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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in common carotid blood flow (CCF) and resistance index (RI), calculated from velocity waveforms by a noninvasive pulsed Doppler technique, were measured during apneic episodes and voluntary breath holding in five sleep apnea patients (SA) and during breath holding in five normal subjects (N). During apneic episodes averaging 27 s, CCF was reduced by 9% and RI increased by 4%, both trends being related to apneic duration. Internal carotid artery measurements in one SA indicated more dramatic changes in blood flow and RI than noted in CCF. During breath holding, CCF decreased significantly in SA but not in N, and RI showed a smaller reduction in SA. These changes in CCF and RI during sleep apnea are similar to those noted in anesthetized dogs where vasomotor waves and associated apneas were induced by elevating intracranial pressure. Previously reported recordings of ventilatory and systemic cardiovascular responses in SA are similar to these recordings in dogs, and it is therefore proposed that vasomotor responses to intermittent cerebral ischemia and hypercapnia may be the principle event in SA and periodic breathing only a secondary consequence of the prevailing autonomic dysfunction.
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PMID:Sleep apnea and autonomic cerebrovascular dysfunction. 310 21

Heart rate varies with breathing patterns, especially in sleep apnea. To assess the effects on heart rate of recurrent apneas interrupting tidal breathing, we studied five normal awake male subjects. These subjects voluntarily changed their breathing pattern from regular tidal breathing to tidal breathing interrupted by breath holding at end expiration. This recurrent apneic breathing pattern did not change mean heart rate but increased its variance significantly. In addition, the variations in heart rate formed a cyclic pattern of oscillation with a mean cycle length identical to both arterial O2 saturation (SaO2) (R = 0.95; P less than 0.01) and ventilation (R = 0.92; P less than 0.01). Cyclic changes in either SaO2 or ventilation reproduced the oscillatory patterns of heart rate seen with tidal breathing interrupted by multiple apneas, but the amplitude of the variance in heart rate was smaller. Finally, preventing the cyclic declines in SaO2 with supplemental O2 did not significantly alter the heart rate changes seen in tidal breathing interrupted by apneas.
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PMID:Changes in heart rate during breathing interrupted by recurrent apneas in humans. 403 Jun 7

To determine the characteristics of and mechanisms causing the bradycardia during sleep apnea (SA), both patients with SA and normals were studied. Evaluation of six consecutive SA patients demonstrated that bradycardia occurred during 95% of all apneas (central, obstructive, and mixed) and became marked with increased apnea length (P less than 0.01) and increased oxyhemoglobin desaturation (P less than 0.01). Heart rate slowed 9.5 beats per minute (bpm) during apneas of 10-19 s in duration, 11.4 bpm during 20-39s apneas, and 16.6 bpm during 40-59-s apneas. Sleep stage had no effect unexplained by apnea length or degree of desaturation. Oxygen administration to four SA patients completely prevented the bradycardia although apneas lengthened (P less than 0.05) in three. Sleeping normal subjects did not develop bradycardia during hypoxic hyperpnea but, instead, HR increased with hypoxia in all sleep stages, although the increase in HR was not as great as that which occurred while awake. Breath holding in awake normals did not result in bradycardia during hyperoxia (SaO2 = 99%), but was consistently (P less than 0.01) associated with heart rate slowing during room air breath-holds (-6 bpm) at SaO2 = 93%, with more striking slowing (-20 bpm) during hypoxic breath-holds (P less than 0.01) at SaO2 = 78%. Breath holding during hyperoxic hypercapnia had no significant effect on rate. Breath holding in awake SA subjects demonstrated similar findings. We conclude that the bradycardia of SA is a consistent feature of apnea and results from the combined effect of cessation of breathing plus hypoxemia.
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PMID:Bradycardia during sleep apnea. Characteristics and mechanism. 708 75

Although breath holding during diving has been studied extensively in seals, the recent observation that these mammals also exhibit long-duration apnea while apparently sleeping has not been systematically examined. This project examined sleep apnea in northern elephant seal pups (Mirounga angustirostris). The animals exhibited a sequential sleep pattern of wakefulness-slow-wave sleep (SWS)-rapid eye movement (REM) sleep that resembled the normal pattern of mammalian sleep. The typical respiratory pattern during sleep in 4-mo-old pups consisted of short periods of continuous breathing separated by periods of apnea of up to 12 min. Several cycles of apnea and eupnea could occur during a single sleep episode. Breathing during a sleep cycle occurred only in SWS, never during REM sleep. The eupneic heart rate was characterized by significant sinus arrhythmia, and the apneic heart rate was similar to the minimum value during normal sinus arrhythmia. Patterns of change in breathing and heart rate associated with wakefulness and sleep were similar in seals sleeping underwater and on land. When sleeping underwater, the seals raised their heads to the surface to breathe without awakening. The changes in heart rate associated with normal sinus arrhythmia, sleep apnea, and diving apnea appear to be similar, suggesting regulation by a common homeostatic control mechanism.
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PMID:Patterns of respiration and heart rate during wakefulness and sleep in elephant seal pups. 816 Aug 82

