Electrolyte distrubance Flashcards
Discuss the effects of hyperkalaemia on the ECG
Potassium is vital for normal electrical activity of the heart. Hyperkalaemia leads to mycocardial excitability while depressing pacemaker cells and conduction tissue
Leads to suprression of impulse by the SA and progressive blocking of the AV node and purkinjes leading to bradycardia and conduction blocks and ultimately cardiac arrest
K>5.5 peaked T waves
K>6.5 associated with progressive paralysis of the atria - P wave widens and flattens, PR sement lengthens and p wave eventually disappear
K>7 – Prolonged QRS with bizarre morphology, high grade AV block with slow junctional and AV escape rhythm - leads to any conduction block, slow AF, SINE wave preterminal
K> 9 - asystole, VF, PEA with bizarre wide complex rythym
Discuss the effects of hypokalaemia on the ECG
Decreased extracellular potassium leads to an increase in hyperexcitability with the potential to develop re-entrant arryhthmias
ECG changes begin when K+ <2.7
- Increased amplitude and width of the P wave
- prolongation of the PR interval
- T wave flattening and inversion
- ST depression
- Prominent u waves
Worsening hypokalaemia
- Frequent supraventricular and ventricular ectopics
- Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
- Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes
Discuss the effects of hypernatraemia and hyponatraemia on the ECG
NIL
Discuss effects of hypocalcaemia on the ECG
-Hypocalcaemia causes QTc prolongation primarily by prolonging the ST segment.
-The T wave is typically left unchanged.
Dysrhythmias are uncommon, although atrial fibrillation has been reported.
-Torsades de pointes may occur, but is much less common than with hypokalaemia or hypomagnesaemia.
Discuss effects of hypercalcaemia on the ECG
- The main ECG abnormality seen with hypercalcaemia is shortening of the QT interval
- In severe hypercalcaemia, Osborn waves (J waves) may be seen
- Ventricular irritability and VF arrest has been reported with extreme hypercalcaemia
Discuss effects hypomagnesiumia on the ECG
- The primary ECG abnormality seen with hypomagnesaemia is a prolonged QTc.
- Atrial and ventricular ectopy, atrial tachyarrhythmias and torsades de pointes are seen in the context of hypomagnesaemia, although whether this is a specific effect of low serum magnesium or due to concurrent hypokalaemia is uncertain.
- Nevertheless, correction of serum magnesium to >1.0 mmol/L (with concurrent correction of serum potassium to >4.0 mmol/L) is often effective in suppressing ectopy and supraventricular tachyarrhythmias, while a rapid IV bolus of magnesium 2g is a standard emergency treatment for torsades de pointes
List common reasons for hyperkalaemia to develop
Spurious- haemolysed sample
- renal failure
- acidosis
- cell death
- drugs
Discuss management of hyperkalaemia
IV calcium stabilizes the cardiac membrane by restoring the electrical gradient - it increases the depolarization threshod and the calcium gradient across teh cardiac membrane
Intracellular shift can be achieved with insulin dextrose, salbutamol and normal saline
- insulin onset at 15 minutes with a peak at 30-60 minutes
- salbutamol high doses 15-20mg measureable effect at 15 minutes and lowers K by 0.5 to 1
- saline infusion stimualte Na/k atpase pump leading to an inward shift of potassium
Removal
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Discuss hypokalaemia
Most common electrolyte abnormality
Moderate is defined as 2.5-3 and severe is less than 2.5
Causes
- Renal loss (diuretic use, steroid, metabolic acidosis, RTA, hyperaldosteronism, DKA, alcohol)
- Increased non renal losses - sweating diarrhoea vomiting laxative use
- decreased intake
- intracellular shift
- endocrine (cushing, bartters, insulin
Discuss management of hypokalaemia
As potassium is an intracellular cation a low serum potassium level almost alwasy reflects a signifaicnt total body K deficit
Most patient with mild to moderate hypokalaemia will need only oral replacement
- chlorvescent which has 8mmol of chloride and 14mmol of K
- Span K 8 and 8 mmol of K and CL
Can safely replace 10-20mmol of IV K an hour - if needing to go faster than this will require central access
Hypokalaemia is often associated with hypomagnesemia. Without Mg potassium will not move intracellulary and will be lost through excretion. Magnesium should be replaced along side K
Discuss hypernatraemia
Serum sodium above 145
Rarely seen in previously healthy patients and usually portends a poor prognosis. It can be subdivided into three phssiological pairing
1) hypernatraemia with dehydration and low total body sodium
-Heat stroke
-increased insensible losses - burns sweating
- GIT loss
-osmotic diuresis
2) hypernatraemia with low total body water and normal total body sodium
- DI
- Neurogenic
- Elderly with rest osmostat
- hypothalamic dysfunction
- suprasella or infrasellar tumors
- renal disease
- Drugs
3) hypernatraemia with increased total body sodium
-Salt tablet ingestion
-salt water ingestion
-saline infusions
-IV sodium bicardb
-primary hyperaldosteronisms
-cushings
conns
Discuss the management of hypernatremia
Three independent goals
1) quickly correct underlying shock, hypoperfusion or significant hypovoalemia with normal saline
2) Treat underlying cause of hypernatreamia
- Central DI can be treated with DDAVP (desmopressin) initial dose is 1-2 microg
3) Carefully lower the serum sodium level usually by replacement of TBW
Almost all patient with hypernatraemia will have chronci hypernatraemia
- Na should be lowered no more than 0.5mmol/hr or 10-12 mmol/day
- IV saline for initial fluid resus to correct 1 than either 0.45% saline or 5% dextrose to correct at the rate above
List causes of diabetes insipidus
Central
- Idiopathic
- familial disease
- paraneoplastic
- hypoxic encephaloapthy
- infiltravitive disorders
- post SVT
- Anorexia nervosa
Nephrogenic
- CKD
- PCKD
- Lithium toxicity
- Hypercalcaemia
- hypokalaemia
- Hereditary
- sickle cell disease
Discuss hyponatraemia
Most patients present asymptomatic
two groups of patient will require acute treatment in the ED
1) those with severe hyponatrameia with sodium level of 110 or lower
2) those with Na level below 120 who are symptomatic
When neurons are subjected to a hyponatremic environement they become depleted of sodium and potassium in an attempt to limite their own osmolarity to prevetn intracellular fluid shift that would lead to cerebral oedema. If fluid therapy raises extracellular sodium levels two quickly fluids shift out of the neurons and can cause diffuse demyelination. This can result in a flaccid paralysis and death due to central pontine myelinolysis
List causes of hyponatraemia
Pseudohyponatraemia
- hyperlipidaemia
- hyperproteinemia
- Hyperglycaemia* - dilutional hyponatreamia
Hypovolaemic
- Body fluid losses - sweating, vomtiing, diarrhoea, gastrointestinal suction
- Third spacing - bowel obsturction, burns, pancreatitis, rhabdo
- Renal - diuretics, mineralocorticoid deficiency, osmotic diuresis,, RTA, salt wasting nephropathies
Hypervolaemic
- heart failure
- chornic renal failure
- hepatic failure and cirrhosis
Euvolemic
- SIADH
- Drugs causing SIAHD (diuretics, barbiturates, carbamazepine, chlorpropmaide, clofibrate, opioids, tolbutamide, vincristine)
- psychogenic polydipsia
- beer potomaniea
- hypothyroidism
- adrenalin insufficiency
- MDMA
- Cerebral salt wasting
