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.     

Comparison of the utility of the classic model (the Henderson-Hasselbach equation) and the Stewart model (Strong Ion Approach) for the diagnostics of acid-base balance disorders in dogs with right sided heart failure

Classically, the acid-base balance (ABB) is described by the Henderson-Hasselbach equation, where the blood pH is a result of a metabolic components--the HCO3(-) concentration and a respiratory component--pCO2. The Stewart model assumes that the proper understanding of the organisms ABB is based on an analysis of: pCO2, Strong Ion difference (SID)--the difference strong cation and anion concentrations in the blood serum, and the Acid total (Atot)--the total concentration of nonvolatile weak acids. Right sided heart failure in dogs causes serious haemodynamic disorders in the form of peripheral stasis leading to formation of transudates in body cavities, which in turn causes ABB respiratory and metabolic disorders. The study was aimed at analysing the ABB parameters with the use of the classic method and the Stewart model in dogs with the right sided heart failure and a comparison of both methods for the purpose of their diagnostic and therapeutic utility. The study was conducted on 10 dogs with diagnosed right sided heart failure. Arterial and venous blood was drawn from the animals. Analysis of pH, pCO2 and HCO3(-) was performed from samples of arterial blood. Concentrations of Na+, K+, Cl(-), P(inorganic), albumins and lactate were determined from venous blood samples and values of Strong Ion difference of Na+, K+ and Cl(-) (SID3), Strong Ion difference of Na+, K+, Cl(-) and lactate (SID4), Atot, Strong Ion difference effective (SIDe) and Strong Ion Gap (SIG4) were calculated. The conclusions are as follows: 1) diagnosis of ABB disorders on the basis of the Stewart model showed metabolic alkalosis in all dogs examined, 2) in cases of circulatory system diseases, methodology based on the Stewart model should be applied for ABB disorder diagnosis, 3) if a diagnosis of ABB disorders is necessary, determination of pH, pCO2 and HCO3(-) as well as concentrations of albumins and P(inorganic) should be determined on a routine basis, 4) for ABB disorder diagnosis, the classic model should be used only when the concentrations of albumins and P(inorganic) are normal.     

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.     

Ventilatory and Metabolic Compensation in Dogs With Acid-Base Disturbances

Ventilatory and metabolic compensation to acid-base disturbances is reviewed. The mechanisms for compensation as well as the values obtained from several studies using normal dogs and dogs with experimentally induced diseases are provided. Compensation is not the same in dogs and human beings. Dogs have a better ability to adapt to most respiratory disorders, and human beings adapt better to metabolic acidosis. In metabolic alkalosis and chronic respiratory acidosis there is no difference in compensation between these species. Ventilatory compensation for metabolic disorders in dogs is the same whether they have metabolic acidosis or metabolic alkalosis, whereas metabolic compensation in respiratory disturbances is less effective in acidosis. Values for the expected changes in PCO₂ in dogs with metabolic acidosis and metabolic alkalosis, and for bicarbonate concentration (HCO₃-) in dogs with acute and chronic respiratory alkalosis and acidosis are presented.     

The use of the standard exercise test to establish the clinical significance of mild echocardiographic changes in a Thoroughbred poor performer

A 4-year-old Thoroughbred gelding racehorse was referred to the Onderstepoort Veterinary Academic Hospital (OVAH) with a history of post-race distress and collapse. In the absence of any obvious abnormalities in the preceding diagnostic work-up, a standard exercise test was performed to determine an underlying cause for the post-race distress reported. In this particular case oxygen desaturation became evident at speeds as slow as 6 m/s, where PO2 was measured at 82.3 mm Hg. Similarly at a blood pH of 7.28, PCO2 had dropped to 30.0 mm Hg indicating a combined metabolic acidosis and respiratory alkalosis. The cause of the distress was attributed to a severe hypoxia, with an associated hypocapnoea, confirmed on blood gas analyses, where PO2 levels obtained were as low as 56.6 mm Hg with a mean PCO2 level of 25.4 mm Hg during strenuous exercise. Arterial oxygenation returned to normal immediately after cessation of exercise to 106.44 mm Hg, while the hypocapnoeic alkalosis, PCO2 25.67 mm Hg, persisted until the animal's breathing normalized. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise. The combination of an aortic stenosis and a mitral valve insufficiency may have resulted in a condition similar to that described as high-altitude pulmonary oedema, with respiratory changes and compensation as for acute altitude disease. The results obtained were indicative of a dynamic cardiac insufficiency present during exercise and substantiate the fact that an extensive diagnostic regime may be required to establish a cause for poor performance and that the standard exercise test remains an integral part of this work-up.     

