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.     

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).     

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.     

Clinical Applications of Quantitative Acid-Base Chemistry

Stewart used physicochemical principles of aqueous solutions to develop an understanding of variables that control hydrogen ion concentration (H+) in body fluids. He proposed that H+ concentration in body fluids was determined by PCO₂, strong ion difference (SID = sum of strong positive ion concentrations minus the sum of the strong anion concentrations) and the total concentration of nonvolatile weak acid (A_tot) under normal circumstances. Albumin is the major weak acid in plasma and represents the majority of A_tot. These 3 variables were defined as independent variables, which determined the values of all other relevant variables (dependent) in plasma, including H+. The major strong ions in plasma are sodium and chloride. The difference between Na+ and Cl^- may be used as an estimation of SID. A decrease in SID below normal results in acidosis (increase in H+) and an increase in SID above normal results in alkalosis (decrease in H+). Unidentified strong anions such as lactate will decrease the SID, if present. Equations developed by Fencl allow Stewart's work to be easily applied clinically for evaluating the metabolic (nonrespiratory) contribution to acid-base balance. This approach separates the net metabolic abnormality into components, and allows one to easily detect mixed metabolic acid-base abnormalities. The Fencl approach provides insight into the nature and severity of the disturbances that exist in the patient. Sodium, chloride, protein, and unidentified anion derangements may contribute to the observed metabolic acid-base imbalance.     

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.     

Effect of changes in ionized calcium concentration in arterial blood and metabolic acidosis on the arterial partial pressure of oxygen in dogs

OBJECTIVE: To evaluate the effects of metabolic acidosis and changes in ionized calcium (Ca2+) concentration on PaO2 in dogs. ANIMALS: 33 anesthetized dogs receiving assisted ventilation. PROCEDURE: Normal acid-base status was maintained in 8 dogs (group I), and metabolic acidosis was induced in 25 dogs. For 60 minutes, normocalcemia was maintained in group I and 10 other dogs (group II), and 10 dogs were allowed to become hypercalcemic (group III); hypocalcemia was then induced in groups I and II. Groups II and IV (5 dogs) were treated identically except that, at 90 minutes, the latter underwent parathyroidectomy. At intervals, variables including PaO2, Ca2+ concentration, arterial blood pH (pHa), and systolic blood pressure were assessed. RESULTS: In group II, PaO2 increased from baseline value (96 +/- 2 mm Hg) within 10 minutes (pHa, 7.33 +/- 0.001); at 60 minutes (pHa, 7.21 +/- 0.02), PaO2 was 108 +/- 2 mm Hg. For the same pHa decrease, the PaO2 increase was less in group III. In group I, hypocalcemia caused PaO2 to progressively increase (from 95 +/- 2 mm Hg to 104 +/- 3 mm Hg), which correlated (r = -0.66) significantly with a decrease in systolic blood pressure (from 156 +/- 9 mm Hg to 118 +/- 10 mm Hg). Parathyroidectomy did not alter PaO2 values. CONCLUSIONS AND CLINICAL RELEVANCE: Induction of hypocalcemia and metabolic acidosis each increased PaO2 in anesthetized dogs, whereas acidosis-induced hypercalcemia attenuated that increase. In anesthetized dogs, development of metabolic acidosis or hypocalcemia is likely to affect ventilatory control.     

Venous blood gas and lactate values of mourning doves (Zenaida macroura), boat-tailed grackles (Quiscalus major), and house sparrows (Passer domesticus) after capture by mist net, banding, and venipuncture

Blood gas partial pressures, pH, and bicarbonate and lactate concentrations were measured from the basilic vein of mourning doves (Zenaida macroura) and the jugular vein of boat-tailed grackles (Quiscalus major) and house sparrows (Passer domesticus) to assess immediate impacts of mist net capture and handling for banding and venipuncture. Mourning doves and house sparrows exhibited mild acidemia (median [minimum-maximum] venous blood pH(41 degrees C) = 7.394 [7.230-7.496] and 7.395 [7.248-7.458], respectively), relative to boat-tailed grackles (Quiscalus major; 7.452 [7.364-7.512]), but for different reasons. Mourning doves exhibited relative metabolic acidosis (lower venous blood pH, higher lactate concentrations, lower bicarbonate, and no significant differences in partial pressure of CO2 (pCO2) or partial pressure of O2 (pO2) compared with boat-tailed grackles). House sparrows exhibited relative respiratory acidosis (lower venous blood pH, higher pCO2, lower pO2, and no significant differences in bicarbonate and lactate concentrations compared with boat-tailed grackles). All birds captured by mist net and handled for banding and venipuncture experienced some degree of lactic acidemia; and values were greater in mourning doves (lactate, 7.72 [3.94-14.14] mmol/L) than in boat-tailed grackles (5.74 [3.09-8.75] mmol/L) and house sparrows (4.77 [2.66-12.03] mmol/L), despite mourning doves resisting least and being easiest to disentangle from the mist net. House sparrows were more susceptible to respiratory acidosis, warranting particular care in handling birds <30 g to minimize interference with ventilation. The different sample collection site for mourning doves may have affected results in comparison with the other two species, due to activity of the wing muscles. However, despite the higher lactate concentrations, pCO2 was relatively low in doves. The metabolic, respiratory, and acid-base alterations observed in this study were minor in most cases, indicative of the general safety of these important field ornithology techniques. The effect of other adverse conditions, however, could be additive.     

