[Non-respiratory acidosis observed in infants and children during general anesthesia. I. Acid-base imbalance during induction of anesthesia].
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Acid-Base Imbalance↗
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Crdiovascular effects of lidocaine during acid-base imbalance.
Although lidocaine HCl is often given to critically ill patients with ventricular tachyarrhythmias, it use is not without hazard. To investigate whether acid-base disturbances and their subsequent effects on molecular ioization influence cardiovascular (CV) response to lidocaine, dogs in normal acid-base balance, metabolic acidosis, respiratory acidosis, and respiratory alkalosis were given 2 or 4 mg/kg lidocaine IV. Heart rate (HR), PR and QT intervals, MAP, LVEDP, LV dp/dt, and LV dp/dt divided by CPIP were measured at intervals. In all groups a slight increase in mean HR occurred after 2 mg/kg. Generally, myocardial contractile force was depressed in direct proportion to dose. Essentially, the CV response to lidocaine was not altered by any clinically remarkable degree by pH disturbances. Responses differing from those observed during normal acid-base conditions could not be significantly correlated with changes in pH or PaCO2. Results suggest that, in the intact animal, the CV effects of lidocaine, administered in therapeutic doses, are not appreciably influenced by clinically encountered states of acid-base imbalance.
Acid-Base Imbalance↗
The correction of acidosis with tris(hydroxymethyl) aminomethane. Treatment of metabolic acidosis mixed respiratory and metabolic acidosis with tris(hydroxymethyl) aminomethane.
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Acidosis↗
Fundamentals of clinical acid-base evaluation.
The final diagnosis of acid-base perturbations relies on laboratory analyses. The major direct tools of assessment are arterial pH and PCO2 and serum electrolytes. From these values, a diagnosis of metabolic acidosis, respiratory acidosis, metabolic alkalosis, and respiratory alkalosis with or without an excess anionic gap and with or without a proper compensatory response is made.
Acid-Base Imbalance↗
Acid-base balance in heart failure.
In end-stage heart failure, various acid-base disorders can be discovered due to the renal loss of hydrogen ions and hydrogen ion movements into cells, the reduction of the effective circulating volume, hypoxemia and renal failure. This justifies the occurrence of metabolic alkalosis, metabolic acidosis, respiratory alkalosis, as well as respiratory acidosis alone or in combination. Several studies have been published on the acid-base state in heart failure. In a 1951 study, Squires et al analyzed the distribution of body fluid in congestive heart failure by taking into consideration the abnormalities in serum electrolyte concentration and in acid-base equilibrium. A recent study by Milionis et al, analyzed 86 patients with congestive heart failure receiving conventional treatment; the majority of these patients exhibited hypokalemia, hyponatremia, hypocalcemia and hypophosphatemia. Disorders in acid-base balance were noted in 37.2% of patients. In a recent study, 70 patients with severe congestive heart failure before heart transplantation showed high-normal pH, slightly reduced pCO 2 and a slight loss of hydrogen ions. After heart transplantation, stability of blood pH and hydrogen ion concentrations was found. In contrast, bicarbonate and pCO 2 increased significantly. The data led us to formulate the diagnosis of a mixed acid-base disorder that includes respiratory alkalosis and metabolic alkalosis before heart transplantation. In heart failure, the presence of acid-base imbalance associated with the activation of mechanisms that lead to salt and water retention reveals evidence concerning the pivotal role of the kidney in determining the outcome of these patients.
Acid-Base Equilibrium↗
Enterococcus faecalis exacerbates burn injury-induced host responses in rats.
Pathophysiology of burn injury with complications of gram-positive infections is not well characterized. We have developed an in vivo rat model to study the effects of burn injury along with intra-abdominal inoculation of Enterococcus faecalis. We hypothesized that although burn injury or E. faecalis inoculation by itself may not induce significant pathophysiological responses, the combination of the two can lead to adverse pathophysiological consequences. Sprague-Dawley rats were divided into 4 groups: group 1(C), controls; group 2(B), burn injury on 30% total body surface area; group 3(EF), intra-abdominal implantation of bacterial pellet impregnated with E. faecalis; group 4(B+EF), burn injury plus bacterial pellet implantation. The mortality was 25% and 60% on day 1 and 2 in Group 4(B+EF), respectively; no significant mortality was observed in other groups. In group 4(B+EF), metabolic acidosis, respiratory alkalosis, and a hyperdynamic state developed on day 1, and metabolic and respiratory acidosis and a hypodynamic state on day 2. There were no significant alterations in metabolic or hemodynamic measurements in other groups. Intestinal microvascular permeability to albumin on day 1 and 2 was increased in group 4(B+EF). In group 2(B), microvascular permeability was not increased significantly. Although the permeability was increased on day 1 in group 3(EF), it declined on day 2. The metabolic and hemodynamic alterations were correlated with increased intestinal microvascular permeability to albumin. E. faecalis appeared to be involved in initiating a vicious cycle of burn injury-mediated disruption of intestinal integrity along with metabolic and hemodynamic derangements.
