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<HTML><HEAD> <META NAME="GENERATOR" CONTENT="Adobe PageMill 2.0 Win"> <TITLE>Untitled Document</TITLE></HEAD><BODY TEXT="#bafddc" BGCOLOR="#006666" LINK="#ffcc66" ALINK="#fb1814" VLINK="#5cf373">(Numbered text commentary matches the numberson the ischemic chest pain algorithm.) <A NAME="anchor1"></A> <H2><A NAME="anchor89668"></A>1. Chest Pain: PainSuggestive of Ischemia</H2>Patients whose initial complaints suggest the possibility of one of theacute coronary syndromes must receive a prompt and targeted evaluation.The single most common symptom of infarction is retrosternal chest discomfort.This pain may be perceived as more of a pressure than an actual pain. Inaddition, heart attack warning signs may include <A NAME="anchor2"></A> <UL> <LI>Uncomfortable pressure, fullness, squeezing, or pain in the center of the chest lasting several minutes (usually more than 15 minutes) <LI>Pain spreading to the shoulders, neck, arms, jaw; or pain in the back or between the shoulder blades <LI>Chest discomfort with lightheadedness, fainting, sweating, nausea, or shortness of breath <LI>A global feeling of distress, anxiety, or impending doom</UL>The clinician must estimate the likelihood that the presenting conditionis an AMI or one of AMI's potentially lethal mimics. Although many conditionsare possible, the most important conditions that must be considered as thepatient is assessed and treated for an acute coronary syndrome include <A NAME="anchor3"></A> <UL> <LI>Aortic dissection <LI>Acute pericarditis <LI>Acute myocarditis <LI>Spontaneous pneumothorax <LI>Pulmonary embolism</UL>An emergency cardiac care provider should continue to think of thesealternative diagnostic possibilities even while proceeding down the managementoutlined in the rest of the algorithm. <A NAME="anchor4"></A> <H2><A NAME="anchor228808"></A>2. Immediate Assessment(<10 minutes)</H2>Every ED must establish a protocol approach for patients who presentwith chest pain and suspected AMI. Clinicians have referred to the intervalfrom the patient's arrival in the ED, determination of eligibility for reperfusiontherapy, and start of thrombolytic agents as the "door-to-drug"interval. EDs should aim for the goal of no more than 30 minutes to assessand begin reperfusion treatment for patients with evidence of coronary thrombosisand no reasons for exclusion. To help meet this goal, the items listed underimmediate assessment should be performed, whenever possible, within 10 minutes. <A NAME="anchor5"></A> Defined ED protocols should cover both assessment and the start of immediategeneral treatment. Team members should have predetermined roles that includethese tasks: <A NAME="anchor6"></A> <UL> <LI>Measurement of vital signs, including oxygen saturation (the "fifth vital sign") <LI>Attachment of a cardiac monitor <LI>Starting one to two intravenous infusion lines <LI>Drawing initial blood studies while the intravenous lines are being started. Serum cardiac markers, electrolytes, and coagulation studies can be drawn and labeled but not necessarily sent for laboratory processing in these initial 10 minutes. <LI>Portable chest x-rays are generally indicated and should be included for most patients, if not immediately then soon.</UL>One member of the emergency team must be identified as the person toobtain the initial 12-lead ECG. This person should operate under standingorders to obtain a 12-lead ECG on all patients triaged for chest pain andsuspected of an acute coronary syndrome. The 12-leadECG stands at the center of the decision pathway in the management of patientswith ischemic chest pain, and delays in obtaining the 12-lead ECG must beeliminated. EDs should have a dedicated ECG machine in the departmentand should not depend on a device coming from another location in the facility. <A NAME="anchor7"></A> <H2><A NAME="anchor229971"></A>3. Immediate GeneralTreatment</H2>Four agents are now recommended routinely for patients with ischemic-typechest pain, unless allergies or contraindications exist: <A NAME="anchor8"></A> <UL> <LI>Oxygen at 4 L/min. Use mask or nasal cannula. <LI>Nitroglycerin sublingual or IV (if the systolic blood pressure is greater than 90 mm Hg). Followed by: <LI>Morphine IV. Use small (1- to 3-mg) IV doses of morphine sulfate, repeated at 5-minute intervals as needed for those patients who do not get complete pain relief from nitroglycerin. Meperidine provides an acceptable alternative. Pain relief is a high priority. <LI>Aspirin PO. The routine use of aspirin (160 to 325 mg) is strongly recommended for all AMI patients (Class I), including those who receive thrombolytic therapy.</UL>ACLS instructors use the phrase "MONA greetsall patients" as a memory aid to help ACLS providers rememberthis list of immediate treatments. Unless contraindicated, "MONA"(morphine, oxygen, nitroglycerin, aspirin)is recommended for all three subsets of patients suspected of having ischemicchest pain: those with ST elevation, those with ST depression, and thosewith nondiagnostic ECG changes. The major contraindications to these agentsare hypotension for morphine and nitroglycerin (in particular hypotensionfrom a right ventricular [RV] infarction) and allergies to aspirin. <A NAME="anchor9"></A> <H2><A NAME="anchor230953"></A>4. Emergency MedicalServices Systems</H2>It is critical to recognize that only about 50% of the patients withischemic chest pain will arrive at the ED after calling 911 and receivingEMS care and transport. Major educational efforts to increase the percentageof people who recognize the warning signs of possible heart attack and call911 are under way in the United States. Much of the initial assessment andimmediate general treatment can be easily and appropriately started by EMSpersonnel. <A NAME="anchor10"></A> Through both standing protocols and as-needed contact with medical controlphysicians, EMS personnel can start intravenous lines, measure vital signsand oxygen saturation, obtain a targeted history with a chest pain checklistto determine eligibility for thrombolytic therapy, and obtain an initial12-lead ECG. The MONA treatments can be