The acid-base equilibrium and carbohydrate metabolism during infection with Eperythrozoon suis

Following on from clinical observations which point to severe metabolic disturbances in association with acute Eperythrozoon (E.) suis infection, the parameters of acid-base balance (pO2, pCO2, pH, actual bicarbonate, standard bicarbonate, base excess) as well as the glucose-, lactate- and pyruvate levels, were measured in venous blood during the course of eperythrozoonotic infection. Glucose consumption was investigated in in vitro experiments with differing numbers of pathogens. Acute E. suis infection is accompanied by a severe acidosis and hypoglycaemia. In vitro experiments showed that a rapid breakdown of glucose follows in E. suis infected blood. No significant reduction in glucose concentration was established in control blood in a comparable time period. The results give rise to the assumption that E. suis is capable of independent glucose breakdown. Both the increase in lactate concentration (metabolic component) and a disturbance of pulmonary gaseous exchange (respiratory component) are regarded as the cause of the acidosis.     

Acid-base equilibrium values in the blood of dogs during training and work stress

Separate components of acid-base balance in blood (ABR)-pH, pCO2, BE, SB, BB-were studied during the long-term drill of service dogs of two age categories. These service dogs were included in two different work strain groups (patrol dogs and searching dogs). The results of long-term drill demonstrated, in particular, significant changes in dynamics of pH and pCO2. The pH values were permanently raised as compared with reduced pCO2 values during the whole period of 130-days exercise and as compared with the initial values. Other components of acid-base balance in blood do not show such variations (patrol and searching dogs) and these components justify that the adaptation of organism to the given strain gained suitable stabilisation. For studying the psychical and physical strain in service dogs it is recommended to include pH and pCO2 in the tests.     

Experimental determination of net protein charge and A(tot) and K(a) of nonvolatile buffers in canine plasma

Acid-base abnormalities frequently are present in sick dogs. The mechanism for an acid-base disturbance can be determined with the simplified strong ion approach, which requires accurate values for the total concentration of plasma nonvolatile buffers (A(tot)) and the effective dissociation constant for plasma weak acids (K(a)). The aims of this study were to experimentally determine A(tot) and K(a) values for canine plasma. Plasma was harvested from 10 healthy dogs; the concentrations of quantitatively important strong ions (Na+, K+, Ca2+, Mg2+, Cl-, L-lactate) and nonvolatile buffer ions (total protein, albumin, phosphate) were determined; and the plasma was tonometered with CO2 at 37 degrees C. Strong ion difference (SID) was calculated from the measured strong ion concentrations, and nonlinear regression was used to estimate values for A(tot) and K(a), which were validated with data from an in vitro and in vivo study. Mean (+/- SD) values for canine plasma were A(tot) = (17.4 +/- 8.6) mM (equivalent to 0.273 mmol/g of total protein or 0.469 mmol/g of albumin); K(a) = (0.17 +/- 0.11) x 10(-7); pK(a) = 7.77. The calculated SID for normal canine plasma (pH = 7.40; P(CO2) = 37 mm Hg; [total protein] = 64 g/L) was 27 mEq/L. The net protein charge for normal canine plasma was 0.25 mEq/g of total protein or 0.42 mEq/g of albumin. Application of the experimentally determined values for A(tot), K(a), and net protein charge should improve understanding of the mechanism for complex acid-base disturbances in dogs.     

