Henry Ford Hospital Medical Journal Henry Ford Hospital Medical Journal

Volume 39 Number 3 Article 7

9-1991

Prehospital Care of Acute Myocardial Infarction: A Review Prehospital Care of Acute Myocardial Infarction: A Review

Asit R. Gokli

Jay L. Kovar

Terry Kowalenko

Richard M. Nowak Henry Ford Health System, rnowak1@hfhs.org

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Recommended Citation Recommended Citation Gokli, Asit R.; Kovar, Jay L.; Kowalenko, Terry; and Nowak, Richard M. (1991) "Prehospital Care of Acute Myocardial Infarction: A Review," Henry Ford Hospital Medical Journal : Vol. 39 : No. 3 , 170-175. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol39/iss3/7

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Therapy

Prehospital Care of Acute Myocardial Infarction: A Review

Asit R. Gokli, MD,* Jay L. Kovar, MD,* Terry Kowalenko, MD,* and Richard M. Nowak, MD*

Each year more than 1 million people in the Uniled States suffer from acute myocardial infarction (Ml) with most ofthe deaths occurring within hours of symptom onset. Over the last 25 years, different prehospital systems have evolved throughout the world which allow early cardiac monitoring and treatment of acute Ml patients. Thrombolytic therapy in acute Ml has heen shown to decrease mortality and preserve left ventricular function when administered early after onset of symptoms. The potential role of Emergency Medical Services or Mohile Coronary Care Units in achieving early thrombolysis is under investigation. Several studies of prehospital interventions to achieve early thrombolysis are reviewed. The use of thrombolytics by prehospital personnel has been found to he feasible, safe, and effective in reducing time delays. However, whether this translates into clinical benefit remains to he seen. (Heniy Ford Hosp Med J1991:39:170-5)

M yocardial infarction (MI) affects more than 1 million peo­ple per year in the United States and accounts for over

25% of overall annual deaths (1). Most deaths from acute M l oc­cur shortly after the onset of symptoms and therefore outside of the hospital (2). Recognition of this has led to the development of efficient prehospital care over the last 25 years which has proved to be lifesaving in terms of treating chest pain and seri­ous dysrhythmias with medicafions and defibrillafion.

Over the last decade it has become known that early lysis of an occluding thrombus in the setfing of an acute M I results in improved left ventricular (LV) function (3-6), reduction in im­mediate mortality (7,8), and enhancement of long-term survival (9,10). This has renewed medical interest in the prehospital care of acute M I . Several studies are under way to better define the role of prehospital care of acute M I . The important questions to be answered are: Should thrombolytic therapy be begun in the prehospital setfing? Is it feasible, safe, and effective? How can prehospital care of acute M I contribute to early diagnosis and the decision to use thrombolyfic therapy?

Developments in Prehospital Care of Acute MI in the United States

The standardization of prehospital emergency medical ser­vices (EMS) is a relatively new component of health care. A l ­though the roots of prehospital care date back to military cam­paigns in the 18th century and hospital transport in the 1860s, prehospital services did littie to provide therapeutic interven­tions and reduce mortality and morbidity until the mid 1960s.

In 1967, in Belfast, Northem Ireland, the first mobile coro­nary care unit (MCCU) was established. Utilizing cardiac moni­

tors and defibrillation capabilities, the Belfast group showed positive benefits by prompt and skillful treatment early in the course of acute M I before the patient reached the critical care unit (CCU) in the hospital (11).

Over the years, the administration of antiarrhythmic agents and defibrillation have become well established prehospital in­terventions. Early defibrillation has been shown to be the single most beneficial prehospital intervention (12). However, the ben­efits of early prehospital care of acute M I are multifactorial. These include: 1) relief of chest pain; 2) cardiac monitoring for early recognition and prompt treatment of dysrhythmias by pharmacologic agents, defibrillation, and electrical cardiac pac­ing; and 3) control of blood pressure and heart rate (2). Treat­ment of autonomic dysfunction (hypotension and bradycardia) associated with acute M I in the prehospital setting has been shown to decrease ultimate mortality and morbidity (13). Be­sides decreasing mortality, effective, early prehospital care may also prevent extension of M I and the later development of pump failure (2).

Different systems have evolved throughout the world over the last 25 years to treat acute M l during the prehospital phase. In the United States, mobile coronary care has largely been in­corporated into the EMS system which is staffed by emergency medical technicians (EMTs) and paramedics (EMTs with spe­cialized training including advanced cardiac life support and an

Submitted for publication: September 13, 1991, Accepled for publication: Oclober 30, 1991, *Departmenl of Emergency Medicine, Henry Ford Hospital, Address correspondence lo Dr, Gokli, Department of Emergency Medicine, Henry Ford

Hospilal, 2799 W Grand Blvd, Detroit, Ml 48202,

170 Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Prehospital Care of Acute Ml—Gokli el al

upgraded level of skills). Timely assessment and therapeutic in­tervention, not limited to resuscitation, includes treatment of secondary complications of acute MI such as hypotension, hy­poxia, bradycardia, pulmonary edema, ventricular fibrillation, and cardiac arrest (14). Thus, in the United States, prehospital care of acute MI is provided by paramedics or EMTs or a combi­nation of both.

