Beat-by-beat modulation of AV conduction. II. Autonomic neural mechanisms

1986 ◽  
Vol 251 (6) ◽  
pp. H1134-H1142 ◽  
Author(s):  
M. R. Warner ◽  
J. M. deTarnowsky ◽  
C. C. Whitson ◽  
J. M. Loeb
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Intrinsic Rate ◽  
Conscious State ◽  
Neural Mechanisms ◽  
Parasympathetic Activity ◽  
Atrial Pacing ◽  
Rate Dependent ◽  
Av Conduction ◽  
Electrocardiogram Ecg

We examined the mechanism by which autonomic neural activity associated with respiration and blood pressure modulates atrioventricular (AV) conduction in conscious dogs. Mongrel dogs were anesthetized and instrumented under sterile conditions to record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded continuously, and heart rate and AV interval were plotted graphically as a function of time. To delineate the role(s) of sympathetic and parasympathetic activity, AV conduction was studied during abrupt and linear changes in heart rate after administration of atropine, propranolol, or both. In the basal state and after propranolol, AV interval oscillated with respiration both in the absence of atrial pacing and at pacing rates 10–100 beats/min above control. Following atropine, oscillations in AV interval associated with respiration were abolished; however, linear and abrupt heart rate increases resulted in AV conduction changes that were associated with fluctuations in blood pressure. In contrast, after both atropine and propranolol, alterations in blood pressure or respiration did not influence AV conduction and rate-dependent prolongation of AV conduction occurred. We conclude that in the basal state, AV conduction is influenced predominately by changes in parasympathetic activity which is the major determinant of respiratory-related AV interval oscillations; after atropine, sympathetic activity produces fluctuations in both AV conduction and blood pressure; and intrinsic rate-dependent properties of the AV node are modulated continually by both divisions of the autonomic nervous system.

Beat-by-beat modulation of AV conduction. I. Heart rate and respiratory influences

1986 ◽  
Vol 251 (6) ◽  
pp. H1126-H1133 ◽  
Author(s):  
M. R. Warner ◽  
J. M. Loeb
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oscillatory Activity ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Sinus Arrhythmia ◽  
Heart Rates ◽  
Av Conduction ◽  
Wide Range ◽  
Cyclic Changes

We examined the integration of heart rate and neural influences at the atrioventricular (AV) node in conscious dogs. Animals were anesthetized and, under sterile conditions, instrumented to chronically record atrial and ventricular electrograms and blood pressure. In the conscious state, electrocardiogram (ECG), respiration, blood pressure, and electrograms were recorded on a beat-by-beat basis, and heart rate and AV interval were plotted graphically as a function of time. Resting animals exhibited both respiratory sinus arrhythmia and marked oscillations in AV conduction time associated with respiration. During inspiration AV interval was shortened, and during expiration AV interval was prolonged. To obviate the effect of cyclic changes in heart rate, atrial pacing was used to increase heart rate over a wide range both abruptly and linearly. Regardless of the pattern of heart rate change, AV interval oscillated at the respiratory frequency at pacing rates 10-100 beats/min above control. Higher levels of atrial pacing resulted in AV conduction patterns that were correlated with changes in blood pressure. Thus in the conscious dog variations in AV conduction time occur on a beat-by-beat basis in conjunction with respiration; oscillatory activity of AV conduction is not dependent on simultaneous changes in heart rate; and during atrial pacing, autonomic neural activity associated with respiration and blood pressure appears to dynamically modulate AV conduction with respiratory effects predominating at low heart rates and blood pressure effects at high heart rates.

scholarly journals Atenolol’s Inferior Ability to Reduce Central vs Peripheral Blood Pressure Can Be Explained by the Combination of Its Heart Rate-Dependent and Heart Rate-Independent Effects

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Tuuli Teeäär ◽  
Martin Serg ◽  
Kaido Paapstel ◽  
Mare Vähi ◽  
Jaak Kals ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Pacemaker ◽  
Atrial Pacing ◽  
Brachial Blood Pressure ◽  
Rate Dependent ◽  
Mechanistic Approach ◽  
Independent Effects ◽  
Single Blind ◽  
Peripheral Blood Pressure