Blood gas and acid-base status during tiletamine/zolazepam anaesthesia in dogs

OBJECTIVE: To evaluate the effect of the tiletamine/zolazepam (TZ) combination (Zoletil 100; Virbac, Carros, France) with and without atropine on blood gas values and acid-base status in dogs. STUDY DESIGN: Randomized cross-over experimental study. ANIMALS: Six healthy adult cross-bred dogs, weighing 11.0-18.5 kg. MATERIALS AND METHODS: Each dog received four different drug treatments at intervals of at least 15 days: (i) 5 mg kg(-1) intravenous (IV) TZ (TZ.IV); (ii) 10 mg kg(-1) intramuscular (IM) TZ (TZ.IM); (iii) atropine, 20 microg kg(-1) IV, followed 5 minutes later by 5 mg kg(-1) TZ IV (A.TZ.IV); and (IV) atropine (same dose) given 5 minutes before 10 mg kg(-1) TZ IM (A.TZ.IM). Arterial blood samples were collected from each dog before drug administration (baseline) at induction of anaesthesia (time 0) and 2, 5, 10 and 30 minutes thereafter. RESULTS: Transient hypoxaemia and respiratory acidosis were observed just after induction. PaO(2) and SaO(2) dropped, while H(+) concentration and PaCO(2) rose significantly above baseline values. In groups TZ.IV and A.TZ.IV, PaO(2) values as low as 6.0-6.4 kPa (45-48 mm Hg) were recorded. However, there was no significant difference in blood gas variables among the groups encountered during the evaluation period. The overall change in [HCO(3) (-)] and base excess (BE) was not significant among groups. Atropine did not affect the above variables. CONCLUSIONS AND CLINICAL RELEVANCE: Tiletamine/zolazepam injection may induce transient hypoxaemia and respiratory acidosis, but acid-base status changes are clinically unimportant. Particularly, close observation of dogs is recommended during the first 5-10 minutes after induction with TZ, especially in animals with cardiopulmonary disease. TZ should perhaps not be used in animals intolerant of tachycardia.     

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.     

Eperythrozoon infection in swine: effect on the acid-base balance and the glucose, lactate and pyruvate content of venous blood

The influence of latent and of splenectomy-induced clinically manifest Eperythrozoon suis infection on the following parameters of the carbohydrate metabolism and the acid-base status was tested in venous blood of German Landrace pigs: Levels of glucose, lactic and pyruvic acid, blood-pH, base excess, actual bicarbonate concentration, standard bicarbonate concentration, pCO2, pO2. The latent E. suis infection resulted in a consistent decrease of blood glucose level. 23 days after infection, blood glucose was reduced by 25% of the initial value. The other parameters were not changed by latent E. suis infection. Acute Eperythrozoonosis induced severe hypoglycaemia (means Gluc, = 39.7 mg/dl and blood acidosis (means pH = 7.13). In vitro experiments showed that break-down of glucose in E. suis infected blood occurs very rapidly. There was no significant reduction of the glucose concentration in control blood that had been treated accordingly. There was an increase of lactic acid (means = 62.7 mg/dl), pyruvic acid (means = 1.86 mg/dl), and pCO2 (means = 82.1 mm Hg). The concentrations of actual bicarbonate (means = 24.8 mmol/l) and standard bicarbonate (means = 20.9 mmol/l) were lowered, and there was a negative base excess (means = -3.56 mmol/l). The ratio of lactic and pyruvic acid changed from 11:1 to 30:1. It seems likely that E. suis itself is able to metabolize glucose. Acidosis is considered to result from both the increase of lactic acid (metabolic component) and an impairment of pulmonary gas exchange (respiratory component).     

The effect of arterial blood sampling sites on blood gases and acid-base balance parameters in calves.

In 21 healthy calves, 1-6 months old, the interrelationship and comparability of acid-base balance variables (pH, HCO3-, BE) and blood gases (pCO2, pO2, and sat-O2) were evaluated in arterial blood collected from a larger, centrally localised (the a. axillaris) and a smaller peripheral artery (the a. auricularis caudalis). Sampling was done by direct puncture of the vessels without local anaesthesia. Except for blood pH, significant differences were observed in the average values of pCO2, pO2, HCO3-, sat-O2 (P < 0.001), and BE (P < 0.05). Analyses of blood from the a. axillaris showed higher pH, pO2, and sat-O2 values, and lower pCO2, HCO3-, and BE values compared with that from the a. auricularis caudalis. Despite statistically significant differences between some variables, in all indices high and significant correlation relationships were recorded (R = 0.928-0.961; P < 0.001). Therefore, from the biological and clinical point of view, these differences are unimportant and the presented method of peripheral arterial blood sampling can be considered suitable for evaluating blood gases and acid-base status.     

