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Top Ten (or 11) EKG Killers

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Presentation on theme: "Top Ten (or 11) EKG Killers"— Presentation transcript:

1 Top Ten (or 11) EKG Killers
Micelle Haydel, MD LSUHSC New Orleans

2 Credit to Amal Mattu, MD Lectures: Books: ACEP EmedHome Podcasts
Visiting Lectures Books: ECG's for the Emergency Physician 1 by Mattu & Brady ECGs for the Emergency Physician 2 by Mattu & Brady Electrocardiography in Emergency Medicine by Amal Mattu

3 The EKG must be interpreted in the clinical context.
Don’t order a test unless you know what to do with the results…

4 The Normal Adult EKG Majority QRS complexes are positive (have tall R waves) Except AVR & V1-2; r-wave progression across the precordium T wave in V1 should be small, flat or flipped

5 Differential Dx of Tall R waves in V1
Posterior MI RBBB Right Strain PE COPD Cor Pulmonale RBBB mimics Brugada ARVD WPW Pediatric EKG (tall R-wave and flipped t-wave V1-3)

6 Specific causes of non-specific flipped T-Waves
CAD/ischemia Cardiomyopathies Myocarditis, pericarditis PE Valvular disorders CNS bleed LVH, BBB, paced

7 Differential Diagnosis: Tall t-waves
Hyperacute T-waves/ischemia HyperKalemia BER LVH, BBB, Paced

8 Low voltage: qrs <10mm precordial
Obese patient The New Orleans’ Special Restrictive cardiomyopathy Pericardial effusion Hypothyroid Hypothermia Myocarditis

9 The EKG must be interpreted in the clinical context.
Don’t order a test unless you know what to do with the results…

10 EKG in Syncope, PreSyncope, Palpitations

11 Is it Syncope-- or is it a sentinel death event??
Cardiomyopathies Dilated Hypertrophic Restrictive ARVD/C Arrhythmogenic Right Ventricular Dyplasia/Cardiomyopathy Primary arrhythmic syndromes WPW QT intervalopathies Brugada ARVD CPVT Catecholaminergic Polymorphic Ventricular Tachycardia Not-so BER Other Biggies MI Pulmonary Embolism

12 Sudden Cardiac Death: unexpected death within 1 hour of symptoms Final, common pathway: Vtach/fib 90% ~300,000/yr in US Over 35 years ~80% due to CAD ~15% Cardiomyopathy NEJM Huikuri et al. 345 (20): 1473,  November 15, 2001

13 Sudden Cardiac Death: 1-35 yrs Final, common pathway: Vtach/fib 90%
~3,000/yr U.S. ~70% have a structural abnormality Cardiomyopathies Coronary Anomalies Myocarditis Valvular Disorders Primary arrhythmic syndromes Accessory pathways QT intervalopathies Ion channelopathies

14 EKG findings in Sentinel Death Events
Cardiomyopathies: (flipped T waves plus…) Hypertrophic Cardiomyopathy (LVH) Dilated (LVH) Restrictive cardiomyopathy (low voltage,a-fib, conduction disturbances) Arrhythmogenic Right Ventricular Dysplasia /Cardiomyopathy (Epsilon waves, RBBB pattern)

15 EKG findings in Sentinel Death Events
Primary arrhythmic syndromes Brugada coved/saddle deformity ST V1 &V2 WPW Delta waves, short PR interval, RBBB pattern Prolonged/shortened QT Not so-BER inferior-lateral j-point elevation Catecholaminergic Polymorphic Ventricular Tachycardia: Normal RESTING EKG/ECHO with recurrent syncope starting in childhood related to exertion/emotions.

