Describing blood acid-base response in dogs with acute haemorrhagic diarrhoea syndrome using three different methods

Abstract

Objective: To describe blood acid-base response in dogs with acute haemorrhagic diarrhoea syndrome (AHDS) using three different methods of analysis. Hypothesis: Dogs with AHDS have increased unmeasured strong anions compared to healthy dogs. Design: Prospective, observational study. Setting: Private referral hospital. Animals: A total of 20 dogs used in two groups as follows: 10 healthy age-, weight- and breed-matched dogs and 10 dogs with AHDS. Interventions: Blood that was collected from healthy dogs were used to establish an expected normal range (minimum and maximum limits of the ranges were calculated as mean ± 2 standard deviations). Jugular venous blood, AHDS index scores (0 – 3: insignificant disease; 4 – 5: mild AHDS; 6 – 8: moderate AHDS; 9 – 18: severe AHDS) and intravenous fluid infusion volumes (mL/kg) were collected at presentation (0H) and then at set hour-intervals post presentation (4H, 8H, 12H, 16H, 20H, 24H, 36H, 48H and 60H). Blood was analysed to measure or calculate acid-base variables used in three different methods of analysis: 1) traditional, 2) Stewart theory, and 3) semi-quantitative theory approaches. Longitudinal data were compared using a general lineal mixed model with post-hoc comparisons using Dunnett's method (control variable: values at 0H) and significance was P < 0.05 and data were reported as median (minimum – maximum). Measurements and main results: The pH, at 0H, was 7.31 (7.22 – 7.49) and classified as acidaemic with a wide anion gap of 24.6 (13.1 – 27.6) mmol/L because of a raised venous carbon dioxide tension [48 (26 – 51) mmHg], negative base excess of extracellular fluid [-5.4((-8.0) – (-2.4)) mmol/L] and acidaemic lactate effect [-3.5 ((-5.4) – (-1.2)) mmol/L]. The pH normalised by 4H (P < 0.0001) in response to fluid administration where 37 (29 – 63) mL/kg was given over the 4-hour period. Whereas the AHDS clinical index score was classified as ‘insignificant disease’ by 48H. The pH remained within normal reference intervals until 60H and fluid rates were 3 mL/kg/hour from 8H onwards. The bicarbonate and haemoglobin buffer systems played a role in blood acid-base homeostasis. Conclusions: The acidaemia at presentation in dogs with AHDS was related to hypovolaemia and all derangements were corrected by fluid resuscitation. All three methods of analysis were useful in interpreting the complex interplay between acidifying and alkalinising effects and blood buffers.