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ECG in ED
“Advances in ACS
ECG”
By
Hesham A.K.Ibrahim,
MCEM, EgFEM,
ED Registrar, Poole Hospital, UK.
- To Discuss the value of ST elevation in aVR.
- To learn how to anticipate ST elevation
before it happens.
- To learn how to diagnose STEMI on top of
BBB & in paced rhythm.
- To learn how to differentiate between STEMI
& Pericarditis ECG.
Objectives
Basic
Knowledge
-isoWhere is the
electric line??
“ST elevation”
“Key information”
(American College of Cardiology Foundation/AHA)
“2013 guidelines”
point.-STE should be measured at the J-
“not 40 msec after it”
Diagnostic ST elevation is defined as:-
STE of 1 mm or more in at least 2 contiguous leads
(except V2-V3) in absence of LBBB or LVH.
:3V-2Regarding V-
- in males, should be 2 mm or more.
- in females, should be 1.5 mm or more.
“Coronary
Circulation”
“Localization of the site of injury”
”aVR“ST Elevation in
1) ST elevation in aVR.
2) ST elevation in V1 (< STE in aVR).
3) ST depression in most of the chest & limb leads.
)3)(2(”aVR“Value of ST elevation in
In ST elevation in aVR + ST depression in
multiple other leads, PLEASE consider:
1) LMCA occlusion, especially if:
- ST elevation in aVR > V1.. (highly specific)
- ST elevation in aVR & aVL..
2) Proximal LAD occlusion.
3) Triple vessel disease.
Why is it BAD?
1) ST elevation in aVR is directly proportionate
to the mortality rate:
- 0.5 mm 10.8 %
- 1 mm 13.8 %
- 1.5-2.5 mm 22.2 %
- > 3 mm 50 %
2) Mortality is 70% without immediate PCI.
3) Medical treatment including thrombolysis
does not improve the mortality!!!
4) Emergency PCI may decrease the mortality
to 40%.
5) Time delay to PCI is the only predictor of
survival. (consider early transfer)
Some cardiology literatures recommended
“not to give Clopidogril” in presence of
ST elevation in aVR as the patient most
probably will need a surgical intervention
(urgent CABG surgery).
“Kosuge, American Journal Cardiology, 2011”
”aVR“ST Elevation in
”1& VaVR“ST Elevation in
”aVL&aVR“ST Elevation in
“SVT”
“Exclusions”
1) In presence of SVT & rapid AF, it is expected
to see STE in aVR & diffuse STD.
(transient)
2) Significant HTN causes non specific ST
changes including STE in aVR due to
increased myocardial strain.
3) When there is QRS widening in LBBB &
sever LVH.
4) Asymptomatic patients or patients with no ST
changes of ischemia.
“Just Before ST
elevation”
“Is it possible to
anticipate?”
“Case 1”
58 years old male patient presented to ED
with a history of cardiac sounding chest pain
12 hours before presentation
He is now pain free..
His 12 hours Troponine is negative..
No old ECGs..
This is his ECG now,,,
“Wellens’ Syndrome” (4)(5)
- First described by Dr. Hein Wellens in 1982.
in thespecific T wave changesIt describes a-
mid precordial leads (V2-5).
- Highly specific for sever stenosis in proximal
.LAD
Diagnostic Criteria
1) Deeply-inverted or biphasic T waves in V2-3 (may
extend to V1-6).
2) Isoelectric or minimally-elevated ST segment
(<1mm).
3) No precordial Q waves.
4) Preserved precordial R wave progression.
5) Recent history of angina.
6) ECG pattern present in pain-free state.
7) Normal or slightly elevated serum cardiac markers.
Rhinehart et al (2002)
- 75% of the patients will develop anterior
wall STEMI within few weeks if treated
medically (5).
- Present in 2 patterns…
(A):1Type
- Deep & symmetric T wave inversion in the mid-
precordial leads.
- More common (75%).
(B):2Type
- Biphasic T wave in the mid-precordial leads.
- Less common (25%).
N.B.
The T waves evolve over time from the symmetrical to the
biphasic pattern.
N.B.
There is a confusion in the literature regarding
the naming of the T wave patterns, with some
authors using Type 1 for inverted T waves and
Type 2 for biphasic.
It may be better to just describe the T wave
pattern!
’ SyndromeWellensTypes of
http://www.aliem.com/wellens-syndrome-is-it-on-your-radar/
”1“Type
”2“Type
“Mimics to Wellens’
Syndrome”
“Pseudo Wellens’ Syndrome”
Hypokalemia)1
T wave in Wellens’ $ is “Up then Down:
T wave in hypokalemia is “Down then Up” i.e inverted T followed
by U.
