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PubMedDate not supplied

The effects of nalorphine and Micoren on blood oxygenation and acid-base equilibrium in patients with myocardial infarction treated with neuroleptanalgesia II.

Sixty-five patients with myocardial infarction were observed for comparison of the values of nalorphine and Micoren in prevention of respiratory depression caused by fentanyl. The patients were divided into 4 groups receiving NLA II with or without nalorphine, morphine or Micoren. In all cases paO2, paCO2 and acid-base equilibrium were determined before and after administration of drugs. In the group receiving only NLA II paO2 fell in 50% of cases, in other groups receiving nalorphine or Micoren it increased in most cases. The paCO2 increased in most cases in groups receiving only NLA II or NLA II with nalorphine with or without morphine and respiratory acidosis developed in 4 cases. In the group receiving NLA II with Micoren paCO2 fell. The results indicate the necessity of administration of respiratory stimulants with NLA II and Micoren appears to be preferable to nalorphine in this respect.

Acid-Base Equilibrium↗
PubMed1988

The plasma potassium concentration in metabolic acidosis: a re-evaluation.

The purpose of these investigations was to describe the mechanisms responsible for the change in the plasma [K] during the development and maintenance of hyperchloremic metabolic acidosis. Acute metabolic acidosis produced by HCI infusion resulted in a prompt rise in the plasma [K], whereas no change was observed during acute respiratory acidosis in the dog. After 3 to 5 days of acidosis due to NH4Cl feeding, dogs became hypokalemic; this fall in the plasma [K] was due largely to increased urine K excretion. Despite hypokalemia, aldosterone levels were not low, and the calculated transtubular [K] gradient was relatively high, suggesting renal aldosterone action. Thus, rather than anticipating hyperkalemia in patients with chronic metabolic acidosis due to a HCl load, the finding of hyperkalemia should suggest that the rate of urinary K excretion is lower than expected (ie, there are low aldosterone levels or failure of the kidney to respond to this hormone).

Acidosis↗
PubMed1982

Effect of acute respiratory alkalosis and acidosis on intestinal ion transport in vivo.

The effects of acute respiratory alkalosis and acidosis on intestinal electrolyte transport were studied in adult Sprague-Dawley rats. During in situ intestinal perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2, creating states of alkalosis (pH 7.64 +/- 0.01), normocapnia (pH 7.45 +/- 0.01), or acidosis (pH 7.26 +/- 0.01), respectively. The plasma bicarbonate concentration decreased 2.0 mM during alkalosis and increased 2.1 mM during acidosis. The jejunum did not respond to the acid-base disturbances. In both the ileum and colon, alkalosis decreased the net absorption of water (-16%), sodium (-23%), and chloride (-42%) and the net secretion of bicarbonate (-33%), whereas acidosis had the opposite effect, i.e., the net absorption of water (41%), sodium (39%), and chloride (32%) increased as did net bicarbonate secretion (33%) (ileal values given). Changes in sodium chloride movement could be correlated with changes in systemic pH and CO2 tension (PCO2), and bicarbonate secretion paralleled changes in the plasma bicarbonate concentration. The acid-base disorders had no effect on ileal and colonic net potassium secretion and transmural potential difference. These studies suggest that systemic pH and/or PCO2 regulate sodium chloride absorption, and the plasma bicarbonate concentration regulates bicarbonate secretion.

Acidosis, Respiratory↗
PubMed1997

The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo.

We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7-10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux (JHCO3) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([HCO3-]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion (FEHCO3) increased threefold, but LOH JHCO3 was unchanged. In ARA, blood pH fell to 7.2, and blood [HCO3-] rose from 28 to 34 mM; FEHCO3 was reduced to < 0.1%, but LOH JHCO3 was unaltered. In CRA, blood pH fell to 7.2, and blood [HCO3-] increased to > 50 mM, whereas FEHCO3 decreased to < 0.1%. JHCO3 was reduced by approximately 30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH JHCO3 increased (by 30%) to normal. These results suggest that LOH JHCO3 is affected by the blood-to-tubule lumen [HCO3-] gradient and HCO3- backflux. When the usual perfusing solution at 20 nl/min was made HCO3- free, mean JHCO3 was -34.5 +/- 4.4 pmol/min compared with 210 +/- 28.1 pmol/min plus HCO3-. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 x 10(-4) M, to abolish H(+)-dependent JHCO3) was used, JHCO3 was -112.8 +/- 5.6 pmol/min. Comparable values for JHCO3 at 10 nl/min were -35.9 +/- 5.8 and -72.5 +/- 8.8 pmol/min, respectively. These data indicate significant backflux of HCO3-along the LOH, which depends on the blood-to-lumen [HCO3-] gradient; in addition to any underlying changes in active acid-base transport mechanisms, HCO3- permeability and backflux are important determinants of LOH JHCO3 in vivo.

