Disturbances Of Acid-base Balance Research Articles

Supplementation with alkaline minerals reduces symptoms in patients with chronic low back pain

The cause of low back pain is heterogeneous, it has been hypothesised that a latent chronic acidosis might contribute to these symptoms. It was tested whether a supplementation with alkaline minerals would influence symptoms in patients with low back pain symptoms. In an open prospective study 82 patients with chronic low back pain received daily 30 g of a lactose based alkaline multimineral supplement (Basica®) over a period of 4 weeks in addition to their usual medication. Pain symptoms were quantified with the “Arhus low back pain rating scale” (ARS). Mean ARS dropped highly significant by 49% from 41 to 21 points after 4 weeks supplemention. In 76 out of 82 patients a reduction in ARS was achieved by the supplementation. Total blood buffering capacity was significantly increased from 77.69 ± 6.79 to 80.16 ± 5.24 mmol/L (mean ± SEM, n = 82, p < 0.001) and also blood pH rose from 7.456 ± 0.007 to 7.470 ± 0.007 (mean ± SEM, n = 75, p < 0.05). Only intracellular magnesium increased by 11% while other intracellular minerals were not significantly changed in sublingual tissue as measured with the EXA®-test. Plasma concentrations of potassium, calcium, iron, copper, and zinc were within the normal range and not significantly influenced by the supplementation. Plasma magnesium was slightly reduced after the supplemention (-3%, p < 0.05). The results show that a disturbed acid-base balance may contribute to the symptoms of low back pain. The simple and safe addition of an alkaline multimineral preparate was able to reduce the pain symptoms in these patients with chronic low back pain.

Direct modulation of basal and angiotensin II-stimulated aldosterone secretion by hydrogen ions.

Disturbances in acid-base balance in vivo are associated with changes in plasma aldosterone concentration, and in vitro changes in extracellular pH (pH(o)) influence the secretion of aldosterone by adrenocortical tissue or glomerulosa cells. There is considerable disparity, however, as to the direction of the effect. Furthermore, the mechanisms by which pH(o) independently affects aldosterone secretion or interacts with other secretagogues are not defined. Thus, bovine glomerulosa cells maintained in primary monolayer culture were used to examine the direct effects of pH(o) on cytosolic free calcium concentration ([Ca(2+)](i))( )and aldosterone secretion under basal and angiotensin II (AngII)-stimulated conditions. pH(o) was varied from 7.0 to 7.8 (corresponding inversely to changes in extracellular H(+) concentration from 16 nM to 100 nM). Whereas an elevation of pH(o) from 7.4 to 7.8 had no consistent effect, reductions of pH(o) from 7.4 to 7.2 or 7.0 caused proportionate increases in aldosterone secretion that were accompanied by increases in transmembrane Ca(2+) fluxes and [Ca(2+)](i). These effects were abolished by removal of extracellular Ca(2+). A decrease in pH(o) from 7.4 to 7.0 also enhanced AngII-stimulated aldosterone secretion. This effect was more pronounced at low concentrations of AngII and was manifested as an increase in the magnitude of the secretory response with no effect on potency. In contrast to its effect on AngII-stimulated aldosterone secretion, a reduction of pH(o) from 7.4 to 7.0 inhibited the Ca(2+) signal elicited by low concentrations (</=1x10(-10) M) of AngII, but did not affect the increase in [Ca(2+)](i) caused by a maximal concentration (1x10(-8) M) of AngII. These data suggest that pH(o) (i.e. H(+)) has multiple effects on aldosterone secretion. It independently increases aldosterone secretion through a mechanism involving Ca(2+) influx and an increase in [Ca(2+)](i). Also, it modulates the action of AngII by both decreasing the magnitude of the AngII-stimulated Ca(2+) signal and increasing the sensitivity of a more distal site to intracellular Ca(2+). The latter action appears to be a more important determinant in the effects of pH(o) on AngII-stimulated aldosterone secretion.