LVH)2
http://lifeinthefastlane.com/ecg-library/wellens-syndrome/
BER)3
Usually the patient will be:
- Young athlete.
- Afro-Caribbean.
- almost always male.
- high voltage ECG.
- fish hook pattern in some leads.
“Case 2”
58 years old male patient presented to ED
with a cardiac sounding chest pain.
This is his ECG,,,
“De Winter sign” (6), (7)
http://lifeinthefastlane.com/ecg-library/de-winters-t-waves/
- First Described by De Winter & Wellens in 2008
in an article in The New England Journal of
Medicine.
It is:-
J point depression + up sloping ST segment +
tall symmetrical T waves + in precordial
leads. (similar to hyperkalaemia)
“Value of De Winter sign”
“Acute Proximal LAD occlusion”
- Possibly a new indication for cath lab
activation as STEMI equivalent.
(not in the guidelines yet).
proximal LAD occlusion,,subacute,,$Wellens-
treat urgently..
proximal LADacute,,De Winter sign-
occlusion,, treat emergently.
http://lifeinthefastlane.com/ecg-library/de-winters-t-waves/
“ST-T wave changes”
- Hyperacute T-wave changes may be observed
in the very early phase of STEMI, before the
development of ST elevation. (1)
- Straightening of the upslope of the T wave is an
early sign that you can use to anticipate ST
elevation.
- Get Serial ECG.
“Intra-ventricular
Conduction Defect,
Bundle Branch Block
(BBB)”
“Case 1”
67 years old female patient presented to ED
with a cardiac sounding chest pain.
She is known to have LBBB.
This is her ECG,,,
Note absence of “septal-q” in V6; andT wave pointing
in direction opposite to QRS (2 repolarization effect)
Broad
S wave
Broad
R wave
(Lead I
similar)
Complete LBBB Pattern
V1 V6
http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/
)9), (8(Sgarbossa Criteria
“Case 2”
Complete RBBB Pattern
V1 V6
rsR’
Complex
In V1
Broad
S wave in V6
(Lead I
similar)
Criteria of RBBB
1) Wide complex.
2) Tall R or RSR’ in V1.
2) Wide S wave in lateral leads.
3) ST depression & T wave inversion in V1-3.
Any ST elevation in RBBB is always
abnormal.
STEMI + RBBB
“STE in a Paced Rhythm”
Sgarbossa Criteria
“STEMI vs Acute
Pericarditis”
“Case”
33 years old male patient presented to ED with
chest pain continuous for the last 6 hours.
central, dull, more with inspiration, notPain was
related to a specific position or a particular
movement, non reproducible.
His observations at presentation were:
BP: 125/82 P: 110 Temp: 37 RR: 18
Sat: 98%
An ECG was requested.
(10), (11), (12)
An Approach to ST
elevation in ECG
Approach to differentiate STEMI
from acute Pericarditis
Is it STEMI??)1
“5 signs to check”
??pericarditisIs it possible acute)2
“5 signs to check”
Factors that strongly favor
STEMI (5)
1) Presence of reciprocal changes,
(ST Depression other than in aVR & V1).
2) STE III > STE II (progressive – sign of RCA lesion).
3) ST elevation is not concave, i.e convex or
horizontal “although it could be concave”.
4) New Q waves.
5) “Checkmark sign”
i.e.QR-T sign (expert opinion)
Factors that strongly favor
Pericarditis (5)
1) Widespread ST elevation & PR segment
depression in most of the limb leads & in
V2-V6.. (This discordance is characteristic)
2) ST elevation is concave upwards (saddle
shape).
3) Reciprocal ST depression & PR segment
elevation in aVR & V1.
4) Spodick’s Sign.
5) Sinus tachycardia, due to pain +/_ effusion.
ECG changes in acute
pericarditits.
PR segment depression reflects atrial
inflammation
http://lifeinthefastlane.com/ecg-library/basics/pericarditis/
“Spodick’s sign”
is a down-sloping of the T-P segment
STEMI vs Acute
Pericarditis
Acute Pericarditis
Never to consider Pericarditis
in presence of:
- ST depression other than in aVR & V1.
- Convex or horizontal ST elevation.
If in doubt:
“Serial ECGs”
Value of Serial ECGs
- 11% of patients with STEMI present with non
diagnostic ECGs.
- 72% of them develop ST elevation within
90 min.
Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-
hospital outcomes for patients with ST-segment elevation myocardial
infarction presenting with non-diagnostic initial electrocardiogram: A report
from the American Heart Association Mission: Lifeline program. Am Heart J.
23237133. PMID:56–50):1(165;2013
“Amal Mattu, MD, FAAEM, FACEP”
Professor of Emergency
Medicine.
University of Maryland.
Baltimore, Maryland, USA.
Summary
- Take care of the value of ST elevation in aVR.
- Always keep in mind Wellens’s $, De Winter sign
& the the ST-T wave changes as signs that you can
use to anticipate ST elevation.
- You can use Sgarbossa criteria to diagnose STEMI
on top of LBBB & in paced rhythm.
- Always have an approach to differentiate between
STEMI & acute pericarditis ECG & never to
consider pericarditis in presence of ST depression.
References
(1) 2013 ACCF/AHA Guideline for the Management of ST Elevation Myocardial
Infarction.
(2) Barrabes JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic
value of lead aVR in patients with a first non ST-segment elevation acute
myocardial infarction. Circulation 2003; 108: 814 – 819
(3) Aygul N, Ozdemir K, Tokac M, Aygul MU, Duzenli MA, Abaci A et al. Value
of lead aVR in predicting acute occlusion of proximal left anterior
descending coronary artery and in-hospital outcome in ST
elevation myocardial infarction: an electrocardiographic predictor of poor
prognosis. J Electrocardiol. 2008 Jul-Aug;41(4):335-41
(4) Wellen's syndrome: An ominous EKG pattern Nicole E Mead, Kelly P
O'Keefe. J Emerg Trauma Shock. 2009 Sep-Dec; 2(3): 206–208.
(5) De Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic
pattern indicating a critical stenosis high in left anterior descending
coronary artery in patients admitted because of impending myocardial
infarction. Am Heart J. 1982.
(6) De Winter R, Verouden N, Wellens H, Wilde A. A new ECG sign of proximal
LAD occlusion. N Engl J Med 2008;359:2071–3.
(7) Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-segment
elevation myocardial infarction equivalent pattern? Prominent T wave and
J-point depression in the precordial leads associated with ST-segment
elevation in lead aVr. Am J Emerg Med. 2014 Mar;32(3):287
(8) Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol
EJ, Califf RM, and Wagner GS. Electrocardiographic diagnosis of
evolving acute myocardial infarction in the presence of left bundle-branch
block. GUSTO-1 (Global Utilization of Streptokinase and Tissue
Plasminogen Activator for Occluded Coronary Arteries) Investigators. N
Engl J Med 1996 Feb 22; 334(8) 481-7.
(9) Klimczak A, Wranicz JK, Cygankiewicz I, Chudzik M, Goch JH, and
Baranowski R. Electrocardiographic diagnosis of acute coronary
syndromes in patients with left bundle branch block or paced rhythm.
Cardiol J 2007; 14(2) 207-13. pmid:18651461.
(10) Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in
Emergency Medicine and Acute Care. Elsevier 2005
(11) Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books
2008.
(12) Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th
edition), Saunders 2008.
“Thank you”
ECG in Emergency Department - Advances in ACS ECG

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ECG in Emergency Department - Advances in ACS ECG

  • 1. ECG in ED “Advances in ACS ECG” By Hesham A.K.Ibrahim, MCEM, EgFEM, ED Registrar, Poole Hospital, UK.
  • 2. - To Discuss the value of ST elevation in aVR. - To learn how to anticipate ST elevation before it happens. - To learn how to diagnose STEMI on top of BBB & in paced rhythm. - To learn how to differentiate between STEMI & Pericarditis ECG. Objectives
  • 5.
  • 7. “Key information” (American College of Cardiology Foundation/AHA) “2013 guidelines” point.-STE should be measured at the J- “not 40 msec after it” Diagnostic ST elevation is defined as:- STE of 1 mm or more in at least 2 contiguous leads (except V2-V3) in absence of LBBB or LVH. :3V-2Regarding V- - in males, should be 2 mm or more. - in females, should be 1.5 mm or more.
  • 9. “Localization of the site of injury”
  • 10.
  • 11. ”aVR“ST Elevation in 1) ST elevation in aVR. 2) ST elevation in V1 (< STE in aVR). 3) ST depression in most of the chest & limb leads.
  • 12. )3)(2(”aVR“Value of ST elevation in In ST elevation in aVR + ST depression in multiple other leads, PLEASE consider: 1) LMCA occlusion, especially if: - ST elevation in aVR > V1.. (highly specific) - ST elevation in aVR & aVL.. 2) Proximal LAD occlusion. 3) Triple vessel disease.
