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Nocturnal hypertension in the obstructive sleep apnea syndrome: spectral analysis and a simple model
173
Implication of cardiopulmonaW reflexes at onset of dynamic exercise R.L.H. Sprangers, A.D.J. ten Harkel, B.P.M. Imholz, R. van der Kley and W. Wieling Departments of Cardiology and Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
We analysed the circulatory responses to 3 s of upright bicycle exercise in young adults to substantiate the hypothesis that the initial fall in blood pressure (BP) is elicited by cardiopulmonary reflexes reacting to overfilling of the heart. Three protocols were used. In protocol 1 ( N = 8)intra-arterial, right atrial (RA) and esophageal pressures were measured. Beat-to-beat stroke volume (SV) changes were derived from the pressure wave form using a pulse contour method and then cardiac output (CO) and total peripheral resistance (TPR) were computed. The subjects were trained to perform the manoeuvres during breath-holding without straining. In protocols 2 and 3 finger BP was measured using a Finapres device. In protocol 2 ( N = 8) forearm blood flow was obtained by venous occlusion plethysmography and forearm vascular resistance (FVR) was computed. In protocol 3 ( N = 4) cycling was performed before and after fl-blockade with 10 mg propranolol i.v. and before and after administration of 0.04 m g / k g atropine i.v. In protocol 1, mean BP decreased, with a maximum fall at 10 s of 26 mm Hg. SV increased with a maximum of 50% at 7 s and decreased again in 7 s to control values. The combined increase in heart rate and SV resulted in an immediate cardiac output rise to 80% above control. T P R decreased abruptly to 50% below control in 7 s and returned to control values 20 s after the start of the manoeuvre. The BP fall was preceded by an abrupt rise in RA pressure of 10 mm Hg without a significant change in esophageal pressure. In protocol 2 FVR dropped to 40% in 7 s lasting for about 13 s after the onset of the manoeuvre. In protocol 3 the fall in BP after cycling was not abolished by fl-blockade or atropine. The finding that the resistance fall also occurred in tissue areas without active muscles (forearm) points to a general reflex mechanism. The unchanged BP fall at the onset of cycling after atropine excludes a pure cholinergic-mediated response. The combined data substantiate the hypothesis that a release in vasoconstrictor tone initiated by an abrupt overfilling of the heart mediated by cardiopulmonary reflexes contributes to the BP fall observed at the onset of cycling.
Nocturnal hypertension in the obstructive sleep apnea syndrome: spectral analysis and a simple model J.G. van den Aardweg and J.M. Karemaker Department of lnternal Medicine and Physiology, Academic Medical Centre, Amsterdam, The Netherlands
The obstructive sleep apnea syndrome has been associated with hypertension, in the form of both daytime essential hypertension and blood pressure (BP) elevations during sleep. This unexplained nocturnal hypertensipn generally manifests itself as periodic rises in BP together with large swings in heart rate (HR) during periods of repetitive apneas. In eight patients with a diagnosis of obstructive sleep apnea syndrome, we measured continuous finger arterial pressure, both during wakefulness and sleep. Power spectra and cross-spectra of beat-to-beat values of systolic, diastolic and pulse pressure and R R interval (from the ECG) were obtained by a Fast Fourier Transform.
174
All patients had normal blood pressures during wakefulness, while in seven of them we observed strong oscillations in BP and H R during sleep, corresponding to peaks in the power spectra of all measured parameters in the 0.02-0.05 Hz band. The one patient without similar swings in BP and H R had atrial fibrillation. In the sleep recordings of the others, all with sinus rhythm, BP and H R seemed to fluctuate almost in phase, with lowest values during apneas and highest values in the periods of respiration. Cross-spectral analysis provided a more precise picture of these phase relationships: in six patients, the sequence of changes was 1) diastolic, 2) systolic and 3) pulse pressure, with mutual delays of about 1-4 s, while this sequence was inverted in one patient. Phase relationships between BP parameters and RR interval varied from 2 s (interval leading) to 16 s (interval following), calculated as the shortest delay between interval and diastolic pressure. These phase relationships could not easily be explained by feedback influence from BP on H R (as by the baroreflex), but could be simulated by assuming an oscillating factor (not influenced by BP) that is capable of lengthening R R interval and, about 2 - 4 beats later, increasing total peripheral resistance. Such a factor could be the action of arterial oxygen desaturation through peripheral chemoreceptors, that can increase vagal outflow to the heart and, probably after a short time delay, increase sympathetic influence on peripheral resistance.