started, and the initial 12-leadECG can be transmitted via cellular or landline telephone. ComputerizedECG interpretation, available on field 12-lead ECGs, can be read orallyto the receiving ED, alerting hospital personnel to patients with acuteECG changes and arrhythmias. <A NAME="anchor11"></A> Whether EMS personnel should actually initiate thrombolytic therapy inthe prehospital setting is addressed in several prospective clinical trials.Positive benefit occurs in settings where there is a delay of 60 to 90 minutesbefore the start of thrombolytic therapy in the ED. In rural settings wheretransport times are often long, prehospital thrombolytic therapy is appropriate.Improved ED triage with routine door-to-needle times of 30 minutes or lesshas tended to offset the value or prehospital thrombolytic therapy, unlessthere are going to be delays. These short door-to-needle times are oftendue to the alerting function of the prehospital 12-lead ECG, which is becomingroutine in EMS systems in most cities. <A NAME="anchor12"></A> <H2><A NAME="anchor231903"></A>5. Assess Initial 12-LeadECG</H2>Today the 12-lead ECG stands at the center ofdecision making. Patients suspected of AMI and ischemia shouldhave a 12-lead ECG obtained and reviewed by the responsible clinician asquickly as possible, within 10 minutes of arrival at the ED, unless specialcircumstances intervene. The AHA Committee on Emergency Cardiovascular Care,the National Heart Attack Alert Program, and the ACC/AHA Task Force on AMIall place the highest priority on being able to classify patients into oneof three groups: <A NAME="anchor13"></A> <UL> <LI>ST-segment elevation <LI>ST depression or T-wave inversion <LI>Nondiagnostic ECG</UL>During medical observation in suggestive clinical circumstances, obtainrepeat ECGs (serial or continuous ECGs or ST-segment monitoring). If a patient'sserial ECG changes from one group's characteristics to another, eg, fromnondiagnostic ECG to ST elevation, change the therapeutic approach to followthe new classification. <A NAME="anchor14"></A> <H2><A NAME="anchor232713"></A>6. ST Elevation orNew or Presumably New BBB</H2>This group of chest pain patients now receives major clinical focus —these are the patients who benefit from acute reperfusion therapy. Numeroustrials of reperfusion therapy over the last decade have confirmed the unequivocalvalue of either thrombolytic therapy or acute angioplasty for this groupof patients. <A NAME="anchor15"></A> The clinician must search for ST elevation that is equalto or greater than 0.1 mV (1 mm on ECG calibrated to 10 mm/1 mV) in twoor more anatomically contiguous leads. This is a Class I indicationfor thrombolytic therapy if the patient is less than 75 years of age andthe time to therapy is 12 hours or less. <A NAME="anchor16"></A> ST-segment elevation must be measured correctly <A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch09/fig09_06.htx"TARGET="_blank">(see Fig 6)<IMG SRC="Book_ACLS/ACLS_Source_Art/ico09_06.gif" WIDTH="44" HEIGHT="32" ALIGN="BOTTOM" NATURALSIZEFLAG="3"></A>: <A NAME="anchor17"></A> <UL> <LI>Measure at 0.04 sec (1 mm) after the J-point. <LI>The J-point is the position of juncture (angle change) between the QRS complex and the ST wave. <LI>The baseline for this measurement traditionally has been the PR segment, but a baseline drawn from the start of the P wave to the end of the T wave is now considered more accurate, particularly for those patients who have either "coved" or "concave" ST segments and hyperacute T waves.</UL>Infarct Localization <A NAME="anchor18"></A> Clinicians who evaluate 12-lead ECGs for ST changes should develop theskill to estimate the location of the infarction, ischemia, or injury andto predict the coronary artery or arteries most likely to be thrombosed.In particular, clinicians who will administer thrombolytic agents must understandthe concept of anatomically contiguous leads. This topic of infarct localizationis discussed further in Infarct Localization: Usingthe 12-Lead ECG to Locate Ischemia, Injury, and Infarct, below<A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch09/fig09_07.htx" TARGET="_blank">(see Fig 7, A through I) <IMG SRC="Book_ACLS/ACLS_Source_Art/ico09_07.gif" WIDTH="58" HEIGHT="32" ALIGN="BOTTOM"NATURALSIZEFLAG="3"></A>. This skill helps identify those patients who willbenefit the most from thrombolytic therapy and helps predict specific complicationsthat are more likely to develop in one infarct location than in another. <A NAME="anchor19"></A> In particular, all patients with inferior injury or infarction shouldreceive a right precordial lead ECG as soon as the inferior abnormalitiesare recognized. The ECG will help identify patients with possible RV infarction.These patients should not, in general, receive nitroglycerin, morphine,or diuretics. <A NAME="anchor20"></A> Exceptions to the ST-Segment Elevation Rule <A NAME="anchor21"></A> Some subsets of patients may be eligible for thrombolytic therapy eventhough they do not present with ST-segment elevation or new BBB. Thrombolytictherapy is appropriate for these patients, especially if ischemic chestpain continues unabated or recurs after initial treatment: <A NAME="anchor22"></A> <UL> <LI>Posterior current of acute injury. Circumflex artery occlusions of the left coronary artery or posterior descending branch occlusions of the right coronary artery may produce a posterior LV infarction. This may be manifested only with marked ST-segment depression confined to leads V1 through V4. <LI>Tall, hyperacute T waves. In the most early phases of acute infarction the ECG may show only giant, hyperacute T waves, without ST-segment elevation.