Acidosis, Respiratory↗
PubMed1979

Myths, morbidity, and mortality in asthma.

Persistence of outmoded concepts or "myths" concerning the diagnosis and treatment of asthma probably is responsible for large economic losses, overutilization of hospital beds, and many preventable deaths. There have been many worthwhile studies refuting these myths, leading to the following conclusions: Asthma consists of much more than wheezing and in many cases must be treated long after wheezing stops. There is no convincing evidence relating the chronic pulmonary changes of asthma to the psyche. Modern methods of prescribing theophylline have not made it universally effective and safe. Intermittent postive-pressure breathing is rarely justified in asthma. Respiratory acidosis may be corrected only by improving alveolar ventilation. Corticosteroids are usually essential for control of severe asthma and may be used safely. Severe asthmatics need careful monitoring because sudden respiratory failure may occur.

Acidosis, Respiratory↗
PubMed1964

ACID-BASE DISORDERS. THE CLINICAL USE OF THE ASTRUP METHOD OF DETERMINING PH, PCO2 AND BASE EXCESS.

The Astrup method for determination of arterial pH, pCO(2), and "base excess" provides a simple and accurate means for quantitation of acid-base disorders. The "base excess" value, a measure of metabolic acidosis or alkalosis, gives the clinician a valuable tool with which to estimate electrolyte replacement. The pCO(2) is a measure of respiratory acidosis or alkalosis. The pH is used as a measure of the adequacy of compensation. Several representative cases illustrate the use and interpretation of the test.

Acid-Base Equilibrium↗
PubMed1997

[Pathogenesis and diagnosis of systemic acidosis in animals with conclusions for effective forms of therapy].

Intermediary metabolism produces daily approximately 285 mmol hydrogen ions per kilogramm metabolic body weight (BWkg 0.75). If the lung fails to eliminate the volatile acid H2CO3 sufficiently and/or if the kidneys do not eliminate the also produced nonvolatile acids a retention of acids in the organism results. This way, as well as increased acid production through metabolic processes, leads to a systemic acidosis. Systemic acidosis develops after a primary dysfunction of an organ. If there is only one cause of an acid-base-disturbance, e.g. metabolic acidosis, the organism will respond with compensation by the correspondent organ, e.g. the lung, which reduces the drop in the pH. If metabolic and respiratory acidosis occur simultaneously normal compensation is impaired and the fall in the pH is greater by additive effects. This can lead to a severe, life-threatening decline in the blood-pH (< 7.00). If the pH falls from normal value of 7.40 below 7.20, buffer therapy is necessary. Most alkalinizing agents in veterinary medicine, such as bicarbonate, lactate or acetate are only effective after increased pulmonary elimination of CO2 produced in buffer reactions. These substances are not suitable and are even contraindicated in therapy of primary respiratory or mixed respiratory-metabolic acidosis. New buffer agents, e.g. an equimolar mixture of NaHCO3 and Na2CO3 (= Carbicarb) open new promising possibilities in the treatment of acidotic disorders in animals. However clinical trials to determine the efficacy of Carbicarb in animals are still to be conducted.

Acid-Base Equilibrium↗
PubMed1988

[Comparative studies of general anesthesia of sheep with ketamine and etomidate].

The studies were carried out on 48 sheep, 2-6 years old, weighing 33-67 kg. The animals were divided into two groups, 24 sheep each. From these 24, 16 sheep were tested for the plasma electrolytes contents, and 8 were tested for the acid-base balance and the oxygenation level of the arterial blood. Sheep from the first group were given xylasine in the dose of 0.1-10.3 mg/kg od body weight and etomidate (1 mg/kg of body weight). Sheep from the second group were given diazepam in the dose of 0.5 mg/kg of body weight and ketamine (20 mg/kg of body weight). In the first group the surgically effective anaesthesia lasting 15-20 minutes was obtained. During the anaesthesia a respiratory depression together with the decrease of oxygen saturation of the blood was observed. Also, a respiratory insufficiency leading to a respiratory acidosis, hypokalemia, hypocalcemia, hypomagnesemia and hypochloremia of plasma were observed. In the second group of sheep treated with ketamine and diazepam the increased pulse rate, respiratory insufficiency, hypokalemia, hypocalcemia and hypophosphatemia were observed. It has been said that respiratory and blood oxygenation disorders are the result of the forced long lasting position on one side. After treating with diazepam and ketamine bigger changes were observed. Usually all these changes and disorders recessed at the end of the experiment.

