Autonomic mechanisms in the heart rate response to coughing

1987 ◽  
Vol 72 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Claudio CaRdone ◽  
Federico Bellavere ◽  
Marcello Ferri ◽  
Domenico Fedele
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
Muscular Contraction ◽  
Diabetic Patients ◽  
Cough Test ◽  
Before And After ◽  
Autonomic Blockade ◽  
Expiratory Muscles

1. To differentiate between the possible reflex and mechanical components in the heart rate response to cough, eight healthy subjects performed a standardized cough test before and after pharmacological autonomic blockade; to test the clinical usefulness of the cough manoeuvre two groups of diabetic patients (without and with autonomic neuropathy) were compared with a group of age-matched normal subjects. 2. Because of the use of abdominal and expiratory muscles during cough, the cardioacceleratory response was compared with that induced by an intense contraction of the arm muscles (handgrip). 3. The cardioacceleratory response was completely abolished by atropine while propranolol failed to affect it. The diabetic patients with autonomic neuropathy showed a response similar to that after cholinergic blockade. The response was similar to that induced by muscular contraction for 4 s, after which it differed showing a continued cardioacceleration. The patterns of recovery were not different. 4. The cough-induced cardioacceleration is essentially reflex in nature and under cholinergic control; initially the mechanism may be partially related to the intense contraction of abdominal and expiratory muscles; later, the arterial hypotension related to the cough may contribute to the more sustained shortening of the R–R interval. 5. The cough test may be useful for the evaluation of cardiac parasympathetic integrity.

Heart-Rate Response to Sustained Hand Grip: Comparison of the Effects of Cardiac Autonomic Blockade and Diabetic Autonomic Neuropathy

1979 ◽  
Vol 56 (3) ◽  
pp. 287-291 ◽  
Author(s):  
L. Hume ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
S. R. Reuben ◽  
B. F. Clarke
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
Diabetic Autonomic Neuropathy ◽  
Initial Increase ◽  
Hand Grip ◽  
Before And After ◽  
Autonomic Blockade ◽  
Later Phase

1. The heart-rate response during sustained hand grip was studied in four normal subjects before and after intravenous atropine, propranolol and combined cardiac autonomic blockade with both drugs. The results suggest that the increase in heart rate during the first 30 s is due to parasympathetic withdrawal, whereas the further increase between 30 s and 180 s is probably mediated by a combination of parasympathetic withdrawal and sympathetic stimulation. 2. The increases in heart rate during each minute of sustained hand grip were compared in 26 normal subjects, 37 diabetic subjects without and 24 diabetic subjects with proven autonomic neuropathy. In the diabetic subjects with autonomic neuropathy the increase in heart rate during the first minute was impaired, whereas the increases during the second and third minutes were similar in all three groups. 3. The initial increase in heart rate over the first 30 s of hand grip and the later increase between 30 s and 180 s were compared in nine normal subjects, ten diabetic subjects without and six diabetic subjects with autonomic neuropathy. The increase during the first 30 s was impaired in the diabetic subjects with autonomic neuropathy, whereas the later phase of the response was similar in all three groups. 4. It is concluded that impairment of the heart-rate response to sustained hand grip in diabetic autonomic neuropathy is mainly due to impairment of the early parasympathetic phase, but that the presence of cardiac sympathetic damage can also be detected.

Autonomic Control of the Immediate Heart Rate Response to Lying Down

1982 ◽  
Vol 62 (1) ◽  
pp. 57-64 ◽  
Author(s):  
F. Bellavere ◽  
D. J. Ewing
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Normal Subjects ◽  
Muscular Exercise ◽  
Diabetic Patients ◽  
Normal Pattern ◽  
Sympathetic Control ◽  
The Third ◽  
Steady Level ◽  
Lying Down

