Electrolytes Flashcards
Potassium
Potassium is a predominantly intracellular ion
Normal range is between 3.5 and 5.0mmol/l
It is absorbed from the small intestine
It’s entry into cells is controlled by the Na/K ATPase pump
It is 90% renally excreted
It regulates acid base balance and maintains the RMP
Hypokalaemia - Causes
Hyperkalaemia = K <3.5mmol/l and causes include:
- Redistribution: alkalosis, hypoMg, refeeding syndrome, drugs (beta agonists, catecholamines, insulin)
- Abnormal intake: inadequate intake or supplementation
- Abnormal losses: Urinary - steroids, DKA, hyperaldosteronism, diuretics, diuretic phase of AKI & GI - vomiting and diarrhoea
Hypokalaemia - Clinical Features
CNS: Weakness, cramps, paralysis, hyporeflexia
CVS: Hypertension (Na retention), dysrhythmias, tall wide P waves, T wave flatting and inversion, ST depression, U waves, prolonged QT, progression to ventricular arrhythmias
GI: Nausea, vomiting, constipation, ileus
Hypokalaemia - Management
Principles include:
- An A-E approach
- Replace potassium (and magnesium if necessary)
- Monitor ECG and electrolytes
- Prevent recurrence
Hyperkalaemia - Causes
Hyperkalaemia = K >5.5mmol/l and causes include:
- Redistribution: Acidosis, Rhabdomyolysis, tumour lysis, insulin deficiency (including DKA), haemolysis, drugs (sux, digoxin, beta-blockers)
- Abnormal intake: High potassium foods, blood transfusion
- Abnormal losses: Urinary - renal failure, adrenal insufficiency, drugs (potassium sparing diuretics, ACEi, ARBs)
Hyperkalaemia - Clinical Features
CVS: Hypotension, arrhythmias, wide flat P wave, prolonged PR, wide QRS, AV and conduction blocks, bradyarrhythmia, PEA or VFib
GI: Nausea, vomiting
Hyperkalaemia - Management
General principles include:
- An A-E approach
- Stop administration/ treat underlying cause
- Move potassium into cells: Salbutamol, Insulin-Glucose
- Protect the myocardium (calcium)
- Remove the potassium (diuretics/ RRT)
- Prevent recurrence
Magnesium
Magnesium is a predominantly intracellular ion
Normal range is 0.7-1.0mmol/l
Absorbed in the small intestine
50-60% stored in bone
Only a small amount renally excreted
Involved in enzyme systems such as ATPase, antagonises calcium
Hypomagnesaemia - Causes
Hypomagnesaemia is defined as a Mg <0.7mmol/l
Redistribution: Refeeding syndrome, insulin, post- parathyroidectomy
Abnormal intake: TPN, malabsorption, alcoholism (malnutrition)
Abnormal losses: Urinary: RTA, diuretics, polyuria, hyperaldosteronism, hypercalcaemia & GI: Vomiting, acute pancreatitis, diarrhoea
Hypomagnesaemia - Clinical features
Often co-exists with hypoCa, hypoK
CNS: Weakness, ataxia, tremor, coma
CVS: Hypertension, angina, arrhythmia, prolonged QT, signs of hypoK, VT (incl. Torsades)
GI: nausea, vomiting, abdominal pain
Hypomagnesaemia - Management
General principles include:
- Replace Mg
- Monitor ECG & electrolytes
- Prevent recurrence
Hypermagnesaemia - Causes
Hypermagnesaemia is defined as a Mg >1.0mmol/l
It is invariably iatrogenic
- Abnormal intake: excess supplementation, think obstetrics
- Abnormal losses: Urinary - renal failure
Hypermagnesaemia - Clinical Features
Magnesium antagonises Ca entry into cells
CNS: Weakness, coma
CVS: Conduction abnormalities
GI: Nausea/ vomiting
Hypermagnesaemia - Management
General principles include:
- An A-E approach
- Stop administration
- Give calcium (antagonises Mg)
- Monitor ECG and electrolytes
- Prevent recurrence
Phosphate
A predominantly intracellular ion
Normal phosphate is 0.85-1.4mmol/l
Absorbed in the small intestine
85% found in bone
PTH causes phosphate resorption from bone and reduces reabsorption in PCT
Calcitonin, Mg, Bicarbonate increase excretion
Needed for ATP
Hypophosphataemia - Causes
Defined as a PO4 <0.85mmol/l
Redistribution: Refeeding syndrome, respiratory alkalosis, insulin in DKA, glucagon, cortisol, adrenaline (causes intracellular shift)
Abnormal intake: Malnutrition, phosphate binders, malabsorption, TPN
Abnormal losses: Urinary: RTA, hyperaldosteronism; GI: diarrhoea; Other: Sweat, burns, bleeding
Hypophosphataemia - Clinical Features
Often an incidental finding and co-exists with hypoK, hypoMg
Neuro: Proximal myopathy, weakness, smooth muscle dysfunction
CVS: Acute cardiomyopathy
Hypophosphataemia - Management
- Replace phosphate
- Monitor (watch for hypoCa also)
- Prevent recurrence
Hyperphosphataemia - Causes
Defined as a PO4 >1.4mmol/l
Redistribtion: Rhabdomyolysis, tumour lysis, malignant hyperpyrexia, haemolysis, acidosis
Abnormal intake: Increased intake, enemas, VitD intoxication