Accuracy of a portable blood gas analyzer incorporating optodes for canine blood

The accuracy of a portable blood gas analyzer (OPTI 1) was evaluated using canine blood and aqueous control solutions. Sixty-four arterial blood samples were collected from 11 anesthetized dogs and were analyzed for pH, partial pressure of carbon dioxide (PCO2) partial pressure of oxygen (PO2), and bicarbonate concentration ([HCO3-]) values by the OPTI 1 and a conventional blood gas analyzer (GASTAT 3). The conventional analyzer was considered as a standard against which the OPTI 1 was evaluated. Comparison of OPTI 1 results with those of GASTAT 3 by linear regression analysis revealed a high degree of correlation with the GASTAT 3 (r = .90-.91). The mean +/- SD of the differences between OPTI 1 and GASTAT 3 values was -0.008 +/- 0.017 for pH, -0.88 +/- 3.33 mm Hg for PCO2, 3.71 +/- 6.98 mm Hg for PO2, and -0.34 +/- 1.45 mEq/L for [HCO3-]. No statistically significant difference was found between the OPTI 1 and the GASTAT 3. Agreement between these 2 methods is within clinically acceptable ranges for pH, PCO2, PO2, and [HCO3-]. The coefficients of variation for measured pH, PCO2, and PO2 values of 3 aqueous control solutions (acidic, normal, and alkalotic) analyzed by the OPTI 1 ranged from 0.047 to 0.072% for pH, 0.78 to 1.81% for PCO2, and 0.73 to 2.77% for PO2. The OPTI 1 is concluded to provide canine blood gas analysis with an accuracy that is comparable with that of conventional benchtop blood gas analyzers.     

Calculation of the total plasma concentration of nonvolatile weak acids and the effective dissociation constant of nonvolatile buffers in plasma for use in the strong ion approach to acid-base balance in cats

OBJECTIVE: To determine values for the total concentration of nonvolatile weak acids (Atot) and effective dissociation constant of nonvolatile weak acids (Ka) in plasma of cats. SAMPLE POPULATION: Convenience plasma samples of 5 male and 5 female healthy adult cats. PROCEDURE: Cats were sedated, and 20 mL of blood was obtained from the jugular vein. Plasma was tonometered at 37 degrees C to systematically vary PCO2 from 8 to 156 mm Hg, thereby altering plasma pH from 6.90 to 7.97. Plasma pH, PCO2, and concentrations of quantitatively important strong cations (Na+, K+, and Ca2+), strong anions (Cl-, lactate), and buffer ions (total protein, albumin, and phosphate) were determined. Strong ion difference was estimated from the measured strong ion concentrations and nonlinear regression used to calculate Atot and Ka from the measured pH and PCO2 and estimated strong ion difference. RESULTS: Mean (+/- SD) values were as follows: Atot = 24.3 +/- 4.6 mmol/L (equivalent to 0.35 mmol/g of protein or 0.76 mmol/g of albumin); Ka = 0.67 +/- 0.40 x 10(-7); and the negative logarithm (base 10) of Ka (pKa) = 7.17. At 37 degrees C, pH of 7.35, and a partial pressure of CO2 (PCO2) of 30 mm Hg, the calculated venous strong ion difference was 30 mEq/L. CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that at a plasma pH of 7.35, a 1 mEq/L decrease in strong ion difference will decrease pH by 0.020, a 1 mm Hg decrease in PCO2 will increase plasma pH by 0.011, and a 1 g/dL decrease in albumin concentration will increase plasma pH by 0.093.     

Evaluation of colostral IgG1 absorption in newborn calves after treatment with alkalinizing agents.