Albumins↗
Severe diaphragmatic necrosis in 4 horses with degenerative myopathy.
Severe diaphragmatic necrosis occurred in horses with degenerative myopathy due to polysaccharide storage myopathy (n = 2), nutritional myopathy (n = 1), and vasculitis (n = 1). Blood gas analysis performed in 1 horse indicated development of respiratory acidosis. Respiratory muscle necrosis can be severe in horses with degenerative myopathy and can lead to respiratory failure.
Animals↗
Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions.
To establish the overall frequency distribution and combination of acid-base and electrolyte disturbances as they occur in a general population requiring hospital care, we studied arterial blood gases and plasma electrolytes (sodium, potassium and chloride) in 110 consecutive patients (age = 68 +/- 8 SE; 64 M, 46 F) at the time of admission to a general medical ward. Disturbances were defined on the basis of the standard pH/pCO2 plot and the normal (mean +/- 2 SD) electrolyte range for our laboratory. Sixty-two patients (56%) showed a disturbance in acid base equilibrium: acidosis: respiratory 16, metabolic 6; alkalosis: respiratory 26, metabolic 10; in 4/62 the acid base disturbance was mixed. In 47 of the 62 patients, the acid base imbalance were associated with electrolyte derangements (low PNa+, 12; high PNa+, 1; low PK+, 10; high pK+, 7; increased anion gap, 17). Electrolyte disturbances with a normal acid base status were detected in only 2 patients. Of significance, in 7 of the 58 individuals considered to have a "pure" acid base disturbance on the basis of the pH/pCO2 plot (5 respiratory alkalosis; 1 respiratory acidosis; 1 metabolic alkalosis), a widened anion gap revealed that the acid-base change was mixed, i.e. there was a concomitant component of metabolic acidosis. Thus, the total number of mixed acid base equilibrium disorders were eleven. This study emphasizes the frequent incidence of acid base and electrolyte disorders, very often in combination, among unselected adult patients admitted to a general medical ward. In addition it reinforces that a high prevalence of hidden cases of mixed acid base disturbances can be recognized by concomitant analysis of acid base and electrolyte parameters, including anion gap calculation.
Acid-Base Imbalance↗
Response of protein synthesis to hypercapnia in rats: independent effects of acidosis and hypothermia.
Acute metabolic acidosis has been shown to inhibit muscle protein synthesis, although little is known on the effect of acidosis of respiratory origin. The aim of this study was to investigate the effect of acute respiratory acidosis on tissue protein synthesis. Rats (n = 8) were made acidotic by increasing the CO2 content of inspired air to 12% for 1 hour. Similar rats breathing normal air served as controls (n = 8). Muscle and liver protein synthesis rates were then measured with L-[ 2H5 ]phenylalanine (150 micromol per 100 g body weight, 40 mol%). The results show that protein synthesis is severely depressed in skeletal muscle (-44% in gastrocnemius, -39% in plantaris, and -24% in soleus muscles, P < .01) and liver (-20%, P < .001) in acidotic animals. However, because breathing CO2 -enriched air was found to lower body temperature by approximately 2 degrees C, in a second experiment (n = 10), the difference in body temperature between treated and control animals was minimized by gently wrapping rats breathing CO2 -enriched air in porous cloths. This second experiment confirmed that respiratory acidosis depresses protein synthesis in muscle (-22% in gastrocnemius, P < .001; -19% in plantaris, P < .01; and -4% in soleus, P = NS). However, no effect on liver protein synthesis could be detected, suggesting that liver protein synthesis may be sensitive to changes in body temperature but is not affected by acute respiratory acidosis for 1 hour. The results show that respiratory acidosis inhibits protein synthesis in skeletal muscle and indicates that acidosis, whether of metabolic or respiratory origin, may contribute to loss of muscle protein in patients with compromised renal or respiratory function.
Acidosis↗
Intestinal ion transport and intracellular pH during acute respiratory alkalosis and acidosis.
