Prophylactic Lidocaine The use of prophylactic lidocaine to protect patients with suspected acute myocardial infarction from the development of malignant dysrhythmias and death has been debated for more than 30 years. ~ Early studies of hospitalized patients documented the ability of prophylactic lidocaine to suppress malignant dysrhythmias, 2-4 while other studies from this era reported no positive effect f r o m its use.S, 6 One of the reasons for the lack of a concise answer stems from a lack of standardization of most studies. Different patient groups, numbers of patients, routes of drug administration, dose regimens, and outcome measurements have been studied. Nonetheless, most studies have suggested that lidocaine does not reduce mortality.7, s Because of this, the prophylactic use of lidocaine in the coronary care unit, where the development of malignant dysrhythmias can be rapidly treated, has essentially been abandoned. 9 The initial studies on the use of prophylactic lidocaine in the prehospital setting were undertaken to determine whether such use could reduce mortality by suppressing the early development of malignant dysrhythmias and subsequent sudden death. 1° This was a reasonable undertaking at the time because prehospital response systems with providers who could monitor cardiac rhythms and treat emerging malignant dysrhythmias were not yet a reality. Although early studies lo reported a reduction in mortality, later studies 11 and meta-studies 8 have suggested that the prehospital use of prophylactic lidocaine does not reduce mortality. This is not an unexpected finding in view of the fact that most of these studies were carried out in prehospital systems that employed paramedics who could definitively treat emergent malignant dysrhythmias. The prehospital setting in this instance had become analogous to the coronary care unit, where the use of prophylactic lidocaine had been shown to have a negligible effect on the reduction of mortality. J
See related article, p 1274.
If one accepts the fact that the use of both prehospital and inpatient prophylactic lidocaine does not affect mortality, one is left with the issue of whether it may be more efficacious to suppress the development of malignant dysrhythmias in the less controlled prehospital setting, with its limited armamentarium of antidysrhythmic agents. 12 The answer to this question remains uncertain. It is clear, however, that in the prehospital setting the patients who need to be studied are those with suspected myocardial infarction who have no signs of dysrhythmia, a group that has not been singled out by most prior studies. In this issue of Annals, Hargarten et al present the findings of administering prophylactic lidocaine to such patients, a continuation of their pilot study published in 1986.~1 They conducted a nonblinded, randomized, prospective study of 1,427 patients presenting with suspected 19:11 November 1990
myocardial infarction w i t h o u t " w a r n i n g a r r h y t h m i a . " Seven hundred four patients received lidocaine and 723 did not. There were 236 patients who were diagnosed with acute myocardial infarction in the lidocaine-treated group and 200 such patients in the nontreated group. Seven patients in each group developed a malignant dysrhythmia. There were 57 deaths in the lidocaine-treated group and 48 in the nontreated group. The authors state that there was no statistically significant difference in the development of malignant dysrhythmias or mortality in the two groups and conclude that because prophylactic lidocaine had no effect on either, its use is unwarranted. This is an important study and the authors are to be commended for their efforts in studying the appropriate group of patients, those persons with suspected acute myocardial infarction but without any sign of dysrhythmia. Ironically, this fact leads to an important shortcoming of this study. The authors point out that there was a statistically significantly greater number (18%) of patients with diagnosed myocardial infarctions in the group of patients treated with lidocaine. This is an important point because if the treatment group did, in fact, have more patients with infarctions, then one would have predicted that this group should have had more patients with malignant dysrhythmias if the use of prehospital prophylactic lidocaine had no effect. The authors report, however, that there was no numerical or statistical difference in the incidence of malignant dysrhythmias in the two groups. One conclusion that can be drawn from these data is that lidocaine treatment could have suppressed the development of malignant dysrhythmias in these patients but statistical significance was not reached because the development of such dysrhythmias