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)

Although morphine depresses respiration the mechanism of this depression remains unknown. Accordingly, ventilatory responses to hypoxia and to hypercapnia were measured before and after administration of 7.5 mg of morphine sulfate subcutaneously in six normal subjects. This procedure produced resting hypoventilation manifested as a peak rise in alveolar carbon dioxide tension from 42.9 plus or minus 1.7 to 45.4 plus or minus 1.5 mm Hg (plus or minus S.E.M.) at 30 minutes ( greater than 0.01). Hypoxic ventilatory drive, measured by an index of the relation between ventilation and hypoxia (parameter A), decreased from a control of 108 plus or minus 17.6 to 42.8 plus or minus 5.3 at 60 minutes after morphine (p greater than 0.01); Hypercapnic ventilatory drive, measured as the slope of the ventilatory response to hypercapnia, also decreased from 1.69 plus or minus 0.24 to 0;98 plus or minus 0.20 (p greater than 0.01) 75 minutes after morphine. Decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.
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PMID:Diminished ventilatory response to hypoxia and hypercapnia after morphine in normal man. 112 55

IV magnesium sulfate was administered to a 72-year-old man with acute respiratory failure secondary to a severe asthma attack. The patient had clinically deteriorated despite aggressive standard treatment and evidenced acidosis and hypercarbia by arterial blood gas determination. An IV dose of 1 g MgSO4 produced rapid clinical and arterial blood gas improvement and enabled management of the patient without endotracheal intubation and mechanical ventilation. This is the first reported case of the use of IV MgSO4 to prevent intubation and assisted ventilation in a patient with acute respiratory failure complicating asthma.
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PMID:Intravenous magnesium sulfate in the management of acute respiratory failure complicating asthma. 291 86

The effects of halothane and isoflurane on regional cerebral blood flow (CBF) were studied in 18 New Zealand White rabbits anesthetized with nitrous oxide (N2O) and morphine sulfate (MS) at three different levels of PaCO2. CBF was measured using the hydrogen clearance technique. Monitored variables were intracranial pressure (ICP), central venous pressure, heart rate, mean arterial pressure, electroencephalogram, arterial blood gases, end-tidal (ET) volatile anesthetic, and ET CO2. Addition of 1 MAC halothane to the N2O/MS background anesthetic caused flow to increase significantly in all three regions studied (cortex, dorsal hippocampus, white matter) at all three levels of PaCO2 (low: 20-25 mmHg; normal: 35-40 mmHg; high: 50-55 mmHg). Addition of 1 MAC isoflurane to the background anesthetic caused CBF to decrease significantly in all regions during hypocapnia. During normocapnia, CBF was unchanged with the addition of 1 MAC isoflurane in all regions and during hypercapnia, CBF increased significantly only in the dorsal hippocampus following addition of 1 MAC isoflurane to the MS/N2O background anesthetic. Volatile anesthetic administration was associated with significant, although small, increases in ICP at all PaCO2 levels. We conclude that 1 MAC concentrations of halothane and isoflurane have opposite effects on CBF when added to a N2O/MS anesthetic during hypocapnia and that the effects of isoflurane on regional CBF are dependent on PaCO2 in rabbits under the anesthetic conditions of this experiment.
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PMID:Isoflurane, halothane, and regional cerebral blood flow at various levels of PaCO2 in rabbits. 308 28

The relationship between the electrical and mechanical activity of the nasal dilator muscle was assessed in 8 pentobarbital-anesthetized, tracheostomized, supine dogs. Alae nasi electromyograms (EMGs) were recorded with bipolar fine wire electrodes, and respiratory changes in muscle length were recorded contralaterally using sonomicrometry. During both resting and stimulated breathing, the intrabreath pattern of muscle shortening closely paralleled the intrabreath pattern of EMG activity. Increases in both alae nasi EMG and alae nasi inspiratory shortening occurred in response to single-breath airway occlusions, brief periods of asphyxia, progressive hyperoxic hypercapnia, and intravenous nicotine sulfate administration. With all interventions, the increases in mechanical activation of the alae nasi paralleled the increases in alae nasi electrical activity. These results indicate that alae nasi EMGs, closely reflect respiratory changes in alae nasi length under conditions in which no mechanical load is placed in the nasal muscle.
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PMID:Effects of respiratory stimulation on alae nasi electromyograms and respiratory changes in length in dogs. 356 23