16 EKG findings in Sentinel Death Events
Myocarditis (diffuse flipped T waves) Congenital coronary-artery anomalies (large p waves) Coronary artery disease: (Wellen’s Sign, Hyperacute T waves, Too tall T-waves) Valvular disorders (AS: LVH; MVP: normal or flipped T waves inferiorly)

17 Heart racing, I feel ok now…

18 WPW Delta waves, short PR interval tall R-waves in V1, RBBB pattern
Pseudoinfarction pattern inferiorly

19 Fainted…

20 Prolonged qt interval

21 Prolonged QT

22 QT interval Depending on the rate, ~normally about the size of two big blocks

23 Woozy, I feel ok now…

24 Congenital SHORT QT syndrome (<320ms) --- vtach, syncope, SCD
HyperCalcemia

25 Weekend warrior, passed out

26 Hypertrophic CardioMyopathy
The most common ECG abnormalities left ventricular hypertrophy abnormal ST-segments Deeply flipped T-wave, tall R apical leads, deep Q waves laterally Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion) Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall

27 Hypertrophic CardioMyopathy
Asymmetrical thickening of the ventricular septum Patients may experience syncope, angina, palpitations, dyspnea Patients may also experience syncope, angina, palpitations, dyspnea (often associated with exertion) Thickening is usually asymetric, involving the septum to a greater extent than the free ventricular wall

28 Chief Complaint: Palpitations

29 Restrictive cardiomyopathy: Low Voltage with flipped anterior Twaves
Shortness of breath (at first with exercise; but over time it occurs at rest). Fatigue (feeling overly tired). Inability to exercise. Swelling of the legs and feet Weight gain Nausea, bloating and poor appetite (related to fluid retention). Palpitations (fluttering in the chest due to abnormal heart rhythms). Less common symptoms: Fainting (caused by irregular heart rhythms, abnormal responses of the blood vessels during exercise, or no cause may be found). Chest pain or pressure (occurs usually with exercise or physical activity, but can also occur with rest or after meals).

30 Restrictive cardiomyopathy:
Amyloidosis, sarcoidosis, hemochromatosis, etc Ventricles become rigid and lack the flexibility to expand during diastole. SOB, fatigue, palpitations & syncope other common findings : atrial fib, conduction delays Shortness of breath (at first with exercise; but over time it occurs at rest). Fatigue (feeling overly tired). Inability to exercise. Swelling of the legs and feet Weight gain Nausea, bloating and poor appetite (related to fluid retention). Palpitations (fluttering in the chest due to abnormal heart rhythms). Less common symptoms: Fainting (caused by irregular heart rhythms, abnormal responses of the blood vessels during exercise, or no cause may be found). Chest pain or pressure (occurs usually with exercise or physical activity, but can also occur with rest or after meals).

31 Specific causes of non-specific flipped T-Waves
CAD/ischemia Cardiomyopathies Myocarditis, pericarditis PE Valvular disorders CNS bleed LVH, BBB, paced

32 The eye does not see what the mind does not know...

33 Seizure vs. syncope…

34 Brugada Na ion channelopathy that predisposes to v-tach/fib
Na ion channelopathy that predisposes to v-tach, fib. Familial. Na ion channelopathy that predisposes to v-tach/fib Coved or Saddle types

35 Almost passed out, I feel ok now…
arrhythmogenic right ventricular dysplasia/ cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue. Patients usually present with arrhythmias of right ventricular origin that range from isolated premature ventricular beats to nonsustained or sustained VT and ventricular fibrillation. Other clinical manifestations include global or regional right ventricular dysfunction, ECG changes, and late evolution to right or biventricular heart failure. Tachycardia is due to reentry and has a LBBB morphology

36 Arrhythmogenic Right Ventricular Dysplasia/ Cardiomyopathy
Replacement of RV muscle by fibro-fatty tissue Associated with VT and ventricular fibrillation arrhythmogenic right ventricular dysplasia/ cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue. Patients usually present with arrhythmias of right ventricular origin that range from isolated premature ventricular beats to nonsustained or sustained VT and ventricular fibrillation. Other clinical manifestations include global or regional right ventricular dysfunction, ECG changes, and late evolution to right or biventricular heart failure. Tachycardia is due to reentry and has a LBBB morphology

37 Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy AVRD/C
May have Epsilon waves: sharp discrete deflections at the terminal portion of the QRS complex in V1-2 Inverted T waves in the anterior leads Incomplete or complete RBBB arrhythmogenic right ventricular dysplasia/ cardiomyopathy, is characterized by replacement of the right ventricular muscle by fatty and fibrous tissue. Blips or wiggles in the terminal part of the QRS

38 Passed out, I feel better now…

39 BER vs Not-so-Benign Early Repolarization
Classically BER is found in the mid- precordial leads Notching, smiley face upward deflection Not-so BER: NEJM 358: Haïssaguerre et al, showed that inferior-lateral ST elevation was associated with v tach/fib.

