scholarly journals Distinct impacts of heart rate and right atrial-pacing on left atrial mechanical activation and optimal AV delay in CRT

2018 ◽  
Vol 41 (8) ◽  
pp. 959-966 ◽  
Author(s):  
Andreas Kyriacou ◽  
Christopher A. Rajkumar ◽  
Punam A. Pabari ◽  
S.M. Afzal Sohaib ◽  
Keith Willson ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mechanical Activation ◽  
Left Atrial ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Av Delay

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.

Effect of cervical vagal stimulation on chicken heart rate and atrioventricular conduction

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw
Keyword(s):  
Heart Rate ◽  
Vagal Stimulation ◽  
Atrioventricular Conduction ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Chicken Heart ◽  
Av Conduction ◽  
Supramaximal Stimulation ◽  
The Right ◽  
Stimulation Of

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.

Right Atrial Pacing Increases Maximal Heart Rate But Does Not Alter Vo2Max Or Maximal Exercise Performance In Healthy Humans

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 163
Author(s):  
Gregers Munch ◽  
Magnus Christensen ◽  
Niels Secher ◽  
Jesper H. Svendsen ◽  
José González-Alonso ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Performance ◽  
Maximal Exercise ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Maximal Heart Rate ◽  
Healthy Humans

"Summation" of the increase in heart rate from stimulation of atrial receptors

1980 ◽  
Vol 58 (6) ◽  
pp. 666-672
Author(s):  
P. V. Greenwood ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Superior Vena ◽  
Right Atrial ◽  
Propranolol Hydrochloride ◽  
Superior Vena Caval ◽  
The Right ◽  
Atrial Receptors ◽  
Stimulation Of ◽  
Wire Cage

In dogs anaesthetized with chloralose, application of stimuli which are likely to activate left atrial (L.A.) and right atrial (R.A.) receptors (complex unencapsulated endings) has been shown to result in an increase in heart rate. The present investigation was undertaken to determine whether the response elicited by the application of one stimulus (i.e., to the left atrium) could be enhanced by the application of a second stimulus (i.e., to the right atrium) in the same animal.The L.A. receptors were stimulated by distending a small balloon at the right upper pulmonary vein-L.A. junction and the R.A. receptors by "expanding" a spherical wire cage positioned at the superior vena caval (S.V.C.)-R.A. junction. Pressures in the S.V.C., R.A., L.A., and femoral artery were measured and the electrocardiogram monitored.In eight dogs stimulation of L.A. receptors resulted in an increase in heart rate (H.R.) of 18.5 beats/min (SEM 6.0; N = 23). In the same animals stimulation of R.A. receptors resulted in an increase in H.R. of 14.6 beats/min (SEM 2.0; N = 25). Application of both stimuli simultaneously resulted in an increase of 32.2 beats/min (SEM 8.0; N = 13). In four dogs propranolol hydrochloride (0.5 mg/kg) markedly diminished the response. In three dogs the response was abolished by bretylium tosylate (10 mg/kg).It is concluded that the increase in H.R. resulting from the application of these two stimuli could be "summated" and these findings support the proposition that the receptors in the two atria act as a functional entity.

Hypertrophic Cardiomyopathy: Non-Invasive Assessment of Diastolic and Systolic Functional Parameters in Relation to Heart Rate

1985 ◽  
Vol 24 (05) ◽  
pp. 196-200
Author(s):  
R. P. Spielmann ◽  
M. Geiger ◽  
A. Clausen ◽  
K.-H. Kuck ◽  
R. Montz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Hypertrophic Cardiomyopathy ◽  
Radionuclide Ventriculography ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Heart Rates ◽  
Ventricular Compliance ◽  
The Individual ◽  
Left Ventricular Compliance

