Syncope and SCD in young patients ECG features

1. ECG in young
Mohamed Elwakil, MD
MRCEM, EGYBEM
Associate consultant of emergency medicine.

2. Who should be the expert in ECG
interpretation?
 Cardiologists are often considered the experts and the gold standard in ECG interpretation and the final
word in diagnosing the cause of STE on an ECG.
 Study: Differentiating ST-Elevation Myocardial Infarction From Nonischemic ST-Elevation in Patients With
Chest Pain. Tran V, Huang HD, Diez JG, et al, Am J Cardiol. 2011;108:1096-1101
 The researchers collected 84 ECGs showing STE in at least 2 contiguous leads from a database of patients
for whom catheterization lab activation had occurred because of presumed STEMI.
 The ECGs were given to 7 "experienced interventional cardiologists" and they were asked to analyze the
ECGs to determine whether they would recommend activation of the catheterization lab for presumed
true STEMI.
 Results: on average these experienced interventional cardiologists missed 29% of the STEMIs and
incorrectly diagnosed STEMI in 37% of the cases of NISTE.

3.  In 2009, a publication by Jayroe and colleagues.
 researchers asked 15 experienced cardiologists to interpret 116 ECGs for evidence of STEMI. In that
study, only 8 patients (7% of the total) had true STEMI. The researchers once again found large
variations in the sensitivity (50% to 100%; mean 75%) and specificity (71% to 97%; mean 85%) in
detecting the true STEMIs.
 The researchers concluded, "If experienced readers using the current criteria and guidelines cannot
accurately and consistently distinguish between STEMI and [non-STEMI], less experienced readers
cannot be expected to do so.”
 Perhaps there really are no true gold standards for ECG interpretation.

4. As ER doctors
 We need to be the BEST in our respective houses of medicine at reading ECGs
 If you think someone else will answer your questions about ECGs, you are mistaken. That person
may just be wrong, so YOU must strive to become THE expert
 We all have to drop the veil of ego, and blame that is so prevalent in our medical culture. As
these studies point out, even the "experts" are far from perfect.

5. SCD
The incidence of sudden cardiac death (SCD) among young athletes is estimated to be 1-3 per
100,000 person years, and may be underestimated.
the risk in male athletes being up to 9 times higher than in female athletes.
Br J Sports Med. 2009 Sep;43(9):644-8. doi: 10.1136/bjsm.2008.054718.

7. Case #1
A 26-year old man presents to ED by ambulance after
an episode of syncope while playing soccer. On arrival,
he is dizzy and slightly pale with a BP of 85/60.

8. ECG on
arrival

9. ECG as the patient becomes unconscious on
the trolley

10. Two cycles of CPR and 100 joules of (biphasic) electricity later, he wakes
up with a start and pushes the resuscitating team off his chest.

11. Two cycles of CPR and 100 joules of (biphasic) electricity later, he wakes
up with a start and pushes the resuscitating team off his chest.

12. Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC)
 Arrhythmogenic Right Ventricular Dysplasia (ARVD)
 An inherited myocardial disease associated with paroxysmal ventricular
arrhythmias and sudden cardiac death.
 fibro-fatty replacement of the right ventricular myocardium.
 The second most common cause of sudden cardiac death in young people (after HOCM),
causing up to 20% of sudden cardiac deaths in patients < 35 yrs of age.
 More common in men than women (3:1)

13. Diagnosis of ARVC
 ARVC causes symptoms due to ventricular ectopic beats or
sustained ventricular tachycardia (with LBBB morphology) and typically
presents with palpitations, syncope or cardiac arrest precipitated by
exercise.
 The first presenting symptom may be sudden cardiac death.
 Over time, surviving patients also develop features of right ventricular
failure, which may progress to severe biventricular failure and dilated
cardiomyopathy.
 There is usually a family history of sudden cardiac death.

14. ECG features
 Epsilon wave (most specific finding, seen in 30% of patients)
 T wave inversions in V1-3 (85% of patients)
 Prolonged S-wave upstroke of 55ms in V1-3 (95% of patients)
 Localised QRS widening of 110ms in V1-3
 Paroxysmal episodes of ventricular tachycardia with LBBB morphology.

