Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assessed ventricular performance during exercise in 16 COPD patients and 8 normal control subjects by means of radionuclide equilibrium angiography using technetium-99m as a tracer. Supine exercise on a bicycle ergometer was performed until symptom-limited exhaustion. Data were accumulated for 300 heart beats at rest and 150 heart beats during exercise. We used the standard voxel count method to calculate the ventricular volumes. Age, FEV1.0%, %VC, PaO2 and PaCO2 of the COPD patients were 63 +/- 8 yr, 46 +/- 11%, 69 +/- 18%, 68 +/- 11 Torr and 44 +/- 7 Torr (mean +/- SD), respectively. Systolic dysfunction of both the left and right ventricles was well confirmed in the present study. In 12 patients who also underwent hemodynamic studies, resting total pulmonary vascular resistance index (TPVRI) and mean pulmonary artery pressure (Ppa) significantly correlated with right ventricular end-systolic volume index (RVESVI) obtained by RI angiography; gamma = 0.769 (p less than 0.01) and gamma = 0.631 (p less than 0.05), respectively. A significant relationship was also observed between left ventricular dysfunction and the degree of hypercapnia. In response to exercise testing, 10 of 16 patients exhibited insufficient augmentation of stroke volume, and both left and right end-diastolic volumes decreased in half of 10 patients. It is suggested that cardiac function may be disturbed by mechanical factors such as pulmonary hyperinflation in COPD patients.
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PMID:[Ventricular performance during exercise in patients with chronic obstructive pulmonary disease (COPD)]. 162 97

We performed inhalation anesthetic therapy in an attempt to produce improvement in cause of life-threatening asthma, which were standard pharmacological therapy. We analysed the results obtained in 6 cases given inhalation anesthetic therapy (4 cases were treated with halothane and 2 cases with enflurane). The following observations were made: 1) The criteria for starting inhalation anesthetic therapy were persistent hypoxycemia or hypercapnia, persistently high inspiratory intra-airway pressure, clinical exhaustion and bronchial toilet with bronchofiberscope. 2) We treated the patients with halothane concentrations of between 1.0 and 2.0% and enflurane concentrations of between 1.0 to 4.2%. 3) No major complications were observed in inhalation anesthetic therapy.
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PMID:[Halothane or enflurane treatment in life-threatening asthma]. 179 65

We have previously shown that the exercise performance of patients with severe chronic obstructive pulmonary disease (COPD) can be increased with the administration of oral morphine (0.8 mg.kg-1). The purpose of this study was to determine whether the administration of dextromethorphan (DXT), an antitussive structurally similar to codeine, would result in increased exercise performance and decreased dyspnoea in patients with COPD, without the side-effects of opiates. Six eucapnic patients (mean age = 66 +/- 3.8 yrs) with COPD (mean forced expiratory volume in one second (FEV1) = 1.01 +/- 0.07 l) underwent two incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following first the oral administration of placebo (P) and then dextromethorphan (60 mg) in a single-blind fashion. There was no statistically significant difference in the maximal exercise performance, perceived dyspnoea (modified Borg scale), breathing pattern or expired gases after the two different treatments. In addition, the ventilatory response to CO2 production during exercise (delta VE/VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after DXT as compared with after P. Indeed the exercise performance was poorer and the ventilatory responses were brisker after DXT. We conclude from this study that the administration of this opiate analogue does not improve the exercise capacity or decrease the ventilatory response of patients with COPD.
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PMID:Lack of effect of dextromethorphan on breathlessness and exercise performance in patients with chronic obstructive pulmonary disease (COPD). 193 24

CO2 reactivity of the brain vessels was investigated in 33 patients (Grade I-III after Hunt and Hess) with cerebral vasospasm after an aneurysmal subarachnoid haemorrhage (SAH) and after early operation within 72 hours. In all cases, transcranial Doppler sonography was used to measure flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) and vasomotor reactivity to CO2 changes. Vasospastic conditions lead to higher flow velocities through the narrow segment, lower peripheral stream resistance due to the post-stenotic pressure drop and lower vasodilating capacities of arterioles under hypercapnia. In severe vasospastic conditions, the peripheral stream bed is already maximally dilated and the hypercapnic response is weak. On the other hand, the peripheral vascular bed reacts normally to hypocapnia in all vasospastic situations. Our results point out two dangerous conditions of vasospastic disease: 1) exhaustion of peripheral vasodilating capacities, and 2) hyperventilatory therapy. Both of these situations can result in a reduction of CBF to brain tissue, mainly for two reasons: 1) In the former, a further increase in vasospasm cannot be compensated for anymore when the peripheral arterioles are maximally dilated, and 2) in the latter, hypocapnia produces a strong peripheral vasoconstrictor response with further reduction of CBF.
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PMID:CO2 reactivity of cerebral vasospasm after aneurysmal subarachnoid haemorrhage. 250 Aug 37

