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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypocapnia contributes to the genesis of Cheyne-Stokes respiration and central sleep apnoea in patients with congestive heart failure (CHF) and is associated with increased mortality. However, the cause of hypocapnia in patients with chronic stable CHF is unknown. Since pulmonary congestion can induce hyperventilation via stimulation of pulmonary vagal afferents, the present study tested the hypothesis that in patients with CHF (carbon dioxide tension in arterial blood (Pa,CO2)) is inversely related to pulmonary capillary wedge pressure (PCWP), and that alterations in PCWP would cause inverse changes in Pa,CO2. In 11 CHF patients undergoing diagnostic cardiac catheterization, haemodynamic variables and arterial blood gas tensions were measured simultaneously at baseline. In three patients, these measurements were repeated after coronary angiographic dye infusion and nitroglycerine infusion. At baseline, Pa,CO2 correlated inversely with PCWP (r=-0.80, p=0.003). In the three patients in whom multiple measurements were made, acute alterations in PCWP caused inversely proportional changes in Pa,CO2. The present study concludes that in patients with congestive heart failure, pulmonary capillary wedge pressure is an important determinant of carbon dioxide tension in arterial blood. These findings imply that hypocapnia in patients with chronic stable congestive heart failure is a respiratory manifestation of elevated left ventricular filling pressures.
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PMID:Relationship of carbon dioxide tension in arterial blood to pulmonary wedge pressure in heart failure. 1184 25

Cheyne-Stokes respiration is frequently observed in congestive heart failure. Among other factors, prolongation of circulation time, hypocapnia and hypoxia are thought to underlie this sleep-related breathing disorder. Primary pulmonary hypertension (PPH) is also characterized by reduced cardiac output and blood gas alterations. Therefore, the aim of the present study was to determine whether a nocturnal periodic breathing (PB) occurs in PPH. A total of 20 consecutive patients with PPH who had been admitted for pharmacological investigation of pulmonary vasoreactivity were investigated by lung function testing, right heart catheterization and full-night attended polysomnography. PB was detected in six patients (30%) (mean +/- SEM: apnoea/hypopnoea index 37 +/- 5 h(-1); arterial oxygen saturation was <90% during 56 +/- 6.5% of total sleep time). The patients with PB had more severe haemodynamic impairment than those without. They also had a more marked reduction in the pulmonary diffusion capacity and greater arterial hypoxia. PB was markedly improved or even eradicated by nasal oxygen during the night. Periodic breathing occurs in patients with advanced primary pulmonary hypertension and can be reversed by nocturnal nasal oxygen. The clinical and prognostic significance of periodic breathing in primary pulmonary hypertension needs to be determined by further studies.
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PMID:Nocturnal periodic breathing in primary pulmonary hypertension. 1199 95

Nocturnal periodic breathing (PB) closely resembling Cheyne-Stokes respiration in congestive heart failure has been reported to occur in end-stage primary pulmonary hypertension (PPH). We herein describe the clinical course of a 56-year-old female patient with PPH and severe hypoxemia, hypocapnia, and right ventricular compromise in whom sleep-disordered breathing (SDB) resolved after successful double-lung transplantation. This case illustrates the crucial roles of blood gas alterations and hemodynamic impairment in the emergence of PB in PPH, and is in favor of a genuine association between advanced right heart failure and the development of SDB.
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PMID:Reversal of nocturnal periodic breathing in primary pulmonary hypertension after lung transplantation. 1471 66

Central sleep apnoea with a Cheyne-Stokes pattern of respiration is a disorder commonly observed in patients with established symptomatic congestive heart failure (CHF). It is associated with hyperventilation and hypocapnia which are likely to result from either increased pulmonary vagal afferent nerve stimulation due to pulmonary oedema or from upregulation of chemoreceptors induced by increased sympathoneural activity. Treatment should be aimed at improving underlying cardiac function which may include angiotensin-converting enzyme inhibitors, nasal continuous positive airway pressure (CPAP) or possibly supplemental oxygen.
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PMID:Heart failure and central apnoea. 1531 May 5

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).
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PMID:[Pulmonary hypertension and sleep-related breathing disorders]. 1594 1

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

Central sleep apnoea (CSA) is highly prevalent in the evolutionary course of chronic heart failure. Such a ventilatory pattern during sleep is independently associated with poor prognosis in people with congestive heart failure. Chronic hyperventilation and daytime hypocapnia are the main mechanisms underlying the frequent association between CSA and cardiac failure. Simplified diagnostic strategies allowing easier recognition of CSA among people with severe heart failure are obviously needed but remain to be validated. Treatment of CSA is essentially aimed at improving cardiac function. When CSA persists, after appropriate adjustment of medication and resynchronisation therapy when indicated, specific ventilatory support during sleep should be considered. Continuous positive airway pressure (CPAP), oxygen, adaptive Servo-ventilation (ASV) and non-invasive ventilation have been proposed. Large randomised trials demonstrating survival and time free from heart transplantation are lacking.
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PMID:Cheyne-Stokes respiration with central sleep apnoea in chronic heart failure: proposals for a diagnostic and therapeutic strategy. 1637 89

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


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