Acid-Base Physiology

Case 6 : A COAD patient with Acute abdominal pain


A 54 year old obese woman presented at night with a history of sudden onset of left upper quadrant and epigastric pain. Past history included ‘moderate chronic obstructive airways disease’ and polymyositis. She had an exercise tolerance of about 10 meters because of breathlessness. Usual medication was prednisone 5mg, nebulised salbutamol and Atrovent.

At urgent laparotomy, a perforated duodenal ulcer was oversewn. Postoperatively, she was transferred intubated and ventilated to ICU. An epidural was inserted the next morning and the patient was weaned and extubated later that day (the 15th). A frusemide infusion was commenced. She became agitated and difficult to manage about 3 days postop (on the 17th). Increasing respiratory distress developed and she was re-intubated and ventilated 4 days postop (on the 18th). Intravenous acetazolamide (1G tds) was started.

Serial Blood Gas Results in Case 6

































































The structured assessment below is on the the FIRST set of results only.

Firstly: Initial clinical assessment

A respiratory acidosis, possibly chronic (ie CO2 retention) is very likely. Acute onset of upper abdominal pain will cause increased respiratory effort and possibly a respiratory alkalosis. Excessive steroid use could cause a metabolic alkalosis. Unfortunately no drug history is given.

Secondly: The acid-base diagnosis

  1. pH: A pH of 7.39 indicates either no acid-base disorder or a mixed disorder with compensating acid-base disorders.
  2. Pattern: Both pCO2 and HCO3 are elevated: this indicates either a respiratory acidosis or a metabolic alkalosis (or both)
  3. Clues: Unfortunately, no biochemistry results are given. It is essential to have at least a set of electrolytes with urea and creatinine results.
  4. Compensation: This lady has a respiratory acidosis. If this was acute, the expected HCO3 would be 25 mmol/l (by rule 1: the 1 for 10 rule). If this was chronic, the expected HCO3 would be 28mmol/l (by rule 2: the 4 for 10 rule).
  5. Formulation: This lady has a respiratory acidosis. What are we to make of the elevated [HCO3]? The most likely situation is that she has a chronic respiratory acidosis causing this. Evidence supporting this is:
    • There is little evidence in the history of the common causes for a metabolic alkalosis (ie no vomiting, thiazide use, steroid excess syndromes) The current prednisone dose is not sufficient to cause a metabolic alkalosis
    • History of very poor effort tolerance due to breathlessness
  6. Confirmation: One way to confirm chronic CO2 retention is by checking for previous results in the patient's clinical record. In particular look for elevated bicarbonate results on biochemistry profiles. Important information to urgently check for this presentation are biochemistry results (electrolytes, urea, creatinine, anion gap) and medication history (eg for any diuretic use, recent higher doses of prednisone)

Finally: The Clinical Diagnosis

Unfortunately, interpretation of this case is made more difficult because of the lack of key information.

The most likely situation is this:

Consider the following hypothesis: The patient normally has a pCO2 of say 59mmHg with an elevated [HCO3] of 31 mmol/l (estimate using rule 2). The acute pain has resulted in a drop of pCO2 by 10mmHg and a drop in [HCO3] to 29mmol/l (estimate using rule 3). This matches the actual results for pCO2 and [HCO3]. The drop in [HCO3] has less effect on the pH than the drop in pCO2 so the pH has returned to within the normal range.

(See also Section 4.5.4)

Note that only one respiratory disorder can be present at any one time. (See section 9.4) In this case it would be WRONG to say the patient probably has a chronic respiratory acidosis (due to severe COAD) and an acute respiratory alkalosis (in response to acute painful condition). We can however consider the processes that are occurring as we attempt to understand what is happening.


The sequence of blood-gas results in this patient is interesting. While ventilated postop, the pCO2 fell to 39 mmHg and [HCO3] returned to normal. Following extubation, a severe respiratory acidosis developed over the next few days (3rd to 8th set of results). The [HCO3] increased as the acidosis became chronic because the kidneys retained bicarbonate. At 1200hrs on the 18th just before reintubation, a severe chronic respiratory acidosis was present. At this time, the maximum compensation (by Rule 2) predicted a [HCO3] = 24 + (4 x 4) = 40mmol/l. The frusemide infusion has increased the rate at which the bicarbonate level increased by adding a component of metabolic alkalosis to the picture. This explains why the maximal level of renal compensation was achieved in less than the usual 3 or 4 days.

Following reintubation and controlled ventilation, the pCO2 and [HCO3] both fell rapidly and the acetazolamide was almost certainly not required in this case. Even if a significant metabolic alkalosis was present, the preferred management is to correct the problem causing maintenance of the disorder.