Objective. Whether the inferior ability of atenolol to reduce central (aortic) compared to peripheral (brachial) blood pressure (BP) is related to its heart rate (HR)-dependent or -independent effects, or their combination, remains unclear. To provide further mechanistic insight into this topic, we studied the acute effects of atenolol versus nebivolol and ivabradine on systolic blood pressure amplification (SBPA; peripheral systolic BP minus central systolic BP) in a model of sick sinus syndrome patients with a permanent dual-chamber cardiac pacemaker in a nonrandomized single-blind single-group clinical trial. Methods. We determined hemodynamic indices noninvasively (Sphygmocor XCEL) before and at least 3 h after administration of oral atenolol 50 or 100 mg, nebivolol 5 mg, or ivabradine 5 or 7.5 mg during atrial pacing at a low (40 bpm), middle (60 bpm), and high (90 bpm) HR level in 25 participants (mean age 65.5 years, 12 men). Results. At the low HR level, i.e., when the drugs could exert their HR-dependent and HR-independent effects on central BP, only atenolol produced a significant decrease in SBPA (mean change 0.74 ± 1.58 mmHg (95% CI, 0.09–1.40; P=0.028)), indicating inferior central vs peripheral systolic BP change. However, we observed no significant change in SBPA with atenolol at the middle and high HR levels, i.e., when HR-dependent mechanisms had been eliminated by pacing. Conclusion. The findings of our trial with a mechanistic approach to the topic imply that the inferior ability of atenolol to reduce central vs peripheral BP can be explained by the combination of its heart rate-dependent and -independent effects. This trial is registered with NCT03245996.

scholarly journals Differential effects of the blood pressure state on pulse rate variability and heart rate variability in critically ill patients

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Elisa Mejía-Mejía ◽  
James M. May ◽  
Mohamed Elgendi ◽  
Panayiotis A. Kyriacou
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Pulse Rate ◽  
Pulse Transit Time ◽  
Pulse Rate Variability ◽  
Physiological Factors ◽  
Ecg Signals ◽  
Non Invasive ◽  
Electrocardiogram Ecg

AbstractHeart rate variability (HRV) utilizes the electrocardiogram (ECG) and has been widely studied as a non-invasive indicator of cardiac autonomic activity. Pulse rate variability (PRV) utilizes photoplethysmography (PPG) and recently has been used as a surrogate for HRV. Several studies have found that PRV is not entirely valid as an estimation of HRV and that several physiological factors, including the pulse transit time (PTT) and blood pressure (BP) changes, may affect PRV differently than HRV. This study aimed to assess the relationship between PRV and HRV under different BP states: hypotension, normotension, and hypertension. Using the MIMIC III database, 5 min segments of PPG and ECG signals were used to extract PRV and HRV, respectively. Several time-domain, frequency-domain, and nonlinear indices were obtained from these signals. Bland–Altman analysis, correlation analysis, and Friedman rank sum tests were used to compare HRV and PRV in each state, and PRV and HRV indices were compared among BP states using Kruskal–Wallis tests. The findings indicated that there were differences between PRV and HRV, especially in short-term and nonlinear indices, and although PRV and HRV were altered in a similar manner when there was a change in BP, PRV seemed to be more sensitive to these changes.

Influence of cardiac innervation on intrinsic heart rate in dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1132-H1137 ◽  
Author(s):  
J. M. Evans ◽  
D. C. Randall ◽  
J. N. Funk ◽  
C. F. Knapp
Keyword(s):  
Heart Rate ◽  
Intrinsic Rate ◽  
Conscious State ◽  
Autonomic Innervation ◽  
Autonomic Activity ◽  
Cardiac Innervation ◽  
Cardiac Denervation ◽  
Ganglionic Blockade ◽  
Intrinsic Heart Rate

Intrinsic heart rate is defined as the rate at which the heart beats when all cardiac neural and hormonal inputs are removed. We determined the effect of prevailing autonomic innervation of the heart on the intrinsic heart rate in chronically maintained, sedated, normally innervated dogs (n = 14), and in 14 other dogs that had previously (greater than 12 day) undergone complete surgical cardiac denervation. Intrinsic rate was determined in both groups using the following two procedures: 1) pharmacological effector blockade; and 2) pharmacological ganglionic blockade. The intrinsic rate determined by effector blockade was 142.9 +/- 7.2 (SE) beats/min in the dogs with intact cardiac innervation. When the same treatment was given after total surgical cardiac denervation, intrinsic rate was 97.9 +/- 4.8 beats/min. Intrinsic heart rate was significantly (P less than 0.05) lower in surgically denervated dogs. Ganglionic blockade in surgically denervated animals yielded an intrinsic rate of 90.0 +/- 8.5 beats/min, which was again significantly lower than the corresponding value of 128.4 +/- 5.5 beats/min in normal dogs. There was no difference in the intrinsic heart rate as determined by effector vs. ganglionic blockade in either group of dogs. An additional six dogs were subjected to selective surgical sinoatrial nodal parasympathectomy; their intrinsic rate (effector blockade) in the conscious state was 115.8 +/- 4.3 beats/min; this was significantly lower than the corresponding value for normal dogs and significantly greater than in dogs subject to total surgical cardiac denervation. The lower rate observed in the totally denervated and selectively denervated dogs after effector and/or ganglionic blockades implies that intrinsic heart rate depends on the level or nature of prevailing autonomic activity.