Fluid therapy for cats 2. Restoring fluid and electrolyte balance

FLUID therapy will be beneficial for any animal that has developed, or is at risk of developing, a disturbance in fluid, electrolyte or acid-base balance. In general terms, fluid therapy...

Increased Optic Nerve Head Blood Flow After 1 Week of Twice Daily Topical Brinzolamide Treatment in Dutch-Belted Rabbits

Objectives: Using a three-way crossover study design, we compared the effects of brinzolamide 2%, dorzolamide 2%, and placebo (vehicle) on microvascular optic nerve head (ONH) blood flow, intraocular pressure (IOP), blood pressure, heart rate, and acid-base balance in nine acepromazine-tranquilized Dutch-belted rabbits. Methods: Baseline measurements were taken before treatment and after drug-free washout periods of 7–14 days. Microvascular ONH blood flow was measured with a fundus camera-based laser Doppler flowmeter (LDF). Intraocular pressure was measured with a Tono-Pen XL. One drop of brinzolamide, dorzolamide, or vehicle was administered twice daily (9 a.m. and 5 p.m.) in right eyes only for 7 days. Experimental measurements were made 90 minutes after the 9 a.m. topical dose was administered on day 8. Results: ONH blood flow was significantly increased (P ≤ 0.05) in carbonic anhydrase inhibitor (CAI)-treated rabbits, as compared with vehicle-treated controls. The percent increase from baseline was 11.2 ± 1.8% in brinzolamide-treated animals and 8.4 ± 4.3% in dorzolamide-treated animals. Compared with controls, IOP in the brinzolamide- and dorzolamide-treated groups was significantly decreased (P ≤ 0.05). The changes in ONH blood flow and IOP were not significantly different between the CAI treatment groups. Small but significant changes in systemic blood gas tensions and pH were present in both CAI treatment groups, as compared with the vehicle group. Systemic blood pressure and heart rate were not significantly changed. Conclusions: Topical ocular CAI treatment for 1 week with either brinzolamide or dorzolamide significantly reduced IOP and significantly increased ONH blood flow in tranquilized Dutch-belted rabbits, while eliciting minimal systemic acid-base balance disturbances.

Acid-base and electrolyte abnormalities in patients with acute leukemia.

Disturbances of acid-base balance and electrolyte abnormalities are commonly seen in patients with acute leukemia. Our study aimed at illuminating the probable pathogenetic mechanisms responsible for these disturbances in patients with acute leukemia admitted to our hospital. We studied 66 patients (24 men and 44 women) aged between 17 and 87 years old on their admission and prior to any therapeutic intervention. Patients with diabetes mellitus, acute or chronic renal failure, hepatic failure, patients receiving drugs that influence acid-base status and electrolyte parameters during the last month, such as corticosteroids, cisplatin, diuretics, antacids, aminoglycosides, amphotericin, penicillin, and K(+), PO(4)(3-), or Mg(2+) supplements were excluded. Forty-one patients had at least one acid-base or electrolyte disturbance. There were no significant differences in the incidence of acid-base balance and electrolyte abnormalities between patients with acute myeloid leukemia (AML) and patients with acute lymphoblastic leukemia (ALL). The most frequent electrolyte abnormality was hypokalemia, observed in 41 patients (63%), namely in 34 patients with AML, and 7 with ALL; the main underlying pathophysiologic mechanism was inappropriate kaliuresis. Furthermore, hypokalemic patients more frequently experienced concurrent electrolyte disturbances (i.e., hyponatremia, hypocalcemia, hypophosphatemia, and hypomagnesemia), as well as various acid-base abnormalities compared to normokalemic patients. Hypokalemia in patients with acute leukemia may serve as an indicator of multiple concurrent, interrelated electrolyte disturbances, especially in patients with AML.