1. The initial heart rate response to lying down was analysed in 18 younger (23–36 years) and 10 older (48–67 years) normal subjects, and consisted of an immediate shortening of the R—R interval reaching a maximum around the third or fourth beat after lying, followed by a lengthening beyond the resting value to reach a steady level around beats 25–30. In six diabetic patients with autonomic neuropathy, no cardiac acceleration occurred and the deceleration was markedly diminished. 2. In eight young normal subjects the pattern of response was altered by atropine, which abolished the initial shortening of the R—R interval over the first 10 beats. Thereafter slow but steady lengthening of the R—R interval occurred. With additional propranolol the later part of the response was further attenuated. Propranolol alone did not affect the normal pattern of response. 3. Six young normal subjects performed short periods of muscular exercise, lying, sitting and standing, and the heart rate patterns were compared with that after lying down. After both manoeuvres R—R interval shortened and then lengthened back to the resting level within 10–15 beats. Thereafter it remained steady after muscular exercise, but continued to lengthen after lying down. 4. In four young normal subjects, no initial R—R interval shortening occurred during fast or slow ‘passive’ tilting from the 80° head-up position to horizontal, whereas shortening was seen both with fast and slow ‘active’ lying down. 5. It is concluded that the immediate part of the heart rate response to lying down (during the first 10 beats) is under vagal control and the later part predominantly under sympathetic control. The first part of the response is probably due to a ‘muscle—heart’ reflex which occurs during the change in posture.

Preservation of the Hypoxic Drive to Breathing in Diabetic Autonomic Neuropathy

1982 ◽  
Vol 63 (1) ◽  
pp. 17-22 ◽  
Author(s):  
P. M. A. Calverley ◽  
D. J. Ewing ◽  
I. W. Campbell ◽  
P. K. Wraith ◽  
H. M. Brash ◽  
...  
Keyword(s):  
Heart Rate ◽  
Autonomic Neuropathy ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Diabetic Autonomic Neuropathy ◽  
Co2 Production ◽  
Diabetic Patients ◽  
Normal Range ◽  
Peripheral Chemoreceptors ◽  
Carotid Chemoreceptors

1. Unexplained cardiorespiratory arrests have been reported in patients with diabetic autonomic neuropathy and these could be due to denervation of the carotid chemoreceptors. 2. We have studied the ventilatory response to transient hypoxia () during exercise in 22 male diabetic patients, six with symptomatic and cardiovascular evidence to suggest diabetic autonomic neuropathy (DAN+) and 12 without these features (DAN−). 3. There was no difference in the ventilatory response to transient hypoxia between the different groups of diabetic patients ( in DAN+ patients = −0·9 ± 0·2 litre min−1 kPa−1; in DAN− patients = −1·2 ± 0·6 litres min−1 kPa−1) even allowing for differences in the level of exercise achieved (CO2 production in DAN+ patients = 743 ± 103 ml/min; CO2 production in DAN– patients = 800 ± 144 ml/min). These results fell within our normal range for ventilatory response to transient hypoxia at this level of exercise. 4. The heart rate response to transient hypoxia varied within the groups but was significantly (P < 0·05) less in the patients with established diabetic autonomic neuropathy. 5. We conclude that the peripheral chemoreceptors are intact in diabetic autonomic neuropathy and that other mechanisms must be implicated in the unexpected cardiorespiratory arrests seen in these patients.

scholarly journals Cardiovascular Autonomic Neuropathyin Chronic Kidney Diseases

2010 ◽  
Vol 49 (178) ◽  
Author(s):  
L Thapa ◽  
P Karki ◽  
SK Sharma ◽  
BK Bajaj
Keyword(s):  
Diabetes Mellitus ◽  
Chronic Kidney Disease ◽  
Heart Rate ◽  
Kidney Disease ◽  
Autonomic Neuropathy ◽  
Autonomic Function ◽  
Heart Rate Response ◽  
Kidney Diseases ◽  
Diabetic Patients ◽  
Age And Sex

