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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dopamine is a direct-acting catecholamine with a short half-life that has many advantages in treating visceral hypoperfusion states such as shock and refractory heart failure. Unlike other inotropic drugs, dopamine directly dilates the mesenteric, renal, and cerebral vessels and redirects blood flow to essential viscera. This dopaminergic effect is prominent with doses of 100-700 mug/min in adults and is attenuated by phenothiazines and haloperidol. At doses of 700-1400 mug/min, dopamine also has a significant beta-adrenergic, inotropic effect, increasing myocardial contractility. The inotropic effect is equivalent to that of isoproterenol, epinephrine, and norepinephrine, but tachycardia, tachyarrhythmias, and angina may be less frequent with dopamine. In doses greater than 1400 mug/min, dopamine is a vasoconstrictor with pressor effects usually equivalent to that of norepinephrine. Dopamine dilates pupils, does not dilate bronchi, and does not shunt blood from viscera to skeletal muscles as does isoproterenol. Because dopamine increases myocardial contractility, selectively redistributes perfusion to essential viscera and allows a pharmacologic titration of effect, it is a logical first-choice catecholamine for treatment of shock and refractory heart failure.
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PMID:The clinical use of dopamine in the treatment of shock. 0 63

Hemodynamic effects of isoproterenol, dopamine, and epinephrine were studied before and after acute beta-adrenergic blockade in 16 open-chest, anesthetized mongrel dogs. Beta blockade was induced with 1 mg. per kilogram of intravenous propranolol. Cardiac output measurements were obtained by thermal dilution, and pressure recordings were obtained in the right ventricle, pulmonary artery, left atrium, left ventricle, and aorta. Derived parameters included stroke volume, pulmonary and systemic vascular resistances, and peak left ventricular dP/dt. In the presence of propranolol, epinephrine became a lethal drug in large doses and did not increase cardiac output in standard doses. Dopamine, in 25 to 50 mcg. per kilogram per minute doses, increased arterial pressure and systemic resistance; cardiac output was diminished compared with dopamine, 10 mcg. per kilogram per minute, prior to propranolol, as a result of increased resistance and decreased LV contractility. Isoproterenol, 0.6 to 0.9 mcg. per kilogram per minute, 15 to 20 times standard dosages, had moderately positive inotropic effects and increased cardiac output. Left ventricular systolic pressure with isoproterenol after propranolol was reduced when compared with effects of smaller doses prior to propranolol. These observations suggest that none of the catecholamines studied would be optimal for circulatory support in heart failure in the presence of propranolol. The present results define a pharmacologic basis for design of appropriate drug combinations for circulatory support in beta-blocked animals.
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PMID:Pharmacologic antagonism of beta-adrenergic blockade in dogs. I. Hemodynamic effects of isoproterenol, dopamine, and epinephrine in acute propranolol administration. 3 98

The hemodynamic response to a dopamine HCl infusion (10 microgram/kg per min) was measured in 25 adult patients with severe sepsis: there were 6 patients with circulatory hyperdynamic states, 9 patients with myocardial failure, and 10 with hypovolemia. Each patient also had acute respiratory failure. Changes of intrapulmonary shunt fraction (Qs/Qt), arterial and mixed venous oxygen tension (PaO2 and PvO2), oxygen transport, and oxygen consumption (VO2) were evaluated before and after dopamine infusion. Dopamine infusion produced clinical improvement and increased cardiac output. The hemodynamic response seemed to differ slightly according to the pattern of circulatory failure: chronotropic effect appeared to be predominant in hyperdynamic states, whereas inotropic effect appeared to be predominant in myocardial failure or hypovolemia. Moreover, in hypovolemic patients we noted a rise in pulmonary capillary wedge pressure suggesting an additional increase in venous return. During this treatment, we also noted a worsening of the Qs/Qt despite the increase in pulmonary blood flow; this worsening did not prevent significant improvements in VO2, but the improvement in PVO2 was offset by increased Qs/Qt and PaO2 remained unchanged.
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PMID:Effect of dopamine on intrapulmonary shunt fraction and oxygen transport in severe sepsis with circulatory and respiratory failure. 44 60

The effects of intravenous dopamine were evaluated in 10 patients with severe but stable coronary artery disease, 17 consecutive patients with primary cardiogenic shock and 3 with severe congestive heart failure and oliguria. Dopamine infusion at 10 mug/kg.min in the 10 patients increased cardiac output by 35%, left ventricular peak dP/dt by 38%, left ventricular minute work index by 44% and mean systolic ejection rate by 7% (P < 0.01); heart rate, aortic pressure, left ventricular end-diastolic pressure and tension-time index were unchanged. For oxygen, potassium and lactate, arterial and coronary sinus values, coronary arteriovenous oxygen differences and myocardial extraction were unchanged. Hemodynamically 13 of the 17 patients in shock responded favourably to dopamine infusion (0.5 to 15 mug/kg.min), with decrease in heart rate, increase in systolic arterial pressure from 75 to 100 mm Hg (P <0.001), decrease in ventricular filling pressure from 20 to 16 mm Hg (P < 0.01) and increase in urine output from 10 to 100 ml/h (P < 0.01). Eleven of those patients survived the shock episode. A close relation was observed between the hemodynamic response to dopamine, survival from the shock episode and the time between onset of shock and initiation of therapy. Low rates of dopamine infusion induced diuresis in the three patients with severe cardiac failure.Dopamine thus seems to improve the mechanical efficiency of the heart in coronary artery disease. Cardiac output is selectively increased and myocardial ischemia does not appear to be induced; those beneficial effects as well as presumably specific action on renal flow and natriuresis, improve immediate survival from cardiogenic shock and severe heart failure.
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PMID:Hemodynamic and therapeutic effects of intravenous dopamine. 60 65