Elevated endorphin levels in patients with COPD may act to diminish the sensation of dyspnea. Exogenous opioids decrease exertional dyspnea and increase exercise capacity in COPD patients. The purpose of this study was to determine the effects of endogenous opioids on the exercise capacity and control of breathing in patients with COPD. We hypothesized that naloxone, an opioid antagonist, would block the endogenous endorphins and decrease the exercise capacity of our patients. Six patients (mean age, 58.8 +/- 3.2 years) with COPD (mean FEV1, 1.28 +/- 0.46 L) underwent identical incremental cycle ergometer tests to exhaustion (Emax) and assessment of their hypercapnic and hypoxic ventilatory responses and mouth occlusion pressure responses following the IV administration of naloxone (0.4 mg/kg) (N) or placebo (P) in a randomized, double-blind fashion. Perceived dyspnea (modified Borg scale), breathing patterns, and expired gas levels were compared at rest and at maximal workload (WL). There was no significant difference after N compared with after P in the WL or the duration of work. At Emax there were no significant differences after N compared with after P in ventilation, the level of dyspnea, P0.1, VO2, or VCO2. The ventilatory response to CO2 production during exercise (delta VE/delta VCO2) and the ventilatory and mouth occlusion pressure responses to hypoxia and hypercapnia did not differ significantly after N compared with after P. This study does not support the hypothesis that endogenous opioids play a significant role in dampening dyspnea and facilitating exercise in patients with COPD.
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PMID:Effect of naloxone on maximal exercise performance and control of ventilation in COPD. 267 90

Eight healthy volunteers performed gradational tests to exhaustion on a mechanically braked cycle ergometer, with and without the addition of an inspiratory resistive load. Mean slopes for linear ventilatory responses during loaded and unloaded exercise [change in minute ventilation per change in CO2 output (delta VE/delta VCO2)] measured below the anaerobic threshold were 24.1 +/- 1.3 (SE) = l/l of CO2 and 26.2 +/- 1.0 l/l of CO2, respectively (P greater than 0.10). During loaded exercise, decrements in VE, tidal volume, respiratory frequency, arterial O2 saturation, and increases in end-tidal CO2 tension were observed only when work loads exceeded 65% of the unloaded maximum. There was a significant correlation between the resting ventilatory response to hypercapnia delta VE/delta PCO2 and the ventilatory response to VCO2 during exercise (delta VE/delta VCO2; r = 0.88; P less than 0.05). The maximal inspiratory pressure generated during loading correlated with CO2 sensitivity at rest (r = 0.91; P less than 0.05) and with exercise ventilation (delta VE/delta VCO2; r = 0.83; P less than 0.05). Although resistive loading did not alter O2 uptake (VO2) or heart rate (HR) as a function of work load, maximal VO2, HR, and exercise tolerance were decreased to 90% of control values. We conclude that a modest inspiratory resistive load reduces maximum exercise capacity and that CO2 responsiveness may play a role in the control of breathing during exercise when airway resistance is artificially increased.
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PMID:Effect of inspiratory resistive loading on control of ventilation during progressive exercise. 310 83

The oxygen extraction fraction (OEF) at maximally vasodilated tissue in patients with chronic cerebrovascular disease was evaluated using positron emission tomography. The vascular responsiveness to changes in PaCO2 was measured by the H2(15)O autoradiographic method. It was correlated with the resting-state OEF, as estimated using the 15O steady-state method. The subjects comprised 15 patients with unilateral or bilateral occlusion and stenosis of the internal carotid artery or middle cerebral artery or moyamoya disease. In hypercapnia, the scattergram between the OEF and the vascular/responsiveness to changes in PaCO2 revealed a significant negative correlation in 11 of 19 studies on these patients, and the OEF at the zero cross point of the regression line with a vascular responsiveness of 0 was 0.53 +/- 0.08 (n = 11). This OEF in the resting state corresponds to exhaustion of the capacity for vasodilation. The vasodilatory capacity is discussed in relation to the lower limit of autoregulation.
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PMID:Oxygen extraction fraction at maximally vasodilated tissue in the ischemic brain estimated from the regional CO2 responsiveness measured by positron emission tomography. 312 86

