An 80 year old lady (wt 40 kgs) was admitted to the Intensive Care Unit following a motor vehicle accident.
She was the driver and was wearing a seat-belt. She had run off the road in her car and hit a tree. She remembered the accident and was not knocked out. Injuries were a left anterior flail segment, a fractured left patella and facial bruising. She was haemodynamically stable but had respiratory distress with paradoxical movement of her left anterior chest wall. There was no head or neck injury. Recently she had had several unexplained blackouts. Only significant past history was of hypertension for which she took propranolol 120 mgs/day.
She was intubated and ventilated in the Casualty department because of respiratory distress. Initial ventilation was tidal volume 1,000mls at a rate of 10 breaths/min with 100% oxygen. Arterial gases (below) were obtained half an hour later. Peripheral perfusion was good. An intravenous infusion was commenced.
Previous health was good apart from recent 'blackouts'. She was on no regular medication.
Arterial Blood Gases |
pH 7.56 |
pCO2 23 mmHg |
pO2 508 mmHg |
HCO3 21 mmol/l |
History is of an acute disorder. The controlled ventilation settings are delivering a tidal volume of 25mls/kg and a minute volume of 250mls/kg. An acute respiratory alkalosis is very likely.
The final acid-base diagnosis is acute respiratory alkalosis due to mechanical hyperventilation. The cause of her ‘blackouts’ needs appropriate investigation.
This result is consistent with her previous good health, lack of diuretic therapy and good peripheral perfusion. Her gases normalised when minute ventilation was decreased.
The probable sequence of events here was an old lady who had a ‘blackout’ and crashed her car. Because of respiratory difficulty due to the flail chest, she was managed with intubation and controlled ventilation. The initial gas results show a predictable acute respiratory alkalosis due to mechanical over-ventilation. She was receiving a very high tidal volume.
It is not uncommon for intubated patients in an Accident & Emergency Department to be initially over-ventilated as the priority is to ensure adequate oxygenation and to adjust alveolar ventilation later (based on arterial pCO2). In addition, multi-trauma patients often develop a metabolic acidosis and the over-ventilation will mimic the body's compensatory response. Whether this is initially useful is uncertain as the body's compensatory response does take some time to develop. Arterial blood gases should be checked soon after institution of controlled ventilation.