Prof. Dr. Andres Ricardo Perez Riera M.D.Ph.D.Disciplina de Cardiologia - Chefe do Setor de Eletrovetorcardiografia

Faculdade de Medicina do ABC Fundação do ABCSanto André – São Paulo – Brasil

First Advanced Virtual Course of Electrocardiology: New frontiers for a century-old discipline.

Sociedad Latinoamericana de Estimulación Cardíaca y Electrofisiología (SOLAECE)

Class 1 – Value of Eletrocardiogram in the 21st Century

Twelve-lead ECG and derived methodologies is still current in the 21st century as one of the first pillars of cardiological diagnosis: the clinical pillar (interrogation and physical examination), ECG and transthoracic echo. Figure 1. More than 95% of diagnoses in cardiology are made without requiring other supplementary methods.In spite of the centennial, it is still the basis of the supplementary rationale for cardiologists, internists, family doctors, intensivists, in the ER and in pediatrics. There are several scenarios where the ECG is the gold standard: when making a decision on the management before clinical symptoms compatible with acute coronary syndrome. Figure 2. In this scenario, the presence or not of ST segment elevation is a watershed for the indication of invasive study or just pharmacological behavior. Figure 3Decisive in the cases of heart failure refractory to proper medication and resynchronization management. The following are predictive parameters of good response, sinus rhythm, absence of P wave suggesting interatrial conduction disorder, pattern of complete left bundle branch block with QRS duration ≥130 ms (men) and 140 ms (women). In the presence of hypertrophic or dilated LV, the duration criteria for CLBBB (≥120 ms) presents a low specificity. Strict LBBB criteria associated to notch in at least 2 leads in V1-V2 or V5-V5, I and aVL presents high sensibility and specificity. Figures 4 and 5.In the diagnosis of genetic channelopathies without structural heart disease, class 1 indication in the diagnosis of syncope(1), in cardiomyopathies and myocarditis, congenital heart diseases and in the identification of artifacts.

Value of Electrocardiogram in the 21st Century

History

Physical examination

ECG

ECHO o chext X-ray

Lab tests

THE FIVE PILLARS OF CARDIOLOGICAL DIAGNOSIS

Figure 1

Fundamental in the diagnosis and management in the presence of arrhythmias. It allows to identify the focus (supraventricular, junctional or ventricular) and offers a guide on therapy (pharmacological, cardioversion, radiofrequency or hybrid).

Main scenarios in which ECG may be decisive or helpful for the diagnosis and/or therapy

1. In acute coronary syndrome. Figures 2 and 32. In indication of cardiac resynchronization in the case of refractory

CHF3. In symptoms of syncope (class I indication)4. In arrhythmias5. In the diagnosis of inherited channelopathies6. In the diagnosis of cardiomyopathies and myocarditis7. In the clinical and epidemiological screening of chronic chagasic

myocarditis8. In electrolytic disorders and effect of drugs9. In acyanotic and cyanotic congenital heart diseases 10.In the identification of artifacts.2

Chest pain causes

Cardiac causes Non-cardiac causes

Ischemic Non-ischemic GastroesophagealNon-

gastroesophageal

StableAngina

Unstable Angina

Acute MyocardialInfarction

Gastroesophageal Reflux

Esophageal spasm

Peptic Ulcer

Acute Coronary Syndrome

Pericarditis Valvular

Acute aortic dissection

PneumothoraxAcute Pulmonary

EmbolismMuscle/skeletal Psychoemotional

≈ 5%of total

Figure 2

UnstableAngina

UnstableAngina

Non-Q AMINon-Q AMI

Q- wave AMIQ- wave AMI Non-Q AMINon-Q AMI

Acute Coronary SyndomeAcute Coronary Syndome

NSTEMINSTEMI

ELECTROCARDIOGRAM

NEGATIVE BIOMARKERS

POSITIVE BIOMARKERS

Thrombolytics or primary coronary angioplasty

New LBBBNew LBBB True posterior AMI pattern

True posterior AMI pattern

STEMI> 2 mm in V1, V2 or V3 or > 1 mm in other leads

STEMI> 2 mm in V1, V2 or V3 or > 1 mm in other leads

*

* Actual basal inferior.

Figure 3

Multisite Cardiac Resynchronization: Relevant Electrocardiographic Aspects

Figure 4

There are 2 types of implantable devices for CHF: Multisite resynchronization pacemaker with leads in the LV, RV and RA, called CRT. There is a more complete modality that associates automatic cardioverter defibrillator (CRT-D). Both devices help to coordinate the pump function of the heart and to improve blood flow. They improve the performance of the pump by increasing systolic discharge.

Figura 5

Electrocardiographic factors associated to low ejection fraction in the presence of CLBBB

The following ECG parameters are associated to low EF in the presence of CLBBB.

1. P wave of duration ≥120 ms

2. Final negative component of P wave in V1 with positive Morris criteria (deep and slow)

3. QRS electrical axis in the frontal plane with extreme shift to the left (>30º) or right (>+90º)

4. QRS duration ≥160 ms

5. Deep S waves in V3-V4

6. Notches in inferior leads.

The presence of 2 or 3 or these alterations present PPV of 98.0% and NPV of 60.4% for reduced LVEF(2).

