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1. Potassium imbalance
Narasumber :
Prof. Dr. dr. Maimun Syukri, SpPD., KGH, FINASIM
dr. Abdullah, SpPD., KGH, FINASIM
dr. Desi Salwani, SpPD., KGH
dr. Fitrah Sari
Program Studi Sp-1 Ilmu Penyakit Dalam
Fakultas Kedokteran Universitas Syiah Kuala/ RSUD dr. Zainoel Abidin Banda Aceh

2. Distribution of electrolytes
in ICF dan ECF

3. Introduction
 Homeostatic mechanisms maintain plasma K concentration between 3.5 and 5.0 mmol/L, despite
marked variation in dietary K+ intake.
 In a healthy individual at steady state, the entire daily potassium intake is excreted, approximately
90% in the urine and 10% in the stool; thus, the kidney plays a dominant role in potassium
homeostasis.
 More than 98% of total-body potassium is intracellular, chiefly in muscle; buffering of extracellular
K+ by this large intracellular pool plays a crucial role in regulating plasma K+ concentration.
 Changes in the exchange and distribution of intra- and extracellular K+ can thus lead to marked
hypo- or hyperkalemia.
 Changes in whole-body K+ content are primarily mediated by the kidney, which reabsorbs filtered
K+ in hypokalemic, K+deficient states and secretes K+ in hyperkalemic, K+ replete states.

4. Hypokalemia

5. Hypokalemia
• Hypokalemia, defined as a plasma K+ concentration of <3.5 mmol/L, occurs in up to 20% of
hospitalized patients.
• Hypokalemia is associated with a 10-fold increase in-hospital mortality, due to adverse effects on
cardiac rhythm, blood pressure, and cardiovascular morbidity.
• Mechanistically, hypokalemia can be caused by redistribution of K+ between tissues and the ECF or
by renal and nonrenal loss of K+.
• Systemic hypomagnesemia can also cause treatment-resistant hypokalemia, due to a combination
of reduced cellular uptake of K+ and exaggerated renal secretion.
• Spurious hypokalemia or “pseudohypokalemia” can occasionally result from in vitro cellular uptake
of K+ after venipuncture, for example, due to profound leukocytosis in acute leukemia.

6. Causes of hypokalemia

7. Causes of hypokalemia

8. Signs and symptoms
 Hypokalemia has prominent effects on cardiac, skeletal, and intestinal muscle cells.
 In particular, hypokalemia is a major risk factor for both ventricular and atrial arrhythmias.
 Electrocardiographic changes in hypokalemia include broad flat T waves, ST depression, and QT
prolongation; these are most marked when serum K+ is <2.7 mmol/L.
 Hypokalemia can thus be an important precipitant of arrhythmia in patients with additional genetic
or acquired causes of QT prolongation.
 Hypokalemia also results in hyperpolarization of skeletal muscle, thus impairing the capacity to
depolarize and contract; weakness and even paralysis may ensue.
 The paralytic effects of hypokalemia on intestinal smooth muscle may cause intestinal ileus.

9. Degree of hypokalemia

10. Diagnostic approach
of hypokalemia

11. Management of
hypokalemia

12. Hyperkalemia

13. Hyperkalemia
• Hyperkalemia is defined as a serum or plasma potassium level above the upper limits of normal,
usually greater than 5.0 mEq/L.
• While mild hyperkalemia is usually asymptomatic, high potassium levels may cause life-threatening
cardiac arrhythmias, muscle weakness, or paralysis.
• Symptoms usually develop at higher levels, > 6.5 mEq/L, but the rate of change is more important
than the numerical value.
• Patients with chronic hyperkalemia may be asymptomatic at increased levels, while patients with
dramatic, acute potassium shifts may develop severe symptoms at lower ones.
• Infants have higher baseline levels than children and adults.

14. Hyperkalemia
• Pseudohyperkalemia is quite common and represents a false elevation in measured potassium due
to specimen collection, handling, or other causes.
• Hyperkalemia should always be confirmed before aggressive treatment in cases where the serum
potassium is elevated without explanation.
• True hyperkalemia may be caused by increased potassium intake, transcellular movement of
intracellular potassium into the extracellular space, and decreased renal excretion.
• The urgency of therapy depends on symptoms, serum levels, and causes of hyperkalemia.

15. Causes of
hyperkalemia

16. Diagnostic approach
of hyperkalemia

17. Sign and symptoms of hyperkalemia
• Physical exam findings may include hypertension and edema in the setting of renal disease.
• There may also be signs of hypoperfusion.
• Muscle tenderness may be present in patients with rhabdomyolysis.
• Jaundice may be seen in patients with hemolytic conditions.
• Patients may have muscle weakness, flaccid paralysis, or depressed deep tendon reflexes.

18. Evaluation of hyperkalemia
• The first test that should be ordered in a patient with suspected hyperkalemia is an ECG since the
most lethal complication of hyperkalemia is cardiac condition abnormalities which can lead to
dysrhythmias and death.
• Elevated potassium causes ECG changes in a dose-dependent manner:
• K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves
• K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves
• K = 7 to 8 ECG mEq/L will show widening of the QRS complex
• K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

19. Evaluation of hyperkalemia
• It should be noted that the rate of rising serum potassium is a greater factor than the level.
• Patients with chronic hyperkalemia may have relatively normal EGCs even at high levels, and
significant ECG changes may be present at much lower levels in patients with sudden spikes in
serum potassium.
• ECG features of hyperkalemia include:
• Small or absent P wave
• Prolonged PR interval
• Wide QRS
• Peaked T waves

20. Evaluation of hyperkalemia
Additional laboratory testing should include :
• Serum blood urea nitrogen and creatinine to assess renal function and urinalysis to screen for renal
disease.
• Urine potassium, sodium, and osmolality may also help evaluate the cause.
• In patients with renal disease, the serum calcium level should also be checked because hypocalcemia
may exacerbate the cardiac effects of hyperkalemia.
• A complete blood count to screen for leukocytosis or thrombocytosis may also be helpful.
• Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected
acidosis.
• Lactate dehydrogenase should be ordered in patients with suspected hemolysis.
• Creatinine phosphokinases and urine myoglobin should be ordered in patients with suspected
rhabdomyolysis.
• Uric acid and phosphorus should be ordered in patients with suspected tumor lysis syndrome.
• Digoxin toxicity may cause hyperkalemia, so serum levels should be checked in patients on digoxin.
• Since pseudohyperkalemia is so common, confirmation should be obtained in asymptomatic patients
without typical ECG changes before initiating aggressive therapy.

21. Management of hyperkalemia

22. Thank you