INTRODUCTION: This study was conducted to explore cardiovascular autonomic neuropathy and its pattern in chronic kidney disease patients. METHODS: Autonomic function using five standard tests was examined in 20 diabetic patients with CKD, 20 age and sex matched diabetic patients without CKD and 20 age and sex matched controls. Analysis of difference between the autonomic function was done in the three groups using Chi-square test or Fischer's test. RESULTS: Total 20 (100%) diabetic CKD patients were found to have autonomic neuropathy. Of these, 2 (10%) patients had early parasympathetic damage, 8 (40%) patients had definite parasympathetic damage, and 10 (50%) patients had combined damage. Heart rate response to standing was statistically significant (p = 0.014) among diabetic CKD patients when compared with diabetic patients without CKD. Combined form of autonomicdysfunction was more frequent in advanced stages of diabetic CKD. Three (42.85%) patients in stage 3 CKD, 4 (66.66%) patients in stage 4 CKD and 5 (71.42%) patients in stage 5 CKD, had combined autonomic failure. CONCLUSIONS: Autonomic neuropathy is common in native Nepalese diabetic CKD patients. Heart rate response to standing is significantly abnormal in diabetic CKD patients in comparison with diabetes mellitus patient without CKD. Severity of autonomic dysfunction increases with severity of CKD..  KEYWORDS: cardiovascualr autonomic neuropathy, chronic kidney disease, diabetes mellitus.

Near-maximal voluntary hyperpnea and ventilatory muscle function

1984 ◽  
Vol 57 (6) ◽  
pp. 1742-1748 ◽  
Author(s):  
T. R. Bai ◽  
B. J. Rabinovitch ◽  
R. L. Pardy
Keyword(s):  
Muscle Function ◽  
Low Frequency ◽  
Normal Subjects ◽  
Pressure Time ◽  
Before And After ◽  
Expiratory Muscles ◽  
Four Levels ◽  
Frequency Relationship ◽  
Low Frequency Power ◽  
Relationship Of

Because of its potential relevance to heavy exercise we studied the ventilatory muscle function of five normal subjects before, during, and after shortterm near-maximal voluntary normocapnic hyperpnea. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made at four levels of ventilation: 76, 79, and 86% maximal voluntary ventilation (MVV) and at MVV. Measurements of pleural and abdominal pressures and diaphragm electromyogram (EMG) during hyperpnea and of maximum respiratory pressures before and after hyperpnea were made. The pressure-stimulation frequency relationship of the diaphragm obtained by unilateral transcutaneous phrenic nerve stimulation was studied in two subjects before and after hyperpnea. Decreases in maximal inspiratory (PImax) and transdiaphragmatic (Pdimax) strength were recorded posthyperpnea at 76 and 79% MVV. Decreases in the pressure-frequency curves of the diaphragm and the ratio of high-to-low frequency power of the diaphragm EMG occurred in association with decreases in Pdimax. Analysis of the pressure-time product (P X dt) for the inspiratory and expiratory muscles individually indicated the increasing contribution of expiratory muscle force to the attainment of higher levels of ventilation. Demonstrable ventilatory muscle fatigue may limit endurance at high levels of ventilation.

Comparison of phenylephrine bolus and infusion methods in baroreflex measurements

1990 ◽  
Vol 69 (3) ◽  
pp. 962-967 ◽  
Author(s):  
J. T. Sullebarger ◽  
C. S. Liang ◽  
P. D. Woolf ◽  
A. E. Willick ◽  
J. F. Richeson
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Baroreflex Sensitivity ◽  
Heart Rate Response ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Arterial Pressure ◽  
Normal Subjects ◽  
Vagus Nerves ◽  
Baroreflex Control

Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

Effect of radiofrequency catheter ablation of accessory pathways on autonomic tone in children

1999 ◽  
Vol 9 (4) ◽  
pp. 377-383 ◽  
Author(s):  
Ruchir Sehra ◽  
Joyce E. Hubbard ◽  
Susan P. Straka ◽  
Naomi S. Fineberg ◽  
Douglas P. Zipes ◽  
...  
Keyword(s):  
Heart Rate ◽  
Catheter Ablation ◽  
Supraventricular Tachycardia ◽  
Radiofrequency Catheter Ablation ◽  
Autonomic Function ◽  
Accessory Pathways ◽  
Non Invasive ◽  
Autonomic Changes ◽  
Before And After ◽  
Autonomic Blockade

