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ST-Elevation Myocardial Infarction: The First 24 Hours -- Early Arrhythmia Management Jamie B. Conti, M.D., F.A.C.C.; C. Richard Conti, M.D., M.A.C.C. Cardiosource. 2008; ©2008 American Posted Abstract Cardiac arrhythmias are common in patients with ST-elevation myocardial infarction (STEMI) and occur most frequently early after the development of myocardial infarction. These arrhythmias include those due to electrical instability ( Table 1 ), pump failure/excess sympathetic tone ( Table 2 ), and bradyarrhythmias ( Table 3 ). Contrary to prior belief, primary ventricular fibrillation (VF) appears to be associated with significantly higher in-hospital mortality, but for patients who survive to hospital discharge, particularly if primary VF occurred within the first 4 hours after STEMI, they appear to have the same long-term prognosis as patients who do not experience primary VF.[1] Treatment of most arrhythmias during the first 24 hours after acute myocardial ischemia is similar to management strategies in nonischemic patients. When in doubt about appropriate treatment strategies, there are two sets of guidelines available with very specific evidence-based recommendations: the 2004 revision of the ACC/AHA STEMI guidelines[2] and the 2006 ACC/AHA/ESC guidelines for managing patients with ventricular arrhythmias and preventing sudden cardiac death, which includes a discussion on the management of arrhythmias that occur after acute coronary syndromes (ACS).[3] Guidelines-Based Management Because lethal ventricular arrhythmias may develop abruptly in patients with STEMI, the ACC/AHA guidelines suggest all patients be monitored with electrocardiography (ECG) on arrival in the emergency department (ED). If the initial ECG is nondiagnostic or if symptoms recur, the guidelines note that it is important to examine serial tracings approximately 5-10 minutes apart. ST elevation also may be detected by intermittent visual inspection of the oscilloscope or auditory alarms in systems with continuous ST-segment monitoring capability. Prophylaxis with lidocaine may reduce the incidence of VF associated with ACS, but this approach appears to be associated with increased mortality, likely owing to bradycardia. Therefore, lidocaine prophylaxis has largely been abandoned. The more common approach today is routine prophylactic beta-blockers in the setting of acute MI, which reduces the incidence of VF. This practice is encouraged when appropriate. In the absence of contraindications, the guidelines note, it is reasonable to initiate beta blockade intravenously, followed by an oral regimen. Suitable regimens include intravenous (IV) metoprolol at 5 mg every 2 minutes for three doses, if tolerated, followed by 50 mg orally twice daily for at least 24 hours and then increased to 100 mg twice per day. An alternative regimen is atenolol 5 to 10 mg IV followed by 100 mg orally on a daily basis. Similarly, in terms of preventing arrhythmias, correction of hypomagnesemia and hypokalemia is encouraged because of the potential contribution of electrolyte disturbances to VF. Specifically, the STEMI guidelines state that it is sound clinical practice to maintain serum potassium levels >4.0 mEq/l and magnesium levels >2.0 mEq/l in patients with acute MI. It may be reasonable to treat VF or shock-refractory VF with boluses of intravenous procainamide, although this approach has limited value owing to the length of time required for administration. Also, it should be noted, prophylactic administration of antiarrhythmic therapy is not recommended when using fibrinolytic agents, specifically lidocaine. Electrophysiologic testing (EP) testing is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. Electrical instability is one of the specific considerations for primary percutaneous coronary intervention (PCI) for STEMI. Therefore, assessment for evidence of obstructive coronary heart disease (CHD) and active ischemia is essential, especially in patients with left main and proximal left anterior descending coronary artery disease. If obstructive CHD is complicated by serious ventricular arrhythmias, the guidelines suggest there is a reasonable likelihood that routine PCI will reduce the frequency and complexity of the arrhythmias and, in some patients, revascularization will eliminate such arrhythmias. Primary VF should be distinguished from secondary VF, with the latter occurring in the presence of severe heart failure or cardiogenic shock. Late VF develops >48 hours after onset of STEMI. Primary VF occurs in 3-5% of patients in the first 4 hours of STEMI onset, with incidence declining markedly thereafter. VF or pulseless ventricular tachycardia (VT) should be treated with an unsynchronized electric shock with an initial monophasic shock energy of 200 J; if unsuccessful, a second shock of 200 to 300 J should be given, and then, if necessary, a third shock of 360 J. VT and Other Arrhythmias Wide-QRS tachycardia should be presumed to be VT if the diagnosis is unclear (class I recommendation). Cardioversion is always indicated for episodes of sustained (more than 30 seconds or causing hemodynamic collapse), hemodynamically compromising VT. For hemodynamically stable VT, class I recommendations include amiodarone (must not exceed 2.2 g over 24 hours) or synchronized electrical cardioversion starting at monophasic energies of 50 J. Revascularization and beta blockade, followed by IV antiarrhythmic drugs are recommended for patients with recurrent or incessant polymorphic VT due to acute myocardial ischemia (Figure 1 and Figure 2). Figure 1 Acute Management of Recurrent or Incessant VT After STEMI
Figure 2 Acute Management of Recurrent or Incessant VT After STEMI (Cont.)
