1. ♣Que ,Francesca ♣ Lin, Yun Hsing ♣Reyes, Elaine
HYPERKALEMIA WORSHOP
♣Que ,Francesca ♣ Lin, Yun Hsing ♣Reyes, Elaine

2. POTASSIUM IN THE BODY Potassium: major ion of the body.
Nearly 98% intracellular ( Na+/K+–ATPase pump)
The ratio of intracellular to extracellular potassium is important in determining the cellular membrane potential.
A balance of GI intake and renal potassium excretion achieves long-term potassium balance.
Normal potassium level: mEq/L,
Total body potassium stores are approximately 50 mEq/kg (3500 mEq in a 70-kg person).

3. HYPERKALEMIA defined as a potassium level greater than 5.5 mEq/L
Ranges are as follows:
mEq/L - Mild condition
mEq/L - Moderate condition
7.0 mEq/L and greater - Severe condition

4. CAUSES OF HYPERKALEMIA

5. A. Decreased or impaired potassium excretion
Decreased GFR (eg, acute /chronic renal failure) - most common
Decreased mineral corticoid activity (Addison’s dse)
Defect in tubular secretion (eg, renal tubular acidosis II and IV)
Drugs (eg, NSAIDs, cyclosporine, potassium-sparing diuretics)
B. Excessive endogenous potassium load
Internal hemorrhage/ Hemolysis
Rhabdomyolysis
C.Exogenous potassium load
Parenteral administration
Excess in diet
Potassium supplements/Salt substitutes
D.Transmembrane shifts / Redistribution
Metabolic Acidosis (uncontrolled DM)
Insulin deficiency
Drugs (e.g.beta-blockers,digoxin,succinylcholine)
E.Factitious or pseudohyperkalemia
Hemolysis (in lab tubes) / Venipuncture - most common
Thrombocytosis , Leukocytosi

6. HISTORY TAKING Generalized fatigue Weakness Paresthesias Paralysis
Hyperkalemia can be difficult to diagnose clinically because complaints may be vague.
Frequently is discovered as an incidental laboratory finding.
Patients may be asymptomatic or report the following:
Generalized fatigue
Weakness
Paresthesias
Paralysis
Palpitations
Hyperkalemia is suggested in any patient with a predisposition toward elevated potassium level.

7. PHYSICAL EXAMINATION Evaluation of vital signs
(to determine hemodynamic stability & presence of arrhythmias)
Cardiac examination may reveal extrasystoles, pauses, or bradycardia.
Neurologic examination may reveal diminished deep tendon reflexes or decreased motor strength.
In rare cases, muscular paralysis and hypoventilation may be observed.
Search for the stigmata of renal failure, such as edema, skin changes, and dialysis sites.
Look for signs of trauma that could put the patient at risk for rhabdomyolysis

8. CASE SCENARIO
A 62 year old male diabetic with chronic kidney disease and a creatinine level of 3.5 mg.dl with an estimated GFR of of 15ml/min. He has been eating fruits with each meal for the past two weeks . he consulted because of inability to lift himself from a chair.
On PE, he was conscious with BP 110/ 70. PR 90/min, RR 28/min. He had pale, palpebral conjunctivae, poor skin turgor, and marked proximal weakness. The rest of the findings were normal.
12L ECG showed peak T-waves and some widening of the P wave and QRS complex. Lab exams showed Na 130 meq/L, K 8.5 meq/L, Cl 98 meq/L, HCO 7meq/L , SCr 3.5 mg/dl . Arterial pH 7.30, CBG 400 mmol/L , serum acetone (+).

9. SALIENT FEATURES 62 year old diabetic chronic kidney disease
poor skin turgor
marked proximal weakness
12L ECG : peak T-waves
widening of the P wave and QRS complex
CHIEF COMPLAINT : inability to lift himself from a chair .

