Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were conducted on cats; inactivation of carboanhydrase with diamox prevented developmento f hypocapnia and disturbances of the rhythmic activity of the respiratory neurons associated with it in acute hypoxia. However, comparision of electrophysiological data, external respiration indices, of the acid-base balance, pO2 and pCO2 of arterial blood demonstrated that, preventing development of pathological Cheyne-Stokes respiration under conditions of hypoxia, inactivation of carboanhydrase with diamox caused dissociation of the thoracic and abdominal respiration and dyspnea. The latter led to shifts in the metabolic processes and to disturbance of the electrolyte metabolism at the cell level.
 ...
PMID:[External respiration and the functional state of the respiratory center in hypoxia developing against a background of inactivated carbonic anhydrase]. 127 3

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR-CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.
 ...
PMID:Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure. 795 21

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.
 ...
PMID:Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure. 814 43

In order to determine which patients with congestive heart failure (CHF) develop Cheyne-Stokes respiration (CSR) during sleep, we compared the cardiorespiratory profiles of CHF patients with CSR to those of CHF patients without CSR. Overnight polysomnography and continuous transcutaneous PCO2 (tc PCO2) monitoring, estimation of left ventricular ejection fraction (LVEF), pulmonary function tests, and chest radiograph were performed on 16 consecutive patients with chronic, stable CHF. The tc PCO2 monitor (Kontron 7640) was calibrated so that measurements reflected arterial PCO2 values. A mean value was calculated for wakefulness (W) and total sleep time (TST). Circulation time (CT) from the lung to the carotid body was estimated from the end of an apnea or voluntary breath-hold to the nadir of oxygen desaturation recorded on an ear oximeter. The duration of CSR was expressed as a percent of TST. Nine patients developed CSR during sleep (52.5 +/- 31.6 percent TST) (group 1) and 7 did not (group 2). All patients were male and both groups were a similar age (64 +/- 8 vs 63 +/- 4 years) and weight (body mass index, 28.1 +/- 3.5 vs 25.4 +/- 3.4 kg/m2). There were no significant intergroup differences between LVEF (22 +/- 5.2 vs 24.1 +/- 5.2 percent), CT (19.1 +/- 3.6 vs 15.9 +/- 6.7 s), SaO2 (W) (94 +/- 1.2 vs 92.4 +/- 2.1 percent), and SaO2 (TST) (90.8 +/- 2.7 vs 92.4 +/- 2.1 percent). The tc PCO2 (W) was lower in group 1 (34.4 +/- 3.5 vs 38.1 +/- 1.9 mm Hg), increased during sleep by a similar amount in both groups (1.6 +/- 1.5 vs 2.1 +/- 2.2 mm Hg), and was significantly lower during sleep in group 1 (36.1 +/- 3.4 vs 40.2 +/- 2.2 mm Hg). We conclude that CHF patients with CSR hyperventilate during sleep and wakefulness and that CHF patients with awake hypocapnia are more likely to develop CSR during sleep. These findings indicate that arterial PCO2 is important in determining which CHF patients develop CSR.
 ...
PMID:Pathogenesis of Cheyne-Stokes respiration in patients with congestive heart failure. Relationship to arterial PCO2. 840 70

Cheyne-Stokes respiration (CSR) is a form of sleep-disordered breathing seen in approximately 40% of congestive heart failure patients with a left ventricular ejection fraction of < 40%. It is characterized by a crescendo-decrescendo alteration in tidal volume separated by periods of apnea or hypopnea. Sleep is generally disrupted, often with frequent nocturnal arousals. Clinical features include excessive daytime sleepiness, paroxysmal nocturnal dyspnea, insomnia, and snoring. Proposed mechanisms include the following: (1) an increased CNS sensitivity to changes in arterial PCO2 and PO2 (increased central controller gain); (2) a decrease in total body stores of CO2 and O2 with resulting instability in arterial blood gas tensions in response to changes in ventilation (underdamping); and (3) an increased circulatory time. In addition, hyperventilation induced hypocapnia seems to be an important determinant for the development of CSR. Mortality appears to be increased in patients with CSR compared to control subjects with a similar degree of left ventricular dysfunction. Therapeutic options include medically maximizing cardiac function, nocturnal oxygen therapy, and nasal continuous positive airway pressure. The role that other therapeutic modalities, such as inhaled CO2 and acetazolamide, might have in the treatment of CSR associated with congestive heart failure has yet to be determined.
 ...
PMID:Cheyne-Stokes respiration during sleep in congestive heart failure. 904 98