Routine use of prophylactic antiarrhythmic therapy is not indicated when fibrinolytic agents are administered. Nor is treatment recommended of isolated ventricular premature beats, couplets, and nonsustained VT. Previously, it was believed that ventricular warning arrhythmias preceded VF, but careful monitoring has refuted this concept. Treatment of the conduction disturbances and resulting bradyarrhythmias can have either a prophylactic or therapeutic focus. The purpose of prophylactic pacing is to prevent symptomatic or catastrophic bradycardia by selecting and placing a transcutaneous or transvenous temporary pacemaker. This requires the clinician to predict which patients will develop sudden complete heart block with an inadequate ventricular escape mechanism. Fortunately, conduction disturbances generally occur in a stepwise fashion, so that knowledge of the specific ECG pattern can be used to estimate the risk of developing complete heart block and thus to guide the need for prophylactic temporary pacing ( Table 4 ). The pharmacological treatment of bradycardia and atrioventricular conduction disturbances during STEMI is a therapeutic, not prophylactic, measure. Pharmacotherapy centers on the use of atropine at doses of 0.6 to 1.0 mg IV repeated every 5 minutes until there is the desired effect or a total dose of 0.04 mg/kg (2 mg for a 50kg person) has been reached. When there is infranodal block, however, atropine may increase the sinus rate without affecting infranodal conduction, and so the effective ratio of conduction may decrease, and the ventricular rate may decrease. Other pharmacotherapies to treat bradyarrhythmias, such as isoproterenol and aminophylline, are not recommended because they are arrhythmogenic and increase myocardial oxygen demand. Glucagon has been used to treat bradycardia caused by beta-blockers and calcium antagonists, although principally only when these agents have been used in toxic doses, particularly in combination. Continued Management There are no firm data to help define an optimal management strategy for preventing recurrent VF in patients who have sustained an initial episode of VF in the setting of STEMI. The guidelines acknowledge that it seems prudent to correct any electrolyte and acid-base disturbances and to administer beta-blocking agents to inhibit increased sympathetic nervous system tone and prevent ischemia. Clinical trials of amiodarone studied bolus administration of amiodarone only during the arrest setting. Thus, in the absence of arrhythmia recurrence, the guidelines state that antiarrhythmic drugs should not be maintained beyond a 6-24-hour period. They should then be discontinued so that the patient's ongoing need for antiarrhythmic treatment can be reassessed. A reduced ejection fraction (EF) remains the critical measurement to determine whether a post-STEMI patient is at high risk for late ventricular arrhythmia. However, the EF criteria used to define a degree of Finally, the 2006 arrhythmia guidelines suggest that statin therapy may be beneficial in patients with CHD to reduce the risk of vascular events and possibly reduce the occurrence of ventricular arrhythmias and sudden cardiac death. (A class I recommendation with a level of evidence of A.) For example, in a study to evaluate the effect of statin therapy on the risk of nonsustained VT occurring after acute STEMI, investigators found that only in patients not on statin treatment was the occurrence of nonsustained VT associated with a significant and marked increase in 1-year mortality. In this interview, Jamie B. Conti, MD, FACC, reviews early arrhythmia management after STEMI, including specific recommendations and how the management of these patients has changed over time. Dr. C. Richard Conti: I'm at the Annual Scientific Sessions of the Dr. Jamie Conti: When I was first asked to address this question at these Scientific Sessions, I wondered: what I could I tell attendees that would be different than just the general management of arrhythmias? In looking into arrhythmia management of patients with acute myocardial infarction, there are guidelines published in 2004 in JACC and Circulation with Dr. Elliott Antman as the principal author. These guidelines, on acute myocardial infarction, have a section on arrhythmia management during the first 24 hours. Dr. C. Richard Conti: What are some of the general recommendations? Dr. Jamie Conti: Adjunctive therapy is the first issue to focus on when managing arrhythmias that occur during acute myocardial infarction. We certainly want to take care of arrhythmias but, at the same time, we should be addressing the primary problem, which is the myocardial infarction. Therefore, while we're managing the arrhythmia, our interventionalists should be gearing up to revascularize the patient. Dr. C. Richard Conti: That's good advice. What about specific recommendations? Let's say a patient fibrillates. Obviously, defibrillate first; then what? Dr. Jamie Conti: Yes, shock first and then, clearly, that's one situation where opening the artery is really how you're going to most effectively resuscitate that patient. Dr. C. Richard Conti: What about the arrhythmia when you open an artery; the accelerated ventricular rhythm? Do you do anything about that? Dr. Jamie Conti: We see a lot of accelerated idioventricular rhythms (AIVR) with reperfusion and we worry a lot about those. We also worry about nonsustained ventricular tachycardia or frequent PVCs. That really pertains to the older notion that there's a warning arrhythmia or a rhythm problem that predicts that the patient is going to fibrillate in the near future, which suggests you really need to do something about it emergently. However, that theory really has been overturned; there's no validity to it. If you see AIVR, don't treat it because, if you do, you may end up with nothing underneath