ECGs by diagnosis: Difference between revisions
(Created page with "==Arrythmias== See Cards: Arrythmias (DDX) ==MI== -T wave usu tracks w/ the QRS, thus if QRS primarily negative, twi is not necessarily abnl (nl twi in V1). -ST elevatio...") |
No edit summary |
||
| Line 1: | Line 1: | ||
==Arrythmias== | ==Arrythmias== | ||
See Cards: Arrythmias (DDX) | See Cards: Arrythmias (DDX) | ||
==MI== | ==MI== | ||
#T wave usu tracks w/ the QRS, thus if QRS primarily negative, twi is not necessarily abnl (nl twi in V1). | |||
#ST elevation non-specific, also w/ LVH & strain, LBBB, CA spasm, pericarditis, "early repol", hyperK, dig/TCA's, CVA, Vent. aneurysm, hypothermia. | |||
#Non-transmural: ST dep at least 1.0mm, twi. | |||
#II, II, AVF for inf. MI | |||
#V1-3 for anteroseptal inf. | |||
#I, AVL, V4-6 for lat. wall inf. | |||
#V1 or V2-6 anterolat. | |||
#Large R and ST depression in V1-V2= POST. INFARCT! Post MI usu seen w/ inf MI b/c RCA supplies both in 90% of pts! | |||
#Pts w/ inf. infarction +/or post wall mi often also have RV mi, need R sided leads!! | |||
#STE >/= 1mm in V3R or V4R suggest RV MI! | |||
#STE > 2wks= poss vent aneurysm! | |||
#STE in avR and avL = LMA stenosis | |||
#STE in avR and V1 = LAD or LMA stenosis | |||
#if STE > 1.5 mm in avR pt has 75% mortality from AMI --> activate cath lab (unless pt is in SVT, then STE is allowed) | |||
===Infarct notes=== | |||
#inf wall: recip. In 1 and AVl. Downward sloping ST in AVl is often first sign. | |||
#Any ST depression in V1 to V3 in a LBBB is pathological and suggestive of a post. Wall MI. | |||
#Poor r waves progression-no r's by V4 | |||
#persistent t-wave elevation 6 wks post mi-vent. Anyeursm.anteroseptal with biphasic/inverted t wave | |||
==Pericarditis== | ==Pericarditis== | ||
#Stage I: ST elevated in precordial leads, esp. V5-6 & I-II. Isoelectric or depressed ST in V1. PR depression in II, AVF, V4-6. | |||
#Stage II: ST returning to baseline. T wave amplitude decreases. | |||
#Stage III: ST isoelectric. TWI where prior STE. | |||
#Stage IV: Resolution of T wave changes. | |||
#Also ST:T ratio >0.25 in V6 | |||
(Depressed PR, Diffuse ST elevation, Scooping upwardly concave ST segments, Notching at the end of the QRS) | (Depressed PR, Diffuse ST elevation, Scooping upwardly concave ST segments, Notching at the end of the QRS) | ||
==HyperK== | ==HyperK== | ||
#5.5-6.6 -> tall peaked T, deep S in I and V6, QRS nml | |||
#7.0-8.0 -> QRS widens, slurred initial and term QRS, ST elevation, low wide P's, AV blocks, SA arrest, bradycardia. | |||
#>8.0 -> widened QRS, Vfib, asystole. | |||
==HypoK== | ==HypoK== | ||
#3.0-3.5 no change or flat T' sand U's in V2-3, QT interval and QRS nml. | |||
#2.7-3.0 U taller, T smaller, esp. V2-3 | |||
#<2.6 ECG change includes tall U's, QT and QRS wnl. | |||
==HyperCa== | ==HyperCa== | ||
#Increased QRS duration (slight) | |||
#ST short or absent | |||
#Short corrected QT. | |||
#PR long | |||
==HypoCa== | ==HypoCa== | ||
#slight decrease in QRS. | |||
#ST and corrected QT long | |||
#PR short. | |||
#T's flat to inverted. | |||
==CNS== | ==CNS== | ||
#SAH, IC bleed, stroke, can see diffuse wide deep, blunted inverted T's. and QT prolonged | |||
==Pacemakers== | ==Pacemakers== | ||
#Should be in the apex of R vent. | |||
#ECG should mimic LBBB, w/ L axis. | |||
==PE== | ==PE== | ||
#S1Q3T3 | |||
##(good specificity, poor sensitiviy) | |||
(good specificity, poor sensitiviy) | |||
==Source== | ==Source== | ||
DONALDSON 17/09 (Adapted from Niemann/Lampe) | DONALDSON 17/09 (Adapted from Niemann/Lampe) | ||
[[Category:Cards]] | [[Category:Cards]] | ||
Revision as of 16:46, 12 March 2011
Arrythmias
See Cards: Arrythmias (DDX)
MI
- T wave usu tracks w/ the QRS, thus if QRS primarily negative, twi is not necessarily abnl (nl twi in V1).
