I've summarized below the relavent parts of the newly released ACC guidelines for the management of acute MI (1). Any commentary on my part is set off in brackets to distinguish it from the official recommendations. I have left out sections pertaining to indications for pacemaker placement, in-patient management, indications for catherterization, secondary prevention etc. in order to focus on aspects of treatment that are more relevant to ED care. I have also deliberately left out drug dosages as these are already widely known. This document answers questions that have been repeatedly raised in this forum including 1) the use of O2, morphine and nitrates in acute MI 2) prehospital thrombolysis 3) whether earlier use of ASA (say in the prehospital setting) would improve outcomes 4) the use of atropine for intra- and infra- HIS blocks 5) contraindications to the use of lysis including chronic anticoagulation and hypertension 6) the 'optimal' lytic agent under various circumstances etc. I have not reproduced the recommendations verbatim and thus some degree of interpretation on my part is incorporated. If I have misinterpreted the original document please let me know. I apologize in advance if the length of this post causes your server to crash. A. Prehospital considerations: In a tiered response system first responder defibrillation programs are recommended. AEDs are a good way of implementing this recommendation. The use of a prehospital checklist and field 12 lead ECGs are an effective way of expiditing the management of patients with acute MI. No trial has shown a mortality advantage of prehospital thrombolysis but a meta-analysis demonstrated a 17% improvement in 'outcome.' Routine implentation of prehospital thrombolysis is not recommended except in certain circumstances, specifically when physicians are available in the prehospital setting or transport times are longer than 90 minutes. B. Intial ED Dx and Management: The goal should be a door-to-needle time of 30 minutes or less. CXR is listed as an intial diagnotic maneuver but the issue of whether lysis should be with-hekd pending its completion is not addressed. Except as noted below the only criteria for thrombolysis is the presence of ST elevation or new BBB. Primary PTCA, as well, is of unknown benefit in their absence. Serial ECG tracings are encouraged in the ED setting to detect early signs of myocardial injury. CK MB lacks complete specificity for acute MI and, thus, false positives will occasionally occur. Its sensitivity on the first 6 to 8 hours is also quite low. An elevated MB band in the presence of a normal total CK is of unknown significnace. Improved sensitivity and specificity may be achieved by the use of CK subform analysis (CKMB2 > 1 or CKMB2/CKMB1 > 1.5). Troponin I and T are elevated earlier and persist longer than CK. An elevated level of Troponin I on presentaiton correlates with subsequent cardiac events. Myoglobin is a reliable early marker of MI but, because of a lack of specificity, requires a confirmatory test. [The observation about the uncertianly of normal CK/elevated MB is interesting in view of the documentation in the literature of confirmed MI in this setting.] Although its benefits are uncertain, the use of supplemental oxygen in the first 2 to 3 hours of an acute MI is recommended. Rationale for the utilization of oxygen include the observation that it may decrease ST segment elevation, that many patients are hypoxemic in the early stages and that the administration of nitroglycerine may worsen V/Q mismatching. The effect of oxygen on morbidity and mortality is unknown. Beyond the first 3 hours, oxygen need not be administered unless hypoxemia exists. Drawbacks to the use of oxygen include its vasoconstrictive properties and potential CO2 retention. ALL patients with acute ischemic syndromes should reiceve at least 1 sublingual NTG unless SBP is less than 90. Intravenous NTG is indicated when acute MI is complicated by CHF, persistant ischemia or HTN. Considerably less evidence exists for the routine use of IV NTG in ALL patients with acute MI. Noteworthy is the fact that NTG, alone, should not be relied upon to control ischemic pain which, instead should be managed, concurrently with analgesics. IV morphine should not be with-held under the assumption that its use will mask symtoms of ischemia. Although no evidence exists of a critcal time-dependant benefit in the use of ASA (unlike thrombolysis) it should be administered as soon as possible and certainly within the first 24 hours in a dose of 160 to 325 mg. Chewable ASA is absorbed more rapidly and ASA suppositories may be used in cases of vomiting. [From the standpoint of prehospital use of ASA this answers the question of whether earlier use is benefical or necessary.] Atropine is indicated for symptomatic sinus bradycardia and Mobitz I 2nd degree AVB and complete AVB occuring at the nodal level such as during an IWMI. Mobitz II AVB and 3rd degree AVB below the nodal level (manifested by a wide escape rythum, rarely responds to atropine which may, in fact, increase the degree of block. Atropine may also be used for treatment of nausea and vomiting resulting from the administration of morphine. Thrombolysis is only indicated in the presence of ST segment elevation or new BBB. The presence of hyperacute T wave changes or right precordial ST segment depression indicative of posterior infaction constitute 