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

Parameter Patient value    Normal range
 FiO2                                0.4  
  pH                                        7.5                               7.35 – 7.45        
 PaO2                                         58.0 mmHg (7.6 kPa)          
 PaCO2                                  47* mmHg (6.2 kPa)           35 – 45 (4.6 – 6.0)     
 HCO3                                      34.8* mmol/l                22 – 27    
Base Excess               10.2*                  -2.0 – +2.0         
Sodium                        137 mmol/l                  135 – 145               
 Potassium                        2.5* mmol/l                  3.5 – 5.0                
 Chloride                       92* mmol/l                  95 – 105                     

a) Describe the acid-base disturbance(s)

b) List the potential causes of the acid-base abnormalities in this patient

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College Answer

a)
Metabolic alkalosis with respiratory compensation 

b)
Diuretic therapy 
Steroid therapy 
Vomiting from gastric outlet obstruction 
Post hypercapnoeic alkalosis

 

Discussion

This question is a fairly straightforward ABG interpretation exercise.

I could add nothing more to these answers. The question plainly states there has been profuse vomiting.

Let us dissect these results systematically.

  1. The A-a gradient is high:
    PAO2 = (0.4 × 713) - (47 × 1.25) = 155.05
    Thus, A-a = (155.05 - 58) = 97.05mmHg.
  2. There is alkalaemia
  3. The PaCO2 is compensatory
  4. The SBE is 10.2, suggesting a metabolic alkalosis
  5. The respiratory compensation is reasonable - the expected PaCO2(0.7 × 34.8) + 20 = 44.36mmHg, which is within +/- 5mmHg of the recorded value
  6. The anion gap is normal: (137) - (92 + 34) = 11, or 13.5 when calculated with potassium

Thus, this patient has a metabolic alkalosis - likely due to vomiting. A diagnostic approach to metabolic alkalosis is offered elsewhere, and goes through this in some detail. In brief, potenial causes include the following:

  • Gastric losses by vomiting or drainage
  • Diuretics:
    • loop diuretics
    • thiazides
  • diarrhoea
  • posthypercapneic state (chronic compensatory renal loss)
  • Primary hyperaldosteronism
  • Mineralocorticoid oversupplementation
  • Licorice (glycyrrhizic acid)
  • β-lactam antibiotics
  • Liddle syndrome
  • Severe hypertension
  • Bartter and Gitelman syndromes
  • Laxative abuse
  • Clay ingestion
  • Recovery from starvation
  • Hypoalbuminemia
  • Hypercalcemia of malignancy
  • Milk-alkali syndrome

References

References

Khanna, Apurv, and Neil A. Kurtzman. "Metabolic alkalosis." J NEPHROL 2006; 19 (suppl 9): S86-S96

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.