40 BER, with inferior-lateral J point elevation
Similar j point elevation & notching has been noted in ARVD, WPW & Brugada. The jury is still out: BER in the inferior-lateral leads can be considered benign, unless the patient presents with syncope, palpitations, family hx sudden death.

41 Is it Syncope-- or is it a sentinel death event??
Cardiomyopathies Dilated Hypertrophic Restrictive ARVD/C Arrhythmogenic Right Ventricular Dyplasia/Cardiomyopathy Primary arrhythmic syndromes WPW QT intervalopathies Brugada ARVD CPVT Catecholaminergic Polymorphic Ventricular Tachycardia Not-so BER Other Biggies MI Pulmonary Embolism

42 EKG in Chest Pain and/or SOB
Ischemia Pericarditis/Myocarditis PE Tamponade

43 Passed out, I feel ok now…
How is this different from the flipped Twaves in HCM? In pe, we have right axis deviation.

44 PE S1,Q3,T3 Rt strain (RBBB pattern) Flipped anterior t-waves
How is this different from the flipped Twaves in HCM? In pe, we have right axis deviation.

45 Dogma: The most common ECG abnormalities in PE are tachycardia and nonspecific T wave abnormalities.
Recent studies: The most common ECG finding in PE is anterior T-wave inversion. Mattu: the combination of flipped t-waves anteriorly and inferiorly is very specific for PE. Flipped Twaves are a prognosticator of badness in PE. The more flipped=more rt strain. This likely represents reciprocal changes reflecting infero-posterior ischemia due to compression of the right coronary artery (RCA) as a result of pressure overload in the right ventricle (RV).

46 Flipped T waves in Pulmonary Embolism
Number of Leads with T Wave inversion correlating with RV dysfunction on Echo: ≤ 3 = 47% 4-6 = 92% ≥ 7 = 100% Kosuge et al. Circ J 2006 Flipped Twaves are a prognosticator of badness in PE. The more flipped=more rt strain.

47 Severe Shortness of breath

48 Tamponade Electrical alternans, pericardial effusion leads to low voltage

49 Low voltage: qrs <10mm precordial
Obese patient The New Orleans’ Special Restrictive cardiomyopathy Pericardial effusion Hypothyroid Hypothermia Myocarditis

50 I had chest pain, but I am ok now…

51 Wellen’s Sign Associated with a critical, proximal LAD lesion
Classically, occurs during a pain-free period Wellens' syndrome is a pattern of ECG T-wave changes associated with critical, proximal left anterior descending artery (LAD) lesion. Classically, the ECG findings of Wellens' occur during the pain free period of angina.

52 Chest Pain

53 HyperAcute T-waves HyperAcute T-waves in the anterior leads
Poor R- wave progression T-waves are asymmetrical and broad-based Follows a pattern of injury

54 Differential Diagnosis: Tall t-waves
Hyperacute T-waves (broad, asym) HyperKalemia (narrow, pointy) BER (usually associated with tall r-waves) LVH (usually assoc with prwp) LBBB (prwp, wide)

55 I had chest pain, but I am ok now…
Today PE: s1q3t3, flipped t’s, RBBB, rt strain. One week ago

56 HyperAcute T-wave in V1 The normal ECG has a small, flat or inverted T-wave in lead V1 and if upright or larger in V1 than V6 in the setting of ACS: Suggests significant underlying CAD or acute ischemia if new may precede other expected ECG changes Tall t-waves don’t belong in V1 except: LBBB LVH

57 Chest Pain

58 ST elevation in V1, plus ST elevation AVR

59 AVR & Left Main lesions: is it magic or is it simply reversal of V6?
Fu, et al, The American Journal of Cardiology, Volume 99, Issue 7 reported higher mortality risk in patients with flipped T & ST depression in the V5-6.

