0592. Metabolic acidosis induced by haemorrhage and hydrochloric acid generates different cardiorespiratory responses

  • G Sabbatini
  • A Dyson
  • M Singer
Open Access
Poster presentation


Metabolic Acidosis Thigh Muscle Blood Withdrawal High Tidal Volume Tissue Hypoperfusion 
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Metabolic acidosis is classically thought to induce an enhanced ventilatory pattern, irrespective of the underlying aetiology.


To induce a similar level of acidaemia in a rat model, by either infusion of an acidic solution or by blood withdrawal, and to assess the physiological responses to these insults.


Isoflurane-anaesthetised, tracheotomized rats were instrumented with left common carotid arterial and right jugular venous lines for blood sampling/BP monitoring and fluid/blood administration, respectively. OxyliteTM probes (Oxford Optronix, UK) placed in thigh muscle were used to monitor tissue oxygen tension (tPO2). Animals were subjected to either continuous 0.1 M hydrochloric acid (HCl) infusion or 60% withdrawal of estimated blood volume in six 10% steps over three hours to induce an equivalent fall in arterial base excess (BE). All animals (including a control group) received n-saline throughout. Hourly measurements were made of haemodynamics, tPO2 and arterial blood gas analysis.


See figure 1.
Figure 1

Results. BL= baseline, SaO2= arterial oxygen saturation. Data shown as mean (SEM). Hydrochloric acid (HCl) n=6, Haemorrhage n=8, Controls n=10/group, *p< 0.05 comparing treated to controls, §p< 0.05 comparing haemorrhage to HCl. Statistics: repeated measures two-way ANOVA and Bonferroni's test for multiple comparisons.

HCl induced a metabolic acidosis with arterial hypoxaemia yet a preserved muscle tPO2, no tachypnoea nor fall in PaCO2. By contrast, haemorrhage to achieve a similar acidaemia, resulted in significant falls in blood pressure and tPO2, hyperlactataemia, a small rise in SaO2 and a decrease in respiration rate with a concomitant fall in PaCO2 probably related to higher tidal volumes.


Tissue hypoperfusion (and not just acidaemia per se) is an important component that triggers an enhanced ventilatory drive.

Copyright information

© Sabbatini et al; licensee Springer. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Authors and Affiliations

  • G Sabbatini
    • 1
  • A Dyson
    • 1
  • M Singer
    • 1
  1. 1.University College LondonBloomsbury Institute of Intensive Care MedicineLondonUnited Kingdom

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