Underlying Causes of High Output Heart Failure

In the U.S., each year, there are more than 500,000 new cases of all types of heart failure. With high output cardiac failure, there is an elevated cardiac output associated with several conditions and diseases, including obesity, chronic anemia, systemic arterio-venous fistula, hypercapnia, mitochondrial dysfunction, and hyperthyroidism. The underlying pathophysiologic mechanisms relate to a reduction in systemic vascular resistance from arterio-venous shunting or peripheral vasodilation. Often there is a decrease in systemic arterial blood pressure and neurohormonal activation leading to heart failure symptoms of dyspnea and fatigue. In a persistent high output state, patients may experience tachycardia, valvular abnormalities, and ventricular dilatation and/or hypertrophy. In this article, there is a review of high output heart failure, including the prevalence, pathophysiology, and common clinical causes of this disease.

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Percutaneous Embolization of Congenital Portosystemic Venous Fistula in an Infant with Down Syndrome

Case Reports in Vascular Medicine ◽

10.1155/2013/127023 ◽

2013 ◽

Vol 2013 ◽

pp. 1-4 ◽

Cited By ~ 1

Author(s):

Pattaraporn Tanya Chun ◽

Terrence Chun ◽

Matthew Files ◽

Nghia Vo ◽

Ryan M. McAdams

Keyword(s):

Heart Failure ◽

Down Syndrome ◽

Portal Vein ◽

Vascular Malformations ◽

Male Infant ◽

Percutaneous Embolization ◽

Left Hepatic Vein ◽

High Output Heart Failure ◽

Venous Fistula ◽

High Output

Congenital intrahepatic portosystemic venous shunts are rare vascular malformations often associated with severe complications. We describe a term male infant with Down syndrome with high output heart failure secondary to a congenital arterial to portal venous fistula that was diagnosed by Doppler ultrasound. Percutaneous embolizations of the left hepatic vein, portal vein, and communicating fistulas were performed without complications, resulting in clinical improvement. A subsequent hepatic ultrasound demonstrated resolution of the pathologic fistulous communication and shunting effects.

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Atrial natriuretic factor release and natriuresis in rats with high-output heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1990.259.5.h1374 ◽

1990 ◽

Vol 259 (5) ◽

pp. H1374-H1379 ◽

Cited By ~ 1

Author(s):

R. Garcia ◽

D. Lachance ◽

G. Thibault

Keyword(s):

Heart Failure ◽

Atrial Natriuretic Factor ◽

Left Ventricular ◽

Heart Weight ◽

Main Peak ◽

Arterial Blood ◽

Natriuretic Factor ◽

High Output Heart Failure ◽

High Output ◽

Atrial Natriuretic

We investigated whether rats with high-output heart failure [aortocaval (AC) shunts] release atrial natriuretic factor (ANF) and excrete sodium after moderate volume expansion (VE) as do sham-operated controls. Mean arterial blood pressure was lower (92.5 +/- 4.4 vs. 114.0 +/- 1.3 mmHg) and relative heart weight was higher (545.6 +/- 35.1 vs. 253.8 +/- 9.8 mg/100 g body wt) in animals with AC shunts than in their controls. Central venous pressure (CVP) was elevated (3.61 +/- 0.36 vs. 0.37 +/- 0.94 mmHg) and heart rate decreased (332.5 +/- 8 vs. 370.0 +/- 9.9 beats/min) in AC rats. This group also presented lower basal urinary sodium excretion (UNaV), urinary volume, and hematocrit than their sham-operated controls. Basal plasma COOH- and NH2-terminal ANF levels were greatly elevated in AC shunt animals (165.43 +/- 55.73 and 1,692.98 +/- 305.63 fmol/ml, respectively) when compared with the controls (14.27 +/- 1.49 and 331.67 +/- 29.84 fmol/ml, respectively). VE was performed in conscious rats 3 times at 15-min intervals with human plasma protein fraction. The effect of VE on CVP, left-ventricular end-diastolic pressure, the increases in plasma COOH- and NH2-terminal ANF, and the diuretic and natriuretic responses were similar in both experimental groups. U(NA)V was positively correlated with plasma COOH- (r = 0.50, P less than 0.01) and NH2- (r = 0.60, P less than 0.001) terminal ANF only in the controls. One main peak of immunoreactive ANF corresponding to the elution time of a small peptide such as ANF-(99-126) was detected in the plasma of AC animals after VE. We conclude that ANF release and natriuresis are conserved after moderate VE in a rat model of moderate high-output experimental heart failure.

