The mixed acid-base disturbances of severe canine babesiosis

Thirty-four dogs suffering from severe babesiosis caused by Babesia canis rossi were included in this study to evaluate acid-base imbalances with the quantitative clinical approach proposed by Stewart. All but 3 dogs were severely anemic (hematocrit <12%). Arterial pH varied from severe acidemia to alkalemia. Most animals (31 of 34; 91%) had inappropriate hypocapnia with the partial pressure of CO2 < 10 mm Hg in 12 of 34 dogs (35%). All dogs had a negative base excess (BE; mean of - 16.5 mEq/L) and it was below the lower normal limit in 25. Hypoxemia was present in 3 dogs. Most dogs (28 of 34; 82%) were hyperlactatemic. Seventy percent of dogs (23 of 33) were hypoalbuminemic. Anion gap (AG) was widely distributed, being high in 15, low in 12, and normal in 6 of the 33 dogs. The strong ion difference (SID; difference between the sodium and chloride concentrations) was low in 20 of 33 dogs, chiefly because of hyperchloremia. Dilutional acidosis was present in 23 of 34 dogs. Hypoalbuminemic alkalosis was present in all dogs. Increase in unmeasured strong anions resulted in a negative BE in all dogs. Concurrent metabolic acidosis and respiratory alkalosis was identified in 31 of 34 dogs. A high AG metabolic acidosis was present in 15 of 33 dogs. The lack of an AG increase in the remaining dogs was attributed to concurrent hypoalbuminemia, which is common in this disease. Significant contributors to BE were the SID, free water abnormalities, and AG (all with P < .01). Mixed metabolic and respiratory acid-base imbalances are common in severe canine babesiosis, and resemble imbalances described in canine endotoxemia and human malaria.     

Chloride Ion in Small Animal Practice: The Forgotten Ion

The Physiology of chioride ion and its relationship to clinical disorders in small animall practice is reviewed. Chioride is the major anion in the extracellular fluid and is important in the metabolic regulation of acid-base balance. A new clinical approach is used to assess chloride ion changes after accounting for changes in free water. Using this approach chloride disorders can be divided into corrected and artifactual. Changes in free water are solely responsible for the chioride ion changes in artifactual disorders, whereas in corrected chloride disorders, chloride ion itself changes. Corrected hypochioremia is associated with increases in the strong ion differece (SID) and metabolic alkalosis and is caused by administration of solution containing a high concentration of sodium relative to chioride (e.g., Sodium bicarbonate) or the excessive loss chioride relative to sodium (e.g., vomiting of stomach contents). Administration of chioride is correction of hypochioremic metabolic alkalosis. Corrected hyperchioremia is associated with a decreased SID and metabolic acidosis and is usually the result of excessive loss of sodium relative to chloride (e.g., diarrhea), chioride retention (e.g., renal tubular acidosis), or therapy with solutions containing a high concentration of chioride relative to sodium (e.g.,0.9% sodium chloride;3–24% hypertonic saline). Treatment with sodium bicarbonate should be attempted in patients with corrected hyperchioremia and a plasma pH beiow 7.2.     

Serum ionized calcium in dogs with chronic renal failure and metabolic acidosis

BACKGROUND: Chronic renal failure (CRF) is a common disease in dogs, and many metabolic disorders can be observed, including metabolic acidosis and calcium and phosphorus disturbances. Acidosis may change the ionized calcium (i-Ca) fraction, usually increasing its concentration. OBJECTIVE: In this study we evaluated the influence of acidosis on the serum concentration of i-Ca in dogs with CRF and metabolic acidosis. METHODS: Dogs were studied in 2 groups: group I (control group = 40 clinically normal dogs) and group II (25 dogs with CRF and metabolic acidosis). Serum i-Ca was measured by an ion-selective electrode method; other biochemical analytes were measured using routine methods. RESULTS: The i-Ca concentration was significantly lower in dogs in group II than in group I; 56% of the dogs in group II were hypocalcemic. Hypocalcemia was observed in only 8% of dogs in group II when based on total calcium (t-Ca) concentration. No correlation between pH and i-Ca concentration was observed. A slight but significant correlation was detected between i-Ca and serum phosphorus concentration (r = -.284; P = .022), as well as between serum t-Ca and i-Ca concentration (r = .497; P < .0001). CONCLUSION: The i-Ca concentration in dogs with CRF and metabolic acidosis varied widely from that of t-Ca, showing the importance of determining the biologically active form of calcium. Metabolic acidosis did not influence the increase in i-Ca concentration, so other factors besides acidosis in CRF might alter the i-Ca fraction, such as hyperphosphatemia and other compounds that may form complexes with calcium.     