The present studies evaluate the effect of acute hypercapnia on distal nephron H+ secretion (DNH+S) in vivo by means of the urine-blood PCO2 difference (U-B PCO2) in alkaline urine. Bicarbonaturia was induced by either a sodium bicarbonate infusion or L-lysine administration. Our results demonstrate that the U-B PCO2, as a function of the urinary bicarbonate concentration, was significantly lower during acute respiratory acidosis; this effect was not dependent on changes in glomerular filtration rate and/or fractional excretion of sodium, potassium, and chloride. Infusion of the sodium salts of sulfate, a nonreabsorbable anion, did not correct the diminished U-B PCO2. Amiloride caused the U-B PCO2 to fall in normocapnic dogs but not in hypercapnic dogs. When hypercapnia was superimposed in dogs with extracellular fluid volume contraction, there were no changes in the U-B PCO2. This study indicates that acute hypercapnia in the intact dog decreases DNH+S and is compatible with an effect of hypercapnia on the voltage-dependent component of urine acidification. The mechanism appears to be direct rather than secondary to factors that influence the rate of sodium delivery to the distal nephron.
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PMID:Decreased distal acidification in acute hypercapnia in the dog. 629 83

Morphine reduces ventilation (VE) in exercising man. The mechanism of this ventilatory depression remains unclear. Recent evidence suggests that morphine may reduce exercise VE by simultaneously reducing exercise metabolic rate. We measured exercise VE in six normal subjects after intravenous injection of either saline or 0.1 mg/kg morphine sulfate. During treadmill walks requiring 1/3 and 2/3 of the maximal oxygen uptake, morphine reduced VE (P < 0.05), while it left metabolic rate unchanged. Morphine treatment elevated end-tidal PCO2 at both work levels (P < 0.05). Lower VE and higher PETCO2 in exercise after morphine persisted after elevation of alveolar PO2 to 200 torr. Thus, morphine left unchanged the contribution of the hypoxic chemoreflex to normoxic exercise VE. In addition, morphine failed to alter the ventilatory responses to hypercapnia measured at each exercise level. These results suggest that analgesic dosages of morphine reduce the ventilatory response to exercise through a mechanism other than alterations in metabolic rate or chemical ventilatory responses.
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PMID:Morphine reduces ventilation without changing metabolic rate in exercise. 677 68

In seven studies on three dogs exercising on a treadmill (1.6 km/h), we studied the effect of ozone on ventilatory responses to hypercapnia and to hypoxia. After ozone exposure (0.67 +/- 0.02 ppm by vol; 2 h), the responses of minute volume of ventilation (VE) to progressive hypercapnia and hypoxia were not changed, but the breathing pattern in response to these stimuli changed. We analyzed the breathing pattern by plotting the relationship between VE and tidal volume (VT). During progressive hypercapnia, the slope of VE-VT relationship increased from a control value of 36.1 +/- 1.6 (mean +/- SE) to 93.5 +/- 8.9 min-1 after ozone (n = 7, P less than 0.005); during hypoxia, the slope increased from a control value of 46.1 +/- 8.6 to 142.7 +/- 18.3 min-1 after ozone (n = 6, P less than 0.005). The ozone-induced tachypneic responses to hypercapnia and hypoxia were not affected by inhalation of atropine sulfate or isoproterenol aerosols, but were completely abolished by bilateral vagal blockade. These findings indicate an effect of ozone on the vagal receptors located in the airways and lungs that causes reflex tachypnea during hypercapnia and hypoxia.
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PMID:Mechanism of ozone-induced tachypneic response to hypoxia and hypercapnia in conscious dogs. 735 69

