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PubMed1995

Permissive hypercapnia in ARDS and its effect on tissue oxygenation.

Many experimental studies have shown that mechanical ventilation with high tidal volumes (Vt) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal lung injury and probably an inflammatory response. Low volume ventilation with permissive hypercapnia has been used in an attempt to avoid such injury in ARDS. Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-oxygen dissociation curve during acute respiratory acidosis may increase venous oxygen tension (PvO2) which could allow increased O2 uptake in ischaemic tissues. Acidosis may reduce intrapulmonary shunt (Qs/Qt) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing PvO2 and CvO2, but the increase in cardiac output (CO) may tend to increase Qs/Qt as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Qs/Qt. Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs. Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive hypercapnia with increased CO, reduced arterio-venous O2 content difference and reduced blood lactate concentration. However, acute hypercapnia per se can reduce lactate production. Further studies are required of this complex issue.

Acidosis, Respiratory↗
PubMed1987

A comparison of the effects of maternally administered meptazinol and pethidine on neonatal acid-base status.

A randomized double-blind study compared the effects of equi-analgesic doses of maternally administered meptazinol (1.5 mg/kg) and pethidine (1.5 mg/kg) on neonatal acid-base status. Heel-prick samples were taken for assessment of acid-base status at 10 and 60 min after delivery. Maternal antenatal history, details of labour and neonatal status at delivery were also recorded. Meptazinol produced less neonatal respiratory depression than pethidine: the mean 10 min acid-base data from 16 infants whose mothers received pethidine were indicative of a respiratory acidosis (pH 7.13, SD 0.08, PCO2, 9.11, SD 2.2 kPa; standard bicarbonate 22.3, SD 3.1 mmol/l). This was not evident in the mean acid-base data from 16 infants whose mothers received meptazinol (pH 7.23, SD 0.07; PCO2 6.83, SD 1.6 kPa; standard bicarbonate 20.9, SD 4.2 mmol/l). The mean pH and PCO2 in the two treatment groups were significantly different (P less than 0.002) at 10 min but not at 60 min after delivery.

Acid-Base Equilibrium↗
PubMed1968

Arterial blood gas tensions and pH in acute asthma in childhood.

Studies of the arterial blood gas tensions and pH in 21 children during 24 acute attacks of asthma showed that all were hypoxic on admission to hospital, and in 10 there was evidence of carbon dioxide retention. Cyanosis, invariably present when the So(2) was below 85%, and restlessness in patients breathing air were the most reliable indices of the severity of hypoxia. There were no reliable clinical guides to the Pco(2) level. Conventional oxygen therapy in tents (25-40%) did not always relieve hypoxia, and in three cases the administration of oxygen at a concentration of 40% or over failed to produce a normal arterial oxygen tension. Uncontrolled oxygen therapy may aggravate respiratory acidosis, and three of our patients developed carbon dioxide narcosis while breathing oxygen. The necessity for blood gas measurements in the management of severe acute asthma in childhood is emphasized.

Acid-Base Equilibrium↗
PubMed1992

Acid base changes in arterial and central venous blood during cardiopulmonary resuscitation.

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.

Acid-Base Imbalance↗
PubMed1984

Effect of arterial carbon dioxide tension on amiloride-sensitive sodium absorption in the colon.

To examine the nature of the electroneutral sodium chloride absorptive process affected by arterial carbon dioxide tension (PCO2), we measured the effects of amiloride on colonic sodium absorption at concentrations (0.75 mM) known to inhibit cell membrane sodium-hydrogen ion exchange. During sequential in situ perfusions of distal colon with amiloride-free and amiloride-containing solutions, water and electrolyte transport was measured in anesthetized, mechanically ventilated rats during normocapnia, respiratory alkalosis, or respiratory acidosis. During amiloride-free perfusions, alkalosis decreased and acidosis increased net water, sodium, and chloride absorption without changing the transmural potential difference. Perfusion of amiloride (0.75 mM) caused a similar fractional decrease in net sodium absorption in alkalotic (-53.3 +/- 10.2%), normocapnic (-46.3 +/- 6.5%), and acidotic rats (-57.2 +/- 5.2%). Net water (-43%) and chloride absorption also exhibited equivalent fractional reductions in the three acid-base states during amiloride perfusion, although net chloride absorption was reduced only about 20%. These results suggest that the specific colonic sodium absorptive process affected by arterial PCO2 is an amiloride-sensitive, sodium-hydrogen ion exchange process. Arterial PCO2 probably also affects a mucosal chloride-bicarbonate exchange process that results in its overall effect on electroneutral sodium chloride absorption by the distal colon.

