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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of respiration on the cerebrovascular response to elevated intracranial pressure (ICP) was studied in anesthetized dogs. Total and regional cerebral blood flows were measured using labelled microspheres. In spontaneously breathing dogs total and regional cerebral blood flows increased when cerebral perfusion pressure was reduced to 20 mm Hg. The increase in regional flows was greater in the infratentorial areas than in the supratentorial areas. The increase in cerebral flow in spontaneously breathing dogs was associated with the development of hypoxemia and respiratory acidosis secondary to depression of ventilation. Elevation in ICP while regulating PO2, PCO2, and pH by controlled ventilation resulted in decrease in the total and regional cerebral blood flows. The decrease in regional flows was greater in the supratentorial areas. Induction of respiratory acidosis during elevated ICP in the controlled ventilated dogs with a 5% CO2 in air gas mixture, reversed the decrease in cerebral flows. The results suggest that the increase in cerebral blood flow during elevated ICP in spontaneously breathing dogs is secondary to the development of hypoxemia and respiratory acidosis since cerebral vessels retain responsiveness to increased PaCO2 when the vessels are dilated due to elevated ICP. The results also indicate that the regional cerebrovascular response to elevated ICP is non-uniform.
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PMID:Respiratory influence on the total and regional cerebral blood flow responses to intracranial hypertension. 84 90

The role of sympathetic mechanisms in mediating the pulmonary vasoconstrictor response to respiratory acidosis was studied in intact dogs. Arterial oxygen tension and ventilation were maintained at resting levels and the response was studied during a constant level of alpha- and beta-adrenergic blockade. There were significant increases in the pulmonary vascular resistance (PVR) and pulmonary perfusion pressure and no change in pulmonary blood flow (Q) when the dogs breathed 5% CO2 for 10 min. The alpha-adrenergic blocking agent, phenoxybenzamine, did not significantly alter the pulmonary vascular response, while the beta-adrenergic blocking agent, propranolol, enhanced the response. Phenoxybenzamine significantly reduced the resting pulmonary perfusion pressure from control values, while propranolol did not alter it. Both propranolol and phenoxybenzamine produced comparable decreases in the resting Q from control values. The resting PVR increased to a greater extent with propranolol than with phenoxybenzamine. These results indicate that adrenergic mechanisms do not play a role in mediating rise in PVR induced by respiratory acidosis. The finding that the pulmonary vasoconstrictor response to respiratory acidosis is enhanced during beta-adrenergic blockade suggests that vasoconstrictor alpha-receptors may be unmasked during beta-adrenergic blockade. Finally, the studies suggest that both alpha- and beta-receptors contribute to maintaining the resting PVR.
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PMID:Adrenergic mechanisms and the pulmonary vascular response to respiratory acidosis. 93 80

In anesthetized dogs electrocardiogram and monophasic action potentials (MAPs) were recorded from the right atrium and the right ventricle by intracardiac suction electrode technique. The animals were subjected, by means of ventilation with CO2 and hyperventilation, to periods of respiratory acidosis and respiratory alkalosis, respectively. Pronounced respiratory acidosis induced an increased sympathetic activity followed by a decrease in heart rate and prolongation of the A-V conduction time whereas the shape and duration of the atrial and ventricular MAPs remained unaltered. Arterial hypoxia in combination with pronounced respiratory acidosis did not influence the MAP durations. Respiratory alkalosis resulted in an increased sympathetic influence on the heart activity whereas the shape and duration of the atrial and the ventricular MAPs remained unaffected. During pronounced hyperventilation with increasing central venous pressure an increased parasympathetic influence on the heart activity with decrease in the heart rate, prolongation of the A-V conduction time and shortening of the atrial MAP duration was recorded.
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PMID:Effects of respiratory alkalosis and acidosis on myocardial excitation. 94 1

Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When the urinary chloride level is only moderately low, the alkalosis is probably not due to gastric loss of H+. This form of alkalosis (saline-resistant) does not respond well to administration of saline solution and requires use of potassium in treatment. Apprpriate compensatory responses to acidosis or alkalosis are critical to survival. Compensation for metabloic acidosis consists of hyperventilation and enhanced renal excretion of H+, chiefly as ammonium. In metabolic alkalosis, compensation is mainly renal excretion of bicarbonate. Respiratory acidosis is due to alveolar hypoventilation. In chronic situations, a compensatory rise in serum bicarbonate concentration is expected. Management consists of treatment of the cause of hypoventilation. Respiratory alkalosis is due to hyperventilation. Treatment requires identification and correction of the cause of hyperventilation.
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PMID:Acute acid-base disorders. 2. Specific disturbances. 98 Oct 88

Rats have been placed for periods from two hours to 22 days in a chamber, the atmosphere of which was enriched in CO2 (FICO2: 0.10). The acute phase of hypercapnia induces multidirectional changes of many plasma amino acids. Some of these changes lessen or become of an opposite direction during the first days of exposure; most of them disappear when the hypercapnic acidosis is partly compensated. The variety of these reactions seems due to the fact that CO2 brings into play various mechanisms of synthesis, circulation and catabolism.
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PMID:[Effects of long term hypercapnia on plasma amino acids in the rat (author's transl)]. 101 69