Recent advances in thrombolytic therapy in acute MI and its time-dependent character have led to a new emphasis on the pre­hospital care of acute MI.

Historical Review of Thrombolytics in Acute MI Acute transmural MI is a thrombotic process (15). Coronary

artery thrombus causing total occlusion of the infarct-related vessel is present in 80% to 90% of patients with acute Ml. In about 15% to 20% of patients, an intraluminal thrombus is pres­ent which causes subtotal occlusion of the infarct-related vessel.

DeWood et al (16), performing cardiac catheterization and coronary angiograms in 210 Ml patients wilhin 6 hours of the onset of symptoms, found that 87% of patients had total occlu­sion ofthe infarct-related vessel.

Working with animal models, Reimer and Jennings et al (17, 18) studied the time course of myocardial necrosis after coro­nary occlusion. They demonstrated that coronary artery occlu­sion followed by variable lengths of ischemia and then by reper­fusion resulted in predictable degrees of myocardial necrosis. This myocardial necrosis proceeds from the subendocardial to the subepicardial layers ofthe myocardium in a wavefront of ne­crosis in a time-dependent manner. Early reperfusion occurring within minutes of occlusion ofthe vessel resulted in minimal to no myocardial necrosis, whereas reperfusion occurring later in the time course resulted in a variable amount of subendocardial necrosis.

Initial human studies with thrombolytic agents utilized intra­coronary administration of streptokinase (SK). In 1979, Feit and Rentrop (19) demonstrated reestablishment of distal blood flow after administration of SK directly into the coronary thrombus. Anderson et al (20) studied 50 patients and demonstrated that intracoronary SK administered at 2.7 hours after the onset of symptoms resulted in a seven-point difference in ejection frac­tion (EF) and thus significant myocardial salvage compared to patients with acute MI who received roufine CCU care. Khaja et al (21) studied 40 patients who received intracoronary SK at an average of 4.8 hours afterthe onset of symptoms of acute MI. No improvement was seen in EF compared to the control group. The difference in improvement in EF in the Anderson (20) and Khaja (21) studies was mainly due to a significant difference in time to treatment (2.7 versus 4.8 hours). The Westem Washing­ton randomized trial demonstrated that intracoronary SK ad­ministered within the first 6 hours of the onset of symptoms re­duced 30-day mortality rates. This benefit persisted at one-year postinfarction when intracoronary SK had resulted in total coro­nary reperfusion (8,22).

Emergency cardiac catheterization and coronary angiograms involve significant time delay, usually about 90 to 180 minutes. Many hospitals are not equipped for cardiac catheterization and

so this mode of therapy is available to few patients with acute Ml. Thus, medical research has focused on the intravenous (IV) administration of thrombolytics.

The Intravenous Streptokinase in Acute Myocardial Infarc­tion study found that patients treated within 1.5 hours ofthe on­set of symptoms had significantly shorter time to peak creat­inine kinase (CK) interval, smaller area under CK-MB curve, and higher global or infarct-related regional EEs compared to patients treated within 1.5 to 4 hours after acute Ml (23).

Fine et al (24) found that IV thrombolytic therapy admini­stered within 2 hours of symptoms in patients with acute ante­rior wall MI resulted in smatier infarct size compared to patients treated within 2 to 4 hours from time of symptoms.

Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto Miocardico (GISSl), a multicenter, placebo-controlled, randomized trial, also utilized IV SK (25). This study conclu­sively showed a reduction in overall mortality of 18% in patients treated with IV SK compared to patients who received routine CCU care. Patients treated within 3 hours of the onset of symp­toms had a 23% reductton in in-hospital mortality. In patients who received IV SK within 1 hour of the onset of symptoms, the in-hospital mortality was reduced by 47% compared to the con­trol group. This survival advantage persisted at one-year follow-up.

Thus, IV thrombolytic therapy given to patients with acute MI appears to lyse the occluding thrombus, reestablish perfu­sion to the ischemic myocardium, and prevent or limit myocar­dial necrosis in a time-dependent manner. The "golden period" appears to be the first 2 to 4 hours after the onset of symptoms, during which maximum benefit could be achieved from throm­bolytic therapy as indicated by reduction in mortality and pres­ervation of residual LV function.