Effects of isovolemic resuscitation with hemoglobin-based oxygen carrier Hemoglobin glutamer-200 (bovine) on systemic and mesenteric perfusion and oxygenation in a canine model of hemorrhagic shock: a comparison with 6% hetastarch solution and shed blood

OBJECTIVE: To study Hemoglobin glutamer-200 bovine (Hb-200), 6% hetastarch (HES) and shed whole blood (WB) resuscitation in canine hemorrhagic shock. STUDY DESIGN: Prospective laboratory investigation. Animals Twelve adult dogs [29 +/- 1 kg (mean +/- SD)]. METHODS: Anesthetized dogs were instrumented for recording systemic and mesenteric hemodynamic parameters and withdrawal of arterial, mixed and mesenteric venous blood, in which hematological, oxygenation, blood gas and acid-bases variables were determined. Recordings were made before [baseline (BL)], after 1 hour of hypovolemia and immediately and 3 hours post-resuscitation with 30 mL kg(-1) of either Hb-200, HES, or WB. RESULTS: Blood withdrawal (average 34 +/- 2 mL kg(-1)) caused significant hemodynamic changes, metabolic acidosis and hyperlactatemia characteristic for hemorrhagic shock. Only WB transfusion restored all variables. Hemoglobin glutamer-200 bovine infusion returned most hemodynamic parameters including cardiac output and mesenteric arterial blood flow to BL but increased mean arterial pressure above BL (p < 0.05). However, Hb-200 failed to restore total Hb and arterial oxygen content (CaO2), leaving systemic (DO2I) and mesenteric O2 delivery (DO2Im) below BL (p < 0.05). Nevertheless, acid-base variables recovered completely after Hb-200 resuscitation, and met-hemoglobin (Met-Hb) levels increased (p < 0.05). Hetastarch resuscitation returned hemodynamic variables to or above BL but further decreased total Hb and CaO2, preventing recovery of sDO2I and mDO2I (p < 0.05). Thus, systemic and mesenteric O2 extraction stayed above BL (p < 0.05) while acid-base variables recovered to BL, although slower than in Hb-200 and WB groups (p < 0.05). CONCLUSIONS AND CLINICAL RELEVANCE: Resuscitation with Hb-200 seemed to resolve metabolic acidosis and lactatemia more rapidly than HES, but not WB; yet it is not superior to HES in improving DO2I and DO2Im. The hyperoncotic property of solutions like Hb-200 that results in rapid volume expansion with more homogenous microvascular perfusion and the ability to facilitate diffusive O2 transfer accelerating metabolic recovery may be the key mechanisms underlying their beneficial effects as resuscitants.     

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.     

Osmolal and anion gaps in dogs with acute endotoxic shock

Serum osmolalities, biochemical concentrations, osmolal and anion gaps, blood lactate concentrations, and acid base status were evaluated in anesthetized, healthy control dogs and in dogs with endotoxic shock. The osmolal gap was not affected by endotoxemia. Compared with control dogs, dogs with endotoxic shock had mildly, though insignificantly, increased anion gaps and significantly increased blood lactate concentrations. The anion gap in dogs with endotoxic shock was positively (r = 0.77) and significantly correlated with the blood lactate concentration. Therefore, the blood lactate concentration of a dog in endotoxic shock may be estimated by use of the equation: lactate = 0.27 (anion gap) - 1.46. Confidence limits for this estimation were calculated. Dogs with endotoxic shock developed a lactic acidosis and hyperchloremic metabolic acidosis, with hyperventilation.     

Lymphocyte subpopulations and hematologic variables in dogs with congestive heart failure

Alterations in lymphocyte subpopulations and in other hematologic variables have been documented in people with heart failure. The purpose of the current study was to compare flow cytometric and hematologic variables in dogs with congestive heart failure (CHF) to healthy controls. CD4+ peripheral blood mononuclear cells (PBMC) and CD8+ lymphocytes were analyzed by flow cytometry, and white blood cell count, platelet count, hematocrit, and hemoglobin were determined by a complete blood count. Twenty-five dogs with CHF (International Small Animal Cardiac Health Council [ISACHC] class 2 [n = 12] and ISACHC class 3a [n = 13]) and 13 healthy controls were enrolled in the study. Compared with the controls, dogs with CHF had markedly lower percentages of CD4+ PBMC, CD8+ lymphocytes, hematocrit, and hemoglobin, but markedly higher leukocytes, neutrophils, and platelets. There were no differences in these variables between dogs with dilated cardiomyopathy (n = 6) and those with chronic valvular disease (n = 19). Dogs in ISACHC class 3a had a markedly lower total lymphocyte number, CD4+ and CD8+ cells, and hematocrit, but markedly higher leukocyte and neutrophil numbers relative to the control group. CD4+ and CD8+ subpopulations and other blood cell variables are altered in dogs with CHF. Future studies to determine possible clinical implications of these changes are warranted.