Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

The effect of standard cardiac resynchronisation therapy (CRT) on the severity of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure was studied. It was hypothesised that CRT, through its known beneficial effects on cardiac function, would stabilise the control of breathing and reduce CSR. Twenty-eight patients who were eligible for CRT and receiving optimised medical treatment for congestive heart failure were referred for overnight polysomnography, including monitoring of thoracic and abdominal movements to identify CSR and obstructive sleep apnoea events. Patients underwent repeat polysomnography after 6 months of CRT to re-evaluate sleep quality and sleep-disordered breathing. Twelve of the 28 patients had significant CSR (43%); 10 patients had a successful implantation and underwent repeat polysomnography a mean+/-SD 27+/-7 weeks after continuous biventricular pacing. Six of the 10 patients experienced a significant decrease in CSR severity following CRT, associated with correction of congestive heart failure-related hyperventilation and hypocapnia. Circulation time, oxygen saturation, frequency of obstructive apnoeas and sleep quality did not change. In conclusion, cardiac resynchronisation therapy is associated with a reduction in Cheyne-Stokes respiration, which may contribute to improved clinical outcome in patients treated with cardiac resynchronisation therapy.
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PMID:Improvement in Cheyne-Stokes respiration following cardiac resynchronisation therapy. 1638 57

Heart failure is a highly prevalent disorder, with significant economic impact, and is associated with excess morbidity and mortality. One factor that may contribute to the progressively declining course of heart failure is the occurrence of recurrent episodes of apnea and hypopnea. There are two major kinds of sleep-related breathing disorders: obstructive and central sleep apnea. In patients with heart failure, in contrast to the general population, central sleep apnea is the most common form of sleep-related breathing disorder. Episodes of apnea, hypopnea, and the subsequent hyperpnea cause sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure. These pathophysiologic consequences of sleep-related breathing disorders have deleterious effects on the cardiovascular system, and may be even more pronounced in the setting of established heart failure and coronary artery disease. Therefore, sleep apnea in heart failure should be treated. Central sleep apnea may be treated with nocturnal supplemental nasal oxygen, theophylline, or nasal-positive pressure devices, such as nasal continuous positive airway pressure (CPAP). The treatment of choice for obstructive sleep apnea is nasal CPAP. Although long-term controlled trials of the effect of treatment of sleep apnea on mortality in patients with heart failure are still pending, treatment of sleep apnea, both obstructive and central, does result in a decrease in sympathetic activity and an improvement in systolic function, which are known surrogates of mortality. Therefore, diagnosis and treatment of sleep-related breathing disorders may increase survival of patients with heart failure.
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PMID:Prevalence and treatment of breathing disorders during sleep in patients with heart failure. 1600 60

The ventilatory responses to immersion and changes in temperature are reviewed. A fall in skin temperature elicits a powerful cardiorespiratory response, termed "cold shock," comprising an initial gasp, hypertension, and hyperventilation despite a profound hypocapnia. The physiology and neural pathways of this are examined with data from original studies. The respiratory responses to skin cooling override both conscious and other autonomic respiratory controls and may act as a precursor to drowning. There is emerging evidence that the combination of the reestablishment of respiratory rhythm following apnea, hypoxemia, and coincident sympathetic nervous and cyclic vagal stimulation appears to be an arrhythmogenic trigger. The potential clinical implications of this during wakefulness and sleep are discussed in relation to sudden death during immersion, underwater birth, and sleep apnea. A drop in deep body temperature leads to a slowing of respiration, which is more profound than the reduced metabolic demand seen with hypothermia, leading to hypercapnia and hypoxia. The control of respiration is abnormal during hypothermia, and correction of the hypoxia by inhalation of oxygen may lead to a further depression of ventilation and even respiratory arrest. The immediate care of patients with hypothermia needs to take these factors into account to maximize the chances of a favorable outcome for the rescued casualty.
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PMID:Respiratory responses to cold water immersion: neural pathways, interactions, and clinical consequences awake and asleep. 1671 16

We tested the hypothesis that, following exposure to high altitude, cerebrovascular reactivity to CO2 and cerebral autoregulation would be attenuated. Such alterations may predispose to central sleep apnea at high altitude by promoting changes in brain PCO2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound) and arterial blood pressure during wakefulness in conditions of eucapnia (room air), hypocapnia (voluntary hyperventilation), and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (1,400 m) and at high altitude (3,840 m) in five individuals. At each altitude, sleep was studied using full polysomnography, and resting arterial blood gases were obtained. During wakefulness and polysomnographic-monitored sleep, dynamic cerebral autoregulation and steady-state changes in MCAv in relation to changes in blood pressure were evaluated using transfer function analysis. High altitude was associated with an increase in central sleep apnea index (0.2 +/- 0.4 to 20.7 +/- 23.2 per hour) and an increase in mean blood pressure and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness, whereas there was a greater decrease during sleep at high altitude compared with low altitude (-9.1 +/- 1.7 vs. -4.8 +/- 0.7 cm/s; P < 0.05). At high altitude, compared with low altitude, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged (5.5 +/- 0.7 vs. 5.3 +/- 0.7%/mmHg; P = 0.06), while it was lowered in the hypocapnic range (3.1 +/- 0.7 vs. 1.9 +/- 0.6%/mmHg; P < 0.05). Dynamic cerebral autoregulation was further reduced during sleep (P < 0.05 vs. low altitude). Lowered cerebrovascular reactivity to CO2 and reduction in both dynamic cerebral autoregulation and MCAv during sleep at high altitude may be factors in the pathogenesis of breathing instability.
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PMID:Alterations in cerebral dynamics at high altitude following partial acclimatization in humans: wakefulness and sleep. 1705 2

