ECG Changes in Myocardial Infarction Clerk Karen G. Amoloza

Myocardial Infarction Death or necrosis of myocardial cells Diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes Ischemia  Injury  Infarction Occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. Myocardial infarction occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis. Ischemia at this critical threshold level for an extended time period results in irreversible myocardial cell damage or death.1-3

ECG on diagnosis of MI cornerstone in diagnosis of acute and chronic IHD Factors: Nature of the process: reversibility (ischemia vs infarction) Duration: acute vs chronic Extent: transmural vs subendocardial Localization: anterior vs inferoposterior Presence of other underlying abnormalities: chamber enlargement/hypertrophy, conduction defects The ECG is a cornerstone in the diagnosis of acute and chronic ischemic heart disease. The findings depend on several key factors: the nature of the process [reversible (i.e., ischemia) versus irreversible (i.e., infarction)], the duration (acute versus chronic), extent (transmural versus subendocardial), and localization (anterior versus inferoposterior), as well as the presence of other underlying abnormalities (ventricular hypertrophy, conduction defects).

Ischemia Decrease in the perfusion of a certain area of the myocardium Temporary, reversible reduction of blood supply Earliest manifestation of reduced coronary blood flow

Ischemia: ECG changes T wave Normal T waves ventricular repolarization Same direction as and smaller than QRS complex Upright, asymmetrical T wave changes Deeply inverted, symmetrical

Ischemia: ECG changes Pseudonormalization of the T wave Reversal to a normal upright T wave Acute ischemia in patients with pre-existing T wave inversion from a past event

Injury Acute, prolonged, reduction in blood supply to the myocardium Reversible

Injury: ECG changes ST segment elevation Subepicardial injury (outer ventricular wall) Minutes to hours of an acute event “Coved” or convex upward displacement of the ST segment from the baseline Factors: Atherosclerosis with sudden clot formation Coronary Artery Spasm (Prinzmetal’s Angina)

Injury: ECG changes ST segment depression Subendocardial injury (inner ventricular wall) Small penetrating branches of the superficial epicardial coronary arteries Poor perfusion First area of the myocardium to sustain injury

Injury: ECG changes ST segment depression Clinical indicator of coronary artery disease during stress test Assessment of Severity Morphology (magnitude ands slope) during exercise Duration of ST segment depression after exercise

Infarction: ECG Changes Q waves Indicate a loss of viable myocardium May develop 1 to 2 hours after the onset of symptoms but can take anywhere from 12 to 24 hours to develop

Infarction: ECG Changes Q waves Insignificant Q waves Small Q waves <25% of the height of the adjacent R wave Normal: Leads I, aVL, V5, V6 Result from the normal process of septal depolarization Significant Q waves Deeper than 25% of the height of the adjacent R wave >0.04s in duration

Infarction: ECG Changes

Infarction: ECG Changes R wave progression

Localizing Ischemia, Injury and Infarction Leads Site of occulusion Anterior V1 – V4 LAD Septal V1 – V2 Lateral I, aVL, V5, V6 Circumflex, RCA High Lateral I, aVL Inferior II, III, aVF RCA, circumflex Posterior RCA

Anterior Infarction Anterior infarction I II III aVR aVL aVF V1 V2 V3 Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL. Left coronary artery

Inferior Infarction Inferior infarction I II III aVR aVL aVF V1 V2 V3 Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node. Right coronary artery

Lateral Infarction Lateral infarction I II III aVR aVL aVF V1 V2 V3 Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL. Left circumflex coronary artery

Evolution of ECG Changes in AMI Development of acute ECG changes with gradual reversion of the ST segments and T waves to normal over time.

The Hyper-acute Phase Less than 12 hours “ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996) The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal Usually occurs within a few hours of infarction May vary in severity from 1mm to ‘tombstone’ elevation

The Fully Evolved Phase 24 - 48 hours from the onset of a myocardial infarction ST segment elevation is less (coming back to baseline). T waves are inverting. Pathological Q waves are developing (>2mm)

The Chronic Stabilised Phase Isoelectric ST segments T waves upright. Pathological Q waves. May take months or weeks.

Reciprocal Changes II, III, aVF I, aVL, V leads Are seen as ST depression in the opposite leads from where the ST elevation is seen Leads II, III and aVF are opposite to Leads I, aVL, and all of the V leads Therefore, if there is ST elevation in leads II, III and aVF any ST depression (if present) would be seen in leads I, aVL and any of the V leads II, III, aVF I, aVL, V leads

Reciprocal Changes ST elevation Reciprocal ST depression ST segment depression seen in the opposite leads from ST segment elevation Highly sensitive as an indicator of acute MI Frequently seen in larger infarctions ST elevation Reciprocal ST depression

Thrombolytic Therapy Indications ST segment elevation in two or more leads associated with acute chest pain Time between onset of chest pain to initiation of therapy less than 24 hours (optimal time to initiate therapy is less than 6 hours, and the earlier the better).

Thrombolytic Therapy Absolute Contraindications History of cerebrovascular hemorrhage at any time History of non cerebrovascular hemorrhage, stroke or other CV event within 1 year Marked hypertension (SBP > 180 or DBP > 110) at any time during acute presentation Suspicion of aortic dissection Active internal bleeding including menses

Thrombolytic Therapy Relative Contraindications Current use of any anti-coagulant (INR ≥ 2) Recent (< 2 weeks) invasive or surgical procedure or prolonged (> 10 min) CPR Pregnancy Hemorrhagic ophthalmic condition (ie. Hemorrhagic DM nephropathy) Active PUD History of severe hypertension that is adequately controlled Streptokinase with preceding 5 days to 2 years (allergic reaction)