Myocardial Infarction - ECGpedia

8/17/2019 Myocardial Infarction - ECGpedia

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Myocardial Infarction

Contents [hide]

1 Risk assessment of Cardiovascular disease

2 Risk assessment of ischemia

3 Diagnosis of myocardial infarction

4 The location of the infarct

5 Development of the ECG during persistent ischemia

6 Subendendocardial Ischemia

7 References

8 External Links

Author(s) I.A. C. van der Bilt, MD

Moderator I.A. C. van der Bilt, MD

Supervisor

some notes about authorship

Ischemia occurs when part of the heart muscle, the myocardium, is deprived of oxygen andnutrients. Common causes of ischemia are:

Narrowing or obstruction of a coronary artery.

A rapid arrhythmia, causing an imbalance in supply and demand for energy.

A short period of ischemia causes reversibleeffects: The heart cells will be able to recover. When

the episode of ischemia lasts for a longer period of time, heart muscle cells die. This is called

a heart attack or myocardial infarction. That is why it is critical to recognize ischemia on the

ECG in an early stage.

Severe ischemia results in ECG changes within minutes. While the ischemia lasts, several ECG

changes will occur and disappear again. Therefore, it may be difficult to estimate the duration of

the ischemia on the ECG, which is crucial for adequate treatment.

Signs and symptoms of myocardial ischemia:

Crushing pain on the chest (angina pectoris), behind the sternum, often radiating to the lower

jaw or the left arm

Fear of dying

Nausea

Shock (manifesting as paleness, low blood pressure, fast weak pulse) shock

Rhythm disturbances (in particular, increasing prevalence of ventricular ectopia, ventricular

tachycardia, AV block)

Risk assessment of Cardiovascular disease

Narrowing of the coronary artery, leading to a myocardial infarction, usually develops over severalyears. An increased risk of cardiovascular disease, which may lead to a myocardial infarction or

cerebrovascular accident, can be estimated usingSCORE system which is developed by the

European Society of cardiology (ESC). As shown in the figure, the most important risk factors for

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ST elevation is measured at the junctional or J-

point

myocardial infarction are:

Male sex

Smoking

Hypertension

Diabetes Mellitus

Hypercholesterolemia

Risk assessment of ischemia

An exercise test such as a bicycle or treadmill test, may be useful in detecting myocardial ischemia after

exercise.[1] In such a test, continuous ECG monitoring is performed during exercise. The ST-segment,

blood pressure and clinical status of the patient (i.e. chest complaints) are monitored during and after

the test.

An exercise test is positive for myocardial ischemia when the following criteria are met:

Horizontal or downsloping ST-depression of >1mm, 60 or 80ms after the J-point

ST elevation of > 1.0 mm

Diagnosis of myocardial infarction

The diagnosis of acute myocardial infarction is not

only based on the ECG. A myocardial infarction is

defined as:[2]

Elevated blood levels of cardiac enzymes

(CKMB or Troponin T) AND

One of the following criteria are met:

The patient has typical complaints,

The ECG shows ST elevation or depression.

pathological Q waves develop on the ECG

A coronary intervention had been performed

(such as stent placement)

So detection of elevated serum cardiac enzymes is

more important than ECG changes. However, the

cardiac enzymes can only be detected in the serum

5-7 hours after the onset of the myocardial

infarction. So, especially in the first few hours after

the myocardial infarction, the ECG can be crucial.

ECG Manifestations of Acute Myocardial Ischaemia (in Absence of LVH and LBBB)are [3]:

ST elevationNew ST elevation at the J-point in two contiguous leads with the cut-off points: ≥0.2 mV in men or ≥

0.15 mV in women in leads V2–V3 and/or ≥ 0.1 mV in other leads.

ST depression and T-wave changes.

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An overview of the

coronary arteries. LM =

'Left Main' = mainstem;

LAD = 'Left Anterior

Descending' artery; RCX

= Ramus Circumflexus;

RCA = 'Right Coronary

Artery'.

Overview of the separate

ECG leads. The lead

with ST segment

elevation 'highlights' the

infarct. An infarction of

the inferior wall will result

in ST segment elevation

in leads II, III and AVF. A

lateral wall infarct results

in ST segment elevation

in leads I and AVL. An

Anterior wall infarct

results in ST segment

elevation in the

precordial leads.

New horizontal or down-sloping ST depression >0.05 mV in two contiguous leads; and/or T

inversion ≥0.1 mVin two contiguous leads with prominent R-wave or R/S ratio ≥ 1

A study using MRI to diagnose myocardial infarction has shown that more emphasis on ST segment

depression could greatly improve the yield of the ECG in the diagnosis of myocardial infarction

(sensitivity increase from 50% to 84%).[4]

Myocardial infarction diagnosis in left or right bundle branch block can be difficult, but it is explained in

these seperate chapters:

MI diagnosis in left bundle branch block or paced rhytm

MI Diagnosis in RBBB

The location of the infarct

The heartmuscle itself is very limited in its

capacity to extract oxygen in the blood that is

being pumped. Only the inner layers (the

endocardium) profit from this oxygenrich blood.