Interventional Delays in Thrombolytic Therapy The optimal goal of thrombolytic therapy in acute MI is to

administer the thrombolytic agent at the earliest fime, within minutes if possible, and most certainly within the first 2 to 4 hours of the onset of symptoms. Unfortunately, only a small proportion of patients receive thrombolytic therapy within this fime frame (27-29).

The causes of delay in initiating thrombolytic therapy are multifactorial and include: 1) patient delay in recognizing acute MI symptoms and seeking medical help; 2) EMS delays in re­sponse time, on-scene time, and transport time; and 3) delays in the Emergency Department (ED).

Patient delay Investigations in patient recognition and response times have

revealed that up to 44% of acute MI patients do not seek medical assistance until more than 4 hours after the onset of symptoms (30). Older patients and those from lower socioeconomic groups wait longer prior to seeking medical help (31). Only 30% to 50% of patients with acute Ml activate EMS; the remainder use other means of transport and walk in to the ED (32). The most common reason for delay in seeking medical care is patient de­nial. Other reasons include mistaking symploms of acute Ml for

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Prehospital Care of Acute Ml—Gokli et al 171

more benign medical conditions, being alone at home at time of symptom onset and thus being unable to activate EMS, and at­tempting to contact personal physician first (33). Limited public awareness campaigns conducted in Sweden (34) and America (35) have failed to produce significant increases in the number of Ml patients who present early for medical treatment. To be ef­fective, public awareness programs need to be of longer dura­tion and repeated frequently.

EMS delay The EMS "response time," or time from system activation to

EMS arrival at the patient's side, averaged about 8 minutes in one multicenter study (36). Difficult access to the pafient due to physical barriers at the scene can contribute to long response times (37). Also, there are limitations due to weather and traffic conditions.

The "on-scene time" is the time from EMS arrival at the pa­tient's side until transport is initiated. This time involves evalua­tion of patient by history and physical examination, electrocar­diographic data acquisition, insertion of IV lines, base station contact with a controlling physician, and initial in-field ther­apies. In a review of eight major prehospital study groups, Kereiakes et al (36) demonstrated an average on-scene time of 26 minutes for patients with chest pain.

The EMS "transport time," time from initiation of patient transport to arrival in the ED, averaged 13 minutes in a mul­ticenter urban study. In rural areas transport times can be much longer especially if aeromedical transport is not available.

Emergency Department delay Once the patient suffering from an acute MI arrives in the ED,

whether conveyed by EMS or private transport, rapid diagnosis and administration is fraught with delays. Factors contributing to the delay include registration and collection of demographic data, triage by a nurse and initial physician evaluation, IV ac­cess, collection of blood, ECG and a chest x-ray, consultation with the patient's private physician or cardiologist, and acquisi­tion of the thrombolytic agent from the pharmacy. Sharkey et al (38) reported an average 20-minute wait after arrival in the ED before the initial ECG was obtained, and an additional 70 ± 40 minutes before thrombolytics were administered.

Prehospital Thrombolytics Thrombolytic therapy in the setting of an acute Ml can re­

duce mortality and morbidity, but its effectiveness is inversely related to time (10,25). Maximum benefit of thrombolytic ther­apy is achieved when it is administered within 2 to 4 hours ofthe onset of symptoms (10,25). Significant time delay to treatment could be prevented if thrombolytic therapy could be initiated by the first trained medical team to come in contact with the patient. In the prehospital setting, this would be either paramedic-staffed EMS or physician-staffed MCCU. Several studies have focu.sed on the feasibility, safety, and effectiveness of prehospital ad­ministration of thrombolytics in acute MI.

Koren et al (39) studied the use of IV SK in the prehospital setting. The MCCU physician was able to obtain and interpret

an initial ECG in the field and begin thrombolytic treatment with IV SK. The average time from onset of symptoms to treat­ment was 1.7 ± 0.8 hours. Patients who received treatment in the first 1.5 hours of symptom onset, versus those who received treatment between 1.5 and 4 hours of symptom onset, had a sig­nificantiy higher global LVEF (56% + 15% versus 47% ± 14%) and infarct-related regional EF (51 % ± 19% versus 34% ± 20%).

Weiss et al (26) showed similar results with prehospital thrombolytics using IV SK. The time from onset of symptoms to administration of IV SK averaged 63 ± 19 minutes in the field compared to 114 ± 54 minuies for a similar group of acute MI patients who received IV tbrombolyfics in-hospital. This study also showed smaller infarct size and better residual EF in the prehospital SK group compared to the in-hospital SK group.

