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PubMed2006

A prospective study on esophageal Doppler hemodynamic assessment in the ED.

We sought to determine whether physicians' estimates of critically ill patients' hemodynamics are accurate as compared with esophageal Doppler probe (EDP) measurements and whether provision of measured hemodynamic profiles produces treatment changes and changes in physician confidence. At an urban county ED, we enrolled 55 critically ill adults with pulmonary edema of unclear etiology, sustained hypotension, or lactic acidosis. Physicians estimated cardiac output (CO) and systemic vascular resistance (SVR), categorized shock, stated treatment plans, and rated confidence in assessment and treatment plans. Physicians were informed of EDP hemodynamic measurements (CO, SVR, stroke volume, and contractility), and they repeated their assessments and plans. Weighted kappa values between physician estimates and EDP measurements of CO and SVR were 0.57 (95% confidence interval [CI] = 0.77-0.36) and 0.40 (95% CI = 0.64-0.16), respectively. Shock characterization changed in 52%, confidence increased significantly (pre-EDP mean = 3.3 +/- 0.9; post-EDP mean = 4.0 +/- 0.6; P = .0001), and stated treatment plans changed in 68% of the patients. Chart review demonstrated that similar proportions of control subjects had treatment changes, with a mean difference of 20% (95% CI = -2 to 42). Physician assessments of hemodynamic variables were moderately accurate. We conclude that EDP hemodynamic profiles change assessments and increase confidence in assessments but may not alter treatment.

Acidosis, Lactic↗
PubMed2002

Lithium dilution measurement of cardiac output and arterial pulse waveform analysis: an indicator dilution calibrated beat-by-beat system for continuous estimation of cardiac output.

Lithium dilution cardiac output (LiDCO trade mark; LiDCO, London, UK) is a minimally invasive indicator dilution technique for the measurement of cardiac output. It was primarily developed as a simple calibration for the PulseCO trade mark (LiDCO, London, UK) continuous arterial waveform analysis monitor. The technique is quick and simple, requiring only an arterial line and central or peripheral venous access. These lines would probably already have been inserted in critical care patients. A small dose of lithium chloride is injected as an intravenous bolus, and cardiac output is derived from the dilution curve generated by a lithium-sensitive electrode attached to the arterial line. Studies in humans and animals have shown good agreement compared with results obtained with other techniques, and the efficacy of LiDCO trade mark in pediatric patients has also been proven. Compared with thermodilution, lithium dilution showed closer agreement in clinical studies with electromagnetic flow measurement.PulseCO trade mark is a beat-to-beat cardiac output monitor that calculates stroke volume from the arterial pressure waveform using an autocorrelation algorithm. The algorithm is not dependent on waveform morphology, but, rather, it calculates nominal stroke volume from a pressure-volume transform of the entire waveform. The nominal stroke volume is converted to actual stroke volume by calibration of the algorithm with LiDCO trade mark. Initial studies indicate good fidelity, and the results from centers in the United States and the United Kingdom are extremely encouraging. The PulseCO trade mark monitor incorporates software for interpretation of the hemodynamic data generated and provides a real-time analysis of arterial pressure variations (ie, stroke volume variation, pulse pressure variation, and systolic pressure variation) as theoretical guides to intravascular and cardiac filling.

Adult↗
PubMed1993

Pulmonary vascular impedance vs. resistance in hypoxic and hyperoxic dogs: effects of propofol and isoflurane.