Integration of heart rate and sympathetic neural effects on AV conduction

1988 ◽  
Vol 254 (4) ◽  
pp. H651-H657
Author(s):  
J. M. Loeb ◽  
J. M. deTarnowsky
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Sinoatrial Node ◽  
Conduction Time ◽  
Atrial Pacing ◽  
Sympathetic Stimulation ◽  
Sympathetic Activation ◽  
Direct Effects ◽  
Av Node ◽  
Av Conduction

Sympathetic activation increases heart rate (HR) and reduces atrioventricular interval (AVI), whereas atrial pacing alone increases AVI. We sought to differentiate the direct effects of sympathetic activation on atrioventricular (AV) conduction time from the indirect changes associated with concurrent alterations in HR. We recorded electrocardiograms, blood pressure (BP), and intracardiac electrograms from chloralose-anesthetized autonomically decentralized dogs. Beat-by-beat HR and AVI data were collected continuously. Sympathetic stimulation (0.25-2.5 Hz; mean 0.81 Hz) resulted in a HR change of +60 beats/min after 60 s. This tachycardia was associated with a mean decrease in AVI of 22 ms. Computer-driven atrial pacing to reproduce the HR associated with control sympathetic stimulation caused a mean AVI increase of 10 ms. Propranolol (200 micrograms) was then administered via the sinoatrial node artery and sympathetic stimulation repeated. Although HR remained constant, AVI decreased by 14.8 ms. The AVIs associated with an identical HR achieved by two different mechanisms (sympathetic stimulation and atrial pacing) were significantly different. Although removal of the contribution of sympathetically induced HR changes on AV conduction might be expected to result in potentiation of neural effects at the AV node, none was evident. Thus sympathetic activity restricted to the AV node is less effective in influencing AV conduction than the response that occurs when HR changes occur concurrently. Therefore, the opposing actions of HR and sympathetic tone on AV conduction may not be predicted by a simple linear relationship.

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.

Evidence of Parasympathetic Activity of the Angiotensin Converting Enzyme Inhibitor, Captopril, in Normotensive Man

1985 ◽  
Vol 68 (1) ◽  
pp. 49-56 ◽  
Author(s):  
B. C. Campbell ◽  
Alessandra Sturani ◽  
J. L. Reid
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Enzyme Inhibitor ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Pressure Change ◽  
Parasympathetic Activity ◽  
Valsalva Manoeuvre ◽  
The Difference ◽  
Normal Increase

1. Captopril (50 mg orally) produced a significant fall in systolic and diastolic blood pressure in six normotensive sodium replete subjects, without a rise in heart rate. 2. On captopril, there was no change in the expected normal increase in heart rate on standing. Supine plasma noradrenaline was not reduced by captopril and normal postural increases were maintained. 3. Atropine (0.04 mg/kg i.v.) reduced the difference in blood pressure change between captopril and placebo. 4. Facial immersion in water produced a bradycardia. This change was abolished by atropine and attenuated both by captopril and edrophonium (10 mg i.V.), a cholinesterase inhibitor. 5. Lying down after 6 min standing produced an immediate transient tachycardia, which was abolished by atropine and attenuated by captopril. 6. Blood pressure and heart rate rose after a cold pressor test on both captopril and placebo. 7. The tachycardia during the Valsalva manoeuvre was inhibited by edrophonium and to a lesser extent by captopril. The effects of captopril and edrophonium were additive. 8. Parasympathetic activity of captopril may contribute to its haemodynamic profile.

