scholarly journals Centralversusperipheral control of cardiac output in humans: insight from atrial pacing

2012 ◽  
Vol 590 (20) ◽  
pp. 4977-4978 ◽  
Author(s):  
Stéphane P. Dufour ◽  
Ellen A. Dawson ◽  
Eric J. Stöhr
Keyword(s):  
Cardiac Output ◽  
Atrial Pacing

scholarly journals Peripheral vasodilatation determines cardiac output in exercising humans: insight from atrial pacing

2012 ◽  
Vol 590 (8) ◽  
pp. 2051-2060 ◽  
Author(s):  
A. A. Bada ◽  
J. H. Svendsen ◽  
N. H. Secher ◽  
B. Saltin ◽  
S. P. Mortensen
Keyword(s):  
Cardiac Output ◽  
Atrial Pacing ◽  
Peripheral Vasodilatation

scholarly journals Maximum heart rate does not limit cardiac output at rest or during exercise in the American alligator (Alligator mississippiensis)

2018 ◽  
Vol 315 (2) ◽  
pp. R296-R302 ◽  
Author(s):  
William Joyce ◽  
Ruth M. Elsey ◽  
Tobias Wang ◽  
Dane A. Crossley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Venous Return ◽  
Reciprocal Relationship ◽  
Alligator Mississippiensis ◽  
Right Atrial ◽  
Atrial Pacing ◽  
American Alligator ◽  
Maximum Heart Rate

In most vertebrates, increases in cardiac output result from increases in heart rate (fH) with little or no change in stroke volume (Vs), and maximum cardiac output (Q̇) is typically attained at or close to maximum fH. We therefore tested the hypothesis that increasing maximum fH may increase maximum Q̇. To this end, we investigated the effects of elevating fH with right atrial pacing on Q̇ in the American alligator ( Alligator mississippiensis) at rest and while swimming. During normal swimming, Q̇ increased entirely by virtue of a tachycardia (29 ± 1 to 40 ± 3 beats/min), whereas Vs remained stable. In both resting and swimming alligators, increasing fH with right atrial pacing resulted in a parallel decline in Vs that resulted in an unchanged cardiac output. In swimming animals, this reciprocal relationship extended to supraphysiological fH (up to ~72 beats/min), which suggests that maximum fH does not limit maximum cardiac output and that fH changes are secondary to the peripheral factors (for example vascular capacitance) that determine venous return at rest and during exercise.

Distribution of fetal cardiac output: importance of pacemaker location

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
Author(s):  
PT Pitlick ◽  
SE Kirkpatrick ◽  
WF Friedman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Left Atrial ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Foramen Ovale ◽  
Rate Versus ◽  
Left Ventricular Output ◽  
The Right

Important questions exist about the relative roles of changes in heart rate versus extent of myocardial shortening in regulating fetal cardiac output, because increases in heart rate created by left atrial pacing have been shown to increase right ventricular output and decrease left ventricular output. Since the pacemaker site could importantly influence foramen ovale flow and, hence, each ventricle's output, changes in individual ventricular outputs were examined when both the right and left atria were paced at a rate of 270 beats/min in five acute and in eight chronically instrumented fetal lamb studies. With pacing of either atrium, total cardiac output was unchanged compared to control values. However, the right ventricle contributed more to total cardiac output with left atrial pacing (73% acute, 65% chronic) than with right atrial pacing (51% acute, 57% chronic). Converse changes were observed in left atrial pacing (27% acute, 35% chronic) as compared to right atrial pacing (49% acute, 43% chronic). Thus the disparity that exists normally in the contributions of the right and left ventricles to total cardiac output is accentuated with left atrial pacing and minimized with right atrial pacing. Pressure measurements demonstrated changes in the atrial pressure relations that would be expected to alter flow across the foramen ovale depending on the chamber initially activated. Previous experimental differences can, therefore, be attributed to changes in the magnitude of shunting across the foramen ovale and depend on pacemaker location.

Temporary biventricular pacing after cardiac surgery: a method of supporting cerebral perfusion

2014 ◽  
Vol 5 (4) ◽  
pp. 104-109
Author(s):  
Aleksey Borisovich Naumov ◽  
Maksim Viktorovich Didenko ◽  
Sergey Pavlovich Marchenko ◽  
Vitaliy Vladimirovich Suvorov ◽  
Igor Igorevich Averkin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiac Surgery ◽  
Right Ventricle ◽  
Right Atrium ◽  
High Efficiency ◽  
Biventricular Pacing ◽  
Open Heart Surgery ◽  
Atrial Pacing ◽  
Cardiac Operation ◽  
Temporary Pacing