AbstractBackgroundRadiofrequency catheter ablation is standard treatment for children with re-entrant supraventricular tachycardias. Autonomic changes have been noted after such ablation for atrioventricular nodal re-entry tachycardia, but not as well documented with atrioventricular re-entry over an accessory pathway.Methods and resultsIn 10 normal paediatric volunteers and 12 children referred for electrophysiologic testing and radiofrequency ablation of supraventricular tachycardia, non-invasive autonomic function tests and tilt-table testing were performed, and the variability in 24-h heart rate was analysed. Patients with supraventricular tachycardia underwent these tests both 24–72 h before and 24 h after ablation. Patients with tachycardia underwent additional autonomic testing to assess the sensitivity of baroreceptors and the intrinsic heart rate with autonomic blockade immediately before and after ablation. One non-invasive autonomic function test, namely handgrip, demonstrated significant differences (p < 0.05) in diastolic blood pressure before and after ablation, though these values did not differ from controls. Significant decreases were noted in two indexes of the variability of heart rate before and after ablation (p < 0.05). Certain tilt test variables also demonstrated significant differences between controls and those with tachycardia subsequent to ablation. Intracardiac testing demonstrated changes (p < 0.05) in sinus cycle lengths, effective refractory periods and/or blood pressures at baseline and during testing of the sensitivity of baroreceptors before and after ablation. These changes were consistent with increased sympathetic or decreased parasympathetic tone. With autonomic blockade, these differences were abolished.ConclusionsCatheter ablation of accessory pathways in children was associated with changes consistent with increased sympathetic or decreased parasympathetic tone. These autonomic changes persisted 24 h after the ablation procedure.

scholarly journals Intravenous adenosine and dyspnea in humans

2005 ◽  
Vol 98 (1) ◽  
pp. 180-185 ◽  
Author(s):  
Nausherwan K. Burki ◽  
Wheeler J. Dale ◽  
Lu-Yuan Lee
Keyword(s):  
Heart Rate ◽  
Heart Rate Response ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Peripheral Chemoreceptor ◽  
C Fibers ◽  
Group Data ◽  
Lung Resistance ◽  
Time Latency ◽  
Stimulation Of

Intravenous adenosine for the treatment of supraventricular tachycardia is reported to cause bronchospasm and dyspnea and to increase ventilation in humans, but these effects have not been systematically studied. We therefore compared the effects of 10 mg of intravenous adenosine with placebo in 21 normal subjects under normoxic conditions and evaluated the temporal sequence of the effects of adenosine on ventilation, dyspnea, and heart rate. The study was repeated in 11 of these subjects during hyperoxia. In all subjects, adenosine resulted in the development of dyspnea, assessed by handgrip dynamometry, without any significant change ( P > 0.1) in lung resistance as measured by the interrupter technique. There were significant increases ( P < 0.05) in ventilation and heart rate in response to adenosine. The dyspneic response occurred slightly before the ventilatory or heart rate responses in every subject, but the timing of the dyspneic, ventilatory, and heart rate responses was not significantly different when the group data were analyzed (18.9 ± 5.8, 20.3 ± 5.5, and 19.7 ± 4.5 s, respectively). During hyperoxia, adenosine resulted in similar effects, with no significant differences in the magnitude of the ventilatory response; however, compared with the normoxic state, the intensity of the dyspneic response was significantly ( P < 0.05) reduced, whereas the heart rate response increased significantly ( P < 0.05). These data indicate that intravenous adenosine-induced dyspnea is not associated with bronchospasm in normal subjects. The time latency of the response indicates that the dyspnea is probably not a consequence of peripheral chemoreceptor or brain stem respiratory center stimulation, suggesting that it is most likely secondary to stimulation of receptors in the lungs, most likely vagal C fibers.

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