0592. Metabolic acidosis induced by haemorrhage and hydrochloric acid generates different cardiorespiratory responses
© Sabbatini et al; licensee Springer. 2014
Published: 26 September 2014
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.
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.
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