Acidosis, Respiratory↗
PubMed1990

Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver.

Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.

Acid-Base Equilibrium↗
PubMed1982

[K+]o accumulation and electrophysiological alterations during early myocardial ischemia.

Double-barreled valinomycin K+-sensitive electrodes and floating microelectrodes were used to monitor extracellular K+ concentration ([K+]o) and intracellular potential, respectively, in the isolated arterially perfused rabbit interventricular septum, under conditions of global ischemia without collateral flow and hypoxia with maintained flow. During ischemia [K+]o reproducibly increased at rates of 0.5-1 mM/min, usually in a triphasic pattern, and was accompanied by shortening of the action potential duration (APD) and an increase in conduction time (CT). Hyperkalemia, equivalent to that occurring during ischemia, in combination with respiratory acidosis (pH 6.2-6.5) and catecholamines reproduced quantitatively the ischemia-induced changes in APD and CT. None of these factors alone produced quantitatively comparable electrophysiological changes. Faster heart rates increased [K+]o accumulation during ischemia and accentuated the changes in APD and CT during ischemia. These findings suggest that local hyperkalemia, intracellular acidosis, and catecholamines release during early ischemia may account for electrophysiological changes predisposing to the development of reentrant arrhythmias.

Acidosis, Respiratory↗
PubMed1975

Peritubular pH and PCO'2 in renal tubular acidification.

The influence of peritubular capillary pH and PCO'2 on renal tubular acidification was studied in rats by luminal and peritubular perfusion techniques. Luminal stopped-flow microperfusions were carried out with bicarbonate or alkaline phosphate solutions and luminal pH continuously measured by antimony micorelectrodes. Peritubular calpillary microperfusions were carried out with mammalian Ringer solution kept at different pH and PCO'2. The acidification process was assessed in terms of 1)maximal pH differences, 2)rates of pH change, and 3)rates of bicarbinate reabsorption or H'+ ion secretion. During peritubular perfusions at physiological pH and PCO'2 tubular acidifying capacity was maintained at near-normal levels. Perfusingcapillaries at high pH and low PCO'2, especially with bicarbonate Ringer, acidification was markedly depressed; it was moderately reduced at a peritubular pH of 5.6. At a capillary pH of 7.4, acidification was similiar at low and physiological PCO'2and enhanced at elevated PCO'2. Systemic respiratory acidosis enhanced acidification in the proximal tubule, but reduced it in distal segments.

Acid-Base Equilibrium↗
PubMed1983

Effect of hypercapnia and cerebral perfusion pressure on cerebrospinal fluid production in cat.

Brain ventricles of anesthetized cats were perfused with an artificial cerebrospinal fluid (CSF) containing inulin (or [14C]dextran) and 3H-labeled sucrose while each animal respired in turn either room air or an 8-11% CO2-in-air gas mixture. Perfusion inflow (Vi) and outflow (Vo) rates and concentrations of the test molecules were measured to calculate steady-state CSF production (Vf), CSF absorption (Va), and ependymal sucrose permeability (Ksuc). During respiratory acidosis Vf varied inversely as a function of normocapnic Vf, Ksuc increased, and Va was the same as during normocapnia. Vf increased with cerebral perfusion pressure (CPP) during normocapnia but was inversely related to it during hypercapnia. When a normocapnic animal's CPP is high in the range 70-105 Torr, its Vf will also be high, but it will increase its Vf little or not at all during hypercapnia. In the same range, if its CPP is low, its Vf will also be low, but its Vf will increase predictably fourfold or more when it breathes CO2. CPP is an influential determinant of Vf at any level of acid-base balance, possibly due to variations in blood flow at CSF production sites.

Acidosis, Respiratory↗
PubMed1983

Decreased distal acidification in acute hypercapnia in the dog.

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.

Acidosis, Respiratory↗
PubMed1987

Effect of acute hypercapnia on PTH-stimulated phosphaturia in dietary Pi-deprived rat.