</UL>New or Presumably New LBBB <A NAME="anchor23"></A> BBBs tend to obscure the ECG diagnosis of MI, left BBB more so than right.BBB distorts the ST segment. Therefore, significant ST-segment elevation,as defined above, cannot be identified. New LBBB is considered the moreserious of the two types of BBB. LBBBs are caused by occlusion of the septalbranch of the left anterior descending branch of the left coronary artery.In most patients, right bundle branch blocks (RBBBs) are caused by occlusionof a branch of the right coronary artery. In general, old RBBB should notobscure the ability to interpret the ECG for ischemic and injury changes.New RBBB in the appropriate clinical setting of ischemic-type chest painwithout ST-segment elevation is a Class IIb indication for thrombolytictherapy. <A NAME="anchor24"></A> Determination of "new or presumably new" requires copies orreports of previous ECGs. Often these tracings will be difficult to obtain.Inability to determine old versus new BBB requires clinical judgment andassessment of the risks and benefits of thrombolytic therapy. In this clinicalsituation most clinicians let the story of onset of symptoms and the degreeof severity weigh heavily in the final determination. The more it appearsthat the pain and associated signs and symptoms are due to an AMI, the morelikely the BBB is to be new. <A NAME="anchor25"></A> Known Old LBBB: How to Read New Ischemic Changes <A NAME="anchor26"></A> Some studies have identified ECG criteria for reading ischemic changesin patients with old LBBB. The sensitivity and specificity of these criteriaremain under review. The management of these patients, in particular decisionsabout the best reperfusion strategy, should be undertaken in consultationwith a cardiologist. <A NAME="anchor27"></A> <H2><A NAME="anchor234045"></A>7. Consider AdjunctiveTreatments</H2>Patients with acute ischemic pain and ST elevation or new LBBB who havenot yet received aspirin and nitroglycerin should have those agents administered.At this point, pain control with intravenous morphinefor those patients who do not achieve complete pain relief from oxygenand nitroglycerin is a major goal. In addition, clinicians should consideradministration of the following adjunctive treatments: <A NAME="anchor28"></A> <UL> <LI>ß-Adrenoceptor blocking agents (ß-blockers) <LI>Nitroglycerin IV <LI>Heparin IV <LI>Angiotensin-converting enzyme (ACE) inhibitors</UL>These agents are placed in an algorithm box ahead of "Select a reperfusionstrategy." This does not mean that each adjunctive treatment must begiven before reperfusion therapy. In fact, ACE inhibitors, for example,are an adjunctive therapy that usually is started in the coronary care unit,after thrombolytics. The highest priority shouldbe on instituting definitive reperfusion therapy at the earliest possibletime after the onset of symptoms of infarction. <A NAME="anchor29"></A> <H3>ß-Adrenoceptor Blocking Agents (ß-Blockers)</H3>ß-Blockers increase myocardial salvage in the anatomic area ofthe infarct-related artery by reducing the size of the ischemic penumbraor shadow. ß-Blockers prevent extension of infarction by reducingoxygen consumption and the demands on threatened, ischemic myocardium. ß-Blockersalso reduce short-term and long-term mortality in AMI survivors. The agentsreduce the incidence of VF and "electrical storm." <A NAME="anchor30"></A> Recommended(patients with ST-segment elevation): <A NAME="anchor31"></A> <UL> <LI>All patients without a contraindication to ß-adrenoceptor blocker therapy if treated within 12 hours of onset of infarction (Class I) <LI>This means that ß-blockers are given not only as an adjunct to thrombolytic agents but also as agents with independent benefit</UL>Relative contraindications: <A NAME="anchor32"></A> <UL> <LI>Heart rate <60 bpm <LI>Systolic blood pressure <100 mm Hg <LI>Moderate or severe LV failure <LI>Signs of peripheral hypoperfusion <LI>PR interval >0.24 seconds <LI>Second- or third-degree block <LI>Severe chronic obstructive pulmonary disease <LI>History of asthma <LI>Severe peripheral vascular disease <LI>Insulin-dependent diabetes mellitus</UL><H3>Nitroglycerin IV</H3>Although extensively studied in large clinical trials, the exact rolefor intravenous nitroglycerin in AMI patients with ST-segment elevationhas not been established. In particular, the value of giving intravenousnitroglycerin to patients also receiving thrombolytic therapy is indeterminate. <A NAME="anchor33"></A> Nevertheless, nitroglycerin is appreciated for vasodilation of the coronaryarteries adjacent to sites of recent plaque disruption and for positivehemodynamic effects on the peripheral arteries and venous capacitance vessels.The ACC/AHA Practice Guidelines make the following recommendations: <A NAME="anchor34"></A> Recommended: <A NAME="anchor35"></A> <UL> <LI>Nitroglycerin IV is Class I for the first 24 to 48 hours in patients with AMI that is complicated by any of the following: <UL> <LI>CHF <LI>Large anterior infarction <LI>Persistent ischemia <LI>Hypertension </UL> <LI>Intravenous nitroglycerin infusion should be started early in the patients noted above, but this infusion should not delay start of reperfusion strategy (see precautions). <LI>For AMI patients without hypotension, bradycardia, or tachycardia, intravenous nitroglycerin is considered acceptable but only possibly helpful (Class IIb).</UL>Precautions: <A NAME="anchor36"></A> <UL> <LI>Avoid systemic hypotension because this will worsen myocardial ischemia and perfusion. <LI>Limit the drop in systolic blood pressure to 10% of the initial level if the patient is normotensive and to 30% if the patient is hypertensive; avoid a drop in systolic blood pressure below 90 mm Hg. <LI>Do not use pain as a way of titrating the infusion rate of nitroglycerin. <LI>Do not use nitroglycerin as a substitute for narcotic analgesics to achieve pain control — patients will often require both. <LI>Exercise extreme caution in the use of nitroglycerin in patients who may have RV infarction. These patients are particularly sensitive to nitroglycerin, diuretics, morphine, and any vasodilators. At highest risk for RV infarction are patients with ECG changes of inferior injury: ST-segment elevation in the inferior leads (II, III, aVF). These patients may experience profound hypotension because the infarction compromises RV function.