- ST elevation non-specific, also w/ LVH & strain, LBBB, CA spasm, pericarditis, "early repol", hyperK, dig/TCA's, CVA, Vent. aneurysm, hypothermia.
- Non-transmural: ST dep at least 1.0mm, twi.
- II, II, AVF for inf. MI
- V1-3 for anteroseptal inf.
- I, AVL, V4-6 for lat. wall inf.
- V1 or V2-6 anterolat.
- Large R and ST depression in V1-V2= POST. INFARCT! Post MI usu seen w/ inf MI b/c RCA supplies both in 90% of pts!
- Pts w/ inf. infarction +/or post wall mi often also have RV mi, need R sided leads!!
- STE >/= 1mm in V3R or V4R suggest RV MI!
- STE > 2wks= poss vent aneurysm!
- STE in avR and avL = LMA stenosis
- STE in avR and V1 = LAD or LMA stenosis
- if STE > 1.5 mm in avR pt has 75% mortality from AMI --> activate cath lab (unless pt is in SVT, then STE is allowed)
Infarct notes
- inf wall: recip. In 1 and AVl. Downward sloping ST in AVl is often first sign.
- Any ST depression in V1 to V3 in a LBBB is pathological and suggestive of a post. Wall MI.
- Poor r waves progression-no r's by V4
- persistent t-wave elevation 6 wks post mi-vent. Anyeursm.anteroseptal with biphasic/inverted t wave
Pericarditis
- Stage I: ST elevated in precordial leads, esp. V5-6 & I-II. Isoelectric or depressed ST in V1. PR depression in II, AVF, V4-6.
- Stage II: ST returning to baseline. T wave amplitude decreases.
- Stage III: ST isoelectric. TWI where prior STE.
- Stage IV: Resolution of T wave changes.
- Also ST:T ratio >0.25 in V6
(Depressed PR, Diffuse ST elevation, Scooping upwardly concave ST segments, Notching at the end of the QRS)
HyperK
- 5.5-6.6 -> tall peaked T, deep S in I and V6, QRS nml
- 7.0-8.0 -> QRS widens, slurred initial and term QRS, ST elevation, low wide P's, AV blocks, SA arrest, bradycardia.
- >8.0 -> widened QRS, Vfib, asystole.
HypoK
- 3.0-3.5 no change or flat T' sand U's in V2-3, QT interval and QRS nml.
- 2.7-3.0 U taller, T smaller, esp. V2-3
- <2.6 ECG change includes tall U's, QT and QRS wnl.
HyperCa
- Increased QRS duration (slight)
- ST short or absent
- Short corrected QT.
- PR long
HypoCa
- slight decrease in QRS.
- ST and corrected QT long
- PR short.
- T's flat to inverted.
CNS
- SAH, IC bleed, stroke, can see diffuse wide deep, blunted inverted T's. and QT prolonged
Pacemakers
- Should be in the apex of R vent.
- ECG should mimic LBBB, w/ L axis.
PE
- S1Q3T3
- (good specificity, poor sensitiviy)
Source
DONALDSON 17/09 (Adapted from Niemann/Lampe)
