ST ELEVATION Flashcards

1
Q

DDX

A

4 BAD THINGS
STEMI
Hyperkalemia
Spasms (Prinzmetal Angina)
Brugada

4 STEMI MIMICS
Pericarditis
LVH
LV Aneurysm
BER

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2
Q

STEMI

A

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

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

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.

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

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3
Q

DDX: STEMI EQUIVALENTS

A

De Winter’s T’s
Wellen’s
ST Elevation in aVR with diffuse STD
MI in LBBB: Sgarbossa
MI in RBBB

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4
Q

deWINTER’s

A

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

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5
Q

WELLEN’S

A

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

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6
Q

ST Elevation in aVR with diffuse STD

A

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

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7
Q

LBBB LV Pacer with Smith Modified Sgarbossa

A

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

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8
Q

HYPERKALEMIA

A

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

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9
Q

SPASMS (PRINZMETAL ANGINA)

A

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

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10
Q

BRUGADA

A

RSR’ with coved ST
V1-V3

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11
Q

PERICARDITIS

A

Sharp / Pleuritic
Relieved sitting forward
Radiating towards the trapezius ridge (virtually pathoognomonic)

Stage 1 – widespread concave STE AND PR depression in all leads EXCEPT aVR and V1 (occurs during the first two weeks). Evolution is SLOW.

Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks)

Stage 3 – flattened T waves become inverted (3 to several weeks)

Stage 4 – ECG returns to normal (several weeks onwards)

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12
Q

STEMI VS. PERICARDITIS: A STEPWISE APPROACH

A
  1. Factors that strongly favour STEMI:
    i. STD except in V1 or aVR: ignore V1 or aVR
    ii. STE in III>II
    iii. Horizontal or convex upwards STE or checkmark signs NOT concave

Factors strongly favouring AP:
v. friction rub
vi. Downsloping or PR depression in multiple leads (only reliably seen in viral AP, transient, NOT PATHOGNOMONIC)
Additional factor favouring STEMI:
iv. R-T signs (checkmark sign)

Additional factor favouring AP:
vii. Spodick sign: downsloping of T-P segment

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13
Q

LV ANEURYMS

A

Persistent, concave STE in chest leads (V1-V6)
AND
Small T waves
Q Waves with poor R wave progress V1-V6
No Reciprocal changes
No change over time

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14
Q

LVH VS. STEMI: STEPWISE APPRAOCH

A

Factors that favour LVH:
ST Elevations V1-V3
STE / R-S Ratio < 25%
<3 leads with STE
NO V1-V3 T-wave Inversions Present

Factors that favour STEMI:
STE / R-S Ratio > 25%
>/3 leads with STE
V1-V3 T-wave Inversions Present

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15
Q

BER

A

Concave STE limited to V leads
Slur, notch and high take off patterns
No Qs and no T wave inversions
Large T waves proportional to STE

Other:
Degree of STE may vary but generally stable over time with no Qs and no T wave inversion
Large T waves proportional to STE

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16
Q

LVH

A

Sokolov-Lyon criteria:
S wave depth in V1 + tallest R wave height in V5-V6 > 35 mm

Non-Voltage Criteria:
STE Concave limited to V1 – V3
STE is modest in relation to large voltages
STD and strain (T Wave Inversion) lateral leads (V5, V6, I, aVL)
STD are downslope due to subendocardial ischemia
Changes to LBBB over time

Precordial Leads:
R wave in V4, V5 or V6 > 26 mm

Limb Leads:
R wave in lead I + S wave in lead III > 25 mm
R wave in aVL > 11 mm
R wave in aVF > 20 mm
S wave in aVR > 14 mm