has an extremely low incidence. This appears to be the case as only 14 of the 436 patients who were subsequently diagnosed with myocardial infarction had malignant dysrhythmias. Based on this, one would have expected to see only 1.5 more dysrhythmias in the lidocaine-treated group if the use of lidocaine had no effect. The incidence of malignant dysrhythmias in the population that needs to be studied is extremely low. In view of this, the authors cannot rule out the possibility that they have made a Type 2 error. In order to adequately demonstrate that pretreatment with lidocaine has no effect on the d e v e l o p m e n t of m a l i g n a n t dysrhythmias, a larger number of patients must be enlisted. If one uses standard power formulas to determine how many patients need to be studied, 10,000 patients would be required in each group if the use of prophylactic lidocaine suppressed the development of 30% of the potential malignant dysrhythmias at a confidence level of 95% ([P < .05] x 2 analysis of a 2 x 2 contingency table with the Yates correction). The authors address this question but reject it on the basis of subjecting a large number of patients to the potential adverse effects of lidocaine. This may be true, but the only way this question will be answered scientifically will be
Annals of Emergency Medicine
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EDITORIALS
to test enough patients to ensure against a Type 2 error at an acceptable power. U n t i l this is done, the s t a t e m e n t that lidocaine does n o t suppress the development of malignant dysrhythmias cannot be made. What really needs to be posed is whether this question actually needs to be answered. If the answer is affirmative, then a large, m u l t i c e n t e r study will be required to enlist enough patients to ensure against m a k i n g a Type 2 error if the n u l l hypothesis is accepted. However, the negative may be more appropriate. Although it has not been proven statistically, there is a suggestion that lidocaine t r e a t m e n t m a y increase mortality.S, 12 Further, both in the prehospital and i n p a t i e n t settings, it has been proven statistically that the prophylactic use of lidocaine in patients w i t h suspected acute m y o c a r d i a l i n f a r c t i o n does n o t reduce the mortality of such patients. If one accepts this, t h e n there m a y be little justification for pursuing the issue further because c u r r e n t prehospital advanced life support providers can effectively treat emerging life-threatening dysrhythmias. Perhaps the analogy between the i n p a t i e n t and prehospital setting should be extended to where, as i n the inpatient e n v i r o n m e n t , the r o u t i n e use of prophylactic lidocaine is abandoned. W i l l i a m G Baxt, M D U n i v e r s i t y o f Califorrfia San Diego
1. WeissWA: Intravenoususe of lidocainefor ventriculararrhythmias. An-
esth Analg 1960;39:369-38t.
2. Lie KI, WellensHJ, van Capelle FJ, et al: Lidocainein the preventionof primary ventricular fibrillation.N Engl J Med 1974;291:1324-1326. 3. Pitt A, Lipp H, AndersonST: Lignocainegiven prophylacticallyto patients with acute myocardialinfarction. Lancet 1971:612~616. 4. DeSilva RA, Hermekens CH, Lown B, et al: Lignocaineprophylaxis in acute myocardial infarction: An evaluation of randomised trials. Lancet 1981:855-85K 5. Bennett MA, WilnerJM, Pentecost BL: Controlledtrial of lignocainein prophylaxisof ventriculararrhythmias complicatingmyocardialinfarction. Lancet 1970:909~911. 6. Darby S, Bennett MA, Crnickshank JC, et al: Trial of combined intra~ muscular and intravenouslignocainein prophylaxisof ventricular tachyarrhythmias. Lancet 1972:817-819. 7. MacMahonS, Collins R, Peto R, et al: Effects of prophylactic lidocaine in suspected acute myocardialinfarction: An overviewof results from the randomized, controlled trials. JAMA 1988;260:1910-1916. 8. Hine LK, Laird N, Hewitt P, et al: Meta-analyticevidence against prophylactic use of lidoeainein acute myocardialinfarction.Arch Intern Med 1989;149:2694-2698. 9. Garruth JE, SilvermanME: Ventricular fibrillation complicatingacute myocardial infarction: Reasons against the routine use of lidocaine. Am Heart J 1982;104:545-550. 10. ValentinePA, FrewJL, Mashford ML, et al: Lidocainein the prevention of sudden death in the pre-hospital phase of acute infarction: A doubleblind study. N Engl J Med 1974;291:1327-1331. 11. Hargarten KM, Aprahamian C, Stueven HA, et al: Prophylactic lidocaine in the prehospital patient with chest pain of suspected cardiac origin. Ann Emerg Med 1986;15:881-885. 12. Koster RW, Dunning AJ: Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospitalizationphase of acute myocardial infarction. N Engl J Med 1985;313:1107-1110.