Circumstances under which the use of oxygen-therapy in lung disease can be effective and harmless, depend upon a careful evaluation of its indications: they are suggested by the clinical need of correction of hypoxaemia as well as by the awareness of factors determining respiratory failure and of problems concerning O(2) transport and supply to tissues in health and disease. Blood gases monitoring enables to control the effects of treatment on arterial O2 and CO2 tensions thus giving all the useful data for oxygen administering particularly as far as components of hyperoxygenated mixtures, flow rate, duration, use of very effective low-risk devices (Venturi masks) are concerned. Correction of hypoxaemia involves the reduction of hypertension of the pulmonary circulation and hyperglobulia, improvement of tolerance of exertion, and attention to the metabolic compensation of respiratory acidosis. These results are influenced by the nature of the pathogenetic factors behind broncho-obstructive disease, which may lead to either a primarily "bronchitis" or a primarily "emphysematous" syndrome. An interesting feature relates to prognosis in the case of patients making home use of hyperoxygenated mixtures as part of a rehabilitation program, or to improve their quality of life. The cost and benifits of such treatment should be carefully weighed. Lastly, in the event of protracted treatment, attention must be paid to the possibility of toxicity and the means to be adopted for its prevention.
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PMID:[Oxygen therapy in pneumology]. 101 8

Isometric, electrically paced strips of cardiac ventricle from two species of fish (plaice, Pleuronectes platessa; cod, Gadus morrhua) with different tolerance to hypoxia were compared with respect to effects of hypercapnic acidosis. Acidosis was induced by altering the equilibrating gas mixture for the muscle strip chamber from 3% CO2 in 97% 02 to 15% CO2 in 85% O2. The pH was varied further by changing the NaHCO3 content of the Cortland-Ringer solution used in the muscle chamber. After onset of acidosis with the highest buffer value of the Cortland-Ringer solution (35.7 mM NaHCO3), the force decay was similar for the initial 10 min of exposure to high Pco2. Subsequently the cod heart continued to lose force at the same rate, whereas the plaice heart regained a cardiac contractile force that after 40 min even exceeded prehypercapnic values. When buffer values were varied by changing the bicarbonate content of the Cortland-Ringer solution in steps from 0.0 to 35.7 mM NaHCO3, the cod heart showed steep force decays at all buffer values during hypercapnic acidosis. The plaice heart showed a similar decline at low buffer values but at a bicarbonate concentration above 23.8 mM NaHCO3, the initial force decline was reversed and prehypercapnic force restored.
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PMID:Adaptive tolerance of fish myocardium to hypercapnic acidosis. 111 31

The effects of arterial PCO2 on plasma activity was studied in chloralose anesthetized dogs undergoing carefully controlled respiratory acidosis. Plasma renin activity, measured by radioimmunoassay, was enhanced (P less than 0.001) during inhalation of CO2 despite insignificant changes in renal blood flow and arterial pressure. Although underlying mechanism remained to be investigated, activation of sympathetic nervous system and intrarenal effects of CO2 seemed to be involved in this enchancement.
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PMID:The effects of respiratory acidosis on plasma renin activity in the dog. 119 7

Periodic apnea and exercise hypoventilation were observed in a 14-year-old boy. Hyperphagia, obesity, serum hyperosmolality without diabetes insipidus or appropriate thirst, and retardation of growth and sexual development indicated a hypothalamic disorder. Neurologic evaluation was normal except for electroencephalographic changes induced by apnea. Pulmonary function tests, resting arterial blood gases in the wakeful state, and ventilatory response to inhaled CO2 were also normal. Acute hypoxemia and respiratory acidosis occurred with apnea during sleep and with insufficient ventilation during exercise. The central origin of sleep apneas was shown by esophageal pressure monitoring. The hypothalamic dysfunction and exercise hypoventilation distinguish this patient from others with obesity and periodic apnea.
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PMID:Periodic apnea, exercise hypoventilation, and hypothalamic dysfunction. 125 44

Twenty-seven patients in cardiopulmonary arrest had simultaneous measurements of arterial and central venous blood gases during cardiopulmonary resuscitation (CPR) with a pneumatic chest comparison and ventilation device. Mean central venous and arterial hydrogen ion concentrations, PCO2 and calculated bicarbonate concentrations were significantly different (P less than 0.01) at all sampling times (0, 10 and 20 min). Central venous blood samples predominantly showed a respiratory acidosis in contrast to a mixed disturbance in arterial samples inclined towards a metabolic acidosis. The mean difference between central venous PCO2 (pcv CO2) and arterial PCO2 (pa CO2) ranged from 5.18 to 5.83 kPa reflecting the low blood flow in patients undergoing CPR. Measurement of arterial Po2 indicated adequate oxygenation using the pneumatic device. Arterial blood gas analysis alone does not reflect tissue acid base status. Bicarbonate administration during CPR may have adverse effects and any decision as to its use should be based on central venous blood gas estimations.
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PMID:Acid base changes in arterial and central venous blood during cardiopulmonary resuscitation. 132 75


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