Roth et al (40) studied recombinant tissue-type plasminogen activator (rt-PA) use in acute MI in the prehospital MCCU (n = 74) and in-hospital (n = 44) setting and found prehospital use of rt-PA safe and feasible. However, this study failed to show sig­nificant clinical advantage of prehospital administration of rt-PA over in-hospital rt-PA administrafion (time to treatment = 94 ± 36 minutes versus 137 ± 15 minutes).

Applebaum et al (41) used IV SK in 13 patients suffering from acute Ml in the prehospital setting using a MCCU. In this study, patients waited 33 ± 17 minutes after onset of acute MI symptoms to call the ambulance. Ambulance arrival time was 5 + 3 minutes. An additional 32 minutes were required before IV SK therapy was initiated. Thus, time from onset of acute MI symptoms to initiation of thrombolytic therapy averaged 66.7 minutes. No major complications were noted. A reduction in time delay of 30 to 60 minutes was achieved by prehospital use of thrombolytics. These investigators concluded that prehospi­tal thrombolytic therapy is safe and reduces time delay to treat­ment.

Castaigne et al (42,43) conducted a two-part study to deter­mine the feasibility and safety of prehospital thrombolytics and whether prehospital thrombolytics caused delay in the patient's arrival to the hospital. Phase 1 of the study evaluated the diag­nostic accuracy of MCCU physicians. Of the 294 patients evalu­ated and judged as having unstable angina or acute MI in the field. 282 were confirmed in the hospital with a low false-posi­tive rate (12 of 294). Of the 62 patients determined to be candi­dates for thrombolytics in the field by the MCCU team, all cases upon arrival at the hospital were confirmed as candidates for thrombolysis by the in-hospital leam. Phase II of this study was a randomized, placebo-controlled trial. Patients who were di­agnosed in the field as having acute MI (n = 100) received ei­ther anisoylated plasminogen streptokinase activator complex (APSAC) (n - 57) or placebo (n = 43). Patients who received placebo in the field received APSAC upon arrival in the hospital if indicated. APSAC was given in the field with a median time delay of 131 minutes after the onset of acute MI symptoms whereas the median time delay to in-hospital administration of APSAC was 180 minutes. Thus, there was an average savings of 50 minutes in the prehospital group. No difference was observed in the complication rate in each treatment group regarding ar­rhythmias, hypotension, hemorrhage, or death. In-field admini­stration of APSAC did not delay patient arrival to the hospital.

172 Henry Ford Hosp Med J—Vol 39, Nos 3 & 4. 1991 Prehospital Care of Acule MI—Gokli el al

However, this study failed to show any difference in the early post APSAC EF in the two groups. This study demonstrates that prehospital thrombolytic use is feasible and safe and signifi­cantiy reduces time delay to treatment.

In the above studies, all ambulances/MCCUs were staffed by physicians. Physicians evaluated the patients on the scene, ob­tained and interpreted ECGs, initiated thrombolytic therapy, and managed complications. In the United States, prehospital care is rendered by highly trained paramedics. The question then arises as to whether specially trained paramedics working in col­laboration with physicians can safely initiate thrombolytic ther­apy in the field.

With the ability of transmitting 12-lead ECGs from the field to a base hospital where a physician can interpret the ECG and make decisions regarding in-field thrombolysis, prehospital thrombolytic therapy has become a real possibility.

Cellular ECG equipment can provide hard copies of the 12-lead ECGs to the paramedic as well as to the physician at the base hospital. At the same time, the paramedic can relay perti­nent patient medical history and other information to the physi­cian. Based on all of the previous data, the base physician then decides whether thrombolytic therapy should be begun in the field. Grim et al (44,45) demonstrated the feasibility and accu­racy of cellular telephone transmission of a 12-lead ECG from the transporting ambulance to the hospital. Aufderheide et al (46) demonstrated that paramedics were able to obtain prehospi­tal ECGs 94.6% of the time (157 of 166 eligible patients). The paramedic-performed ECGs required one-third the time of that needed to perform ECGs in the ED (8.4 + 5.1 minutes versus 24.2 + 21.6 minutes). The prehospital ECGs increased on-.scene time by an average of 5.2 minutes compared to a retrospectively evaluated group of paramedic-transported patients (26.8 ± 7.8 minutes versus 21.6 ± 7.6 minutes). There was a high concor­dance between prehospital and ED 12-lead ECG diagnosis (99.3% for acute MI and 92.8% for angina). This study also demonstrated that prehospital 12-lead ECGs were diagnostic in 54.2% of all acute MI patients with a specificity of 99.2% and positive predicfive value of 92.8%. These values far exceed those achieved by paramedics using single-lead telemetry (posi­tive predictive value 32.7%).

Grim et al (47) demonstrated that emergency physicians can accurately make the decision to administer thrombolytic ther­apy in the field based on the 12-lead ECG and historical infor­mation provided by the paramedics. However, only 4.2% of pa­tients evaluated for chest pain (2 of 48) were actually candidates for in-field thrombolysis.

