Ischemic Heart Disease EKG (Costa) PDF

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ISCHEMIC HEART DISEASE Coronary Arteries: - Right: comes off of R cusp, wraps around R AV grooves to supply posterior descending branch in R dominant heart (POSTERIOR) - Left: comes off of L cusp, supplies LAD down front of heart, perforators, and diagonal branches (ANTERIOR) - Left Circumflex: wraps around L AV groove and supplies obtuses marginal branches to the lateral wall (LATERAL)

ST Segment

STEMI: occlusive thrombus  no perfusion; clinical syndrome with characteristics EKG changes and release of biomarkers for myocardial necrosis SUMMARY: - Clinical syndrome (symptoms of MI + EKG - ST segment concave, no notching - Anatomic Distribution - QT prolongation not normal with classic STEMI Guidelines: - Classic: > 1 mm ST elev in 2 contiguous leads - ANTERIOR: V1-V4 (ST elevation in V2-V3 >2 mm in men, > 1.5 mm in women - INFERIOR: II, III, aVF - LATERAL: I, aVL, V5, V6 - Other - Transmural posterior: ST depression in 2 precordial leads (V1-V4) - L main/Proximal LAD: multi-lead depression with ST elevation in aVR - Early STEMI: hyperacute T wave changes - Consider reciprocal changes in leads opposite those with ST elevation Repolarization Plateau - time b/w end of V depolarization & beginning of repolarization - ventricles active, but no electrical activity - Is myocardium getting enough blood/O2?

Myocardial Infarction MI Evolution

NSTEMI: thrombus forms, but not occlusive; still compromises blood flow

A. Normal B. ST Elevation w/ hyperacute T waves (appears as if the T wave was just pulled up) C. ST Elevation D. Evolving Q wave, resolving ST elevation, T wave inversion E. Q wave & T wave inversion F. Q wave

Normal: isoelectric (same at baseline) - J point to T wave

Q Waves

- Sign of old transmural infarction - Permanent damage/scarring of myocardium - Significant: 1 mm wide (small box) or 1/3 QRS height & in consecutive leads - Q waves follow pattern Old Infarction:  30 ms (40 ms = 1 small box) - Anteroseptal MI: V1-V3 - Anterior MI: V2-V4 - Inferior MI: II, III, aVF - Lateral MI: I, aVL

Old Inferior MI: Q waves in inferior leads

Age Indetermined Anterior MI: Q wave & no R wave V1-V4, sudden 10mm R wave in V5 (anterior myocardium infarcted) STEMI

Clinical Syndrome - sxs of myocardial ischemia (chest pain, etc) - due to occlusive thrombus - biomarkers of myocardial necrosis - can cause complic (complete heart block) ECG Findings -  1 mm ST elevation in 2 contiguous leads - **consider reciprocal changes ( 0.5 mm) - hyperacute T waves may appear before ST elevation in early phase STEMI Hints - ST segment: - Concave or convex? Convex frown  MI - J point notching? Not STEMI - Normal ST elevation variants in V1-V6: males  1 mm, females  1 mm - In V2-V3 –>2 mm (M), >1.5 mm (F) - Anatomic distribution (blood supply): - Does ST elevation pattern make sense? - QT prolongation? - Seen in repolarization abnormalities, ischemia, & myocarditis (“RIM”) - **Not in normal variant ST elevation - Rhythm: - Pacing spikes? You usually won’t see ST elevations with pacing spikes - Atrial dysrhythmia? STEMI & NSTEMI Tx: “triple A” - Antiplatelet (Aspirin) - revascularization - Antithrombotic – prevent clotting - Antianginal - increase perfusion

STEMI (acute MI) - ST elevation in contigous leads (V1-V4) - ST depression in reciprocal leads (II, III, aVF)

convex (frown): more likely STEMI

Anterior STEMI

LAD occlusion - V1-V4 - V2-V3: men  2 mm, women  1.5 mm - reciprocal ST depression in inferior leads (II, III, aVF) Anterior STEMI (V1-V4) w/ reciprocal changes in inferior leads (II, III, aVF)

Anterior STEMI w/ atrial pacing (spike before P wave) & slight RBBB; ST elev in V2-V5, recip ST dep