15. Epsilon waves
 The epsilon wave is a small
positive deflection (‘blip’) buried
in the end of the QRS complex.
 It is the characteristic finding in
arrhythmogenic right ventricular
dysplasia (ARVD).
 Also in hypothermia

16. overview
 ECHO is needed and MRI is modality of choice
 endomyocardial biopsy or at autopsy, provides a definitive diagnosis but
is impractical, and for those patients diagnosed at post-mortem… far too
late!
 high risk of sudden death if they have any of the following:
1. A history of syncope due to cardiac arrest
2. Recurrent arrhythmias not suppressed by anti-arrhythmic drug therapy
3. A family history of cardiac arrest in first degree relatives

17. Treatment
 In patients with no high risk features, initial treatment is with anti-
arrhythmic drugs such as beta-blockers or amiodarone to suppress
cathecholamine-triggered ventricular arrhythmias. Currently, the most
effective drug for this is sotalol.
 Patients with any high risk features require urgent insertion of an
implantable cardioverter-defibrillator (ICD).
 In patients with persistent symptomatic arrhythmias, radiofrequency
ablation of conduction pathways may be attempted.
 Heart failure is treated in the usual way, with diuretics, ACE inhibitors and
anticoagulants. In severe cases, cardiac transplantation may be required.

18. Case #2
A 30-year old man presented with exertional
lightheadedness and palpitations

20. Hypertrophic Cardiomyopathy Overview
 HCM is the number one cause of sudden cardiac death in young athletes.
 It is a heterogeneous disorder, produced by mutations in multiple genes coding
 The chief abnormality associated with HCM is left ventricular hypertrophy (LVH),
occurring in the absence of any inciting stimulus such as hypertension or aortic
stenosis.
 The most commonly observed pattern is asymmetrical septal hypertrophy. This pattern
is classically associated with systolic anterior motion (SAM) of the mitral valve and
dynamic left ventricular outflow tract (LVOT) obstruction. However, in the majority of
cases (75%), HCM is not associated with LVOT obstruction (hence the name change
from HOCM to HCM).
 Other less common patterns of LVH include concentric hypertrophy (20% of cases) and
apical hypertrophy (10%).

21. Cross-sectional views. A, Normal
ventricular septal anatomy. B,
Asymmetric septal hypertrophy found in
hypertrophic cardiomyopathy

22. Clinical features
 Exertional syncope or pre-syncope — this is the most worrying
symptom, suggesting dynamic LVOT obstruction ± ventricular
dysrhythmia, with the potential for sudden cardiac death.
 Symptoms of pulmonary congestion (e.g. exertional dyspnoea, fatigue,
orthopnoea, paroxysmal nocturnal dyspnoea) due to left ventricular
dysfunction.
 Chest pain — may be typical anginal pain due to increased demand
(thicker myocardial walls) and reduced supply (aberrant coronary arteries).
 Palpitations due to supraventricular or ventricular arrhythmias.

23. Pathophysiology of Hypertrophic
Cardiomyopathy
Dynamic obstruction of the LVOT.
Left ventricular diastolic dysfunction resulting from impaired
relaxation and filling of the stiff and hypertrophied left ventricle
(often associated with increased filling pressures).
Abnormal intramural coronary arteries with thickened walls and
narrowed lumens.
Chaotic, disorganised left ventricular architecture (“cellular disarray”)
predisposing to abnormal transmission of electrical impulses and
thus serving as a substrate for arrhythmogenesis.

24. ECG features
Left atrial enlargement
Left ventricular hypertrophy with associated ST segment / T-
wave abnormalities
Deep, narrow (“dagger-like”) Q waves in the lateral > inferior
leads
Giant precordial T-wave inversions in apical HCM
Signs of WPW (short PR, delta wave).
Dysrhythmias: atrial fibrillation, supraventricular tachycardias,
PACs, PVCs, VT

25. Left atrial enlargement (LAE)
Broad (>110ms), bifid P wave in lead II (P
mitrale) with > 40ms between the peaks
P waves with terminal portion > 1mm
deep in V1

26. Left Ventricular Hypertrophy
 This results in increased R wave amplitude in the left-sided ECG leads (I,
aVL and V4-6)
 increased S wave depth in the right-sided leads (III, aVR, V1-3).
 The thickened LV wall leads to prolonged depolarisation (increased R
wave peak time)
 delayed repolarisation (ST and T-wave abnormalities) in the lateral leads.