One of the main aims in postoperative period after cardiac surgery is the improving good systemic hemodynamics. In this connection after the cardiac operation it is necessary to use temporary pacing. In literature we can find a lot of methods of application temporary pacing, but what is better we don’t know. Routinely, in cardiac surgical procedures, epicardial pacing leads are placed on the right atrium and right ventricle in case of significant bradycardia or the development of atrioventricular block. It has been reported previously that right atrium - right ventricle pacing may induce left ventricle dyssynchrony and hemodynamic compromise compared with atrial pacing alone. On the other hand, it has recently been suggested that right atrio-biventricular pacing may improve hemodynamics in postcardiac surgery patients. However, this conclusion is not clear in the clinical setting. And may be we will be able to reduce the doses of inotropes, if we will be use method of right atrio-biventricular pacing [16, 20]. Temporary atrio-biventricular pacing improves cardiac output after open-heart surgery and whether ventricular pacing optimization increases cardiac output in this setting. We will examine which forms of cardiac dysfunction benefit from temporary pacing using direct and indirect measures of perfusion and cardiac function. We will also analyze hemodynamics effect after cardiac operation with different setting of pacemaker. The results of our study demonstrate the high efficiency of temporary biventricular pacing, achieved the best hemodynamic effect compared with other methods of temporary pacemaker.

Cardiac Function in Chronic Bronchitis: Effects of Pacing and Plasma Expansion

1981 ◽  
Vol 60 (4) ◽  
pp. 371-375 ◽  
Author(s):  
H. Valette ◽  
B. Raffestin ◽  
A. Lockhart
Keyword(s):  
Cardiac Output ◽  
Plasma Volume ◽  
Volume Expansion ◽  
Past History ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Plasma Volume Expansion ◽  
History Of ◽  
Wedge Pressure

1. We have investigated left ventricular function in 25 selected patients with chronic bronchitis by use of atrial pacing and plasma volume expansion. Nine subjects had a past history of acute respiratory failure. None had either clinical or electrocardiographic signs of coronary heart disease. Paradoxical pulse was absent, since the difference between the highest and lowest systolic arterial pressure throughout the respiratory cycle was 5.4 ± 1.5 mmHg. 2. During atrial pacing, at a mean rate of 145 ±15, about 80% of the predicted maximal rate, none of the patients showed anginal pain or ventricular repolarization abnormality. Cardiac output remained unchanged compared with control values. 3. Plasma volume expansion was achieved by intravenous injection of 1 litre of gelatin over 30 min. Cardiac output, pulmonary wedge pressure and right atrial pressure rose as reported in literature for normal subjects. In four patients cardiac output did not increase although wedge pressure and right atrial pressure did; two of these four patients also had an overshoot in pulmonary wedge pressure just after atrial pacing, suggesting left ventricular dysfunction. Three out of 25 patients had high control right atrial pressures, probably in relation to impaired right ventricular function. No paradoxical pulse occurred during plasma volume expansion. Therefore competition for space in the pericardium between ventricles was unlikely. 4. Our data suggest that left ventricular dysfunction is rare in patients with chronic obstructuve pulmonary disease. There was no significant difference between subjects with and without a past history of acute respiratory failure.

Temporary Atrial Pacing for Cardiac Output After Pediatric Cardiac Surgery

2013 ◽  
Vol 34 (7) ◽  
pp. 1605-1611 ◽  
Author(s):  
Gregory M. Barker ◽  
Jeremy Affolter ◽  
Jessica Saenz ◽  
Casey S. Cox ◽  
Joseph M. Forbess ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Cardiac Surgery ◽  
Pediatric Cardiac Surgery ◽  
Atrial Pacing

Capacitive function of the heart: influence of acute changes in heart volume on mean right atrial pressure

1997 ◽  
Vol 272 (1) ◽  
pp. H553-H558 ◽  
Author(s):  
D. D. Sheriff ◽  
Z. Luo
Keyword(s):  
Cardiac Output ◽  
Blood Volume ◽  
Normal Sinus Rhythm ◽  
Mean Value ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Pacing ◽  
Normal Sinus ◽  
Rapid Pacing