</UL><H3>Heparin IV (patients with ST-segment elevation)</H3>Recommended: <A NAME="anchor37"></A> <UL> <LI>Patients receiving TPA and Retevase (Class IIa) <LI>Patients for whom the reperfusion strategy is PTCA or surgical revascularization (Class I)</UL>Precautions: <A NAME="anchor38"></A> <UL> <LI>Same contraindications as for thrombolytic therapy: <UL> <LI>Active bleeding <LI>Recent intracranial, intraspinal, or eye surgery <LI>Severe hypertension <LI>Bleeding disorders <LI>Gastrointestinal bleeding </UL> <LI>Sensitivity to heparin may be decreased when it is used concomitantly with intravenous nitroglycerin. Higher doses may be needed to achieve anticoagulation end point. Risk of bleeding is increased if nitroglycerin is stopped and heparin continues.</UL><H3>ACE Inhibitors</H3>Large clinical trials have confirmed a role for ACE inhibitors in reducingmortality from MI. This reduction occurs whether or not thrombolytic agentsare used, especially when ACE inhibitors are given early (in the first 12to 24 hours). In these trials ACE inhibitors have been particularly helpfulin patients with larger or anterior AMIs and with CHF without hypotension. <A NAME="anchor39"></A> Recommended(patients with ST-segment elevation): <A NAME="anchor40"></A> <UL> <LI>Patients whose suspected AMI is associated with ST-segment elevation in two or more anterior precordial leads <LI>Patients who during their AMI develop LV ejection fraction less than 40% <LI>Patients who during their AMI develop clinical signs of heart failure due to systolic pump dysfunction</UL>Precautions: <A NAME="anchor41"></A> <UL> <LI>In general, ACE inhibitors are not started in the ED but are started within the first 24 hours, after thrombolytic therapy has been completed and blood pressure has stabilized.</UL><H2><A NAME="anchor35509"></A>8. Time From Onset ofSymptoms?</H2>Onset of symptoms is defined as thebeginning of continuous, persistent discomfort that led to the patient'sdecision to call 911, come to the ED, or otherwise seek help. Frequently,however, patients will present with a "stuttering" or "on-off"pattern of pain, thus making the onset of symptoms difficult to determine.In general, for onset time, the physicianshould use the time of the experience that prompted the patient to seekcare. <A NAME="anchor42"></A> Patient delays in decision making after the onset of symptoms continueto present a major barrier to realizing the full benefits of reperfusiontherapy. The key principle is this: the earliertherapy begins, the better the outcome. Greatest benefit in survivaland LV function occurs when therapy is given within the first 3 hours. <A NAME="anchor43"></A> Studies have shown, however, that significant survival benefit occursup to at least 12 hours after onset of symptoms. Because management forthe two groups is different, the ischemic chest pain algorithm attemptsto divide patients by whether onset of symptoms is less than or greaterthan 12 hours. <A NAME="anchor44"></A> <H2><A NAME="anchor37503"></A>9. Select a ReperfusionStrategy</H2>Thrombolytic therapy is a Class I intervention if <A NAME="anchor45"></A> <UL> <LI>Clinical complaints are consistent with ischemic-type pain <LI>ST elevation <IMG SRC="Book_ACLS/ACLS_Source_Art/a_GreaterThen.gif" WIDTH="6" HEIGHT="10" ALIGN="BOTTOM" NATURALSIZEFLAG="3">1 mm in at least two anatomically contiguous leads <LI>There are no contraindications (<A HREF= "http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch09/ta09_03.htx" TARGET="_blank">see Table 3<IMG SRC="Book_ACLS/ACLS_Source_Art/ACLS_table_icon.GIF" ALIGN="BOTTOM" WIDTH="32" HEIGHT="23" NATURALSIZEFLAG="3"></A>) <LI>Patient is less than 75 years of age</UL>Patient Is More Than 75 Years of Age.For patients older than 75, thrombolytic therapy drops to a Class IIa intervention.The risks of thrombolytic therapy increase in this age group (primarilyintracranial hemorrhage), but so does the risk of untreated AMI. These patientsshould still be treated with thrombolytics even though the relative benefitof therapy is reduced. <A NAME="anchor46"></A> Time to Therapy Is Greater Than 12 Hours. The algorithm indicates that these patients areno longer candidates for an immediate reperfusion strategy. Clinical studiesindicate only a small benefit of either thrombolytic therapy or primaryPTCA for these patients. Sometimes, however, patients may give a story oflong duration (>12 hours), but on presentation they still have pain andST elevation. It is reasonable to conclude that myocardial cells are stillinfarcting. Thrombolytic therapy is therefore considered a Class IIb intervention(may offer some benefit) for this specific group of patients who displaycontinuing ischemic pain plus extensive ST elevation. <A NAME="anchor47"></A> <H2><A NAME="anchor51743"></A>10. Thrombolytic TherapySelected (No Contraindications)</H2>As of July 1997 there are three approved thrombolytic agents available(see the AHA Handbook of Emergency Cardiac Care for more details): <A NAME="anchor48"></A> <H3>Tissue Plasminogen Activator (TPA): Alteplase</H3>The GUSTO study and other recent clinical trials suggest that alteplase, given as an accelerated infusion,AND combined with intravenousheparin, is currently the most effectivetherapy to achieve early coronary reperfusion. This therapy produces superiorsurvival benefits. Alteplase, however, is much more expensive than streptokinaseand carries a greater risk of intracranial hemorrhage. The cost-benefitratio favors alteplase when patients present early with large areas of damageand low risk of brain hemorrhage. The recommendedaccelerated infusion dose is <A NAME="anchor49"></A> <UL> <LI>15-mg bolus IV <LI>Then 0.75 mg/kg over the next 30 minutes (not to exceed 50 mg) <LI>Then 0.50 mg/kg over the next 60 minutes (not to exceed 35 mg)</UL><H3>Streptokinase</H3>Streptokinase is the agent of choice for patients with a greater riskof brain hemorrhage and with a smaller potential for survival benefit (thosepatients with longer times from onset of symptoms and smaller areas of injury).Avoid reuse of streptokinase for at least 2 years (preferably indefinitely).This is because of a high prevalence of potentially neutralizing antibodies.The standard dose is <A NAME="anchor50"></A> <UL> <LI>1.5 million IU in a 1-hour infusion</UL><H3>Reteplase (Recombinant Retevase)</H3>Retevase is the newest thrombolytic agent to receive approval for clinicaluse in the United States (late 1996). Initial data from the GUSTO-III trialindicate that it is equal in efficacy to TPA. Retevase has the advantageover current treatment regimens that it is administered as a double bolus.Retevase dosing is not based on weight. Regimen is double-dose dosing forall patients: <A NAME="anchor51"></A> <UL> <LI>10 units IV plus a 10-unit IV bolus over 2 minutes, 30 minutes apart</UL>Heparin and aspirinshould probably be administered conjunctively because all clinical trialshave been conducted with conjunctive heparin and aspirin. An infusion pumpis not required, and administration is complete in 30 minutes. <A NAME="anchor52"></A> <H2><A NAME="anchor52982"></A>11. Patients Selectedfor Primary PTCA or With Contraindications to Thrombolytic Therapy</H2>At this time both primary PTCA and thrombolytic therapy are consideredClass I interventions for acute, developing MI. Some experts, however, thinkprimary PTCA is superior to thrombolytic agents alone. See the ACC/AHA PracticeGuidelines for more on this issue. <A NAME="anchor53"></A> Consideration of thrombolytic therapy requires a thorough review forcontraindications. One or more of several contraindications may be discovered.At this point in decision making the clinician faces a patient with <A NAME="anchor54"></A> <UL> <LI>ST-segment elevation or new or presumably new BBB <LI>Less than 12 hours from onset of symptoms <LI>But thrombolytic therapy is contraindicated for any of a number of reasons.</UL>This clinical scenario constitutes an indication for primary PTCA. Theclinician, in collaboration with the responsible cardiologist, should arrangefor the patient to go quickly to the catheterization laboratory. Arrangementsfor transfer should be initiated if these facilities are unavailable atthe hospital of initial presentation. MONA and adjunctive therapy shouldcontinue to be administered when indicated. <A NAME="anchor55"></A> <H2><A NAME="anchor54103"></A>12. Primary PTCA Selected— Goal: Door-to-Dilatation Interval or Arrival-in–CatheterizationLab Interval <60 Minutes</H2>Early Primary PTCA: an Equivalent Alternativeto Early Thrombolytic Therapy. The ischemic chest pain algorithmshows equal status for angioplasty and thrombolytics as reperfusion strategies.This equivalence exists, however, only if the primary angioplasty can beperformed rapidly (interval from arrival at the ED ["door time"]to arrival in the catheterization suite less than 60 minutes or to inflationof the catheter balloon less than 90 minutes ["dilatation time"]).In addition, the ACC/AHA Practice Guidelines require other stringent conditionsbefore PTCA can be considered an equivalent alternative to thrombolytictherapy: <A NAME="anchor56"></A> <UL> <LI>Operators must be skilled in the procedure (defined as having performed more than 75 PTCA procedures per year) <LI>The PTCA center must be high volume (performs more than 200 PTCA procedures per year) <LI>The PTCA operators and centers must operate within a specified "corridor of outcomes" defined by flow rates attained and low complication rates (defined in the 1996 ACC/AHA Practice Guidelines, page 1349)</UL>Twenty percent of US hospitals have cardiac catheterization laboratories;a portion of these centers can perform emergency PTCA. The emphasis in ACLStraining therefore will continue to be on rapid identification of thosepatients who qualify for thrombolytic therapy and rapid initiation of thrombolyticagents. <A NAME="anchor57"></A> PTCA. More than 70% of patients are within 30 minutes of a catheterizationlaboratory. Emergency coronary catheterization with possible angioplastymust be considered early in the following situations: <A NAME="anchor58"></A> Recommended (patients with ST-segmentelevation): <A NAME="anchor59"></A> <UL> <LI>Patients with signs and symptoms of a large AMI for less than 12 hours who should receive thrombolytic therapy but have a contraindication to thrombolytic therapy because of a risk of bleeding (Class I) <LI>Patients with possible "stuttering" infarction, with ECG changes, but without clear indication for thrombolytic therapy (Class IIa) <LI>Patients with AMI who develop cardiogenic shock or pump failure within 18 hours (Class IIa) <LI>Patients with a history of previous coronary artery bypass graft (CABG) surgery in whom a recent occlusion of a vein graft may have occurred (Class IIa) <LI>Patients with a possible AMI in the hospital that is an observed AMI with rapid access to a catheterization facility (Class IIb). <LI>Patients who receive thrombolytic therapy for appropriate reasons but who fail to reperfuse and who develop or continue symptoms</UL><H2><A NAME="anchor55305"></A>13. ST Depression orT-wave Inversion: ECG Strongly Suspicious for Ischemia</H2>Clinical trials have observed no benefit and even harm when thrombolyticagents have been administered to acute coronary syndrome patients with onlyST-segment depression or T-wave inversion. These patients are members ofa dynamic subgroup who merit at least one repeat ECG during evaluation.Most of these patients will need to be admitted to the CCU or other monitoredlocation. Serum markers of myocardial necrosis are not helpful in decisionmaking for these patients during the first hours of their evaluation unlessthe levels are abnormally elevated. These patients will usually need admissionregardless of normal serum enzyme markers. <A NAME="anchor60"></A> They should be rapidly treated as outlined further in the algorithm andshould be assessed quickly for whether they fall into a high-risk clinicalcategory. <A NAME="anchor61"></A> Posterior current of injury? Marked ST-segment depression that is confined toleads V1 through V4may indicate an occlusion of a circumflex artery producing damage in theposterior portion of the left ventricle. Thrombolytic therapy should beconsidered for these patients, especially if ischemic chest pain continuesunremittingly. <A NAME="anchor62"></A> <H2><A NAME="anchor56696"></A>14. Consider AdjunctiveTreatments (ST Depression or T-wave Inversion: ECG Strongly Suspicious forIschemia)</H2>With the exception of thrombolytic therapy, ischemic chest pain patientswith ST-segment depression or new T-wave inversion receive the same adjunctivetherapy as that administered to patients with ST-segment elevation. Thereare some differences in indication as discussed below. <A NAME="anchor63"></A> In the first several hours of management, it is unclear where to placethese patients in the acute coronary syndromes — whether they willhave positive serum markers (thus defining an AMI) or negative serum markers(thus defining unstable angina) or whether the patients with positive serummarkers will develop Q waves or non–Q waves. <A NAME="anchor64"></A> <H3>Heparin IV</H3>Recommended: <A NAME="anchor65"></A> <UL> <LI>If there are no contraindications, chest pain patients with acute ST-segment depression and T-wave inversions should receive heparin IV under the assumption that they have unstable angina.