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PubMed1991

Hemodynamic and metabolic effects of aortic unclamping following emergency surgery for traumatic thoracic aortic tear in shunted and unshunted patients.

Nine cases of traumatic aortic tear treated during 1986-1987 were reviewed. Two patients had functioning Gott shunts, six patients had simple crossclamp, and one patient had a Gott shunt placed which was nonfunctional. Anesthetic management was similar in all patients. Clamp times ranged in unshunted patients from 25 to 38 minutes, and in shunted patients from 42 to 50 minutes. The crossclamp time of the patient with the nonfunctional shunt was 42 minutes. Declamping was accompanied in unshunted patients by decreases in core temperature of up to 1 degree C and acute decreases in PaO2. Marked respiratory and metabolic acidosis occurred with declamping. Respiratory acidosis resolved within 30 minutes with hyperventilation, but metabolic acidosis persisted despite bicarbonate therapy (mean = 1.2 mEq/kg) up to 6 hours after declamping. Associated elevations in serum potassium resolved as pH returned to baseline. Acid-base and electrolyte abnormalities were less marked in patients who were shunted.

Acid-Base Equilibrium↗
PubMed1986

Functional role of carbonic anhydrase in intestinal electrolyte transport.

We examined the role of carbonic anhydrase activity in intestinal transport by measuring the effect of systemic pH and PCO2 on electrolyte transport in the presence and absence of luminal acetazolamide. Adult Sprague-Dawley rats were anesthetized, and ileal and colonic segments were perfused with Ringer solution that was acetazolamide-free or that contained 0.1 mM sodium acetazolamide. Consecutive states of acute respiratory alkalosis and acidosis were created by changing the inspired CO2 from 0% (room air) to 8% CO2. In the ileum, acetazolamide perfusion did not affect the increment in net sodium and chloride absorption caused by a reduction in systemic pH. Mucosal carbonic anhydrase activity in this segment was measurable, although very low. In both the ascending and descending colon, acetazolamide perfusion reduced the increment in net sodium absorption caused by an increase in systemic PCO2. In addition, acetazolamide increased the chloride absorptive response to PCO2 in the ascending colon but did not affect the chloride response at all in the descending colon. Colonic mucosal carbonic anhydrase exhibited a proximal-to-distal gradient of activity: levels in the ascending colon were severalfold greater than in the descending colon. These findings suggest a functional role for carbonic anhydrase in mediating the colonic but not the ileal absorptive response to changes in systemic acid-base balance.

Acetazolamide↗
PubMed1988

Intracellular pH and inorganic phosphate content of heart in vivo: a 31P-NMR study.

Studies were performed to determine the contribution of red blood cells to the 31P-nuclear magnetic resonance (NMR) spectrum of the canine heart in vivo and the feasibility of measuring myocardial intracellular phosphate and pH. This was accomplished by replacing whole blood with a perfluorochemical perfusion emulsion blood substitute, Oxypherol, and noting the difference in the 31P-NMR spectrum of the heart. NMR data were collected with a NMR transmitter-receiver coil on the surface of the distal portion of the left ventricle. These studies demonstrated that a small (approximately 10%) contribution from 2,3-diphosphoglycerate (2,3-DPG) and phosphodiesters in the blood could be detected. The magnitude and shift of these blood-borne signals permitted the relative quantification of intracellular inorganic phosphate (Pi) content as well as intracellular pH. Under resting conditions, the intracellular ATP/Pi was 7.0 +/- 0.8 (n = 19). This corresponds to a free intracellular Pi content of approximately 0.8 mumol/g wet wt. The intracellular pH was 7.10 +/- 0.01 (n = 19). Acute respiratory alkalosis and acidosis, with the arterial pH ranging from approximately 7.0 to 7.7, resulted in only small changes in the intracellular pH (approximately 0.1 pH unit). These latter results demonstrate an effective myocardial intracellular proton-buffering mechanism in vivo.

Acidosis, Respiratory↗
PubMed1992

Effects of acid-base status on acute hypoxic pulmonary vasoconstriction and gas exchange.

