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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
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PMID:Mechanisms of arrhythmias in chronic obstructive lung disease. 1 Feb 30

Unanesthetized and unrestrained rats, chronically cannulated in the carotid artery, were exposed to normal air (NA) and Helox (21% O2, 79% He) at ambient temperatures (Ta) of 22 and -10 degrees C. In Helox at Ta = 22 degrees C, the Vo2 was 1.39 ml O2/g-h and the Vco2 0.98 ml CO2/g-h, 145 and 126%, respectively, of the values in NA at Ta = 22 degrees C. The arterial Pao2, Paco2, and pH were comparable in Helox and NA at Ta = 22 degrees C. In Helox at Ta = -10 degrees C, rats invariably became hypothermic after exposure of 0.75 to 1.5 h. During the induction of hypothermia the decrease of Vo2 and Vco2 was oscillatory, Pao2 and pH increased, and Paco2 decreased significatnly (P less than 0.05). Minimum Vo2 and Vco2 during hypothermia averaged 0.71 ml O2/g-h and 0.50 ml CO2/g-h, 23 and 22%, respectively, of the values in normothermic animals at Ta = -10 degrees C. Minimum body temperature during hypothermia was clamped at 21.7 +/- 0.3 degrees C (X +/- SE) by increasing Ta to 19 degrees C. When Helox was replaced by NA, hypothermic rats rewarmed spontaneously, returning to normothermia within 4 h. The data suggest that hypothermia induced by Helox plus cold does not seem to be due to respiratory failure, as systemic hypoxia or hypercapnia were not observed. The controlled hypothermia cycle reported here provides a model for dynamic studies of thermogenic mechanisms both at the normothermic and hypothermic states without the interference of drugs and other nonphysiological treatments.
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PMID:Metabolic and respiratory responses during Helox-induced hypothermia in the white rat. 24 22

Direct assessment of tracheal circumference, which permits evaluation of constriction and dilatation in vivo, was made continuously in intact, pentobarbital-anesthetized, spontaneously breathing dogs. Immediate response to induction of hypercapnia included tracheal constriction and cessation of normal, vagus-dependent rhythmicity of airway tone. The characteristic constrictor response to acetylcholine was exaggerated significantly during hypercapnic acidosis and returned to normal when arterial pH, but not CSF pH, was corrected by NaHCO3 infusion. Epinephrine produced significant tracheal dilatation (infrequently followed by constriction) and isoproterenol produced only dilatation at normal pH. The catecholamine-induced dilatation was decreased significantly during hypercapnic acidosis, but improved after NaHCO3 infusion. Responses to acetylcholine and epinephrine were the the same as control during alkalemia, whereas the response to isoproterenol was unexplainedly diminished. Thus alkalemia may inhibit the action of isoproterenol; acidemia enhances parasympathomimetic constriction and reduces sympathomimetic dilatation; and correction of arterial pH returns these responses to normal, even if hypercapnia and CSF acidosis persist.
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PMID:Arterial pH, airway caliber and response to acetylcholine and catecholamines in vivo. 50 32

A patient with end-stage renal disease (ESRD) developed metabolic alkalosis and alkalemia from protracted vomiting. As a result of the absence of the alkali excretory capacity in this patient with ESRD, the alkaline load accumulated rapidly. Once the amount of acid lost from vomiting exceeded the amount of acid gained from metabolism, alkalemia supervened. The initial arterial blood gas on room air revealed hypercarbia, hypoxia and alkalemia. Her serum bicarbonate was greater than 50 mEq/l. Compensatory hypoventilation occurred. In this report, the extent of compensatory hypoventilation in the setting of metabolic alkalosis in patients treated for ESRD and therapeutic approaches to this problem will be discussed. Treatment was aimed at correcting the primary disorder, namely metabolic alkalosis. Conventional bicarbonate dialysis was shown to be effective in improving acid-base homeostasis in this patient.
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PMID:Hypoventilation in a dialysis patient with severe metabolic alkalosis: treatment by hemodialysis. 176 Jan 42

Metabolic alkalosis is defined as a primary increase in plasma bicarbonate concentration. As a consequence of this increase, systemic alkalemia and secondary hypercapnia develop. In most instances metabolic alkalosis arises from loss of acid through the kidney or gastrointestinal tract. The causes of metabolic alkalosis can be separated into two groups. Those forms of alkalosis responsive to chloride salt administration (e.g., vomiting), are associated with extracellular fluid volume and chloride depletion. In contrast, alkalosis resistant to administration of chloride salt (e.g., primary aldosteronism), is usually associated with extracellular fluid volume expansion and a urine chloride above 20 mEq/L (mmol/L). Metabolic alkalosis; causes; diagnosis; clinical manifestations.
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PMID:[Water-electrolyte and acid-base disorders. VII. Metabolic alkalosis]. 222 26

Adequate oxygenation of apneic subjects can be maintained by constant flow transtracheal oxygen (TTO), but this method alone is associated with hypercapnia. The "bellows" effect of external chest compressions (ECC) might prevent this problem if the airway were kept open by TTO. In dogs, we investigated the utility of TTO delivered at 15 L/min by a percutaneously placed intratracheal catheter, plus ECC (TTO/ECC) as an alternative method of ventilation during CPR. TTO was applied to anesthetized, paralyzed dogs in normal sinus rhythm (NSR) at various rates of ECC and during ventricular fibrillation (VF) at an ECC rate of 80/min. During NSR and VF, hypercapnia did not develop and arterial oxygen saturations were maintained above 90 percent. During NSR, the PaCO2 decreased and the pH increased as the ECC rate increased. For many of the animals, coronary perfusion pressure remained above 20 mm Hg during VF, suggesting that these animals could be resuscitated to NSR. In another phase, after 15 min of VF using TTO/ECC, seven of nine animals were defibrillated. We conclude that ventilatory and hemodynamic support adequate to permit successful resuscitation to NSR is provided by the combination of TTO/ECC to apneic dogs during VF.
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PMID:Continuous transtracheal oxygen delivery during cardiopulmonary resuscitation. An alternative method of ventilation in a canine model. 249 66

