Electrolytes Flashcards by Sam Clark

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

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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

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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

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Hypokalaemia - Management

Principles include:

An A-E approach
Replace potassium (and magnesium if necessary)
Monitor ECG and electrolytes
Prevent recurrence

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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)

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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

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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

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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

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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

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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

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Hypomagnesaemia - Management

General principles include:

Replace Mg
Monitor ECG & electrolytes
Prevent recurrence

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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

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Hypermagnesaemia - Clinical Features

Magnesium antagonises Ca entry into cells

CNS: Weakness, coma
CVS: Conduction abnormalities
GI: Nausea/ vomiting

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Hypermagnesaemia - Management

General principles include:

An A-E approach
Stop administration
Give calcium (antagonises Mg)
Monitor ECG and electrolytes
Prevent recurrence

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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

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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

1. Replace Ca (Nb Ca Chloride contains 3x calcium ions as Ca Gluconate) 2. Monitor 3. 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

1. IV hydration 2. Bisphosphonates 3. Loop Diuretics 4. Monitor 5. 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

1. A-E approach 2. Oral water (or IV 5% glucose) fluid replacement: Calculate free water deficit and replace 50% in first 24h 3. Monitor Na: 2mmol/l/h drop in first 2-3h followed by 0.5mmol/l/h thereafter 4. 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