Acute respiratory alkalosis and acidosis alter rat ileal and colonic but not jejunal electrolyte transport. To examine the role of altered intracellular pH, pHi, and HCO3 concentration, (HCO3)i, we measured pHi in mucosa scraped from the jejunum, ileum, and colon of anesthetized, mechanically ventilated Sprague-Dawley rats. During states of respiratory alkalosis (Pco2 24.9 +/- 0.8 mmHg, pH 7.586 +/- 0.014), respiratory acidosis (Pco2 67.8 +/- 1.2 mmHg, pH 7.228 +/- 0.007), and normocapnia (Pco2 41.1 +/- 0.7 mmHg, pH 7.401 +/- 0.006), pHi was measured by determining the distribution of 5,5-dimethyl[2-14C]oxazolidine-2,4-dione, using [3H]inulin as a marker of extracellular space. (HCO3)i was calculated using portal vein Pco2. In the ileum, the pHi of 6.901 +/- 0.029 was similar in alkalosis [(HCO3)i 5.4 +/- 0.3 mM], acidosis [(HCO3)i 12.4 +/- 0.6 mM], and normocapnia [(HCO3)i 8.6 +/- 0.8 mM). In both the jejunum and colon, pHi was increased in alkalosis [pHi 6.998 +/- 0.038, (HCO3)i 6.7 +/- 0.6 mM] and decreased in acidosis [pHi 6.789 +/- 0.024, (HCO3)i 10.4 +/- 0.6 mM] as compared with normocapnia [pHi 6.915 +/- 0.026, (HCO3)i 8.9 +/- 0.7 mM] (colon data given). Net electrolyte transport measured by in vivo perfusion revealed that ileal and colonic, but not jejunal, net Na and Cl absorption was decreased during alkalosis and increased during acidosis. These data suggest that, during respiratory acidosis and alkalosis, pHi is maintained in a qualitatively similar way in the jejunum, ileum, and colon with quantitatively greater or lesser changes in (HCO3)i.(ABSTRACT TRUNCATED AT 250 WORDS)
Acidosis, Respiratory↗
The respiratory control system: analysis of steady state solutions for metabolic and respiratory acidosis-alkalosis and increased metabolism.
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Acidosis, Respiratory↗
Simple acid-base disorders.
The body regulates pH closely to maintain homeostasis. The pH of blood can be represented by the Henderson-Hasselbalch equation: pH = pK + log [HCO3-]/PCO2 Thus, pH is a function of the ratio between bicarbonate ion concentration [HCO3-] and carbon dioxide tension (PCO2). There are four simple acid base disorders: (1) Metabolic acidosis, (2) respiratory acidosis, (3) metabolic alkalosis, and (4) respiratory alkalosis. Metabolic acidosis is the most common disorder encountered in clinical practice. The respiratory contribution to a change in pH can be determined by measuring PCO2 and the metabolic component by measuring the base excess. Unless it is desirable to know the oxygenation status of a patient, venous blood samples will usually be sufficient. Metabolic acidosis can result from an increase of acid in the body or by excess loss of bicarbonate. Measurement of the "anion-gap" [(Na+ + K+) - (Cl- + HCO3-)], may help to diagnose the cause of the metabolic acidosis. Treatment of all acid-base disorders must be aimed at diagnosis and correction of the underlying disease process. Specific treatment may be required when changes in pH are severe (pH less than 7.2 or pH greater than 7.6). Treatment of severe metabolic acidosis requires the use of sodium bicarbonate, but blood pH and gases should be monitored closely to avoid an "overshoot" alkalosis. Changes in pH may be accompanied by alterations in plasma potassium concentrations, and it is recommended that plasma potassium be monitored closely during treatment of acid-base disturbances.
Acid-Base Equilibrium↗
Amine buffers in the management of acidosis. Study of respiratory and mixed acidosis.
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Acidosis↗
Interaction of acidosis and increased extracellular potassium on action potential characteristics and conduction in guinea pig ventricular muscle.
We studied the individual and combined effects of extracellular acidosis and increases in extracellular potassium on action potential characteristics and conduction in order to gain a better understanding of the effects of acute ischemia. At each level of potassium between 2.7 and 17 mm, acidosis induced by increasing Pco2 (respiratory acidosis) and by decreasing HCO3- (metabolic acidosis) decreased resting membrane potential, the maximum rate of rise of the action potential upstroke (Vmax), and slowed conduction. Metabolic acidosis consistently and significantly lengthened the steady state action potential duration whereas respiratory acidosis did not. Respiratory acidosis caused changes in resting membrane potential, Vmax, and conduction velocity; which occurred more rapidly and were of greater magnitude than the changes induced by metabolic acidosis. The changes in Vmax induced both types of acidosis were due to a change in the resting membrane potential-Vmax relationship as well as to the changes in the resting membrane potential. The conduction slowing induced by acidosis was greater when potassium was 9 and 13 mM than when potassium was 5.4 mm. Our results suggest that acidosis causes important changes in the electrophysiological properties of ventricular fibers and that many of the known electrophysiological effects of acute ischemia can be mimicked by the combined effects of extracellular acidosis and an increase in extracellular potassium.