Clinical signs, diagnosis, and treatment of alkalemia in dogs: 20 cases (1982-1984)

Alkalemia (pH greater than 7.50) was measured in 20 dogs admitted over a 3-year period for various clinical disorders. Alkalemia was detected in only 2.08% of all dogs in which blood pH and blood-gas estimations were made. Thirteen dogs had metabolic alkalosis (HCO3- greater than 24 mEq/L, PCO2 greater than 30 mm of Hg), of which 8 had uncompensated metabolic alkalosis, and of which 5 had partially compensated metabolic alkalosis. Seven dogs had respiratory alkalosis (PCO2 less than 30 mm of Hg, HCO3- less than 24 mEq/L); 4 of these had uncompensated respiratory alkalosis and 3 had partially compensated respiratory alkalosis. Ten dogs had double or triple acid-base abnormalities. Dogs with metabolic alkalosis had a preponderance of clinical signs associated with gastrointestinal disorders (10 dogs). Overzealous administration of sodium bicarbonate or diuretics, in addition to anorexia, polyuria, or hyperbilirubinemia may have contributed to metabolic alkalosis in 8 of the dogs. Most of the dogs in this group had low serum K+ and Cl- values. Two dogs with metabolic alkalosis had PCO2 values greater than 60 mm of Hg, and 1 of these had arterial hypoxemia (PaO2 less than 80 mm of Hg). Treatments included replacement of fluid and electrolytes (Na+, K+, and Cl-), and surgery as indicated (8 dogs). Six dogs with respiratory alkalosis had a variety of airway, pulmonary, or cardiac disorders, and 3 of these had arterial hypoxemia. Two other dogs were excessively ventilated during surgery, and 1 dog had apparent postoperative pain that may have contributed to the respiratory alkalosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Physiologic responses in healthy Labrador Retrievers during field trial training and competition

Ten healthy Labrador Retrievers (4 females and 6 males aged 3-6.5 years [mean, 4.5 years]) training with a professional trainer were studied. The dogs were in training during the entire study. Dogs were monitored within 5 minutes after retrieving birds on land and in water on 2 consecutive days during training and on 2 consecutive days at the Atlanta Retriever Club Fall Field Trial. Baseline samples were taken in the morning on a separate day before the dogs were loaded onto a truck. Venous samples were analyzed with a portable blood analyzer. Measurements included hematocrit, sodium, potassium, chloride, blood urea nitrogen (BUN), glucose, lactate, blood pH, Pco2, Po2, HCO3, and TCO2 plus rectal temperature, pulse rate, and respiratory rate. Ambient temperatures were recorded. Distances and times were estimated. Compared to baseline, significant increases occurred in rectal temperature, pulse rate, respiratory rate, chloride, lactate, and pH postexercise (P < .05): sodium, potassium, BUN, Pco2, and TCO2 were significantly decreased postexercise. Blood pH was markedly higher after retrieves on land than after retrieves in water. Estimated mean speeds were 11.4 mph (18.3 km/h) during a triple retrieve on land and 5.6 mph (9.0 km/h) during a retrieve in water. Maximal ambient temperatures were 84-86 degrees F (29-30 degrees C). In summary, Labrador Retrievers training with a professional trainer had evidence of hyperthermia, respiratory alkalosis, hypocapnia, and mild metabolic acidosis monitored within 5 minutes postexercise during training and field trial competition when maximal ambient temperatures were 85 degrees F (29 degrees C). The results provide a baseline against which physiologic responses of dogs with poor performance can be compared.     

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.     

Some physiological and biochemical effects of the intravenous administration of five different electrolyte solutions in the dog

Some physiological effects of the intravenous administration of five different commercial electrolyte solutions were studied in healthy conscious dogs. Measurements were taken before, during and up to 3 h after fluid administration. The measurements included temperature, heart rate, respiratory rate, systolic and diastolic arterial pressure, central venous pressure, pO₂, pCO₂, pH, packed cell volume, haemoglobin, total plasma protein, sodium, potassium, chloride, bicarbonate, base excess and creatinine. There were no significant changes in temperature, respiratory rate, systolic pressure, pO₂ or pCO₂. All dogs showed a similar rise in central venous pressure and a fall in packed cell volume, haemoglobin and total plasma protein in response to the fluid administration. Two saline solutions produced a metabolic acidosis, a fall in plasma potassium values and a rise in chloride. Administration of multi-electrolyte solutions resulted in the least disturbance in acid-base and electrolyte balance.     

