Rules

1. approach
to
Hyperkalemia
Dr Vilas Naik
DM (nephrology)
Fellowship in Nephrology (Toronto, Canada)

2. Hyperkalemia: Life threatening Emergency
Common
Treatable

3. K physiology
• Total body K stores are approximately 3000 meq
• K: primarily intracellular cation {98 % of body K}
• Ratio of the K concentrations in the cells and outside:
major determinant of the resting membrane potential
across the cell membrane
• Generation of the action potential: essential for
normal neural and muscle function
• K abnormalities: Muscle weakness and arrythmia

4. Regulation of urinary potassium excretion
Connecting segment & Cortical duct
Na comes here
Lumen
Negative
ROMK
Electrical gradient
For K secretion
Na-K ATPase
Electrical and
chemical gradient for
Na reasbsorption

5. Regulation of urinary potassium excretion
Stimulation of K secretion by principal cells
• An increase in plasma potassium
concentration and/or potassium intake
• An increase in aldosterone secretion
• Enhanced delivery of sodium and water to the
distal potassium secretory site

6. An increase in plasma potassium
concentration and/or potassium intake

7. An increase in aldosterone secretion
Hyperkalemia
Renin angiotensin
Aldosterone system
(RAAS)
Na channel
Aldosterone deficiency,
blockade

8. Enhanced delivery of sodium and water to
the distal potassium secretory site
We need Na and
Water here.
No distal Na (decresed GFR),
No K secretion
e.g Renal failure
Increased distal flow,
Increased Na delivary,
Increased K secretion
Eg diuretics

9. Distribution of potassium between the cells
and the extracellular fluid
98 % K intracellular
Maintained by this
pump
Pump block
eg digitalis toxicity
Beta blockers
Pump stimulation
Insulin, beta2 stimulation

10. Distribution of potassium between the cells
and the extracellular fluid

11. Distribution of potassium between the cells
and the extracellular fluid

12. Hyperkalemia
• Increased intake: K adaptation, rapid
• Shift: intracellular to extracellular, alone again not
enough to sustain hyper K.
• Decrease excretion: almost always present
– Aldosterone
– Decreased distal delivery of Na/ water
– Renal dysfunction

13. Case 1
• 52/ male, DM and HT- 15 yrs
• Uncontrolled HT, Edema 3+
• Recent change in medications
• Adm: rapid onset quadriparesis over last 24
hours

14. Case1: examination
• ECG: HR of 30, broad QRS, CHB like pattern
• Rest vitals stable
• Higher functions normal
• Quadriparesis (grade 2 power, absent reflexes)

15. Case 1: Labs
• Na 129
• K 8.7
• Cl 96
• HCO3 16
• AG 17
• Creat 4.4
• Glucose 600
• CBC leucocytosis
• Urine
• Sugar- 4+
• Ketones- nil
• Plenty pus cells

16. Hyperkalemia appraoch
• Intake
• Shift
• Impaired excretion

17. Case: analysis
• Intake: propably reduced (UTI, blood sugars)
• Shift:
– Severe hyperglycemia
– Insulin deficiency
– Acidosis

18. Case analysis
• Decreased renal excretion (almost always)
• Was started on ramipril (ACEI) for HT
– RAAS blockade (decreased aldosterone)
Decreased GFR
so decreased distal delivery of Na and water,
no Na reabsorption, no electronegative potential in lumen
No secretion of K

19. Na+
--
--
--
--
--
K+

20. Case analysis
• The patient was also
started on
spironolactone which
blocked aldosterone
action
• NSAIDS for fever
– Deceased GFR
– Renal failure

21. More mechanisms
• K loading increases ROMK expression and insertion into
CCD luminal membrane
• ? May be gut signal to kidney to change ROMK
• Another K channel in CCD
– High capacity K channels (big K or Maxi K)
– Activated of high flow (water and Na delivery)
– Activated by K depletion
– Aldosterone independent action

22. Another K channel: intercalated cells
• H-K exchanger in IC cells
of CCD
• Activated in K depletion
• Absorbs K+ and
secretion of H+

23. Evaluation of hyperkalemia
• Exclude Pseudohyperkalemia
– potassium movement out of the cells during or
after the blood collection
– Torniquet
– Thrombocytosis, high WBC counts (leukemias)

24. Assessing K excretion
• Kidneys can vary K excretion from < 5 Meq/L to 400
Meq/L, with decreased or increased intake
• Urine K/ Creatinine ratio
– < 15 mmol/gm in K depletion
– >200 mmol/gm in hyperkalemia
–

25. Case 1
• Urine Na- 120 Meq/L
• Urine K- 15 Meq/L
• SO distal delivery of Na is adequate
• Severely impaired K excretion
• Aldosterone deficiency: hyporeninemic
hypoaldosteronism in DM
• Drugs blocking aldosterone production and action
• Decreased GFR

26. Case 1
• NSAIDS: worsening of RFT (GFR)
• PG synthesis inhibited
– PG inhibit renin –reduce aldosterone
• So in this patients, almost all things to
increase his K has been done
– ACEI, aldosterone blockade
– NSAIDS

27. Treatment of severe hyperkalemia
• Calcium: if hypocalcemia or ECG changes
• Shift inside the cells:
– Insulin alone (hyperglycemia) or with 25 %
Dextrose
– B2 agonist
– Bicarbonate if acidosis

28. Treatment
• Excretion
– Saline, especially if depleted
– Thiazide and loop diuretic
– K binding resins, small effect, increasing GI
excretion, given with lactulose
• Dialysis- the most rapid and effective means in
the presence of renal dysfuction and fluid
overload

29. Case 1
• We started the patient on dialysis, normal
sinus rhythem in 45 minutes
• Stopped implicated drugs, treated UTI
• Baseline creatinine of 2 mg % on follow up.
• K normal

30. Thanks for your patience