Electrolytes Case 2

Answer the questions at the bottom of the page when all data has been reviewed

History & Examination

An 18 year old woman attends the ER/ED with generalised weakness and episodes of collapse without loss of consciousness. In the past 24 hours she has experienced frightening palpatations. She has spent much of her life in foster-homes and various institutions. She is not on any medications and has not noticed any GI symptoms. There is little else of note in the history.

There are no abnormal findings on examination of the systems. Her dentition is poor and there are areas of ulceration in the oropharynx. She is 5’6” tall and weighs 140 pounds. Her chest is clear. 


Course 1 Case 2 bloods

hypok now

Chest X ray requested


potassium obs

 Potassium fluid


Q1. What abnormalities are present on her blood tests?

Q2. What abnormalities are present on her EKG/ECG?

Q3. Outline the key points in her initial management.

Q4. What are the possible underlying diagnoses and how would you distinguish between them?


Q1. What abnormalities are present on her blood tests? 

1. Severe hypokalemia (serum [K+]: 1.9 mmol/l). Serum [K+] normal range: 3.5 – 5.0 mmol/l. Hypokalemia may be classified as mild, moderate or severe.

mild: 3.0 -2.4 mmol/l

moderate: 2.0 – 2.9 mmol/l

severe: <2.0 mmol/l

2. Metabolic alkalosis

C2 bloods vbg

Hopefully, you realised that this is  a ‘venous blood gas-a VBG’. This is clearly a venous sample as the pO2 is very low. We know from clinical examination and her observation chart that her chest is clear, she is not tachypnoeic and her SpO2 is normal.

The pO2 on a VBG bears no useful relationship to the paO2 on an ABG. However, VBGs are useful as the pH and bicarbonate concentration are a reliable indicator of events in the extracellular fluid (ECF) (see VBG v ABG comparison below).

In our patient, there is clear evidence of a metabolic alkalosis with a high pH associated with a high bicarbonate concentration. This is useful information. Assuming the metabolic alkalosis is secondary to the electrolyte abnormalities (very likely), it implies that the changes in electrolyte levels are not acute. They have been present long enough to allow the kidney adjust the threshold for bicarbonate excretion.Acute severe falls in K+ levels generally do not result in a pH disturbance.

There is currently a plague of VBGs in clinical practice and you will need to know about them. They are obtained by placing a venous, as opposed to arterial, sample in the blood gas analyser. The big advantage is the much lower level of patient discomfort in obtaining the sample. When you are confident that the arterial oxygenation is not a concern and are interested in the patients metabolic status, it is a very reasonable test to do.

ABG v VBG comparisons

pH is more acidic on the VBG than the ‘true’ arterial pH, add 0.035 pH units to the pH on a VBG to estimate the arterial pH.

pCO2 When above 45 mmHg (6 kPa) on the VBG, this is a reliable indicator of presence of hypercarbia (100% sensitive, allegedly).  However, the correlation between actual values above this range on a VBG and an ABG is poor. So, VBG can be used to identify the presence of hypercarbia but not to assess the response of hypercarbia to treatment.

HCO3 Decent correlation with ABG levels (+/- 6 mmol/l compared to arterial bicarbonate)

pO2 on a VBG is useless

Lactate levels on a VBG bear a somewhat complicated relationship with those on an ABG. Within the normal range of lactate concentration, there seems to be a good correlation between the two. Therefore, in clinical practice people say that if the lactate concentration on a VBG is normal, lactate will not be elevated on an ABG. Clinical experience suggests that a lactate level on a VBG above the normal range quoted for an ABG should be interpreted with caution.

Electrolytes Be careful when looking at the electrolyte concentrations on a VBG. The sample is not screened for hemolysis and release of potassium from in vitro hemolysed red cells, if present, can cause spuriously high measurements.

VBG has no role in

Analysis of mixed pH disturbances

Critically ill/Shock/ICU setting

Q2. What abnormalities are present on her EKG/ECG? 

  • Electrode misplacement
  • ‘Pseudo’ QT prolongation due to prominent U waves
  • Widespread T wave inversion


Her initial ECG (shown above) is highly abnormal. It is suggestive of the presence of hypokalemia. It also raises an interesting side issue: electrode misplacement. Electrode misplacement is common in clinical practice and can be very misleading.

Electrode misplacement


We will deal with the electrode misplacement first. Notice the curious appearance of lead III. The P waves in this lead are inverted (circle). Also, on initial analysis the T waves in the inferior leads appear to be inverted (box), although I suspect from their timing, that these are in fact U waves (vide infra). Also, the initial deflections of the qrs complex are deeply negative, are these pathological Q waves (example outlined by blue lines)? All of this is unexpected, nothing in the history points towards intrinsic heart disease. When you see this type of pattern in the standard limb leads (more negative deflections than you expect and findings out of clinical context)  always consider the possibility of electrode misplacement.

The suspicion of electrode misplacement was confirmed when a repeat ECG was performed (shown below). The morphology of lead III is completely normal on the second ECG (taken shortly after the ECG above). However, even with the electrodes correctly positioned, overall the ECG is grossly abnormal demonstrating several important findings which must not be missed.

EM repeat Csi

Aside: we can use Einthoven’s triangle to determine which electrodes were reversed on the original ECG. It is not critical but if you are interested?

ECG changes of hypokalemia

Intriguingly, the computer interpretation (CI) on her initial ECG considers her to have a markedly prolonged QT interval (circled in blue below, QTc: 643 ms). While we always look at the CI, we never completely trust it. In fact, her ECG demonstrates beautifully the phenomenon of ‘pseudo’ QT prolongation.