27. Diagnosis of LVH
 The most commonly used are the Sokolov-Lyon criteria (S wave depth in
V1 + tallest R wave height in V5-V6 > 35 mm).
 Voltage criteria must be accompanied by non-voltage criteria to be
considered diagnostic of LVH.
 Non Voltage Criteria: Increased R wave peak time > 50 ms in leads V5 or
V6 and ST segment depression and T wave inversion in the left-sided
leads(I, aVL and V4-6): the left ventricular ‘strain’ pattern

28. Left Ventricular Hypertrophy
LVH by voltage criteria: S wave in V2 + R
wave in V5 > 35 mm
LV strain pattern: ST depression and T
wave inversion in the lateral leads

29. LVH
Markedly increased LV voltages: huge
precordial R and S waves that overlap with
the adjacent leads (SV2 + RV6 >> 35
mm).
R-wave peak time > 50 ms in V5-6 with
associated QRS broadening.
LV strain pattern with ST depression and
T-wave inversions in I, aVL and V5-6.
ST elevation in V1-3.
Prominent U waves in V1-3.
Left axis deviation.

30. Apical HCM
uncommon form of HCM is seen
most frequently in Japanese
There is localised hypertrophy of
LV apex
giant T-wave inversion in the
precordial leads.
Large precordial voltages.
Inverted T waves are also seen in
the inferior and lateral leads.

32. Take home
T wave inversion in otherwise athlete ECG should raise suspicion of:
 HCM
 Anabolic drug abuse
 Recreational drug usage

34. Case #3
a 33 yr old male.
Presented to the
ED following an
episode of
collapse

36. Brugada Syndrome
 First described in 1992 by the Brugada brothers
 Brugada Syndrome is an ECG abnormality with a high incidence of sudden death in
patients with structurally normal hearts.
 is due to a mutation in the cardiac sodium channel gene. This is often referred to as a
sodium channelopathy.
 Common males, Asian descent, 30-50 years
 Diagnosis depends on a characteristic ECG finding AND clinical criteria.
 Definitive treatment = ICD.

37. Types
Type I coved shape Type II saddle shape
is the only ECG abnormality that is potentially diagnostic.

38. ECG changes can be transient with Brugada syndrome and can also be augmented by multiple factors:
1. Fever
2. Ischaemia
3. Multiple Drugs
1. Sodium channel blockers eg: Flecainide, Propafenone
2. Calcium channel blockers
3. Alpha agonists
4. Beta Blockers
5. Nitrates
6. Cholinergic stimulation
7. Cocaine
8. Alcohol
4. Hypokalaemia
5. Hypothermia
6. Post DC cardioversion

39. Diagnosis
ECG abnormality must be associated with one of the following clinical criteria :
1. Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
2. Family history of sudden cardiac death at <45 years old .
3. Coved-type ECGs in family members.
4. Syncope.
5. Nocturnal agonal respiration.

40. Management
 The only proven therapy is an implantable cardioverter – defibrillator (ICD). Quinidine has
been proposed as an alternative in settings where ICD’s are unavailable
 Undiagnosed, Brugada syndrome has been estimated to have a mortality of 10% per
year. Does this mean that a diagnosis in ED mandates admission? Probably yes for all
type 1 patients if they present with suggestive clinical criteria.