Acidosis↗
Urinary inhibitor of the ammoniagenic response to acute acidosis is a prostaglandin.
Both acute respiratory acidosis and acute metabolic acidosis stimulate NH3 production by the isolated perfused rat kidney. This stimulatory effect is abolished if the urine is drained back into the recirculating perfusate rather than collected. To determine whether the urinary inhibitor is a cyclooxygenase product, studies were carried out using prostaglandin synthetase inhibitors. Kidneys perfused with 0.5 mmol/L glutamine and urine reinfusion were subjected to acute respiratory acidosis (30% CO2, pH 6.8). With either indomethacin (20 mumol/L) or meclofenamate (20 mumol/L) in the perfusate, NH3 production increased significantly in response to acute respiratory acidosis despite urine reinfusion. The increment in NH3 production was comparable to that in studies with urine collection, indicating that a cyclooxygenase product can account completely for the urinary inhibitor. To further characterize the urinary prostaglandin inhibitor, studies were performed with both the isolated perfused kidney and renal cortical tubules. Prostaglandin E2 (PGE2) did not exhibit an inhibitory effect on NH3 production with either experimental model. Prostaglandin F2 alpha at low doses inhibited NH3 production in response to acute acidosis by the isolated kidney, but an effect was not apparent with higher concentrations. PGF2 alpha inhibited the stimulatory effect of a low pH (7.1) on NH3 production by isolated tubules, and had no effect on ammoniagenesis at pH 7.4. Thus a prostaglandin, which is not PGE2 and may be PGF2 alpha, appears to be the previously unidentified urinary inhibitor of the ammoniagenic response to acute acidosis found with the isolated perfused kidney.
Acidosis, Respiratory↗
The effect of carbon dioxide on cerebral blood flow and cerebral metabolism in dogs.
In 11 normally oxygenated, normotensive mongrel dogs, blood flow and oxidative metabolism of the brain was studied during normocapnia and during respiratory alkalosis and respiratory acidosis. During respiratory alkalosis (mean PaCO2 17.8 mm Hg) CBF decreased significantly from 61.0 to 33.9 ml/100 g/min (44%) while arteriovenous-substrate differences increased and the rates of oxygen and glucose metabolism remained constant. Cerebral venous-arterial difference of lactate was increased significantly as compared with the resting state. During hypercapnia CBF increased significantly from 61.0 (resting state) to 115.7 ml/100 g/min (89%) (mean PaCO2 64.7 mm Hg). The arteriovenous-substrate differences decreased while the cerebral metabolic rates remained constant. The data show that the relationship between PaCO2 and CBF in the range 20-65 mm Hg PaCO2 is expressed by a linear relationship: y = 2.88 + 1.69x; in this range, the oxidative metabolism of the brain is unchanged and the increased cerebral lactate production in respiratory alkalosis is not necessarily linked to tissue hypoxia.
Acidosis, Respiratory↗
Respiratory acid-base disorders.
Both respiratory acidosis and respiratory alkalosis are most likely to occur in combination with some metabolic acid-base disturbance, particularly in the hospitalized patient. After a review of the pulmonary and renal cellular events involved in these complex electrolyte imbalances, principles of diagnosis and treatment are illustrated by means of clinically representative cases.
Acid-Base Imbalance↗
Electrolyte composition of cerebrospinal fluid in acute acid-base disorders.
Electrolyte composition of cisternal CSF was measured during 4 hours of respiratory and metabolic acid-base disturbance in anesthetized dogs. Three groups of dogs were studied: (1), isocapnic metabolic alkalosis; (2), acute respiratory acidosis; and (3), combined respiratory acidosis and metabolic alkalosis. Cisternal CSF [K+] remained unchanged despite significant changes in plasma [K+], PCO2 and [HCO3-]; suggesting that mechanisms involved in regulation of CSF [K+] continue to operate normally under such conditions. Cisternal [Na+] and osmolality remained unchanged with almost identical reciprocal equimolar changes in CSF concentration of Cl- and HCO3- during the acid-base disorders studied. The regulatory mechanisms involved in this Cl- -HCO3- exchange may be different in different acid-base disorders, but since CSF [Na+] is kept constant, CSF [HCO3-] in any acid-base disorder equals the difference between CSF [Na+] and CSF [Cl-].
Acid-Base Imbalance↗