and that's more of an emergency than AIVR. Since there are no warning arrhythmias, one of the changes in practice that we should be aware of is that the prophylactic administration of antiarrhythmic drugs is no longer recommended; in fact, it's a class III recommendation. It's just not appropriate. Dr. C. Richard Conti: That doesn't mean you can never use lidocaine in certain circumstances in which you can't control a ventricular tachycardia. Correct? Dr. Jamie Conti: Correct, I do not mean to imply that you don't treat arrhythmias appropriately. Ten years ago, we had patients being transported to the emergency room in an ambulance and the paramedics were giving thrombolytic therapy at the same time they were infusing lidocaine, to prophylax against VF. But that's no longer appropriate. Dr. C. Richard Conti: Twenty years ago, or even longer than that, we were giving lidocaine and atropine as a bolus injection just to prevent bradycardia and tachycardia. Interesting. You mentioned nonsustained VT. It is something cardiologists worry about when they see it in the immediate post-infarction state. What do we do about it? Did the CAST trial tell us anything about what to do in these patients? Dr. Jamie Conti: Remember, the CAST trial was not looking at patients in the first 24 hours after myocardial infarction. They were looking at remote myocardial infarction in patients with congestive heart failure. So, it's a little different population, but in that population we were looking to suppress PVCs as an attempt to decrease mortality. As everybody knows, suppression of PVCs was, in fact, detrimental... Dr. C. Richard Conti: ...with encainide and flecainide. What about stable VT in the first 24 hours? What do we do about that? Dr. Jamie Conti: We don't want to leave somebody in ventricular tachycardia for a prolonged period of time, especially an ischemic patient because of the demand on the myocardium and the oxygen supply. On the other hand, if they're stable, if they're talking to you, if they are maintaining their blood pressure, it's sort of an emergency but not enough of an emergency to shock people while they're awake. One of the things we emphasize in our training institutions is that if the patient is mentating and talking to you and apparently perfusing all their vital organs, you have time to get anesthesia to put the patient to sleep before you shock them. Dr. C. Richard Conti: What about drug therapy? Dr. Jamie Conti: Certainly you can use drug therapy and follow standard advanced cardiac life support guidelines, with IV amiodarone now the drug of first choice. Dr. C. Richard Conti: What about beta blockade? Dr. Jamie Conti: Beta-blockers decrease the number of arrhythmias that patients will have during the first 24 hours of myocardial infarction. So, yes, beta blockers are clearly indicated. Dr. C. Richard Conti: What if they had the arrhythmia on beta blockade? Then I guess that's an indication for amiodarone or some other drug. Dr. Jamie Conti: That's correct. Asymptomatic arrhythmia is treated as any other arrhythmia would be treated. Dr. C. Richard Conti: And you make an important point: If they're stable and you need to shock them then do it because you don't want them to be in ventricular tachycardia for a long time because ventricular tachycardia begets more cardiomyopathy. What about the unstable patient? Dr. Jamie Conti: Unstable ventricular tachycardia would be treated as any unstable rhythm and cardioverted urgently. Dr. C. Richard Conti: So, that's no different whether they just had a myocardial infarction or not. Dr. Jamie Conti: There's no difference. Dr. C. Richard Conti: How about atrial fibrillation or SVT, supraventricular tachycardia, in these patients? Dr. Jamie Conti: The treatment of supraventricular arrhythmias is essentially the same as in other patients, again with the caveat that the underlying problem is ischemia and that should be fixed urgently. In patients with atrial fibrillation, one thing you want to consider carefully is whether the heart rate is controlled because rapid ventricular response with atrial fibrillation will only worsen the ischemia situation. Dr. C. Richard Conti: Let's finish up with the patient with heart block. Dr. Jamie Conti: Heart block is the most complicated issue addressed in the guidelines. Fortunately, there's a really good table in the STEMI guidelines (Table 9) that I'd refer all our listeners to. It specifically outlines who needs atropine; who needs transcutaneous pacing; who needs transvenous pacing; and it gives you the level of recommendation. It is an important table for clinicians struggling with that decision-making process. For example, for a patient with anterior myocardial infarction, periods of ventriculoatrial Wenckebach, and a new right bundle branch block, it shows you exactly what to do based on the evidence. I recommend it highly. (To access the STEMI guidelines, click here.) Dr. C. Richard Conti: We'll end on that note, Jamie. Thanks very much for coming to ACCEL. Dr. Jamie Conti: Thank you. Guidelines Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48:e247-346. Antman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction – executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:671-719. References: ST-Elevation Myocardial Infarction: The First 24 Hours – Early Arrhythmia Management Table 1. Arrhythmias During Acute Phase of STEMI: Electrical Instability Table 2. Arrhythmias During Acute Phase of STEMI: Pump Failure/Excess Sympathetic Tone Table 3. Arrhythmias During Acute Phase of STEMI: Bradyarrhythmias Table 4. Arrhythmias During Acute Phase of STEMI: AV Conduction Disturbances References
Jamie B. Conti, M.D., F.A.C.C. Assoc Prof of Medcn, Shands Hospital University of Florida Disclosure: Jamie B. Conti, M.D., F.A.C.C. Research Grants: Medtronic.
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