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Chronic captopril and losartan (DuP 753) administration in rats with high-output heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.3.h833 ◽

1992 ◽

Vol 263 (3) ◽

pp. H833-H840 ◽

Cited By ~ 4

Author(s):

G. Qing ◽

R. Garcia

Keyword(s):

Heart Failure ◽

Cardiac Hypertrophy ◽

Renin Angiotensin System ◽

Left Ventricular ◽

Right Atrial ◽

Angiotensin Converting Enzyme Inhibition ◽

Arterial Blood ◽

High Output Heart Failure ◽

Regression Of Cardiac Hypertrophy ◽

High Output

We investigated the role of atrial natriuretic factor (ANF) and the renin-angiotensin system as well as the effects of losartan in rats with aortocaval (AC) shunts. Right atrial and left ventricular end-diastolic pressures (LVEDP) were higher and mean arterial blood pressure (MAP) was lower in AC shunt animals than in their controls. AC shunt rats presented marked cardiac hypertrophy, decreased right atrial ANF concentration, and increased ventricular ANF content and concentration. Plasma ANF levels were elevated, and hematocrit was lower in AC shunt animals than in controls. Captopril or losartan treatment decreased MAP and returned LVEDP to sham-operated control values. A clear regression of cardiac hypertrophy was evident in both treated AC shunt groups, with plasma ANF levels tending to follow those in sham-operated rats. Plasma COOH-terminal ANF levels were decreased and urinary volume and hematocrit were increased in losartan-treated AC shunt animals. We conclude that chronic angiotensin converting enzyme inhibition and angiotension II receptor antagonism improved hemodynamic conditions, diminished water retention, reversed cardiac hypertrophy, and restored plasma and tissue ANF to more “normal” levels in rats with moderate high-output heart failure.

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Systematic nocturnal atrial demand pacing results in high-output heart failure

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.5.1803 ◽

1992 ◽

Vol 72 (5) ◽

pp. 1803-1809 ◽

Cited By ~ 6

Author(s):

M. I. Talan ◽

B. T. Engel ◽

P. H. Chew

Keyword(s):

Heart Failure ◽

Cardiac Function ◽

Venous Pressure ◽

Control Period ◽

Peripheral Resistance ◽

Left Ventricular ◽

Central Venous ◽

Arterial Blood ◽

High Output Heart Failure ◽

High Output

Beat-to-beat parameters of heart rate (HR), intra-arterial blood pressure (BP), central venous pressure, and derived indexes of cardiac output and total peripheral resistance were recorded 18 h/day (from 1800 to 1200 h the following day) in four monkeys (Macaca mulatta) during 20 control days followed by 20 days of atrial demand pacing. The pacing rate was set at approximately 10 beats/min above the fastest hourly average HR recorded during the control period, i.e., sufficient to prevent the normal nocturnal fall in HR. Nocturnal pacing resulted in progressive weekly increases in central venous BP and arterial BP. Analyses of levels and diurnal trends in hemodynamic parameters and cardiac function curves across consecutive 5-day periods of nocturnal pacing revealed a hemodynamic pattern characteristic of high-output heart failure, which progressively increased (week by week) during the early morning hours (0500–0700). Sustained elevated left ventricular work resulting from the prevention of a nocturnal fall in HR may have been responsible for the reduction in cardiac function seen in this experimental model.

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High output heart failure due to an iatrogenic arterio-venous fistula after lumbar disc surgery

Acta Neurochirurgica ◽

10.1007/s00701-007-1397-5 ◽

2007 ◽

Vol 149 (12) ◽

pp. 1243-1247 ◽

Cited By ~ 12

Author(s):

M. Gallerani ◽

G. Maida ◽

B. Boari ◽

R. Galeotti ◽

T. Rocca ◽

...

Keyword(s):

Heart Failure ◽

Lumbar Disc ◽

Lumbar Disc Surgery ◽

Disc Surgery ◽

High Output Heart Failure ◽

Venous Fistula ◽

High Output

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A case report: percutaneous management of high-output heart failure from iatrogenic aortocoronary venous grafting to the coronary sinus

The Egyptian Heart Journal ◽

10.1186/s43044-021-00186-1 ◽

2021 ◽

Vol 73 (1) ◽

Author(s):

Akarsh Parekh ◽

Vivek Sengupta ◽

Ryan Malek ◽

Mark Zainea

Keyword(s):

Heart Failure ◽

Coronary Sinus ◽

Saphenous Vein Graft ◽

Left Ventricular ◽

Heart Catheterization ◽

Covered Stents ◽

Bypass Grafting ◽

Output State ◽

State Management ◽

High Output

Abstract Background Aortocoronary arteriovenous fistula (ACAVF) due to iatrogenic bypass grafting to a cardiac vein is an exceedingly rare complication resulting from coronary artery bypass grafting (CABG) surgery. If not identified in a timely fashion, ACAVF has known significant clinical consequences related to left to right shunting and possible residual myocardial ischemia. Case presentation An 82-year-old male with a history of CABG, presented with dyspnea. Over the span of 2 years following CABG, the patient experienced progressive exertional dyspnea and peripheral edema. The patient was found to have a new cardiomyopathy with a severely reduced ejection fraction at 30–35%. The patient underwent diagnostic left heart catheterization, and an ACAVF was discovered between a saphenous vein graft and the coronary sinus. The patient underwent successful percutaneous coiling of the ACAVF with no residual flow. Follow-up echocardiography at 3 months revealed restoration of left ventricular systolic function to 50% and significant improvement in heart failure symptoms. Conclusions ACAVF is an exceedingly rare iatrogenic complication of CABG that may result in residual ischemia from the non-grafted myocardial territory and other sequelae relating to left to right shunting and a high-output state. Management for this pathology includes but is not limited to the use of percutaneous coiling, implantation of covered stents, graft removal and regrafting, and ligation.

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