Clin Path: Potassium balance Flashcards
What are the normal serum Potassium Levels
3.5 - 5.3 mmol/L
What are the three mechanism by which Potassium levels can change in the body
In order of importance:
Kidney -Retention and excretion of Potassium in the loop of henle
Intracellular/extracellular movement
GI absorption/Loss
What regulates Kidney excretion of potassium
The Renin-angiotensin-aldosterone system (RAAS)
Renin excreted from JGA (in response to Low Na or low BP) converts angiotensiogen to Ang-1
Ang 1 is converted to Ang-2 by ACE in the lung
Ang-2 induces Aldosterone release by the Adrenals
in turn, aldosterone causes increased Na+ intake by the cells.
this causes an electrical imbalance with the lumen (becoming more -ve). K+ travels down the gradient (to equilibrate) into the lumen and is excreted
High potassium can also directly induce Aldosterone production
What are the main causes of Hyperkalemia
Renal Impairment
Medication
Low aldosterone
release from cells
Hyperkalemia is mostly caused by low/improper aldosterone-either an issue with the RAAS or the Aldosterone receptors
Renal impairment- Low GFR causes reduced JGA flow- limits renin production
Similarly, NSAIDS and T4 tubular acidosis can directly reduce Renin production
Medication- all those reducing the RAAS - antihypertensives (e.g.: ACEi or ARB’s) or Spirolactone (Aldosterone antagonist)
Low aldosterone can also be caused by -addisons disease /hypoaldosteronism
Extracellular release -
rhabdomyolysis- cellular death causes release of k+
Acidosis- K+ is released to counter the pH
Why does low aldosterone cause hyperkalemia?
When K+ is high, aldosterone is produced to increase its excretion by the kidneys
When aldosterone production is blocked (by having an inefficient RAAS system), or by blocking its receptors, there is no increase possible to excrete the K+ -leading to hyperkalemia
What are the ECG changes associated with hyperkalemia
Peaked T waves (early sign) Broad QRS (more than 120ms) Flat p-waves Prolonged PR interval and bradycardia Sine wave
What is the immediate management of hyperkalemia
1 protective, 2 to reduce K+
Protective -10ml of 10% 1) calcium gluconate -protects myocardium of the heart
Reduce K+ -
1) 10U of insulin -
Need to give sugar to not get hypoglycemia -100ml of 20% Dextrose *
2) Nebulised Salbutamol
Treat Underlying cause
- old text books might mention 50ml of 50% dextrose but rarely used in practice
What are the causes of Hypokalemia
GRRR
1) GI-Gi loss via vomiting and diarrhoea
2) Renal losses-
MR excess -cushings, Conns,
Excess Na delivery to distal collecting tubule
Osmotic diuresis
3) redistribution within cells
Insulin/insulinomas
B-agonists
Alkalosis
4) rare causes:
Renal tubular acidosis T1/2
Hypomagnesia
Why does excess Na in the tubular cause Hypokalemia?
Usually this is caused by a diuretic -either the triple transporter (frusemide) or co-transporter (thiazides_ is blocked.
This leads to increased levels of Na in the distal collecting tubule
The Na is reabsorbed efficiently, but causes a more -ve lumen -which leads to potassium excretion and loss down the lumen
What are the clinical features of Hypokelmia?
Muscle weakness
Cadiac arrhythmia
ECG changes- ST depression, flat T waves and U waves
Polyuria and Polydypsia (caused by nephrogenic DI)
What is a diagnosis that needs to be investigated in a patient with Low K+ and Hypertension? What is the gold standard investigation?
if this patient is not taking any medication:
Must exclude CONN’s syndrome
aldosterone: renin ration is gold standard -the ratio would be RAISED in Conn’s
How do you manage hypokalaemia?
Mild- 3.0-3.5mmol/L
Oral SandoK supplements But needs monitoring of K+ levels
Severe (<3.0)
IV KCL at a max rate of 10mmol/h in peripheral veins
+ treat underlying cause