Intraoperative continuous hemofiltration for metabolic management in acute aortoiliac occlusion

Acute aortoiliac occlusion, or Leriche’s syndrome, carries a risk of the development of severe ischemia-reperfusion injury, characterized by electrolyte and acid-base balance disturbances. These injuries are often fatal, because of the rapid deterioration of multiple organ systems. We present a case in which we intraoperatively and postoperatively treated hyperkalemia and metabolic acidosis by high-volume, continuous, veno-venous hemofiltration, which is a recently developed form of continuous renal replacement therapy.

Osmoregulation and salinity effects on the expression and activity of Na+,K(+)-ATPase in the gills of European sea bass, Dicentrarchus labrax (L.).

The European sea bass, Dicentrarchus labrax, tolerates salinities ranging from freshwater (FW) to hypersaline conditions. In two experiments, we analysed changes in plasma ions, muscle water content (MWC), gill Na+,K(+)-ATPase activity, and alpha-subunit mRNA expression during the course of acclimation from 15 ppt salt water to FW or high salinity seawater (HSSW). In Experiment 1, fish (6.2 +/- 1.1 g) were acclimated from 15 ppt to either FW, 5, 15, 25, 50, or 60 ppt SW and sampled after 10 days. Gill Na+,K(+)-ATPase activity was stimulated in FW- and in 50 and 60 ppt SW-groups relative to the 15 ppt control group. In Experiment 2, subgroups of fish (89 +/- 7 g) were transferred from 15 ppt SW to FW or 50 ppt SW, and sampled 1, 2, 4, and 10 days later. Plasma osmolality, [Na+] and [Cl-] decreased in the FW-group and increased in the HSSW-group one day after transfer and lasting until day 10. This was accompanied by a pronounced increase in MWC in the FW-group and an insignificant decrease in the HSSW-group. The plasma [Na+]:[Cl-]-ratio increased markedly in the FW-group and decreased slightly in the HSSW-group, suggesting acid-base balance disturbances after transfer. Gill Na+,K(+)-ATPase activity was unchanged in 15 ppt SW but doubled in FW- and HSSW-groups after transfer. In both groups, this was preceded by a 2- to 5-fold elevation of the gill alpha-subunit Na+,K(+)-ATPase mRNA level. Thus increased expression of alpha-subunit mRNA is part of the molecular mechanism of both FW and SW acclimation in sea bass. Gill Na+,K(+)-ATPase Na(+)-, K(+)-, and ouabain-affinity were similar in fish acclimated to FW, 15 ppt, and HSSW, suggesting that identical isoforms of the catalytic subunit of the enzyme are expressed irrespective of salinity.

Vascular resistance and the efficacy of red cell substitutes in a rat hemorrhage model.

We have compared polyethylene glycol-modified bovine hemoglobin (PEG-Hb; high O2 affinity, high viscosity, high oncotic pressure) and human hemoglobin cross-linked between the alpha-chains (alpha alpha-Hb; low O2 affinity, low viscosity, low oncotic pressure) with a non-O2-carrying plasma expander (pentastarch, high viscosity and oncotic pressure) after a 50% (by volume) exchange transfusion followed by a severe (60% of blood volume) hemorrhage. Mean arterial pressure and systemic vascular resistance rose significantly in the alpha alpha-Hb but not in the PEG-Hb animals. Two-hour survival was greater in the PEG-Hb animals (93%) than in control (35%), pentastarch (8%), or alpha alpha-Hb (6%) animals. In the PEG-Hb animals, there was no disturbance of acid-base balance, significantly less accumulation of lactic acid, and higher cardiac output than in the other groups. The data suggest that the rise in vascular resistance that follows alpha alpha-Hb exchange transfusion offsets the additional O2 transport provided by the cell-free hemoglobin. When resistance does not rise, as with PEG-Hb, even relatively small amounts of cell-free hemoglobin appear to be a very effective blood replacement.