SummaryHypertrophic cardiomyopathy (HC) is characterized by reduced left ventricular compliance and subsequent filling abnormalities. To study the pathophysiologic changes in parameters of left ventricular systolic and diastolic performance as a function of increasing heart rate 14 patients with HC (32 ± 12 yrs; 11 M, 4 F) and 4 normal individuals were subjected to equilibrium radionuclide ventriculography (99mTc-labelled red blood cells) at rest and during incremental right atrial pacing; heart rate was increased in steps of 20 beats per min from basal state to the individual symptom-limited endpoint. Mean symptom-limited heart rate was 141 ± 28 in HC and 160 in normals (p <.01.). At each pacing level filling and ejection parameters as well as the left ventricular endsystolic (LVESV) and enddiastolic volume (LVEDV) were determined relative to resting volumes at a heart rate of 78 ± 8. At the individual maximal pacing rate HC revealed a decline in LVEDV to 61 ± 4 % (p C.001) and an increase in LVESV to 117 ± 14% (p <.001) resulting in decreasing ejection fractions at heart rates above 120. Peak LV filling rates initially increased but subsequently decreased steeply at heart rates above 100; peak LV ejection rates in HC showed a similar pattern with increasing frequency. Time inter- vais to peak ejection and peak filling rate did not differ from normal. Thus, patients with HC demonstrated combined left ventricular diastolic and systolic abnormalities with increasing heart rate leading into a low-input low-output circulatory state. This probably explains not only the symptoms associated with HC, but also supports the concept of “hemodynamic syncope” in HC.

Right and left atrial diameters during incremental atrial pacing in pigs

1991 ◽  
Vol 260 (3) ◽  
pp. H973-H978
Author(s):  
E. Leistad ◽  
G. Christensen ◽  
A. Ilebekk
Keyword(s):  
Heart Rate ◽  
Confidence Interval ◽  
Left Atrial ◽  
Atrial Pacing ◽  
Ultrasonic Technique ◽  
Heart Rates ◽  
Open Chest ◽  
Maximal Diameter ◽  
V Wave ◽  
The Relationship

The relationship between right and left atrial diameters and heart rate was examined in 14 open-chest barbiturate-anesthetized pigs by an ultrasonic technique. The maximal atrial diameter was read at the top of the v wave, which decreased in both atria when heart rate was increased from 124 (118-130) to 159 (156-160) (median and 95% confidence interval) beats/min. Right and left atrial maximal diameter fell significantly from 25.7 (23.6-32.6) to 24.9 (22.9-29.5) mm and from 30.8 (25.1-37.2) to 29.8 (23.4-36.3) mm, respectively, when heart rate was increased from 124 to 180 (177-182) beats/min. At higher pacing frequencies, both right and left atrial maximal diameter progressively increased, and at 220 (216-221) beats/min the maximal diameter regained the values obtained at 124 beats/min. The minimal atrial diameter, which was read at the end of the a wave, remained unchanged at heart rates below 180 beats/min but rose significantly at higher rates. Our findings indicate progressively reduced atrial filling with increasing heart rate and hampered atrial emptying and atrial distension at the highest heart rates.

Atrial systolic pressure, as well as stretch, is a principal stimulus for release of ANF

1997 ◽  
Vol 272 (2) ◽  
pp. H820-H826
Author(s):  
G. Christensen ◽  
E. Leistad
Keyword(s):  
Atrial Fibrillation ◽  
Heart Rate ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Av Block ◽  
Open Chest ◽  
Atrial Contraction

The mechanism for increased secretion of atrial natriuretic factor (ANF) during tachycardia and atrial fibrillation has remained unsettled. In seven open-chest pigs, the plasma concentration of ANF increased from 49.8 +/- 12.4 to 131.8 +/- 15.7 pg/ml when heart rate was increased from 133 +/- 13 to 212 +/- 4 beats/min by atrial pacing. Right atrial maximal diameter, recorded by ultrasonic technique at the maximal atrial filling, did not increase. During pacing tachycardia, the atrial contraction (a wave) occurs during atrial filling, and the a wave becomes superimposed on the v wave. In the present study the systolic atrial pressure (a wave) increased from 5.8 +/- 0.8 to 9.6 +/- 0.5 mmHg. The significance of this pressure rise was subsequently examined. After complete atrioventricular (AV) block, the AV delay was progressively increased, without altering heart rate, until the a wave was similar to the the a wave during the preceding tachycardia. Plasma ANF increased to 113.8 +/- 14.7 pg/ml, which showed that the increase in atrial pressure during atrial systole is a stimulus for ANF release. In the second part of the study, atrial fibrillation was induced in six open-chest pigs by rapid atrial pacing after complete AV block. Plasma ANF increased from 83.5 +/- 7.2 to 269.0 +/- 45.4 pg/ml during atrial fibrillation. No increase in atrial dimensions occurred during atrial fibrillation, but atrial pressure was substantially elevated. Thus, although passive atrial stretch stimulates ANF release during blood volume expansion, the present study shows that the increase in atrial pressure during atrial contraction is a stimulus for release of ANF during tachycardia and atrial fibrillation.