10. Lab Results 130 meq/L HYPONATREMIA 8.5 meq/L HYPERKALEMIA 98 MEQ/LCl
( meq/L)
98 MEQ/L
NORMAL
HCO3
(21-30 meq/L)
7meq/L
METABOLIC ACIDOSIS pH
( )
7.30
Crea
(<1.5 mg/dL)
3.5 mg/dL

11. What are the most likely factors responsible for the elevation of the plasma K+ concentration?
Diabetes
Insulin deficiency and hypertonicity (e.g. hyperglycemia)
promote K+ shift from ICF to ECF
Chronic kidney disease
↓ renal K+ excretion: impaired secretion or diminished distal solute delivery
↓ K+ secretion by principal cells: impaired Na+ reabsorption or ↑ Cl- reabsorption
in acute oliguric renal failure: ↑ K+ release from cells (acidosis, catabolism) and ↓ excretion
in chronic renal insufficiency: ↑ distal flow rate and K+ secretion per nephron compensate for decreased renal mass --- adaptive mechanisms eventually fail to maintain K+ balance when GFR falls below ml/min or oliguria ensues
Eating fruits with each meal for the past 2 weeks
↑ K+ intake
rarely the sole cause of hyperkalemia since the phenomenon of potassium adaptation ensures rapid K+ excretion in response to increases in dietary consumption

12. 2. How do you know that this is not pseudohyperkalemia?
artificially elevated plasma K+ concentration due to K+ movement out of cells immediately prior to or following venipuncture
Contributing factors
prolonged use of a tourniquet with or without repeated fist clenching
hemolysis and marked leukocytosis or thrombocytosis: elevated serum K+ concentration due to release of intracellular K+ following clot formation
should be suspected in an otherwise asymptomatic patient with no obvious underlying cause.
If proper venipuncture technique is used and a plasma (not serum) K+ concentration is measured, it should be normal.

13. Signs & Symptoms

14. 3. What are the signs and symptoms of hyperkalemia in this patient?
Explain the pathophysiology.
A. Marked proximal weakness
Increase in membrane excitability
RMP closer to threshold potential
 depolarization
Na channel become inactivated
Decrease in excitability

15. Inhibits ammoniagenesis
B . Metabolic Acidosis
Hyperkalemia
Inhibits ammoniagenesis
Reabsorption of NH4
Impaired net acid secretion
K moves out of the cell

16. Peaked T waves – ventricular repolarization
C. ECG changes
Peaked T waves – ventricular repolarization
Widening of the P wave – atrial depolarization
& QRS complex – ventricular depolarization
decrease membrane potential
Decreases upstroke velocity
Slows intraventricular conduction
Depression of conduction in myocardium

17. Peaked t-waves in hyperkalemia

18. Widened QRS interval in hyperkalemia

19. Treatment

20. 2. Emergency treatment – reversal of membrane abnormalities by giving:
1. Immediate discontinuation of all sources of potassium intake and agents that affect potassium homeostasis
2. Emergency treatment – reversal of membrane abnormalities by giving:
Calcium gluconate (Decrease membrane excitability)
10mL of 10% solution infused in 2-3min
repeat if no change in electrocardiogram after 5-10min
Hypertonic sodium chloride
(for hyponatremic patients)

21. 3. Redistribution of potassium from extracellular space to intracellular space using:
Intravenous sodium bicarbonate
Insulin and glucose
Stimulation of β2 adrenergic
receptors
Salbutamol + nebulization

22. 4. External removal of potassium through:
Stools
Sodium polystrene sulfonate is a cation exchange resin that promotes the exchange of sodium for potassium in the GIT
Urine
Loop + thiazide diuretics enhances renal excretion if renal function is adequate.
Dialysis
Hemodialysis
Most rapid & effective
Peritoneal dialysis
15 – 20% as effective as
hemodialysis

23. 5. Treatment of underlying cause:
Dietary modification
Correction of metabolic acidosis
Volume expansion
Administration of exogenous mineralocorticoid