V4 5

She is profoundly hypokalemic and hypokalemia results in a number of ECG changes, one of which is the development of prominent U waves (illustrated in blue on the magnification above). As in this case, the U waves may fuse with the preceding T wave (outlined in red above) to generate what appears to be a prolonged biphasic T wave. The computer has been fooled, measuring the QT interval between the first thick black line and the second solid black line as illustrated above. Unlike the computer, you are aware of the clinical context and won’t fall into this trap. The true QT interval is approximated by the distance to the dotted black line. Always interpret the ECG in clinical context.

As you know, particularly in young adults, T wave inversion in leads V1 and V2 may be a normal finding (‘persistent juvenile pattern’). You will note, however, that the T waves are inverted well beyond this limit in our patient. On the first ECG they are inverted all the way out to lead V6. ST changes may be a prominent feature of hypokalemia.

Hypokalemia may result in a range of abnormalities on the ECG (illustrated below).


Q3. Outline the key points in her initial management.

1. ABC (airway, breathing circulation)

Attention to the basics of life support is essential. Remember severe hypokalemia may compromise muscle function to the extent that respiratory effort is compromised. Provided her SpO2 is satisfactory on room air I would probably not subject her to an ABG. The fact that the pvCO2 on the VBG is in the normal range for paCO2 is also to some extent reassuring that she is not hypoventilating as, in a given patient, at a given moment in time, the pvCO2 tends to be higher than the paCO2.

2. Cardiac monitor/IV access

She is at risk of arrhythmia. Also we will be giving her IV potassium (vide infra). Intravenous potassium replacement is dangerous. It can result in a rebound hyperkalemia which can induce lethal arrhythmias. The patient must be on a cardiac monitor with a trained person looking at the monitor not just the patient in the opposite cubicle.

3. Replace potassium

Protocols will differ around the world. Most cases of mild hypokalemia (3.0 – 3.4 mmol/l) will respond to treatment of the cause without potassium supplementation while in cases of moderate hypokalemia (2.5 – 2.9 mmol/l) oral replacement therapy will suffice. However, severe cases (<2.5 mmol/l) will generally require IV supplementation. Remember in hypokalemia, don’t be fooled by the absence of ECG changes. Unlike hyperkalemia, the presence or absence of ECG changes does not predict the risk of dangerous arrhythmias.

As a general rule, 20 mmol of potassium diluted in 1L normal saline is given IV over one hour. Certainly, no more than 40 mmol should be administered in one hour. Potassium should never be given by IV push.

Following administration of IV potassium, the serum potassium is rechecked. The infusion may be repeated as necessary.

4. Check serum magnesium

Low serum magnesium levels commonly accompany hypokalemia. Low magnesium levels make it difficult to correct low serum potassium levels. Serum magnesium concentration should, therefore, be checked and corrected if low.

5. Remove offending cause

If possible (not in this case).

Q4. What are the possible underlying diagnoses and how would you distinguish between them?

Until proven otherwise, this apparently normal young woman with severe chronic hypokalemia is suffering from Bulimia nervosa.

Bulimia nervosa typically begins in adolescence and has a predilection for women. The disorder is characterised by binge eating and purging. Repeated self-induced vomiting results in hypokalemia due to increased potassium losses in the urine and is associated with a metabolic alkalosis. Most patients with Bulimia are of normal weight, most have a co-existing psychiatric condition and there is an association with substance abuse. In terms of investigation, laboratory tests can help us (we should also ask her of course).

Hypokalemia investigation

Hypokalaemia is extremely common. It’s presence is often not suspected clinically and is picked up on blood tests. Hypokalemia may result in muscle weakness, which if severe, may affect ventilation. In addition, hypokalemia increases the risk of cardiac arrhythmia. The chance of these problems developing increases with the degree of hypokalemia.

Particularly in elderly patients, the cause of hypokalemia is usually obvious and the abnormality does not require extensive investigation. Diuretic therapy is a common culprit in middle aged to elderly patients while loss of potassium due to vomiting or diarrhoea is usually an obvious clinical cause in patients of any age. Therefore, in most patients and particularly the elderly, there is usually no need to chase a cause.

In the rare cases of hypokalemia where we need to look for a cause, we divide the possibilities into two categories.

1) Renal causes manifesting as loss of K+ in the urine.

2) Extra-renal causes. Usually associated with avid retention of K+ by the kidney and, therefore, low urinary K+ levels.

In theory, if we measure the urinary potassium and it is low, this implies the presence of an extra-renal cause and we investigate appropriately. If the urinary K+ is high, this implies a renal cause and we focus investigations accordingly. However, we need to be cautious. In the presence of active  vomiting, low K+ levels are actually due to loss of this cation in the urine not the vomitus and, therefore, urinary K+ levels may be high! If the bouts of purging are intermittent the urinary K+ may be low if measured  between episodes. As with many medical tests, interpretation of urinary K+ level depends on clinical context.

In this patient’s case urinary K+ was elevated. This is not inconsistent with our clinical impression of Bulimia nervosa.

We should also check:

serum magnesium: frequently low in cases of hypokalemia and can aggravate the tendency towards tachyarrhythmia.

thyroid function: T4 drives potassium into cells. It would be a shame to miss hyperthyroidism in a woman of this age.

toxicology screen: there is an association between Bulima and substance abuse.

Subsequent Course


These things rarely end well.