Thirteen patients with severe cardiac failure underwent a single crossover study of dopamine and dobutamine in order to compare the systemic and regional hemodynamic effects of the two drugs. The dose-response data demonstrated that dobutamine (2.5--10 microgram/kg/min) progressively and predictably increases cardiac output by increasing stroke volume, while simultaneously decreasing systemic and pulmonary vascular resistance and pulmonary capillary wedge pressure. There was no change in heart rate or premature ventricular contractions (PVCs)/min at this dose range. Dopamine (2--8 microgram/kg/min) increased the stroke volume and cardiac output at 4 microgram/kg/min. Dopamine at less than 4 microgram/kg/min provided little additional increase in cardiac output and increased the pulmonary wedge pressure and the number of PVCs/min. At greater than 6 microgram/kg/min, dopamine increased heart rate. During the 24-hour maintenance-dose infusion of each drug (dopamine 3.7--4, dobutamine 7.3--7.7 microgram/kg/min), only dobutamine maintained a significant increase of stroke volume, cardiac output, urine flow, urine sodium concentration, creatinine clearance and peripheral blood flow. Renal and hepatic blood flow were not signfiicantly altered by the maintenance dose of either drug. Systemic and regional hemodynamic data suggest that dobutamine has many advantages over dopamine when infused in patients with cardiac failure.
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PMID:Comparative systemic and regional hemodynamic effects of dopamine and dobutamine in patients with cardiomyopathic heart failure. 67 37

To assess the circulatory effects of afterload reduction and inotropism individually and in combination as rational therapy for refractory heart failure, nitroprusside and dopamine were administered to 13 patients with severe cardiac decompensation. Dopamine at average doses of 3 and 7 microgram/kg per min produced increases in cardiac output and reductions in peripheral resistance. At doses of 15 microgram/kg per min, dopamine increased heart rate, peripheral arterial pressure and side effects. Nitroprusside alone decreased left-sided filling pressures and increased cardiac output. When the agents were administered together, the increases in cardiac output were significantly greater than with either agent alone and there was physiologic improvement in overall circulatory function. The relations among changes in afterload (systemic impedence), preload (filling pressures) and cardiac index help to explain the salutary effects of combined therapy in patients with refractory heart failure.
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PMID:Combined nitroprusside-dopamine therapy in severe chronic congestive heart failure. Dose-related hemodynamic advantages over single drug infusions. 68 39

15 patients have been treated with dopamine (2.0--6.0 gamma/kg/min) in the initial phase of cardiogenic shock after cardiac surgery. Indication was a systolic blood pressure of less than 85 mmHg associated with oligurie and peripheral vasoconstriction. 12 patients survived the cardiocirculatory crisis and the early postoperative period. Dopamine alone increased the arterial blood pressure in 6 patients from 52.4 to 80.1 mmHg and the urine flow from 25.2 ml/hr to 181.2 ml/hr. To obtain an optimal perfusion pressure additional application of Noradrenalin was used in 8 patients. In these patients the urine flow rose from 9.1 ml/hr to 131 ml/hr. In one patient no reaction, neither to dopamine, nor in combination with Noradrenalin was seen. The effect of pulse rate, central venous pressure and arterial oxygen tension has been discussed. Dopamine seems to be a useful substance in surgical patients with temporary cardiac insufficiency.
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PMID:[Clinical experiences with dopamine after heart surgery]. 108 Oct 33

Dopamine exerts marked positive inotropic effects in the dog with no effect on heart rate. This effect is abolished by propranolol, reduced by reserpine, and unaffected by atropine. Dopamine exhibits similar inotropic activity in the normal guinea pig and in guinea pigs with experimentally induced heart failure. In the isolated perfused hamster heart, dopamine caused marked increases in left ventricular pressure with slight increases in heart rate. However, in the failing heart of the myopathic Syrian hamster, dopamine caused moderate increases in left ventricular pressure with much greater increases in heart rate. The total heart work of the failing heart under the influence of dopamine is significantly higher than that of the normal heart. The energy utilization under this condition is equal in both hearts. Therefore, the calculated efficiency of the failing heart treated with dopamine is much higher than that of the normal heart treated similarly.
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PMID:Cardiovascular effects of dopamine in the normal and failing heart of experimental animals. 119 88

The Authors report their experience with a new vasodilator drug (Urapidil) employed in the management of serious cardiac failure, in a patient who previously didn't respond in a satisfactory manner to a therapy with Dopamine alone. After several days of continuous treatment, the patient was discharged, without any sign of toxic or metabolic reactions.
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PMID:[Urapidil and dopamine in severe heart failure. A clinical case]. 129 8

Beta-adrenergic stimulants (Dobutamine and Dopamine) and recently introduced phosphodiesterase inhibitors (PDI) such as Amrinone, Milrinone, Enoximone and Piroximone are the principal inotropic agents for the treatment of acute cardiac failure. Most of the hemodynamic effects of these drugs are comparable, but peripheral vasodilatation is more marked with PDI. A potential advantage of the latter group is the lack of development tolerance, which occurs within 48 to 72 hours after beta-stimulants. On simultaneous administration, additive effects can be observed. Short term clinical results with PDI are good, especially in patients with postoperative cardiocirculatory failure, including cardiogenic shock. In contrast, long-term oral treatment with Amrinone, Milrinone and Enoximone in recent studies was disappointing. Efficacy was not superior to Digoxin, and unwanted side effects were frequent. Intermittent instead of continuous administration of positive inotropic agents should be evaluated in patients with severe congestive heart failure not responding to vasodilators and diuretics.
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PMID:[New positive inotropic drugs in acute and chronic heart failure]. 135 9


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