Several studies have shown that the acquisition of the prehos­pital ECGs and their transmission to base hospital and protocol-driven assessment of history, physical examination, and risk factors for administration of thrombolytic therapy do not in­crease either on-scene or transport fime (14,48). Grim et al (47) reported an average time from arrival at the scene to arrival at the hospital of 28 ± 6 minutes in the prehospital ECG group compared to 27 + 6 minutes in the control group withoul prehos­pital ECG. The Field Ambulance Study of Thrombolysis in Myocardial Infarction demonstrated a significant decrease in the average time delay to initiation of thrombolyfic therapy in

Henry Ford Hosp Med J—Vol 39. Nos 3 & 4. 1991

the hospital by prehospital ECGs (48 ± 12 minutes with prehos­pital ECG compared to 68 ± 29 minutes for pafients without pre­hospital ECGs) (48). Thus, prehospital acquisifion of ECG with either its transmission to the base hospital or by presenting the 12-lead ECG upon the pafient's arrival to the ED can signifi­cantiy reduce ED time delay to thrombolytic therapy without in­creasing EMS on-scene or transport time.

Using strict criteria for the diagnosis of acute MI of I) 1 mm ST elevation in contiguous ECG leads, 2) "reciprocal" ST de­pression of at least 0.5 mm in at least one ECG lead, and 3) an interpretive comment suggesting "injury" or "infarction," O'Rourke et al (49) demonstrated lhat paramedic diagnosis of acute MI was feasible and accurate without telemetry, provided that patients with prior Q wave infarctions were excluded.

The actual administration of thrombolytic therapy in the pre-ho.spital setting, either on-scene or during transport, has reduced average time delay to treatment by 30 to 86 minutes (31,40,48). SK, rt-PA, and APSAC all have been studied in the prehospital setting and show no reduction in safety or efficacy (32). Initial studies were conducted using continuous IV infusion of SK. Castaigne et al (42) have suggested APSAC for use in the pre­hospital setting since the single IV bolus dose obviates the need of continuous infusion. Purvis et al (50) and McKendall et al (51) have demonstrated high (exceeding 90%) infarct artery pa­tency rate on coronary angiograms performed 90 minutes after an initial bolus of rt-PA. The more common complicattons of hypotension and reperfusion arrhythmias are usually self-lim­ited and easily treated in the field by the paramedics (52).

Of the 2,472 patients prospectively evaluated for chest pain during phase I of the Myocardial Infarction Triage and Interven­tion (MITI) trial, 677 (27%) had clinical findings suggestive of acute MI (53). Of the 522 patients in whom in-field ECGs were obtained, 107 were eligible for prehospital thrombolytic therapy based on diagnostic changes of acute MI on ECG. Thus only 107 (4.2%) of the 2,472 chest pain patients evaluated were po­tenfial candidates for prehospital thrombolytics. The Cincinnati Heart Project also showed a low accrual rate of acute MI patients with only 20 (4.2%) acute Mis identified out of 477 patients evaluated for chest pain (54). In the Nashville prehospital rt-PA trial, only three (3.5%) of the 85 patients were found to be actual candidates for rt-PA in the field over a six-month period (54).

Studies to date have conclusively shown reduction in time de­lay to treatment of 30 to 70 minutes with prehospital throm­bolytics. However, data on clinical benefit from this fime saving is not clear. Randomized trials of prehospital thrombolytics have shown improved survival without improved residual LV funcfion (55), improved LV funcfion with no difference in sur­vival (43), and no difference in survival or LV function (56). Data from the MITI and European Myocardial Infarction Pro­ject (EMIP) trials which are currently in progress will hopefully yield a more definitive answer regarding whether reduction in fime delay to treatment of 30 to 70 minutes by prehospital thrombolytic therapy translates into improved survival and im­proved residual LV funcfion. Phase 11 of the MITI trial, which began in October 1988, is a prospective evaluation of the benefit of paramedic administration of rt-PA (53). A total of 800 pa­tients will be randomized lo receive rt-PA in the field or in the

Prehospital Care of Acute Ml—Gokli et al 173

hospital after prehospital diagnosis of acute MI by 12-lead ECGs. LVEFs will be measured to judge the benefit of prehos­pital versus in-hospital thrombolytic therapy. The main goal of EMIP, a prospective, double-blind, randomized, multicenter in­temational study, is to evaluate the benefit/risk ratio of prehos­pital thrombolytic therapy compared with in-hospital thrombol­ysis, with total mortality as the major endpoint. Patients sus­pected of having acute MI receive APSAC in the field or in the hospital. The goal is to include 10,000 pafients in this study.