Evaluating Toxic Alcohol Poisoning in the Emergency Setting

Ingestion of a toxic alcohol often occurs when an alcoholic patient cannot obtain ethanol and thus, seeks an ethanol substitute. Methanol produces visual disturbances, while ethylene glycol produces pulmonary and renal disturbances. Ingestion of isopropanol results in acetone production that can lead to central nervous system depression. Unlike methanol and ethylene glycol poisoning, however, isopropanol poisoning generally does not produce major disturbances in acid-base balance. Most clinical laboratories do not perform toxic alcohol analyses. Thus, the clinician relies on interpretation of other clinical laboratory data to ascertain the presence or absence of a toxic alcohol.

Potassium homoeostasis in the elderly.

The mechanisms which are involved in potassium potassium excretion by enhancing potassium homeostasis maintain the serum level within the secretion. relatively narrow normal range of 3.5–5.0 mEq/l Increased renal delivery of sodium5 and water6 to despite widely varying dietary intake and relatively the distal tubule may enhance renal potassium excrehuge intracellular potassium stores (98% of total tion, e.g. following loop diuretics,7 but the physiobody potassium). Abnormalities in renal excretion logical importance of this is uncertain. Conversely, and/or interference with the physiological control of decreased delivery of sodium chloride to the distal intracellular to extracellular potassium gradient may tubule during periods of avid sodium retention upset this fine balance, resulting in abnormalities in hinders potassium secretion, e.g. prerenal azotemia serum potassium.1,2 A complex interaction of renal or severe congestive heart failure.8 Arginine vasopresand extrarenal mechanisms are involved in mainsin secretion also significantly influences potassium taining this balance. Physiological changes associexcretion.9 ated with increasing age would tend to predispose Systemic acidosis and alkalosis exert a powerful the elderly to hyperkalaemia. However, potassium impact on renal potassium balance.10 During homeostasis in the elderly has not been well studied periods of systemic acidosis, hydrogen ion is to date. buffered intracellularly, with a resultant shift of In this commentary, renal and extrarenal potaspotassium from the intracellular to the extracellular sium homeostasis are summarized. Age-related fluid to maintain electrical neutrality. Thus, the alterations in these mechanisms are highlighted, and potassium concentration within the distal tubular the possible clinical implications of such changes cells falls, as does the concentration gradient are discussed. towards the tubular lumen, which culminates in a reduction in potassium secretion. Conversely, a shift of potassium into distal renal tubular cells in systemic alkalosis enhances renal tubular secretion, Renal mechanisms which contributes to an increase in potassium excretion. The above effects are however modified The renal tubules can normally adapt to wide fluctuby the duration of disturbance of acid-base balance, ations in potassium intake. The renal excretory e.g. prolonged acidosis alters fluid delivery, and this capacity for potassium is not exceeded by a dietary complicates the above picture. intake of 6 mEq/kg/day.3 The distal convoluted tubule The late distal convoluted tubule and cortical and collecting ducts constitute the sites which control collecting duct contain intercalated and principal renal potassium excretion (Figure 1). Dietary potascells which serve distinct transport functions.11 The sium loading results in both direct4 and indirect (via a and b subtypes of intercalated cells secrete hydroincreased aldosterone secretion3) stimulation of Na+K+ ATPase. This results in a prolonged increase in gen and bicarbonate ions into the lumen, respect-

Neuromuscular transmission and its pharmacological blockade. Part 2: Pharmacology of neuromuscular blocking agents.

Clinically, neuromuscular blockade is induced with either depolarizing or non-depolarizing relaxants. Suxamethonium is the only depolarizing relaxant still in use. It is hydrolysed in the plasma by pseudo-cholinesterase (plasma cholinesterase). In some patients and in particular diseases the plasma cholinesterase activity is low and hence the effect of suxamethonium prolonged. Suxamethonium is characterized by side-effects such as myalgia, fasciculations and increase in intraocular, intracranial and intragastric pressure. More serious adverse reactions are masseter muscle spasm and potassium release, in patients with some neuromuscular diseases and increase in extrajunctional acetylcholine receptors. As non-depolarizing muscle relaxants benzylisoquinolines and steroidal compounds are mainly used. Each relaxant has its own pharmacological characteristics. The effect of most relaxants depends on liver and renal function because the pharmacokinetic behaviour is strongly dependent on these organs. Also, acid base balance disturbances, change in temperature, and neurological diseases have an effect on the profile of the relaxants. A number of drugs (anaesthetics, antibiotics, antiepileptics, etc.) have an effect on neuromuscular transmission, and thus interact with the relaxants. Some non-depolarizing relaxants cause histamine release and cardiovascular effects.