</UL><H3>Nitroglycerin IV</H3>Recommended: <A NAME="anchor66"></A> <UL> <LI>If pain is not controlled with up to 3 sublingual nitroglycerin tablets, 3 metered spray doses, or nitroglycerin paste <LI>If pain recurs after initial abatement <LI>If blood pressure is elevated after giving ß-blockers <LI>If signs of CHF develop</UL>Relative Contraindications: <A NAME="anchor67"></A> <UL> <LI>Hypotension (systolic blood pressure <90 mm Hg <LI>Inferior ECG changes (suspected RV infarction)</UL><H3>ß-Adrenoceptor Blocking Agents (ß-Blockers)</H3>Recommended: <A NAME="anchor68"></A> <UL> <LI>Patients with continuing or recurrent ischemic pain <LI>Patients with tachyarrhythmias, such as atrial fibrillation with a rapid ventricular response</UL>Relative contraindications: <A NAME="anchor69"></A> <UL> <LI>Same as listed under box 7</UL>Calcium Channel Blockers (if ß-blockade is inadequate ornot tolerated). Most cardiologists consider calcium channel blockers tobe an overprescribed medication for the AMI patient. The ACC/AHA PracticeGuidelines list calcium channel blockers as an adjunctive treatment butonly for a limited list of indications: <A NAME="anchor70"></A> Recommended: <A NAME="anchor71"></A> <UL> <LI>(Class IIa) Calcium channel blockers are a second-line agent (after ß-blockers, nitroglycerin, and analgesics) for continuing ischemia or control of heart rate in patients with atrial fibrillation. Avoid in patients with CHF, LV dysfunction, or AV block. Use when ß-blockers are contraindicated. <LI>(Class IIb) It is acceptable to give diltiazem routinely to patients without ST-elevation AMI if they lack LV dysfunction, pulmonary congestion, or CHF. Do not start until after the first 24 hours.</UL>Contraindications: <A NAME="anchor72"></A> <UL> <LI>Do not use nifedipine as routine treatment in AMI (negative inotropic effects, harmful reflex sympathetic activation, tachycardia, and hypotension). <LI>Do not use diltiazem or verapamil in AMI patients if they have associated LV dysfunction or CHF.</UL><H2><A NAME="anchor58696"></A>15. Assess ClinicalStatus</H2>At box 15 the clinician is dealing with an ischemic chest pain patientwith ST-segment depression or T-wave inversion or a patient with ST-segmentelevation but more than 12 hours from onset of symptoms. The critical decisionmaking at this point is to determine whether these patients fit into a high-riskcategory or are clinically stable. This distinction has important therapeuticimplications. <A NAME="anchor73"></A> <H2><A NAME="anchor59850"></A>16. High-Risk Patient</H2>Patients who are assessed as high risk at this point (abnormal ECG) willneed cardiac catheterization. A patient should be considered high risk ifhe or she <A NAME="anchor74"></A> <UL> <LI>Experiences recurrent (stuttering) breakthroughs of ischemic pain despite morphine, nitroglycerin, and ß-blockers (Class I indication for angiography) <LI>Exhibits signs of depressed LV function, shock, and pulmonary congestion (Class I) <LI>Continues to have unremitting, persistent ischemic discomfort that has not been controlled with aggressive use of morphine, nitroglycerin, and ß-blockers (Class II) <LI>Displays ECG changes of ST depression in multiple leads, suggesting extensive cardiac ischemia (Class IIa) <LI>Has a history of two or more risk factors for coronary artery disease, including prior AMI, prior angioplasty, or prior CABG (Class IIa)</UL>The ACC/AHA Practice Guidelines recommend taking these high-risk patientsto the cardiac catheterization suite for diagnostic and therapeutic purposes.For the more than 80% of US hospitals that are not equipped for cardiaccatheterization, the clinician should consider transfer to a medical centerthat has such capabilities. <A NAME="anchor75"></A> <H2><A NAME="anchor61007"></A>17. Perform CardiacCatheterization: Anatomy Suitable for Revascularization?</H2>The goal here is to identify, first of all, those high-risk patientswho have a coronary artery lesion that can be effectively treated with balloonangioplasty or stent placement or both. If the angioplasty fails, the patientbecomes a potential candidate for CABG. Second, many of these high-riskpatients will have left main coronary stenosis or severe multivessel diseasethat may be treatable by emergent or urgent CABG. The catheterization providesanatomic information to the vascular surgeon. <A NAME="anchor76"></A> <H2><A NAME="anchor62374"></A>18. Revascularization:</H2><UL> <LI>PTCA <LI>CABG</UL>When indicated, PTCA may producedramatic results with immediate relief of pain and cardiac dysfunction onthe catheterization table. CABG comesinto play primarily for those patients with left main coronary artery stenosisand severe multivessel disease when other therapies have failed. The indicationsfor urgent CABG surgery in patients with anatomy suitable for surgery are <A NAME="anchor77"></A> <UL> <LI>Failed angioplasty with persistent pain (Class I) <LI>Hemodynamic instability (Class I) <LI>Ischemia refractory to medical therapy plus the patient is not a candidate for catheter intervention (Class I) <LI>Cardiogenic shock (Class IIa) <LI>Failed PTCA with a small area of myocardium at risk (Class IIb)</UL><H2><A NAME="anchor63679"></A>19. Clinically Stable(ST-Segment Depression or T-wave Inversion)</H2>These patients, presenting with ischemic chest pain and ST-segment depressionor T-wave