[Intravenous nitroglycerin therapy in low cardiac output syndrome resulting from left ventricular failure after open heart surgery].
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Aim of this short report is to present a simple and fast technique to pace in VDD mode patients with acute myocardial infarction associated with third degree AV block and haemodynamic deterioration. VDD pacing was obtained using atrial electrogram recorded by trans-oesophageal catheter and a Medtronic Thera VDD pace-maker as temporary pace-maker.
OBJECTIVE: We sought to determine whether a critical cardiac output and oxygen delivery exist in normal pregnancy. We also sought to determine the role of fetoplacental oxygen demand on maternal oxygen transport variables in response to decreased maternal cardiac output. STUDY DESIGN: We studied 10 adult female sheep, 5 nonpregnant and 5 pregnant. We placed a flow-directed thermodilution catheter in the pulmonary artery and a balloon-tipped catheter in the right atrium of the sheep. We also placed a catheter for pressure monitoring and blood sampling in the descending thoracic aorta in both the mother and fetus. We decreased maternal cardiac output by incremental inflation of the right atrial balloon. We measured maternal cardiac output by intravenous bolus thermodilution technique. We also measured maternal and fetal acid-base status and serum lactate concentrations. We calculated a variety of maternal cardiorespiratory variables, including systemic oxygen delivery, systemic oxygen consumption, and fractional whole body tissue oxygen extraction. RESULT: The nonpregnant sheep displayed a critical cardiac output below which there was an abrupt decrease in oxygen consumption. In contrast, there was no critical level of cardiac output in the pregnant sheep. Maternal oxygen consumption was linearly dependent on cardiac output. Maximum fractional oxygen extraction was significantly lower in the pregnant sheep than in the nonpregnant sheep. CONCLUSION: States of low cardiac output in the pregnant sheep are associated with a lack of a critical cardiac output; the flow-dependent oxygen consumption observed is the result of either an impairment in tissue oxygen extraction or some degree of metabolic arrest or a combination of both. If this unique cardiac output-oxygen consumption relationship is seen in human pregnancy, it could have significant implications in the care of the critically ill obstetric patient.
Post-operative low cardiac output states remain a major cause of mortality following cardiac surgery in infants and children. Since 1979 we have used moderate induced whole-body hypothermia in the management of low-output states refractory to conventional modes of therapy. This is based not only upon the relationship between body temperature and oxygen consumption, but also on experimental work showing a beneficial effect of cooling upon myocardial contractility, particularly when there is pre-existing impairment of ventricular function. Between July 1986 and June 1990, 20 children with refractory low-output states were cooled by means of a thermostatically controlled water blanket to a rectal temperature of 32-33 degrees C. The median age was 12 months (1 week-11 years) with a median weight of 6 kg (3.5-33 kg). Ten children survived to leave hospital while a further two made a haemodynamic recovery. There was a marked reduction in heart rate (P < 0.001). The mean arterial pressure rose (P = 0.037) while there was a fall in mean atrial pressure (P < 0.001). There was a significant improvement in the urine output (P = 0.002). A fall in the platelet count (P < 0.001) was not accompanied by any change in the white cell count (P = 0.15). Although it is impossible to say whether cooling influenced the outcome in any of these children, it was usually effective in stabilising their clinical condition. The technique is simple and has a sound theoretical basis.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the haemodynamic effects of dopexamine hydrochloride, a beta 2-adrenergic agonist with dopaminergic (DA1) activity, in 20 patients with low cardiac output following surgery for coronary artery bypass grafting and/or valve replacement or repair. Following titration of four doses (1, 2, 4 and 6 micrograms.kg-1.min-1), the dose producing the optimal response was infused for up to 48 h (five patients). During the infusion, significant increases in cardiac index and stroke volume were accompanied by significant decreases in systemic vascular resistance. Heart rate increased significantly up to 6 h and thereafter returned to control levels. Mean blood pressure was reduced but did not fall below 60 mmHg. However, in five patients treated for 48 h mean blood pressure had returned to control levels. Unwanted effects (tachycardia and hypotension) were seen chiefly at higher doses, leading us to conclude that infusion rates of 4 micrograms.kg-1.min-1 or less will be useful in the treatment of low cardiac output following cardiac surgery.
