in function occurred before relief of pain. It is concluded that the action of nitroglycerin on the left ventricle in patients without acute ischemia is to increase ejection fraction by an equal decrease in end-diastolic and end-systolic volumes with little change in stroke volume. A reduction in left ventricular function during acute ischemia precedes complaints of pain and is associated with an increase in end-systolic and end-diastolic volumes and a decrease in ejection fraction and stroke volume. In these patients, nitroglycerin appeared to contribute to relief of pain by decreasing end-diastolic volume and systolic blood pressure.

Variability in response to norepinephrine in acute myocardial infarction

Twenty-seven patients with acute myocardial infarction were studied by infusion of graded levels of norepinephrine at rates of 1 to 3, 3 to 5, 5 to 8 and 8 to 10 <i>μ</i>g/min. Twelve patients subsequently died of pump failure during hospitalization. Control levels of stroke work produced excellent separation between survivors and nonsurvivors. The magnitude of maximal stroke work response during norepinephrine infusion in the two groups was also significantly different, but did not further separate the groups. However, the maximal percent change in stroke work in the two groups was similar, thus suggesting that, even in the presence of large infarcts, the remaining viable myocardium remains responsive to inotropic agents. Qualitatively the response of survivors and nonsurvivors was similar at low dose rates, but at a rate of 8 to 10 <i>μ</i>g/min, survivors exhibited predominantly an increase in stroke volume with little change in peripheral vascular resistance, whereas nonsurvivors showed predominantly an increase in peripheral vascular resistance with little change in stroke volume. We conclude that the initial level of ventricular function determines both the nature and magnitude of response to inotropic agents in acute myocardial infarction. Clinically, the usefulness of norepinephrine in this disease may be limited, since patients most likely to receive the drug would be expected to respond with a small increase in flow and a significant increase in afterload.

Factors affecting arterial pressures and blood flow from the heart in intact, unrestrained lingcod, Ophiodon elongatus

1. 1. Increases in temperature resulted in large increases in heart rate but caused little change in stroke volume. Injections of atropine into the pericardial cavity caused an increase in heart rate, a decrease in stroke volume but little change in cardiac output. 2. 2. Injections of adrenaline into the dorsal aorta resulted in a rise in dorsal aortic blood pressure and a fall in heart rate and cardiac output. In the atropinized fish, adrenaline injections into the dorsal aorta caused a rise in dorsal aortic blood pressure, a fall in cardiac output but no change in heart rate. Blockade of α-adrenergic receptors with phenoxybenzamine abolished the circulatory changes associated with adrenaline injections. Addition of adrenaline to the water in which the fish was situated resulted in an increase in cardiac output and stroke volume, with little change in heart rate. 3. 3. Cardiovascular changes associated with swimming were similar to those that occurred when the animal was disturbed. There was a bradycardia, with little change in stroke volume. In the atropinized fish, exercise was associated with an increase in cardiac output and stroke volume with little change in heart rate.

Influence of sympathetic nerve stimulation on right ventricular outflow-tract pressures in anesthetized dogs.

Stellate ganglion stimulation in the anesthetized, open-chest dog consistently resulted in the generation of pressure differences which averaged 20 mm Hg across the infundibular region of the right ventricle. Before stimulation, peak systolic pressures in the sinus and conus were closely matched. Peak sinus pressure showed an average increase of 184 and 162% during stimulation of the left and right stellate ganglia, respectively. Simultaneously, peak conus pressure showed average increases of 88 and 61% during left and right stellate ganglion stimulation, respectively. In addition, the maximal rate of intrasinus pressure development (dP/dt) was usually elevated above conus dP/dt, and this change contributed to the generation of early systolic pressure differences. Cervical vagosympathetic nerve stimulation following atropine administration also resulted in the generation of infundibular pressure differences, but the latter were less marked than those elicited during stellate ganglion stimulation. Elevations in main pulmonary arterial resistance abolished the induced pressure differences by allowing peak conus pressure to rise to the same extent as peak intrasinus pressure. Simultaneous electromagnetic flow recordings of pulmonary arterial blood flow during stellate ganglion stimulation revealed two- to five-fold increases in maximum flow acceleration with relatively little change in stroke volume. Infundibular pressure gradients which developed in early systole were associated with maximum flow changes in the pulmonary artery.

Cardiovascular and blood gas responses to hyperbaric oxygenation

Ten normal subjects were studied while they breathed air and 100% oxygen at 1 and 3.04 atmospheres. Oxygen inhalation at 3.04 atmospheres was associated with a significant increase in arterial and venous pO 2 and O 2 content. Hemoglobin in the venous circulation was completely saturated in 8 of 10 subjects. Oxygen inhalation at 3.04 atmospheres produced a small but significant increase in venous pCO 2, presumably due to the loss of the buffering effect of reduced hemoglobin. Heart rate and cardiac output fell significantly with little change in stroke volume during oxygen inhalation at 3.04 atmospheres, indicating that the decrease in cardiac output was rate-dependent. There was little change in mean arterial pressure but an increase in calculated peripheral resistance during oxygen inhalation at 3.04 atmospheres. Two subjects who demonstrated signs of acute oxygen intoxication did not differ significantly from the group as a whole either in terms of blood gas values or patterns of hemodynamic response.