The effects of alkalinizing agents, administered prior to feeding colostrum, on blood-gas and acid-base values and on absorption of IgG1 were determined in 40 newborn Holstein calves. Two treatments, sodium bicarbonate (3 mEq/kg of body weight, IV) and doxapram HCl (2 mg/kg, IV), were evaluated, using a randomized complete-block experimental design. These treatments resulted in significant (P less than 0.01) alteration of blood-gas and acid-base values, generally in the direction of normal values for adult cattle. Significant least squares mean effects were detected for sodium bicarbonate treatment on blood pH (+ 0.04 units, P less than 0.01), PCO2 (+ 4.1 mm of Hg, P less than 0.01), and HCO3 concentration (+ 4.4 mEq/L, P less than 0.01). Significant least squares mean effects were detected for doxapram HCl treatment on blood pH (+ 0.06 pH units, P less than 0.01) and PCO2 (-5.2 mm of Hg, P less than 0.01). Absorption of colostral IgG1 was not affected by the treatments given or by the altered blood-gas and/or acid-base status.     

Changes in oxygen content and acid-base balance in arterial and portal blood in response to the dietary electrolyte balance in pigs during a 9-h period after a meal

The effect of two dietary electrolyte balance (dEB, Na+ + K+ - Cl-) levels on arterial and portal blood oxygen content, blood pH, and acid-base status in pigs was studied during a 9-h period after a meal, using a crossover experimental design. The dEB levels were established by changing the Cl- level in the diets. Four pigs with a mean weight of 45 kg were surgically fitted with catheters in the carotid artery and portal vein. Two dEB levels (-100 and 200 mEq/kg) were evaluated in two periods of 1 wk each. Feed was given at 2.6 times the maintenance requirement for energy in two meals per day. Water was freely available. Blood samples were taken at 0, 0.5, 1, 1.5, 2, 3, 4, 6, and 9 h after feeding. Blood hemoglobin; O2 pressure; O2 saturation; O2 content; pH; PCO2; HCO3-; base excess; and Na+, K+, and Cl- contents were measured. Oxygen contents in arterial and portal blood were lower (P < 0.008) in the -100 mEq/kg group (5.78 and 4.82 mmol/L respectively) compared to the 200 mEq/kg group (6.18 and 4.99 mmol/L respectively). This was related to the lower hemoglobin content in the blood of animals in the -100 mEq/kg group. Arterial and portal blood pH were lower (P < 0.003) at -100 mEq/kg (7.46 and 7.37) than at 200 mEq/kg (7.49 and 7.43). The difference in blood pH between the two groups was sustained throughout the sampling period. The average values of arterial and portal blood for base excess and HCO3- content were higher (P < 0.001) at high dEB (6.96 and 31.0 mmol/L, respectively, for -100 mEq/kg and 12.54 and 35.9 mmol/ L, respectively, for 200 mEq/kg). The Na+ concentration in the blood was increased and K+ and Cl- concentrations were decreased (P < 0.02) by increasing dEB from -100 mEq/kg to 200 mEq/kg. Blood electrolyte balance level was higher (P < 0.001) in the 200 mEq/kg dEB group than in the -100 mEq/kg dEB group. In conclusion, dEB changed blood oxygen content and pH, and influenced the acid-base buffer system in pigs. Also, within each group, pigs maintained a relatively constant blood pH level during the 9-h period after feeding.     

Qualification of the Stewart variables for the assessment of the acid-base status in healthy dogs and dogs with different diseases

Peter Stewart criticized the traditional theory of the acid-base status by Henderson-Hasselbalch as too simple and incomplete. He developed a new model with 3 independent variables: (1) pCO2, (2) SID (strong ion difference) and (3) Atot (Acid total). In healthy and ill dogs the diagnostic usefulness of both acid-base models were compared. This study included n=58 healthy dogs and 3 clinical cases of sick dogs.The age of the healthy dogs was 5.0 (2.0-7.0) years (= median (1.-3. quartil)).The 3 clinical cases included (1) a dog with septic shock, (2) with acute renal insufficiency, and (3) with hypovolaemic shock due to gastric torsion.Venous blood was taken of all dogs and the acid-base parameters were determined within < or =30 minutes. Electrolytes and albumin were determined in blood serum and used for calculation of the Stewart variables. Limits of reference intervals (x+/-1.96 - s) were determined for the healthy dogs yielding pCO2 = 3.6-6.5 kPa, [SID3] = 33.1-50.9 mmol/l resp. [SID4] = 31.8-49.6 mmol/l and [Al = 8.5-13.1 mmol/l. In Case 1 the Henderson-Hasselbalch parameters demonstrated the presence of a strong metabolic acidosis with mild respiratory influence (pH, [HCO3-], [BE] and PCO2 at upper range of normal). Analysis of the Stewart variables [SID3] resp. [SID4] revealed an electrolyte imbalance with [Cl-] and [lactate-] as the reason for metabolic acidosis. Case 2 showed a metabolic acidosis with respiratory compensation (pH, [HCO3-], [BE] and PCO2). Analysis of the Stewart variables with [SID3] resp. [SID4 caused by [K+], [Na+] and [lactate-]demonstrated the acidotic metabolism due to a renal malfunction. Case 3 had a metabolic acidosis (pH-value in the lower range) caused by electrolyte imbalances ([SID4]. The Stewart variables allow a better understanding of the causes of acid-base-disturbances in animals with implications for successful therapy via infusion.     

