Significant Increase In Stroke Volume Research Articles

Usefulness of Doppler echocardiography in cardiac pacing: assessment of mitral regurgitation, peak aortic flow velocity and atrial capture.

Doppler echocardiographic studies were performed in 14 patients with dual chamber pacemakers. Transmitral flow studies (12 patients) revealed absence of mitral regurgitation (MR) or no change in MR severity in 6, new development or increased MR during VVI and/or short or long AV interval lengths compared to more normal AV intervals (150-160 ms) in 5, and appearance of MR when the pacing mode was changed from VVI to DVI with a fixed AV interval of 250 ms in 1 patient. Aortic peak flow velocity measurements (7 patients) showed significant increases in stroke volume (range 9 to 25%, mean 19.5%) in all patients with DVI/VDD pacing compared to VVI pacing (4 patients) or to shortest available AV interval (3 patients). Presence of Doppler left atrial systolic flow correlated with evidence of atrial depolarization in all 7 patients in whom high quality 12-lead surface electrocardiograms were obtained. Our preliminary study demonstrates the value of Doppler echocardiography in the "fine tuning" of cardiac pacemaker parameters by assessment of presence, absence, or change in severity of MR, estimation of relative changes in stroke volume, and determination of atrial capture in different pacing modes and at various AV intervals.

Prenalterol, an oral beta-1 adrenoceptor agonist, in the treatment of chronic heart failure.

The haemodynamic effects of prenalterol, a new beta-1 agonist, were studied in 10 patients with chronic heart failure. Following intravenous prenalterol infusions of 1 mg, 2.5 mg and 5 mg at 15 min intervals, oral slow release prenalterol 20 mg, 30 mg and 50 mg was given at 2 h intervals and then 50-100 mg bid for one month. There were no significant changes in heart rate or blood pressure. Cardiac output increased significantly from control of 4.4 +/- 0.91/min to a maximum of 5.8 +/- 1.81/min (p less than 0.01) following the 5 mg prenalterol infusion and this increase was maintained following oral prenalterol on Days 1 and 2 and at 1 month. Significant increases in stroke volume and stroke work indices and reduction in systemic vascular resistance were also observed. Maximum increases in cardiac output and stroke work index following intravenous prenalterol correlated significantly with maximum increases observed following oral prenalterol on Day 2. Non-invasive evaluation showed no change in echocardiographic left ventricular end-diastolic dimension but a significant reduction in left ventricular end-systolic dimension on Day 30. PEP/LVET was significantly reduced from control of 0.56 +/- 0.15 to 0.47 +/- 0.12 (p less than 0.05) on Day 2 and 0.49 +/- 0.09 (p less than 0.05) at 1 month. Treadmill exercise duration was significantly improved for the group at 1 month and no adverse effects were noted. Oral slow release prenalterol is a potentially useful new drug for patients with chronic heart failure.

Effect of bromocriptine on cardiac function and coronary blood flow.

The present study was designed to investigate the effects of bromocriptine, a dopamine receptor agonist, on systemic and coronary hemodynamics and to determine the mechanisms involved in the action of this compound. Intravenous infusion of bromocriptine (1 microgram/kg/min for 20 min) to pentobarbital-anesthetized dogs produced significant decreases in blood pressure, heart rate, total peripheral resistance, peak dP/dt, left ventricular pressure, and coronary blood flow. There were significant increases in stroke volume and coronary vascular resistance, whereas the index of contractility was unaffected. Cardiac output was decreased 30 min after the termination of bromocriptine infusion. The cardiovascular actions of bromocriptine were significantly antagonized by the dopamine receptor antagonist, sulpiride. Bromocriptine also failed to exert these effects when administered to animals that were treated with ganglionic blocking agents. These results suggest that the hypotensive action of bromocriptine is mainly due to a decrease in total peripheral resistance. In addition, the actions of bromocriptine on cardiac function are the result of activation of presynaptic dopamine receptors and the drug does not have any direct action on the myocardium.

Clinical Pharmacology of Prazosin and Phentolamine in Patients with Heart Failure

In a controlled crossover study we assessed the effects of an initial single oral dose of 150 mg phentolamine or 2 mg prazosin on the haemodynamics and plasma concentrations of noradrenaline in 12 patients with mild to moderate cardiac dysfunction in cardiomyopathy (NYHA Classes I-III). Nine of these patients continued chronic oral treatment with either 300-450 mg phentolamine or 7.5-15 mg prazosin for a period of 4-6 weeks each in randomised order. The effects on both haemodynamics and plasma noradrenaline were essentially the same under the treatment with both drugs. The acute effect on reduction of exercise-induced elevation of diastolic pulmonary artery pressure was abolished after chronic treatment. However, significant increase in stroke volume—on average, from 83 ± 7.2 to 100 ± 6.0 ml (phentolamine) and 99 ± 6.7 ml (prazosin)—occurred only after chronic treatment. Increased sympathetic activity, as expressed in plasma noradrenaline concentrations, was similar under both phentolamine and prazosin. There was no direct evidence for the clinical relevance of the more pronounced presynaptic α-blockade with phentolamine as compared with the almost pure postsynaptic α-blocking properties of prazosin. Development of tolerance seemed to occur with both drugs; however, haemodynamic benefit in terms of increased stroke volume could only be achieved after chronic treatment.

