Electrolytes Flashcards
How do you classify hyponatraemia
By the volume:
Hypovolaemic, euvolaemic or hypervolaemic
The concentration of sodium depends on the level of both sodium and water in the body.
How much of the body is water, and what proportion of this is extracellular vs intacellular
60%- 2/3 is intracellular, 1/3 is extra
Distinguish the osmolarity and sodium concentration between intracellular and extracellular fluid
What is the most abundant anion in the extracellular vs intracellular space
Osmolarity is equal between the two
Sodium concentration is much higher extracellularly than intracellularly
But potassium and magnesium concentrations are the most common cations intracellularly
In EC space, chloride most abundant, but IC this is Po43- and negative plasma proteins
Broad two principles for hyponatraemia mechanisms, and the 3 classifications that follow
Sodium is more a measure of fluid status than salt concentration
Losing more sodium than water
Gaining more water than sodium
- Hypervolaemic hyponatreamia (gaining lots of water but small amount of sodium)
- Euvolaemic hyponatreamia (increasing H20 with a normal Na+, i.e. contrary to the name!)
- Hypovolaemic hyponatraemia (losing both sodium and water, but more sodium than water)
Causes of hypervolaemic hyponatraemia
Congestive heart failure
Cirrhosis
Nephrotic syndrome
Outline pathophysiology of hypervolaemic hyponatraemia
Leakage of fluid out into vessels leading to oedema and low circulating volume.
This causes ADH to be released which just reabsorbs water via collecting ducts
It also leads to aldosterone release, which retains Na+ but also water.
Overall, more water is gained than sodium
Causes of hypovolaemic hyponatraemia
Diarrhoea and vomiting (where enterocytes put Na+ into gut lumen, and these are not reabsorbed)
Diuretics (when Na+ remains in the tubule and goes into the urine)
Cerebral salt wasting
What type of electrolyte imbalance can cerebral salt wasting lead to and why
HYPOVOLAEMIC HYPONATRAEMIA
This condition disrupts the SNS activation of sodium reabsorption in the kidneys.
Can follow meningitis
Definition recap and causes of euvolaemic hyponatraemia
It actually means INCREASED H2O and normal Na+
The reason it’s called this is because you DON’T have fluid pouring into the interstitial space so no oedema
There are some causes with DILUTE urine (think about this as when the body has lots of water):
- Adrenal insufficiency
- Drinking too much (water, or beer!)
Some with CONCENTRATED URINE:
- Syndrome of inappropriate ADH secretion leads to H2O retention
- Hypothyroidism (mechansim not understood)
Why is there euvolaemic hyponataemia in the case of adrenocortical failure
Remember that euvolaemic hyponatraemia actually means the total body sodium is normal, but that there is just too much water (but NOT leading to oedema)
Hyponatremia is mediated by increased release of antidiuretic hormone (ADH) which results in water retention and a reduction in the plasma sodium concentration (even though there isn’t actually less Na+, because BNP is released which reabsorbs this in the PCT)
What is false hyponatraemia
Body sodium and water are normal
But excess lipids (e.g. hypertriglyveridaemia) or proteins (e.g. multiple myeloma) which affect the lab machinery to give a false hyponatraemia
Symptoms of hyponatreamia
Nausea and vomiting, muscle cramps
Sever (<120mEq/L):
1) cerebral oedema leading to confusion, coma and death
2) raised ICP, which can squash the blood vessels leading to ischaemia/herniation
Why is there cerebral oedema in hyponatramiea
Water moves from the EC to the IC compartment (cells in CNS swell up and die)
What investigations for hypotraemia
-Low serum osmolarity shows true hyponatramia
-Urine osmolality to differentiate the two types of euvolaemic hyponatramia:
(if urine really concentrated >100mOsm/kg), could be SIADH, whereas if it’s dilute it could be (<100mOsm/kg) could be due to taking in too much fluid/adrenocortical failure
-Urine Na+:
20-40mEq/l- suggests SIADH and cerebral salt wasting
-<20mEq- suggests hypovolaemia
What type of hyponatramiea do the following signs suggest:
- Oedema
- Dehydration
Odema- hypervolaemic hyponatramia
Dehydration- Hypovolaemic hyponatramia
How to manage severe hyponatraemia, why must you be careful?