To investigate the relationship between hypoxic pulmonary vasoconstriction and respiratory and metabolic acidosis and respiratory alkalosis, the pulmonary gas exchange and pulmonary hemodynamic responses were measured in anesthetized, paralyzed, and mechanically ventilated dogs in two sets of experiments (series A, n = 6; series B, n = 10). The animals were treated with acute hypoxia, CO2 inhalation, hyperventilation, and dinitrophenol in various combinations. Multiple regression analysis indicated that mean pulmonary arterial pressure (Ppa) was significantly correlated with end-tidal PO2, mixed venous PO2, and the mean pulmonary capillary pH (average of arterial and mixed venous pH) as independent variables [series A: r = +0.999, standard error of estimate (SEE) = 0.4 mmHg; series B: r = +0.98, SEE = 1.4 mmHg]. Similar analyses of mean values published by other authors from an acute study on humans with exercise at sea level and simulated altitudes of 10,000 and 15,000 ft also indicated a good relationship (n = 14, r = +0.98, SEE = 2.1 mmHg). The mean data (n = 19) obtained in Operation Everest II at various exercise loads and simulated altitudes gave a correlation of r = +0.87, SEE = 6.1 mmHg. These empirical analyses suggest that variations in the rise of Ppa with hypoxia can be accounted for in vivo by the superimposed acid-base status. Furthermore, ventilation-perfusion inhomogeneity, as estimated in the dogs from end-tidal and arterial O2 and CO2 differences and assuming no true shunt or diffusion impairment, was highly correlated with Ppa and mean pulmonary capillary pH (r = +0.999 in series A, r = +0.77 in series B). The human data from the above studies also showed significant correlations between Ppa and directly measured ventilation-perfusion (standard deviation of perfusion obtained from inert gas measurements). These observations indicate that the beneficial effects of hyperventilation during hypoxia may be related to the marked alkalosis that serves to reduce Ppa and improve pulmonary gas exchange efficiency.

2,4-Dinitrophenol↗
PubMed1991

[Application of positive end expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) in the treatment of asthma].

Two intubated young adults with respiratory failure and acidosis due to severe asthma attack were treated by mechanical ventilation with PEEP. Two hours after using of PEEP the expiratory resistance decreased from 35 to 14 cmH2O/L/Sec and 56 to 18 cmH2O/L/Sec respectively, and within two days they were successfully weaned from mechanical ventilation. Another fifteen patients with moderate asthmatic attack were treated with CPAP via a mask from Siemens 900C ventilator. Twenty minutes later the FEV1 and VC were significantly increased from 1.19 +/- 0.69 L to 1.36 +/- 0.73 L and 2.41 +/- 0.97 to 2.65 +/- 0.94 L respectively. We concluded that, PEEP and CPAP have mechanical bronchodilative effect on spasm bronchi, and could be used as a effective way to treat severe asthma attack.

Acidosis, Respiratory↗
PubMed1988

Does diazepam really reduce the cardiotoxic effects of intravenous bupivacaine?

The effect of diazepam on the cardiovascular toxicity of bupivacaine was investigated in a rat model. Under chloral hydrate (400 mg/kg intraperitoneal) anesthesia, unilateral femoral venous and bilateral femoral arterial cannulae were placed for administration of drugs, for blood sampling, and for continuous qualitative monitoring of arterial blood pressure. Lead II ECG was continuously recorded and a tracheostomy performed to increase FIO2 by use of a "T-piece." Four groups of 24 to 36 rats each were studied. All rats received IV bupivacaine 2 mg/kg, within 10 seconds. Group I, the control group, received only bupivacaine. Groups II and III received IV diazepam 0.2 mg/kg, or diazepam vehicle in an equivalent volume, respectively. Five minutes after this pretreatment, groups II and III received IV bupivacaine 2 mg/kg. Group IV was given diazepam, 0.2 mg/kg, 30 seconds after injection of 2 mg/kg bupivacaine. A marked respiratory and metabolic acidosis occurred in all rats but was significantly worse in groups II and III. No rat in the study became hypoxemic. Serious arrhythmias (ventricular or supraventricular tachycardia) were noted in all groups, but the incidence was significantly higher in the group of rats given diazepam pretreatment than in the other three groups. It is concluded that IV diazepam 0.2 mg/kg given 5 minutes before administration of IV bupivacaine 2 mg/kg increases the incidence of serious cardiac arrhythmias. Second, this increase is not solely due to increased acidosis, because the rats receiving the vehicle (group III) developed equivalent acidosis but did not develop increased arrhythmias.

Acidosis, Respiratory↗
PubMed1987

[Critical study of erythrocyte bilirubin and predictive factors of kernicterus in premature low birth weight infants].