2 exceptions to the requirement for ST elevation provided that they are reliably diagnosed. Thrombolysis is not useful in the setting of nondiagnostic ST segment changes, and may in fact be harmful in some instances where acute MI manifests with ST segment depression alone. The benefit of thrombolysis is more evident for AWMI. It is of less benefit in IWMI unless right vedntricular infarction is also present. Therapy may be given up to 12 hours after onset of infarction. Ongong pain with persistant ST segment elevation may extend the period of beneift from 12 to 24 hours. The presence of a blood pressure greater than 180/110 *at presentation* is a relative contraindication to lysis as it increases the risk of ICH which is fatal in 1/2 to 2/3 of cases. It is unknown whether pre-lysis treatment of elevated BP would reduce this risk but attempts should be made to do so nonetheless. In addition to the usual contraindications, the presence of therapeutic anticoagulation (INR 2 -3) is considered to be a *relative* contraindication to lysis. Active internal bleeding, excepting menses is also a contraindication for lysis. PTCA is an alternative to thrombolysis but only if can be performed in a timely fashion. Transfer to a facility with angiographic capabilites in lieu of thrombolysis is generally not warranted because any benefit of PTCA will be offset by delay in treatment that results from transfer. PTCA is also indicated in patients who are not candidates for lysis because of a risk of bleeding complications. In earlier studies the survival benefit of PTCA vs thrombolysis was largely due to the increased risk of bleeding with the latter. [Most recently a study found no difference in survival between the two modalities.] [Contraindications to thrombolysis are either absolute (such as history of previous ICH) or relative (such as therapeutic anticoagulation). How does one weigh the risk/benefit ratio if relative contraindications exist? No guidance is given. Certainly if the patient has multiple relative contraindications and presents with a 'low-risk' MI--say uncomplicated IWMI--then treatment is probably not indicated. On the other hand, in the presence of a single relative contraindication and high risk features such as anterior infarction, sinus tachycardia, hypotension, diabetes, previous infarction etc. then the risk/benefit ratio may well tilt toward treatment.] Which thrombolytic agent should be chosen? The issue is not addressed except to observe that many other factors, some modifiable, others not, have a much greater influnce on mortality than does the precise agent chosen. Patients presenting early or with large anterior MIs may benefit more from tPA. Those with risk factors for ICH, from streptokinase. C. Complications: Pericarditis may occur from 24 hours to several weeks after infarction. Ibuprofen and steriods are effective for pain relief but may cause thinning of the scar and myocardial rupture. Heparin may be continued, generally, if pericarditis occurs but the patient should be closely observed for complications. Left ventricular dysfunction may be treated early on with IV NTG as ischemia is often implicated. For more severe LV failure NE should be used for SBP < 80. Above this level it is appropriate to start dopamine. When SBP reaches 90 dobutamine may be ADDED. Nonrandomized studies have yielded encouraging results of PTCA in cardiogenic shock unresponsive to lysis. IWMI may be complicated by right ventricular infaction which dramatically increases the mortality rate. The presence of jugular venous distention on exam and ST elevation in V4R are the most specific findings. ECHO may be useful diagnostically in equivical cases. Volume loading (1 -2 L NS) followed by dobutamine is specific therapy. Sustained polymorphic VT (greater than 30 sec) should be treated with *unsynchromized* countershok. Nonsustained VT (less than 5 beats) does not require treatment. Sustained polymorphic VT associated with hypotension, angina or pulmonary edema should be treated with *synchronized* countershock. Uncomplicated sustained monomorphic VT should be treated with lidocaine, procainamide, amiodarone and synchronized shock in that order provide that the rate is less than 150. For rates greater than 150 intial countershock is recommended. Accelerated idioventriculr rhythum usually has a good prognosis and does not require treatment other than observation. Prohylactic use of lidocaine is not indicated as mortality is not effected by this therapy. The reduced incidence of primary v-fib is offest completely by an increased incidence of asystole and EMD when this drug is used. D. Pharmacotherapy. Nitrates reduce the odds of death after acute MI by 35%. NTG may interfere with the actions of heparin and require larger doses of the latter for efficacy. Patients with a history of bleeding peptic ulces may be given rectal aspirin suppositories. Doses less than 160 mg acutely (orally) are needed for prompt antiplatelet effect. Patients undergoing lysis with tPA should concomitantly receive weight based heparin (70 u/kg bolus 15 u/kg/hr drip) titrated to PTT 1.5 to 2.0 times control. Those treated with stereptokinase should also receive heparin *only if* they are at high risk for systemic emboli (AWMI, atrial fib, previous embolus or LV thrombus). ROUTINE use of heparin in low risk patients traeted with steptokinase is not indicated. The evidence for the use of