The effects of respiratory acidosis on renal inorganic phosphate (Pi) handling are controversial. Clearance experiments, therefore, were performed in fasted, chronically parathyroidectomized (PTX), dietary Pi-deprived rats. The objectives were twofold: to study the effects of compensated and uncompensated hypercapnia per se on renal Pi excretion and to examine the interaction between acute hypercapnia, dietary Pi, and parathyroid hormone (PTH) on the renal handling of Pi. Acute hypercapnia increased the plasma Pi (delta 2.82 +/- 0.65 mg/dl, P less than 0.05) without altering the glomerular filtration rate (GFR). The FEPi increased (delta 7.26 +/- 0.48%, P less than 0.001) but the TRPi/GFR also increased. PTH (3 U X kg-1 X h-1) superimposed on hypercapnia resulted in a plasma Pi comparable to hypercapnia alone. The FEPi (7.56 +/- 0.78 vs. 24.43 +/- 2.20%; P less than 0.001) was higher and the TRPi/GFR (117 +/- 4 vs. 80 +/- 2 micrograms/min, P less than 0.01) lower, in the former group. PTH infusion during normocapnia resulted in a lower FEPi (0.20 +/- 0.10 vs. 24.43 +/- 2.20%, P less than 0.001) and a higher TRPi/GFR (106 +/- 2 vs. 80 +/- 2 micrograms/min, P less than 0.01) compared with PTH infusion during hypercapnia. Urinary adenosine 3',5'-cyclic monophosphate (cAMP) excretion was similar between the groups. During hypercapnia, when the extracellular acidemia was neutralized, the phosphaturic action of PTH persisted. These studies offer direct evidence that in chronically PTX, dietary Pi-deprived rats, the phosphaturic action of PTH is restored by hypercapnia per se. This effect appears to be independent of extracellular acidemia, changes in the plasma Pi and calcium, urinary pH and Na and cAMP excretion.

Acidosis, Respiratory↗
PubMed1992

Ventilatory failure induced by tracheal banding in the hamster.

Previous animal models of hypercapnic ventilatory failure are limited in that the resistive load has only been applied acutely and often in anesthetized animals. We therefore developed a chronic animal model of hypercapnic ventilatory failure by increasing airway resistance via tracheal banding over several days. To test the efficacy of this model, we compared arterial blood gases, pulmonary function, and internal area of the trachea 6 days after the banding or sham procedure in 20 hamsters. Six days later, banded animals had an increased airway resistance as indicated by a 66% reduction in internal cross-sectional area of the trachea and a 6.5-fold increase in pulmonary resistance compared with control hamsters. The increased airway resistance resulted in a severe respiratory acidosis and hypoxemia in the awake banded hamsters. Banded hamsters were also hyperinflated. This animal model will be useful for investigating the various mechanisms that contribute to hypercapnic ventilatory failure and interventions that may promote recovery.

Acidosis, Respiratory↗
PubMedDate not supplied

Double-blind comparison of the respiratory effects of parenteral lorazepam and diazepam in patients with chronic obstructive lung disease.

The effects on the respiratory function of two tranquillising drugs, lorazepam and diazepam, have been compared in 20 patients with chronic obstructive lung disease. Both drugs induce a respiratory depression (decrease in tidal volume and minute ventilation with acceleration of the respiratory frequency) with slight respiratory acidosis, but lorazepam causes no significant hypoxemia and has a shorter duration of action than diazepam. Nevertheless, if tranquillisers are indicated in such patients, they have to be used with care.

Acidosis, Respiratory↗
PubMed2004

Limited extracellular but complete intracellular acid-base regulation during short-term environmental hypercapnia in the armoured catfish, Liposarcus pardalis.

Environmental hypercapnia induces a respiratory acidosis that is usually compensated within 24-96 h in freshwater fish. Water ionic composition has a large influence on both the rate and degree of pH recovery during hypercapnia. Waters of the Amazon are characteristically dilute in ions, which may have consequences for acid-base regulation during environmental hypercapnia in endemic fishes. The armoured catfish Liposarcus pardalis, from the Amazon, was exposed to a water P(CO(2)) of 7, 14 or 42 mmHg in soft water (in micromol l(-1): Na(+), 15, Cl(-), 16, K(+), 9, Ca(2+), 9, Mg(2+), 2). Blood pH fell within 2 h from a normocapnic value of 7.90+/-0.03 to 7.56+/-0.04, 7.34+/-0.05 and 6.99+/-0.02, respectively. Only minor extracellular pH (pH(e)) recovery was observed in the subsequent 24-96 h. Despite the pronounced extracellular acidosis, intracellular pH (pH(i)) of the heart, liver and white muscle was tightly regulated within 6 h (the earliest time at which these parameters were measured) via a rapid accumulation of intracellular HCO(3)(-). While most fish regulate pH(i) during exposure to environmental hypercapnia, the time course for this is usually similar to that for pH(e) regulation. The degree of extracellular acidosis tolerated by L. pardalis, and the ability to regulate pH(i) in the face of an extracellular acidosis, are the greatest reported to date in a teleost fish. The preferential regulation of pH(i) in the face of a largely uncompensated extracellular acidosis in L. pardalis is rare among vertebrates, and it is not known whether this is associated with the ability to air-breathe and tolerate aerial exposure, or living in water dilute in counter ions, or with other environmental or evolutionary selective pressures. The ubiquity of this strategy among Amazonian fishes and the mechanisms employed by L. pardalis are clearly worthy of further study.