A refractory low-cardiac-output syndrome is, in pediatric patients, most often due to impaired myocardial function after corrective surgery in congenital heart disease. Therapy has to focus on postoperative adaptation, which usually takes place within a few days. We report on three therapeutic strategies to "bridge" this phase of postoperative adaptation. Improving the contractile state of the myocardium using enoximone was attempted in 16 neonates with low-cardiac-output syndrome refractory to catecholamines (Dosage: loading-dose 1 mg/kg in 10 min intravenously, followed by an infusion of 10 mcg/kg/min). In 12/16 neonates cardiac index increased by more than 20% ("responder"), while in 4/16 neonates cardiac index remained unchanged ("non-responder"). All non-responders succumbed due to refractory low-cardiac-output syndrome, while only one responder died in low-cardiac-output syndrome. Hemodynamically, enoximone resulted in an increase of cardiac index and stroke volume (p < 0.003), a reduced systemic vascular resistance (p < 0.0022), and reduced right and left atrial pressures (p < 0.003). Heart rate and mean arterial pressure remained unchanged. No rhythm disturbances were observed. Another therapeutic approach to postoperative low-cardiac-output syndrome is atrial decompression by creating an atrial septal defect. Due to the possibility of later transcatheter closure of these defects, the acceptance for the intraoperative creation of an atrial communication to decompress the right or left atrium is increased. The defect size is critical and should be below 9 mm, so that the Rashkind-PDA-Occluder can be used for later transcatheter closure. We performed such a "surgical-interventional" decompression in 18 patients (age: 2 weeks to 7 years). In six patients the atrial defect was created because of an underdeveloped left ventricle (body weight 2.9-9.2 kg), in 12 patients for right atrial decompression during a total cavopulmonary shunt (body weight 15.2-54.2 kg). A spontaneous closure of the defect did not occurred in any of the patients, thus, transvenous closure of the defect was performed 2 to 10 weeks postoperatively. In the follow-up period of 4 to 22 months no complications such as thrombus formation, thromboembolic events or infections occurred. In low-cardiac-output syndrome refractory to all therapeutic measures mechanical circulatory support is the final method to keep the patient alive. In 11 children with refractory low-cardiac-output syndrome mechanical circulatory support was performed. In three of these, extracorporal membrane oxygenation (ECMO) was used, in eight children a ventricular assist device (Berlin Heart) was used.(ABSTRACT TRUNCATED AT 400 WORDS)
Forty patients developed low cardiac output states after surgery for mitral valve disease or with associated cardiac disease and were randomly allocated to two treatment groups, one group to receive Dobutamine (D) and the other Enoximone (E), a phosphodiesterase inhibitor. Haemodynamic assessment covered a 24 hour period but treatment was continued for as long as was necessary. An improvement was observed from the 15th minute of treatment. At the second hour, the cardiac index had increased by 55% in Group E and by 59% in Group D whilst the heart rate increased by only 12% in Group E compared to 30% in Group D. The right and left heart filling pressures decreased by 25 to 27% in the 2 groups. The systemic arterial resistances fell by 36 to 37% without any significant changes in systemic or pulmonary arterial pressures. No significant difference was demonstrated in the haemodynamic responses to Dobutamine and Enoximone in this study. The duration of treatment was significantly shorter in Group E than in Group D (59 +/- 22 hrs vs 86 +/- 49 hrs) as was the patient's stay in the intensive care unit (92 +/- 37 hrs vs 155 +/- 129 hrs). The duration of assisted ventilation was the same in the two groups. These results suggest that Enoximone is as effective as Dobutamine in the treatment of low cardiac output after mitral valve surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