Cardiopulmonary effects of butorphanol tartrate intravenously administered for placement of duodenal cannulae in isoflurane-anesthetized yearling steers

Cardiopulmonary effects of IV administered butorphanol tartrate (BUT) were assessed in 7 yearling steers medicated with atropine and anesthetized with guaifenesin, thiamylal sodium, and isoflurane in O2 for surgical placement of duodenal cannulae. Heart rate, respiratory rate, arterial blood pressures, pHa, PaCO2, PaO2, arterial [HCO3-], esophageal temperature, and end-tidal isoflurane concentrations were measured before and after IV administration of BUT (10 mg). Mean respiratory rate increased significantly (P less than 0.05) only at 45 and 60 minutes after BUT administration. Mean respiratory rate was 26 +/- 6.3 breaths/min before BUT administration and 46 +/- 12.1 breaths/min 60 minutes after BUT administration. Arterial blood pressures were increased significantly (P less than 0.05) at all times, except 5 minutes after BUT administration. The mean value for mean arterial pressure was 76 +/- 9.6 mm of Hg before BUT injection and 117 +/- 12.6 mm of Hg 60 minutes after BUT injection. Mean values for pHa and arterial [HCO3-] were significantly (P less than 0.05) higher at 60 minutes after BUT administration (baseline, pH = 7.25 +/- 0.04 and [HCO3-] = 29.9 +/- 3.5 mEq/L; 60 minutes after BUT, pH = 7.28 +/- 0.03 and [HCO3-] = 33.0 +/- 1.8 mEq/L). Although some statistically significant changes were recorded, IV administration of BUT to these steers did not have a marked effect on the cardiopulmonary variables measured.     

A Comparison of Simultaneously Collected Arterial, Mixed Venous, Jugular Venous and Cephalic Venous Blood Samples in the Assessment of Blood-Gas and Acid-Base Status in the Dog

Blood samples were collected simultaneously from the pulmonary artery, jugular vein, cephalic vein, and carotid artery in awake dogs. Blood-gas and acid-base values were measured from these blood samples in normal dogs and in dogs after production of metabolic acidosis and metabolic alkalosis. The values obtained from each of the venous sites were compared with those obtained from arterial blood to determine if venous blood from various sites accurately reflected acid-base balance and could therefore be used in the clinical patient. The results of this study demonstrated significant differences between the blood from various venous sites and the arterial site for PCO2 and pH in all acid-base states. Significant differences for standard bicarbonate (SHCO3) were found only when jugular and cephalic venous blood were compared with arterial blood in dogs with a metabolic acidosis. No significant differences were found for BE when blood from the venous sites was compared with arterial blood. The values for pH, HCO3, TCO2, BE, and SHCO3 measured on blood collected at the various venous sites were found to correlate well with those obtained from arterial blood, with a correlation coefficient of 0.99 for HCO3, TCO2, BE, and SHCO3. These correlation coefficients, together with similar values in BE at all collection sites, indicate that, in the dog with normal circulatory status, blood from any venous site will accurately reflect the acid-base status of the patient.     

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.     