Regulation of the insulin-like growth factor system by acute acidosis.

Many catabolic conditions are characterized by disturbances in acid-base balance and concomitant alterations in the insulin-like growth factor (IGF) system. However, the influence of acidosis per se on the various components of the IGF system has not been extensively examined. The purpose of the present study was to determine the effect of acute metabolic acidosis on the plasma and tissue concentrations of IGF-I and the various IGF-binding proteins (IGFBPs). Conscious unrestrained fasted rats were infused iv with either 0.2 N HCl or an equal volume of saline for 4 h. The arterial blood pH decreased within 60 min after starting the HCl infusion and remained lower than time-matched control values for the entire experimental protocol. Although the plasma IGF-I concentration fell gradually and was reduced by 30%, compared to time-matched control values, GH levels were unaltered. The IGF-I content of tissues collected at the conclusion of the experiment was increased in liver (35%) and kidney (63%), and unchanged in skeletal muscle. However, whereas acidosis moderately increased IGF-I messenger RNA abundance in liver, no significant alteration in IGF-I expression was detected in kidney. Acidosis also increased the plasma levels of IGFBP-1 and -2 as well as the IGFBP-1 content of liver and kidney. In contrast, the concentration of intact IGFBP-3 was decreased in acid-infused rats, and this reduction was associated with an increased rate of IGFBP-3 protease activity. Acidotic rats demonstrated unremarkable changes in the plasma concentrations of glucose and insulin, but corticosterone levels were elevated throughout the experiment. The results of the present study demonstrate that in the absence of underlying pathology, acute metabolic acidosis decreases circulating levels of IGF-I, probably by increasing renal clearance of the peptide, not by decreasing hepatic IGF-I synthesis.

Complications of laxative abuse.

Laxative abuse is an uncommon but clinically important cause of chronic diarrhea, a condition often associated with other gastrointestinal symptoms, as well as with disturbances in electrolyte and acid-base balance. A high index of suspicion, a detailed history, and the detection of laxative in stool and/or urine will establish the diagnosis once routine laboratory, endoscopic, and radiologic investigations have excluded common causes of chronic diarrhea. Confirmation of the diagnosis may rule out the need for more extensive, invasive, and costly investigations. However, management is frequently difficult owing to the laxative abuser's complex underlying psychopathology.

Cyclic Decrease in Mixed Venous Oxygen Saturation for the Early Diagnosis of Seizure Complications After Cardiac Surgery

Cyclic Decrease in Mixed Venous Oxygen Saturation for the Early Diagnosis of Seizure Complications After Cardiac Surgery

