ST Elevation in Various Syndromes

Early Afterdepolarization vs ST-Elevation

Early After Depolarizations

QRS Morphology 1. Are there any pathological Q waves as a sign of previous MI? Yes/No? 2. Are there signs of LV or RV Hypertrophy: Yes/No? 3. Does the QRS complex show Microvoltage (< 5mV): Yes/No? 4. Is the Conduction normal or prolonged ( > 0.12s): Yes/No? 5. Is the R wave propagation normal? **(Normal R waves become larger from V1-V5 (Max @ V5)) a. Is R-Wave amplitude @ V2 > R-Wave amplitude @ V3? Yes? could be a sign of a (previous) posterior MI + others *If all these items are normal you can go on to the next step: ST morphology

STT Elevation #1 = Acute Ischemia Early Repolarization Acute Pericarditis: SE Elevation @ All Leads (Except AVR) Pulmonary Embolism: St Elevation @ V1 + AVRr Hypothermia: St Elevation @ V3, V4, V5, V6, II, III, + AVF HCM @ V3, V4, V5, (V6)

K (Hyperkalemia): @ V1, V2 (V3)

During Acute Neurologic Events: @ All Leads, (Primarily V1-V6) Acute Sympathic Stress: @ Leads Leads, (Especially V1-V6) Brugada Syndrome. Cardiac Aneurysm Cardiac Contusion LV-Hypertrophy Idioventricular Rhythm Including Paced Rhythm

The T wave= morphologically variable but give hints

Flat T wave < 0.5 mm / Concordance @ Leads I, II, V3, V4, V5 or V6

Inverted T wave > 0.5 mm @ leads I, II, V3, V4, V5 or V6

Possible causes of T wave changes: Ischemia & MI Pericarditis Myocarditis Cardiac Contusion Acute Neurologic event (ex SAH) Mitral valve prolapse (MVP) Digoxin effect Straining RV/LV-Hypertrophy

STT Depression #1 = Ischemia Reciprocal STsD (If one lead shows STsE another must show STsD Straining LV-Hypertophy Digoxin effect K, Mg

Post tachycardia) During acute neurologic events

P Wave Morphology can reveal RA-Hypertrophy, LA-Hypertrophy + Atrial arrhythmias best determined @ leads II and V1 during sinus rhythm.

Normal P-Wave: P-Wave max height = 2.5 mm @ leads II or III P-Wave duration < 0.12 seconds P-Wave: Lead II: , AVF: , V1: Biphasic

Abnormal P wave 1. Elevation or Depression of the PTa segment PTa seg = between the p wave and QRS complex can result from atrial infarction or pericarditis. 2. If the p-wave is enlarged, the Atria are enlarged. 3. Inverted P-Wave = ectopic atrial rhythm

PTa seg = between the p wave and QRS complex Atrial infarction or PericarditisElevation or Depression of the PTa segment

STT = ST Seg = ventricular repolarizationRepolarization follows Contraction and Depolarization.

During Repolarization -Cardiomyocytes elongate and prepare for the next heartbeat -Repolarization takes much more time than the depolarization.

-Elongation is not passive Repolarization Starts @ J point, Ends @ T wave. Normally the STs @ or near the isoelectric line **Minor STT changes are not necessarily associated with cardiac ischemia[1].

The T wave is usually "CONCORDANT" e.g. QRS = T-Wave for a given lead

The T wave is normally in Lead I, II, AVL, AVF, V3-V6.

The T wave is normally in V1 & AVR.

The T wave is in V2 (in Blacks V3)

The T wave angle LV Endocardium repolarizes 22msec slower LV Epicardium Repolarization = Current from the Endocardium Epicardium

Interpreted as a signal on the ECG

Early repolarization = STE w/o without underlying disease.Probably has nothing to do with actual early repolarization. Commonly seen in young and understand that ER Ischemia

EKG Morphology

P-Wave?PTa Seg?QRS?STT?T-Wave?

Denition of a pathologic Q wave Any Q-wave @ leads V2V3 0.02s or QS complex in leads V2 and V3 Q-wave 0.03 s and > 0.1 mV deep or QS complex in leads I, II, aVL, aVF, or V4V6 in any two leads of a contiguous lead grouping (I, aVL,V6; V4V6; II, III, and aVF) R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive T-wave in the absence of a conduction defect