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
2018 ◽  
Vol 315 (2) ◽  
pp. R296-R302 ◽  
Author(s):  
William Joyce ◽  
Ruth M. Elsey ◽  
Tobias Wang ◽  
Dane A. Crossley

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.


1989 ◽  
Vol 256 (6) ◽  
pp. H1621-H1626 ◽  
Author(s):  
J. F. Liard

The selective V2-agonist 4-valine-8-D-arginine vasopressin (VDAVP) increases cardiac output and heart rate and decreases total peripheral resistance in dogs. The mechanism of these hemodynamic effects was examined in the present studies. When infused into the left coronary artery of six conscious dogs for 1 h, VDAVP (10 ng.kg-1.min-1) increased cardiac output and decreased total peripheral resistance more than when given intravenously in the same animals. Administration of VDAVP into the carotid circulation elicited effects that did not differ significantly from those after intravenous infusion at the same rate in six conscious dogs. After destruction of the central nervous system in five dogs anesthetized with pentobarbital, VDAVP failed to increase cardiac output and heart rate but lowered mean arterial pressure and total peripheral resistance. Finally, infusion of VDAVP into the femoral artery of six anesthetized dogs increased femoral blood flow at rates of 1, 5, and 10 ng.kg-1.min-1, whereas none of these rates increased femoral blood flow when given intravenously. Thus the hemodynamic effects of VDAVP appear to result primarily from a peripheral vasodilatory action, with possible contribution from a positive inotropic effect. We found no evidence that central effects of VDAVP were importantly involved in its cardiovascular action.


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

1976 ◽  
Vol 231 (1) ◽  
pp. 204-208 ◽  
Author(s):  
PT Pitlick ◽  
SE Kirkpatrick ◽  
WF Friedman

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.


1988 ◽  
Vol 255 (6) ◽  
pp. H1443-H1451 ◽  
Author(s):  
U. Freyschuss ◽  
P. Hjemdahl ◽  
A. Juhlin-Dannfelt ◽  
B. Linde

Cardiovascular, sympathoadrenal, and subjective responses to mental stress induced by a color-word conflict test (CWT) were studied in 30 healthy males before and after intravenous administration of either placebo, beta 1-blockade by metoprolol (0.15 mg/kg), or nonselective beta-blockade by propranolol (0.15 mg/kg). CWT responses were reproducible. Mean arterial pressure increased by 20%. A mainly heart rate-dependent 65% increase in cardiac output (thermodilution) was associated with 25% decreases of both systemic (SVR) and calf vascular (CVR) resistances. Arterial plasma epinephrine (Epi) was doubled, and norepinephrine (NE) increased by 50%. Self-evaluated stress score correlated positively with changes in cardiac output and inversely with changes in SVR during CWT. Both metoprolol and propranolol halved heart rate responses; whereas increases in mean arterial pressure, Epi, and NE were uninfluenced. Metoprolol reduced the increase in stroke volume, and propranolol abolished it. SVR and CVR responses were attenuated by metoprolol and abolished by propranolol. The results suggest that mental stress accelerates the heart through neurogenic mechanisms and that peripheral vasodilatation is achieved through the concerted actions of reduced vasoconstrictor activity and elevated circulating Epi.


2015 ◽  
Vol 40 (6) ◽  
pp. 605-614 ◽  
Author(s):  
Felipe A. Cunha ◽  
Adrian W. Midgley ◽  
Pedro P. Soares ◽  
Paulo T.V. Farinatti

This study investigated postexercise hypotension (PEH) after maximal cardiopulmonary exercise testing (CPET) performed using different exercise modalities. Twenty healthy men (aged 23 ± 3 years) performed 3 maximal CPETs (cycling, walking, and running), separated by 72 h in a randomized, counter-balanced order. Systolic (SBP) and diastolic blood pressure (DBP), heart rate, cardiac output, systemic vascular resistance (SVR), autonomic function (spontaneous baroreflex sensitivity (BRS) and heart rate variability (HRV)), and energy expenditure (EE) were assessed during a 60-min nonexercise control session and for 60 min immediately after each CPET. Total exercise volume (EE during CPET plus 60 min recovery) was significantly higher in running versus cycling and walking CPETs (P ≤ 0.001). Compared with control, only SBP after running CPET was significantly reduced (Δ = −6 ± 8 mm Hg; P < 0.001). Heart rate and cardiac output were significantly increased (P < 0.001) and SVR significantly decreased (P < 0.001) postexercise. BRS and HRV decreased after all CPETs (P < 0.001), whereas sympatho-vagal balance (low- and high-frequency (LF:HF) ratio) increased significantly after all exercise conditions, especially after running CPET (P < 0.001). Changes in SVR, BRS, sympathetic activity (low-frequency component of HRV), and LF:HF ratio were negatively correlated to variations in SBP (range −0.69 to −0.91; P < 0.001) and DBP (range −0.58 to −0.93; P ≤ 0.002). These findings suggest that exercise mode or the total exercise volume are major determinants of PEH magnitude in healthy men. Because of the running CPET, the PEH was primarily related to a decrease in SVR and to an increase in sympatho-vagal balance, which might be a reflex response to peripheral vasodilatation after exercise.


2014 ◽  
Vol 5 (4) ◽  
pp. 104-109
Author(s):  
Aleksey Borisovich Naumov ◽  
Maksim Viktorovich Didenko ◽  
Sergey Pavlovich Marchenko ◽  
Vitaliy Vladimirovich Suvorov ◽  
Igor Igorevich Averkin ◽  
...  

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.


1981 ◽  
Vol 60 (4) ◽  
pp. 371-375 ◽  
Author(s):  
H. Valette ◽  
B. Raffestin ◽  
A. Lockhart

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.


2013 ◽  
Vol 34 (7) ◽  
pp. 1605-1611 ◽  
Author(s):  
Gregory M. Barker ◽  
Jeremy Affolter ◽  
Jessica Saenz ◽  
Casey S. Cox ◽  
Joseph M. Forbess ◽  
...  

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