Acid-Base Physiology - Examples for 9.6
Case History  26 : A man with a gunshot wound & a cardiac arrest

 

Clinical Details
A 26 year old man was shot in the abdomen. He arrested in the ambulance and resuscitaion was commenced. Sinus rhythm with normal QRS complexes was restored. Aggressive volume loading in the Emergency Department resulted in a systolic pressure of 70 mmHg just prior to transfer to theatre for immediate laparotomy. External cardiac massage and volume loading were continued as pulseless electrical activity due to hypovolaemia continued. Adequate circulation was restored following surgical control of bleeding and volume loading with colloid. Hyperventilation with 100% was continued and initial blood gases were collected 20 minutes later.

Serial Blood Gas Results

Number

 1

 2

 3

 4

 5

Time

 1320 hrs

 1350 hrs

 1510 hrs

 1930 hrs

 2320 hrs

Place

 Theatre

 Theatre

 Theatre

 ICU

 ICU

FIO2

 1.0

 1.0

 1.0

 1.0

 ?

pH

 7.16

 7.36

 7.37

 7.40

 7.39

pCO2 (mmHg)

 33

 27

 28

 31.2

 38.1

HCO3 (mmol/l)

 12

 15

 16

 18.7

 22.7

pO2 (mmHg)

 414

 546

 490

 353

 205.2

Lactate (mmol/l)

 NR

 NR

 NR

 2.6

 1.0

(All gas results measured and reported at 37C)

When the initial gas results were received, management was to increase the minute ventilation to lower the pCO2 further and to continue volume resuscitation with colloid, crystalloid and red cell concentrate to achieve an endpoint of systolic BP greater then 110 systolic. Urine output was good. Bicarbonate was not given. Postoperatively, the patient was transferred ventilated to the Intensive Care Unit. Total intraoperative fluids was about 20 litres including 16 units of packed red cells.

Assessment
Firstly, initial clinical assessment (on the first gas results only):
This patient has had an arrest associated with hypovolaemia & poor tissue perfusion so the expected result would be a lactic acidosis. The initial gases were collected 20 minutes after the circulation was restored and any respiratory acidosis could have been corrected in this time. Indeed, the Anaesthetist should be hyperventilating the patient (to help restore the pH towards normal) so there may be a respiratory alkalosis. 

Secondly, the acid-base diagnosis: 
1. pH:  Severe acidaemia indicates a severe acidosis.
2. Pattern:  The pattern of a low bicarbonate in conjunction with a low pCO2 occurs in metabolic acidosis and in respiratory alkalosis. As an acidosis is present, then this indicates a severe metabolic acidosis
3. Clues:  No electrolyte or other biochemistry results are available.
4. Compensation:  If the patient was spontaneously ventilating, respiratory compensation would be expected to produce an arterial pCO2 of (1.5 x 12 + 8) = 26mmHg. The actual pCO2 is higher then this.
5. Formulation: A severe metabolic acidosis, presumably a lactic acidosis, is present.
6. Confirmation: A lactate level would confirm the diagnosis. Electrolytes should be measured to allow calculation of the anion gap and to check the [K+]

Finally, the Clinical Diagnosis:
Abdominal trauma (due gunshot wound) resulting in hypovolaemic cardiac arrest & lactic acidosis (due to poor perfusion).

Comments
What is the respiratory acid-base status?
Such a metabolic acidosis in a conscious patient would cause compensatory hyperventilation. As this patient is unconscious with controlled ventilation then respiratory compensation in the usual sense of it being a physiological response is not possible. The Anaesthetist is hyperventilating the patient but this has resulted in a pCO
2 lower than 40mmHg, but higher than that expected at physiologically maximal compensation. As this hyperventilation is an externally controlled event it is a 'primary process' (& not due to the acidosis) so a pCO2 of 33mmHg would indicate a respiratory alkalosis

However, if this patient had been hyperventilating as a physiological response then a pCO2 of 33mmHg would be higher then the 26mmHg expected at maximal compensation and this would be called a respiratory acidosis (and this situation of a combined metabolic & respiratory acidosis would be invoked to explain why the pH was so low). In any case though, maximal compensation takes 12 to 24 hours to reach so a pCO2 of 33mmHg may well be quite appropriate at this early stage and there would be no respiratory disorder present. 

So what is the correct situation: a respiratory alkalosis, acidosis or no respiratory acid-base disorder?
Clearly it cannot be all three. The above discussion illustrates that in a patient on controlled ventilation it is really a semantic issue in deciding on the respiratory compensation status. But, to return to basics: the whole purpose of any acid-base assessment is to understand the situation & and attempt to improve the outcome for the patient. The above discussion cannot help to achieve this so is not useful. I find that a practical approach is to predict the maximal respiratory compensation that would be achieved (using the formula as above) and aim to achieve this. This approach is neither proven nor disproven by controlled trials but the effect will be to lessen the deviation of pH from normal and hopefully lessen the adverse effects of this.

Other comments: 
Lactic levels were not measured on the initial gases. Many modern automated blood-gas analysis machines can now measure electrolytes and lactate and provide these useful results automatically with every gas analysis. When finally measured (1930hrs), the lactate level was not particularly elevated. 

Bicarbonate was not given in this case. The main indication for bicarbonate in organic forms of metabolic acidosis is to treat life-threatening hyperkalaemia. A set of electrolytes, esp for K+ should be measured urgently. Bicarbonate probably does have a role in management of mineral forms of acidosis.

The second set of gas results show a significant improvement in pH towards normal due to increased bicarbonate level (subsequent to improved circulation) and the increased alveolar ventilation (introduced by the Anaesthetist). Subsequent gas results show continued resolution of the metabolic acidosis and minute ventilation was decreased allowing an elevation in arterial pCO2.

 

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