Need for advanced cardiac life-support training in rural, community hospitals

To define the relative needs of the staffs of rural, community hospitals for training in advanced cardiac life support (ACLS), identify weaknesses, and modify a standard ACLS course to meet these needs. Prospective assessment of knowledge and skills relating to the practice of ACLS. Rural, community hospitals in southern Wisconsin. None. A well-validated, multiple-option, precourse test for life-support knowledge and clinical judgment was administered to the staff nurses, respiratory therapists, and practicing physicians of 12 rural, community hospitals in southern Wisconsin before their participation in a modified, extended, ACLS course, using the pre-1992 American Heart Association standards and guidelines. Testing was accomplished over 4 yrs. Detailed item analysis of the test was performed. A total of 461 persons participated. Overall, physicians performed better (p < .001) than did the nurses. Precourse difficulties included electrocardiographic rhythm strip interpretation, particularly with identification of the atrioventricular (A-V) blocks. Only 39.6% of the nurses and 64.1% of the physicians correctly identified third-degree A-V block. One third of the nurses and 22% of the physicians did not correctly identify coarse ventricular fibrillation. The pharmacologic properties and utility of atropine and epinephrine were not understood. Propranolol was selected for treatment of third-degree A-V block by 31.6% and 22.8% of the nurses and the physicians, respectively. Neither group was able to accurately distinguish between the components of disturbances in acid-base balance. The esophageal obturator airway tube was not a familiar tool to any of the groups. No improvement in overall performance on pretests occurred across the calendar years of the study. There is a need for ACLS training in community hospitals. Educational programs for physicians and staffs should be designed to meet that need.

Effect of advanced cardiac life-support training in rural, community hospitals

To define the effectiveness of training personnel in rural, community hospitals in advanced cardiac life support (ACLS) and the changes that result in the process and quality of care to patients with ischemic heart disease that can be attributed to participation by team members in an ACLS course. Case-controlled, retrospective abstraction of hospital records of 869 consecutive patients with ischemic heart disease, who were admitted during the year preceding and the year following the ACLS course. Seven rural, community hospitals in Wisconsin. Physicians, nurses, and other critical care staff (others). Training in ACLS using 12 3-hr sessions in an interdisciplinary format by a multidisciplinary faculty. Rates of successful attainment of the terminal behavior objectives by physicians and nurses were 84.0% and 78.8%, respectively. Less than 50% of others achieved a satisfactory level of competence. Performance on an examination of cognitive ability improved significantly for all groups (p < .005 for nurses; p < .05 for physicians). Enhancement of knowledge base and integrative skills occurred in all areas of designated ACLS content. Difficulty remained apparent relative to the pharmacologic effects of epinephrine and atropine. No statistically significant deterioration in didactic knowledge base could be detected 1 to 2 yrs after completion of the ACLS course. Slight deterioration in intubation and defibrillation skills occurred in < 3 months after completion of the course. Substantial costs were encumbered by the hospitals, despite the free training provided to the institutions. After ACLS training had been given, overall mortality rates decreased from 17.4% to 13.4% (p < .05). A pooled estimate of the decrease in the mortality rate was 1.4 +/- 3.8%/quarter. Across the entire spectrum of severity of illness, the probabilities for survival increased at a given severity of illness following completion of the course (p = .06). When extremes of severity of illness were excluded from the analysis, the differences in probability for survival over the midrange of severity were statistically significant (p < .05). Training directed to the entire team likely to participate in the provision of ACLS in the community hospital favorably affects the overall practice of ACLS and the survival rate of patients with ischemic heart disease.

Effects of heat stress on Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of broiler chickens vital organs.

Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of brain, heart, kidney, and small and large intestinal mucosa of broiler chickens exposed to heat stress (41 degrees C, 65% relative humidity for 6 h) and thermoneutral (25 degrees C, 65% relative humidity) conditions were determined. Brain and kidneys were found to have significantly higher Na+,K(+)-ATPase activities than those of heart and intestinal mucosa. Mg(2+)-activated ATPase and Na(+)-ATPase activities in the intestinal mucosa were higher than those of brain, kidneys, and heart under thermoneutral conditions. While there was a significant inhibition of total ATPase, Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activity of small and large intestinal mucosa of broiler chickens exposed to heat stress, the inhibitory effect was limited to total ATPase and Na+,K(+)-ATPase enzymes in kidneys. Heat stress produced a significant increase only in Mg(2+)-activated ATPase activity of the heart, without a remarkable change in all forms of ATPase activity in the brain. Heat stress significantly decreased the ratio of Na+,K(+)-ATPase to Mg(2+)-ATPase in the heart, kidneys, and small and large intestinal mucosa. The percentage of Na(+)-ATPase in Na+,K(+)-ATPase of brain, heart, and kidneys did not significantly change during heat stress, but the ratio in small and large intestinal mucosa increased significantly during heat stress. The severe disturbances in both serum electrolytes and acid-base balance observed in previous heat stress studies could partly be mediated by direct or indirect effects of heat stress on Na+,K(+)-ATPase, Mg(2+)-activated ATPase, and Na(+)-ATPase activities of kidneys, and small and large intestinal mucosa of broiler chickens.