The pulmonary vascular effects of inhaled anesthetics have been reported variably. We compared the effects of intravenous anesthesia (propofol) and inhalational anesthesia (isoflurane) on multipoint mean [pulmonary arterial pressure (Ppa)-pulmonary arterial occluded pressure (PpaO)]/cardiac output (Q) plots and on pulmonary vascular impedance (PVZ) spectra in eight dogs alternatively ventilated in hyperoxia [inspired O2 fraction (FIO2) 0.4] and in hypoxia (FIO2 0.1). Q was altered by a manipulation of venous return. During propofol, hypoxia increased (Ppa-PpaO) by an average of 2-3 mmHg over the entire range of Q studied, from 1 to 2.5 l.min-1 x m-2. This hypoxic pulmonary vasoconstriction (HPV) was associated with insignificant changes in PVZ. Decreasing Q in hypoxia and hyperoxia did not affect PVZ. Compared with propofol, isoflurane decreased (Ppa-PpaO) by an average of 2-5 mmHg at all levels of Q studied in both hypoxia and hyperoxia but did not affect HPV. During isoflurane anesthesia, 0 Hz PVZ was lower (P < 0.01) in hypoxia, but otherwise the PVZ spectrum was not different from that recorded during propofol anesthesia. We conclude that, in dogs, 1 degree general anesthesia with isoflurane alone decreases pulmonary vascular tone without inhibition of HPV and that 2 degrees pressure/Q plots in the time domain are more sensitive than those in the frequency domain to subtle hemodynamic changes induced by hypoxia or isoflurane at the periphery of the pulmonary vasculature.

Anesthesia↗
PubMed1991

Redistribution of intraorgan blood flow in acute, hyperdynamic porcine endotoxemia.

In a standardized porcine model of acute, hyperdynamic endotoxemia the distribution of intraorgan blood flow within heart, kidney and brain was analyzed. Twelve pigs received either short-term (23 min) or long-term (205 min) continuous intravenous infusion of endotoxin (Salmonella abortus equi). A high cardiac output/low peripheral resistance state was maintained throughout the 3.5 h observation period. Total organ blood flow in heart, kidney and brain remained high; however, already small amounts of endotoxin provoked a significant redistribution of intraorgan blood flow within the left ventricle and the kidney. These characteristic alterations were absent in a control group of 5 animals subjected to the same protocol, but receiving 0.9% saline instead of endotoxin. Deterioration of respiratory function developed exclusively after continuous intravenous endotoxin infusion over 205 min, indicating incipient organ failure. Using electron microscopy, endothelial cells swelling and entrapment of blood cells in capillaries of the midmyocardium as well as severe ultrastructural damage in the kidney could be demonstrated already after 90 min of endotoxemia in two additional animals. It is concluded that already in the initial phase of acute endotoxemia, in the presence of high cardiac output and high global organ blood flow microcirculatory deterioration and organ failure develops. As small amounts of endotoxin are capable of inducing these alterations, earliest possible diagnosis of endotoxemia should be achieved in critically ill patients.

Acute Disease↗
PubMed1995

Noninvasive investigation of infantile hepatic hemangioma: a case study.

A preterm infant presented with high-output cardiac failure. Color Doppler imaging of the liver revealed a large hepatic hemangioma. Pulsed-wave Doppler of the proximal aorta was used to monitor noninvasively the reduction in flow through the arteriovenous malformation in response to steroid therapy. The hemangioma resolved completely by 7 weeks of age.

Aorta↗
PubMed1994

Hemodynamics of mitral stenosis: a review.

This review discusses the latest developments in the hemodynamics of mitral stenosis. English-language journal articles, reviews, and textbooks from the clinical, physiology, and engineering literature related to mitral valve stenosis were identified and reviewed. The main conclusions are: (1) the hemodynamics of mitral stenosis are determined by the complex anatomical and pathophysiologic features of the valve apparatus, (2) the properties of the left ventricle, atrium, and pulmonary vasculature also have a major impact on the hemodynamic significance and the clinical syndrome of mitral stenosis, (3) the valve and the cardiac chambers have a functional reserve that become exhausted as the stenosis worsens and/or the compensatory mechanisms of the chambers fail, and (4) a careful approach to data acquisition and analysis will lead to an accurate assessment of the hemodynamics of mitral stenosis before and after therapeutic interventions.

Atrial Function↗
PubMed1996

Cardiovascular disease in peritoneal dialysis.

