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

1992 ◽  
Vol 72 (5) ◽  
pp. 1803-1809 ◽  
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.

Effect of nocturnal atrial demand cardiac pacing on diurnal hemodynamic patterns

1992 ◽  
Vol 72 (5) ◽  
pp. 1798-1802 ◽  
Author(s):  
B. T. Engel ◽  
M. I. Talan ◽  
P. H. Chew
Keyword(s):  
Central Venous Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Control Period ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Central Venous ◽  
Arterial Blood ◽  
Early Evening

Heart rate (HR), stroke volume (SV), intra-arterial blood pressure, and central venous pressure were recorded on a beat-to-beat basis, 18 h/day (1800–1200 h the following day), for approximately 2 mo in four monkeys (Macaca mulatta). Cardiac output, left ventricular work, and total peripheral resistance were derived from these primary measurements. During the 1st mo we measured these parameters under control conditions, and during the 2nd mo the animals were studied while HR was paced by atrial demand pacing sufficient to prevent the normal nocturnal fall in HR (approximately 10 beats/min above the fastest hourly average rate recorded during the control condition). The main hypothesis of this study was that when HR is prevented from falling, SV, which normally does not fall overnight, would fall; this hypothesis was confirmed. In addition, we observed that, during the period of pacing, relative to the control period, SV was approximately 14% greater during the early evening and 4% lower during the early morning; total peripheral resistance was similar during the early evening but was 13% higher by morning. Throughout the night, systolic pressure was approximately 4% greater, diastolic pressure was 17% higher, central venous pressure was 43% greater, and left ventricular work was 27% higher. These findings show that when HR is prevented from falling overnight by atrial demand pacing, even to a relatively modest degree, there can be very significant sustained changes in cardiovascular function.

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

1990 ◽  
Vol 259 (5) ◽  
pp. H1374-H1379 ◽  
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.

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

1992 ◽  
Vol 263 (3) ◽  
pp. H833-H840 ◽  
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.

CARDIORENAL EFFECTS OF LARGE INFUSIONS OF DEXTRAN IN DOGS

1954 ◽  
Vol 32 (1) ◽  
pp. 559-566 ◽  
Author(s):  
C. W. Gowdey ◽  
I. E. Young
Keyword(s):  
Cardiac Output ◽  
Peripheral Resistance ◽  
The Body ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
The Right ◽  
Dextran Solution ◽  
High Output

The production of hypervolemic dilution anemia in intact, anesthetized dogs by the continuous intravenous infusion of 6% dextran solution caused large increases in the cardiac output and urine flow. No consistent changes were observed in pulse rate or arterial blood pressure. The right auricular mean pressure usually increased early in the infusion, but later there was no consistent relation between right auricular pressure and cardiac output. The total peripheral resistance, glomerular filtration rate, and renal blood flow decreased. With infusion volumes exceeding 10% of the body weight, acute high-output heart failure occurred. The observed hemodilution was consistently greater than that expected from the volume of the infusion, because the dextran solution was, presumably, hypertonic.

Development of High-Output Heart Failure after Correction of Central Venous Occlusion: A Case Report

Renal Failure ◽  
2011 ◽  
Vol 33 (8) ◽  
pp. 833-836 ◽  
Author(s):  
Kenan Turgutalp ◽  
Mehmet Horoz ◽  
Turkay Ozcan ◽  
Altan Yildiz ◽  
Ebru Gok Oguz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Case Report ◽  
Venous Occlusion ◽  
Central Venous ◽  
High Output Heart Failure ◽  
Central Venous Occlusion ◽  
High Output

scholarly journals Underlying Causes of High Output Heart Failure

2020 ◽  
pp. 1-4
Author(s):  
Qiuhua Shen ◽  
Qiuhua Shen ◽  
John B. Hiebert ◽  
Janet D. Pierce
Keyword(s):  
Heart Failure ◽  
Neurohormonal Activation ◽  
Chronic Anemia ◽  
Output State ◽  
Arterial Blood ◽  
High Output Heart Failure ◽  
Underlying Causes ◽  
Venous Fistula ◽  
High Output ◽  
Pathophysiologic Mechanisms

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.

Peripheral vascular effects of nitroglycerin in a conscious rat model of heart failure

1982 ◽  
Vol 243 (6) ◽  
pp. H974-H981
Author(s):  
S. F. Flaim
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Arterial Blood Flow ◽  
Vascular Effects ◽  
Conscious Rat ◽  
Arterial Blood ◽  
Caudal Artery

The effects of intravenous nitroglycerin (NG; 2, 8, 32 micrograms/kg) on cardiocirculatory dynamics were evaluated in control normal (C) and chronically volume-overloaded [high-output heart failure (aortocaval fistula), HCO] conscious rats. Pressures were recorded in the left ventricle, the caudal artery, and the right atrium. Regional blood flows were determined by radioactive microsphere injection into the left ventricle with reference sampling from the caudal artery. Cardiac output (CO) was 289 ml . min-1 . kg in C and did not change with NG; however, in HCO systemic CO was decreased 31, 23, and 23% by NG from 350 ml . min-1 . kg. In both groups left ventricular end-diastolic pressure was reduced (C, 8.4–5.0; HCO, 19.8–12.7 mmHg); however, central venous pressure was reduced only in C (1.2–0.3 mmHg). During NG primarily at 2 and 8 micrograms/kg, arterial blood flow was lower and vascular resistance was higher in HCO compared with C in the following regions: kidney, ileum, jejunum, skin, heart, spleen, stomach, and testes, whereas no major differences were noted in the cerebellum, cerebrum, liver, or skeletal muscle. Thus acute NG infusion is a more potent regional vasodilator in C than in HCO. It is suggested that this difference is related to a more powerful NG-induced sympathetic reflex activation in the HCO group, which strongly attenuates the direct vasodilator effect of NG that was apparent in C.

