ELECTROCARDIOGRAPHIC DIAGNOSIS OF ACUTE

MYOCARDIAL INFARCTION“CURRENT CONCEPTS

FOR CLINICIANS”DR ASADULLAH SOOMRO

CARDIOLOGISTKING FAHAD HOFUF HOSPITAL

KINGDOM OF SAUDI ARABIAEmail;hssbasadsoomro@gmail.

com

INTRODUCTIONThe electrocardiogram remains a

crucial tool in the identification and management of acute myocardial infarction. EKG is single most often used most effective diagnostic test in Cardiology, despite introduction of computerized EKG interpretation yet most frequently misinterpreted in clinical practice

• The early and accurate analysis of “ST segment deviation “ may influence decision regarding use of

"reperfusion therapy “ and may identify infarct related artery and proximal occlusion result in most extensive and sever myocardial damage. It is crucial in decision regarding urgency of revascularization.

• 12 lead ECG is of central importance in the management of acute MI because there is strong evidence that patients with

“ST segment elevation” benefit from reperfusion therapy.

• current data suggest that there is no role of

“ thrombolytic therapy” in non ST elevation MI however

role of glycoprotein chopidogrel followed

by primary angioplasty / CABG is now well established.

Some EKG leads are “underutilized” in clinical practice , but can be very helpful in discriminating infarct related artery especially during inferior injury with ST segment elevation in V7—V9 and ST depression in AVR are probably related to left “Circumflex “ occlusion.

Coronary occlusion will result in widely different EKG manifestations depending on ,

1) Artery size

2) Artery length

3) Occlusion level

4) Presence of collaterals

5)Previous heart damage

6)Intraventricular conduction disorders

7)Position of heart in chestThus 12 lead EKG is only moderately accurate to

determine the anatomic location of acute MI.

EKG Angiographic Correlations

The most frequent infarct related artery among patients admitted with chest pain or discharge after MI is ,

1) LAD 44% to 56%

2) RCA 27% to 39%

3) LCX 17%

SIGNIFICANCE OF ST ELEVATION IN “ V1”Lead V1 area ( Rt paraseptal area) is supplied by

septal branches of the “LAD” .In some patients the septum is additionally protected by blood supply from conal branch of the “RCA” ( double circulation ) ,that’s why approximately 2/3 of patients with anterior MI have,

“ NO ST ELEVATION IN V1”.

In 7% of patients with ST elevation in lead V1 through V4 who undergo coronary angiogram this St elevation is secondary to RCA occlusion.

INFERIOR INJURY WITH ST ELEVATION IN “ V1”ST elevation in V1 along with ST elevation in 11,111 & avf , indicates

1) Large RV infarction

2) Proximal RCA occlusion

PROXIMAL “LAD” OCCLUSION

In anterior wall MI maximum ST elevation is in V2-V3 ,how ever additional signs recorded recently by Brinbaum & colleagues as powerful predictor of proximal occlusion includes,

1) ST ELEVATION IN AVL2) ST DEPRESSION IN III & AVF

INFERIOR INFARCTION“RCA OR LCX “

ST elevation in 11,111,avf occlusion is in “RCA”

in 80% to 90% of cases and is in the “LCX” in remaining patients.

ST depression in avl is almost always

determined by RCA occlusion , injury in leads 11 111 & avf without STdepression in avl indicate” proximal LCX occlusion”

Precordial ST depression accompanying inferior injury is more likely to develop from “ RCA or LCX” with large ischemic burden.

• An autopsy study found that ST segment depression of 1mm in the initial EKG was a sensitive sign for infarction of a papillary muscle . Inferior ST depression was seen exclusively in infarctions of the “ Antero lateral “papillary muscle ,where as ST

depression in leads 1,aVL occurred only

after infarction of the “Postero medial papillary muscle.

PAPILLARY MUSCLE INFARCTION

PAPILLARY MUSCLE INFARCTION

It is usually a small MI, frequently single vessel

disease. The blood supply to “posteromedial” derived only from PDA, is more tennous than that “ anterolateral” which has double supply

(LAD & LCX ) ,consequently 90% of pappilary muscle rupture involve posteromedial group.

It has usually multiple heads in contrast to anterolateral with single head. Rupture of individual head is survivable

• RV infarction is always associated with occlusion of “proximal segment of right coronary” artery. The most sensitive EKG sign of RV infarction is ST segment elevation of more than 1 mm in lead V4R .This sign is rarely present more than 12 hours after infarction.54% of inferior MI have ST elevation in V4R.18% of Pts with acute inferior MI had ST elevation in lead V1,which is highly specific sign of RV infarction. It is usually associated with large infarct size and higher incidence of major in hospital atrial & ventricular arrhythmias and high grade AV block

RIGHT VENTRICULAR INFARCTION

CAUSES OF ST ELEVATION IN “ V4R”

1) Acute “RV “myocardial infarction

2) Acute pulmonary embolism

3) Left ventricular hypertrophy

4) Pericarditis

5)Previous MI with aneurysm

• ST segment elevation in leads 1 ,aVL,V5 & V6 and St segment depression in V1 ,V2 & V3 suggest concomitant infarction of the

posterior wall ,however ,ST elevation in V7 & V9 is always detected and is more specific than pre cordial leads in posterior MI .When St elevation is more than 2mm it is probably a sign of “ Mega artery related “ ( either RCA or LCX ) infarction with a large ischemic burden .

LATERAL & POSTERIOR INFARCTION

ANTERIOR PLUS INFERIOR MI

• The combination of anterior plus inferior ST elevation in the EKG may give the impression of a critical mass of myocardial injury .How ever, it often results from

distal occlusion of long LAD after D1 , which “Wraps around“ the cardiac apex ( ST segment elevation in V1,V2 & V3 along with ST elevation in 11, 111,& aVF.

NON DIAGNOSTIC EKG• 15 to 18% of patients with MI do not have changes

in initial EKG & an additional 25% show non specific changes ,( often associated with branch arteries.) The probability of detecting MI does increase by recording serial EKGS . However because reperfusion therapies are more effective when administered early.

• Approximately 8% of patients with cardiac pain will display ST elevation only in posterior leads (V7 through V9 ) or right precordial leads ( V3R through V6R ) leads .These patients may not be offered reperfusion if 12 lead EKG is used for decision making.

• It is reasonable to assume that a systematic examination of lead aVR may increase sensitivity for acute infarction.

CONCLUSION•Plethora of data currently available on

electro cardiographic changes accompanying chest pain should allow clinicians to make faster and better decisions than ever before .

• It is now clear that isolated ST depression in leads V1 through V3 may indicate “ Left Circumflex “ occlusion and potentially benefit from thrombolysis.

• Entirely non diagnostic EKG may become diagnostic when serial or previous EKGS are obtained or when posterior and right precordial leads are recorded.

• A few hospitals around the world are

already using the “15 or 16” lead EKG for routine admission workups.

• Cardiologists and emergency physicians should make an effort to incorporate these leads in both teaching and clinical practice and request EKG machine vendors that EKG be set to provide a panoramic display of

frontal plane leads including a “ AVR “

• The 12 lead EKG is only moderately accurate to determine the anatomic location of AMI hence some patient may not be offered revascularization if 12 lead ECG is used for decision making how ever 15 lead EKG recording i- e “V4R V8 –V9 “ Increases the probability of detecting ST elevation in “RV and posterior wall MI”.