Cardiovascular morbidity and mortality remain high in ESRD patients. Lipid abnormalities in CAPD may be more important than in hemodialysis. Vessel calcification may have a role in atherosclerotic heart disease, but this is only an inference from several clinical observations, and it remains to be defined more clearly as a risk factor. Left ventricular hypertrophy is frequent in this patient population, and is associated with specific clinical patterns and an increased risk of death. Erythropoietin treatment of anemia and tight blood pressure controls have proved to help in reversing severe left ventricular hypertrophy. Finally, we describe a syndrome of the hypertrophic, high cardiac output hemodialysis heart, which is characterized by a high cardiac output in hemodialysis patients. It is associated with left ventricular hypertrophy and eventually right ventricular hypertrophy with tricuspid insufficiency. This may require fistula revision and even a switch peritoneal dialysis.

Cardiovascular Diseases↗
PubMed1991

Effect of ventilatory strategy on cardiac output during high frequency jet ventilation.

STUDY OBJECTIVE: The aim was to study the effects of changes in ventilation variables on cardiac function during high frequency jet ventilation. DESIGN: Controlled changes in mean airway pressure (2-10 cm H2O), tidal volume (4 and 8 ml), and frequency (4-8 Hz) were used to assess the effects of ventilatory variables on cardiac output in cats with normal and reduced lung compliance during high frequency jet ventilation. Cardiac output was continuously measured with an electromagnetic flow probe placed around the aorta. Respiratory compliance was reduced by lung lavage. EXPERIMENTAL MATERIAL: Seven anaesthetised adults cats, weight 3.0(SEM 0.2) kg, were used in the study. MEASUREMENTS AND MAIN RESULTS: Cardiac output fell as mean airway pressure was raised from 2 to 10 cm H2O at all frequencies and tidal volumes. At identical levels of minute ventilation and mean airway pressure, cardiac output was improved with combinations of smaller tidal volumes and higher frequencies. Reducing respiratory compliance by lung lavage dampened the effect of mean airway pressure on cardiac output, but maintained the relationship between ventilatory variables observed before lavage. CONCLUSION: At identical settings of minute ventilation and mean airway pressure, cardiac output may be improved with smaller tidal volumes during high frequency jet ventilation.

Airway Resistance↗
PubMed1999

The effects of chronic prostacyclin therapy on cardiac output and symptoms in primary pulmonary hypertension.

OBJECTIVES: This study evaluated the response to prostacyclin dose reduction in patients with primary pulmonary hypertension (PPH) who developed high cardiac outputs. BACKGROUND: Patients on prostacyclin require chronic upward dose titration to overcome tolerance to the medication. No upper limit of effective dose has been described. METHODS: We studied 12 patients with PPH treated with chronic prostacyclin therapy who presented in high cardiac output states. Each patient underwent prostacyclin dose reduction under hemodynamic guidance targeted to reduce the cardiac index to < or =4 liter/min/M2, unless rebound pulmonary hypertension occurred. Following dose reduction, patients were observed for changes in the effectiveness of the prostacyclin. RESULTS: Patients were treated for 39 +/- 20 months, resulting in a 71% reduction in pulmonary vascular resistance compared to baseline. At the time of their most recent evaluation their cardiac outputs were increased to 10.1 +/- 2.3 liter/min. The patients underwent a 39% dose reduction (range 12% to 78%) resulting in a change of mean PAP from 45 to 46 mm Hg (p = NS), cardiac index from 7.4 +/- 1.4 to 4 +/- 0.74 liter/min/M2 (p = 0.01), and pulmonary vascular resistance from 3.7 +/- 1.7 to 4.7 +/- 1.5 units (p < 0.001). In no instance did rebound pulmonary hypertension occur. However, the patients all retained their clinical benefit without a return of tolerance. CONCLUSIONS: Excessive prostacyclin in PPH can lead to a high cardiac output state, suggesting it has important positive inotropic effects. In this circumstance, reducing the dose can allow the cardiac output to return to normal without worsening the clinical state.

