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.

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

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.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

"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.

Role of cardiac output in mediating arterial blood pressure oscillations

1996 ◽  
Vol 271 (3) ◽  
pp. R641-R646 ◽  
Author(s):  
D. S. O'Leary ◽  
D. J. Woodbury
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Low Frequency ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Power ◽  
Av Block ◽  
Arterial Blood ◽  
Low Frequency Oscillations

The objective of this study was to determine the role of cardiac output in mediating spontaneous fluctuations in mean arterial pressure (MAP) conscious dogs. Dogs were chronically instrumented to monitor MAP and cardiac output. Atrioventricular (AV) block was induced, and left ventricular and right atrial electrodes were implanted. After recovery, MAP was observed for 5 min under two conditions: 1) normal variation in heart rate and cardiac output via triggering the ventricular stimulator with each atrial depolarization (effectively reversing the AV block, AV-linked stimulation) and 2) computer control of ventricular rate to maintain cardiac output constant on a by-beat basis at the same level as observed during normal variations in heart rate and cardiac output. When cardiac output was held constant, large-amplitude, low-frequency oscillations in MAP were readily apparent. Spectral analysis by fast Fourier transform revealed that during constant cardiac output the power observed at low frequencies in the MAP spectrum represented 95.0 +/- 2.7% of the total power compared with 75.5 +/- 4.6% during normal variations in heart rate and cardiac output (P < 0.05). In addition, when cardiac output was held constant, the power observed at higher frequencies markedly decreased from 24.5 +/- 4.6% of total power during AV-linked stimulation to only 5.0 +/- 2.7% of total power during constant cardiac output (P < 0.05). We conclude that low-frequency oscillations in MAP are due to changes in peripheral resistance, whereas a significant amount of high-frequency changes in MAP stems from spontaneous changes in cardiac output.

Cardiovascular effects of positive-pressure ventilation in normal subjects

1979 ◽  
Vol 47 (2) ◽  
pp. 453-461 ◽  
Author(s):  
S. S. Cassidy ◽  
W. L. Eschenbacher ◽  
C. H. Robertson ◽  
J. V. Nixon ◽  
G. Blomqvist ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
Positive Pressure Ventilation ◽  
Normal Subjects ◽  
Left Ventricular ◽  
Right Atrial ◽  
Positive Pressure ◽  
Right Ventricular Filling ◽  
Ventricular Filling

In normal subjects during 15-min positive-pressure ventilation with 10 cmH2O end-expiratory pressure (PEEP), cardiac output fell 19% due to a fall in stroke volume. Transmural mean right atrial pressure rose 3.1 cmH2O and right ventricular end-diastolic diameter increased 15%. Simultaneously, left ventricular end-diastolic diameter decreased 21%, ejection time increased 11%, and velocity of circumferential fiber shortening fell 30%. Thus, right ventricular filling increased and left ventricular filling decreased. The function of the right ventricle was impaired and the function of the left ventricle may have been impaired. Cardiac output gradually increased due to a 7% increase in heart rate as PEEP was continued for 1 h and transmural mean right atrial pressure also increased further by 2.4 cmH2O. Compensation for the reduced stroke volume occurred as filling pressures and heart rate rose, but ventricular function remained impaired for the entire duration of PEEP. On resuming spontaneous breathing, cardiac output and ventricular function returned to base-line levels. We conclude that the reduced cardiac output during PEEP is not due to a direct mechanical reduction in right ventricular filling.

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.

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.

Influence of alterations in heart rate on left ventricular echocardiographic measurements in healthy cats

2016 ◽  
Vol 19 (8) ◽  
pp. 841-845 ◽  
Author(s):  
Keisuke Sugimoto ◽  
Yoko Fujii ◽  
Yuto Ogura ◽  
Hiroshi Sunahara ◽  
Takuma Aoki
Keyword(s):  
Heart Rate ◽  
Wall Thickness ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Free Wall ◽  
Left Ventricular Free Wall ◽  
Linear Fashion ◽  
Significant Relationships

Objectives The purpose of this study was to evaluate the effect of sudden alterations in heart rate (HR) on left ventricular (LV) wall thickness and dimensions determined by echocardiography in healthy cats. Methods Six experimental cats were used. All cats were anaesthetised and HR was controlled with right atrial pacing. The interventricular septum and left ventricular free wall thickness at end diastole (IVSd and LVFWd, respectively), left ventricular end-diastolic and end-systolic diameter (LVIDd and LVIDs, respectively) and shortening fraction (FS) of each cat were assessed using echocardiography at pacing rates of 120, 130, 140, 150, 160, 170 and 180 ppm. Results There were significant relationships between HR and IVSd, LVFWd, LVIDd, LVIDs and FS. As the HR increased, LV wall thickness increased and chamber dimensions got smaller in a linear fashion. The maximum and minimum differences in wall thickness between 120 ppm and 180 ppm were 2.0 mm and 0.7 mm in single measurements, respectively. Conclusions and relevance LV wall thickness and dimensions were significantly influenced by alterations in HR.

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