  • 13. Why is it BAD? 1) ST elevation in aVR is directly proportionate to the mortality rate: - 0.5 mm 10.8 % - 1 mm 13.8 % - 1.5-2.5 mm 22.2 % - > 3 mm 50 % 2) Mortality is 70% without immediate PCI. 3) Medical treatment including thrombolysis does not improve the mortality!!!
  • 14. 4) Emergency PCI may decrease the mortality to 40%. 5) Time delay to PCI is the only predictor of survival. (consider early transfer)
  • 15. Some cardiology literatures recommended “not to give Clopidogril” in presence of ST elevation in aVR as the patient most probably will need a surgical intervention (urgent CABG surgery). “Kosuge, American Journal Cardiology, 2011”
  • 20. “Exclusions” 1) In presence of SVT & rapid AF, it is expected to see STE in aVR & diffuse STD. (transient) 2) Significant HTN causes non specific ST changes including STE in aVR due to increased myocardial strain. 3) When there is QRS widening in LBBB & sever LVH. 4) Asymptomatic patients or patients with no ST changes of ischemia.
  • 21. “Just Before ST elevation” “Is it possible to anticipate?”
  • 22. “Case 1” 58 years old male patient presented to ED with a history of cardiac sounding chest pain 12 hours before presentation He is now pain free.. His 12 hours Troponine is negative.. No old ECGs.. This is his ECG now,,,
  • 24. - First described by Dr. Hein Wellens in 1982. in thespecific T wave changesIt describes a- mid precordial leads (V2-5). - Highly specific for sever stenosis in proximal .LAD
  • 25. Diagnostic Criteria 1) Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6). 2) Isoelectric or minimally-elevated ST segment (<1mm). 3) No precordial Q waves. 4) Preserved precordial R wave progression. 5) Recent history of angina. 6) ECG pattern present in pain-free state. 7) Normal or slightly elevated serum cardiac markers. Rhinehart et al (2002)
  • 26. - 75% of the patients will develop anterior wall STEMI within few weeks if treated medically (5). - Present in 2 patterns…
  • 27. (A):1Type - Deep & symmetric T wave inversion in the mid- precordial leads. - More common (75%). (B):2Type - Biphasic T wave in the mid-precordial leads. - Less common (25%). N.B. The T waves evolve over time from the symmetrical to the biphasic pattern.
  • 28. N.B. There is a confusion in the literature regarding the naming of the T wave patterns, with some authors using Type 1 for inverted T waves and Type 2 for biphasic. It may be better to just describe the T wave pattern!
  • 33. Hypokalemia)1 T wave in Wellens’ $ is “Up then Down: T wave in hypokalemia is “Down then Up” i.e inverted T followed by U.
  • 35. BER)3 Usually the patient will be: - Young athlete. - Afro-Caribbean. - almost always male. - high voltage ECG. - fish hook pattern in some leads.
  • 36. “Case 2” 58 years old male patient presented to ED with a cardiac sounding chest pain. This is his ECG,,,
  • 37. “De Winter sign” (6), (7) http://lifeinthefastlane.com/ecg-library/de-winters-t-waves/
  • 38. - First Described by De Winter & Wellens in 2008 in an article in The New England Journal of Medicine. It is:- J point depression + up sloping ST segment + tall symmetrical T waves + in precordial leads. (similar to hyperkalaemia)
  • 39. “Value of De Winter sign” “Acute Proximal LAD occlusion” - Possibly a new indication for cath lab activation as STEMI equivalent. (not in the guidelines yet). proximal LAD occlusion,,subacute,,$Wellens- treat urgently.. proximal LADacute,,De Winter sign- occlusion,, treat emergently.
  • 40.
  • 43. - Hyperacute T-wave changes may be observed in the very early phase of STEMI, before the development of ST elevation. (1) - Straightening of the upslope of the T wave is an early sign that you can use to anticipate ST elevation. - Get Serial ECG.
  • 45. “Case 1” 67 years old female patient presented to ED with a cardiac sounding chest pain. She is known to have LBBB. This is her ECG,,,
  • 46.
  • 47. Note absence of “septal-q” in V6; andT wave pointing in direction opposite to QRS (2 repolarization effect) Broad S wave Broad R wave (Lead I similar) Complete LBBB Pattern V1 V6
  • 50.
  • 51.
