Question 4

The following arterial blood gas and biochemistry results are from a patient  with chronic cardiac and respiratory disease and recent profuse vomiting.

FiO2   0.4  
pH   7.5  
PaO2                     58.0 mmHg  
PaCO2                  47.0mmHg  
HCO3-                 34.8 mmol/L (22 - 27)
BE 10.2 mmol/L   (-2.0 to +2.0)
Na+ 137mmol/L (135 - 145)
K+ 2.5mmol/L (3.5 - 5.0)
Cl-             92mmol/L   (95 - 105)

a)  Describe the acid-base and the metabolic disturbance.

b)  List the potential causes of these abnormalities in this patient.

c)  Outline the management of the metabolic and acid-base disturbance

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College Answer

The major abnormalities are:

a)  Metabolic alkalosis with respiratory compensation

b)  Hypokalemia and hypochloremia

c)  Normal anion gap

d)  An increased apparent strong ion difference [(Na + K) – Cl] = 47

Possible causes in this patient include

a)  Diuretic therapy

b)  Steroid therapy

c)  Vomiting from gastric outlet obstruction

d)  Post hypercapnic alkalosis

Outline the management of the metabolic and acid-base disturbance.

1) Normal saline administration

2) K supplements

3) Acetazolamide


Let us dissect these results systematically.

  1. The A-a gradient is high:
    PAO2 = (0.4 × 713) - (47 × 1.25) = 226.45
    Thus, A-a = ( 226.45 - 58) = 168.mmHg.
    But you did not need to know the A-a gradient to recognise that the patient is hypoxic.
  2. There is alkalaemia
  3. The PaCO2 is compensatory
  4. The SBE is 10.2, suggesting a metabolic alkalosis
  5. The respiratory compensation is adequate - the expected PaCO2( 0.7 × 34.8) + 20 = 44.4mmHg, and this falls within the +/- 5mmHg error range of this blood gas rule. If we were to use the Copenhagen rules, the expected PaCO2 would be around 50mmHg (40+ SBE).

Thus, this is a reasonably well compensated metabolic alkalosis.

There is also hypochloraemia and hypokalaemia.

The patient has chronic cardiac and respiratory disease, and has been vomiting.

Thus, the broad list of potential causes of metabolic alkalosis can be narrowed to the following:

  • Diuretics (for CCF)
  • Corticosteroids (for COPD)
  • Gastric secretion loss though vomiting
  • β-lactam use (for exacerbation of COPD)
  • Post-hypercapneic alkalosis is possible, but less likely (because this metabolic alkalosis is well-compensated, and with post-hypercapneic alkalosis the respiratory compensation is by definition inadequate, i.e. the calculated "expected" PaCO2 should be higher than the measured PaCO2)

The college then go on to suggest three uninspired management options. For instance, they want to replace potassium, which is a sensible reaction to a low potassium, but not an elegant solution to any underlying problem. Similarly, acetazolamide and sodium chloride may seem essentially cosmetic measures, as they only serve to improve the appearance of the blood gas. 

Management of metabolic alkalosis is discussed in greater detail elsewhere. Most of the detail can be found in the following literature sources:

In brief:

  • Address the underlying problem:
    • Stop the diuretics, treat the hyperaldosteronism, etc etc.
  • Correct volume depletion - ideally with normal saline
  • Correct hypokalemia - ideally with potassium chloride
  • Alternative strategies if the patient is fluid-overloaded:
    • Acetazolamide
    • Hydrochloric acid (HCl)
    • Infusions of cationic amino acids such as lysine and arginine
    • Correction of hypoalbuminaemia


Tripathy, Swagata. "Extreme metabolic alkalosis in intensive care." Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine 13.4 (2009): 217.


Galla, John H. "Metabolic alkalosis." Journal of the American Society of Nephrology 11.2 (2000): 369-375.


Pahari, D. K., et al. "Diagnosis and management of metabolic alkalosis."JOURNAL-INDIAN MEDICAL ASSOCIATION 104.11 (2006): 630.


Palmer, Biff F., and Robert J. Alpern. "Metabolic alkalosis." Journal of the American Society of Nephrology 8.9 (1997): 1462-1469.


Gennari, F. John. "Pathophysiology of metabolic alkalosis: a new classification based on the centrality of stimulated collecting duct ion transport." American Journal of Kidney Diseases 58.4 (2011): 626-636.


Ferrara, A., et al. "[Physiopathological and clinical data on post-hypercapnic metabolic alkalosis. A case of severe hypercapnia treated with drugs and in an" iron lung"]." Minerva medica 70.1 (1979): 67-73.


Banga, Amit, and G. C. Khilnani. "Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay." COPD: Journal of Chronic Obstructive Pulmonary Disease 6.6 (2009): 437-440.

Webster, Nigel R., and Vivek Kulkarni. "Metabolic Alkalosis in the Critically III." Critical reviews in clinical laboratory sciences 36.5 (1999): 497-510.