Effects of oral caffeine on post-prandial and posturai hypotension in chronic autonomic failure E. A r m s t r o n g , L. W a t s o n , T . C . H a r d m a n
*, R . B a n n i s t e r a n d C.J. M a t h i a s
Department of Medicine, St Mary's Hospital Medical School/Imperial College and University Department of Clinical Neurology, Institute of Neurology and National Hospital for Nervous Diseases, Queen Square, London, * Department of Therapeutics, Westminster Hospital, London, U.K.
Oral caffeine is reported to reduce post-prandial hypotension in chronic autonomic failure [1]. It is unclear if it also reduces postural hypotension. We therefore studied the effects of caffeine on two groups of patients with primary autonomic failure, five with pure autonomic failure (PAF) and seven with multiple system atrophy (MSA). They were studied on two separate occasions. Drugs were stopped on the study day, except in those who were on Fludrocortisone and Desmopressin. Most took either little or no coffee. Studies were performed after an overnight fast with only water allowed. Blood pressure was measured with an automated sphygmomanometer (Sentron). Blood was taken from an indwelling cannula for measurement of plasma noradrenaline, adrenaline, caffeine, insulin, plasma renin activity and glucose. Measurements were made whilst supine and after head-up tilt to 45 o for 10 rain. After return to the horizontal, measurements were repeated after 5 rain, followed by a liquid meal (66 g carbohydrate, 22 g fat and 18 g protein) made up to 300 ml and administered via a flexible straw. Measurements in the supine position continued for a further 45 min after which head-up tilt to 45 ° was repeated. On the first occasion, no medication was given, while on the second, 5 anhydrous caffeine tablets (250 mg) were given with 50 ml of water, 30 rain before the initial period of tilt and 45 rain before the test meal. In the non-caffeine phase, blood pressure fell with tilt in both PAF and MSA patients. In both groups there was substantial post-prandial hypotension whilst they remained supine, the fall in blood pressure being greater in PAF patients. Post-prandial tilt caused a further fall in blood pressure in both groups. The PAF patients could not maintain the upright position for more than 3 min, while the MSA patients remained upright for 10 rain, but were more symptomatic than previously. Caffeine raised the supine blood pressure in some patients. It had no effect on the responses to head-up tilt, the meal and post-meal
Implication of cardiopulmonaW reflexes at onset of dynamic exercise R.L.H. Sprangers, A.D.J. ten Harkel, B.P.M. Imholz, R. van der Kley and W. Wieling Departments of Cardiology and Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
We analysed the circulatory responses to 3 s of upright bicycle exercise in young adults to substantiate the hypothesis that the initial fall in blood pressure (BP) is elicited by cardiopulmonary reflexes reacting to overfilling of the heart. Three protocols were used. In protocol 1 ( N = 8)intra-arterial, right atrial (RA) and esophageal pressures were measured. Beat-to-beat stroke volume (SV) changes were derived from the pressure wave form using a pulse contour method and then cardiac output (CO) and total peripheral resistance (TPR) were computed. The subjects were trained to perform the manoeuvres during breath-holding without straining. In protocols 2 and 3 finger BP was measured using a Finapres device. In protocol 2 ( N = 8) forearm blood flow was obtained by venous occlusion plethysmography and forearm vascular resistance (FVR) was computed. In protocol 3 ( N = 4) cycling was performed before and after fl-blockade with 10 mg propranolol i.v. and before and after administration of 0.04 m g / k g atropine i.v. In protocol 1, mean BP decreased, with a maximum fall at 10 s of 26 mm Hg. SV increased with a maximum of 50% at 7 s and decreased again in 7 s to control values. The combined increase in heart rate and SV resulted in an immediate cardiac output rise to 80% above control. T P R decreased abruptly to 50% below control in 7 s and returned to control values 20 s after the start of the manoeuvre. The BP fall was preceded by an abrupt rise in RA pressure of 10 mm Hg without a significant change in esophageal pressure. In protocol 2 FVR dropped to 40% in 7 s lasting for about 13 s after the onset of the manoeuvre. In protocol 3 the fall in BP after cycling was not abolished by fl-blockade or atropine. The finding that the resistance fall also occurred in tissue areas without active muscles (forearm) points to a general reflex mechanism. The unchanged BP fall at the onset of cycling after atropine excludes a pure cholinergic-mediated response. The combined data substantiate the hypothesis that a release in vasoconstrictor tone initiated by an abrupt overfilling of the heart mediated by cardiopulmonary reflexes contributes to the BP fall observed at the onset of cycling.