Barriers to Prehospital Thrombolytics About half of all patients suffering from acute Ml activate

EMS while the others arrive in the ED by other means of trans­port (42% in Seattie, 44% in Minneapolis, and 57% in Gote-borg) (38,32,35). Thus prehospital administration of thrombo­lytic therapy would reach only half of all patients with acute MI. Due to adherence to strict inclusion and exclusion criteria for prehospital thrombolytics, only about 4% of patients evaluated for chest pain would be candidates for prehospital thrombolytics (53). This would translate into few prehospital thrombolytic treatments given. Gibler et al (54) noted a decline in paramedic skill because of infrequent use of thrombolytic therapy. Thus it would be necessary to train paramedics to give thrombolytics in the field and then periodically retrain them to prevent decline in their skills. The cost of equipping the ambulance with electro­cardiographic and communication equipment may be prohibi­tive. The costs of stocking the thrombolytic agents in the field and wastage of these agents due to expiration or breakage may also be excessive. There could be additional medicolegal risk for the ED physicians as well as the paramedics due to faulty di­agnosis from inaccurate history and increased complicafions. Interference with cellular telephone transmission could delay prehospital thrombolysis.

Conclusion The time-dependent efficacy of thrombolyfic therapy in

acute MI has revitalized interesi in the prehospital care of acute MI. Thrombolytic therapy within 2 to 4 hours of symptom onset is desirable. Patient delay in seeking medical attention and low usage of the EMS system is a major component in delay to thrombolytic treatment, with as many as one-half of patients waiting 4 or more hours before seeking medical attention. In-hospital time delay to thrombolytic treatment of 60 minutes is common despite enhanced general awareness, transfer of re­sponsibility for initiating thrombolytics to the emergency physi­cians, and stocking of thrombolytic agents in the ED. The acqui­sition of prehospital 12-lead ECG has been shown to reduce hospital time delay to thrombolytic therapy in acute MI patients. Potential time savings of 30 to 60 minutes have been observed with this strategy. Prehospital diagnosis of acute Ml using 12-lead ECG has been found to be feasible and accurate. The use of all three current forms of thrombolytic agents (SK, rt-PA, and APSAC) in the prehospital setting is feasible and safe and re­duces time delay to treatment. However, clinical benefit from this reducfion in time delay has not been conclusively shown. Low public use of EMS, few patients meeting criteria for in­

field thrombolysis, the high cost of equipping the ambulance and training paramedics, along with increased medicolegal risks may make prehospital administration of thrombolytics imprac­tical at the present time. We await the results from ongoing stud­ies of large numbers of patients to help answer this question.

References 1, Braunwald E. ed. Heart Disease: A textbook of cardiovascular medicine,

Philadelphia: WB Saunders. 1988:1222. 2, Geddes JS, Twenty years of prehospital coronary care, Br Heart J 1986;

56:491-5, 3, Rentrop KP, Blanke H, Karsch KR, Effects of nonsurgical coronary reper­

fusion on the left ventricle in human subjects compared with conventional treat­ment: Study of 18 patients with acute myocardial infarction treated with intra­coronary infusion of streptokinase. Am J Cardiol 1982:49:1-8,

4, Smalling RW, Fuentes F, Matthews MW. et al. Sustained improvement in left ventricular function and mortality by intracoronary streptokinase admini­stration during evolving myocardial infarction. Circulation 1983:68:131-8.

5, Sheehan FH. Mathey DG, Schofer J, Krebber HJ, Dodge HT Effect of in­terventions in salvaging left ventricular function in acute myocardial infarction: A study of intracoronary streptokinase. Am J Cardiol 1983:52:431-8,

6, Spann JF, Sherry S, Carabello BA, et al. Coronary thrombolysis by intrave­nous streptokinase in acute myocardial infarction: Acute and follow-up studies, AmJCardiol 1984;53:655-61,

7, GlSSI, Long-term effects of intravenous thrombolysis in acute myocardial infarction: Final report ofthe GISSl study. Lancet 1987:2:871-4,

8, Kennedy JW, Ritchie JL, Davis KB, Fritz JK, Westem Washington ran­domized trial of intracoronary streptokinase in acute myocardial infarction, N Engl J Med 1983:309:1477-82,

9, Mathey DG, Schofer J. Sheehan FH. et al. Improved survival up to four years after early coronary thrombolysis. Am J Cardiol 1988;61:524-9,

10, ISIS-2 (Second Intemational Study of Infarct Survival) Collaborative Group, Randomized trial of intravenous streptokinase, oral aspirin, both, or nei­ther among 17.187 cases of suspected acute myocardial infarction: ISIS 2, Lan­cet 1988;2:349-60,