Abnormal losses: Urinary: Renal failure, hypo parathyroid sim, hypoMg
Hyperphosphataemia - Clinical Features
Binds with calcium to cause HypoCa
Neuro: Tetany
Renal: Calculus formation
Hyperphosphataemia - Management
- Stop administration
- Bind phosphate (aluminium hydroxide)
- Remove phosphate (RRT and volume repletion)
- Monitor
- Prevent recurrence
Calcium
A predominantly extracellular ion
Normal concentration in plasma is 2.2-2.6mmol/l
Exists in plasma as free ions, bound to proteins (40-50%) and diffusible complexes
PTH ensures control of ionised calcium by INCREASING release from bone, reabsorption from DCT, converting VitD to increase GI absorption
Calcitonin released from thyroid opposes PTH
Hyopcalcaemia - Causes
Hypocalcaemia is defined as a serum Ca <2.2mmol/l
Redistribution: Alkalosis, citrate toxicity, blood administration, hyperphosphataemia, pancreatitis, tumour lysis, rhabdomyolysis, hypoparathyroidism, drugs (PPIs, SSRIs)
Abnormal intake: Low dietary Ca, low VitD, phenytoin (increases VitD metabolism)
Abnormal losses: Urinary: ethylene glycol, cisplatin, loop diuretics; Other: bleeding, plasmapheresis, citrate RRT
Hyopcalcaemia - Clinical Features
Neuro: Mental state changes, tetany, facial muscle contracture, carpopedal spasm
CVS: Prolonged QTc, AV block, Torsades
Hypocalcaemia - Management
- Replace Ca (Nb Ca Chloride contains 3x calcium ions as Ca Gluconate)
- Monitor
- Prevent recurrence
Hypercalcaemia - Causes
Defined as a serum Ca >2.6mmol/l
Redistribution: Immobilisation, malignancy, hyperparathyroidism, sarcoid, lithium toxicity, adrenal insufficiency, thyrotoxicosis
Abnormal intake: Calcium, VitA or VitD, hypoMg, hypovolaemia, TPN
Abnormal losses: Urinary: thiazide diuretics
Hypercalcaemia - Clinical Feature
Groans (constipation)
Bones (bony pain)
Moans (psychosis)
Stones (renal calculi)
Also malaise, weakness, hyporeflexia
Hypercalcaemia - Management
- IV hydration
- Bisphosphonates
- Loop Diuretics
- Monitor
- Prevent recurrence
Sodium
Sodium is a major extracellular ion with roles in regulating ECF, preserving osmolality and maintaining tubuloglomerular feedback
Normal range is 135-145mmol/l
Absorbed in the small intestine
Reabsorption in nephron influenced by RAAS, ADH, thirst, beta stimulation at PCT
99% reabsorbed
Hyponatraemia - Causes
Hyponatraemia is defined as a Na <135mmol/l
Unlike other electrolytes - classified according to volume status
Hypovolaemic: Total body water low but with disproportionate Na loss = vomiting, diarrhoea, excess sweating
Euvolaemic: Most common = SIADH, glucocorticoid deficiency, hypothyroid, beer potomania, polydipsia
Hypervolaemic: Essentially dilutional (kidney unable to excrete water) = nephrotic syndrome, CCF, cirrhosis
Hyponatraemia - Clinical features
Neuro: signs result from a change in osmotic gradient which can result in seizures, comas and death (milder symptoms include headache, nausea, poor balance, confusion, muscle fatigue).
Hyponatraemia - Management
Overaggressive treatment risks dymelination!
If severe <115 with severe symptoms then give sodium chloride 3% to increase sodium by 5mmol/l
Otherwise/ thereafter correct slowly (<12mmol/l/24h)
Hypernatraemia - Causes
Defined as a serum sodium >145mmol/l
Abnormal intake (low free water intake): unable to drink water, impaired thirst mechanism (malignancy) Abnormal intake (sodium overload): large volumes of hypertonic NaHCO3 or hypertonic saline; hyperaldosteronism (though usually negated by water intake) Abnormal losses (free water losses): Renal: osmotic diuresis (recovery from AKI, poorly controlled DM, loop diuretics/ mannitol); GI: diarrhoea, vomiting; Other: Burns.
Hypernatraemia - Clinical Features
Neuro: Lethargy, weakness, irritability, seizures, coma, death
PLUS signs of hypovolaemia
Urine osmolality: High (>500) = pure volume depletion; Low (<150) = DI
Serum osmolality: Alway High (>295mosm/kg)
Hypernatraemia - Management
- A-E approach
- Oral water (or IV 5% glucose) fluid replacement: Calculate free water deficit and replace 50% in first 24h
- Monitor Na: 2mmol/l/h drop in first 2-3h followed by 0.5mmol/l/h thereafter
- Treat underlying cause/ co-existing electrolyte abnormalities
Also:
- Desmopressin if DI
- Consider loop diuretic if therapeutic excess
What is the definition of BE?
The amount of acid or alkali to restore 1L of blood to pH 7.4 at PCO2 5.3 and body temperature
What is the StdBE
StdBE is corrected to a Hb concentration of 50g/dL and is defined in terms of a litre of extracellular fluid