Large wrap-around LAD – Anterior STEMI, w/ reciprocal changes in inferior leads Inferior STEMI

R Coronary A occlusion - Could cause papillary muscle rupture (anterolateral papillary muscle only has Q from posterior descending artery)  regurgitation with holocystolic murmur radiating to axilla

- II, III, aVF - reciprocal ST depression (I, aVL, V2, etc) Inf STEMI w/ recip ST dep, CHB, & junctional rhythm

Inferior STEMI w/ pacing spikes before QRS & reciprocal ST depression

Lateral STEMI

Circumflex A occlusion - I, aVL, V5, V6

Inferolateral injury (ST elevation in inferior leads that extends laterally) AD & STEMI

Marfan’s - Aortic dissection: can occur near coronary ostium & cause STEMI - ST elevation w/ neuro findings (paralysis)

Marfan’s  Aortic Dissection  STEMI (rare) ST elevations, wide QRS, RBBB Posterior MI

Transmural Posterior Injury - ST depression in 2 precordial leads (V1-V4) - > 2mm - R & T waves stay upright - portion of circumflex a occluded - most commonly missed STEMI – If there is a suspicious clinical history and normal EKG – ask for posterior EKG to see circumflex occlusion (lateral leads)

Posterior MI: ST dep in V1-V3, R & T waves upright

Large dominant L Circumflex – Posterior MI, w/ reciprocal ST depression (V1-V3) Global Ischemia (L Main/Proximal LAD)

ST depression in multiple leads & reciprocal ST elevation in aVR - L main coronary a or proximal LAD occlusion - Tx: emergent CABG - high risk of v arrhythmias & sudden death

Global ischemia: ST depressions in multiple leads (I, aVL, II, V2-V6) w/ slight reciprocal ST elevation in aVR

ST Elevation ST Elevation (Injury)

Electrolytes (Hyperkalemia)

Causes: “ECG ELEVATION” Electrolytes (hyperkalemia) LBBB & Brugada syndrome Early repolarization Ventricular hypertrophy (LVH) Aneurysm Treatment (pericardiocentesis), Takotsubo Injury (acute MI, contusion), Infection (pericarditis) Osborne waves (hypothermia) Non-occlusive vasospasm Hyperkalemia - ST elevation - tall T wave (affects ability to repolarize) - shortened QT - wide QRS (widens over time) - Timing: 1) peaking of T waves; 2) widening of Pr interval; 3) P wave may disappear; 4) QRS spreads out

If there is ST elevation in leads I & II  90% of time it isn’t MI due to arterial distribution (I and II would be inferior and lateral)

Hyperkalemia: initial ECG, peaking of T waves (christmas trees)

Tx: “triple S” - Stabilize membrane (bicarb & Ca2+) - Shift the K+ (insulin, glucose, B agonist) - Shit (kayexelate to inc K+ excretion)

Hyperkalemia: 8 minutes later – declining status - ST elevation, tall T, shortened QT LBBB & Brugada

LBBB L bundle branch blocked  impulse to R branch  through mm to L side  LV gets delayed impulse - wide QRS  120 ms - broad, deep S: V1-V3 (late forces negative) - broad R: I, V5-V6 (late forces positive) - ST elevation V1-V3 - Assoc w/ - LVH - MI: see reciprocal ST depression - congenital heart disease - degenerative conduction system - rate related on occasion

LBBB: wide QRS, broad deep S (V1-V3), broad R (I, V5 - V6), ST elevation (V1-V3)

-ANY PATIENT with LBBB and CP, suspect MI – if no CP or clinical syndrome, Rlikely just LBBB LBBB & STEMI: ST elevation (II, III) w/ **reciprocal ST depression (V2 – should be elevated)

Brugada Syndrome - mild dyspnea w/o chest pain, HTN, obesity - RBBB pattern w/ persistent ST elevation (V1-V3 shark fin) - recurrent polymorphic VT - recurrent syncope - no structural heart disease - Na channelopathy: abnormal electrolyte channels in the heart - induced by Na channel antagonist (procainamide, flecainide) - sudden cardiac death risk

Brugada Syndrome: RBBB pattern w/ persistent ST elevation (V1-V3 shark fin) Early repolarization