60 Mattu:  aVR A. ST-segment elevation in lead aVR suggestive of LMCA occlusion: in NonSTEACS pts, increased 30 day mortality: Yan, American Heart Journal - Volume 154, Issue 1 B. PR-segment elevation suggestive of acute pericarditis. C. Prominent R′ wave suggestive of TCA poisoning. D. Rapid, regular, narrow QRS complex tachycardia with ST-segment elevation suggestive of WPW-related tachycardia.                    

61 I had chest pain, but I am ok now…
ST segment elevation everywhere with no flipped twave/reciprocal changes. Or is it pr depression????? II elevated greater than III, more likely to be pericarditis. Mattu.

62 Pericarditis ST segment elevation everywhere with no flipped twave/reciprocal changes. Or is it pr depression?????

63 CP, SOB… 25yo, low grade fever, dyspnea, uri symptoms, chest pain…
Combined pericarditis and myocarditis--- ST elevations, tachycardia, nonspecific changes. Both syndromes are characterized by abnormal ECGs and chest x-rays and elevated serum markers. Evolution of the ECG abnormality is consistent with AMI and against the diagnosis of myocarditis; the ECG also shows abnormality within a specific coronary artery territory. In contract, in myocarditis, the findings are diffuse. The clinical features that strongly suggest myocarditis in our patient are the young age, the paucity of risk factors, failure of symptoms to resolve with nitrates and thrombolysis, and the normal coronary arteries. Additional supportive evidence for myocarditis includes the prolonged CK-rise and absence of segmental wall motion abnormalities on echocardiography. Most important, the cTnT was elevated which, in the absence of AMI or acute ischemia, has recently been shown to be a sensitive marker for myocarditis 25yo, low grade fever, dyspnea, uri symptoms, chest pain…

64 Myocarditis: SOB, CP, fever
Diffuse T-wave inversions with or without ST segment abnormality Incomplete atrioventricular conduction blocks or Intraventricular conduction blocks (usually transient) ~60% have fever,

65 EKG in Chest Pain and/or SOB
Ischemia Pericarditis/Myocarditis PE Tamponade

66 EKG in Weak & Dizzy Electrolytes

67 I feel weak…

68 Hyperkalemia

69 “SLOW Vtach”? It ain’t tach, if it ain’t tachy V-tach >120bpm….
Severe hyperkalemia Idioventricular/reperfusion dysrhythmias • Type IA medication toxicity         TCA toxicity         Cocaine toxicity

70 I feel weak…

71 Hypocalcemia– prolonged QT

72 EKG in Weak & Dizzy Electrolytes

73 EKG in Overdose Na Channel Blockade K+ efflux blocker AV nodal blocker
Widen QRS K+ efflux blocker Prolongs qt interval AV nodal blocker Depresses inotropy Depresses chronotropy Digitalis: Na/K pump AV nodal blockage Increased automaticity

74 Depressed, AMS…

75 TCA overdose By far, the most important life-threatening effect is cardiotoxicity from cardiac sodium channel blockade. Sodium channel blockade initially manifests itself as QRS prolongation and terminal 40 milliseconds right axis deviation (terminal R wave in lead aVR and S wave in lead I), but ultimately may cause ventricular dysrhythmias and death. Sodium channel blockade: TCA, Cocaine, Benadryl, anticholinergic, dilantin SALT: shock, AMS, Long QT & Terminal slurring R in AVR

76 Sympathetomimetics/Cocaine
Cocaine has similar cardiac sodium channel blockade Typically more tachy than TCA OD b/c less potassium efflux blockade

77 Depressed, took something….

78 Potassium efflux blockers: Medication induced long qt

79 Medication induced long qt

80 Depressed, AMS…

81 B-blocker/Ca-Channel blocker

82 Digitalis Acute: AV block Chronic: Increased automaticity

83 EKG in Overdose TCA Sympathetomimetics/Cocaine
B-blocker/Ca-Channel blocker Digitalis

84 EKG Stat!! ECG, Willem Einthoven, assigning P, Q, R, S and T to the various deflections and awarded the 1924 Nobel Prize


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