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Hyperkalaemia- Raised Potassium


Hyperkalaemia- Raised Potassium


This chart on A4medicine addresses this common finding of increased potassium level or hyperkalaemia / hyperkalemia. Physiology of potassium regulation and the causes of hyperkalaemia have been shown for a better understanding of this matter. Suggested investigations and ECG findings have been discussed. The management has also been discussed.

Causes of raised potassium plasma levels- Haemolysed blood and prolonged or tight application of torniquet shift of potassium from blood cells to blood plasma by mechanical trauma Lab errors Thrombocytosis Leukocytosis ( ^^ WBC ) Lab errors Infectious mononucleosis Leukaemia Familial psedohyperkalaemia Dietary Supplements Total parenteral nutritional formulas Pencillin G Potassium therapy PRBC tranfusion Once GFR falls < 15-20 sig hyperkalaemia can occur even in abscence of an abnormally large K+ load Potassium sparing diuretics NSAIDs ACE inhibitors Angiotensin receptor blockers Cyclosporine or Tacrolimus Trimethoprim -sulfamethoxazole Heparin Ketoconazole Herbs Diabetes mellitus Sickle cell disease or Trait Lower urinary tract obstruction Adrenal insufficiency Primary Addison’s syndrome ( Autoimmune dis , TB or infarct ) Enzyme deficiencies Genetic disorders Metabolic acidosis Beta adrenergic blockade Acute tubular necrosis Electrical burns Thermal burns Cell depolarization Head trauma Digitalis toxicity Digitalis toxicity Methotrexate Rhabdomyolysis Tumour lysis syndrome Cyclosporine

Approach-Often incidental laboratory finding Rarely associated with symptoms Compains may be vague Ocassionally patients may c/o palpitations , nausea , muscle pain or paraesthesia , generalised fatigue Clinical affects are due to pathological effects of ↑ K+ conc on generation of action potentials in excitable tissues 
( Heart and Neuromuscular tissue )

Assessment –Cardiac function ( eg ECG ) Renal function Kidneys and Urinary tract Hydration status ( fluid over load ) Blood pressure ( vol depletion ) Neurological evaluation Medications

Tests to consider –Glucose Bicarbonate Blood Urea Nitrogen Serum creatinine Serum calcium Full Blood Count ECG All patients K+ value >= 6.0 should have a 12 lead ECG done urgently Cortisol and Alosterone ( r/o Addisons ) Urinalysis ( Rhabdomyolysis ) Creatinine phosphokinase ( CPK ) and Calcium 
( r/o Rhabdomyolysis ) ABG ( r/o acidosis ) Digoxin levels ( if on treatment ) Transtubular potassium gradient ( assessment of renal potassium handling ) Plasma renin activity Urine and plasma osmolality

Threshold for emergency treatment varies but most guidelines recommend that emergency treatment should be given if the serum K+ is >= 6.5 mmol/L with or without ECG changes
 If hyperkalaemia suspected on clinical grounds or ECG changes

ECG Changes-Causes a rapid reduction in resting membrane potential leading to ↑ ed cardiac depolarization and muscle excitability → this causes ECG changes ECG changes do not consistently follow a stepwise , dose-dependent pattern Risk of arrythmias ↑es with K+ values > 6.5 mmol and even a small elevation in K + above this conc can lead to rapid progression from peaked T waves to VF and asystole ECG changes may be normal even in presence of sig hyperkalaemia ECG changes may also be modified by the presence of co-existing metabolic disorders such as metabolic acidosis , Ca conc , Na conc and the rate of ↑ in K+ level It can affect the function of both temporary and permanent pacemakers

Due to ↑ risk of fatal arrythmias , hyperkalaemia needs urgent treament if its causing ECG abnormalities or the plasma K+ level is more than 6.5 mmol/L

Tall tented T waves Can also widen the T wave so that entire ST segment is incorporated into the upstroke of the T waves

May also cause Flattenning and even loss of the P wave ↑ of PR interval Widening of the QRS complex Arrthymias

Emergency treatment-Protect the heart Shift K+ out of cells Remove K+ from body Monitor K+ and glucose Prevent recurrence

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