Bread dough toxicosis in dogs

Objective: To provide information on the ingestion, and subsequent toxicity, of raw bread dough in dogs. Case summary: A report from the ASPCA animal poison control center (APCC) files of 3 cases of ingestion of raw bread dough by dogs. Clinical signs included vomiting, ataxia, blindness, hypothermia, and recumbency. All dogs were successfully treated for ethanol toxicosis. New information: Ingestion of bread dough can cause gastric obstruction, bloat, or ethanol toxicosis. The treatment of ethanol toxicosis, including decontamination, IV fluids, management of metabolic acidosis, and hypoglycemia is discussed. Yohimbine can be used in cases where the dog is comatose or has developed severe respiratory depression.     

Pyometra in the dog--a pathophysiological investigation. VI: Acid-base status and serum electrolytes

Arterial pH, oxygen and carbon dioxide tensions, and standard bicarbonate, as well as serum electrolytes (Na, Cl, K, inorganic P, Ca and anion gap) have been investigated in bitches with pyometra. A respiratory alkalosis was a common finding in the patients, and a smaller group showed a metabolic acidosis of mixed origin superimposed on the respiratory alkalosis. In this group 4 out of 9 patients died. In addition, the patients showed moderate electrolyte disturbances indicating a "sick cell syndrome" and a mild to severe renal dysfunction.     

Renal tubular acidosis in horses (1980-1999)

Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.     

Left displacement of the abomasum in a reticulated giraffe bull in managed care

A 10-y-old giraffe (Giraffa camelopardalis reticulata) bull developed colic after a 3-mo history of reduced feed consumption. Physical examination and management were performed with 2 standing sedations. The giraffe developed metabolic alkalosis and progressive pre-renal azotemia followed by compensatory respiratory acidosis and paradoxical aciduria. A metallic “ping” sound was auscultated on the left side near ribs 10–12. The giraffe was euthanized given the grave prognosis, and postmortem examination confirmed left displacement of the abomasum (LDA) with fluid sequestration (150–190 L [40–50 gal]) within the rumen. Dental disease was evident at postmortem examination and perimortem skull computed tomography. To ensure cases of LDA are not overlooked, the position of the abomasum must be noted during postmortem examination prior to removal of the gastrointestinal tract. The risk factors for the development of LDA in giraffes are not known, and associations such as those of dairy cattle (hypocalcemia, high-concentrate low-fiber diet, and indoor housing) remain to be elucidated.     

Contemporary approach to acid-base balance and its disorders in dogs and cats

The issue of the acid-base balance (ABB) parameters and their disorders in pets is rarely raised and analysed, though it affects almost 30% of veterinary clinics patients. Traditionally, ABB is described by the Henderson-Hasselbach equation, where blood pH is the resultant of HCO3- and pCO2 concentrations. Changes in blood pH caused by an original increase or decrease in pCO2 are called respiratory acidosis or alkalosis, respectively. Metabolic acidosis or alkalosis are characterized by an original increase or decrease in HCO3- concentration in the blood. When comparing concentration of main cations with this of main anions in the blood serum, the apparent absence of anions, i.e., anion gap (AG), is observed. The AG value is used in the diagnostics of metabolic acidosis. In 1980s Stewart noted, that the analysis of: pCO2, difference between concentrations of strong cations and anions in serum (SID) and total concentration of nonvolatile weak acids (Atot), provides a reliable insight into the body ABB. The Stewart model analyses relationships between pH change and movement of ions across membranes. Six basic types of ABB disorders are distinguished. Respiratory acidosis and alkalosis, strong ion acidosis, strong ion alkalosis, nonvolatile buffer ion acidosis and nonvolatile buffer ion alkalosis. The Stewart model provides the concept of strong ions gap (SIG), which is an apparent difference between concentrations of all strong cations and all strong anions. Its diagnostic value is greater than AG, because it includes concentration of albumin and phosphate. The therapy of ABB disorders consists, first of all, of diagnosis and treatment of the main disease. However, it is sometimes necessary to administer sodium bicarbonate (NaHCO3) or tromethamine (THAM).     

A case‐based review of a simplified quantitative approach to acid‐base analysis

Objective – To present a simplified quantitative approach to acid‐base analysis and to demonstrate its clinical utility. Data Sources – Original research articles and textbooks. Data Synthesis – A simplified quantitative approach to acid‐base analysis is presented, which is derived from the Fencl‐Stewart approach and calculates the magnitude of the effect on the standardized base excess (SBE) of 5 separate variables: (1) a free water effect (marked by sodium concentration), (2) an effect marked by the chloride concentration, (3) an albumin effect, (4) a lactate effect, and (5) a phosphate effect. Six clinical cases with acid‐base abnormalities are presented in which the quantitative approach provides information that is not apparent from the traditional approach. Conclusion – This simplified quantitative approach provides a comprehensive evaluation of complex acid‐base disorders, identifies individual processes and their relative influence on SBE, and aids in the development of an appropriate therapeutic plan.     

