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PubMed1991

Pharmacologic support for postoperative low cardiac output.

This review has outlined a rational approach to the understanding and pharmacologic treatment of low output states after cardiac surgery. There are clearly other reasonable schemes for the use of these agents for management of these difficult patients. However, the principles of management remain the same. Data about the specific effects of these drugs must be applied to specific patients whose particular hemodynamic derangements have been analyzed carefully. However, the complex and changing interactions between the heart and the peripheral vascular system and the effects of these agents on both signify that these analyses must be made continuously during the early hours after cardiac surgery. Rational use of these agents requires careful analysis of the specific hemodynamic disorder in a given patient. Pharmacologic inotropic therapy should then be tailored to these abnormalities and based on what is known about the expected effects of these drugs on the heart and peripheral circulation. Careful and repeated follow-up measurements to document both the effects of the drugs and potential changes in the patient's hemodynamic state are required if successful therapy is to be achieved. A rational approach to the selection of the inotropic agents requires not only an understanding of the effects of the drugs, but continuous monitoring of the patient's hemodynamic state and recognition that the patient's condition and needs may change and dictate alteration in subsequent therapy.

Cardiac Output, Low↗
PubMed1986

Comparative effects of combined dopamine and nitroprusside versus dobutamine and nitroprusside infusions for computer-controlled management of low-output cardiac failure after open heart surgery.

In order to evaluate the possible differences in response to two currently preferable inotropic-vasodilator drug combinations, the hemodynamic effects of automated infusions of nitroprusside-dobutamine and nitroprusside-dopamine were studied in two clinically similar groups of patients with low-output syndrome after aorto-coronary bypass surgery. Nitroprusside, when infused in combination with dopamine, was effective in lowering filling pressures of both ventricles and systemic and pulmonary arterial pressures reflecting the reversal of deleterious rise of these parameters including determinants of myocardial oxygen consumption (mean arterial pressure rate by +6%, heart rate by +20%) caused by dopamine (6 micrograms/kg/min) infused alone. The combination of the more cardioselective catecholamine dobutamine with nitroprusside brought about similar increase in cardiac output by 50%, but derived its hemodynamic efficiency from the sum of separate effects of components and produced less in the way of elevation of determinants of oxygen consumption. Dobutamine when infused alone (6 micrograms/kg/min) has not affected systemic and pulmonary arterial pressures and stroke index rose more markedly (+9%) as a result of more moderate heart rate increase (+13%). Nitroprusside contributed in an additive manner to the achieved overall reduction of SVR and PVR by 43% and 50%, resp., the automated infusion being helpful in maintaining these values within close tolerances.

Cardiac Output, Low↗
PubMed1991

Continuous extracorporeal fluid removal in children with low cardiac output after cardiac operations.

Eleven hypervolemic and oliguric children with low cardiac output after cardiac operations were treated by slow continuous ultrafiltration or continuous arteriovenous hemofiltration. A mean negative fluid balance of 1.63 +/- 0.37 ml/kg/hr (standard error of the mean [SEM]) significantly improved the hemodynamic status within 59 +/- 6.1 hours (SEM). Although the central venous pressure decreased significantly from 15.2 +/- 0.84 to 8.8 +/- 0.92 mm Hg (p less than 0.0001), the mean arterial pressure increased significantly from 41.5 +/- 2.54 to 53.5 +/- 2.21 mm Hg (p less than 0.001). In addition, pH increased significantly from 7.31 +/- 0.01 (SEM) to 7.43 +/- 0.001 (SEM) (p less than 0.001) and oxygenation index (arterial oxygen tension/inspired oxygen fraction) from 119 +/- 15.2 (SEM) to 214 +/- 27.0 (SEM) (p less than 0.001). Hemodynamic improvement during slow continuous extracorporeal fluid removal allowed a significant decrease of the catecholamine infusion rate. After normovolemia had been achieved, continuous arteriovenous hemofiltration had to be continued in four children because of persistent anuria. Eight patients could be weaned from artificial ventilation and vasopressor support. Two patients died without recovery of renal function and one with restored renal function. Slow continuous ultrafiltration and continuous arteriovenous hemofiltration improve the cardiovascular function in children with low cardiac output by optimizing the preload conditions of the failing heart. In addition, they improve acid-base balance and pulmonary gas exchange.