Net transfer of blood volume into or out of the cardiac chambers should have the same effect on central venous pressure as does transfer of an equal volume of blood to or from peripheral organs (e.g., spleen, or liver). We studied five pentobarbital sodium-anesthetized open-chest pigs (20-23 kg) to determine whether a reduction in the time-averaged volume of blood contained in the heart, induced by rapid atrial pacing, can raise right atrial pressure. A central premise of our study is that the mean value of right atrial pressure is acutely governed by the volume of blood that distends the central veins, and that atrial contractions primarily determine how atrial pressure varies about its mean value. To prevent changes in cardiac output from altering central blood volume and pressure, cardiac output during rapid pacing (2.36 +/- 0.18 l/min) was made to equal the resting output (2.35 +/- 0.16 l/min). This was achieved by selecting a rate of pacing at which the tendency for more frequent cardiac contractions to raise cardiac output was counterbalanced by the decrease in stroke volume induced by rapid pacing. Autonomic reflex mechanisms were attenuated by pharmacological blockade. Mean arterial pressure was minimally affected in the transition from a normal sinus rhythm (89 +/- 6 beats/min) to rapid atrial pacing (165 +/- 7 beats/min) in four pigs. Mean right atrial pressure rose abruptly from 2.8 +/- 0.5 mmHg during normal sinus rhythm to 3.5 +/- 0.5 mmHg (P = 0.015) at the onset of rapid pacing in these four pigs, presumably owing to decreased cardiac blood volume and a reciprocal expansion of central venous volume. In the fifth pig, a reduction in cardiac output induced by tachycardia led to a larger rise in mean right atrial pressure than did a reduction in cardiac output induced by bradycardia, presumably because tachycardia reduces cardiac blood volume whereas bradycardia raises cardiac volume. We conclude that the heart may play an important role in maintaining or raising its own filling pressure when heart rate rises.

Coherence of cardiac output with rate changes

1982 ◽  
Vol 243 (4) ◽  
pp. H499-H504 ◽  
Author(s):  
J. Melbin ◽  
D. K. Detweiler ◽  
R. A. Riffle ◽  
A. Noordergraaf
Keyword(s):  
Cardiac Output ◽  
Stellate Ganglion ◽  
Atrial Pacing ◽  
Adrenergic Stimulation ◽  
Experimental Conditions ◽  
Circulatory Response ◽  
Atrial Rate ◽  
Anesthetized Dogs ◽  
Linear Version ◽  
Independent Variable

In awake or lightly anesthetized dogs increases in heart rate (HR) induced by atrial pacing affect cardiac output (CO) and stroke volume (SV) in a predictable way that is represented by a SV-HR relationship (dSV/dHR). Under our experimental conditions where normal regulation of atrial rate was bypassed, atrial rate was the independent variable and CO and SV were dependent variables. As HR is increased, CO and SV are modified by reflex and other circulatory regulators. The dSV/dHR relation characterized the circulatory response to increasing HR. A single dSV/dHR curve consistently predicted responses under a number of different conditions (standing, recumbent, awake, various anesthetics, beta-adrenergic stimulation, or depression) and thus appeared as an expression of cardiac function. Alterations of the circulation by stellate ganglion or vagal stimulation, volume loading, aortic compression, and ventricular pacing were not represented by the same dSV/dHR function. The dSV/dHR function (including its linear version as reported by others for anesthetized dogs) showed that, when SVs were larger at low rates, maximum CO occurred at a higher HR. Recognition of this arithmetic-based feature resolves apparent contradictory findings reported in the literature.

Passive effect of reduced cardiac function on splanchnic intravascular volume

1992 ◽  
Vol 262 (5) ◽  
pp. H1361-H1364 ◽  
Author(s):  
D. L. Rutlen ◽  
F. G. Welt ◽  
A. Ilebekk
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Venous Pressure ◽  
Peripheral Circulation ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Intravascular Volume ◽  
Cardiac Filling

It has been hypothesized that lowered cardiac output due to heart failure results in passive redistribution of intravascular volume from the peripheral circulation to the central circulation and that this redistribution acts to support cardiac output. To test this hypothesis, acute heart failure was induced by rapid atrial pacing to raise heart rate from 148 +/- 6 to 232 +/- 1 beats/min for 5 min, while splanchnic intravascular volume was assessed with radionuclide imaging in eight anesthetized pigs that had undergone prior carotid denervation and vagotomy. Cardiac output decreased from 3,350 +/- 410 to 2,170 +/- 290 ml/min (P less than 0.001), mean arterial pressure decreased from 103 +/- 5 to 84 +/- 4 mmHg (P less than 0.001), left atrial pressure increased from 5.9 +/- 0.6 to 10.8 +/- 0.9 mmHg (P less than 0.001), right atrial pressure increased from 2.4 +/- 0.5 to 4.8 +/- 0.9 mmHg (P less than 0.001), total splanchnic intravascular volume did not change (0 +/- 2 ml), splenic intravascular volume decreased 11 +/- 3% (P less than 0.001), hepatic intravascular volume increased 12 +/- 2% (P less than 0.001), and mesenteric intravascular volume did not change (-3 +/- 2%). Thus, when cardiac output is lowered with pacing-induced acute heart failure, lowered perfusion pressure acts to lower splenic intravascular volume and increased central venous pressure acts to increase hepatic intravascular volume; however, total splanchnic intravascular volume does not decrease to support cardiac filling and cardiac output.

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