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Survival after cardiac arrest and severe lactic acidosis (pH 6.61) due to haemorrhage
  1. Craig Spencer1,
  2. John Butler2
  1. 1University Hospitals of South Manchester NHS Foundation Trust, Wythenshawe Hospital, Manchester, UK
  2. 2Department of Critical Care, Manchester Royal Infirmary, Manchester, UK
  1. Correspondence to Dr Craig Spencer, Consultant in Anaesthesia and Critical Care, Royal Preston Hospital, Lancashire Teaching Hospitals NHS Foundation Trust, Sharoe Green Lane, Fulwood, Preston PR2 9HT, UK; docspenc{at}


This paper describes a 21-year-old man who presented to the emergency department with a knife wound to his buttock. He had a witnessed cardiac arrest with pulseless electrical activity in hospital as a result of further haemorrhage. His post-resuscitation arterial blood gas revealed a severe lactic acidosis (pH 6.61, lactate 22.0 mmol/l). Despite poor expectations he went on to make a full neurological recovery. To the authors' knowledge, he had the fourth-lowest pH for a cardiac arrest survivor with normal neurology. Severe lactic acidosis occurs post cardiac arrest due to imbalance between cellular oxygen supply and demand. Severe lactic acidosis is associated with hypoxic brain injury but has a low specificity in its prediction. The case illustrates that, especially in younger adults, severe lactic acidosis may be a poor predictor of outcome if it reflects a period of relative hypoperfusion preceding cardiac arrest.

  • Acidosis
  • lactic
  • anaesthesia
  • haemorrhage
  • heart arrest
  • intensive care
  • musculo-skeletal
  • resuscitation
  • soft tissue injury

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  • Competing interests None.

  • Patient consent Obtained.

  • Provenance and peer review Not commissioned; not externally peer reviewed.