scholarly journals Wide pulse pressure and Quincke’s pulse in high-output heart failure

2021 ◽  
Vol 14 (7) ◽  
pp. e241654
Author(s):  
Katie Lin Berry ◽  
Peter D Sullivan ◽  
André Martin Mansoor
Keyword(s):  
Heart Failure ◽  
Alcohol Use ◽  
Pulse Pressure ◽  
Systolic Function ◽  
Venous Pressure ◽  
Diuretic Therapy ◽  
Vena Cava ◽  
Right Heart Catheterisation ◽  
High Output Heart Failure ◽  
High Output

A 74-year-old man with a history of chronic alcohol use presented with progressive exertional dyspnoea and weight gain. On physical examination, he was noted to have wide pulse pressure, elevated jugular venous pressure, and alternating flushing and blanching of the nail beds in concert with the cardiac cycle, known as Quincke’s pulse. Transthoracic echocardiography demonstrated normal biventricular systolic function and valvular function, but noted a dilated inferior vena cava. Right heart catheterisation revealed elevated filling pressures, high cardiac output and low systemic vascular resistance, consistent with high-output heart failure. Whole blood concentration of thiamine was low, confirming the diagnosis of wet beriberi. The patient abstained from alcohol use and was started on thiamine replacement therapy, resulting in narrowing of the pulse pressure over time and complete resolution of symptoms without the need for diuretic therapy.

Increased ANF secretion after volume expansion is preserved in rats with heart failure

1988 ◽  
Vol 254 (2) ◽  
pp. R185-R191 ◽  
Author(s):  
Y. W. Chien ◽  
R. W. Barbee ◽  
A. A. MacPhee ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Blood Volume ◽  
Volume Expansion ◽  
Diastolic Pressure ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Blood Volume Expansion

To examine whether the failing heart has reached a maximal capacity to increase plasma atrial natriuretic factor (ANF) concentration, the change in plasma immunoreactive ANF level due to acute blood volume expansion was determined in conscious rats with chronic heart failure. Varying degrees of myocardial infarction and thus heart failure were induced by coronary artery ligation 3 wk before study. Compared with controls, infarcted rats had decreases in mean arterial pressure (-10 mmHg, P less than 0.01), cardiac index (-27%, P less than 0.001), renal blood flow (-35%, P less than 0.01), and peak left ventricle-developed pressure after aortic occlusion (an index of pressure generating ability; -15%, P less than 0.01), and increases in central venous pressure (+1.7 mmHg, P less than 0.01), left ventricular end-diastolic pressure (+10 mmHg, P less than 0.001), total peripheral resistance (+28%, P less than 0.01), and plasma ANF level (752 +/- 109 vs. 244 +/- 33 pg/ml, P less than 0.001). Plasma ANF was correlated with infarct size, cardiac filling pressures, and left ventricle pressure-generating ability. At 5 min after 25% blood volume expansion, plasma ANF in rats with heart failure increased by 2,281 +/- 345 pg/ml; the magnitude of the changes in circulating ANF and hemodynamic measurements was similar in controls. The results suggest that plasma ANF level can be used as a reliable index of the severity of heart failure, and that the capacity to increase plasma ANF concentration after acute volume expansion is preserved in rats with heart failure. There was no evidence of a relative deficiency of circulating ANF in this model of heart failure.

Why does pulmonary venous pressure rise after onset of LV dysfunction: a theoretical analysis

1993 ◽  
Vol 265 (5) ◽  
pp. H1819-H1828 ◽  
Author(s):  
D. Burkhoff ◽  
J. V. Tyberg
Keyword(s):  
Heart Failure ◽  
Theoretical Analysis ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Simple Explanation ◽  
Sympathetic Activation ◽  
Dramatic Rise ◽  
Hemodynamic Consequence

One of the most important consequences of acute left ventricular dysfunction (LVD) is pulmonary edema resulting from a rise in pulmonary venous pressure (PVP). It is generally believed that the PVP rise is a direct hemodynamic consequence of LVD. While this paradigm seems plausible, especially if the LV is viewed as a sump pump, there is no specific evidence to support this simple explanation. A theoretical analysis was performed to assess the hemodynamic mechanisms responsible for the dramatic rise in PVP after acute LVD. The ventricles were modeled as time-varying elastances; pulmonary and systemic vascular systems were modeled as series of resistive and capacitive elements. In response to a 50% decrease in LV contractile strength [end-systolic elastance (Ees)], cardiac output (CO) and mean arterial pressure (MAP) dropped substantially, while PVP increased minimally from its baseline of 12 to approximately 15 mmHg. With LV Ees set at 50% of normal, the effects of sympathetic activation were tested. When heart rate and total peripheral resistance were increased, CO and MAP improved, yet PVP still did not rise. The only intervention that caused a substantial increase in PVP was to simulate the decrease in unstressed volume (VU) of the venous system known to occur with sympathetic activation. When VU was decreased by about 15-20% (comparable to experimentally observed shifts with acute heart failure), PVP increased above 25 mmHg. The effects of pericardial constraints were investigated, and the results suggest a major role of this organ in determining the overall hemodynamic response to acute LVD, sympathetic activation, and explaining the responses to therapy. Thus this analysis suggests that elevations of PVP do not occur simply as a direct hemodynamic consequence of acute LVD. Rather, changes in PVP may be dictated more by sympathetic control on venous capacity. If confirmed, recognition of this as a primary mechanism may prove important in directing development of new therapies and in understanding the mechanisms of disease progression in heart failure.

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