42. Case #4
21 years male, palpitation, panic attacks

46. WPW
 Wolff-Parkinson-White Syndrome
 First described in 1930 by Louis Wolff, John Parkinson and Paul Dudley
White.
 Existence of accessory pathway
 Abnormal conduction between atria and ventricles
 Paroxysms of tachycardia, syncope

47. WPW

48. ECG features
 PR interval <120ms
 Delta wave – slurring slow rise of initial portion of the QRS
 QRS prolongation >110ms
 ST Segment and T wave discordant changes – i.e. in the opposite direction to the major component
of the QRS complex
 Pseudo-infarction pattern can be seen in up to 70% of patients – due to negatively deflected delta
waves in the inferior / anterior leads (“pseudo-Q waves”), or as a prominent R wave in V1-3
(mimicking posterior infarction).
 WPW may be described as type A or B.
1. Type A has a positive delta wave in all precordial leads with R/S > 1 in V1
2. Type B has a negative delta wave in leads V1 and V2

49. Type A
•Sinus rhythm with a very short PR interval (<
120 ms).
•Broad QRS complexes with delta wave.
•Dominant R wave in V1 — associated with
a left-sided accessory pathway.
•Tall R waves and inverted T waves in V1-3 .
•Negative delta wave in aVL simulating the Q
waves of lateral infarction — this is referred to
as the “pseudo-infarction” pattern.

50. Type B WPW
Sinus rhythm with very short PR interval (< 120
ms)
Broad QRS complexes with delta wave.
Dominant S wave in V1 —indicates a right-sided
accessory pathway.
Tall R waves and inverted T waves in the inferior
leads and V4-6 mimic the appearance of left
ventricular hypertrophy — this is due to WPW
and does not indicate underlying LVH.

51. Atrial Fibrillation in
WPW
 Atrial fibrillation can occur in up
to 20% of patients with WPW.
 Rapid ventricular rates may result
in degeneration to VT or VF.
 Rapid, irregular, broad complex
tachycardia (overall rate ~ 200
bpm) with a LBBB morphology
(dominant S wave in V1);
however, QRS Complexes change
in shape and morphology
 LBBB usually has fixed width QRS
complexes

52. Management
Stable or unstable

53. Case #5
34 y male, hx of pseudoseizures.

55. later

56. Prolonged QT syndrome
 The QT interval is the time from the start of the Q wave to the end of the T wave.
 It represents the time taken for ventricular depolarisation and repolarisation.
 normal QT = < 440ms (two large squares) – prolonged QT > 450ms
 Shortens as rate increases
 Increased risk with QT > 500 ms
 Increased risk if QT > ½ the R to R

57. Causes
 Congenital
 Acquired
1. Hypomagnesemia
2. Hypocalcemia
3. Hypokalemia
4. Hypothermia
5. Acute ischemia
6. Drug overdose
7. Increased ICP
8. Alcohol intoxication
Risk factors for drug inducted
QT lengthening:
 Hypothermia
 Electrolyte disturbances
 Female sex
 Structural heart disease

59. Long QT and TdP Treatment
Magnesium infusion
Shock
Overdrive pacing
Beta blockade
ICD

60. Key points
Rhythm (non-sinus)
T wave inversion (Widespread)
ST segment elevation
Axis deviation and conduction abnormalities (LBBB)
Tachycardia (QRS widening )

61. Thanks
‫شكرا‬

62. Useful links
 ECG Interpretation of STEMI: Who's the Expert? By Amal Mattu, MD, Medscape.
http://www.medscape.com/viewarticle/760447_1
 https://lifeinthefastlane.com/ecg-exigency-008/
 EPEC(EMERGENCY PHYSICIAN ECG COURSE)/ HTTPS://WWW.FACEBOOK.COM/GROUPS/153446858500774/
 CARDIAC RISK IN THE YOUNG/ Professor Sanjay Sharma/. https://www.youtube.com/user/cryvideos
 ACEP2015/ Syncope: With a Lethal Twist!
 HTTPS://LIFEINTHEFASTLANE.COM/ECG-LIBRARY/BASICS/ARRHYTHMOGENIC-RIGHT-VENTRICULAR-
CARDIOMYOPATHY/
 HTTPS://LIFEINTHEFASTLANE.COM/ECG-LIBRARY/PRE-EXCITATION-SYNDROMES/
 HTTPS://LIFEINTHEFASTLANE.COM/ECG-LIBRARY/BRUGADA-SYNDROME/