In patients with congestive heart failure (CHF), elevated, left ventricular (LV) volume might lead to pulmonary congestion and hypocapnia, which would create a predisposition to the development of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In addition, because LV volume affects cardiac output, it should influence the lengths of hyperpneas. We therefore evaluated LV volumes and transcutaneous PCO2 (PtcCO2) during wakefulness and stage 2 sleep in 16 patients with CHF due to nonischemic dilated cardiomyopathy (NIDC). Data were then compared between those with (n = 7) and those without CSR-CSA (n = 9). LV end-diastolic volume (LVEDV) was significantly higher in patients with than those without CSR-CSA (585 +/- 118 versus 312 +/- 41 ml, p < 0.05). Compared with patients without CSR-CSA, those with CSR-CSA had lower mean stage 2 sleep PtcCO2 (36.3 +/- 2.2 versus 41.2 +/- 1.2 mm Hg, p < 0.05) and a lesser change in PtcCO2 from wakefulness to stage 2 sleep (-0.4 +/- 0.3 versus 2.0 +/- 0.4 mm Hg, p < 0.001). Among patients with CSR-CSA, hyperpnea length was inversely related to LVEDV (R = 0.769, p = 0.043) owing to the direct relationship of cardiac output to LVEDV (R = 0.791, p = 0.034). We conclude that CSR-CSA in patients with CHF due to NIDC is associated with increased LV volumes possibly through the direct or indirect influence of LV volume on PaCO2 and cardiac output.
 ...
PMID:Left ventricular volume in patients with heart failure and Cheyne-Stokes respiration during sleep. 937 74

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
 ...
PMID:[Sleep-related cardiac insufficiency and respiratory disorders. Prevalence, physiopathology, and treatment]. 1033 59

Central sleep apnea with Cheyne-Stokes respiration (CSR) during sleep affects about 40 % of patients with chronic heart failure (CHF). During CSR simultaneous periodic fluctuations in wakefulness and respiration with accompanying changes in blood pressure and heart rate are observed. CSR can be described as an oscillation of the ventilatory feedback loop controlling respiration. The major synergistically acting mechanisms causing this oscillation include reduced body stores of oxygen and carbon dioxide, hyperventilation with concomitant hypocapnia, prolonged circulation time, and a relatively high hypercapnic ventilatory response. The repetitive desaturations and arousals following CSR cause daytime symptoms and an increase in sympathetic activity. In CHF chronically increased sympathetic activity has negative effects on left ventricular function and is associated with reduced exercise tolerance and poor prognosis. Therefore CSR is expected to have an unfavorable influence on the course of CHF. Whether successful treatment of nocturnal CSR has any impact on the high mortality of CHF needs to be resolved in controlled studies with sufficient sample size.
 ...
PMID:Central sleep apnea and chronic heart failure. 1089 7

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
 ...
PMID:[Heart failure and sleep respiratory disorders. Prevalence, physiopathology and treatment]. 1093 1

We have developed a mathematical model of the regulation of ventilation that successfully simulates breathing in the awake as well as in sleeping states. In previous models, which were used to simulate Cheyne-Stokes breathing and respiration during sleep, the controller was only responsive to chemical stimuli, and allowed no ventilation at sub-normal carbon dioxide levels. The current model includes several new features. The chemical controller responds continuously to changes in P(CO(2)) with a lower sensitivity during hypocapnia than in the hypercapnic ranges. Hypoxia interacts multiplicatively with P(CO(2)) over the entire range of activity. The controller in the current model, besides the chemical drive, includes also a neural component. This neural drive increases and decreases as the level of alertness changes, and adds or subtracts from ventilation levels demanded by the chemical controller. The model also includes the effects of post-stimulus potentiation (PSP) and hypoxic ventilatory depression (HVD). While PSP eliminates apneas after a disturbance and also dampens the subsequent dynamics of the respiration, it is not a major factor in the damping of the response. Another finding is that HVD is destabilizing. The model is the first to reproduce results reported in conscious humans after hyperventilation and after acute and longer-term hypoxia. It also reproduces the effects of NREM sleep.
 ...
PMID:Effects of neural drives on breathing in the awake state in humans. 1178 35


1 2 Next >>