Blood Pressure↗
PubMed2006

Nesiritide for treatment of perioperative low cardiac output syndromes in cardiac surgical patients: an initial experience.

The physiologic properties of the b-type natriuretic peptide nesiritide include pulmonary, coronary, and renal arterial vasodilation and lusitropic effects on ventricular myocardium. These effects may be useful during cardiac surgery, particularly when myocardial function and cardiac output (CO) are compromised. Intraoperative hemodynamic data were collected retrospectively before and 5-15 min following completion of a nesiritide loading dose in 15 adult cardiac surgical patients with low CO associated with pulmonary hypertension, low left ventricular ejection fraction, diastolic dysfunction, or left ventricular assist device placement. In seven patients, prior alternative pharmacologic interventions had failed to improve CO, and fluid challenges were ineffective in six patients with diastolic dysfunction. Perioperative nesiritide administration (2 microg.kg(-1) load, followed by 0.01 microg.kg(-1).min(-1) for a maximum of 24 h) resulted in a statistically significant median increase in CO of 35% (P = 0.0006). In conclusion, nesiritide was associated with increased CO in patients with low CO syndromes undergoing cardiac surgery, when other measures failed. This novel agent may offer an additional option to inotropes and fluid challenges for these patients perioperatively. Randomized clinical trials are desirable to determine the risks and benefits of nesiritides and to elucidate its role for the cardiac anesthesiologist.

Aged↗
PubMed1993

Managing low cardiac output states: maintaining volume after cardiac surgery.

Low cardiac output after cardiac surgery may be caused by hypovolemia, myocardial depression, vasoconstriction, and dysrhythmias. Postoperative hypovolemia occurs because of blood volume loss and decreased diastolic filling. Diuresis, intravascular fluid shift into the interstitium, hormonal influences, and bleeding deplete blood volume. Diastolic filling may be compromised by positive end-expiratory pressure, vasodilation, dysrhythmias, and venous return obstruction. The primary indicator of intravascular volume is ventricular preload, which may be measured indirectly with central venous pressure, left atrial pressure, or pulmonary capillary wedge pressure. Recognition of hypovolemia is aided through the use of cardiac pressure trend monitoring and evaluation of noninvasive indicators of hypovolemia. Nursing goals, in response to hypovolemia, are to increase the circulating volume, optimize oxygen delivery, stabilize hemodynamics, improve tissue perfusion, and prevent shock.

Aged↗
PubMed1985

Amrinone in the management of low cardiac output after open heart surgery.

Hemodynamic effects of amrinone were studied in 2 groups of patients after open heart surgery. Group I consisted of 10 patients with moderate heart failure. In the absence of inotropic agents, their mean cardiac index (CI) was 2.02 +/- 0.41 liters/min/m2 and mean pulmonary capillary wedge pressure (PCWP) 19 +/- 3 mm Hg. Amrinone was administered 24 hours postoperatively by bolus injection (2 mg/kg) and by 12-hour infusions (20 micrograms/kg/min). Hemodynamic data and plasma concentrations were obtained 10 and 20 minutes after the bolus injection and at 1, 4, 8 and 12 hours during infusion. Significant beneficial changes were noted in CI, PCWP, right atrial pressure, systemic vascular resistance and pulmonary vascular resistance. Group II consisted of 5 patients in severe cardiogenic shock (mean CI 1.97 +/- 0.3 liters/min/m2, mean PCWP 28 +/- 8 mm Hg) despite adrenergic agonists in all patients and intraaortic counterpulsation in 2. After these measures, amrinone was given intravenously for 36 to 72 hours as additional inotropic support. Significant improvement was observed in CI, PCWP, right atrial pressure, systemic vascular resistance and pulmonary vascular resistance. Four patients in this group were discharged; 1 patient died after 5 days in acute renal failure and coma grade IV. No serious adverse effects of amrinone were observed in any group II patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Inotropic effect of triiodothyronine (T3) in low cardiac output following cardioplegic arrest and cardiopulmonary bypass: an initial experience in patients undergoing open heart surgery.