1. Plasma noradrenaline concentrations are elevated in patients with congestive heart failure; however, the pathogenesis of these elevated noradrenaline levels is controversial. 2. Possible mechanisms for elevated noradrenaline concentrations in patients with congestive heart failure include increased noradrenaline secretion, decreased clearance of noradrenaline, and a combination of increased secretion and decreased clearance. 3. In the present study, plasma noradrenaline clearance and apparent secretion rates were determined using a whole-body steady-state radionuclide tracer method in six otherwise healthy patients with moderate degrees of low-output cardiac failure and in six normal control subjects. 4. The venous plasma noradrenaline level was elevated in the patients with congestive heart failure as compared with the control subjects (4.18 +/- 1.34 versus 1.54 +/- 0.16 nmol/l, P less than 0.05). There was no stimulation of the adrenal medulla as evident by normal plasma adrenaline levels in both groups (0.19 +/- 0.04 versus 0.18 +/- 0.02 nmol/l, not significant). The apparent secretion rate of noradrenaline was elevated in the patients with congestive heart failure (4.75 +/- 1.95 versus 1.78 +/- 0.18 nmol min-1 m-2, P less than 0.05), whereas the clearance rate of noradrenaline was similar in the two groups (1.26 +/- 0.27 versus 1.16 +/- 0.02 l min-1 m-2, not significant). 5. We conclude that the high peripheral venous plasma noradrenaline concentrations in patients with mildly decompensated low-output cardiac failure are initially due to increased secretion, rather than to decreased metabolic clearance, perhaps in response to diminished effective arterial blood volume.
OBJECTIVE: To assess systemic and regional oxygen transport after open heart surgery in patients with the low cardiac output syndrome who are receiving vasoactive drugs and in patients with normal hemodynamics during spontaneous rewarming. DESIGN: Prospective, nonrandomized controlled trial. SETTING: Tertiary care center. PATIENTS: Sixteen patients aged 53.1 +/- 8.4 yrs were studied after coronary artery bypass operations: ten patients with a cardiac index of < 1.75 L/min/m2 and six control patients with a cardiac index of > 1.75 L/min/m2. INTERVENTIONS: The patients with a cardiac index of < 1.75 L/min/m2 received either dobutamine alone (n = 5) or in combination with nitroprusside (n = 5). The control patients with a cardiac index of > 1.75 L/min/m2 did not receive vasoactive treatment. The systemic oxygen consumption was measured by indirect calorimetry and the regional blood flow was measured by primed continuous infusion of indocyanine green. MEASUREMENTS AND MAIN RESULTS: Both splanchnic and femoral blood flows increased (p < .05) in parallel with cardiac output during vasoactive drug therapy. High splanchnic oxygen extraction in patients with low cardiac index and flow-dependent splanchnic oxygen consumption in some patients indicated marginal splanchnic oxygen delivery. In addition, femoral blood flow was low and oxygen consumption changed in parallel with oxygen delivery in patients with the low cardiac output syndrome. CONCLUSIONS: In low cardiac output syndrome after cardiac surgery, splanchnic oxygen delivery was marginal and was maintained at the expense of peripheral oxygen delivery. Dobutamine, both alone and in combination with sodium nitroprusside, improved splanchnic oxygen delivery.