inversion, should not be considered clinically stable unless theyare free of pain and virtually asymptomatic. Morphine, intravenous nitroglycerin,and intravenous ß-blockers may have been required and may still beneeded. These patients display none of the high-risk criteria (box 16).With rare exceptions, these patients will require hospital admission (box20). <A NAME="anchor78"></A> <H2><A NAME="anchor65126"></A>20. Admit to CCU/MonitoredBed</H2><UL> <LI>Continue or start adjunctive treatments as indicated (see box 14) <LI>Obtain serial serum markers <LI>Obtain serial ECGs <LI>Consider imaging study (radionuclide or 2D echocardiography)</UL>Patients have arrived at this point in the ischemic chest pain algorithmfrom three different subsets. All three groups need admission to a monitoredbed, serial serum markers, and serial ECGs. Making these patients pain-freecontinues as a major goal. Adjunctive treatments should continue or be startedbased on specific indications (see box 14). Alternatives to expensive CCUbeds are appropriate for low-risk MI patients, eg, patients presenting morethan 12 hours from onset of symptoms with normal ECGs and normal serum cardiacmarkers in the ED. Consider an imaging study such as radionuclide or two-dimensionalechocardiography as a means to diagnose wall motion abnormalities and tofurther risk-stratify the patient. <A NAME="anchor79"></A> From box 19 <A NAME="anchor80"></A> <BLOCKQUOTE> This group of now clinically stable patients with ST depression or T-wave inversion represents part of the continuum between chronic stable angina and typical AMI with ST-segment elevation. Unlike patients with ST-segment elevation, these patients probably do not have total occlusion of the coronary artery. About half of these patients will have enzymatic evidence of myocardial necrosis; the majority of these will not develop Q waves. <A NAME="anchor81"></A> </BLOCKQUOTE>From box 17 <A NAME="anchor82"></A> <BLOCKQUOTE> This is the group of high-risk patients who have received cardiac catheterization but did not have anatomy suitable for revascularization. Continue or start all indicated adjunctive therapy, in particular aspirin, nitroglycerin, heparin, ß-blockers, or calcium channel blockers, along with continued oxygen and analgesia. If serial ECGs reveal development of ST segment elevation, thrombolytic therapy becomes indicated. <A NAME="anchor83"></A> </BLOCKQUOTE>From box 24 <A NAME="anchor84"></A> <BLOCKQUOTE> These patients with an acute coronary syndrome, admitted because they have evidence of ischemia/infarction but nondiagnostic ECG changes, will probably evolve a non–Q-wave infarction pattern. This is more common in the elderly and in patients with prior MI. The incidence appears to be increasing because of the greater use of aspirin and ß-blockers. <A NAME="anchor85"></A> </BLOCKQUOTE><H2><A NAME="anchor67265"></A>21. Nondiagnostic ECG:Absence of Changes in ST Segment or T Waves</H2>Trials have observed thrombolytic therapy to be ineffective for subgroupsof patients with an acute coronary syndrome and a nondiagnostic ECG withoutchanges in ST segment or T waves. Once a patient with chest pain is notedto have nondiagnostic ECG changes, the patient is no longer a high-prioritycandidate for thrombolytic therapy. <A NAME="anchor86"></A> Patients who have not yet received aspirin,nitroglycerin, and morphineas indicated should immediately have these agents administered, especiallyif pain continues. Control of pain with intravenous morphineand nitroglycerin should be a majorgoal, as it is for all patients with a suspected acute coronary syndrome. <A NAME="anchor87"></A> <H2><A NAME="anchor68656"></A>22. Meets Criteria forUnstable or New-Onset Angina?</H2>This box focuses the clinician on the important branch point of whetherthe patient meets criteria for unstable or new-onset angina. This decisionpoint has major therapeutic implications. Patients who are classified ashaving unstable angina need to be started on intravenous heparin. Otheradjunctive treatments, discussed in box 14, may be indicated. As discussedabove, unstable angina is just one point of the continuum of the acute coronarysyndromes, falling somewhere between stable angina and AMI with ST-segmentelevation. <A NAME="anchor88"></A> Stable Angina. Stable angina is aclinical syndrome usually characterized by a deep, poorly localized chestor arm discomfort that is reproduciblyassociated with physical exertion or emotional stress and that is predictably relieved promptly with restor sublingual nitroglycerin. <A NAME="anchor89"></A> Unstable Angina. In general, unstableangina is a change in the pattern of predictability of stable angina. Thereare three principal presentations of unstable angina: <A NAME="anchor90"></A> <UL> <LI>Rest angina. Angina that occurs at rest, usually prolonged more than 20 minutes. <LI>New-onset angina. Chest pain that starts with physical exertion and that produces marked limitation of ordinary physical activity; occurs on walking one to two blocks on the level and climbing one flight of stairs in normal conditions and pace; symptoms have begun within the past 2 weeks. <LI>Increasing angina. Previously diagnosed angina that is distinctly more frequent, longer in duration, or lower in threshold (refers to the level of activity that reproduces the pain). Changes in threshold (moving from one class to a higher class) can be graded according to these classes: <UL> <LI>Class I: Ordinary physical activity does not cause the angina. Pain requires strenuous, rapid, or prolonged exercise. <LI>Class II: Slight limitation of ordinary activity. Pain occurs on (1) walking or climbing stairs rapidly, walking uphill, stair-climbing after meals, or in the wind or cold or (2) walking more than two blocks or climbing more than one flight of stairs at normal pace. <LI>Class III: Marked limitation of ordinary physical activity. Pain occurs after walking one or two blocks on the level or climbing one or two flights of stairs at a normal pace. <LI>Class IV: Inability to carry on any physical exertion without discomfort. </UL></UL>New-onset Angina Versus AMI? Whatis the distinction