We explained about Hyperkalemia. What pathogenesis behind it and how to treat it. How emergency is it, how to save life from hyperkalemia.

1. By Dr Ankit Agrawal

2.  Pathogenesis of Hyperkalemia.
 Evaluation of Hyperkalemia.
 Management of Hyperkalemia.

3.  A very serious condition in which elevation of serum potassium levels can increase
the risk of sever cardiac abnormalities (like cardiac arrhythmias) and sudden
death.
 Normal serum potassium level is 3.5 mEq/L -5.5 mEq/L.
 Serum potassium level more then 5.5 mEq refer as hyperkalemia.
 Severe hyperkalemia is most often defined as serum levels >6 mEq/L

4.  Internal K+ shift
 External K+ shift

5.  Total K+ in human body can split into 2 components.
 Intercellular K+ (150 mEq/L) 98%.
 Extracelluar K+ (3.5 – 5.5 mEq/L) 2%.
 Because of these concentration difference there is electrochemical gradient across
the cell membrane.
 Internal K+ balance maintained by the Na+/k+ pump present on cell membrane
that send 2K+ ion in the cell for every 3Na+ ion out.
 This electrochemical gradient id extremely important for setting the resting
membrane potential of excitable cell membrane which is needed for normal
contraction od smooth, cardiac and skeletal muscle.

6.  Insulin deficiency
 Acidosis
 Beta-Blockers
 Hyperosmolarity
 Cell Lysis
 Exercise

8. H+
K+

9.  Increese of extracelluar K+ with respect to intracelluar lead to move water from
cell to extracelluar space. Due to less water in intracellular space gradient was
increased and move K+ to blood.
 During exercise cell works harder and use ATP, depletion of ATP trigger K +
channels on the membrane of muscle call to open up
 It move down its Electrochemical gradient and K+ out of cell.
 Usually it is very small but with combination with Beta blocker or kidney issues
lead to hyperkalemia.

10.  Since we know 98% of body K+ present in cell so, due to cell lysis all K+ released to
blood.
 E.g. – Severe Burn
- Rhabdomyolysis
- Tumor lysis sundrome.

11.  Major amount of K+ taken for diet i.e. 50-150mEq per day.
 Usually body excrete most of what taken in.
 These external K+ balancing act by
 Kidney (Excess K+ secreted in tubules that excreted in urine).
 GIT
 Sweat

12.  Decreased K+ excretion
 High Intake K+
 Rapid or excessive infusion of K+ intravenously
 Aldosterone deficiency
 Adrenal insufficiency
 Acute or Chronic kidney disease

15.  Concentration of K+ inside and out side the cells is really super important for
maintaining the resting cell membrane potential and ultimately for allowing a cell
to depolarize in a all types of muscle to contract.
 So in hyperkalemia membrane potential become more positive to the point of
threshold potential meaning that once the muscle depolarizes and contracts it
cant repolarize to allow another contraction.
 In Skeletal muscle
 Weakness
 Flaccid paralysis – starts with lower extremities and moves upwards
 In Cardiac muscle
 Arrhythmias
 Cardiac arrest

16.  By high potassium level in blood = >5.5 mEq/L
 ElectroCardioGram
 Typically shows tall peaked t-waves with a narrow base, best seen in lead V1 – V6.
 Shortened QT interval
 ST segment depression
 In severe cases it can also cause a prolonged PR interval with absent P wave and
widened QRS complex

17.  5.5-6.5 mEq/L: Tall peaked T waves
 6.5-7.5 mEq/L: Loss of P waves
 7.0-8.0 mEq/L: Widening of QRS complexes
 8.0-10.0 mEq/L: Sine wave, ventricular
arrhythmias, asystole

18.  This ECG displays many of the features of hyperkalaemia:
 Prolonged PR interval.
 Broad, QRS complexes — these merge with both the preceding P wave and subsequent
T wave.
 Peaked T waves.
This patient had
a serum K+ of 9.3

19. • Huge peaked T waves.
• Sine wave appearance.
This patient had Severe hyperkalaemia
(K+ 9.0 mEq/L)
secondary to rhabdomyolysis.

20.  Often asymptomatic, but patients may report non-specific symptoms, including
palpitations, nausea, muscle pain, weakness, dyspnea, or paresthesia
 Hyperkalemia can lead to disturbances of cardiac rhythm, which can be fatal.

21. *-Symptoms of hyperkalemia,
changes on electrocardiography,
rapid-onset hyperkalemia, or
underlying heart disease,
cirrhosis, or kidney disease.

22.  Inj Cal gluconate/ Cal chloride
 To neutralized effect of potassium but it not lower the potassium values.
 DOC, 1st line drug
 I/V Insulin drip with 50% dextrose..
 It sent K+ inside to cell, and magnitude is 0.5 – 1 mEq/hr
 Most effective to lower potassium level
 Salbutamol nebulization
 Furosemide – loss of K+ by KALIURIA
 Hemodialysis – most effective method

23.  Patiromer
 sodium zirconium cyclosilicate
 Resin sodium polystyrene sulphonate
 Soda bicarbonate is not routinely (used for management of metabolic acidosis).