Among 217 premature neonates with birth-weights less than or equal to 1,500 g who died, in whom post mortem examination was carried out during the years 1978-1984, 11 cases of kernicterus (5%) were found. A comparative study was undertaken between these 11 children and 42 children of the same population matched for birth-weight, gestational age and life duration. The following clinical and biological perinatal data were found more frequently in the kernicterus group: meningitis (3/11 vs 0/42), p less than 0.01), hyperchloronatremic dehydration (3/11 vs 1/42, p less than 0.05) and hypoglycemia either severe (less than 0.83 mumol/l) (5/11 vs 3/42, p less than 0.01) or prolonged (less than 1.66 mumol/l for at least 36 hrs) (3/11 vs 0/42, p less than 0.01). The mean value of total bilirubin highest levels was 261 +/- 76 mumol/l in cases with kernicterus and 266 +/- 58 mumol/l in the control group (NS). In a case with kernicterus the total bilirubin level was 149 mumol/l (87 mg/l). Erythrocyte bilirubin was repeatedly assayed in 16 children, 4 of which were found to have kernicterus. There was no significant difference in the mean maximum peak of erythrocyte bilirubin between the 2 groups (kernicterus group: 17.8 +/- 3.4 mumol/l in the 4 cases with kernicterus. Finally, hypoglycemia, respiratory and/or metabolic acidosis were found associated with the highest erythrocyte bilirubin level, or during the 24 preceding hours in children with kernicterus only.

Acidosis↗
PubMed1982

Blood pressure responses associated with hemorrhagic shock in anesthetized rats.

Blood pressure responses to noradrenaline were studied in anesthetised rats subjected to hypovolemia by a constant pressure--open reservoir technique. Hypovolemia resulted in a decrease of the noradrenaline response, which correlated well to the length of the hypovolemic period and to the arterial perfusion pressure when lower than 60 mmHg. Early after retransfusion of the shed blood the pressure response to noradrenaline continued to decrease and began to recover only after additional 30-60 min. The decline in blood pressure response to noradrenaline during hemorrhagic shock was not significantly altered by adrenalectomy, infusion of various metabolic substrates, such as fat emulsion, Na-pyruvate or ATP-MgCl2, or by protection against respiratory and metabolic acidosis. The results imply that high levels of circulating catecholamines, substrate exhaustion and acidosis may be regarded as secondary factors rather than primary causes of decreased blood pressure response and development of irreversible hemorrhagic shock, and they stress the importance of adequate tissue perfusion in the protection against these disorders.

Acidosis, Respiratory↗
PubMed1994

Effects of hypercarbic acidotic reperfusion on recovery of myocardial function after cardioplegic ischemia in neonatal lambs.

BACKGROUND: There is continued controversy over the management of pH during ischemia and reperfusion. Calcium overload is an integral feature of the injury resulting from ischemia and reperfusion, and hydrogen ions are known to blunt Ca2+ influx into cells because H+ inhibits the Na(+)-Ca2+ exchange and the slow calcium channels. Hypercarbia is one source of H+, but elevated CO2 level is also known to be a potent coronary vasodilator, which may be beneficial during early reperfusion. This study was designed to explore the effect of respiratory and metabolic acidosis during the initial phases of reperfusion after hypothermic cardioplegic ischemia in the neonatal lamb. METHODS AND RESULTS: Forty isolated, blood-perfused neonatal lamb hearts underwent 2 hours of cold cardioplegic ischemia followed by reperfusion with blood with various pH values. pH was controlled either by altering the FICO2 in the ventilating gas to the oxygenator (groups A through D) or by adding HCl to the reperfusate (group E). pH of the initial reperfusate was 6.8 in group A, 7.1 in group B, 7.5 in group C, and 7.8 in group D. In these groups, pH values were maintained for the initial 5 minutes of reperfusion and then corrected to 7.4 over 20 minutes by changing the FICO2 to the oxygenator. In group E, HCl was added to the reperfusate to give pH 6.8 (metabolic acidosis). pH was corrected after 5 minutes of reperfusion by administration of NaHCO3 and THAM over the next 15 minutes. At 30 and 60 minutes of reperfusion, left ventricular maximum developed pressure, dP/dt, -dP/dt, maximum developed pressure at V10 (volume that gave left ventricular end-diastolic pressure of 10 mm Hg during baseline measurements), and dP/dt at V10 were measured. Coronary blood flow and oxygen consumption (MVO2) were also measured to evaluate the metabolic recovery. Group A showed better functional recovery than groups B, C, or D (maximum dP/dt V10: group A, 88.3 +/- 7.7%; group B, 69.3 +/- 10.8%; group C, 74.6 +/- 10.3%; group D, 66.1 +/- 9.4%; and group E, 73.7 +/- 13.8% at 30 minutes [P < .05]; group A, 76.1 +/- 13.6%; group B, 61.9 +/- 8.6%; group C, 63.8 +/- 5.4%; group D, 57.9 +/- 9.4%; and group E, 62.6 +/- 12.7% at 60 minutes [P < .05]). Coronary blood flow was higher in group A than in other groups (A, 177.2 +/- 29.6%; B, 144.1 +/- 18.1%; C, 127.3 +/- 18.5%; D, 150.4 +/- 24.3%; and E, 106.0 +/- 20.0% [P < .05]). There were no significant differences in MVO2. CONCLUSIONS: These data indicate that hypercarbic reperfusion (pH 6.8) for a short period after ischemia improved functional recovery after cold cardioplegic ischemia in neonatal lamb hearts but that metabolic acidosis to an equivalent pH did not improve postischemic function. Possible mechanisms for this effect include reduction of calcium loading to the myocardium through H+ inhibition of calcium uptake or the induction of coronary vasodilation by hypercarbia.