Acute effects of oral propranolol on hemodynamic responses to upright exercise

Noninvasive measurements of maximal oxygen intake and invasive measurement of systemic and pulmonary arterial pressures, arterial and mixed venous oxygen contents and direct Fick cardiac output are reported for 3 healthy men and 14 men with coronary heart disease. Observations were obtained at supine and sitting rest, during graded levels of upright exercise on a treadmill up to symptom-limited maximal effort and in two periods of recovery. The effects of 40 mg of propranolol orally were ascertained by repeating the measurements 1 to 1 1 2 hours later. The most consistent effect of propranolol was reduction of pressure-rate products at all phases; slowing of heart rate was significant only during exercise and recovery, and the greater slowing was accompanied by a significant increase in stroke volume. These changes were similar in patients with and without evidence of left ventricular impairment greater than 15 percent on exercise testing. Maximal oxygen intake decreased in healthy subjects and decreased slightly in patients with coronary heart disease with less than 15 percent left ventricular impairment or percent deviation of pressure-rate product from age-predicted normal values during the control study. Maximal oxygen intake increased in patients with more than 15 percent left ventricular impairment. Arterial-mixed venous oxygen difference increased after propranolol because of a reduction of mixedvenous oxygen content attributed to greater peripheral extraction of oxygen.

Stroke volume and systolic time interval adjustments during bicycle exercise

By use of the impedance noninvasive method, cardiac output (Q), stroke volume (SV), heart rate (HR), Heather index (HI), and systolic time interval (STI) values were studied in 17 subjects working at 25, 50, and 75% of their maximal oxygen uptake (Vo2 max) on a Monark bicycle. A significant increase in SV at each work load and a concomitant decrease in positive expiratory pressure (PEP), left ventricular ejection time (LVET), and PEP/LVET were observed. The linear regression equation at 75% Vo2 max between LVET and HR and SV confirms the close relationship between these parameters. The significa-t increase of the contractility index (HI) showing the stress response of the myocardium is clearly assessed. At 75% work load, its correlation with SV is low; but the high level of the correlation (r = 0.90) between HI and HR in the stress response. Consequently the changes in STI and HI provide valuable information on SV adjustment during calibrated effort responses. Consequently, the changes in STI and HI, the relationship between STI and SV, and the study of SV, HR, and Q provide valuable information about the adjustment of these parameters during calibrated efforts.

Treatment of cardiogenic shock after acute myocardial infarction with intra-aortic balloon counterpulsation (author's transl)

Intra-aortic balloon counterpulsation (IABP) was used in 20 patients with acute myocardial infarction and cardiogenic shock, after four hours of drug treatment. In all instances the abnormal haemodynamic state had been demonstrated. Four patients were successfully treated and finally discharged home. In two with post-infarction ventricular septal defect and cardiogenic shock, IABP also successfully reversed the shock state, while in seven the shock state was reversed but they died 2-8 days after IABP had been stopped. IABP failed in seven patients who died during its application. In those in whom IABP failed there had been no significant fall in pulmonary-artery pressure and no significant increase in stroke volume. The post-mortem examinations demonstrated that cardiogenic shock was irreversible where more than 50% of the left ventricular myocardium had been infarcted.

Relation between acute changes in pH and PCO 2 and inotropic responses to acetyl strophanthidin

The effects of acutely induced hypercapnic or lactic acidemia on the inotropic responses to acetyl strophanthidin were studied in adult cats. Beta adrenergic blockade was produced with propranolol to eliminate sympathetic influences on the heart. In control animals significant increases in stroke volume, mean ejection rate and rate of rise of left ventricular pressure ( dP dt ) were shown after infusion of acetyl strophanthidin, 15 μg/kg. Similar increases were demonstrated in cats with lactic acidemia (pH 7.0) or hypercapnic acidemia (PCO 2 60 mm Hg). The responses of cats with low pH or high PCO 2 values did not differ significantly within the 2 groups or by comparison with control responses. These results demonstrate (1) that digitalis is effective in producing significant inotropic responses even under these altered metabolic conditions, and (2) that propranolol does not inhibit these responses.