氨氟醚吸入麻醉妊娠犬及其胎儿动脉血药浓度和血气分析

选用 10只妊娠犬 ,实施母体及胎儿股动脉血管插管后 ,测定了氨氟醚麻醉期间母犬及胎儿的动脉血药浓度和血液 p H、PO2 (动脉氧分压 )、PCO2 (动脉 CO2 分压 )、T- CO2 (血浆 CO2 总量 )、HCO- 3 (实际碳酸氢盐 )、SB(标准碳酸氢盐 )、BEb(全血碱超 )、Sat.O2 (血氧饱和度 )。结果 :氨氟醚可透过胎盘进入胎儿血液 ,胎儿血药浓度低于母犬 ,但两者上升和消除变化趋势接近 ;麻醉期间 ,母犬及胎儿血液 p H、BEb下降 (P<0 .0 1或 P<0 .0 5 ) ,PO2 、PCO2 、Sat.O2 升高(P<0 .0 1或 P<0 .0 5 ) ,HCO- 3 、T- CO2 表现升高趋势 (P>0 .0 5 ) ,SB表现下降趋势 (P>0 .0 5 )。结果表明 ,氨氟醚吸入麻醉期间 ,母犬及其胎儿呈现轻度呼吸性酸中毒和代谢性酸中毒并存 ,并随氨氟醚血药浓度的降低而逐渐恢复     

Gastric Conduit Urinary Diversion in Normal Dogs Part II, Hypochloremic Metabolic Alkalosis

Gastric conduit urinary diversion was performed in 10 dogs after complete cystectomy. Four dogs were euthanatized on day 30 because of hypochloremic metabolic alkalosis and renal failure. Hematologic and biochemical changes in six dogs evaluated for 120 days were compatible with hypochloremic metabolic alkalosis. The continuous loss of hydrochloric acid from the gastric conduit resulted in significant increases in arterial blood pH, PaCO2, anion gap, TCO2, and the concentration of HCO3-. There were significant decreases in PaO2 and the serum concentrations of chloride and potassium. Deterioration of renal function resulted in all dogs. It was concluded that hypochloremic metabolic alkalosis makes gastric conduit urinary diversion unsatisfactory for clinical use in dogs.     

Replacement of chloride deficit by use of 1.8% NaCl to correct experimentally induced hypochloremic metabolic alkalosis in sheep.

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour IV treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl- less than or equal to 60 +/- 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced. Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl-1 deficit. Although hydration improved, plasma Cl- decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl- deficit without replacing total volume. Plasma Na+ and Cl- concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the IV replacement of Cl- without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.     

Blood acid-base curve nomogram for immature domestic pigs

The purpose in this study was to characterize the acid-base status of arterial blood from healthy young domestic swine and to construct an acid-base curve nomogram appropriate to such animals. Accordingly, 40 immature, 20- to 31-kg domestic pigs were used to establish acid-base characteristics for arterial blood. Samples were collected from chronically implanted catheters while the animals were maintained under steady-state, near-basal conditions. At a measurement temperature of 38 C, pH averaged 7.496; PCO2, 40.6 mm Hg; [HCO3-], 31.6 mEq/L; PO2, 79.1 mm Hg; hemoglobin, 9.65 g/dl; hematocrit, 0.29; plasma albumin, 25.3 g/L; plasma globulin, 32.3 g/L; and plasma buffer base, 45.4 mEq/L. Hourly measurements over a 6-hour period in 6 of these pigs showed a small, but significant decrease in PO2 with time, but no significant change in acid-base status. The data showed that nomograms or other procedures based on blood characteristics of men were invalid when used to estimate base excess concentration of blood from young pigs. The normal pH of arterial blood was higher in immature pigs than in men; thus, reference values defining zero base excess were not equivalent in men and pigs. Constant PCO2 titrations were performed on arterial samples taken from 10 additional pigs, and the data were used to construct an acid-base curve nomogram in which zero base excess was defined for blood with a pH of 7.50 and a PCO2 of 40 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)     

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).     

Effects of Acute Hyperventilation on Serum Potassium in the Dog

The effects of increasing respiratory rates on arterial pH, PaCO2, HCO3, and potassium (K) were measured in normal anesthetized dogs. Hyperventilation resulted in increased pH, decreased PaCO2, decreased HCO3, and decreased K compared with those parameters in spontaneously breathing dogs. The changes were related quantitatively: each 10 mmHg decrease in PaCO2 was associated with a pH increase of 0.1, a HCO3 decrease of 2.0 mEq/L, and a K decrease of 0.4 mEq/L. There were no cardiac arrhythmias or clinical signs of hypokalemia. After termination of hyperventilation, serum K was slower to return to control values than PaCO2. The ratio of the duration of hyperventilation to the time required for return of serum K to control was 0.67.