ST ELEVATION Flashcards
DDX
4 BAD THINGS
STEMI
Hyperkalemia
Spasms (Prinzmetal Angina)
Brugada
HOCM
4 STEMI MIMICS
Pericarditis
LVH
LV Aneurysm
BER
STEMI
ST-ELEVATION CRITERIA
(Use the J point, 2 contiguous leads)
Men > 40 yo: 2mm in v2-V3 and >/ 1 mm in all other leads
Men < 40 yo: 2.5 mm in v2-v3 and >/ 1 mm in all other leads
Women: 1.5 mm in v2-v3 and >/ 1 mm in all other leads
ST-Segment Elevation in non-AMI vs. AMI:
Draw a line from the J point to the apex of the T-wave
non-AMI: ST-segment-T-wave complex is concave
AMI: ST-segment-T-wave complex is convex or flattened (“bulging upward”)
ANTERIOR STEMI
ST Elevation in precordial leads V1 - V6) +/- High Lateral Leads with subsequent q wave formation
Changes usually preceded by hyper acute t waves
Reciprocal st depression in inferior leads (mainly III and aVF)
The magnitude of reciprocal change in inferior leads is determined by the magnitude of ST elevation in I and aVL (as these leads are electrically opposite III and aVF), and hence may be minimal or absent in anterior STEMIs that do not involve high lateral leads.
LAD. Poorest prognosis.
INFERIOR STEMI
INFERIOR STEMI
STE in leads II, III, and aVF
Hyperacute T waves may preceed these changes
Reciprocal depression in aVL
Progressive Q wave development in II, III, and aVF
RCA (80%),STE III>II, STD I, signs of RV infarction
LCx (18%), STE II = III, NO STD I, signs of lateral infarction
Associated features with Inferior STEMI that confer poor prognosis:
Concomitant right ventricular infarction (40% patients)
Significant bradycardia due to 2nd or 3rd degree heart block
Posterior Infarction due to extension of infarct area
DO NOT IGNORE aVL!!! MAY BE THE ONLY FINDING
Inferior Stemi: ST depression in aVL (reciprocal changes) may preceed STE in II, III, aVF
Ongoing pain -> serial ECG’s
Inferior MI -> get right sided leads -> aggressively give IVF, monitor lung sounds
POSTERIOR STEMI
POSTERIOR STEMI
Horizontal ST dep v1-v3 (the right precordial leads)
Prominent R waves (R/S ratio > 1) and upright T waves in V1-V3
If ST depression >=0.5 m in v1-v3 do posterior leads
Posterior Leads:
ST elevation >= 0.5 mm in V7-V9
Flipped T in aVL (reciprocal of inf/RCA MI)
RECIPROCAL CHANGES
I, aVL are reciprocal to II, III, aVF
RIGHT SIDED STEMI
RIGHT SIDE STEMI
ST-segment elevation V1
ST-segment elevation V1 > V2
Isoelectric OR ST-segment elevation in V1
AND
ST-segment depression in lead V2
ST elevation in III > II
Complicates up to 40% of Inferior STEMI.
Diagnosis confirmed by presence of ST elevation in the right-sided leads (V3R-V6R). The most useful lead is V4R.
ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI
Preload sensitive, can develop severe hypotension in response to nitrates. Treat with fluid loading. Nitrates c/i.
DDX: STEMI EQUIVALENTS
De Winter’s T’s
Wellen’s
ST Elevation in aVR with diffuse STD
MI in LBBB: Sgarbossa
MI in RBBB
deWINTER’s
T Waves are large, peaked, together with STD
Criteria:
Tall symmetric peaked T waves in V1-6
WITH
Upsloaping ST depression > 1 mm at the J point in V1-V6
Quickly evolves into a STEMI
Absence of ST elevation in the precordial leads
Reciprocal ST segment elevation (0.5mm-1mm) in aVR
Proximal LAD Occlusion
~2% of acute LAD occlusions
WELLEN’S
Type A (25%) - Biphasic t wave pattern (initial positivity, terminally negative) in V2-3 (may extend to V1-6)
OR
Type B (75%) - Inverted t wave in V2-3 (may extend to V1-6)
PLUS
ECG pattern is present in a pain free state
May evolve from a Type 1 to Type B over time.
A recent history of chest pain (resolved)
Signifies a Critical LAD occlusion
Inverted T waves are a marker of reperfusion and may occur after an aborted anterior STEMI
Patient’s may be pain free and with minimally elevated or normal cardiac enzymes
patients are at risk of sudden LAD re-occlusion leading to massive anterior STEMI, require invasive therapy
Re-occlusion of the LAD will lead to normalization of the t waves (“pseudo-normalization”) and evolve into a STEMI
ST Elevation in aVR with diffuse STD
ST Segment elevation in aVR that is accompanied by widespread ST depression (>6 leads)
Could indicate a STEMI equivalent
Chronic triple vessel disease and global ischemia are also important causes
The clinical picture is critical
LBBB LV Pacer with Smith Modified Sgarbossa
Concordant STE >/ 1 mm in >/ 1 lead
Concondant STD >/ 1 mm in >/ 1 lead of V1-V3
Proportionally excessive discordant STE in >/1 lead anywhere with >/ 1 mm STE, as defined by >/ 25% of the depth of the preceding wave
HYPERKALEMIA
Syncope
Peaked T Waves
Wide QRS
Loss of the Ps
Bradycardia
Other:
Prolonged PR, Tachycardias, AV blocks, sinus pause,
Pearl:
Hyperkalemia can produce Pseudo-ACS
Rightward Axis Deviation with wide QRS, new BBB
Mimics STE, V Tach, Brugada, Heart Block, Hypothermia
Anterior STE DOES NOT produce Rightward Axis Deviation
Bonus Pearl:
Massive STE can mimic wide QRS, usually a few leads, but NO rightward axis
SPASMS (PRINZMETAL ANGINA)
Chest Pain
A transient STEMI
Reverses spontaneously or with Rx
May occur in young, healthier people
BUT
Most occur on top of CAD
ECG without pain usually normal
BRUGADA
RSR’ with coved ST
V1-V3
HOCM
Large amplitude QRS
Left ventricular hypertrophy with increased precordial voltages
non-specific ST segment and T-wave abnormalities
Deep, narrow (“dagger-like”) Q waves in lateral (I, aVL, V5-6) and/or inferior (II, III, aVF) leads