Adult↗
PubMed2002

Comparison of bedside measurement of cardiac output with the thermodilution method and the Fick method in mechanically ventilated patients.

INTRODUCTION: Bedside cardiac output determination is a common preoccupation in the critically ill. All available methods have drawbacks. We wished to re-examine the agreement between cardiac output determined using the thermodilution method (QTTHERM) and cardiac output determined using the metabolic (Fick) method (QTFICK) in patients with extremely severe states, all the more so in the context of changing practices in the management of patients. Indeed, the interchangeability of the methods is a clinically relevant question; for instance, in view of the debate about the risk-benefit balance of right heart catheterization. PATIENTS AND METHODS: Eighteen mechanically ventilated passive patients with a right heart catheter in place were studied (six women, 12 men; age, 39-84 years; simplified acute physiology scoreII, 39-111). QTTHERM was obtained using a standard procedure. QTFICK was measured from oxygen consumption, carbon dioxide production, and arterial and mixed venous oxygen contents. Forty-nine steady-state pairs of measurements were performed. The data were normalized for repeated measurements, and were tested for correlation and agreement. RESULTS: The QTFICK value was 5.2 +/- 2.0 l/min whereas that of QTTHERM was 5.8 +/- 1.9 l/min (R = 0.840, P < 0.0001; mean difference, -0.7 l/min; lower limit of agreement, -2.8 l/min; upper limit of agreement, 1.5 l/min). The agreement was excellent between the two techniques at QTTHERM values <5 l/min but became too loose for clinical interchangeability above this value. Tricuspid regurgitation did not influence the results. DISCUSSION AND CONCLUSIONS: No gold standard is established to measure cardiac output in critically ill patients. The thermodilution method has known limitations that can lead to inaccuracies. The metabolic method also has potential pitfalls in this context, particularly if there is increased oxygen consumption within the lungs. The concordance between the two methods for low cardiac output values suggests that they can both be relied upon for clinical decision making in this context. Conversely, a high cardiac output value is more difficult to rely on in absolute terms.

Adult↗
PubMed1987

Progressive heart failure secondary to a high output state.

A high cardiac output state has been an infrequent but previously reversible cause of heart failure in patients with hemodialysis fistulas. A patient with two proximal upper extremity fistulas was found to have progressive depression in his left ventricular function and a high output state. His symptoms did not respond to the removal of the most prominent fistula, suggesting that chronic volume overload from the high output state may irreversibly depress left ventricular function.

Adult↗
PubMed2002

Crow-Fukase syndrome associated with high-output heart failure.

A 64-year-old woman was admitted with systemic edema and exertional dyspnea. High-output heart failure was diagnosed by right heart catheterization and she was treated with diuretics. After 3 weeks, her symptoms disappeared but a high cardiac output state persisted. A diagnosis of Crow-Fukase syndrome was made based on the presence of polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes. Her serum vascular endothelial growth factor (VEGF) level was markedly elevated after recovery from heart failure. We suspect that an elevated VEGF level and a high cardiac output state may play a role in the pathogenesis of heart failure in Crow-Fukase syndrome.

Cardiac Output, High↗
PubMed1974

On the role of vasopressin and angiotensin in the development of irreversible haemorrhagic shock.

