hyperkalemia and its management

1. HYPERKALEMIA
UNDER THE GUIDANCE OF :
Dr. Mukesh Rana Sir
Dr. Brijesh Sir
Dr. Asif Akhtar Sir
Dr. Javed Sir
Dr. Rajesh Sir
Presented By:
Abhishek Kumar Yadav
Roll No. - 04
PARA 15

2. Hyperkalemia is defined as a plasma potassium
level of 5.5 mM; and severe hyperkalemia as a
plasma potassium level of >6.0 mM.

3. Causes of Hyperkalemia :
I. Pseudohyperkalemia
II. Intra- to extracellular shift
III. Inadequate excretion

4. I. Pseudohyperkalemia
•Factitious hyperkalemia
•Artifactual increase in serum K+ due to the release
of K+ during or after venipuncture.
•Causes :
(a) Cellular efflux; thrombocytosis, erythrocytosis,
leukocytosis, in-vitro hemolysis
(b)Hereditary defects in red cell membrane
transport

5. II. Intra- to extracellular shift
A. Acidosis
B. Hyperosmolality; radiocontrast, hypertonic
dextrose, mannitol
C. Lysine, arginine, epsilonaminocaproic acid
(structurally similar, positively charged)
D. Digoxin and related glycosides (yellow oleander)
E. Succinylcholine; thermal trauma, neuromuscular
injury, disuse atrophy, mucositis, or prolonged
immobilization
F. Rapid tumor lysis
G. β2-Adrenergic antagonists (noncardioselective
agents)
H. Hyperkalemic periodic paralysis (HYPP)

6. • III. Inadequate excretion
A. Inhibition of RAAS; ↑ risk of hyperkalemia when used
in combination :
 ACE inhibitors, ARBs, Mineralocorticoid receptor
blockers, Blockade of the ENaC
B. Decreased distal delivery eg., CHF
C. Hyporeninemic hypoaldosteronism
1. Tubulointerstitial diseases: SLE, sickle cell anemia
2. Diabetes, diabetic nephropathy
3. Drugs: NSAIDs, β-blockers, cyclosporine
4. Chronic kidney disease, advanced age

7. D. Advanced renal insufficiency eg., CKD, ESRD
E. Primary adrenal insufficiency
1. Autoimmune: Addison’s disease
2. Infectious: HIV, CMV, TB
3. Infiltrative: amyloidosis, malignancy
4. Drug-associated: heparin, LMWH
5. Hereditary: adrenal hypoplasia congenita

8. (A) ACIDOSIS :
Acidemia → cellular uptake of H+ → efflux of K+
- via K+-H+ exchange
- this effect is limited to non–anion gap metabolic
acidosis and, to a lesser extent, respiratory causes of
acidosis;
-does not occur in the anion gap acidoses- lactic
acidosis and ketoacidosis.

9. (B) HYPEROSMOLALITY
- Due to osmotic gradient ("solvent drag" effect) :
- Hyperkalemia due to hypertonic mannitol,
hypertonic saline, and intravenous immune globulin
is due to osmotic gradient.
- Diabetics are also prone to osmotic hyperkalemia
in response to intravenous hypertonic glucose, when
given without adequate insulin.

10. (C) Cationic amino acids, as lysine, arginine, and
the structurally related drug epsilonaminocaproic
acid, cause efflux of K+ and hyperkalemia via
effective cation-K+ exchange.

11. (D) Digoxin → inhibits Na+/K+-ATPase → impairs
uptake of K+ by skeletal muscle, so, digoxin
overdose → hyperkalemia.
• Structurally related glycosides found in yellow
oleander, foxglove and in the cane toad, Bufo
marinus (bufadienolide) act via same pathway and
cause hyperkalemia.

12. (E) Succinylcholine (SCh) → depolarizes muscle
cells→ efflux of K+ through acetylcholine receptors
(AChRs).
•Contraindicated in patients who have sustained
thermal trauma, neuromuscular injury, disuse
atrophy, mucositis, or prolonged immobilization
becasue it leads to an exaggerated efflux of K+ 
acute hyperkalemia.