Effects of asynchrony on myocardial relaxation at rest and during exercise in conscious dogs

1988 ◽  
Vol 254 (5) ◽  
pp. H817-H822 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. J. Vantrimpont ◽  
M. F. Rousseau ◽  
H. Pouleur
Keyword(s):  
Heart Rate ◽  
Right Ventricular ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Ventricular Pacing ◽  
Right Ventricular Pacing ◽  
Relaxation Phase

The effect of left ventricular asynchrony induced by right ventricular pacing on relaxation indexes was studied at rest and during exercise in seven conscious dogs instrumented for chronic measurements of left ventricular pressure, coronary blood flow, and arterial pressure and with right atrial and ventricular pacing electrodes. Increasing heart rate with atrial pacing resulted in an increase in both left ventricular maximum and minimum rates of pressure development, LV dP/dtmax and LV dP/dtmin, respectively, as well as in a decrease in the relaxation constant T. In contrast, increasing heart rate with ventricular pacing resulted in a decrease in LV dP/dtmax, a small increase in LV dP/dtmin, and a significant decrease in T. During exercise with heart rate kept constant with atrial pacing, both LV dP/dtmax and LV dP/dtmin increased and T decreased to the same extent as during exercise in sinus rhythm. In contrast, exercising during right ventricular pacing resulted in a significant increase in T, expressing a slowing of relaxation. It is concluded that increasing heart rate alone in the presence of asynchrony of LV contraction induced by abnormal electrical activation results in a depressed contractile response, while the relaxation phase is not significantly affected. However, during sympathetic stimulation, a condition where synchronization should be improved, the relaxation phase is considerably lengthened.

44 Signal-to-Noise Ratio During Haemodynamic Optimisation of AV Delay is Improved more by Atrial Pacing than by Increasing Heart Rate

Heart ◽  
2015 ◽  
Vol 101 (Suppl 4) ◽  
pp. A25.2-A26
Author(s):  
Alexander Sharp ◽  
Afzal Sohaib ◽  
Keith Willson ◽  
Jamil Mayet ◽  
Alun Hughes ◽  
...  
Keyword(s):  
Heart Rate ◽  
Signal To Noise Ratio ◽  
Atrial Pacing ◽  
Signal To Noise ◽  
Noise Ratio ◽  
Av Delay

Effect of heart rate on left atrial systolic shortening in the dog

1975 ◽  
Vol 38 (6) ◽  
pp. 1110-1116 ◽  
Author(s):  
H. L. Stone
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Atrial Pacing ◽  
Adrenergic Blockade ◽  
Rapid Infusion ◽  
Heart Rates ◽  
Contractile State ◽  
Inotropic State ◽  
Vagal Blockade ◽  
The Relationship

The relationship between heart rate and left atrial end-diastolic diameter (LAEDD) and left atrial systolic shortening (LASS) was investigated in 12 conscious dogs. Atrial pacing, vagal blockade, isoproterenol, and beta-adrenergic blockade were used to change heart rate and the inotropic state of the atrium. LAEDD decreased linearly as heart rate increased. LAEDD averaged 33.0 mm (+/- 0.6 mm SEM) and decreased by 3.2 mm (+/- 0.4 mm SEM) with a change in heart rate of 50 beats/min. The ratio of LASS/LAEDD decreased as LAEDD decreased with increasing heart rate, but there was less of a reduction in the ratio at the extreme levels of LAEDD change with isoproterenol and vagal blockade. Propranolol reduced LASS at any LAEDD. At lower heart rates the reduction of LASS with pacing could be corrected by returning LAEDD to near control levels with a rapid infusion of fluid. It is concluded that LASS is primarily dependent on LAEDD and the inotropic state of the atrium. At higher heart rates, though, some effect of frequency can be observed. Isoproterenol and vagal blockade (increased contractile state) reduced the dependence of LASS on LAEDD.

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