Dr Binula Wickramarachchi

Emergency Registrar

Peer review: Dr Laura Murphy

It’s 4:20am on a night shift, and you’ve finally caught up with the waiting patient list. Just as you’re thinking about where you could source some caffeine, you see a 26 year old male come up on the screen. The triage note reads: “2/7 epigastric pain, can’t sleep tonight”. You barely get a chance to chart the pink lady when a nurse places a venous gas result in front of you. You’re ecstatic, as you realise you might actually be able to use some of those equations you’ve been memorising for your fellowship exams.

What do you do with a metabolic alkalosis?

Is there appropriate respiratory compensation?

The calculation for this is:

Expected PCO2 = (0.7 x HCO3) + 20 = (0.7 x 39) + 20 = 47

The patient’s PCO2 is 37, therefore there is inadequate compensation or a concurrent respiratory alkalosis

The K+ is 2.1! Is this appropriate for the extent of alkalosis?

Correct the K+ for the extent of alkalosis:

Expected K+ for alkalosis = 5 – (1 for every 0.1 increase in pH x 0.5)

There has been a ~0.2 change in pH (7.62 – 7.40), therefore:

Expected K+ = 5 – (2 x 0.5) = 5 – 1 = 4

So the expected K+ level for this pH is 4.0. The above level of 2.1 means the patient is profoundly hypokalaemic.

Why is the chloride so low?

The most common causes for a low chloride that we would see in the ED are due to increased losses: vomiting, sweating or diuretic use. Chloride also tends to move in an opposite direction to HCO3, so the alkalosis itself will also be a contributing factor. Feeling pretty chuffed with yourself for remembering all the equations, you decide to actually go assess the patient.

What are the important differentials to consider?

Going back to basics, metabolic alkalosis can be considered in terms of loss of acid (gastrointestinal or renal) or gain of bicarbonate (exogenous or related hypokalaemia/hypochloraemia). Another approach is to measure the urinary chloride and classify the cause according to that (see references below), but I find the differential tree below a bit more straightforward to start with. Another important concept to keep in mind is that metabolic alkalosis requires both of: 1) an initiation factor, and 2) a maintenance factor that prevents the kidney from correcting the imbalance by excreting excess HCO3. There are a number of processes that can act as maintenance factors, some of which include potassium/chloride depletion, hypovolaemia and steroid use.   The patient tells you that he’s had sharp, constant epigastric pain for the last 2 days, with 3 to 4 vomits each day. His abdominal examination is benign, and bloods including LFT’s, renal function and lipase are unremarkable. On enquiring about whether he takes any medication, he tells you that a friend told him that bicarb soda mixed with water was great for reflux, so that’s all he’s been having for oral fluids through this time!

Putting it all together

The initiation factor in this case was the patient’s exogenous bicarbonate ingestion. Though small to moderate amounts of this would’ve been excreted by the kidney, the hypokalaemia and hypochloraemia caused by the patient’s vomiting would have acted as the maintenance factors that propagated the metabolic alkalosis. The relative respiratory alkalosis in this case was likely related to hyperventilation secondary to pain, as no other concurrent cause was apparent.

Are there any consequences of having metabolic alkalosis?

HCO3 levels below 40 are usually asymptomatic. Levels above 50 can however cause a number of serious complications including severe hypoventilation, decreased cardiac contractility and output, arrhythmias and seizures.


Management, in this case, was to replace potassium and chloride (ideally using IV potassium chloride) and fluid resuscitate using 0.9% NaCl. As the patient had normal renal function, the correction of serum potassium and chloride will allow restoration of the renal excretion of HCO3, consequently resolving the metabolic alkalosis. In more severe or refractory cases, IV acetazolamide may also be used to increase urinary excretion of bicarbonate.

Patient Outcome

The patient was treated with normal saline, with all electrolytes replaced, and their metabolic alkalosis resolved within 24 hours. An abdominal ultrasound was performed which was also unremarkable, and the patient was discharged on a course of pantoprazole and advised to use bicarbonate sparingly in the future!



  1. Galla, J. H. (2000). Metabolic alkalosis. Journal of the American Society of Nephrology11(2), 369-375. Access via DOI: https://doi.org/10.1681/ASN.V112369
  2. Emmett, M. (2020). Metabolic alkalosis: A brief pathophysiologic review. Clinical Journal of the American Society of Nephrology15(12), 1848-1856. Access via DOI: https://doi.org/10.2215/CJN.16041219
  3. EMCRIT: Metabolic Alkalosis – https://emcrit.org/ibcc/metabolic-alkalosis/
  4. Deranged Physiology – Causes of metabolic alkalosis – https://derangedphysiology.com/required-reading/acid-base-disorders/Chapter%20241/causes-metabolic-alkalosis
Binula Wickramarachchi

Binula Wickramarachchi

Emergency Registrar | Education Fellow

Binula is an Emergency Advanced Trainee and Education Fellow at the Alfred Hospital. He grew up among the verdant hills of Auckland, New Zealand, obtaining his medical degree and Postgraduate Diploma in Clinical Education at the University of Auckland. He also has a passion for point of care ultrasound, particularly echo and lung ultrasound.

At home, Binula is a devoted parent to his two feline daughters, and is the household co-lead for the acclimatisation to a new human child.