Acid-Base Equilibrium↗
PubMedDate not supplied

Management of myxedema coma: report on three successfully treated cases with nasogastric or intravenous administration of triiodothyronine.

Three consecutive cases of myxedema coma treated successfully with either nasogastric or intravenous route of administration of I-triiodothyronine, followed by oral thyroxine, are described. All were hypothermic, had biochemical evidence of advanced hypothyroidism (T4 less than 1.0 micrograms/dl, T3 less than 20 ng/dl and TSH greater than 150 microU/ml), severe hypoxemia, respiratory acidosis, hypercarbia and temporary depression of respiratory center responsiveness. In only one patient it was found significant hyponatremia (Na = 127 mEq/l). Two patients were successfully treated with the nasogastric route of administration of T3 (12.5 micrograms/6h) but in a female patient with intestinal atony (ileus) there was no absorption of the orally administered T3. Intravenously administered T3 promptly corrected the hypometabolic state in this patient. It was confirmed that T4 therapy, although promptly correcting low serum T4 concentration, failed to rise serum T3 levels due to lack of peripheral T4 5'-monodeiodination to T3 in these critically ill patients.

Administration, Intranasal↗
PubMed1980

The effect of systemic acidosis on perfusion of replanted extremities.

By measuring skin temperature and muscle pH of replanted rat legs, we found that uncorrected systemic acidosis had a detrimental effect on perfusion of the replanted extremity. Following administration of systemic sodium bicarbonate and correction of acidosis, muscle pH and skin temperature returned to normal with 60 minutes after revascularization. Metabolic acidosis following major extremity replantation and respiratory acidosis after prolonged anesthesia for digital replantation(s) must be corrected to ensure optimal perfusion of the distal capillary bed.

Acidosis↗
PubMed2004

Chemical immobilization of rhebok (Pelea capreolus) with carfentanil-xylazine or etorphine-xylazine.

Twelve adult rhebok (Pelea capreolus) were immobilized using a combination of 0.4 mg/kg xylazine and either 0.01 mg/kg of carfentanil (n = 6) or 0.01 mg/kg etorphine (n = 6), delivered i.m. using a remote injection system. Induction and recovery times, heart rate, respiratory rate, rectal temperature, oxygen saturation, end-tidal CO2 (ETCO2), anesthetic depth, indirect blood pressure, and arterial blood gases were recorded. Rhebok were not intubated but nasal oxygen was administered. Forty minutes after induction, anesthesia was antagonized with naltrexone and yohimbine. Mean initial heart rate was significantly higher in the carfentanil group than in the etorphine group. Mean initial oxygen saturation was consistent with hypoxia in both the carfentanil group and the etorphine group. In both groups, arterial pH decreased and partial pressure of carbon dioxide increased during the first 15 min of anesthesia, and values were similar in both groups. These findings were consistent with respiratory acidosis and decreased ventilation. Values for respiratory rate, temperature, oxygen saturation, ETCO2, and blood pressure were similar for both groups at all time periods. During the first 5 min of anesthesia, rhebok in the carfentanil group were more responsive to stimuli than rhebok in the etorphine group. After administration of antagonists, time to first arousal was significantly shorter in the etorphine group than in the carfentanil group. Although cardiopulmonary values were similar for the two groups, rhebok in the carfentanil group were at a comparatively lighter plane of anesthesia, and some individuals in this group required additional manual and chemical restraint for medical procedures to be performed. In conclusion, for captive adult rhebok, 0.01 mg/kg of etorphine and 0.4 mg/kg of xylazine are recommended over 0.01 mg/kg carfentanil and 0.4 mg/kg xylazine because of qualitatively better anesthetic episodes and shorter recovery times.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

The effects of pathophysiologic state on the metabolism of vasoactive peptides by mammalian lung.