From Pain to Reperfusion: What Role for the Prehospital 12-Lead ECG? Emergency medical services require the rapid arrival of the right p e r s o n n e l w i t h the right e q u i p m e n t . T h e last two decades have witnessed n o t only an increase in the training and skills of paramedics and emergency medical technicians (EMTs) but also an increase in the a m o u n t of e q u i p m e n t they carry to the scene. EMTs in m a n y parts of the c o u n t r y n o w bring either c o n v e n t i o n a l or a u t o m a t e d defibrillators to the patient. Paramedics may enter with pulse oximeters, external pacemakers, m e c h a n i c a l CPR devices, and end-tidal CO 2 m o n i t o r s . In addition, they m u s t carry monitor-defibrillators, v e n t i l a t i o n kits, oxygen tanks, IV fluid and m e d i c a t i o n administration kits, cellular t e l e p h o n e s , a n d radio e q u i p m e n t . In King C o u n t y , Washington, w h e n an evaluation of external pacemakers was proposed to the paramedics, the i m m e d i a t e reply was "only if you provide us with 8herpas." See related article, p 1280. N o w clinicians, manufacturers, and prehospital personnel are i n t e n s e l y i n t e r e s t e d i n the latest candidate for space in the paramedics' arsenal: devices for recording pre164/1343
hospital 12dead ECGs. In particular, interest is focused on small, p o r t a b l e 12-lead u n i t s t h a t p r o v i d e an o n s c e n e p r i n t o u t of the ECG, a computerized interpretation of the recording, and cellular t r a n s m i s s i o n of both the cardiogram and the interpretation. Aufderheide and colleagues, in this issue of A n n a l s , demonstrate that use of 12-lead ECGs by paramedics in Milwaukee is possible in the prehospital setting and m a y contribute to more accurate evaluation of patients w i t h chest pain. Research groups in Seattle-King County, Washington, 1,2 Chicago,3,4 Salt Lake City, 5 and Nashville 6 have also explored the feasibility of prehospital 12-lead ECGs. Two of these locations have assessed the diagnostic i m p a c t of t h e c o m p u t e r i z e d i n t e r p r e t a t i o n . 2-4 T h e s e studies confirm that we n o t only possess the technical capability to o b t a i n and t r a n s m i t 12-lead ECGs, b u t that computerized ECG interpretation is accurate and useful. 2 The s t i m u l u s for these studies has, of course, been the i n t e n s e interest in early t r e a t m e n t of acute myocardial infarction w i t h thrombolytic agents. 7 The M i l w a u k e e study provides positive i n f o r m a t i o n to help answer the u l t i m a t e question: should paramedics administer thrombolytic therapy i n the field? As of 1990 the a n s w e r is unclear.
Annals of Emergency Medicine
19:11 November 1990
See related article, p 1274.
If one accepts the fact that the use of both prehospital and inpatient prophylactic lidocaine does not affect mortality, one is left with the issue of whether it may be more efficacious to suppress the development of malignant dysrhythmias in the less controlled prehospital setting, with its limited armamentarium of antidysrhythmic agents. 12 The answer to this question remains uncertain. It is clear, however, that in the prehospital setting the patients who need to be studied are those with suspected myocardial infarction who have no signs of dysrhythmia, a group that has not been singled out by most prior studies. In this issue of Annals, Hargarten et al present the findings of administering prophylactic lidocaine to such patients, a continuation of their pilot study published in 1986.~1 They conducted a nonblinded, randomized, prospective study of 1,427 patients presenting with suspected 19:11 November 1990