- sharp stabbing chest pain, smoker - can cause sudden cardiac death ECG findings: - J point notching (V4, V5) – or fishhook - PR depression - Tall T waves/prominent concordant T - concave ST elevation (smile) – max in leads w/ tallest R waves Early repolarization: J point notching, ST concave smile elevation, tall T waves

Ventricular hypertrophy (LVH)

LVH - chest pain, HTN - QRS-T wave discordance (esp in lateral leads) - can mimic STEMI due to 2o ST/T changes - concave ST (smile) - LVH w/ IVCD: very common, can further elevate ST segment in V1-V3 - asymmetrical T waves ECG: Left-Axis Deviation (lead I +, aVF -) - high voltage  think inc muscle mass - deep S on V1 - tall R on V6 Males: Females: > 40 yo: Sokolow:

R (aVL) + S (V3) > 28mm R (aVL) + S (V3) > 20mm R (V5 or V6) + S (V1) > 35mm R (aVL) > 11mm

LVH: ST elevation (concave smile, V1-V3), high voltage

Treatment, Takotsubo

Treatment: pericardiocentesis Takotsubo - life altering event  severe chest pain, dyspnea - stress-induced cardiomyopathy: basal portion contracts, apex doesn’t  octopus trap LV appearance in systole - arteries normal – can recover EF with meds - tx like most MI cases - recover in 3-4 wks - can go into cardiogenic shock

Takotsubo: octopus trap LV appearance in systole

Takotsubo: prolonged QRS, ST elevations (V3-V6, I) Injury, Infection

Injury: acute MI (STEMI) - due to occlusive thrombus

STEMI (acute MI): elevated in contigous leads - inferior leads (II, III, aVF)  “inferior STEMI” Infection: Pericarditis - Clinical history: **recent cold/illness, sharp chest pain/pressure - diffuse ST elevation, concave (smile) – not confined to arterial territory, can be global - **no reciprocal ST depression (if there are – this is a likely STEMI) - PR depression, with elevation in aVR - auscultation: pericardial friction rub

Osborne waves

- Stage I: diffuse concave-upward ST elevation, PR depression, low voltage, ST depression in aVR or V1, absence of reciprocal ST changes - Stage II: ST goes to baseline, T wave flattens - Stage III: T-wave inversion - Stage IV: gradual resolution of T wave Pericarditis: diffuse ST concave (smile) elevations inversion w/ PR depression Hypothermia (seen in cold environments, or following hypothermia treatment after cardiac arrets - Osborne waves - “J waves, camel-hump waves” - ST elevations - best seen in inferior & lat precordial leads - become more prominent as body temp drops & regress gradually w/ rewarming - elevated & prominent U waves - prolonged QT - Temps < 86oF: progressive widening of QRS  inc risk of v fib - Temp ~60oF: asystole Hypothermia: Osborne waves (ST elevations)

ST Depression ST Depression (Ischemia)

Causes: “DEPRESSED ST” Drooping valve (MVP) Enlargement of LV with strain Potassium loss (hypokalemia) Reciprocal ST- depression (in I/W AMI) Embolism in lungs (PE) Subendocardial ischemia Subendocardial infarct Encephalon hemorrhage (intracranial) Dilated cardiomyopathy Shock Toxicity of digitalis, quinidine

UA/NSTEMI: ST depression & T wave inversion - non-occlusive thrombus

STEMI & NSTEMI Tx: “triple A” - Antiplatelet (Aspirin) - Antithrombotic - Antianginal (inc perfusion) Global ischemia - ST depressions globally with reciprocal ST elevation in aVR - L main plaque rupture/90% critical narrowing - requires emergent CABG (high risk of v arrhythmias & sudden death)

Global ischemia: ST depressions globally (I, aVL, II, V2V6) with slight reciprocal ST elevation in aVR Transmural Posterior Injury (MI) - ST depression in 2 precordial leads (V1-V4) - > 2mm - R & T waves stay upright - portion of circumflex a occluded - most commonly missed STEMI

Posterior MI: ST depression in V1-V3, R & T waves stay upright

Large dominant L Circumflex – Posterior MI, w/ reciprocal ST depression (V1-V3)...