Acidosis↗
PubMed2003

Management of acidosis during lung-protective ventilation in acute respiratory distress syndrome.

In ARDS, when acidosis complicates LPV, the goal of alkali therapy is to maintain arterial pH at a safe level (> or = 7.20). A pure respiratory acidosis generally does not require alkali therapy. If the Pplat is greater than 30 cm H2O, and the respiratory rate equals the upper limit (35-40 breaths/minute), then V(E) is slowly titrated down by approximately 1 L/hour, so that PaCO2 increases by 10 mm Hg/hour or less. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics. Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. Using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation. Under these circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. When renal failure is present, CRRT is indicated to manage acidosis. When ARDS is complicated by traumatic or hemorrhagic shock, overresuscitation with Cl(-)-rich solutions should be avoided to prevent metabolic acidosis.

Acidosis↗
PubMed1978

Lactic acidosis presenting as acute respiratory failure.

Two patients with chronic obstructive pulmonary disease and chronic respiratory failure who developed acute lactic acidosis are described. The initial arterial blood gas values in both patients had the pattern of acute respiratory failure with no metabolic disturbance. It was the calculation of the "anion gap" that provided the clue to the presence of metabolic acidosis, which was then confirmed with the measurement of serum lactate. We emphasize that complete laboratory data and clinical information may be essential for accurate diagnosis and understanding of mixed acid-base disturbances and, hence, for initiation of appropriate treatment.

Acidosis↗
PubMed2006

Mechanisms of CO2/H+ chemoreception by respiratory rhythm generator neurons in the medulla from newborn rats in vitro.

We investigated mechanisms of CO(2)/H(+) chemoreception in the respiratory centre of the medulla by measuring membrane potentials of pre-inspiratory neurons, which are putative respiratory rhythm generators, in the brainstem-spinal cord preparation of the neonatal rat. Neuronal response was tested by changing superfusate CO(2) concentration from 2% to 8% at constant HCO(3)(-) concentration (26 mm) or by changing pH from 7.8 to 7.2 by reducing HCO(3)(-) concentration at constant CO(2) (5%). Both respiratory and metabolic acidosis lead to depolarization of neurons with increased excitatory synaptic input and increased burst rate. Respiratory acidosis potentiated the amplitude of the neuronal drive potential. In the presence of tetrodotoxin (TTX), membrane depolarization persisted during respiratory and metabolic acidosis. However, the depolarization was smaller than that before application of TTX, which suggests that some neurons are intrinsically, and others synaptically, chemosensitive to CO(2)/H(+). Application of Ba(2+) blocked membrane depolarization by respiratory acidosis, whereas significant depolarization in response to metabolic acidosis still remained after application of Cd(2+) and Ba(2+). We concluded that the intrinsic responses to CO(2)/H(+)changes were mediated by potassium channels during respiratory acidosis, and that some other mechanisms operate during metabolic acidosis. In low-Ca(2+), high-Mg(2+) solution, an increased CO(2) concentration induced a membrane depolarization with a simultaneous increase of the burst rate. Pre-inspiratory neurons could adapt their baseline membrane potential to external CO(2)/H(+) changes by integration of these mechanisms to modulate their burst rates. Thus, pre-inspiratory neurons might play an important role in modulation of respiratory rhythm by central chemoreception in the brainstem-spinal cord preparation.

Acidosis↗