11, Pantridge JF, Geddes JS, A mobile intensive-care unit in the management of myocardial infarction. Lancet 1967:2:271-3,

12, Weaver WD, Copass MK, Bufi D, Ray R. Hallstrom AP. Cobb LA. Im­proved neurologic recovery and survival after early defibrillation. Circulation 1984:69:943-8,

13, Pressley JC. Severance HW Jr, Raney MP. et al, A comparison of para­medic versus basic emergency medical care of patients at high and low risk dur­ing acute myocardial infarction, J Am Coll Cardiol 1988:12:1555-61,

14, Weaver WD. Eisenberg MS. Martin JS. et al. Myocardial infarction triage and intervention project-Phase I : Patient characteristics and feasibility of pre­hospital initiation of thrombolytic therapy, J Am Coll Cardiol 1990;15:925-31,

15, Kennedy JW, Thrombolytic therapy for acute myocardial infarction: A brief review. Heart Lung 1987;16:740-5,

16, DeWood MA. Spores J, Notske R. et al: Prevalence of total coronary oc­clusion during the early hoursof transmural myocardial infarction, NEngI J Med 1980:303:897-902,

17, Reimer KA, Lowe JE, Rasmussen MM, Jennings RB, The wave front phe­nomenon of ischemic cell death, I , Myocardial infarct size versus duration of coronary inclusion in dogs. Circulation 1977:56:786-94,

18, Jennings RB. Reimer KA. Factors involved in salvaging ischemic myo­cardium: Effects of reperfusion of arterial blood. Circulation I983;68(suppl I): 125-36,

19, Feit F. Rentrop KP, Thrombolysis in the treatment of acute myocardial in­farction. In: PetersdorfRG. Isselbacher K, Adams R. et al. eds, Harrison's princi­ples of intemal medicine. Update 6, New York: McGraw-Hill, 1985:147-62,

20, Anderson JL. Marshall HW, Bray BE, et al, A randomized trial of intra­coronary streptokinase in the treatment of acute myocardial infarction, N Engl J Med 1983;308:1312-8,

21, Khaja F. Walton JA Jr, BrymerJF, et al, Intracoronary fibrinolytic therapy in acute myocardial infarction: Report of a prospective randomized trial, N Engl JMed 1983:308:1305-11,

174 Henry Ford Hosp Med J—Vol 39, Nos 3 & 4,1991 Prehospital Care of Acute Ml—Gokli et al

22, Kennedy JW, Ritchie JL. Davis KB, et al, Westem Washington intra­coronary streptokinase trial follow-up, N Engl J Med 1985:312:1073-8,

23, The ISAM Study Group, A prospective trial of intravenous streptokinase in acute myocardial infarction (ISAM): Mortality, morbidity, and infarct size at 21 days, N Engl J Med 1986;314:1465-71,

24, Fine DG. Weiss AT, Sapoznikov D. et al. Importance of early initiation of intravenous streptokinase therapy for acute myocardial infarction. Am J Cardiol 1986:58:411-7,

25, Gruppo Italiano Per Lo Studio Della Streptochinasi Nell'Infarto Miocar­dico (GISSl), Effectiveness of intravenous thrombolytic treatment in acute myo­cardial infarction. Lancet 1986:1:397-402,

26, Weiss AT, Fine DG, Applebaum D. et al. Prehospital coronary thromboly­sis: A new strategy in acute myocardial infarction. Chest 1987;92:124-8,

27, TIMI Study Group, Thrombolysis in myocardial infarction (TIMI) trial: Phase I findings, N Engl J Med 1985;312:932-6,

28, Topol EJ. Califf RM, George BS. et al. A randomized trial of immediate versus delayed elective angioplasty after intravenous tissue plasminogen activa­tor in acute myocardial infarction, N Engl J Med 1987:317:581-8,

29, Topol EJ. Califf RM, Kereiakes DJ, George BS, Thrombolysis and an­gioplasty in myocardial infarction (TAMI) trial, J Am Coll Cardiol 1987:10: 65B-74,

30, Ho M. Eisenberg M, Litwin P, et al. Reasons chest pain patients delay or do not call 911. Circulation 1988;78(suppl II): 187,

31, Sherrid M. Greenberg H. Marsella R. Mathisen D. Lynn S, Dwyer E, A pi­lot study of paramedic-administered, prehospital thrombolysis foracute myocar­dial infarction. Clin Cardiol 1990:13:421-4,

32, Kowalenko T, Kereiakes D. Gilber W, Prehospital diagnosis and treat­ment of acute myocardial infarction: A critical review. Am Heart J (In press),

33, Omato JP, Role of the emergency department in decreasing the time to thrombolytic therapy in acute myocardial infarction. Am J Hosp Pharm 1990:47 (II):Sll-4,

