2014年1月9日 星期四

Hyperkalemia  (Serum K > 5.0 mEq/L or 5 mmol/L)
Signs & Symptoms of Hyperkalemia:
The symptoms of hyperkalemia are related to impaired neuromuscular transmission (nonspecific Sx).
The earliest findings are paresthesias and weakness, which can progress to paralysis affecting respiratory muscles. 鉀多感弱麻痺呼吸肌中樞無恙
These symptoms are similar to those seen with hypokalemia; cranial nerve function, however, characteristically remains unaffected.
EKG changes: increase T, S ,PR interval, QRS interval; decreased P, R, ST segment; 2-3 AV block; atrial or vent. arrhythmia
  • Serum K 5.5 - 6.5 mEq/L: peaked T waves; prolonged PR segment
  • Serum K 6.5 - 8.0 mEq/L: loss of P wave, prolonged QRS complex, ST-segment elevation, ectopic beats and escape rhythms
  • Serum K > 8.0 mEq/L: progressive widening of QRS complex, sine wave, ventricular fibrillation, asystole, axis deviations, bundle branch blocks, fascicular
Figure 1
  • Hyperkalemia ECG

    Hyperkalemia can cause life-threatening arrhythmia and thus recognizing hyperkalemia on the ECG is crucial. The ECG findings of hyperkalemia change as the potassium level increases. From slightly high levels to very high levels, ECG findings include:
    1.  Peaked T waves best seen in the precordial leads, shortened QT interval, and sometimes ST segment depression.
    TWaves2
    2.  Widening of the QRS complex (usually potassium level is 6.5 or greater). This frequently appears as in "non-specific intraventricular conduction delay" or IVCD which is characterized by a widened QRS complex of > 120 ms that does not meet the criteria for a left or right bundle branch block. Frequently an IVCD will look like a left bundle branch block in lead V1 with a rS complex or monomorphic S wave and it appears like a right bundle branch block in leads I and V6 with a broad, slurred S wave.
    CLINICAL PEARL: If you see an IVCD, think of hyperkalemia.
    3.  Decreased amplitude of the P waves, an increase in the PR interval, and bradycardia in the form of AV blocks occur as the potassium level exceeds 7.0.
    CLINICAL PEARL: Supportive measurements like fluids, pacing, and pressors do not work in the setting of hyperkalemia. You must treat the hyperkalemia first.
    4.  Absence of the P waves and eventually a "sine wave" pattern (see below) which is frequently a fatal rhythm.
    Hyperkalemia
    CLINICAL PEARL: Giving intravenous calcium is "cardioprotective" in the setting of hyperkalemia. Frequently instant reversal of all hyperkalemic ECG changes within seconds of administration. Calcium does not decrease the potassium levels, so other therapy like bicarbonate or insulin is needed to do this. Calcium administration can be fatal when digoxin toxicity is causing hyperkalemia and should be avoided.
  • Treatment of Hyperkalelmia   Discontinuance of all medications that adversely affect potassium balance is mandatory in true hyperkalemia, particularly when it is severe (plasma [K+] > 6.0 mEq/L).
    These medications include nonselective beta blockers, ACE inhibitors, potassium-sparing diuretics, NSAIDs, and trimethoprim. Salt substitutes, which contain potassium chloride, should also be avoided. Persons with mild hyperkalemia (plasma [K+] < 6.0 mEq/L) can usually be treated conservatively with reduction of daily intake to less than 2 g and, if indicated, with the addition of a loop diuretic.
    Algorithmic management of Hyperkalemia Is life-threatening hyperkalemia present? (ECG changes?  Serum K > 6.5 mEq/L? High-risk as renal failure, receiving dialysis, causative medications?) A.  If No (Life-threatening hyperkalemia is not present) --> Resin exchange with laxative, loop diuretic as furosemide, dialysis
    • Kayexalate (Na Polystyrene Sulfonate) 30 gm in 100 cc 20% sorbitol PO q3-4h. Kayexalate 50 gm in 200 cc 20% sorbitol retention enema 30- 60 min q 4- 6h (decreased 0.5-1 meqK)