13. (F) Excess Intake or Tissue Necrosis
Following conditions provoke severe hyperkalemia in
susceptible patients :
 Foods rich in potassium include tomatoes, bananas, and
citrus fruits;
 Simple overreplacement with K+-Cl– or the
administration of a K+-containing medication (e.g., K+-
penicillin)
 Red cell transfusion, typically massive transfusions.
 Finally, severe tissue necrosis, as in acute tumor lysis
syndrome and rhabdomyolysis.

14. Clinical Features
-Medical emergency due to its effects on heart, i.e.,
cardiac arrhythmias.
 Other modes of presentation :
• Ascending paralysis, denoted secondary
hyperkalemic paralysis : includes diaphragmatic
paralysis and respiratory failure.
• Patients with familial HYPP develop myopathic
weakness during hyperkalemia induced by
increased K+ intake or rest after heavy exercise.

15. ECG
Electrocardiographic manifestations in hyperkalemia
: (At increasing K+ levels)
>8.0 mM
Sine wave pattern
7.0-8.0 mM
Widened QRS Complex
6.5-7.5 mM
Loss of P waves
5.5-6.5 mM
Tall peaked T waves

16. Diagnostic Approach
•First priority is to assess the need for emergency
treatment, followed by a comprehensive workup to
determine the cause.
•Laboratory tests
- Electrolytes, BUN, creatinine, serum osmolality,
Mg2+ and Ca2+, CBC
- Urinary pH, osmolality, creatinine, and
electrolytes.

17. Trans-tubular potassium gradient (TTKG) :
- index reflecting the conservation of potassium in
the cortical collecting ducts (CCD) of the kidneys.
<3 in the presence of hypokalemia
>7–8 in the presence of hyperkalemia

19. Treatment :
The treatment of hyperkalemia is divided into three stages:
1. Immediate antagonism of the cardiac effects of
hyperkalemia - Intravenous calcium
2. Rapid reduction in plasma K+ concentration by
redistribution into cells
• Insulin
• β2-agonists (most commonly albuterol)
3. Removal of potassium
- using cation exchange resins, diuretics, and/or dialysis.
- Hemodialysis is the most effective and reliable method to
reduce plasma K+ concentration.

20. Drugs Dosage Onset Length of
effect
MOA Cautions
Ca2+
gluconate
10-20 mL of
10% solution
IV over 2-3
minutes
Immediate 30 minutes Protects
myocardium
from toxic
effects of
Ca2+
Can worsen
digoxin
toxicity
Insulin Regular
insulin 10
units IV with
50 mL of
50% glucose
15-30
minutes
2-6 hrs. Shifts K+ out
of the
vascular
space and
into the cells
Consider 5% Dextrose solution infusion at 100 mL/hr to prevent hypoglycemia
with repeated doses. Glucose unnecessary if blood sugar elevated above
250mg/dL
Albuterol
(Ventolin)
10-20 mg by
nebulizer
over 10
minutes (use
conc. form,
5mg/mL)
15-30
minutes
2-3 hrs. Shifts K+
into the
cells,
additive to
the effect of
insulin
May cause a
brief initial
rise in
serum
potassium

21. Furosemide
(Lasix)
20-40 mg IV,
give with
saline if
volume
depletion is a
concern
15 min. - 1
hr.
4 hrs. Increases
renal
excretion of
potassium
Only
effective if
adequate
renal
response to
loop diuretic
Sodium
polystyrene
sulfonate
(Kayexalate)
Oral : 50 g in
30 mL of
sorbitol
solution
Rectal : 50 g
in a retention
enema
1-2 hrs.
(Rectal
route is
faster)
4-6 hrs. Removes
potassium
from the gut
in exchange
for sodium
Sorbitol may
be
associated
with Bowel
necrosis.
Drugs Dosage Onset Length of
effect
MOA Cautions

22. THANK YOU