Variability of Heart Rate and Regulation of Systolic Blood Pressure Evaluated by Fixed Rate Atrial Pacing

1996 ◽  
Vol 91 (s1) ◽  
pp. 13-15
Author(s):  
Joerg Bamstedt ◽  
Kilian Tegethoff ◽  
Aninka Stellmacher ◽  
Jan H. Baumert ◽  
Martin Dambacher ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Systolic Blood Pressure ◽  
Atrial Pacing ◽  
Fixed Rate

scholarly journals Assessment of dynamic cardiac repolarization and contractility in patients with hypertrophic cardiomyopathy

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246768
Author(s):  
Andrew E. Radbill ◽  
Lucy Y. Lei ◽  
Sachin Y. Paranjape ◽  
Daniel J. Blackwell ◽  
Robert L. Abraham ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hypertrophic Cardiomyopathy ◽  
Qt Interval ◽  
Calcium Release ◽  
Cardiac Contractility ◽  
Cardiac Repolarization ◽  
Atrial Pacing ◽  
Ventricular Ectopy ◽  
Rate Dependent ◽  
Rapid Pacing

Aims Arrhythmia mechanisms in hypertrophic cardiomyopathy remain uncertain. Preclinical models suggest hypertrophic cardiomyopathy-linked mutations perturb sarcomere length-dependent activation, alter cardiac repolarization in rate-dependent fashion and potentiate triggered electrical activity. This study was designed to assess rate-dependence of clinical surrogates of contractility and repolarization in humans with hypertrophic cardiomyopathy. Methods All participants had a cardiac implantable device capable of atrial pacing. Cases had clinical diagnosis of hypertrophic cardiomyopathy, controls were age-matched. Continuous electrocardiogram and blood pressure were recorded during and immediately after 30 second pacing trains delivered at increasing rates. Results Nine hypertrophic cardiomyopathy patients and 10 controls were enrolled (47% female, median 55 years), with similar baseline QRS duration, QT interval and blood pressure. Median septal thickness in hypertrophic cardiomyopathy patients was 18mm; 33% of hypertrophic cardiomyopathy patients had peak sub-aortic velocity >50mmHg. Ventricular ectopy occurred during or immediately after pacing trains in 4/9 hypertrophic cardiomyopathy patients and 0/10 controls (P = 0.03). During delivery of steady rate pacing across a range of cycle lengths, the QT-RR relationship was not statistically different between HCM and control groups; no differences were seen in subgroup analysis of patients with or without intact AV node conduction. Similarly, there was no difference between groups in the QT interval of the first post-pause recovery beat after pacing trains. No statistically significant differences were seen in surrogate measures for cardiac contractility. Conclusion Rapid pacing trains triggered ventricular ectopy in hypertrophic cardiomyopathy patients, but not controls. This finding aligns with pre-clinical descriptions of excessive cardiomyocyte calcium loading during rapid pacing, increased post-pause sarcoplasmic reticulum calcium release, and subsequent calcium-triggered activity. Normal contractility at all diastolic intervals argues against clinical significance of altered length-dependent myofilament activation.

Heart rate variability and electrocardiogram waveform as predictors of morbidity during hypothermia and rewarming in rats

2002 ◽  
Vol 80 (9) ◽  
pp. 925-933 ◽  
Author(s):  
C B Matthew ◽  
A M Bastille ◽  
R R Gonzalez ◽  
I V Sils
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Wave Amplitude ◽  
Sodium Pentobarbital ◽  
Sprague Dawley ◽  
T Wave ◽  
Sprague Dawley Rats ◽  
Copper Tubing ◽  
Electrocardiogram Ecg

This study examined electrocardiogram (ECG) waveform, heart rate (HR), mean blood pressure (BP), and HR variability as potential autonomic signatures of hypothermia and rewarming. Adult male Sprague–Dawley rats had telemetry transmitters surgically implanted, and 2 weeks were allowed for recovery prior to induction of hypothermia. Rats were lightly anesthetized (sodium pentobarbital, 35 mg/kg i.p.) and placed in a coil of copper tubing through which temperature-controlled water was circulated. Animals were cooled to a core temperature (Tc) of 20°C, maintained there for 30 min, and then rewarmed. Data (Tc, BP, HR from ECG, and 10-s strips of ECG waveforms) were collected every 5 min throughout hypothermia and rewarming. Both HR and BP declined after initial increases with the drop in HR starting at a higher Tc than the drop in BP (29.6 ± 2.4°C vs. 27.1 ± 3.3°C, p < 0.05). Animals that were not successfully rewarmed exhibited a significant (p < 0.05) increase in the normalized standard deviation of interbeat intervals (IBI) throughout cooling compared with animals that were successfully rewarmed. The T wave of the ECG increased in amplitude and area with decreasing Tc. T-wave amplitude and IBI variability show potential as predictors of survival in hypothermic victims.Key words: hypothermia, rewarming, heart rate variability, ECG, blood pressure.

Sign in / Sign up

Export Citation Format

Share Document