Hyperkalemia 1

HYPERKALEMIA
Dr.M.Salman Fras
Second year resident
Department of Anaesthesia
Stanley Medical College and hospital
Physiology
• Potassium is an intracellular cation
• 98% is intracellular and the remaining 2% is extracellular
• i.e.)140meq/l is intracellular compared to the extracellular
3.5 – 5.5 meq/l
• This is in contrast to sodium , difference in the concentration
between these actions is maintained by the Na- K ATPase
pump in cell membrane.
• Potassium has two major physiological functions:
• It participates in the process of protein and glycogen

synthesis in the cell
• Ratio of K+ concentration in the cell and ECF is the
major determinant of the resting membrane
potential across the cell
HYPERKALEMIA
• It is defined as serum Potassium concentration >5.5
meq/L
• Severe HYPERKALEMIA When serum potassium
exceeds >7 meq/L
• Normally excess K+ is eliminated by renal excretion
• i.e.) 90% in the urine and 10% in the sweat and stool
• Decrease in the renal excretion is the most important
cause for HYPERKALEMIA
Classification of HYPERKALEMIA
• It is classified according to the severity
• Mild HYPERKALEMIA – 5.5 – 6 meq /L

• Moderate HYPERKALEMIA – 6.1 – 6.9 meq/L
• Severe HYPERKALEMIA - > 7 meq/L
Etiology
HYPERKALEMIA
Pseudo True
hyperkalemia
hyperkalemia
Pseudo hyperkalemia
• It can be spuriously elevated if red cells hemolyze in a blood
specimen
• When the leucocyte counts exceed 70,000 or platelets > 1
million
• RBC membrane leaking disorders ( hereditary spherocytosis)
• Blood sample drawing
1. K+ containing collection tubes
2. Prolonged tourniquet application before venepuncture
True hyperkalemia
• Increased intake of potassium
• Decreased urinary excretion of potassium
• Intercompartmental shift of potassium

Condition Serum Plasma ECG
potassium potassium changes
True High High Probably yes
hyperkalemia
Pseudo Falsely high Normal Absent

hyperkalemia
Increased intake of potassium
• Foods such as dried nuts,avocados,seaweed are amongst
the highest levels of total dietary potassium
• Massive blood transfusion
• In normal patients,succinyl choline in a dose of 1mg/kg

when given IV cause increase in sr.potassium of
1mmol/l.but there are conditions where succinyl choline
can cause serious rise in K like burns,trauma,renal failure
and paraplegia
Increased intake of potassium
• Foods such as dried nuts,avocados,seaweed are amongst
the highest levels of total dietary potassium
• Massive blood transfusion Presence of ECG

changes after Suxa
– immediately
• In normal patients,succinyl choline in a dose of 1mg/kg
countered by
when given IV cause increase in sr.potassium of hyperventilation
1mmol/l.but there are conditions where succinyl choline
with increased o2
in addition to drugs
can cause serious rise in K like burns,trauma,renal failure
and paraplegia
Intercompartmental shift of potassium
• Extensive tissue damage – crush injuries with
rhabdomyolysis,hemolysis,internal bleeding
• Metabolic or respiratory acidosis
• Sepsis or dehydration
• Insulin resistance and DKA
• Malignant hyperthermia
• Tumor lysis syndrome
• Acute release of potassium from transplanted organs
Decreased renal excretion of potassium
• Decreased renal excretion of potassium can result from
1. Marked reduction in GFR
2. Decreased Aldosterone activity
3. Defect in k secretion in distal nephron
Marked reduction in GFR
• In renal diseases ,elevations of potassium are not
usually seen until GFR falls below 30ml/min
• So if the GFR is 5ml/min it is definitely associated with
hyperkalemia
Decreased Aldosterone activity
• primary defects in adrenal hormone synthesis like Addison
disease ,isolated 21-hydroxylase adrenal enzyme deficiency
• Defect in the RAAS pathway – drugs interfering with the RAAS have the
potential to cause hyperkalemia particularly in the presence of kidney
disease
1. NSAIDS – inhibit PG mediated renin release
2. ACE /ARB inhibitors
3. Heparin – antagonising the activity of AT II receptors
• If there is an Intrinsic or acquired defect in the distal nephrons ability to

secrete potassium decreases
ECG changes in Hyperkalemia
Management
• Confirm the diagnosis by measuring STAT serum potassium
• Rule out pseudohyperkalemia
• Stop the administration of potassium containing fluids
• Stabilize the myocardium
1. Calcium gluconate or chloride
2. Hyperventilation
• Shift extracellular potassium intracellularly
1. Insulim and glucose
2. Beta 2 agonist
• Increased K+ excretion
1. Diuretic therapy
2. Cation exchange resins
3. hemodialysis
Membrane stabilizer:
• Hyperventilate the patient
• Calcium should be given to depress the membrane threshold potential
• In case of circulatory shock calcium chloride is preferred but it should
not be given in peripheral line (extravasation causes tissue necrosis)
• Calacium should not be mixed in bicarbonate containing solutions it
will precipitate
Transfer of extracellular potassium into the cell:
INSULIN : Administration of 5-10units of insulin along with 25-50g
of dextrose drives the K+ intracellularly by activating the Na-K-
ATPase , insulin decrease K+ by 0.6meq/L
Common regimen : 10units of regular insulin + 50ml of 50%
dextrose
Anaesthetic implication
• Elective surgery should not be undertaken in significant
hyperkalemia
• Anaesthetic management in perioperative patients directed
at both lowering the plasma potassium and to prevent
further increase.
• ECG should be carefully monitored
• Succinylcholine should be avoided
• Avoidance of metabolic or respiratory acidosis Is critical
• Ventilation should be controlled under GA,mild
hyperventilation is desirable
• Neuromuscular function should be monitored closely

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HYPERKALEMIA

• It participates in the process of protein and glycogen

• Mild HYPERKALEMIA – 5.5 – 6 meq /L

• Decreased urinary excretion of potassium

• Intercompartmental shift of potassium

Pseudo Falsely high Normal Absent

• Massive blood transfusion

• In normal patients,succinyl choline in a dose of 1mg/kg

• Massive blood transfusion Presence of ECG

• If there is an Intrinsic or acquired defect in the distal nephrons ability to

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