Hyperkalemia
- causes and risk factors
- signs, symptoms and diagnosis
- pathophysiology
- treatments
- consequences and course
- the patient
- health care team
- community involvement
- resources and references
Hyperkalemia is defined as potassium greater than 5.5 mmol/L. It occurs during 1-10% of hospital admissions.
- 5.5 - 6.0 mmol/L - Mild
- 6.1 - 7.0 mmol/L - Moderate
- 7.0 mmol/L and greater - Severe
Causes and Risk Factors
Cellular Release
|
Increased Intake
|
Decreased Excretion
|
Factitious
|
Signs, Symptoms, and Diagnosis
- history
- physical exam
- ECG changes
- lab investigations
History
A careful history, with emphasis on diet and use of medications and laxatives, should be obtained. "No salt" is KCl, and so is dangerous.
Patients are usually asymptomatic, but can develop:
- nausea
- palpitations
- muscle weakness often starting in legs
- paresthesias
- areflexia
- ascending paralysis
- hypoventilation
Physical Exam
Signs of hyperkalemia include:
- mental confusion
- hypotension
- weakness, paralysis
ECG Changes
Cardiac disturbances and ECG changes do not correlate well with K levels, but are clearly very important. Rate of change may be very important.
- peaked, narrow T waves
- flattened P waves
- prolonged PR interval
- widened QRS, and eventual merging with T wave
- AV block
- ventricular fibrillation
- asystole
Lab Investigations
Repeat blood test to confirm finding.
Estimate GFR (creatinine clearance)
If GFR is normal, calculate transtubular potassium gradient (TTKG) = (UK/PK) / UOsm/POsm)
- TTKG <7 - decreased aldosterone function
- TTKG >7 - normal aldosterone function
Serum and urine should be assayed for electrolytes and osmolality.
In extrarenal hyperkalemia, renal potassium excretion should be greater than 200 mEq/day.
Pathophysiology
The ratio of intracellular to excellular potassium is the major determinant of cell membrane resting potential. As extracellular potential increases, the cell becomes partially depolarized, and the ability to generate action potentials is diminished.
Hyperkalemia is normally dealt with by an increase in ICF potassium stores in muscle, mediated by insulin, epinephrine, and aldosterone. These all increase K uptake by the Na/K pump.
Hyperkalemia also increases K secretion in the urine via action of aldosterone on cells of the CCT.
Treatments
Treatment depends on urgency.
Hold exogenous K and any medications which are K-retaining (furosemide, thiazide)
Cardiac Stabilizatiuon
The most rapid way of reversing cardiac membrane potential is to give calcium Ca gluconate (1-2 amps, 10 mL of 10% solution). It is indicated when QRS is widened, or with loss of P waves. This is short lived (30-60 minutes), however, and does not affect serum K. It must be followed by other therapies to decrease extracellular potassium concentration.
Transcellular shift
K can be moved into cells via many mechanisms:
- insulin R 10-20 units IV, given with 1-2 amp D50W
- onset 15-30 min; duration 1-2h
- bicarbonate 1-3 amps
- onset 15-30 min, transient and less useful
- ventolin 1mcg inhaled, 0.5 mg IV: stimulates Na/K ATPase
- onset 30-90 min; caution with heart disease
- can lower by 0.5-1.5
Enhance K removal
Renal excretion can be enhanced by giving furosemide >40 mg IV; consider IV NS to avoid hypovolemia
Gut excretion via cation-exchange resins: calcium or Kayexalate
Dialysis can be done in renal failure or if life-threatening hyperkalemia is unresponsive to therapy.
Consequences and Course
In muscle, decreased action potentials leads to muscle weakness and paralysis.
Effects on the Heart
As plasma levels rise above 6 mM, T waves become symmetrically tented, with a sharp peak. The P-R interval lengthens and the P wave becomes smaller. Sinus bradycardia and conduction defects can also occur.
Above 8 mM, the P wave disappears and the QRS complex widens and merges with the T wave.
At higher concentrations, ventricular fibrillation can result.
the cell will have an easier time depolarizing if [K]i/[K]o is reduced
References