1. Long-lasting haemorrhagic hypotension (4.5 hr at 35 mmHg) leading to irreversible haemorrhagic shock, has been studied in normal dogs, in dogs treated with a bradykinin potentiating nonapeptide (BPP(9a)), which blocks the conversion of angiotensin I to angiotensin II, and in dogs with experimental chronic diabetes insipidus (DI dogs). BPP(9a) was given by I.V. injection before the start of bleeding (BPP pre-treated group), 45 min after blood pressure had reached 35 mmHg (BPP early treated group) or 2 hr after blood pressure had reached 35 mmHg (BPP late-treated group). After retransfusion of blood all dogs were allowed to recover and observed for a further period of 3 days.2. Untreated control dogs developed haemorrhagic shock with tachycardia, low cardiac output, low total peripheral conductance and low stroke volume. All died within 24 hr of retransfusion, with pathological lesions typical of irreversible haemorrhagic shock.3. BPP pre-treated dogs developed haemorrhagic shock with bradycardia (during early shock), high cardiac output, high peripheral vascular conductance and high stroke volume when compared with the untreated controls. All pre-treated animals survived the 3 day observation period. They were then killed and on post-mortem showed no signs of irreversible haemorrhagic shock.4. BPP early-treated animals behaved like controls before BPP, but like pre-treated animals after the drug. Only one out of eight died within the 3 day observation period.5. BPP late-treated dogs behaved like controls before BPP. They responded to the drug with a rise in cardiac output, peripheral vascular conductance and stroke volume, and with a fall in heart rate. These responses were, however, short-lived. Four out of these eight animals died within the 3 day observation period, with lesions of irreversible haemorrhagic shock.6. DI dogs developed haemorrhagic shock with tachycardia (like controls), but with high cardiac output and peripheral vascular conductance (like BPP pre-treated dogs). The stroke volume of DI dogs was intermediate between those of controls and pre-treated groups. All six dogs survived the 3 day observation period.7. BPP(9a) had no measurable effect on the course of endotoxic shock.8. It is suggested that the normally severe vasoconstriction of the mesenteric vascular bed, which is thought to be responsible for irreversible haemorrhagic shock, is absent or attenuated in the absence of vasopressin or angiotensin. The consequences of this on the development of irreversibility are discussed.

Angiotensin II↗
PubMed2004

Effect of surgical banding of a high-flow fistula on access flow and cardiac output: intraoperative and long-term measurements.

Creation of either a natural arteriovenous graft or a fistula as a vascular access to support long-term hemodialysis can lead to "high-output" cardiac failure. The authors describe a patient who underwent surgical banding of an upper arm arteriovenous fistula. Access flow and cardiac output were measured not only pre- and postoperatively but also intraoperatively using a modified Swan Ganz catheter, originally developed to measure access flows during radiologic procedures. Banding resulted in a significant decrease in access flow and cardiac output, which was sustained for up to 1 year postoperatively.

Arteriovenous Fistula↗
PubMed1994

Reversal of refractory hypotension in septic shock by inhibitor of nitric oxide synthase.

Septic shock is a life-threatening condition that results from exposure to bacterial endotoxin. It is mediated by the release of cytokines. Some of these cytokines cause the release of vasoactive substances. We report the case of a 62-year-old male patient who received redo operation for replacement of the degenerative porcine aortic and mitral prostheses. High cardiac output shock developed on the seventh postoperative day with severe metabolic acidosis and oliguria. Systemic vascular resistance and mean arterial pressure elevated within 5 min and stabilized 60 min after the start of a single dose of intravenous administration of NG-monomethyl-L-arginine (50 mg), a potent and selective inhibitor of nitric oxide synthesis. These findings indicate that nitric oxide overproduction is an important contributor to refractory hypotension in high cardiac output septic shock. Our findings suggested the utilization of nitric oxide synthase inhibitor in the treatment of septic shock in humans.

Amino Acid Oxidoreductases↗
PubMed1991

Congestive heart failure secondary to an arteriovenous fistula from cardiac catheterization and angioplasty.

Arteriovenous (AV) fistulae are well known to cause high output cardiac failure. AV fistulae from cardiac catheterization are as rare as 0.01% in the transfemoral approach. We describe here what we believe is the first reported case of high output cardiac failure from an AV fistula due to percutaneous transluminal coronary angioplasty (PTCA). The patient had reversal of the congestive heart failure with surgical correction of the fistula.

Aged↗