Hypercapnia due to respiratory failure can be more severe when accompanied by coexistent metabolic alkalosis. We therefore tested the hypothesis that hydrochloric acid (HCl) infusion could improve PaCO2 in 15 critically ill patients admitted with mixed respiratory acidosis and metabolic alkalosis, and a pH of between 7.35 and 7.45. HCl was infused at a constant rate of 25 mmol/h until the bicarbonate concentration decreased less than 26 mmol/L, or until the pH decreased less than 7.35 (initial pH greater than 7.40) or 7.30 (initial pH less than 7.40). Administration of 170 +/- 53 mmol of HCl decreased the bicarbonate concentration from 34 +/- 3 to 25 +/- 2 mmol/L (p less than .001), the pH from 7.41 +/- 0.03 to 7.33 +/- 0.02 (p less than .001), and the PaCO2 from 54 +/- 8 to 48 +/- 8 torr (p less than .001). Postinfusion PaCO2 could be predicted accurately from the initial status of the patients (r = .95, p less than .001) except in one patient with fixed hypercapnia. PaCO2 increased from 77 +/- 19 to 94 +/- 24 torr (p less than .001) and PaO2/PAO2 increased from 59 +/- 17 to 66 +/- 17% (p less than .001). The effects of HCl were still present 12 h after the end of the infusion. No complications related to the acid infusion were noted. These results indicate that, even in the absence of alkalemia, active correction of metabolic alkalosis by HCl infusion can improve CO2 and oxygen exchange in critically ill patients with mixed respiratory acidosis and metabolic alkalosis.
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PMID:Hydrochloric acid infusion for treatment of metabolic alkalosis associated with respiratory acidosis. 249 54

To determine the relative contribution of sudden death as a cause of late inpatient mortality in newborns after prolonged mechanical ventilation, we reviewed the charts of 348 patients who received ventilation assistance and who were admitted to the neonatal intensive care unit during a 26-month period. The overall mortality rate for these patients was 25%, with 88% (77/88) of these deaths occurring within 30 days of birth. Eleven infants died after more than 60 days of mechanical ventilation. Seven of these late deaths were sudden, unexpected in-hospital deaths. Sudden deaths occurred at a mean (uncorrected) age of 12 months (range, 4 to 27 months), during periods when infants appeared to be stable or clinically improving, were unrelated to recent respiratory exacerbations, and occurred despite prompt resuscitative efforts. Four infants still required mechanical ventilation, and 4 had tracheostomies at the time of death. All of the infants had chronic hypercarbia (greater than 50 mm Hg) and an elevated serum bicarbonate level (greater than 30 mmol/L), but not hyponatremia, hypochloremia (less than 80 mmol/L), or alkalemia. Left and right ventricular hypertrophy, multiple drug therapy, recurrent cyanotic episodes, and frequent unexplained fevers were common. In comparison with 17 bronchopulmonary dysplasia survivors who required longer than 60 days of ventilation therapy, the late deaths group more frequently had left ventricular hypertrophy and received prolonged combination theophylline anhydrous and beta-adrenergic agonist therapy. We report that sudden death can occur in infants with severe bronchopulmonary dysplasia despite in-hospital cardiopulmonary monitoring and the rapid institution of cardiopulmonary resuscitation, and is a significant cause of late mortality in infants who receive ventilation therapy for longer than 2 months.
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PMID:Late sudden unexpected deaths in hospitalized infants with bronchopulmonary dysplasia. 274 53

Hypoproteinemia by itself produces a metabolic alkalosis. It is not clear whether a respiratory compensation (hypercapnia) develops with this alkalosis; patients with liver cirrhosis, most of them with hypoproteinemia, are known to hyperventilate. We studied 23 clinically stable patients with hypoproteinemia, with very low albumin-to-globulin ratios (range 0.4 to 1.1), who had either liver cirrhosis (n = 12) or other medical conditions (n = 11). In both groups, there was marked hypocapnia, accompanied by alkalemia (PaCO2 values (mean +/- SD) 31 +/- 2 and 32 +/- 3 torr; pH (mean +/- SD) 7.45 +/- 0.03 and 7.47 +/- 0.03, for the patients with cirrhosis and those without, respectively). Hypoxemia was not the stimulus provoking hyperventilation. The lowering of PaCO2 was proportional to the reduction of serum albumin and total protein concentrations; no detectable difference was seen between the patients with cirrhosis and those without cirrhosis in this apparent dependence of PaCO2 on the concentration of serum proteins. Many of these clinically stable patients with hypoproteinemia, with or without liver cirrhosis, had appreciable concentrations of unidentified anions in plasma (inappropriately high anion gap). Whatever the nonrespiratory acid-base status of the patients with hypoproteinemia, their pulmonary ventilation (hypocapnia) appeared excessive when compared with subjects (presumably) without proteinemia who had similar nonrespiratory acid-base states. The mechanism responsible for the hyperventilation in hypoproteinemia and the nature of the unidentified anions in this condition are obscure.
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PMID:Hyperventilation with hypoproteinemia. 318 88

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4


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