INTRODUCTION AND OBJECTIVES: Levosimendan is an inotropic agent that is effective in the treatment of heart failure. However, experience with levosimendan in patients with reduced cardiac output following cardiopulmonary bypass is limited. The objective of this study was to compare the short-term hemodynamic effects of levosimendan with those of dobutamine in managing low cardiac output after cardiac surgery. METHODS: Forty-one patients who had low cardiac output after cardiopulmonary bypass were randomly assigned to dobutamine (n=20), 24-hour infusion of 7.5 microg/kg per min, or levosimendan (n=21), at a loading dose of 12 microg/kg followed by 24-hour infusion of 0.2 microg/kg per min. The following parameters were determined during a 48-hour observation period: arterial, central venous, pulmonary arterial and pulmonary capillary wedge pressure, cardiac index, heart rate, stroke volume, and systemic and pulmonary vascular resistance. RESULTS: Although both dobutamine and levosimendan improved the cardiac index, the increase was significantly greater with levosimendan (2.4 [0.2] l/min per m2 vs 2.9 [0.3] l/min per m2, respectively, at 24 h; P<.05). Moreover, levosimendan significantly reduced systemic and pulmonary vascular resistance, and significantly decreased systemic arterial, pulmonary arterial, pulmonary capillary wedge, and central venous pressure. CONCLUSIONS: Both dobutamine and levosimendan are effective in managing postoperative low cardiac output. However, levosimendan induces non-specific systemic, venous and pulmonary vasodilation which can result in hypotension as a adverse event. In these patients, it is advisable to omit or reduce the loading dose.
We assessed the effect of milrinone on myocardial function in pediatric patients with postoperative low cardiac output syndrome by index of myocardial performance in a prospective, open-label, nonrandomized, consecutive study. Fifteen patients with low cardiac output syndrome following cardiac surgical treatment were studied in the tertiary cardiothoracic pediatric intensive care unit between April 2001 and November 2003 (age range, 0.2-16 months; median, 7; weight, 2.7-11.8 kg; median, 5). Echocardiographic, Doppler-derived, time interval-based index of myocardial performance (Tei index) was used to study cardiac function prior to and while on intravenous milrinone treatment for 18-24 hours. Treatment with milrinone led to improvement in biventricular myocardial function [mean right ventricular index from 0.521 (SD-0.213) to 0.385 (SD-0.215), p = 0.003; mean left ventricular index from 0.636 (SD-0.209) to 0.5 (SD-0.171), p = 0.012). No difference was found in the values of heart rate corrected right or left ventricular ejection time prior to and while on treatment with milrinone (right ventricle: mean, 1.23 (SD-0.42) and 1.14 (SD-0.48), p = 0.29; left ventricles: mean, 1.17 (SD-0.51) and 1.13 (SD-0.48), p = 0.66) Our data support the direct myocardial effect of milrinone as part of the mechanism behind its already proven benefit in children with low cardiac output syndrome following cardiac surgery.
BACKGROUND: Low cardiac output syndrome (LCOS), defined as the need for postoperative intraaortic balloon pump or inotropic support for >30 minutes in the intensive care unit, remains a relatively common complication of aortic valve (AV) surgery. The aim of this study is to identify the preoperative predictors of LCOS in patients undergoing isolated AV surgery. METHODS AND RESULTS: We conducted a retrospective review of data prospectively entered into an institutional database. Between 1990 and 2003, 2255 patients underwent isolated AV surgery with no other concomitant cardiac surgery. The independent predictors of LCOS and operative mortality (OM) were determined by stepwise logistic regression analysis. The overall prevalence of LCOS was 3.9%. The independent predictors of LCOS were (odds ratio in parentheses) renal failure (5.0), earlier year of operation (4.4), left ventricular ejection fraction <40% (3.6), shock (3.2), female gender (2.8), and increasing age (1.02). Overall OM was 2.9%. The OM was higher in patients who experienced LCOS (38% versus 1.5%; P<0.001). The independent predictors of mortality were (odds ratio in parentheses) preoperative renal failure (8.3), urgency of surgery (3.4), previous stroke (2.9), congestive heart failure (2.6), previous cardiac surgery (2.3), hypertension (1.7), and small AV size (1.3). CONCLUSIONS: Low-output syndrome is associated with significantly increased morbidity and mortality. Novel strategies to preserve renal function, optimization of preexisting heart failure symptoms, and avoidance of prosthesis-patient mismatch may reduce the incidence of LCOS and lead to improved results after AV surgery.