Nocturnal hypertension in the obstructive sleep apnea syndrome: spectral analysis and a simple model J.G. van den Aardweg and J.M. Karemaker Department of lnternal Medicine and Physiology, Academic Medical Centre, Amsterdam, The Netherlands
The obstructive sleep apnea syndrome has been associated with hypertension, in the form of both daytime essential hypertension and blood pressure (BP) elevations during sleep. This unexplained nocturnal hypertensipn generally manifests itself as periodic rises in BP together with large swings in heart rate (HR) during periods of repetitive apneas. In eight patients with a diagnosis of obstructive sleep apnea syndrome, we measured continuous finger arterial pressure, both during wakefulness and sleep. Power spectra and cross-spectra of beat-to-beat values of systolic, diastolic and pulse pressure and R R interval (from the ECG) were obtained by a Fast Fourier Transform.
174
All patients had normal blood pressures during wakefulness, while in seven of them we observed strong oscillations in BP and H R during sleep, corresponding to peaks in the power spectra of all measured parameters in the 0.02-0.05 Hz band. The one patient without similar swings in BP and H R had atrial fibrillation. In the sleep recordings of the others, all with sinus rhythm, BP and H R seemed to fluctuate almost in phase, with lowest values during apneas and highest values in the periods of respiration. Cross-spectral analysis provided a more precise picture of these phase relationships: in six patients, the sequence of changes was 1) diastolic, 2) systolic and 3) pulse pressure, with mutual delays of about 1-4 s, while this sequence was inverted in one patient. Phase relationships between BP parameters and RR interval varied from 2 s (interval leading) to 16 s (interval following), calculated as the shortest delay between interval and diastolic pressure. These phase relationships could not easily be explained by feedback influence from BP on H R (as by the baroreflex), but could be simulated by assuming an oscillating factor (not influenced by BP) that is capable of lengthening R R interval and, about 2 - 4 beats later, increasing total peripheral resistance. Such a factor could be the action of arterial oxygen desaturation through peripheral chemoreceptors, that can increase vagal outflow to the heart and, probably after a short time delay, increase sympathetic influence on peripheral resistance.
Effects of oral caffeine on post-prandial and posturai hypotension in chronic autonomic failure E. A r m s t r o n g , L. W a t s o n , T . C . H a r d m a n
*, R . B a n n i s t e r a n d C.J. M a t h i a s
Department of Medicine, St Mary's Hospital Medical School/Imperial College and University Department of Clinical Neurology, Institute of Neurology and National Hospital for Nervous Diseases, Queen Square, London, * Department of Therapeutics, Westminster Hospital, London, U.K.
Oral caffeine is reported to reduce post-prandial hypotension in chronic autonomic failure [1]. It is unclear if it also reduces postural hypotension. We therefore studied the effects of caffeine on two groups of patients with primary autonomic failure, five with pure autonomic failure (PAF) and seven with multiple system atrophy (MSA). They were studied on two separate occasions. Drugs were stopped on the study day, except in those who were on Fludrocortisone and Desmopressin. Most took either little or no coffee. Studies were performed after an overnight fast with only water allowed. Blood pressure was measured with an automated sphygmomanometer (Sentron). Blood was taken from an indwelling cannula for measurement of plasma noradrenaline, adrenaline, caffeine, insulin, plasma renin activity and glucose. Measurements were made whilst supine and after head-up tilt to 45 o for 10 rain. After return to the horizontal, measurements were repeated after 5 rain, followed by a liquid meal (66 g carbohydrate, 22 g fat and 18 g protein) made up to 300 ml and administered via a flexible straw. Measurements in the supine position continued for a further 45 min after which head-up tilt to 45 ° was repeated. On the first occasion, no medication was given, while on the second, 5 anhydrous caffeine tablets (250 mg) were given with 50 ml of water, 30 rain before the initial period of tilt and 45 rain before the test meal. In the non-caffeine phase, blood pressure fell with tilt in both PAF and MSA patients. In both groups there was substantial post-prandial hypotension whilst they remained supine, the fall in blood pressure being greater in PAF patients. Post-prandial tilt caused a further fall in blood pressure in both groups. The PAF patients could not maintain the upright position for more than 3 min, while the MSA patients remained upright for 10 rain, but were more symptomatic than previously. Caffeine raised the supine blood pressure in some patients. It had no effect on the responses to head-up tilt, the meal and post-meal