The outer layers of the heart (the epicardium)

are dependent on the coronary arteries for the

supply of oxygen and nutrients. With aid of an

ECG, the occluded coronary can be identified.

This is valuable information for the clinician,

because treatment and complications of for instance an anterior wall infarction is different

than those of an inferior wall infarction. The

anterior wall performs the main pump function,

and decay of the function of this wall will lead to

decrease of bloodpressure, increase of

heartrate, shock and on a longer term: heart

failure. An inferior wall infarction is often

accompanied with a decrease in heartrate

because of involvement of the sinusnode.

Longterm effects of an inferior wall infarction are

usually less severe than those of an anterior wall

infarction.

The heart is supplied of oxygen and nutrients by

the right and left coronary arteries. The left

coronary artery (the Left Main or LM) divides

itself in the left anterior descending artery

(LAD) and the ramus circumflexus (RCX).

The right coronary artery(RCA) connects to

the ramus descendens posterior (RDP). With

20% of the normal population the RDP is

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The coloured figure

shows contiguous leads

in matching colors

The ST segment

elevation points at the

infarct location. Inferior

MI=ST segment

elevation in red regions

(lead II,III and AVF).

Lateral MI = ST elevation

in blue leads (lead I,

AVL, V5-V6). Anterio MI:

ST segment elevation in

yellow region (V1-V4).

Left main stenosis: ST

elevation in gray area

(AVR)

The coronary blockade

can cause conduction

block, on AV nodal, His

or bundle branch level.

supplied by the RCX. This called left

dominance.

Below you can find several different types of

myocardial infarcation. Click on the specific

infarct location to see examples.

Help with the localisation of a myocardial infarct

localisation ST elevation Reciprocal ST depression coronary

artery

Anterior MI V1-V6 None LAD

Septal MI V1-V4, disappearance of

septum Q in leads V5,V6 none

LAD-septalbranches

Lateral MI I, aVL, V5, V6 II,III, aVF LCX or MO

Inferior MI II, III, aVF I, aVL RCA (80%) or

RCX (20%)

Posterior MI V7, V8, V9 high R in V1-V3 with ST depression

V1-V3 > 2mm (mirror view) RCX

RightVentricle MI

V1, V4R I, aVL RCA

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The evolution of an infarct on the ECG. ST

elevation, Q wave formation, T wave inversion,

normalisation with a persistent Q wave

A pathological Q wave

Wellens syndrome: symmetrical negative T wave

in pre-cordial leads without R loss of R waves can

regularly be observed in early anterior ischemia. Many

patients with Wellens syndrome / sign turn out to have

a critical proximal LAD stenosis[6].

Atrial MI PTa in I,V5,V6 PTa in I,II, or III RCA

The localisation of the occlusion can be adequately visualized using a coronary angiogram (CAG). On

the CAG report, the place of the occlusion is often graded with a number (for example LAD(7)) using

the classification of the American Heart Association.[5]

Development of the ECG during persistent ischemia

The cardiomyocytes in the subendocardial layers

are especcially vulnerable for a decreased

perfusion. Subendocardial ischemia manifests as

ST depression and is usually reversible. In a

myocardial infarction transmural

ischemia develops.

In the first hours and days after the onset of a

myocardial infarction, several changes can be

observed on the ECG. First, large peaked T

waves(or hyperacute T waves), then ST elevation,

thennegative T waves and finally pathologic Q

wavesdevelop.

Wellens syndrome or sign (see image) can be an

early ECG warning sign of critical anterior ischemia

before the development of overt mocardial

infarction.

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Typical negative T waves post anterior myocardial

infarction. This patient also shows QTc prolongation.

Whether this has an effect on prognosis is debated.[7]

[8][9]

Evolution of the ECG during a myocardial infarct

Time from

onset of symptoms

ECG Changes in the heart

minutes hyperacute T waves (tall T waves), ST-elevation reversible ischemic damage

hours ST-elevation, with terminal negative T waves,

negative T waves (these can last for days to months)

onset of myocardialnecrosis

days Pathologic Q Waves

scar formation

Subendendocardial Ischemia

Subendocardial ischemia is ischemia that is not transmural. It is mostly caused by demand ischemia

where energy supply to cardiomyocytes is insufficient for the work force, e.g. during extreme

hypertension, aortic valve stenosis, extreme left ventricular hypertension, anemia, atrial fibrillation with

rapid ventricular response. On the ECG often diffuse ST depression is present. Cardiac enzymes (CK-

MB, Troponine) may or may not be elevated depending on the severity.

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An example of subendocardial ischemia with

diffuse ST depression
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