A significant reduction in plasma free triiodothyronine (T3) (P less than 0.0001) has been observed in patients undergoing open heart surgery. The beneficial effect of T3 would appear to be associated with increased synthesis and utilization of myocardial high energy stores. We have therefore administered T3 (4-10 micrograms iv) to 10 patients either when difficulty was being experienced in weaning from cardiopulmonary bypass (CPB) support (n = 5), or when myocardial function remained extremely poor (n = 5), despite inotropic and intraaortic balloon pump support. Mean preoperative NYHA functional class of the 10 patients was 3.2, left ventricular enddiastolic pressure (LVEDP) 20 mm Hg and ejection fraction (EF) 40%. The mean myocardial ischaemia time was 72 min (range 40-120 min). Within 1 h of T3 administration the mean plasma free T3 level had risen from 1.03 to 3.56 micrograms/ml and CPB was discontinued in all 5 cases. Balloon pump support (n = 2) was no longer essential within 3 h. At 1 h, the mean arterial pressure (MAP) had risen from 42 to 78 mm Hg, and heart rate (HR) from 90 to 104 beats/min; the left atrial pressure (LAP) had fallen from 30 to 14 mm Hg, and the central venous pressure (CVP) from 20 to 11 cm H2O. (All changes significant at P less than 0.0001.) Inotropic support had been significantly reduced or discontinued. To our knowledge, T3 has not been administered previously as an inotropic agent to patients who have undergone cardiac surgery. We believe that T3 may have an important role in the rescue of failing hearts following a period of myocardial ischaemia in patients who have undergone open heart surgery.

Cardiac Output, Low↗
PubMed1999

Low cardiac output complicating pericardiectomy for pericardial tamponade.

Neoplastic involvement of the pericardium resulting in an effusion and subsequent tamponade is an emergency requiring prompt decompression, generally safely accomplished by subxiphoid pericardiectomy. However, the current case report describes a patient with florid pericardial tamponade who underwent surgical decompression with transient hemodynamic improvement, who then rapidly developed progressive, heart failure and death. This paradoxical response to pericardial decompression, similar to that seen occasionally with pericardiectomy in constrictive pericarditis, may be more frequent than currently appreciated. Its cause may relate to the sudden removal of the chronic external ventricular support from the effusion resulting in ventricular dilatation and failure.

Cardiac Output, Low↗
PubMed1992

[Ventricular stimulation triggered by esophageal atriogram: a new technique of temporary physiologic stimulation in the course of acute myocardial infarct complicated by atrioventricular block and low cardiac output].

Advanced atrio-ventricular (AV) block during acute myocardial infarction (AMI) is considered a complicating dysrhythmia as the well as mechanism responsible for occurrence of life-threatening hemodynamic changes. Often, simple VVI pacing can result insufficient in improving the decreased cardiac output. VDD pacing, which preserves atrial contribution, should represent the most effective electrical approach; therefore, it requires intracavitary placement of 2 catheters. In 10 pts (6M, 4F, mean age of 63.8 +/- 6.6 years) with advanced AV block due to AMI (4 inferior, 6 anterior) and without sinus node dysfunction, we performed stable VDD stimulation (mean 16.6 +/- 20.6 hours) using only one catheter positioned in the right ventricle while the atrial impulse, filtered (50-70 Hz) and amplified through a special device, was derived from the esophagus. Such technique is rapid and reliable, avoiding problems associated with atrial sensing and catheterization.

Aged↗