WCT에서 toxic or metabolic condition이 의심되는 경우, empirical Tx of calcium or soidium bicarbonate

Hyperkalemia 치료에서 다른 치료 없이

sodium bicarbonate로 치료를 하면 안되는데

(Given the limited efficacy, we do not recommend the administration of sodium bicarbonate as the only therapy for the acute management of hyperkalemia, even in patients with mild to moderate metabolic acidosis)

아래와 같이 sodium bicarbonate를 주입한 것이 잘못되었다는 내용이 아닙니다.

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Wide QRS tachycardia이어서 Vtach일 수도 있고 아닐 수도 있는데...

이렇게 really wide QRS tachycardia이고 HR가 120회 정도이면(Vtach은 140-160 이상) 아닐 가능성이 높고(toxic 또는 metabolic condition),

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고칼륨혈증을 미리 알 수 없는 상황에서 toxin or metabolic 원인이 의심되는 경우, sodium bicarbonate, calcium bicabonate로 empirical treatment하는 것이 lifesaving할 수 있다는 내용입니다.

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고칼륨혈증임을 알게 된다면 다른 치료에 더하여 투약해 볼 수는 있으며

그러한 경우는 1L dextrose에 150 mEq mix하여 2-4시간에 걸쳐 투약하지만

미리 고칼륨혈증인지 알 수 없는 경우는 1 A bolus 투약해 볼 수 있습니다.

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Beta-2-adrenergic agonists (eg, inhaled albuterol) and intravenous sodium bicarbonate have been studied as potential rapidly acting therapies to reduce the serum potassium in hyperkalemic patients. Although they can be used in addition to calcium, insulin (with glucose), and potassium removal therapy, they should not be used in place of these treatments.

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Sodium bicarbonate

Raising the systemic pH with sodium bicarbonate results in hydrogen ion release from the cells as part of the buffering reaction. This change is accompanied by potassium movement into the cells to maintain electroneutrality. The use of bicarbonate for the treatment of hyperkalemia was mainly based upon small uncontrolled clinical studies. However, in a study that compared different potassium-lowering modalities in 10 patients undergoing maintenance hemodialysis, a bicarbonate infusion (isotonic or hypertonic) for up to 60 minutes had no effect on the serum potassium concentration. This lack of benefit was confirmed in several subsequent studies of hemodialysis patients.

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Given the limited efficacy, we do not recommend the administration of sodium bicarbonate as the only therapy for the acute management of hyperkalemia, even in patients with mild to moderate metabolic acidosis. However, prolonged bicarbonate therapy appears to be beneficial in patients with metabolic acidosis, particularly when administered as an isotonic infusion rather than bolus ampules of hypertonic sodium bicarbonate. In one series, for example, the administration of isotonic sodium bicarbonate in a constant infusion to patients with a baseline serum bicarbonate of 18 mEq/L had little effect at one and two hours but significantly lowered the serum potassium from 6 mEq/L at baseline to 5.4 and 5.3 mEq/L at four and six hours, respectively; the serum bicarbonate increased to 28 mEq/L at one hour and 30 mEq/L at six hours.

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In addition, acute or chronic bicarbonate (alkali) therapy may be warranted to treat acidemia independent of hyperkalemia.

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When bicarbonate is given in the acute setting, we recommend the administration of an isotonic solution (eg, 150 mEq in 1 L of 5 percent dextrose in water over two to four hours), assuming the patient can tolerate the volume load. There is a potential hazard of giving hypertonic solutions, such as the standard ampule of 50 mEq of sodium bicarbonate in 50 mL. In addition, multiple doses can lead to hypernatremia.

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Over the long term, in patients with chronic kidney disease (CKD), there are a variety of benefits from treating metabolic acidosis, and alkali therapy is recommended to maintain a near-normal serum bicarbonate, independent of any effect on the serum potassium concentration.

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REF. UpToDate 2020.01.18

       https://ecgweekly.com/2020/01/amal-mattus-ecg-case-of-the-week-january-13-2020/