myocardial infarction w i t h o u t " w a r n i n g a r r h y t h m i a . " Seven hundred four patients received lidocaine and 723 did not. There were 236 patients who were diagnosed with acute myocardial infarction in the lidocaine-treated group and 200 such patients in the nontreated group. Seven patients in each group developed a malignant dysrhythmia. There were 57 deaths in the lidocaine-treated group and 48 in the nontreated group. The authors state that there was no statistically significant difference in the development of malignant dysrhythmias or mortality in the two groups and conclude that because prophylactic lidocaine had no effect on either, its use is unwarranted. This is an important study and the authors are to be commended for their efforts in studying the appropriate group of patients, those persons with suspected acute myocardial infarction but without any sign of dysrhythmia. Ironically, this fact leads to an important shortcoming of this study. The authors point out that there was a statistically significantly greater number (18%) of patients with diagnosed myocardial infarctions in the group of patients treated with lidocaine. This is an important point because if the treatment group did, in fact, have more patients with infarctions, then one would have predicted that this group should have had more patients with malignant dysrhythmias if the use of prehospital prophylactic lidocaine had no effect. The authors report, however, that there was no numerical or statistical difference in the incidence of malignant dysrhythmias in the two groups. One conclusion that can be drawn from these data is that lidocaine treatment could have suppressed the development of malignant dysrhythmias in these patients but statistical significance was not reached because the development of such dysrhythmias has an extremely low incidence. This appears to be the case as only 14 of the 436 patients who were subsequently diagnosed with myocardial infarction had malignant dysrhythmias. Based on this, one would have expected to see only 1.5 more dysrhythmias in the lidocaine-treated group if the use of lidocaine had no effect. The incidence of malignant dysrhythmias in the population that needs to be studied is extremely low. In view of this, the authors cannot rule out the possibility that they have made a Type 2 error. In order to adequately demonstrate that pretreatment with lidocaine has no effect on the d e v e l o p m e n t of m a l i g n a n t dysrhythmias, a larger number of patients must be enlisted. If one uses standard power formulas to determine how many patients need to be studied, 10,000 patients would be required in each group if the use of prophylactic lidocaine suppressed the development of 30% of the potential malignant dysrhythmias at a confidence level of 95% ([P < .05] x 2 analysis of a 2 x 2 contingency table with the Yates correction). The authors address this question but reject it on the basis of subjecting a large number of patients to the potential adverse effects of lidocaine. This may be true, but the only way this question will be answered scientifically will be
Annals of Emergency Medicine
1342/163
EDITORIALS
to test enough patients to ensure against a Type 2 error at an acceptable power. U n t i l this is done, the s t a t e m e n t that lidocaine does n o t suppress the development of malignant dysrhythmias cannot be made. What really needs to be posed is whether this question actually needs to be answered. If the answer is affirmative, then a large, m u l t i c e n t e r study will be required to enlist enough patients to ensure against m a k i n g a Type 2 error if the n u l l hypothesis is accepted. However, the negative may be more appropriate. Although it has not been proven statistically, there is a suggestion that lidocaine t r e a t m e n t m a y increase mortality.S, 12 Further, both in the prehospital and i n p a t i e n t settings, it has been proven statistically that the prophylactic use of lidocaine in patients w i t h suspected acute m y o c a r d i a l i n f a r c t i o n does n o t reduce the mortality of such patients. If one accepts this, t h e n there m a y be little justification for pursuing the issue further because c u r r e n t prehospital advanced life support providers can effectively treat emerging life-threatening dysrhythmias. Perhaps the analogy between the i n p a t i e n t and prehospital setting should be extended to where, as i n the inpatient e n v i r o n m e n t , the r o u t i n e use of prophylactic lidocaine is abandoned. W i l l i a m G Baxt, M D U n i v e r s i t y o f Califorrfia San Diego
1. WeissWA: Intravenoususe of lidocainefor ventriculararrhythmias. An-
esth Analg 1960;39:369-38t.