HYPERTONIC SALINE
Careful to avoid cerebral pontine myelinolysis
How do you manage each of the following types of hypontraemia:
hypovolaemic
euvolaemic
hypercolaemic
Hypovolaemic: hypertonic saline infusion
Euvolaemic:
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What usually defines hyperkalaemia
Serum K+>5.5mMol/L
Categorise the causes of hyperkalaemia
- Drugs: ACEi/ARBs/Potassium sparing diurectics (spironolactone/amiloride)/NSAIDs/digoxin (in toxicity)/b blockers/trimethoprim/heparin
- Renal failure (inability to excrete K+)
- Iatrogenic:
- drugs,
- over replacement of K+ with IV fluids,
- blood transfusions gives a load of K+ - Excessive release from cells:
- Tissue necrosis (burns, rhabdo, trauma)
- Massive haemolysis (e.g. ABO incompatibility)
- Low insulin (DKA)
- Acidosis - Addison’s disease:
- Lack of aldosterone
Why does heparin/LMW
H cause hyperkalaemia
It causes hypoaldosteronism. Reduces synthesis of aldosterone and blocks ATII receptors on zona glomerulosa
Why does acidosis lead to hyperkalaemia
When the plasma becomes acidotic the body attempts to correct this by promoting muscle cells to absorb hydrogen ions out of the plasma.
This exchange mechanism involves the transfer of potassium ions into the serum, resulting in plasma K+ levels rising.
Symptoms from hyperkalaemia
- Palpitations
- Chest pain
- ARRHYTHMIAS (risk increases with values above 6.5mMol/L
TENTED T WAVES
Investigations for hyperkalaemia
U&Es (renal failure can cause)
FBCs (sudden drop in Hb in acute haemolysis)
ECG (can cause arrhythmia)
Insulin (DKA can cause it)
Serum cortisol (Addison’s disease can cause)
ABG (acidosis can cause)
ECG changes associated with hyperkalaemia
Tall tented T waves
Flattening of P waves
Broad QRS complexes
Acute management of hyperkalaemia
- IN THE EVIDENCE OF ECG HYPERKALAEMIA: Protect heart:
-10mL, 10% calcium gluconate
To stabiolise the myocardium (onset action 1-3 minutes, DOA 30-60mins) - Shift K+ into cells
-Insulin and glucose infusion (Rapidly acting insulin combined with glucose as an infusion helps drive potassium into the cells and out of the serum. The glucose is used to prevent hypoglycaemia whilst the potassium is being shifted intracellularly)
(Onset action 10-20 minutes, DOA 2-6hrs)
AND
-Salbutamol (adjuvant therapy) promites movement of potassium into cells. Onset of action 15-30 minutes. DOA- 4-6hrs
CHECK SERUM POTASSIUM AT 1 / 2 / 6 / 12 hours after treatment
Long term correction of hyperkalaemia
Consider the underlying cause
Think about common cuases:
- Have they recently had IV fluids or blood transfusion
- Are they taking any causative drugs
- Renal impairment
- Acidotic (ABG)
What happens to the total body calcium following acute hyperkalaemia management
Acute management provides only temporary reduction of K+ levels via shifting K+ out of the plasma and into cells, meaning total body K+ levels remain unchanged. As a result, the patient will likely become hyperkalemic once again if the underlying cause is not treated.
Thus you need to assess underlying cause
Any long term hyperkalaemia management medication (other than treating cause)
Calcium resonum
not 1st line.
Proivdes slow method of reducing K+ levels, by binding K+ in the bowel and preventing its reabsorption
Used in patients with resistant hyperkalaemia who require long term management
Most commonly used in those with chronic renal failure
As mentioned above, senior input should be sought before using this drug
As with all drugs that lower K+, there is the risk of causing hypokalaemia
Intermittent confusion, non-specific abdominal pain and constipation is highly suggestive of what electrolyte imbalance
Hypercalcaemic crisis
Why can hyponatraemia be fatal if severe
Severe hyponatraemia is defined as serum sodium < 120 mmol/L and is associated
with neurological symptoms such as seizures, hallucinations, confusion and memory
loss. Hyponatraemia can be fatal if the serum sodium drops acutely over 24-28
hours as this can lead to cerebral oedema, coning and respiratory arrest.
What might lead to an erroneously low sodium reading
The presence of high levels of lipids
or proteins in the sample, which dilutes the aqueous component of the extracellular
compartment thereby decreasing the apparent sodium concentration.
What are the signs of central pontine myelinolysis
Paralysis, dysarthria and dysphagia