between new-onset angina and the pain of a classic AMI?The most frequent presentation of documented AMI is the sudden onset ofsevere, prolonged (more than 15 minutes), substernal chest pain or pressure,most commonly occurring at rest.From the patient's perspective, angina usually appears to have a clearrelation to physical activity and exertion.However, the majority of patients with new-onset angina, as a form of unstable angina, have pain at rest, with coronaryartery spasm occurring in addition to thrombus. The distinction, therefore,between new-onset angina and AMI is impossible to make on history alone.It must be reiterated that the most urgent clinicalobligation is to identify the subset of these patients who have associatedST-segment elevations — these are the reperfusion candidates. <A NAME="anchor91"></A> <H2><A NAME="anchor71790"></A>23. Consider:</H2><UL> <LI>Admission to CCU/intermediate care? <LI>Admission to chest pain observation unit? <LI>Continued ED evaluation? <LI>Appropriate to discharge from ED?</UL>At this point the clinician must make several critical decisions abouta patient who has these features: ischemic-like chest pain on presentationbut is now pain-free either with or without morphine, nitroglycerin, orß-blockers; a nondiagnostic ECG; and absence of criteria for unstableangina. Several observations are critical: <A NAME="anchor92"></A> <UL> <LI>A normal ECG does not rule out MI; the serial ECG changes that indicate an AMI may start within 1 hour or may take up to 24 hours to develop. <LI>The large majority of these patients (approximately 80% to 85%) will not turn out to have an MI. <LI>Serum markers of MI do not begin to become positive until 2 to 4 hours after the tissue damage; the ACC/AHA Practice Guidelines recommend checking the serum markers over 8 to 12 hours when initial enzyme levels are not elevated <A HREF="http://localhost:8032/servlet/lp?url=Book_ACLS/ACLS_ch09/fig09_05.htx" TARGET="_blank">(see Fig 5) <IMG SRC="Book_ACLS/ACLS_Source_Art/ico09_05.gif" WIDTH="62" HEIGHT="32" ALIGN="BOTTOM" NATURALSIZEFLAG="3"></A>. Whether this prolonged ED time will be accepted widely by specialists in emergency medicine is not yet established. <LI>Radionuclide and 2D echocardiographic cardiac imaging can detect wall motion abnormalities early in MI, even earlier than ECG and serum marker changes. <LI>Exercise stress testing of this group of patients has acceptable sensitivity in detecting those who can safely be discharged (nondiagnostic ECG and pain-free).</UL>According to the ACC/AHA Practice Guidelines, it is no longer acceptablefor clinicians to discharge the suspicious ischemic chest pain patient witha nondiagnostic ECG on the basis of history, physical examination, and risk-factorevaluation alone. Instead the clinician is obligated to obtain additionalobjective evidence that myocardial ischemia or infarction has not occurredor is not occurring. This objective evidence can take the form of <A NAME="anchor93"></A> <UL> <LI>Serial serum cardiac markers <LI>Serial or continuous ECGs <LI>2D echocardiography or radionuclide cardiac imaging <LI>Stress testing</UL>A variety of alternatives to the expensive practice of "admit toCCU — rule out AMI" are now being explored. These approaches areacceptable, provided close patient monitoring can be provided. They include <A NAME="anchor94"></A> <UL> <LI>Admission to an intermediate level "telemetry-observation" or "step-down" unit <LI>Admission to a "chest pain evaluation unit" (often a designated area within the ED) where 2D echocardiography, radionuclide cardiac imaging, or stress testing can be performed <LI>Continued evaluation in a monitored ED bed</UL><H2><A NAME="anchor73724"></A>24. Evidence of Ischemiaor Infarction Over 8 to 12 Hours?</H2>The thrust of this decision point is to change explicitly the clinicalpractice in many EDs. An implicit weighing of evidence has been centralin the practice of emergency physicians making the decision to admit ornot admit a patient with chest pain. This decision making now becomes lessdependent on implicit clinical judgment and more dependent on explicit objectiveinformation. Several changes in practice are likely: <A NAME="anchor95"></A> <UL> <LI>Fewer CCU admissions: fewer patients will be immediately admitted to "rule out AMI" as in the past, for they can now be ruled out over 8 to 12 hours in the ED. <LI>Fewer quick ED discharges: fewer patients will be quickly discharged from the ED, for they now need to stay until the 8 to 12 hours have passed. <LI>Longer ED stays: more patients will spend longer time in the ED or "chest pain center" waiting for serial serum markers of MI and serial ECGs. <LI>More complex ED workups: longer stays in the ED allow more evaluations to be performed in the ED, often in conjunction with cardiology outpatient evaluations. <LI>More use of intermediate care units or step-down units or "short hospital stays" (<24 hours): now patients can be placed more accurately into specific risk categories.</UL><H2><A NAME="anchor75256"></A>25. Discharge Acceptable</H2><UL> <LI>Arrange Follow-up</UL>It is acceptable to discharge most patients presenting with ischemic-typechest pain who have nondiagnostic ECG changes and who have had no ECG orserum marker evidence of ischemia/infarction over 8 to 12 hours of monitoring.Note that these patients should have been rendered pain free within minutesof presenting to the ED. If the pain could not be quickly eliminated soonafter ED presentation, then the patient falls into one of the other categoriesof unstable angina, new-onset angina, or high risk. <A NAME="anchor96"></A> Before discharge from the ED, these patients should receive specific,written directions for obtaining prompt follow-up evaluation. Patients shouldbe instructed explicitly to call 911 and to return to the ED should anyof their symptoms recur. Voice-to-voice contact with the physician who willtake responsibility for continued evaluation is recommended if practical.These actions not only comprise appropriate clinical care but also diminishthe marked risk ED physicians face for possible malpractice accusationsand actions.</BODY></HTML>