2. Lie KI, WellensHJ, van Capelle FJ, et al: Lidocainein the preventionof primary ventricular fibrillation.N Engl J Med 1974;291:1324-1326. 3. Pitt A, Lipp H, AndersonST: Lignocainegiven prophylacticallyto patients with acute myocardialinfarction. Lancet 1971:612~616. 4. DeSilva RA, Hermekens CH, Lown B, et al: Lignocaineprophylaxis in acute myocardial infarction: An evaluation of randomised trials. Lancet 1981:855-85K 5. Bennett MA, WilnerJM, Pentecost BL: Controlledtrial of lignocainein prophylaxisof ventriculararrhythmias complicatingmyocardialinfarction. Lancet 1970:909~911. 6. Darby S, Bennett MA, Crnickshank JC, et al: Trial of combined intra~ muscular and intravenouslignocainein prophylaxisof ventricular tachyarrhythmias. Lancet 1972:817-819. 7. MacMahonS, Collins R, Peto R, et al: Effects of prophylactic lidocaine in suspected acute myocardialinfarction: An overviewof results from the randomized, controlled trials. JAMA 1988;260:1910-1916. 8. Hine LK, Laird N, Hewitt P, et al: Meta-analyticevidence against prophylactic use of lidoeainein acute myocardialinfarction.Arch Intern Med 1989;149:2694-2698. 9. Garruth JE, SilvermanME: Ventricular fibrillation complicatingacute myocardial infarction: Reasons against the routine use of lidocaine. Am Heart J 1982;104:545-550. 10. ValentinePA, FrewJL, Mashford ML, et al: Lidocainein the prevention of sudden death in the pre-hospital phase of acute infarction: A doubleblind study. N Engl J Med 1974;291:1327-1331. 11. Hargarten KM, Aprahamian C, Stueven HA, et al: Prophylactic lidocaine in the prehospital patient with chest pain of suspected cardiac origin. Ann Emerg Med 1986;15:881-885. 12. Koster RW, Dunning AJ: Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospitalizationphase of acute myocardial infarction. N Engl J Med 1985;313:1107-1110.
From Pain to Reperfusion: What Role for the Prehospital 12-Lead ECG? Emergency medical services require the rapid arrival of the right p e r s o n n e l w i t h the right e q u i p m e n t . T h e last two decades have witnessed n o t only an increase in the training and skills of paramedics and emergency medical technicians (EMTs) but also an increase in the a m o u n t of e q u i p m e n t they carry to the scene. EMTs in m a n y parts of the c o u n t r y n o w bring either c o n v e n t i o n a l or a u t o m a t e d defibrillators to the patient. Paramedics may enter with pulse oximeters, external pacemakers, m e c h a n i c a l CPR devices, and end-tidal CO 2 m o n i t o r s . In addition, they m u s t carry monitor-defibrillators, v e n t i l a t i o n kits, oxygen tanks, IV fluid and m e d i c a t i o n administration kits, cellular t e l e p h o n e s , a n d radio e q u i p m e n t . In King C o u n t y , Washington, w h e n an evaluation of external pacemakers was proposed to the paramedics, the i m m e d i a t e reply was "only if you provide us with 8herpas." See related article, p 1280. N o w clinicians, manufacturers, and prehospital personnel are i n t e n s e l y i n t e r e s t e d i n the latest candidate for space in the paramedics' arsenal: devices for recording pre164/1343
hospital 12dead ECGs. In particular, interest is focused on small, p o r t a b l e 12-lead u n i t s t h a t p r o v i d e an o n s c e n e p r i n t o u t of the ECG, a computerized interpretation of the recording, and cellular t r a n s m i s s i o n of both the cardiogram and the interpretation. Aufderheide and colleagues, in this issue of A n n a l s , demonstrate that use of 12-lead ECGs by paramedics in Milwaukee is possible in the prehospital setting and m a y contribute to more accurate evaluation of patients w i t h chest pain. Research groups in Seattle-King County, Washington, 1,2 Chicago,3,4 Salt Lake City, 5 and Nashville 6 have also explored the feasibility of prehospital 12-lead ECGs. Two of these locations have assessed the diagnostic i m p a c t of t h e c o m p u t e r i z e d i n t e r p r e t a t i o n . 2-4 T h e s e studies confirm that we n o t only possess the technical capability to o b t a i n and t r a n s m i t 12-lead ECGs, b u t that computerized ECG interpretation is accurate and useful. 2 The s t i m u l u s for these studies has, of course, been the i n t e n s e interest in early t r e a t m e n t of acute myocardial infarction w i t h thrombolytic agents. 7 The M i l w a u k e e study provides positive i n f o r m a t i o n to help answer the u l t i m a t e question: should paramedics administer thrombolytic therapy i n the field? As of 1990 the a n s w e r is unclear.
Annals of Emergency Medicine
19:11 November 1990