Acute physiological responses to the "PO2-Aerobic Exerciser" (AE), a partial rebreathing device designed to stimulate training at altitudes, were studied in seven healthy men [mean VO2max = 56.1 +@- 10.1 (SD) ml X kg-1 X min-1] who performed cycle ergometer exercise to exhaustion in three experimental situations: a control test (C) breathing normal atmosphere: a test with the device (AE); and a test with the AE air supplemented with oxygen (AEO2'). Arterial oxygen saturation at rest for C, AE, and AEO2' studies was 97 +/- 1, 95 +/- 2, and 97 +/- 1%, respectively (P less than 0.05 for C vs AE and AE vs AEO2'), while at exhaustion it was 95 +/- 1, 87 +/- 2, and 95 +/- 1%, respectively (P less than 0.05 for C vs AE and AE vs AEO2'). Maximum work rate decreased from a control value of 1738 +/- 184 kg X min-1 to 1371 +/- 147 kg X min-1 during AE and remained below control levels during AEO2'; 1554 +/- 110 kg X min-1 (P less than 0.05). Beyond 60% of maximum work rate during AE, inspired CO2 increased to 0.026 +/- 0.005. Mouth pressure swings of up to -19.2 +/- 10.2 and 12.7 +/- 5.7 cm H2O were recorded during AE. While the PO2 aerobic exerciser induced a hypoxic stress, the pertubation imposed was not explained fully by arterial oxygen desaturation. Other factors such as hypercapnia and a flow resistive increase in the work of breathing appear to have influenced work capacity during the use of the device.
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PMID:Influence of supplemental oxygen on the physiological response to the PO2 aerobic exerciser. 370 49

Maintenance of cerebral perfusion pressure is a prerequisite for the prevention of cerebral ischemia. Physiological fluctuations in systemic perfusion pressure are compensated by cerebrovascular autoregulation. Cerebral hypoperfusion could result from (1) systemic hemodynamic failure (eg, distal to severe arterial stenosis), overcharging the vasoregulatory capacity; (2) dysfunction and exhaustion of cerebrovascular autoregulation; or (3) both. Ultrasound offers an excellent temporal resolution, is noninvasive, and is easily applicable for follow-up investigations. Despite its poor spatial resolution, transcranial Doppler sonography has been used for determination of cerebral perfusion reserve studies measuring cerebral blood flow velocity (CBFV) during hypercapnia or application of vasoactive agents (eg, acetazolamide). This approach evaluates vasomotor regulation in patients with hemodynamic compromise distal to severe stenosis or occlusion of the brain supplying arteries. Monitoring CBFV during tilt table examinations directly measures cerebral autoregulation. In patients with systemic orthostatic hypotension, maintainance or failure of cerebrovascular compensation and, even more importantly, cerebrovascular dysautoregulation, despite normal systemic blood pressure regulation, may be demonstrated. Vasoneuronal coupling is reflected by CBFV variations during appropriate neuronal stimulation. Neuronal dysfunction is associated with CBFV abnormalities as exemplified by preconditions of focal cerebral dysfunction in the posterior cerebral artery (PCA) in migraineurs with aura, where massive alteration of vasoneuronal coupling and ischemia is threatening during spreading depression. A highly significant asymmetric gain of vasoneuronal coupling in the interictal state may act as a trigger mechanism in these patients. Testing for vasoneuronal coupling within the middle cerebral artery (MCA) territory is more difficult due to the poor spatial resolution with various neuronal stimuli (eg, motorsensory or cognitive paradigms), only eliciting local neuronal areas underrepresented in the MCA CBFV global changes. However, motor stimulation evoked CBFV may be used to indicate dysintegration of vasoneuronal coupling in the course of acute cerebral ischemia with sensorimotor hemiparesis and, moreover, seems to be of prognostic value regarding the motor deficit.
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PMID:Cerebrovascular regulation and vasoneuronal coupling. 769

Non-invasive continuous positive airway pressure (CPAP) seems to decrease the need for intubation in patients with severe cardiogenic pulmonary oedema (CPO) in the intensive care unit. The goals of our study were to delineate indications for CPAP in the emergency department, and to confirm its usefulness in such a setting. We retrospectively assess the evolution of all patients ventilated under CPAP for an acute hypoxaemic respiratory failure over a 1-year period (n = 64 patients). Hypercarbia and respiratory acidosis were present in most patients with CPO (PaCO2 = 54.4+/-22.3 mmHg; pH = 7.27+/-0.13), according to respiratory exhaustion, although initial PaCO2 was low in the pneumonia group. There was a significant improvement of arterial blood gases after 1 hour of ventilation in the CPO group (PaO2 = 254.1+/-121.0 mmHg; PaCO2 = 44.0+/-12.6 mmHg; pH = 7.34+/-0.08; p < 0.0001 for both parameters). In the pneumonia group, oxygenation was also improved but with the persistence of a significant shunt (PaO2 = 157.6+/-84.4 mmHg). Fifty-four patients (84%) were considered as successfully ventilated under CPAP, with no need for intubation and a favourable evolution, mainly in the CPO group. No side effects were reported. In conclusion, CPAP is a useful and easy-to-use ventilatory device in the emergency department. It is now one of our first line treatments during prehospital and emergency care of patients with CPO.
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PMID:Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department. 982 33


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