Central (brainstem) and peripheral (carotid body) respiratory chemoreflexes act in concert to modulate breathing during sleep, maintaining blood gases (PCO2 and PO2) within narrow limits. Increases in both central and peripheral chemoreflex gain have been reported in clinical populations that experience central sleep apnoea and likely underlie the pathophysiology of this disorder. However, how central-peripheral chemoreceptor interaction affects the apparent gain of each chemoreflex is controversial. Data from our laboratory demonstrate that there is a negative interaction between central and peripheral chemoreceptors in the rat, such that brainstem hypocapnia augments peripheral chemoreflex gain in response to both carotid body PCO2 and PO2. We note that a negative interaction may also occur in humans, especially relevant in those experiencing chronic hypocapnia. Interestingly, chronic hypocapnia occurs in populations prone to central sleep apnea, such as congestive heart failure (CHF) patients and individuals sleeping at high altitude. These observations lead us to propose the novel hypothesis that a negative interaction between chemoreceptors results in an augmented peripheral chemoreceptor gain when the central chemoreceptors are hypocapnic, thereby contributing directly to breathing instability during sleep.
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PMID:A negative interaction between central and peripheral respiratory chemoreceptors may underlie sleep-induced respiratory instability: a novel hypothesis. 1808 15

Our previous work showed a diminished cerebral blood flow (CBF) response to changes in Pa(CO(2)) in congestive heart failure patients with central sleep apnea compared with those without apnea. Since the regulation of CBF serves to minimize oscillations in H(+) and Pco(2) at the site of the central chemoreceptors, it may play an important role in maintaining breathing stability. We hypothesized that an attenuated cerebrovascular reactivity to changes in Pa(CO(2)) would narrow the difference between the eupneic Pa(CO(2)) and the apneic threshold Pa(CO(2)) (DeltaPa(CO(2))), known as the CO(2) reserve, thereby making the subjects more susceptible to apnea. Accordingly, in seven normal subjects, we used indomethacin (Indo; 100 mg by mouth) sufficient to reduce the CBF response to CO(2) by approximately 25% below control. The CO(2) reserve was estimated during non-rapid eye movement (NREM) sleep. The apnea threshold was determined, both with and without Indo, in NREM sleep, in a random order using a ventilator in pressure support mode to gradually reduce Pa(CO(2)) until apnea occurred. results: Indo significantly reduced the CO(2) reserve required to produce apnea from 6.3 +/- 0.5 to 4.4 +/- 0.7 mmHg (P = 0.01) and increased the slope of the ventilation decrease in response to hypocapnic inhibition below eupnea (control vs. Indo: 1.06 +/- 0.10 vs. 1.61 +/- 0.27 l x min(-1) x mmHg(-1), P < 0.05). We conclude that reductions in the normal cerebral vascular response to hypocapnia will increase the susceptibility to apneas and breathing instability during sleep.
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PMID:Influence of cerebral blood flow on breathing stability. 1911 58

Cerebral blood flow (CBF) and its distribution are highly sensitive to changes in the partial pressure of arterial CO(2) (Pa(CO(2))). This physiological response, termed cerebrovascular CO(2) reactivity, is a vital homeostatic function that helps regulate and maintain central pH and, therefore, affects the respiratory central chemoreceptor stimulus. CBF increases with hypercapnia to wash out CO(2) from brain tissue, thereby attenuating the rise in central Pco(2), whereas hypocapnia causes cerebral vasoconstriction, which reduces CBF and attenuates the fall of brain tissue Pco(2). Cerebrovascular reactivity and ventilatory response to Pa(CO(2)) are therefore tightly linked, so that the regulation of CBF has an important role in stabilizing breathing during fluctuating levels of chemical stimuli. Indeed, recent reports indicate that cerebrovascular responsiveness to CO(2), primarily via its effects at the level of the central chemoreceptors, is an important determinant of eupneic and hypercapnic ventilatory responsiveness in otherwise healthy humans during wakefulness, sleep, and exercise and at high altitude. In particular, reductions in cerebrovascular responsiveness to CO(2) that provoke an increase in the gain of the chemoreflex control of breathing may underpin breathing instability during central sleep apnea in patients with congestive heart failure and on ascent to high altitude. In this review, we summarize the major factors that regulate CBF to emphasize the integrated mechanisms, in addition to Pa(CO(2)), that control CBF. We discuss in detail the assessment and interpretation of cerebrovascular reactivity to CO(2). Next, we provide a detailed update on the integration of the role of cerebrovascular CO(2) reactivity and CBF in regulation of chemoreflex control of breathing in health and disease. Finally, we describe the use of a newly developed steady-state modeling approach to examine the effects of changes in CBF on the chemoreflex control of breathing and suggest avenues for future research.
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PMID:Integration of cerebrovascular CO2 reactivity and chemoreflex control of breathing: mechanisms of regulation, measurement, and interpretation. 1921 19

