This week we'll focus primarily on the information contained by bradycardia.
1.What are common etiologies of bradydysrhythmias?
2.What are common symptoms of bradycardia?
3.What medications commonly given during anesthesia may result in bradycardias?
4.When and how should bradydysrhythmias be treated?
1 缓慢性心律失常的常见病因有哪些？
2 心动过缓的常见症状？
3 麻醉过程中有哪些药物会导致心动过缓？
4 应该在何时、如何治疗缓慢性心律失常？
1 缓慢性心律失常的常见病因有哪些？
缓慢性心律失常通常与窦房结功能失调有关，包括节性心动过缓、窦性间歇、窦房性传导阻滞和窦性停搏。这些节律可能有症状也可能无症状，也可能导致出现需要起搏器的急症。麻醉干预包括药物、喉镜置入和脊髓麻醉起效均可能引起自主神经功能失调，这些都可能引起上述心率变化。
2 心动过缓的常见症状？
心动过缓的症状包括：
•头晕
•眩晕
•晕厥
•脑缺血症状
•运动耐量受限
•劳力性呼吸困难
•心衰
3 麻醉过程中有哪些药物会导致心动过缓？
据报道很多药物对窦房结或节旁组织有影响，可导致心动过缓
心血管药物：
•β受体阻滞剂
•钙离子拮抗剂
•腺苷
•镁
麻醉药物
•诱导药物
•司可林和甾体类神经肌肉阻断剂
•麻醉药物
4 应该在何时、如何治疗缓慢性心律失常？
对缓慢型心律失常的治疗应该依据于临床表现。如果血流动力学欠佳或血流灌注不足（如心电图有心肌缺血证据）应予以治疗。β1受体激动剂（如异丙肾）和抗毒蕈碱药物（如阿托品和胃长宁）增加心率，然而，阿托品在用于有血流动力学变化的病(态)窦(房结)综合征和钙离子阻滞剂和β受体拮抗剂中毒时效果有限。尽管有报道认为氯化钙（10%氯化钙100-500 mg IV）可能逆转钙离子拮抗剂中毒时的外周血管扩张作用，但观察不到心率增高现象。最近，有研究报道钙和地高辛联合与单独应用钙可能更有效升高收缩压和预防恶性心率失常；在此类药物中毒时选择联合应用可能是比较正确的选择。
在一有争议的病例报道中，Mullins建议钙通道阻滞剂中毒时可应用苯二氮卓拮抗剂。提示心肌苯二氮卓受体存在并且表现出钙通道活性（与苯二氮卓中毒时导致一度房室传导阻滞的报道相一致）。作者因此建议氟马西尼可能是处置钙通道阻滞剂中毒时的有效药物。进一步研究将阐明此种治疗方案的有效性。
在β受体阻滞剂中毒时，可能应用胰高血糖素(2-4 mg IV)，尽管可能出现恶心和呕吐现象且需要防止误吸发生
如果需要，心脏起搏是有效的，可通过经食道或经静脉途径。患者存在与病窦有关的缓慢型心律失常时，最佳处置是术前预防性植入临时起搏器。
英文参考答案
1 What are common etiologies of bradydysrhythmias?
Bradydysrhythmias are often associated with sinus node dysfunction, and may include sinus bradycardia, sinus pause, sino-atrial block, and sinus arrest (1). These rhythms may or may not be symptomatic, and may result in the emergence of alternative pacemakers. Anesthetic interventions, including medications, laryngoscopy and the onset of spinal anesthesia, may create the autonomic imbalance which is often responsible for these changes.
2 What are common symptoms of bradycardia?
Symptomatic bradycardia includes:
•lightheadedness
•dizziness
•near or frank syncope
•manifestations of cerebral ischemia
•limitations in exercise tolerance
•dyspnea on exertion
•congestive heart failure
3 What medications commonly given during anesthesia may result in bradycardias?
A number of drugs have been noted to have an effect on the sinus node or perinodal tissue, causing bradycardias.
Cardiac medications
•beta adrenergic blockade
•calcium channel blockade
•adenosine
•magnesium
Anesthetic medications
•induction agents
•succinycholine and steroidal neuromuscular blockers
•narcotics
4 When and how should bradydysrhythmias be treated?
Therapy for bradydysrhythmias should be dictated by the clinical circumstances. Should hemodynamic compromise or hypoperfusion (such as myocardial ECG evidence of ischemia) occur, treatment is indicated. Beta 1 agonists (such as isoproterenol) and antimuscarinic agents (such as atropine and glycopyrolate) can increase the rate, however, atropine may be of only limited value in managing hemodynamically significant dysrrhythmias in the setting of sick sinus syndrome (2), and calcium channel or beta blocker toxicities (1). Although the use of calcium chloride (IV dose 100-500 mg of 10% calcium chloride) has been noted to be of some value in reversing the peripheral dilation associated with calcium channel blocker toxicity, heart rate increases may not be observed. Most recently, calcium with digoxin was noted to be more effective in raising systolic blood pressure and preventing malignant arrhythmias than calcium alone (3); this may prove to be the combination of choice in such toxicities.
In an provocative case report, Mullins (4) suggested that calcium-channel blocker toxicity may also be treated with benzodiazepine antagonists. Noting that myocardial benzodiazepine receptor ligands exist and appear to affect calcium-channel activity (and consistent with their report of a benzodiazepine overdose resulting in first degree AV block) the authors suggested that flumazenil may be a useful adjunct in the management of calcium channel blocker toxicity. Further work will need to be done to demonstrate the effectiveness of this treatment modality.
In the setting of beta blocker toxicity, glucagon (IV dose of 2-4 mg) may be the drug of choice, although severe nausea and emesis may occur and protection against aspiration should be instituted (5).
Should it be necessary, cardiac pacing is effective and may be initiated by transesophageal or transvenous routes. Patients with preexisting bradydysrhythmias associated with sinus node dysfunction may be best managed by the insertion of a prophylactic temporary pacemaker prior to surgery.
References:
1.Atlee JL. Perioperative cardiac dysrhythmias: diagnosis and management. Anesthesiology 1997;86:1397-424.
2.Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med 2000;342(10):703-9
3.Bania TC, Blaufeux B, Hughes S, Almond GL, Homel P. Calcium and digoxin vs calcium alone for severe verapamil toxicity. Acad Emerg Med 2000;7(10):1089-96.
4.Mullins ME. First-degree atrioventricular block in alprazolam overdose reversed by flumazenil. J Pharm Pharmacol. 1999;51(3):367-70.
5.Love JN, Sachdeva DK, Bessman ES, Curtis LA, Howell JM. A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia. Chest 1998;114(1):323-6.