Despite advancing knowledge of the pathophysiology and treatment of asthma, asthma morbidity and mortality are on the rise. To help avert this trend, clinicians and patients must focus their attention on the early identification and treatment of asthma exacerbations. As in the words of Dr. Thomas Petty: " ... the best treatment of status asthmaticus is to treat it three days before it occurs." (7) Still, there will be asthmatics with life-threatening attacks that require careful assessment and aggressive management. Inhaled beta-agonists, systemic corticosteroids, and oxygen remain the drugs of choice in SA. Anticholinergics play a lesser role in the treatment of acute asthma, and debate continues regarding the efficacy of theophylline in this setting. Available data do not support the routine use of magnesium sulfate or antibiotics in patients with SA. Patients failing drug therapy should be considered early for intubation and mechanical ventilation. A strategy of mechanical ventilation that prolongs TE by limiting VE and decreasing inspiratory time, and that tolerates hypercapnia, avoids excessive lung hyperinflation and barotrauma and should improve the outcome of these most critically ill asthmatics. Intubated and mechanically ventilated patients should be aggressively sedated. Paralytic agents should be used only if adequate control of the cardiopulmonary status cannot be achieved by sedation alone. Minimizing the use of paralytic agents may decrease risk of myopathy and other adverse consequences of muscle paralysis. Finally, after successful treatment of a life-threatening episode of asthma, the treatment team should address prevention of future episodes of SA prior to discharge.
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PMID:The assessment and management of adults with status asthmaticus. 773 78

Despite improved understanding of the basic mechanisms underlying asthma, morbidity and mortality remain high, especially in the "inner cities." The treatment of choice in status asthmaticus includes high doses of inhaled beta 2-agonists, systemic corticosteroids, and supplemental oxygen. The roles of theophylline and anticholinergics remain controversial, although in general these agents appear to add little to the bronchodilator effect of inhaled beta-agonists in most patients. Anti-leukotriene medications have not yet been evaluated in acute asthma. Other therapies, such as magnesium sulfate and heliox, have their advocates but are not recommended as part of routine care. If pharmacological therapy does not reverse severe airflow obstruction in the asthmatic attack, mechanical ventilation may be temporarily required. Based on our current understanding of ventilator-induced lung injury, optimal ventilation of asthmatic patients avoids excessive lung inflation by limiting minute ventilation and prolonging expiratory time, despite consequent hypercapnia. Unless respiratory function is extremely unstable, the use of paralytic agents is discouraged because of the increased risk of intensive care myopathy. Patients who have suffered respiratory failure due to asthma are at increased risk for subsequent death due to asthma (14% mortality at 3 years) and should receive very close medical follow-up. In general, severe asthmatic attacks can best be prevented by early intervention in the outpatient setting. In the words of Dr. Thomas Petty, "... the best treatment of status asthmaticus is to treat it three days before it occurs".
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PMID:Medical and ventilatory management of status asthmaticus. 953 66

The goal of management of patients with respiratory failure is to restore them to a state of quiet breathing, without complication. This goal is often achieved by pharmacotherapy alone. Inhaled albuterol sulfate, oxygen, and systemic corticosteroids are mainstays of acute care drug management, whereas other data support the use of inhaled steroids, ipratropium bromide, magnesium sulfate, theophylline, and heliox. Assisted ventilation by face mask or endotracheal tube may be required in refractory patients. In intubated patients, a ventilatory strategy that prolongs exhalation time and accepts hypercapnia minimizes lung hyperinflation and generally results in a good outcome. Acute asthma often represents failure of outpatient management; key aspects of the outpatient program should be addressed in the acute care setting to help prevent recurrent attacks.
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PMID:Management of respiratory failure in patients with asthma. 1060 30


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