ACUTE MYOCARDIAL ISCHEMIA An acute ST elevation myocardial infarction (MI) presents with a current of injury pattern characterized by elevation

n of the ST se ment in different leads! dependin upon the location of the MI" The earliest chan e! which is not fre#uently seen! is symmetric! hyperacute T waves (defined as amplitude more than $% percent of the & wave in the same lead) in at least two conti uous leads! which reflects a localized increase in plasma potassium concentration '()" Thereafter! the ST se ment elevates with the followin appearance*

upward"

Initially there is elevation of the + point and the ST se ment retains its concave confi uration" ,ver time the ST se ment elevation becomes more pronounced and the ST se ment chan es its morpholo y! becomin more conve- or rounded

potential"

The ST se ment may eventually become indistin uishable from the T wave. the /&S0T comple- can actually resemble a monophasic action

An initial / wave develops and there is a loss of & wave amplitude as the ST se ment becomes elevated"

An abnormal / wave is any / wave in leads 1( to 12 or a / wave 32% msec in leads I! II! a14! a15! or 16 to 17. the / wave must be present in any two conti uous leads and 3( mm in depth '()" (See 89rior myocardial infarction8 below") ,ver time! there is evolution of these :;< chan es* the ST se ment radually returns to the isoelectric baseline. the & wave amplitude becomes mar=edly reduced. the / wave deepens. and the T wave becomes inverted" These chan es enerally occur within the first two wee=s after the event. however! in some patients they occur within a few hours of presentation" The electrocardio raphic chan es that occur in patients who sustain a non0ST elevation MI are different '()" T wave flattenin or inversion typically precedes ST se ment depression" / waves are typically absent but can occur! and the duration of the ST and T waves chan es is variable" The leads affected by these chan es depend upon the location of the infarction*

An acute anterior wall MI presents with the chan es in some or all of the precordial chest leads 1(017 (fi ure ()" &eciprocal :;< chan es

occasionally are observed durin the initial period of the acute infarction! presentin most often as depressions of the ST se ments in the inferior leads (>! 2! and a15)" An acute anteroseptal transmural MI presents with the chan es in leads 1(01> (fi ure >)" &eciprocal :;< chan es occasionally are observed durin

the initial period of the acute infarction! presentin as depressions of the ST se ments in the inferior (>! 2! a15) or lateral leads ((! a14! 1$! and 17)"

An acute anteroapical transmural MI presents with the chan es in leads 12 and 16 (fi ure 2)" &eciprocal :;< chan es occasionally are observed

durin the initial period of the acute infarction! presentin as depressions of the ST se ment in the inferior leads (>! 2! a15)"

An acute anterolateral transmural MI presents with the chan es in leads 1$ and 17! often in association with chan es in leads ( and a14 (fi ure 6)"

&eciprocal :;< chan es occasionally are observed durin the initial period of the acute infarction! presentin as depressions of the ST se ment in the inferior leads (>! 2! a15)! and in some cases in leads 1( and 1>"

An acute lateral transmural myocardial infarction presents with the chan es confined to leads ( and a14 (fi ure $)" &eciprocal :;< chan es

occasionally are observed durin the initial period of the acute infarction! presentin as ST se ment depressions in the inferior leads (>! 2 and a15) or leads 1( and 1>"

An acute inferior wall transmural myocardial infarction presents with the chan es in leads >! 2! and a15 (fi ure 7)" &eciprocal :;< chan es

occasionally are observed durin the initial period of the acute infarction! presentin with ST se ment depressions in leads 1( to 12! (! or a14" The ST se ment chan es in the precordial leads are not reciprocal in some cases! but represent true posterior wall involvement (which may be dia nosed by ST elevation in leads 1? to 1@) '>) or involvement of the ri ht ventricle (which may be dia nosed by ST elevations in ri ht precordial chest leads)" (See A&i ht ventricular myocardial infarctionA")

PRIOR MYOCARDIAL INFARCTION A chronic MI! or infarction of indeterminate a e! is characterized by initial / waves that are deep (B( mm) and broad (B%"%6 seconds)" The / waves may be associated with an inverted T wave" The location of these chan es is dependent upon the location of the MI" (See A9atho enesis and dia nosis of / waves on the electrocardio ramA") Anterior wall MI A chronic anterior wall infarction is dia nosed by the presence of initial deep and broad / waves in any of the precordial leads (fi ure ?)" In some cases there are no / waves! but rather poor & wave pro ression across the precordium (the & wave amplitude does not increase pro ressively from leads 1(012! to 16! 1$ or 17)" This situation must be distin uished from other causes of poor & wave pro ression! includin late transition (cloc=wise rotation) or a normal variant (often seen in women)" (See A:;< tutorial* Miscellaneous dia nosesA") Infre#uently there may be reverse & wave pro ression where the & wave amplitude becomes pro ressively smaller from lead 1> or 12 to lead 17" Similar to the :;< of an acute infarction! the location of the / waves establishes the area of infarcted myocardium. septum (1(01>). ape- (12016). or anterolateral wall (1$0 17)" The ST se ment typically is isoelectric" Cowever! an aneurysm is suspected if it remains elevated reater than three wee=s after the acute event" Anterolateral wall MI An old anterolateral wall infarction typically is dia nosed by the presence of / waves that are deep and broad in the anterolateral precordial leads 16017" Cowever! the / waves may e-tend across the entire precordium and are usually associated with inverted T waves" In addition! there may be / waves and T wave inversions in leads I and a14" ST se ment elevation is indicative of an aneurysm" Lateral wall MI An old lateral wall infarction is dia nosed by the presence of initial / waves which are deep and broad in leads ( and a14 (fi ure D)" If the & wave in these leads is small or absent! it is associated with a ri htward a-is (BE@%F) and is by definition a left posterior fascicular bloc=" Cowever! the ri ht a-is in this situation is actually the result of the / wave infarction and not a conduction system abnormality. it is =nown as a periinfarction bloc=" (See A:;< tutorial* Gasic principles of :;< analysisA! section on 8A-is8") There is also an inverted T wave in these leads" Inferior wall MI An old inferior wall MI is dia nosed by the presence of initial / waves which are deep and broad in the inferior leads >! 2! a15 (fi ure @)" There are usually inverted T wave associated with the / waves" If the & wave amplitude is reduced! the /&S comple- (/r) may appear to have a leftward a-is (B07%F) and by definition a left anterior fascicular bloc=! Cowever! the left a-is is actually the result of the infarction and not a conduction abnormality. it is =nown as a periinfarction bloc=" (See A:;< tutorial* Gasic principles of :;< analysisA! section on 8A-is8") It is not uncommon to see a / wave in lead 2 only in patients who have not had a MI" The depth of this / wave usually varies with respiration (respiratory / wave)" It represents a nonspecific normal findin " A dia nosis of inferior MI can only be made if there are also / waves in either of the other inferior leads" / waves may resolve within one year after an inferior wall MI in up to 2% percent of cases" The only remainin abnormalities in these instances are flattened or inverted T waves and ST se ment chan es"

Posterior wall MI An old posterior wall MI is dia nosed when there is a tall & wave in 1(01> (&HS B("%) (fi ure (%)" 5re#uently there is also evidence of an inferior wall infarction" ,ther causes for a tall & wave in these leads! includin ri ht ventricular hypertrophy or early transition (countercloc=wise rotation)! must be considered in these patients" (See :;< tutorial* Miscellaneous dia nosesA)" The findin of / waves and ST se ment chan es in leads 1? to 1@ is helpful in dia nosin a true posterior MI (table 6) '>)"