■高渗碳酸氢钠被提倡用于治疗钠通道阻滞剂中毒,但它的功效在不同的钠通道阻滞剂中有所不同。本评论解决了高渗碳酸氢钠疗法在心脏毒性药物中毒中的常见陷阱和适当用法。
■血清碱化最好通过高渗碳酸氢钠和过度换气(PCO2~30-35mmHg[0.47-0.6kPa])的协同作用来实现。这减少了实现血清碱化(pH~7.45-7.55)所需的碳酸氢钠剂量,并避免了过量高渗碳酸氢钠的不利影响。
■三环抗抑郁药中毒对碳酸氢钠治疗反应良好,但许多其他钠通道阻滞剂可能不会。例如,阻断细胞间缝隙连接的药物,如安非他酮,对碱化反应不好。对于预期反应未知的钠通道阻滞剂中毒,1-2mmol/kg碳酸氢钠的推注可用于评估对碱化的反应。
■高渗碳酸氢钠可引起电解质异常,如低钾血症和低钙血症,导致QT间期延长和扭转性室性心动过速与具有混合钠和钾心脏通道特性的药物中毒,如羟氯喹和氟卡尼。
■如果在QRS波持续时间<100ms之前给药,通常会出现剂量过多的高渗碳酸氢钠。延长的QRS波持续时间对于钠通道阻滞剂毒性不是特异性的。一些钠通道阻滞剂没有反应,即使有回应,QRS波持续时间需要几个小时才能完全恢复到正常。此外,QRS波延长可能是由于速率依赖性束支传导阻滞。所以,在达到血清碱化(pH~7.45-7.55)后,不应给予进一步的剂量。
■避免患者过量使用高渗碳酸氢钠的进一步策略是设定最大剂量。超过6mmol/kg可能会引起高钠血症,流体过载,代谢性碱中毒,和脑水肿在许多病人和可能是致命的。
■我们建议在钠通道阻滞剂中毒患者中使用高渗碳酸氢钠治疗,这些患者具有临床上明显的毒性,例如癫痫发作,休克(收缩压<90mmHg,平均动脉压<65mmHg)或室性心律失常。我们建议初始推注1-2mmol/kg的高渗碳酸氢钠,如果病人不稳定,可以重复,最大剂量为6mmol/kg。建议与机械通气和过度通气一起使用,以实现血清碱化(PCO2〜30-35mmHg[4-4.7kPa])和pH〜7.45-7.55。反复推注高渗碳酸氢钠,必须监测和纠正钾和钠异常,并观察血清pH值和心电图的变化。
■高渗碳酸氢钠是某些钠通道阻滞剂中毒的有效解毒剂,如三环抗抑郁药,当用于适当的剂量时,它与过度换气协同作用,以实现血清碱化和减少钠通道阻滞。然而,有许多陷阱,可导致过量的碳酸氢钠治疗和严重的不良反应。
UNASSIGNED: Hypertonic sodium bicarbonate is advocated for the treatment of sodium channel blocker poisoning, but its efficacy varies amongst different sodium channel blockers. This Commentary addresses common pitfalls and appropriate usage of hypertonic sodium bicarbonate therapy in cardiotoxic drug poisonings.
UNASSIGNED: Serum alkalinization is best achieved by the synergistic effect of hypertonic sodium bicarbonate and hyperventilation (PCO2 ∼ 30-35 mmHg [0.47-0.6 kPa]). This reduces the dose of sodium bicarbonate required to achieve serum alkalinization (pH ∼ 7.45-7.55) and avoids adverse effects from excessive doses of hypertonic sodium bicarbonate.
UNASSIGNED: Tricyclic antidepressant poisoning responds well to sodium bicarbonate therapy, but many other sodium channel blockers may not. For instance, drugs that block the intercellular gap junctions, such as bupropion, do not respond well to alkalinization. For sodium channel blocker poisonings in which the expected response is unknown, a bolus of 1-2 mmol/kg sodium bicarbonate can be used to assess the response to alkalinization.
UNASSIGNED: Hypertonic sodium bicarbonate can cause electrolyte abnormalities such as hypokalaemia and hypocalcaemia, leading to QT interval prolongation and torsade de pointes in poisonings with drugs that have mixed sodium and potassium cardiac channel properties, such as hydroxychloroquine and flecainide.
UNASSIGNED: Excessive doses of hypertonic sodium bicarbonate commonly occur if it is administered until the QRS complex duration is < 100 ms. A prolonged QRS complex duration is not specific for sodium channel blocker toxicity. Some sodium channel blockers do not respond, and even when there is a response, it takes a few hours for the QRS complex duration to return completely to normal. In addition, QRS complex prolongation can be due to a rate-dependent bundle branch block. So, no further doses should be given after achieving serum alkalinization (pH ∼ 7.45-7.55).
UNASSIGNED: A further strategy to avoid overdosing patients with hypertonic sodium bicarbonate is to set maximum doses. Exceeding 6 mmol/kg is likely to cause hypernatremia, fluid overload, metabolic alkalosis, and cerebral oedema in many patients and potentially be lethal.
UNASSIGNED: We propose that hypertonic sodium bicarbonate therapy be used in patients with sodium channel blocker poisoning who have clinically significant toxicities such as seizures, shock (systolic blood pressure < 90 mmHg, mean arterial pressure <65 mmHg) or ventricular dysrhythmia. We recommend initial bolus dosing of hypertonic sodium bicarbonate of 1-2 mmol/kg, which can be repeated if the patient remains unstable, up to a maximum dose of 6 mmol/kg. This is recommended to be administered in conjunction with mechanical ventilation and hyperventilation to achieve serum alkalinization (PCO2∼30-35 mmHg [4-4.7 kPa]) and a pH of ∼7.45-7.55. With repeated bolus doses of hypertonic sodium bicarbonate, it is imperative to monitor and correct potassium and sodium abnormalities and observe changes in serum pH and on the electrocardiogram.
UNASSIGNED: Hypertonic sodium bicarbonate is an effective antidote for certain sodium channel blocker poisonings, such as tricyclic antidepressants, and when used in appropriate dosing, it works synergistically with hyperventilation to achieve serum alkalinization and to reduce sodium channel blockade. However, there are many pitfalls that can lead to excessive sodium bicarbonate therapy and severe adverse effects.