Obstructive sleep apnea is characterized by repeated upper airway obstruction during sleep and affects between 5% and 20% of the population. Epidemiological studies reveal that sleep apnea and associated intermittent hypoxemia increase the risk for hypertension and vascular disease but the mechanisms underlying these effects are incompletely understood. This review reports the results of rodent models of intermittent hypoxia (IH) and relates them to the observed hemodynamic and vascular consequences of sleep apnea. These animal studies have demonstrated that IH exposure in the absence of any other comorbidity causes hypertension, endothelial dysfunction, and augmented constrictor sensitivity, all due at least in part to increased vascular oxidative stress. Animal studies have used a variety of exposure paradigms to study intermittent hypoxia and these different exposure protocols can cause hypocapnia or hypercapnia-or maintain eucapnia-with accompanying alterations in plasma pH. It appears that these different profiles of arterial blood gases can lead to divergent results but the impact of these differences is still being investigated. Overall, the studies in rodents have clearly demonstrated that the vascular and hemodynamic impact of intermittent hypoxia provides a strong rationale for treating clinical sleep apnea to prevent the resulting cardiovascular morbidity and mortality.
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PMID:Vascular effects of intermittent hypoxia. 1950 14

Cheyne-Stokes respiration (CSR) is a form of central sleep-disordered breathing (SDB) in which there are cyclical fluctuations in breathing that lead to periods of central apneas/hypopnea, which alternate with periods of hyperpnea. The crescendo-decrescendo pattern of respiration in CSR is a compensation for the changing levels of blood oxygen and carbon dioxide. Severe congestive heart failure seems to be the most important risk factor for the development of CSR. A number of pathophysiologic changes, such as sleep disruption, arousals, hypoxemia-reoxygenation, hypercapnia/hypocapnia, and changes in intrathoracic pressure have harmful effects on the cardiovascular system, and the presence of CSR is associated with increased mortality and morbidity in subjects with variable degrees of heart failure. The management of CSR involves optimal control of underlying heart failure, oxygen therapy, and positive airway pressure support. In this review, we initially define and describe the epidemiology of central sleep apnea (CSA) and CSR, its pathogenesis, clinical presentation, diagnostic methods, and then discuss the recent developments in the management in patients with heart failure.
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PMID:Cheyne-stokes respiration in patients with heart failure. 1995 65

The typical respiratory response to hypoxia includes a dramatic facilitation of augmented breaths (ABs) or 'sighs' in the breathing rhythm. We recently found that when acetazolamide treatment is used to promote CO(2) retention and counteract alkalosis during exposure to hypoxia, then the hypoxia-induced facilitation of ABs is effectively prevented. These results indicate that hyperventilation-induced hypocapnia/alkalosis is an essential factor involved in the hypoxia-induced facilitation of augmented breaths. However, acetazolamide is also known to decrease the sensitivity of the arterial chemoreceptors. Therefore, the question remains as to whether acetazolamide prevents the facilitation of ABs during hypoxia by offsetting the effects of respiratory alkalosis, or alternatively by suppressing carotid body afferent activity. In the present study, we addressed this question by studying the effects of treatment with an alternative carbonic anhydrase inhibitor, methazolamide, which has been reported to leave carotid body responsiveness to hypoxia intact. Respiratory variables were monitored before, during and after 2 days of methazolamide treatment (10 mg kg(-1) IP, bid) in unsedated and unrestrained adult male rats. Pre-treatment, the number of ABs observed in a 5 min observation window was 1.2 + or - 0.8 and 17.4 + or - 3.8 in room air and hypoxia, respectively. During methazolamide treatment, the facilitation of ABs in hypoxia was rapidly and reversibly suppressed such that ABs we no longer significantly more frequent than they were in room air. The present results demonstrate that the hypoxia-induced facilitation of ABs can be suppressed via the general effects of carbonic anhydrase inhibition, which are common to both acetazolamide and methazolamide. We discuss these results as they pertain to the mechanisms regulating augmented breath production, and the possible association between hypocapnia/alkalosis and sleep disordered breathing.
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PMID:The hypoxia-induced facilitation of augmented breaths is suppressed by the common effect of carbonic anhydrase inhibition. 2038 75


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