Download - ECG Changes in Myocardial Infarction
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+ECG Changes in Myocardial InfarctionClerk Karen G. Amoloza
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+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
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+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
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+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
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+Ischemia: ECG changesT wave Normal T waves
ventricular repolarization Same direction as and smaller
than QRS complex Upright, asymmetrical
T wave changes Deeply inverted, symmetrical
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+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
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+Injury
Acute, prolonged, reduction in blood supply to the myocardium
Reversible
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+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)
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+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
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+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
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+
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+Infarction: ECG Changes
Q wavesIndicate 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
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+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
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+Infarction: ECG Changes
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+Infarction: ECG Changes
R wave progression
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+Localizing Ischemia, Injury and Infarction
Leads Leads Site of occulusion
Anterior V1 – V4 LAD
Septal V1 – V2 LADLateral I, aVL, V5,
V6Circumflex, RCA
High Lateral
I, aVL Circumflex, RCA
Inferior II, III, aVF RCA, circumflexPosterior V1 – V2 RCA
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+Anterior InfarctionAnterior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left coronary artery
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+Inferior InfarctionInferior infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Right coronary artery
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+Lateral InfarctionLateral infarction
I II III aVR aVL aVF V1 V2 V3 V4 V5 V6
Left circumflexcoronary artery
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+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.
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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
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+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)
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+The Chronic Stabilised Phase
Isoelectric ST segments T waves upright. Pathological Q waves. May take months or weeks.
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+Reciprocal Changes
II, III, aVFI, 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
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+Reciprocal Changes 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
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+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).
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+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
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+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)