  • 53. Complete RBBB Pattern V1 V6 rsR’ Complex In V1 Broad S wave in V6 (Lead I similar)
  • 54. Criteria of RBBB 1) Wide complex. 2) Tall R or RSR’ in V1. 2) Wide S wave in lateral leads. 3) ST depression & T wave inversion in V1-3. Any ST elevation in RBBB is always abnormal.
  • 56. “STE in a Paced Rhythm” Sgarbossa Criteria
  • 58. “Case” 33 years old male patient presented to ED with chest pain continuous for the last 6 hours. central, dull, more with inspiration, notPain was related to a specific position or a particular movement, non reproducible. His observations at presentation were: BP: 125/82 P: 110 Temp: 37 RR: 18 Sat: 98% An ECG was requested.
  • 59.
  • 60.
  • 61. (10), (11), (12) An Approach to ST elevation in ECG
  • 62. Approach to differentiate STEMI from acute Pericarditis Is it STEMI??)1 “5 signs to check” ??pericarditisIs it possible acute)2 “5 signs to check”
  • 63. Factors that strongly favor STEMI (5) 1) Presence of reciprocal changes, (ST Depression other than in aVR & V1). 2) STE III > STE II (progressive – sign of RCA lesion). 3) ST elevation is not concave, i.e convex or horizontal “although it could be concave”. 4) New Q waves. 5) “Checkmark sign” i.e.QR-T sign (expert opinion)
  • 64. Factors that strongly favor Pericarditis (5) 1) Widespread ST elevation & PR segment depression in most of the limb leads & in V2-V6.. (This discordance is characteristic) 2) ST elevation is concave upwards (saddle shape). 3) Reciprocal ST depression & PR segment elevation in aVR & V1. 4) Spodick’s Sign. 5) Sinus tachycardia, due to pain +/_ effusion.
  • 65.
  • 66. ECG changes in acute pericarditits. PR segment depression reflects atrial inflammation http://lifeinthefastlane.com/ecg-library/basics/pericarditis/
  • 67. “Spodick’s sign” is a down-sloping of the T-P segment
  • 68.
  • 70. Never to consider Pericarditis in presence of: - ST depression other than in aVR & V1. - Convex or horizontal ST elevation. If in doubt: “Serial ECGs”
  • 71. Value of Serial ECGs - 11% of patients with STEMI present with non diagnostic ECGs. - 72% of them develop ST elevation within 90 min. Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in- hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with non-diagnostic initial electrocardiogram: A report from the American Heart Association Mission: Lifeline program. Am Heart J. 23237133. PMID:56–50):1(165;2013
  • 72. “Amal Mattu, MD, FAAEM, FACEP” Professor of Emergency Medicine. University of Maryland. Baltimore, Maryland, USA.
  • 73. Summary - Take care of the value of ST elevation in aVR. - Always keep in mind Wellens’s $, De Winter sign & the the ST-T wave changes as signs that you can use to anticipate ST elevation. - You can use Sgarbossa criteria to diagnose STEMI on top of LBBB & in paced rhythm. - Always have an approach to differentiate between STEMI & acute pericarditis ECG & never to consider pericarditis in presence of ST depression.
  • 74. References (1) 2013 ACCF/AHA Guideline for the Management of ST Elevation Myocardial Infarction. (2) Barrabes JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic value of lead aVR in patients with a first non ST-segment elevation acute myocardial infarction. Circulation 2003; 108: 814 – 819 (3) Aygul N, Ozdemir K, Tokac M, Aygul MU, Duzenli MA, Abaci A et al. Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol. 2008 Jul-Aug;41(4):335-41 (4) Wellen's syndrome: An ominous EKG pattern Nicole E Mead, Kelly P O'Keefe. J Emerg Trauma Shock. 2009 Sep-Dec; 2(3): 206–208. (5) De Zwaan C, Bar FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J. 1982. (6) De Winter R, Verouden N, Wellens H, Wilde A. A new ECG sign of proximal LAD occlusion. N Engl J Med 2008;359:2071–3.
  • 75. (7) Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr. Am J Emerg Med. 2014 Mar;32(3):287 (8) Sgarbossa EB, Pinski SL, Barbagelata A, Underwood DA, Gates KB, Topol EJ, Califf RM, and Wagner GS. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996 Feb 22; 334(8) 481-7. (9) Klimczak A, Wranicz JK, Cygankiewicz I, Chudzik M, Goch JH, and Baranowski R. Electrocardiographic diagnosis of acute coronary syndromes in patients with left bundle branch block or paced rhythm. Cardiol J 2007; 14(2) 207-13. pmid:18651461. (10) Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in Emergency Medicine and Acute Care. Elsevier 2005 (11) Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008. (12) Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.