Clinical Details
A 67 year old man presented to a peripheral hospital with a 3 day history of lethargy, vomiting, fever with rigors and increasing dyspnoea. A dry cough was present. There was no pleuritic pain. He was described as a 'previously healthy heavy smoker'. There was a past history of osteoarthritis treated with simple analgesics. No other medication.

On examination, he was sweaty, pale and acutely dyspnoeic. T 38.4C BP 104/70. Pulse oximetry reading was 62% on room air. Bilateral bronchopneumonia was present on chest xray.

Initial pathology: Hb 147 g/l, Na 137, K 4.3, Cl 96, total CO2 32, glucose 7.3, urea 10.2, creatinine 0.11 mmol/l.

Initial arterial gases in table below. He was then intubated and ventilated and transferred to a larger hospital.

The serial results in the table indicate when various significant interventions occurred. A potassium infusion was used when acetazolamide was administered. The patient also received naloxone during this period.

Serial Results & Events in Case 18
Date	Time	pH	pCO2	HCO3	Cl-	K+
29/8	Initial gases	7.29	63		96	4.3
Intubated & ventilated
29/8	1600 hrs	7.32	59.3	29.9
30/8	0620	7.41	50	31.1
	2155	7.34	55.5	29.2
31/8	0640	7.35	58.7	31.5
01/9	0440	7.40	56.7	34.5
Extubated
01/9	0945	7.42	54	34.4
	1700	7.42	61.7	38.9
	2220	7.43	63.3	40.8
02/9	0145	7.38	71.8	41.0
	0900	Acetazolamide 1G IV			98	4.2
	1440	7.38	56.4	32.7	101	3.1
	1500	Acetazolamide 1G
	2100	Acetazolamide 1G
	2230	7.36	49.7	27.5
03/9	0300	Acetazolamide 1G
	0415	7.33	47.3	24.1
04/9	0850	7.42	36.2	22.9	113	3.7
06/9					105	3.4
07/9	Discharged home

Assessment
Firstly, initial clinical assessment (on the first gas results):
A respiratory acid-base disorder is suspected in view of the respiratory distress & low pulse oximeter reading.

Secondly, the acid-base diagnosis:

to be completed
 

1. pH:  
2. Pattern:  
3. Clues:  
4. Compensation:  
5. Formulation:  
6. Confirmation: 

Finally, the Clinical Diagnosis:

Comments
An acidaemia with a significantly elevated pCO2 on the initial gases confirms the clinical suspicion of a respiratory acidosis. The expected bicarbonate would be 26 mmol/l for an acute respiratory acidosis (by rule 1) and 32 mmol/l for a chronic respiratory acidosis (by rule 2). The history does not suggest that this patient has severe chronic airway disease with CO2 retention so the elevation of the [HCO3] has occurred since the onset of the patient’s illness. The actual bicarbonate is a few mmol/l higher than expected with acute respiratory acidosis and this may be due to renal retention of bicarbonate due to a couple of days of elevated pCO2. The clinical diagnosis is an acute bronchopneumonia resulting in acute respiratory failure. The anion gap is not elevated.

The respiratory acidosis worsens following extubation and the bicarbonate level increases significantly. The rise in bicarbonate is rapid and sufficient to keep the pH in the normal range so it is more than the rise expected with acute compensation. This suggests the presence of an acute metabolic alkalosis though the particular cause is not evident from the details given. [K+] and [Cl-] levels are normal.

The carbonic anhydrase inhibitor acetazolamide has been given and the total dose used in this case is excessive. This has resulted in hypokalaemia and a hyperchloraemic metabolic acidosis with a fall in [HCO3]. The result of this (and the naloxone) has been respiratory stimulation and arterial pCO2 has fallen to normal levels in about 30 hours. The naloxone was used to counteract residual effects of narcotic infusion given during the period while the patient was ventilated.

A pulse oximeter reading of 62% is outside the calibrated range but clearly the patient is hypoxaemic on presentation as confirmed on the initial gases.

With significant acute respiratory failure with hypercapnia the kidneys start retaining bicarbonate and this takes several days to reach maximal levels. The respiratory acidosis in this patient is changing from acute to chronic as bicarbonate is retained.

Metabolic alkalosis may develop in ICU for multiple reasons:

use of diuretics

secondary hyperaldosteronism due to low effective circulating intravascular volume

metabolism of citrate following massive blood transfusion

administration of NaHCO3 (eg for management of hyperkalaemia or metabolic acidosis)

development of hypoalbuminaemia

loss of gastric secretions via nasogastric drainage

‘post-hypercapnic alkalosis’

A rise in [HCO3] in compensation for a chronic respiratory acidosis is not a metabolic alkalosis as it is a secondary process but it certainly contributes to any rise in [HCO3] which is occurring for other reasons such as those listed above. Following correction of the hypercapnia (eg with intubation and ventilation), the [HCO3] may remain elevated under certain conditions (eg chloride deficiency, hypovolaemia, reduced GFR). This abnormal situation where the bicarbonate level remains elevated following correction of a respiratory acidosis is often referred to as ‘post-hypercapnic alkalosis’.

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