Pressure-flow studies in man: effect of atrial systole on ventricular function in mitral stenosis.

The effect of atrial contraction on left ventricular function in six patients with varying degrees of mitral stenosis was determined by utilizing the pressure gradient technique to measure instantaneous aortic blood flow and pressure. Aortic flow was measured as ventricular rate was controlled by right ventricular pacing to create A-V (atrioventricular) dissociation at varying rates (90-150 beats/min). At each heart rate, beats with preceding P waves, effective atrial systole, were grouped according to the duration of the P-R interval. Beats without P waves served as controls. There was always a significant increase in stroke volume, created by effective atrial systole, but the P-R interval at which it took place was different for each patient. There was no difference in the stroke volume for beats preceded by P waves having a P-R interval within the range of 0.05-0.20 sec. These beats were grouped for each patient, subjected to regression analysis, and compared to control beats. The absolute and percent change created by effective atrial systole was inversely proportional to the severity of the disease as determined by mitral valve orifice size. Effective atrial systole plays less of a role in augmenting left ventricular function in patients with mitral stenosis than in patients with normal valves.

PHENTOLAMINE FOR VASODILATOR TREATMENT OF SEVERE HEART-FAILURE

Phentolamine, an adrenergic alphareceptor-blocking drug, was administered to twelve patients with severe progressive left ventricular failure due to ischæmic heart-disease. The drug was infused intravenously in a dose of 1-2 mg. per minute, sufficient to lower the systemic arterial blood-pressure by 20-30 mm. Hg. This resulted in a rapid relief of symptoms simultaneously with a substantial reduction in the left ventricular end-diastolic and pulmonary-artery mean pressures, and a significant increase in stroke volume and cardiac output; these changes were maintained throughout the 3-hour infusion. Patients who were able to exercise also reported a significant reduction in breathlessness, an increase in the cardiac output, and a decrease in the left ventricular end-diastolic pressure response to exercise. Chest radiographs showed a conspicuous clearing of pulmonary œdema and reduction in cardiac size after the drug. The benefits of this treatment are probably due to the effects of the drug in lowering the raised systemic vascular resistance and thus reducing cardiac pressureload, and to its positive inotropic action increasing the strength of myocardial contraction. The drug may also directly support the metabolism of the failing heart by release of the suppression of insulin secretion frequently associated with severe heart-failure, and its bronchodilator action may also contribute to the relief of symptoms in patients with cardiac asthma. This approach to the treatment of severe heart-failure may usefully complement conventional treatment with digitalis and diuretics and may be of particular value where digitalis is contraindicated.

Comparison of norepinephrine and isoproterenol in experimental coronary shock: Observations on the effects of dextran infusion

Shock was produced in dogs by embolization of the coronary arteries with microspheres of divinylbenzene. The comparative efficacy of norepinephrine versus isoproterenol in returning hemodynamic function and tissue perfusion toward normal was assessed. In six dogs showing rapidly progressive deterioration within 15 minutes after embolization neither drug was effective. In eight dogs surviving this initial 15 minute period of observation, isoproterenol in large doses resulted in significant increases in stroke volume, cardiac output, body oxygen consumption, and adequacy of tissue perfusion persisting up to 3 hours of therapy. Concomitant lidocaine infusion prevented the development of fatal ventricular arrhythmias. Metabolic studies directed toward assessing adequacy of coronary blood flow during isoproterenol infusion suggest improved over-all myocardial oxygenation but do not exclude continuing or increasing regional myocardial ischemia. In seven other dogs in shock of similar severity, norepinephrine infusion resulted in significant increases in blood pressure and prevented the high incidence of early deaths occurring in a control group of eight untreated shocked dogs, but failed to produce sustained increases in stroke volume, cardiac output, or body oxygen consumption. Systemic excess lactate either increased or remained elevated during norepinephrine infusion. Myocardial metabolic studies suggest that over-all myocardial oxygenation was worsened during norepinephrine therapy of coronary shock, although regional improvements could not be excluded. When shocked dogs initially treated with norepinephrine were given isoproterenol, hemodynamic function and tissue perfusion were significantly improved; when shocked dogs initially treated with isoproterenol were then given norepinephrine, hemodynamic function and tissue perfusion worsened. Dextran infusion in shocked dogs sufficient to increase left ventricular end-diastolic pressure increased cardiac output only when isoproterenol was being given. Generally, similar responses to norepinephrine and isoproterenol therapy were seen in a group of dogs with less severe hemodynamic depression following coronary embolization. From these studies, it is concluded that isoproterenol infusion concomitant with continuous lidocaine infusion and intermittent expansion of blood volume merits clinical evaluation in the therapy of shock due to myocardial infarction.