subcutaneous heparin in the latter instance (7500 to 12500 BID) is equivical. Baring contraindications beta-blockers are indicated in nearly all patients with acute MI. Their efficacy in non Q-wave infarction is unclear. They may reduce mortality if started within 2 hours of symptom onset. ACE inhibitors should be started in all patients with acute MI (baring contraindications) within the first 24 hours of therapy. ACE inhibitors are of greatest value in patients with high risk infarction including, but not limited to, those with impaired ventricular function. Meta-analysis reveals a mortality reduction on the order of 6.5 lives per 1000 patients treated. Verapamil or diltiazem are indicated when beta-blcokers are contraindicated or ineffective for relief of ischemia or control of the ventriclar response in atrial fib. Both drugs are contraindicated in the setting of LV dysfunction or failure. The use of nifedipine is contraindicated in acute MI. Patients with non Q-wave infarction, in the absense of LV dysfunction may benefit from the use of short acting preparations of diltiazem. Magnesium is clearly indicated and effective for torsade-type VT associated with prolonged QT interval. ISIS-4, in contrast to the results of a meta-analysis of 7 other randomized trials, found no benefit to the routine use of magnesium in acute MI. E. Adjunctive Pharmacological therapy: Haloperidol appears to be a safe and effective agent in the setting of acute MI for control of agitation. H. Louzon MD (1) ACC/AHA Guidelines for the Management of Patients with Acute Myocardial Infarction. JACC 1996;28:1328-1419 -------------- I wanted to make several additions and one correction to the MI guidelines: Because of a single typo, the paragraph on the treatment of VT contradicts itself. The correct paragrph is as follows: Sustained polymorphic VT (greater than 30 sec) should be treated with *unsynchromized* countershok. Nonsustained VT (less than 5 beats) does not require treatment. Sustained monomorphic VT associated with hypotension, angina or pulmonary edema should be treated with *synchronized* countershock. Uncomplicated sustained monomorphic VT should be treated with lidocaine, procainamide, amiodarone and synchronized shock in that order provide that the rate is less than 150. For rates greater than 150 intial countershock is recommended. Additions: Prehospital: Patients who are identified in the field as representing a 'high-risk' group by virtue of the presence of shock, pulmonary congestion, tachycardia (> 100) or hypotension (< 100) should be triaged to facilites with catheterization and revascularization facilities. Treatment: NTG (SL or IV) should be avoided in the presence of bradycardia (< 50) or tachycardia and used with extreme caution, if at all, in those with right ventricular infaction. Invasive hemodynamic monitoring, although not essential, is preferred. For purposes of assessing the risk/benefit ratio of thrombolyis when relative contraindications are present consider that high risk IWMI includes not only the presence of right ventricular infarction but those with anterior ST segment depression as well. For MIs in all locations factors that increase risk and thus benefit the most from lysis include diabetes, hypotension (< 100) and tachycardia. As usual, the presence of AWMI is considered a high risk feature in its own right. Although the risk/benefit of lysis is reduced in those over the age of 75 those with ST elevation still benefit from treatment. [Note that the criteria of new BBB was dropped from those over the age of 75. Whether this was deliberate or merely an oversight on their part is speculative.] Factors increasing the risk of ICH with lysis include age over 65, body weight less than 70 kg, HTN at presentation or the use of tPA (vs streptokinase). The presence of multiple risk factors increases the risk proportionately. ACE ihibitors may be particularly beneficial in the following subgroups: those with large or AWMI, CHF in the absence of hypotension and those with prior MI. The optimal time to initiate ACE inhibitors is *after* thrombolytics have been adminstered and the patient's hemodynamic status has stabilized. They are contraindicated in the presence of allergy, hypotension (< 100), renal failure or bilateral renal artery stenosis. The use of morphine is indicated because of its beneficial effects in reducing sympathetic stimulation. There is no indication for treatment of isolated PVCs, couplets, accelerated idioventricular rhythum or nonsustained (less than 5 beats) monomorphic or polymorophic VT. H. Louzon MD ================ Journal of American College of Cardiology site has this entire document at http://www-east.elsevier.com/jac/2805/jac2805toc.htm (Sorry, I haven't figured out how to put links in my e-mail yet) There are probably 200 pages if you try to print it out. For reprints, here is what is listed in the article: "Address for reprints: A single reprint of this document (the complete Guidelines) is available by calling 800-253-4636 (US only) or writing the American College of Cardiology, Educational Services, 9111 Old Georgetown Road, Bethesda, MD 20814-1699. Ask for reprint No. 71-0094. To obtain a reprint of the shorter version (Executive Summary and Summary of Recommendations) published in the November 1 issue of Circulation, ask for reprint No. 71-0092. To purchase additional reprints (specify version and reprint number)"