    • Furosemide (Lasix) 40-80-160 mg IV
    • Dialysis
    B.  If Yes (life-threatening hyperkalemia is present)--> Step 1: Stabilize the myocardium: (IV Calcium infusion) 
    • IV Calcium Chloride (27.2 mg/dL calcium) or Calcium gluconate  (8.8 mg/dL calcium) 10 mL (1 amp) of 10% solution (500-1000 mg)
      IV infusion over 2-3 minutes.
      * Be extra careful when using calcium infusion in patients with concurrent digitalis toxicity, it could worsen brady-arrhythmia and potentially cause cardiac arrest; use EKG monitor.
      - for slow infusion, may give the calcium solution in 250 mL D5W and given over 30 minutes.
    Step 2: Shift potassium into cells:  (IV glucose +/- insulin +/- Na bicarbonate; Albuterol nebulizer Rx or IV infusion)
    • IV 25 - 50 gm of glucose (25-50 g = 1-2 ampules of 50% dextrose D50W or 250-500 mL of D10W solution) +/- IV Regular insulin 10 units
      - may add Na HCO3 7.5% 50 cc amp 1 -2 amp in the setting of substandial metabolic acidosis (bicarbonate <22 mEq/L)
    • Albuterol  nebulizer Rx can be administered at a dosage of 10 to 20 mg in 4 ml of saline by nasal inhalation over 10 minutes or by a 0.5 mg I.V. infusion.
      - Beta-agonists decrease plasma potassium levels.  Albuterol can be given via a nebulizer (10-20 mg in 4 mL of saline) or via IV infusion (0.5mg).  The dosages of B-agonists administered in this setting are relatively high, ranging from 4 to 8 times that recommended for Rx of an acute asthma exacerbation).  The major adverse effects are tremor, tachycardia, anxiety, and flushing.
    Step 3:  Enhance elimination of potassium:  (Kayexalte, Lasix, Dialysis)
    • Resin exchange with laxative: Kayexalate (Na Polystyrene Sulfonate) 30 gm in 100 cc 20% sorbitol PO q3-4h. Kayexalate 50 gm in 200 cc 20% sorbitol retention enema 30- 60 min q 4- 6h (decreased 0.5-1 meqK)
    • Loop diuretic as furosemide (Lasix) 40-80-160 mg IV
    • Hemodialysis - It is the Rx of choice for life-threatening hyperkalemia that is refractory to medical management.  It may decrease the serum K level by 1.0 - 1.5 mEq/L for each hour of dialysis.
    REF: Mayo Clinic Proceedings Dec 2007   * If aldosterone deficiency has been documented in cases of chronic hyperkalemia that are inadequately controlled by diet or diuretics, aldosterone replacement with fludrocortisone acetate may be useful. The combination of fludrocortisone and a loop diuretic may limit the development of hypertension or edema. However, because its onset of action may take several days or longer, this therapy is not sufficiently effective to be used in the treatment of acute, life-threatening hyperkalemia.
  • Diff. Dx:A. Pseudohyperkalemia (Factitious hyperkalemia)
    1. Improper blood collection (lab error)
    2. Hematologic disorder with increased WBC or platelets B. Exogenous potassium load
    1. Oral or IV potassium supplement intake
    2. Potassium containing drugs
    3. Transfusion C. Decreased renal potassium excreation
    1. Renal failure: acute or chronic
    2. Potassium sparing diuretics or ACE-inhibitors
    3. Mineralocorticoid deficiency
        a. Addison's disease or  Bilateral adrenalectomy
        b. Hypoaldosteronism
           (1) Hyporeninemic hypoaldosteronism
           (2) Heparin therapy
           (3) Specific enzyme defect or Tubular unresponsiveness
    4. Congenital adrenal hyperplasia or Primary defect in potassium excretion D. Cellular shift of K+
    1. Tissue damage: trauma, burns, rhabdomyolysis;   Destruction of tumor tissue
    2. Acidosis
    3. Digitalis overdose; Hyperosmolality
    4. Hyperkalemic periodic paralysis
    5. Succinylcholine, Arginin infusion

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