Acid-Base Physiology

Case 14 : A man following an out-of-hospital cardiac arrest

History

A 54 year old man was admitted following an out-of-hospital cardiorespiratory arrest.

His wife said he had complained of indigestion on and off for the past 2 months. He had attended his local doctor the previous day with upper abdominal pain and a cough. He was commenced on an antacid and erythromycin. That night the pain had become much more severe. The After-hours Locum Doctor Service was called; he gave the and he was given IM morphine. The pain was severe again the next day. He collapsed at home at about 1200 hours.

The ambulance arrived about 5 minutes later. The ambulance officers diagnosed a cardiorespiratory arrest because the patient was comatose (GCS 3/15), pulseless and apnoeic. Cardiopulmonary resuscitation was commenced. After 5 minutes, the patient had a palpable pulse and was breathing. On arrival at hospital he was awake and able to give a history. He complained of severe abdominal pain and was guarded in the upper abdomen. Blood pressure of 80 systolic increased with fluid loading. The only past history was of hypertension but he was on no medications. A pneumoperitoneum was seen on a semi-erect chest xray. At urgent laparotomy, a perforated duodenal ulcer and gross peritoneal soiling was found. Fifty mls of 8.4% sodium bicarbonate was given intraoperatively at 1345hrs following arterial gases at 1330hrs. Postoperatively, he was transferred ventilated to the Intensive Care Unit. Serial results are listed in the table.

Serial Biochemistry and Arterial Gases

Time:

1245

1330

1500

1715

0625

0720

Na+

143

 

141

 

 

141

K+

  5.6

 

4.5

 

 

5.3

Cl-

  106

 

108

 

 

115

HCO3-

 7.1

 

10.7

 

 

22

Glucose

 3.6

 

8.1

 

 

 5.4

Urea

 11.4

 

11.0

 

 

13.5

Creatinine

 0.30

 

 0.22

 

 

0.16

Lactate

 9.3

 

 

 

 

 

Anion gap

 30

 

22

 

 

 4

pH

 6.89

 7.14

 

 7.28

 7.38

 

pCO2

32

25

 

32

32

 

[HCO3]

5.6

8.3

 

15.2

18.4

 

pO2

244

283

 

180

144

 

Assessment

The structured assessment below is on the the FIRST set of results only (i.e. results at 1245 hours).

First: Initial clinical assessment

A metabolic acidosis is expected given the a cardiopulmonary arrest and subsequent hypotension possibly indicating poor peripheral perfusion (shock). No other acid base disorder is suggested from the history. The acute abdomen and pneumoperitoneum indicate a perforated viscus.

Second: The acid-base diagnosis

Proceeding systematically:

  1. pH: The pH is very low. A severe acidaemia results from a severe acidosis.
  2. Pattern: The pattern of decreased pCO2 and decreased HCO3 indicates either a metabolic acidosis or a respiratory alkalosis. A severe acidosis is known to be present (from the previous step) so this indicates a severe matabolic acidosis.
  3. Clues: The anion gap is 30 (=143-106-7.1) so a high anion gap metabolic acidosis is present. Lactate is very elevated. Urea and creatinine are elevated. Blood glucose is normal.
  4. Compensation: Compensation for a metabolic acidosis is hyperventilation. By rule 5, the expected pCO2 at maximal compensation is 16.4 (=5.6 x 1.5 + 8), but the time is too short for compensation to develop.
  5. Formulation: A severe metabolic acidosis that is uncompensated due to insufficient time (Respiratory compensation takes 12 to 24 hours to reach its peak value).
  6. Confirmation: No further tests to confirm the diagnosis. Urinalysis to exclude ketouria should be done.

Finally: the Clinical Diagnosis

A lactic acidosis due to poor perfusion and probable sepsis is present. The lactate level was very high indicating a lactic acidosis. Pre-renal renal failure was present and this will probably have contributed to the metabolic acidosis. As an approximate guide, acidosis (and hyperkalaemia) in chronic renal failure does not occur until the GFR is less than 20 mls/min (corresponding to a creatinine level of 0.30-0.35 mmol/l ). The creatinine level in acute renal failure will initially tend to underestimate the actual level of renal impairment as the rise in creatinine takes time to occur.

The decrement in [HCO3] is about 18 mmol/l. This matches the rise in the anion gap (ie from 12 to 30) but is more than the rise in the lactate level. This strongly suggests the presence of acid anions other than lactate. In pure lactic acidosis, the anion gap increment is usually greater than the bicarbonate decrement because of substantial intracellular buffering. The pCO2 is high for the severity of the metabolic acidosis in this patients the predicted pCO2 (by rule 5) is about 16 mmHg. It typically takes about an hour or two for much compensatory hyperventilation to occur, but 12 to 24 hours are required for full respiratory compensation. Assuming the onset of the problem was at the time of the arrest, thewn insufficient time has passed. Upper abdominal guarding due to pain has probably limited the increase in ventilation and there may be a component of respiratory acidosis in this case. The initial pH is critically low reflecting the severity of the acidosis and the lack of ventilatory compensation.

The management consisted of assessment, restoration of the circulation (with volume loading), urgent surgery and postoperative ventilatory support and monitoring in the Intensive Care Unit. It is difficult to provide adequate pain relief following major upper abdominal surgery in an elderly patient without depressing ventilation. A rise in the pCO2 would have caused worsening of the intracellular acidosis and negative inotropic effects with circulatory instability.

The mortality rate associated with a lactate level as found in this patient is about 90%. This patient survived and was discharged from hospital.

Serial results are given in the table to indicate the progression in results in this patient.