Electrolyte and Acid-Base Flashcards
What is the normal range for serum K+?
Potassium is the most abundant intracellular cation with serum concentration kept at 3.5 - 5.0 mmol/L.
Define hyperkalaemia
Moderate hyperkalaemia is defined as serum potassium value >5.0mmol/L.
Significant hyperkalaemia is potassium >6.0mmol/L.
What is the aetiology of hyperkalaemia?
The main causes of hyperkalaemia can be split into ineffective elimination or excessive release from cells.
We consume around 50-150 mmol/L of K+ every day, but only need a plasma concentration of 5.0 mmol/L. This means we need to excrete a lot of potassium. Hyperkalaemia can be caused by ineffective elimination of potassium due to:
- Acute or chronic renal insufficiency - AKI, diabetic nephropathy, CKD.
- Drugs that inhibit potassium excretion such as ACE inhibitors, potassium-sparing diuretics, NSAIDs, trimethoprim. (The combination of ACEi with either NSAIDs or Potassium-sparing diuretics is dangerous).
- Adrenal insufficiency (Addison’s disease, Congenital Adrenal Hyperplasia).
The concentration of K+ inside cells is around 150 mmol/L to set up a strong electrochemical gradient with the extracellular K+ concentration of around 4.5 mmol/L. Hyperkalaemia can also be caused by excessive release from cells:
- Acidosis (metabolic more so than respiratory) as K+ leaves the cell to act as a buffer. To compensate, H+ are moved from the plasma into the cells via H+/K+ co-transporters, causing increased K+ outside the cell. Less pronounced in respiratory acidosis as CO2 can feely move into cells.
- Insulin deficiency -insulin increases Na+/K+ pump function. Without this, less K+ is pumped into the cell, and more K+ leaves the cell.
- Acute digoxin poisoning
- Cell lysis due to severe burns, rhabdomyolysis and chemotherapy.
- Exercise temporarily increases K+. Usually this shift is small, but if combined with other factors, can cause hyperkalaemia.
What are the clinical features of hyperkalaemia?
Serum potassium >7.0mmol/L is a medical emergency and has ECG changes.
Muscle weakness is often the only symptom before cardiac arrest. However, if the cause is due to metabolic acidosis, the patient may exhibit Kussmaul respiration.
Severe hyperkalaemia predisposes to asystolic cardiac arrest. It causes widespread cell depolarisation, leading to decreased cardiac excitability, hypotension,bradycardia and eventually asystole. Bradycardia is often fatal on its own!
Describe the ECG changes seen in hyperkalaemia
An ECG may show changes consistent with hyperkalaemia, which progress with increasing hyperkalaemia:
- Tended T waves (b)
- Reduced P wave with widened QRS complex (c)
- ‘Sine wave’ pattern - pre cardiac arrest (d)
The ECG tends to show bradycardia even without these changes.
Describe the management of hyperkalaemia
Hyperkalaemia is a medical emergency. After fitting the patient with a cardiac monitor, administer:
- Calcium chloride (acute) or calcium gluconate (10ml 10%). It has no effect on plasma potassium, but has an effect on cardiac excitability and treats bradycardia. Works quickly
- 100ml 20% dextrose + 10 units of insulin causes short-term shift in potassium from extracellular to intracellular fluid compartment. Takes half an hour to work and works for 4 hours before potassium starts leaking out.
- 1/2 L of sodium bicarbonate if there is metabolic acidosis. If the patient is acidotic, we may start with this, and may not need the other two.
Then treat the underlying cause.
Define hypokalaemia
Hypokalaemia is defined as a serum potassium level of <3.5mmol/L.
What is the aetiology of hypokalaemia?
Hypokalaemia is mainly caused by either increased potassium entry into cells, and increased excretion of potassium. Very rarely caused by decreased consumption (anorexia).
Increased potassium entry into the cells can occur via various mechanisms:
- Alkalosis (metabolica nd respiratory less so). As H+ leave the cells to compensate, K+ enters the cells to balance electroneutrality.
- Increased beta-adrenergic activity due to beta-adrenergic agonist or catecholamine release during stress. Catecholamines promote the entry of K+ into the cell by increasing the Na+/K+ pump.
- Increased insulin- often if a patient with diabetes takes too much insulin. Insulin also increases Na+/K+ pump action.
Increased excretion of potassium can occur by:
- Hyperaldosteronism (Conn’s syndrome) - extra aldosterone causes increased K+ excretion.
- Diuretics (particularly thiazides and loop diuretics) as these work by inhibiting Na+ reabsorption. However, this delivers more Na+ further downstream the nephron to the principle cells, causing increased Na+/K+ exchange - and more K+ in the urine. Furthermore, as there is more urine in the tubule, the K+ concentration is lower, allowing more K+ to escape via diffusion.
- Vomiting - not much K+ is lost directly, however loss of stomach acid causes metabolic alkalosis, which causes more K+ to leave the plasma.
- Diarrhoea - more potassium is excreted with faeces, so there is more direct loss. This may be due to infection, IBD etc.
- Sweating - exercise in a hot country can cause excess sweating and thus K+ loss.
What are the clinical features of hypokalaemia?
Hypokalaemia causes hyperpolarisation of cells, and therefore reduced contractility. This is felt as muscle weakness.
Hypokalaemia may also cause symptomatic hyponatraemia. They may also have polyuria and polydipsia because hypokalaemia is a cause of nephrogenic diabetes insipidus.
Describe the management of hypokalaemia
Treat the underlying cause such as stopping diuretics or treating vomiting. If diuretic therapy is needed, switch to potassium-sparing diuretics. Acute hypokalaemia may correct spontaneously.
Replace potassium:
- If the serum potassium is between 3.0-3.5 mmol/L- give oral potassium chloride (two SandoK tablets twice daily for 48h). Recheck serum potassium.
- If their serum potassium is below 3.0 mmol/L- give IV potassium chloride at a maximum rate of 10 mmol/h. If you need to give at a greater rate, give via central line as potassium is highly irritating to peripheral veins.
Treat underlying cause.
What investigations would you perform for hypokalaemia?
- Take a thorough history and double check for vomiting or gastrointestinal loss.
- Take a drug history and look for redistribution into cells
ECG features of hypokalaemia:
- U waves (see picture)
- Small or absent T waves (occasionally inversion)
- Prolong PR interval
- ST depression
- long QT
If a patient has hypokalaemia and hypertension (points to hyperaldosteronism) check their Aldosterone:Renin ratio.
What are the ECG features of hypokalaemia?
ECG features of hypokalaemia:
- U waves (see picture)
- Small or absent T waves (occasionally inversion)
- Prolong PR interval
- ST depression
- long QT