34, Heriitz J, Hartford M, Blohm M. et al. Effect ofa media campaign on delay times and ambulance use in suspected acute myocardial infarction. Am J Cardiol 1989:64:90-3,

35, Ho MT. Eisenberg MS, Litwin PE, Schaeffer SM, Damon SK, Delay be­tween onset of chest pain and seeking medical care: The effect of public educa­tion, Ann Emerg Med 1989; 18:727-35,

36, Kereiakes DJ, Weaver WD, Anderson JL. et al. Time delays in the diagno­sis and treatment of acute myocardial infarction: A tale of eight cities. Report from the pre-hospital study group and the Cincinnati heart project. Am Heart J 1990:120:4:773-80,

37, Becker LB. Ostrander MP, Ban-en TJ, Kondos GT. Outcome of CPR in a large metropolitan area: Where are the survivors? Ann Emerg Med 1991:20:355-61.

38, Sharkey SW. Brunette DD. Ruiz E. et al. An analysis of time delays pre­ceding thrombolysis for acute myocardial infarction. JAMA 1989;262:3171-4.

39, Koren G. Weiss AT, Hasin Y, et al. Prevention of myocardial damage in acute myocardial ischemia by early treatment with intravenous streptokinase, N

Engl J Med 1985;313:1384-9, 40, Roth A, BarbashGI, Hod H, etal. Should thrombolytic therapy be admini­

stered in the mobile intensive care unit in patients with evolving myocardial in­farction? A pilot study, J Am Coll Cardiol 1990; 15:932-6,

41, Applebaum D, Weiss AT, Koren G, Ben David Y, Hasin Y. Gotsman MS, Feasibility of pre-hospital Fibrinolytic therapy in acute myocardial infarction. Am J Emerg Med. 1986;4:201-4.

42, Castaigne AD, Herve CH, Duval-Moulin AM, Gaillard M, Dubois-Rande JL, Leilouche D. Pre-hospital thrombolysis, is it useful? Euro Heart J 1990; 11 (suppl F):43-7.

43, Castaigne AD, Herve C, Duval-Moulin AM, et al. Prehospital use of APSAC: Results of a placebo-controlled study. Am J Cardiol 1989;64(suppl A):30A-3,

44, Grim P. Feldman T Martin M, Donovan R, Nevins V. Childers RW, Cel­lular telephone transmission of 12-lead electrocardiograms from ambulance to hospital. Am J Cardiol 1987:60:715-20,

45, Feldman T, Grim P, Childers RW, et al. Prehospital diagnosis and therapy for acute MI, Cardiology 1989:85-8,

46, Aufderheide TP, Hendley GE, Thakur RK, et al. The diagnostic impact of preho,spital 12-lead electrocardiography, Ann Emerg Med 1990; 19:1280-7,

47, Grim PS, Feldman T Childers RW, Evaluation of patients for the need of thrombolytic therapy in the prehospital setting, Ann Emerg Med 1989:18:483-8,

48, Karagounis L, Ipsen SK, Jessop MR, et al. Impact of field-transmitted electrocardiography on time to in-hospital thrombolytic therapy in acute myo­cardial infarction. Am J Cardiol 1990:66:786-91,

49, O'Rourke M, Cook A, Gallager D, et al. Paramedic-initiated pre-hospital thrombolysis using urokinase in acute coronary occlusion (TIC02) (Abstract), J Am Coll Cardiol 1991; I7:246A,

50, Purvis JA, Trouton TG, Dalzell GW, et al, Pre-hospital double bolus al-teplase in acute myocardial infarction (Abstract), Circulation I990;82(suppl III):538,

51, McKendall GR, Woolard R, McDonald MJ, Williams DO, Feasibility of pre-hospital acute myocardial infarction diagnosis: Results of the pre-hospital administration of t-PA (PATS) study (Abstract), Circulation 1990;82(suppl III):667,

52, Breed J, Prehospital administration of thrombolytic therapy, J Emerg Nurs 1989;I5(2):200-4,

53, Kennedy JW. Weaver WD. The potential for prehospital thrombolytic therapy. Clin Cardiol 1990;13:VIII-23-6,

54, Gibler WB, Kereiakes DJ, Dean EN. et al. Prehospital diagnosis and treat­ment of acute myocardial infarction: A north-south perspective. Am Heart J 199I;I21(1):1-1I,

55, Barbash GI, Roth A, Hod H, etal. Improved survival but not left ventricu­lar function with early and prehospital treatment with tissue plasminogen activa­tor in acute myocardial infarction. Am J Cardiol 1990;66:261-6,

56, Schofer J. Buttner J, Geng G, et al. Prehospital thrombolysis in acute myo­cardial infarction. Am J Cardiol 1990;66:1429-33,

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