The pulmonary circulation plays a major role in the metabolism of angiotensin I (AI) and bradykinin through the activity of endothelial cell membrane-bound dipeptidylcarboxypeptidase, converting enzyme of kininase II. This report describes studies which investigate the effects of hypoxia on the function of converting enzyme in vivo in dogs and in endothelial cells in culture. Pulmonary converting enzyme function was assessed by both a blood pressure response technique and radioimmunoassay of bradykinin. Conversion of AI in vivo is decreased during acute alveolar hypoxia. At a PaO2 of 30 mmHg, conversion of AI is decreased to one-half control values. This decrease in AI conversion could not be related to hemodynamic factors in the pulmonary vasculature induced by hypoxia. Clearance of bradykinin by lung converting enzyme decreased from 96% at PaO2 levels above 95 torr to 0% below 26 torr. Hypoxic inhibition of enzyme activity was rapid in onset (less than 2 min), was closely correlated with PaO2 (r = 0.92, p less than 0.001) and reversible within 2 min after return to room air breathing. Converting enzyme activity of the systemic vascular bed also is inhibited by hypoxia. Converting enzyme activity also was studied by adding bradykinin or AI to endothelial cells in culture flasks and measuring residual peptide over time by radioimmunoassay. Hypoxia rapidly (less than 2 min) decreased enzyme activity and room air restored it rapidly. There was no enzyme activity below a PO2 of 30 mmHg. Hypoxia does not affect the activity of purified converting enzyme free of the endothelial cell. Metabolic and respiratory acidosis, as well as metabolic and respiratory alkalosis, had no significant effect on converting enzyme function in vivo in intact animals. While converting enzyme is resistant to a number of pathophysiological insults, it is extraordinarily responsive to acute hypoxia which may have important implications for systemic vasomotor control in conditions associated with clinical hypoxia and hypoxemia.

Acid-Base Equilibrium↗
PubMedDate not supplied

Role of mechanical ventilation in acute severe asthma.

During the last 4 years, fifty-seven patients of acute severe asthma (ASA) were admitted to intensive care unit (ICU). Twenty-three patients required mechanical ventilation (MV) on 25 occasions. Indications to intubate were persistent hypoxia (PaO2 < or = 55 mm Hg) or hypercapnia with respiratory acidosis (64%), abnormal mentation (24%) and respiratory arrest (12%). All the patients were monitored for clinical features, arterial blood gases (ABG) and peak airway pressure (PAP). During MV, there was one case of pneumothorax (4%), seven (28%) cases of transient hypertension and one (4%) patient died. Mean duration of MV was 3 days and the outcome was favourable. Therefore, resorting to aggressive treatment early in the course of disease proves life saving in acute severe asthma.

Acute Disease↗
PubMed1987

Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood.

While maintaining the arterial CO2 tension constant near the normal level of the dog (4.3 kPa), we studied the influence of decreasing cardiac output on both the arterial and mixed-venous blood acid-base status in anaesthetized, artificially ventilated dogs. Cardiac output was manipulated by applying positive end-expiratory pressure (PEEP), and by beta-adrenergic blockade to suppress a compensatory heart rate response. The systemic vascular response was attenuated by alpha-adrenergic blockade. Metabolic rate remained virtually unchanged when cardiac output decreased. Under these conditions a fall in cardiac output led to a shift of the arterial acid-base status in the direction of a metabolic acidosis. The changes occurring in the mixed-venous blood resembled those of an in-vivo CO2 bufferline, with the shift being such as if a respiratory acidosis was developing.

Acid-Base Imbalance↗
PubMed1975

Effect of pH on ionic exchange and function in rat and rabbit myocardium.

The effects of pH variation on ionic exchange and mechanical function were studied in the arterially perfused rat and rabbit septa. The pH and PCO2 of the control perfusate were 7.40 and 39 mmHg, respectively. In the rabbit septum a metabolic acidosis (pH equals 6.82, PCO2 equals 39 mmHg) caused a loss of 16% of control tension in 12 min. Na+ and K+ exchange were unaltered. A comparable respiratory acidosis (pH equals 6.81, PCO2 equals 159 mmHg) caused a 51% loss of tension in 2 min. Na+ exchange was unaltered but K+ efflux fell from 8.9 +/- 0.6 (mean +/- SE) to 4.9 +/- 0.3 mmol/kg dry wt per min (P less than 0.001, n equals 10). A net gain of K+ of 16.9 +/- 1.7 (n equals 14) mmol/kg dry wt occurred and was attributable to a delayed fall in K+ influx relative to efflux over 15 min. The net gain could not be mimicked by epinephrine administration or blocked by propranolol and was absent in the beating rat septum and the quiescent rabbit septum. These results suggest that the net uptake of K+, which appears to be dependent on a period of depolarization, and the changes of contractility are controlled by the H+ ion concentration at a cellular site whose exchange with the extracellular space is characterized by a considerable restriction of diffusion. Changes of contractility are not related to the net uptake of K+.

