T4: Potassium and Hydrogen Ion Homeostasis

Question 1

What is the normal reference range for potassium?

Answer 1

Potassium reference is 3.6 - 5.0 mmol/L.

Values below 3 and above 6 are seriously dangerous. This can lead to cardiac condition defects and abnormal neuromuscular excitability. Many causes are iatrogenic and avoidable.

Question 2

Give examples of situations that can affect serum plasma potassium concentration?

Answer 2

Exchange between intracellular fluid and extracellular fluid significantly affects plasma potassium.
Affected by:
- Acidosis
- Insulin/glucose therapy - this takes potassium into the cell as a transporter - can be useful as a treatment measure
- Adrenaline
- Rapid cellular incorporation - total parental nutrition, can sometimes cause potassium depletion as the cells are going so fast and using up potassium. Also in leukaemia.

Question 3

What is the relationship between potassium and hydrogen ions?

Answer 3

In the cell we have proteins with negative charges on. These negative charges are filled up by potassium ions, hydrogen ions and calcium ions. Changes in pH causes shift in the equilibrium. A change in hydrogen ion displaces the potassium level.

- Acidosis - potassium moves out of the cell - hyperkalaemia 
- Alkalosis - potassium moves into the cell - hypokalaemia

Question 4

Give examples of causes of hyperkalaemia.

Answer 4

Causes of hyperkalaemia:

- Hyperkalaemia is seen very frequently as we can get delayed delivery of the sample. Since it has been sitting around, there may have been haemolysis or the red cell leakage as the red cells are filled with potassium
- Haemolysis can lead to hyperkalaemia. People often use small needles when taking out blood, as the cells goes through the tub, the cells can break up on the edge due to the shear force. The sample then has haemolysis. This can be picked up by a detector. Sometime it is not evident and so we can get falsely high values. 
- Drug therapy - excess in take 

- Renal failure - acute and chronic renal failure. In an acute phase, we are more worried.  In chronic renal failure, the patient usually compensates. 
- Acidosis (intracellular exchange)

- Mineralocorticoid dysfunction - adrenocorticoid failure. Angiotensin is not produced. Angiotensin, increases blood pressure and reduces sodium. It also promotes a diuresis of potassium, protecting against hyperkalaemia. Adrenal failure form excess corticosteroids, treatment of the pituitary and Addison's disease. This is usually chronic. Once treated this it can get better.
- Spironolactone is a potassium sparing diuretic. This can lead to a high potassium  Cell death - cytotoxic therapy. This is seen in oncology wards.

Question 5

What is the treatment of hyperkalaemia?

Answer 5

Treatment of hyperkalaemia

- Correct acidosis if this is the cause
- Stop unnecessary supplements/intake 
- Give glucose and insulin - drive potassium into the cells 
- Ion exchange resins - GIT potassium binding 
- Dialysis - short and long term

Question 6

Give examples of causes of potassium depletion.

Answer 6

• Low intake - a poor diet as we will always lose potassium in urine
  
  • Increased urine loss - diuretic/osmotic diuresis (diabetes), tubular dysfunction (intrinsic renal problems, missing pumps) and mineralocorticoid excess (Cushing’s or Conn’s or high dose therapy).
    Around 10% of patients in the hospital will have an iatrogenic ion disturbance.
  • GIT losses - vomiting, diarrhoea/laxatives and fistulae (bypassing of gut)
    Hypokalaemia without depletion - alkalosis and insulin/glucose therapy - the glucose has been shifted in the cells

Question 7

What are the effects of potassium depletion?

Answer 7

The main effects of potassium depletion (<2.5 mmol/l)

- Acute changes in Intracellular fluid: Extracellular fluid ratios
- Neuromuscular effects include lethargy, muscle weakness and heart arrythmias. 
- Chronic losses from the ICF: lethargy, muscle weakness and heart arrythmias. This can be quiet debilitating or elderly patients for example those on too many diuretics.
- Potassium depletion can mean the kidney does not function well leading to polyuria which can exacerbate the situation 
- Renal acid base disturbances can lead to alkalosis as it affects the way bicarbonates are produced 
- Effect on the vascular system
- Effect on the gut - if very depleted you can get an ileus - this is status of movement of the bowel and often needs suction to get the excess fluid out and ions to move the fluids again

Question 8

How do we detect potassium depletion?

Answer 8

Detection - a high index of clinical suspicion is required
History:
- Diarrhoea, vomiting and drugs (diuretics and digoxin)
- Symptoms of lethargy/weakness
- Cardiac arrythmias
Electrolyte investigation
- Hypokalaemia
- Alkalosis - raised bicarbonate
It is easy to be missed. Regular samples of patients on drips must be taken.

Question 9

Diagnose the following clinical problem:

Patient has Hypertension & Hypokalaemia

Plasma
Na 150 (135-145 mmol/L)
K 2.5 (3.0-5.0 mmol/L)
Urea 5 (3.0 - 8.0 mmol/L)

Urine
Na 5 mmol/L
Urea 50 mmol/L

Answer 9

The kidneys are working. We know this as the urea ratio is 10:1, they are concentrating urine nicely. They are also producing urine. High plasma sodium and a low urine sodium. They have high aldosterone - they are retaining sodium, hypertensive and hypokalaemia. The sodium in the urine should be higher since the sodium level is high in the blood. This is an example of Con’s syndrome - a tumour producing aldosterone in the adrenal gland.

Question 10

Explain the illustrative case:

A 16 year old admitted in coma with a history of severe weight loss, thirst and polyuria over the previous 4 weeks.

Initial tests
Glucose 	35.0 (3.5 - 5.5 mmol/L)
pH	7.01	(7.38 - 7.42)
[H+]  100	(35 - 45 nmol/L)
Sodium 130 (135-145 mmol/L)
Potassium 6.7	(3.5 - 5.0 mmol/L)
Urine ketones +++

Answer 10

The patient is acidotic. Plasma potassium is outside the reference waste. They have thirst and polyurea. The total body potassium is depleted as all the extra potassium is being lost. The intracellular potassium is lower than it should be.

Once you correct acidosis, by giving insulin and stopping ketone break down, potassium suddenly moves into the cell. They then become suddenly hypokalaemia. They can then become hypokalaemia and die. You should therefore start the potassium infusion when the acidosis is correcting and push potassium over the insulin and saline to rehydrate. You then measure potassium continuously to feed back the potassium at the rate of loss.