Mixed acid-base disorders

Mixed acid-base disturbances are combinations of two or more primary acid-base disturbances. Mixed acid-base disturbances may be suspected on the basis of findings obtained from the medical history, physical examination, serum electrolytes and chemistries, and anion gap. The history, physical examination, and serum biochemical profile may reveal disease processes commonly associated with acid-base disturbances. Changes in serum total CO2, serum potassium and chloride concentrations, or increased anion gap may provide clues to the existence of acid-base disorders. Blood gas analysis is usually required to confirm mixed acid-base disorders. To identify mixed acid-base disorders, blood gas analysis is used to identify primary acid-base disturbance and determine if an appropriate compensatory response has developed. Inappropriate compensatory responses (inadequate or excessive) are evidence of a mixed respiratory and metabolic disorder. The anion gap is also of value in detecting mixed acid-base disturbances. In high anion gap metabolic acidosis, the change in the anion gap should approximate the change in serum bicarbonate. Absence of this relationship should prompt consideration of a mixed metabolic acid-base disorder. Finding an elevated anion gap, regardless of serum bicarbonate concentration, suggests metabolic acidosis. In some instances, elevated anion gap is the only evidence of metabolic acidosis. In patients with hyperchloremic metabolic acidosis, increases in the serum chloride concentration should approximate the reduction in the serum bicarbonate concentration. Significant alterations from this relationship also indicate that a mixed metabolic disorder may be present. In treatment of mixed acid-base disorders, careful consideration should be given to the potential impact of therapeutically altering one acid-base disorder without correcting others.     

Respiratory function and extraocular muscle paralysis following administration of pancuronium bromide in dogs

Pancuronium bromide, a neuromuscular blocking agent, was evaluated in canine cataract surgical patients under general anesthesia to determine its effects on respiratory function and globe position. Two paralytic, anesthetic regimes were studied: one using a standard dosage of 0.066 mg kg⁻¹ pancuronium bromide, given intravenously while providing the patient with ventilatory support, and one using a dosage of 0.022 mg kg⁻¹ in which no ventilatory support was provided. Eye position and anterior vitreal position/displacement were recorded by a surgeon who was blinded as to treatment group. Physiological parameters indicative of respiratory function were monitored. Both dosages of pancuronium produced comparable, neutral globe position within 30 s following administration which lasted for 20–30 min. All patients in the standard dose group experienced uneventful anesthetic episodes with physiological parameters well within the normal ranges. Within 5 min after administration, all patients in the low-dose group developed a pronounced respiratory acidosis (mean arterial pH = 7.07 ± 0.08; mean PaCO₂ = 79.8 ± 10.7 mmHg), which exceeded a set of predetermined safety limits, and subsequently these dogs received ventilatory support. We conclude that 0.022 mg kg⁻¹ pancuronium rapidly produces an unacceptable level of respiratory acidosis and, as a result, patients receiving neuromuscular blocking agents should routinely receive ventilatory support.     

Arterial Blood Gases in Dogs with Bacterial Pneumonia

The purpose of this study is to report the aterial blood gas findings in dogs with bacterial pneumonia. Arterial blood gas samples were collected from 62 dogs with culture-confirmed bacterial pneumonia. These results were compared with 46 normal dog arterial blood gas samples. Results demonstrated that respiratory acidosis was not a problem in dogs with pneumonia in this study. Significant evidence of hypoxemia was noted with abnormal mean values in PaO₂ (P<0.001) and the Alveolar-arterial (A-α) gradient (P<0.001).     

绵羊实验性乳酸酸中毒研究——Ⅱ.血气和阴离子隙对乳酸酸中毒的诊断价值

12只2～(?)岁健康绵羊被分为Ⅰ组(3只)、Ⅱ组(?)只)和Ⅲ组(3只),分别按2.5,5.0,10.0g/kg瘤胃内注入50%D-L消旋体乳酸溶液.Ⅱ组羊在恢复期因过度代偿而导致代谢性碱中毒。各实验绵羊血液pH值与HCO3-、BEB、TCO2、BEECF和SB成正相关,可作为绵羊乳酸酸中毒的可靠诊断依据。计算AG能反映绵羊酸中毒的程度。绵羊瘤胃内注入乳酸10.0g/kg体重,AG升高到35mmol/L时,绵羊处于休克状态,AG35mmol/L可作为乳酸酸中毒预后不良的监测指标。     

Metabolic acid-base disorders in the critical care unit.

The recognition and management of acid-base disorders is a commonplace activity in the critical care unit, and the role of weak and strong acids in the genesis of metabolic acid-base disorders is reviewed. The clinical approach to patients with metabolic alkalosis and metabolic acidosis is discussed in this article.