Acid-Base Equilibrium↗
PubMed1994

Prognosis of severely hypoxemic patients receiving long-term oxygen therapy.

Two hundred seventy severely hypoxemic (PaO2 < or = 55 mm Hg: mean +/- SD = 48 +/- 6) COPD patients (232 men) were selected for long-term oxygen therapy (LTOT). They were old (mean = 66 +/- 8 years), with severe airflow limitation (FEV1 = 30 +/- 12 percent of predicted), some CO2 retention (PaCO2 = 47 +/- 9 mm Hg), and compensated respiratory acidosis. Eighteen percent of the patients presented some complicating pleuropulmonary diseases (pleural thickening, sequelae of tuberculosis, etc). Overall survival proportion was poor: 70, 50, and 43 percent at 1, 2, and 3 years, respectively. The Cox model showed that the factors which independently reduced survival were lower CO transfer coefficient, smaller intrathoracic gas volume, more severe bronchial obstruction, the fact that oxygen administration did not increase PaO2 above 65 mm Hg, increasing age, and the presence of chest wall abnormalities. When the patients were divided into three groups according to mortality risk, the mean clinical and functional profile of the high-mortality risk group was consistent with the prevalence of emphysematous lesions. Moreover, the best survivors fitted better into the "bronchitic" type; they showed a higher mean PaCO2, suggesting that some degree of hypoventilation could delay muscular fatigue and improve survival. The difference in the proportion of "emphysematous" and "bronchitic" patients is a possible explanation for the variability of the mortality rate reported in literature.

Acidosis, Respiratory↗
PubMed1997

Pulmonary embolism presenting as seizures.

Two patients with massive pulmonary embolism (PE) presented with generalized seizures. Pathophysiologic abnormalities that explain this clinical syndrome include respiratory acidosis, hypoxemia, and cerebral hypoperfusion due to decreased cardiac output. PE should be considered in the differential diagnosis of new-onset and otherwise unexplained seizures.

Acidosis, Respiratory↗
PubMed2001

Malignant hyperthermia in a patient with Graves' disease during subtotal thyroidectomy.

We report the case of a 31-year-old man with Graves' disease who manifested malignant hyperthermia during subtotal thyroidectomy. His past medical history and family history were unremarkable. Before surgery, his condition was well controlled with propylthiouracil, beta-adrenergic blocker and iodine. During the operation, anesthesia was induced by intravenous injection of vecuronium and thiopental, followed by suxamethonium for endotracheal intubation. Anesthesia was maintained with nitrous oxide and sevoflurane. One hour after induction of anesthesia, his end tidal carbon dioxide concentration (ET(CO2)) increased from 40 to 50 mmHg, heart rate increased from 90 to 100 beats per min and body temperature began to rise at a rate of 0.3 degrees C per 15 min. Suspecting thyroid storm, propranolol 0.4 mg and methylprednisolone 1,500 mg were administered, which, however, had little effect. Despite the lack of muscular rigidity, the diagnosis of malignant hyperthermia was made based on respiratory acidosis. Sevoflurane was discontinued and dantrolene was given by intravenous bolus. Soon after the treatment, ET(CO2), heart rate and body temperature started to fall to normal levels. His laboratory findings showed abnormally elevated serum creatine phosphokinase and myoglobin but normal thyroid hormone levels. Since dantrolene is efficacious in thyrotoxic crisis and malignant hyperthermia, an immediate intravenous administration of dantrolene should be considered when a hypermetabolic state occurs during anesthesia in surgical treatment for a patient with Graves' disease.

Acidosis, Respiratory↗