Preparation of the intensive care patient for major surgery.

Improved methods for monitoring and treating critically ill patients have increased the number of surgical candidates with multiorgan system impairment. Whereas such patients may have been considered "too sick to undergo surgery" in the past, many such patients linger in the intensive care unit unless definitive therapy is accomplished. Specific attention to review of the patient's preoperative preparation for surgery on a system-by-system basis may improve outcome substantially. The need for possible mechanical ventilation prior to transport to the operating room must receive particular attention. Pneumothorax, if present, must be treated prior to institution of positive-pressure ventilation so progression to tension pneumothorax can be avoided. Deficits in the circulating blood volume must be identified and corrected preoperatively if possible. A need for enhancement of cardiac output or alteration of vascular tone requires pulmonary arterial catheterization and indicates an increased operative risk. Metabolic abnormalities such as disturbances of acid-base balance, sodium or potassium concentration, and endocrinopathies are identified and corrected as much as possible prior to operation. Antibiotics are instituted as appropriate. Replacement of the red blood cell mass is dictated primarily by anticipated or actual blood loss. Factors of coagulation are infused on a replacement basis as necessary. Great care must be taken during transport to the operating room, as maintenance of intravascular monitoring devices, therapeutic infusions, and mechanical ventilation must continue during transport. Precautions must be taken to avoid hypothermia during transport and institution of anesthesia. Critical illness mandates specific considerations of the anesthetic agents to be utilized.

Acid-Base Balance Disturbances Following Toxic Doses of Local Anesthetics

The effect of equitoxic doses of three carbamate local anesthetics (pentacaine, carbisocaine and heptacaine), and a derivative of lidocaine (trimecaine) on the acid-base balance of blood was studied in conscious rabbits. In addition, changes in arterial blood pH induced by local anesthetics in relation to lipophilicity of the respective drugs were evaluated. All the drugs administered at the dose of half of LD50 induced a significant decrease in the arterial blood pH as well as in the plasma bicarbonate level and in the blood base excess. The observed acidosis was compensated within a 60 minute period by hyperventilation. The local anesthetic-induced decrease in the blood pH, expressed as AUC, correlated to some extent with the partition coefficient of these agents. These findings suggest that the acidifying effect of local anesthetics may be dependent on their lipophilicity.

Diuretics, Hypochloremia, and Outcome in Bronchopulmonary Dysplasia Patients

We evaluated retrospectively the outcome of patients with severe bronchopulmonary dysplasia who required hospitalization (greater than 90 days) to determine the role of diuretics aminophylline and chloride deficiency in the fatal outcome of these patients. Total cumulative amounts of furosemide, chlorothiazide, spironolactone accrued during hospitalization (dosage per patient per day), and a diuretic index (logarithm of the sum of the cumulative dosage of the three diuretics) were calculated for each patient. Other predetermined variables included in the analysis were birth weight, gestational age, duration of mechanical ventilation, duration of oxygen therapy, caloric intake, fluid and electrolyte intake, echocardiographic data, and duration and type of acid base balance disturbances. No differences were found between survivors and nonsurvivors in diuretic and aminophylline use. Hypochloremia did not discriminate between the groups. Duration of mechanical ventilation, the ratio between days with serum bicarbonate concentration greater than 30 mEq/l and total days of hospitalization, and the difference between head circumference at discharge or death and birth head circumferences were the most important factors which contribute to the difference between survivors and non survivors.