Forms of sleep apnea syndrome: Interrupted breathing and hypoventilation during sleep lead to sleep disorders and to cardiovascular sequelae. In the common obstructive sleep apnea syndrome (OSAS) apneas are related to intermittent obstruction of the upper airways. In the rarer central sleep apnea syndrome certain cardiovascular or central nervous system disorders lead to disturbed regulation of respiration connected with periodic breathing. Signs indicating OSAS: Loud, cyclic snoring, interrupted by cessation of breathing during sleep observed by relatives and excessive daytime to diurnal sleepiness indicate OSAS. Furthermore alteration of personality, headache in the morning, non-refreshing sleep and nocturnal choking sensations may indicate OSAS. When is evaluation necessary? Patients with complaints possibly induced by OSAS should be further evaluated since nocturnal application of continuous positive airway pressure (CPAP) by means of a nose mask and other treatment forms often lead to significant improvement of OSAS. In addition patients with untreated OSAS have an increased risk for car accidents and premature death as consequence of cardiovascular diseases. The type and extent of a supposed respiratory disorder is evaluated by means of a sleep study.
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PMID:[Indications in sleep-apnea syndrome. When and why is further assessment meaningful?]. 919 Jun 46

Several studies have demonstrated a clear association between snoring, sleep apnoea and increased risk of stroke. However, the possible role of sleep apnoea in the pathophysiogenetic mechanisms of cerebrovascular disease is still unknown. Our aim in this study was to investigate cerebral haemodynamic changes during the waking state in eight patients with sleep apnoea syndrome (OSAS) by means of transcranial Doppler (TCD). In particular, we studied cerebral vascular reactivity (CVR) to hypercapnia calculated by means of the breath holding index (BHI). The investigation was performed in the early morning, soon after awakening, and in the late afternoon. Data were compared with those of eight healthy subjects matched for age and vascular risk factors. OSAS patients showed significantly lower BHI values with respect to controls both in the morning (0.56 vs. 1.36; P < 0.0001) and in the afternoon (1.12 vs. 1.53; P < 0.0001). In patients, BHI values in the afternoon were significantly higher than in the morning (P < 0.0001). These data demonstrate a diminished vasodilator reserve in OSAS patients, particularly evident in the morning. This reduction of the possibility of cerebral vessels to adapt functionally in response to stimulation could be linked to hyposensitivity of cerebrovascular chemoreceptors after the continuous stress caused by nocturnal hypercapnia.
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PMID:Impairment of daytime cerebrovascular reactivity in patients with obstructive sleep apnoea syndrome. 984 56

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO(2) and O(2) were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO(2) increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (approximately 4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO(2) retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.
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PMID:Increased pulmonary vascular resistance and reduced stroke volume in association with CO2 retention and inferior vena cava dilatation. 1672 15

We evaluated daily variability in the cardiovascular response to arterial chemoreceptors activation during breath holding in shift workers who were obstructive sleep apnea patients. Ten patients and 10 weight and age-matched control subjects were enrolled in the study. The experimental sessions consisted of 10 episodes of breath holding on inspiration interspersed with 1 min free breathing periods, repeated every 6 h: at 0.00, 6.00, 12.00, 18.00 hours. The subjects were examined under two experimental protocols: after day-shift work and after night-shift work (36 h of sleep deprivation). Blood pressure (System Portapres), ECG, and arterial hemoglobin oxygen saturation were monitored continuously. Data analysis were based on Smietanowski procedures written in the 4-th generation script language of MATLAB environment. The two methods introduced by Smietanowski a enabled symbolic description of cardiovascular regulatory mechanisms as cardiac, vascular, or mixed type control (BBC), and allowed quantifying relative contributions of cardiac and vascular components in the blood pressure variability. During the part of the study conducted after day-shift work, repetitive apneas led to a significantly greater increase in blood pressure in the sleep apnea patients, as compared with the controls. BBC analysis demonstrated that in the patients the domination of vascular influences during breath holding periods reached 70+/-2.0% and was significantly greater in comparison with the control group: 56+/-2.8 (P<0.01). However, contribution of cardiac component in the blood pressure response to breath holding was greater in the control group: 32+/-2% as compared with the 18+/-2% in the group of patients (P<0.01). Under the conditions of sleep deprivation (night-work shift), greater blood pressure responses to breath holding were observed in all subjects, but they were larger in the group of sleep apnea patients. The cardiovascular responses to hypoxia during breath holding showed daily variability: greater responses at 12.00 and 18.00 declined at 0.00 and 6.00 h. BBC analysis indicated a greater domination of vascular component in the blood pressure response in patients: 71+/-2.8% vs. 58+/-2% in controls. The contribution of cardiac component predominated in the control group: 27+/-3% vs. 19+/-1% in patients.
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PMID:Daily changes in cardiac and vascular blood pressure components during breath holding episodes in obstructive sleep apnea patients after day-shift and night-shift work. 1820 83