Acidosis↗
PubMed1983

Acute respiratory alkalosis and acidosis and rabbit intestinal ion transport in vivo.

The effects of acute respiratory alkalosis and acidosis on electrolyte transport in the rabbit ileum, colon, and gallbladder were studied. During in situ perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2 gas, creating states of alkalosis (pH 7.49 +/- 0.01, PCO2 = 27.0 +/- 0.9 mmHg, HCO3 = 21.7 mM), normocapnia (pH 7.38 +/- 0.02, PCO2 = 41.3 +/- 1.1 mmHg, HCO3 = 25.9 +/- 0.4 mM), and acidosis (pH 7.21 +/- 0.01, PCO2 = 66.3 +/- 1.3 mmHg, HCO3 = 28.1 +/- 0.8 mM). In the ileum alkalosis decreased the net absorption of water (-36%), sodium (-44%), and chloride (-27%), whereas acidosis had the opposite effect on water (+69%), sodium (+98%), and chloride (+32%) absorption and reduced bicarbonate secretion. Small changes in net potassium absorption occurred in the direction of water movement. There was no effect on the ileal transmural potential difference (PD). The colon and gallbladder did not respond to the acid-base disorders with changes in electrolyte transport or PD. These results suggest that systemic pH and/or PCO2 affect an electroneutral sodium chloride absorptive process in the rabbit ileum. The simple presence of this absorptive process in the gallbladder was not a sufficient basis for this organ to respond to alterations in systemic pH.

Acidosis, Respiratory↗
PubMed1995

Preliminary evaluation of a new continuous intra-arterial blood gas monitoring device.

Continuous intra-arterial blood gas monitoring is a new technique, possibly offering therapeutic advantages through improved monitoring in patients prone to hypoxaemia, hypercapnia and/or respiratory acidosis. Therefore, we studied the clinical applicability, reliability, precision and side effect of long-term continuous intra-arterial blood gas monitoring in patients suffering from severe acute respiratory distress syndrome. In 10 patients continuous intra-arterial blood gas monitoring based on fluorescent optodes technique was performed. At 4 h intervals, arterial blood samples for in vitro blood gas analyses were drawn, stored in ice, and analysed within 3 min. Evaluation of data retrieved from the continuous intra-arterial blood gas monitoring and in vitro blood gas analysis was based on 596 data points using 10 catheters. Average length of insertion was 281 +/- 215 h, max. lengths of stay was 750 h. Arterial blood gas data obtained in vivo were compared to the mean of in vivo and in vitro arterial blood gases. Inter-catheter bias, expressed as percent difference between continuous intra-arterial blood gas and mean in vitro blood gas analysis was 0.19 +/- 0.23% for pH. 1.1 +/- 5.2% for PaCO2 and 1.6 +/- 5.7% for PaO2. No significant gas partial pressure dependent change in precision was demonstrable. There was no significant time dependent drift in sensor precision over the study period. No negative side-effects related to IABG monitoring were observed. We conclude that long-term use of this new device is possible in patients and represents a reliable alternative to conventional in vitro arterial blood gas analysis, when continuous monitoring of blood gases and/or acid-base balance is critical.

Acid-Base Equilibrium↗
PubMed1985

Differential effects of CO2 and H+ as central stimuli of respiration in the cat.

Effects of H+ and CO2 as independent stimuli of central respiratory chemoreceptors were studied in anesthetized cats in which pH and PCO2 on the ventral surface of the medulla (pHe and PeCO2) could be monitored in response to intravenous acid infusion or CO2 inhalation or to a combination of CO2 inhalation and base infusion that allowed PeCO2 to vary at constant pHe. Respiratory responses to these changes were monitored by measuring tidal volume (VT), respiratory frequency (f), and total ventilation. Respiratory acidosis stimulated ventilation by increasing both VT and f. Mild metabolic acidosis (decrease in pHe less than 0.05) exerted similar effects, but more severe metabolic acidosis failed to produce further stimulation. Increasing or decreasing PeCO2 at constant pHe caused pronounced increases or decreases in respiration mediated both by VT and f. For the same change in PeCO2 the respiratory effects were, however, less pronounced when pHe was kept constant than when pHe was allowed to change with PeCO2. The results suggest that both CO2 and H+ exert independent effects on respiration via central chemoreceptors.

Acidosis↗