Markers of good response in cardiac resynchronization

1. Epidemiological: female gender

2. Non-ischemic etiology

3. Electrocardiographic: CLBBB pattern with duration ≥150 ms for at least >120-130 ms because it is

considered a marker of electrical and mechanic dyssynchrony with exceptions. The pattern and QRS

duration is the only parameter that should be used according to randomized studies.

4. ECG QRSd ≥140 ms for men or ≥130 ms for women associated to middle notch in QRS, in at least 2

leads, I, aVL, V1, V2, V5, and/or V6. (3)

5. QRS >150 ms are the ones that benefit the most with CRT

6. fQRS presents a sensibility of 93% and specificity of 90% respectively, to locate the segment with

dyssynchrony.

7. Biventricular pacing by stimulating the area with greatest delay(4)

8. Choose the site of greater mechanic delay by transvenous approach in tributary veins of the coronary

sinus (rate of success, 90%). The site of greatest delay is evaluated by speckle-tracking imaging in the

latero-dorsal wall.

Markers of poor response in cardiac resynchronization therapy

1) Male gender(5)

2) CRBBB pattern

3) Narrow QRS complex

4) Co-morbidities

• CRF: creatinine clearance < 30ml/min/m2

• Chronic obstructive pulmonary disease (COPD)

• Anemia

• Pulmonary hypertension

5) Coronary artery disease

6) Significant cardiomegaly

7) Previous LVEF ≤23%(1)

8) Previous functional class IV(1)

9) Ischemic patients with previous acute myocardial infarction(6)

10) LV end diastolic diameter >75 mm: severely dilated and remodeled ventricles.

11) Severe mitral valve insufficiency

12) Scars in the area of electrode implant (high thresholds) or large scars affecting >50% of the LV.

13) Inappropriate programming of AV and VV intervals. With mitral annular tissue Doppler, separation of E/A with AV interval optimization.

Cardiac resynchronization therapy is a significant therapeutic modality in symptomatic patients with heart

failure refractory to drugs with CLBBB pattern and wide QRS (≥120 ms) in the electrocardiogram. However,

regrettably wide QRS (considered as a marker of electrical dyssynchrony) is present in just 30% of the

patients with heart failure, which turns most of the patients with heart failure refractory to drugs, non-eligible

for resynchronization therapy.

A significant number of patients with narrow QRS presents echocardiographic evidence of left ventricular

dyssynchrony. However, there are few data on the additional resources in surface ECG that may predict

intraventricular dyssynchrony.

Fragmented QRS (fQRS) is a marker of electrical dyssynchrony, which results in significant intraventricular

dyssynchrony in patients of non-ischemic dilated cardiomyopathy and narrow QRS interval. fQRS locates the

dyssynchronous segment and may be useful in the identification of patients that may benefit from cardiac

resynchronization therapy(7)

Brugada syndrome: The diagnostic confirmation is only possible in the presence of type 1 pattern: ST

segment elevation ≥2 mm, of upper convexity or descending oblique rectilinear followed by negative T in

the right precordial leads (V1-V2 or from V1 through V3) and/or high right leads V1H, V2H and V3H (they

increase diagnostic sensibility). Figure 6.

Value of ECG in the diagnosis of channelopathies without apparent structural heart disease.

Typical type 1 Brugada pattern in the right precordial leads V1 and V2

Figure 6

Long QT syndrome: The LQT1 variant is characterized by wide-base T waves, moderate QT dependence on heart rate modifications and paradoxical prolongation of QT with infusion of low doses of epinephrine. LQT2 is characterized by bifid T waves (T1-T2 >150 ms),

In LQT3, prolonged QT interval by greater ST segment duration and late appearance of T. Figure 7.

LQT1

LQT2

LQT3

Figure 7

Short QT syndrome: very short intervals, J point interval to the apex of T <120 ms: Jp-Tp (1 point)(2) and prolonged Tpeak/Tend (Tpe) >94 ms in men and >92 ms in women when measured in V5, frequent early repolarization, T wave of great voltage, narrow base and high tendency to atrial fibrillation. Figure 8.

Minus-plus T-wave signal

. Very Short QT interval. ST segment is absent or minimal, tall peaked pseudosymmetric T wave or hyperkalemic-like T wave

Figure 8

Catecholaminergic polymorphic ventricular tachycardia. Recurrent syncopes, triggered by physical or emotional stress, consequence of polymorphic VT. In the latter, QRS axis changes from beat to beat from -60º to +120º from and in precordial leads; alternating pattern of LBBB and RBBB. Figure 9.

Female, white, 20-year-old patient; recurrent syncope of uncertain etiology after physical and emotional stress, carrier of familial catecholaminergic cardiomyopathy. Alternating QRS complexes are observed with alternating right and left bundle branch block morphology. The QRS axis shifts from –60º to +120º.

Figure 9

In the diagnosis of hypertrophic cardiomyopathyECG presents a greater sensibility than auscultation and echocardiogram in the detection of hypertrophic cardiomyopathy, main cause of sudden cardiac death between athletes younger than 35 years old; i.e. when the auscultation is negative and normal echocardiogram, ECG may raise the suspicion of existence of hypertrophic cardiomyopathy(8). Figure 10.

In the diagnosis of cardiomyopathies and myocarditis

HCM, non-obstructive form. Apical portion of the septum with 32 mm of diastolic thickness. LAELVE, systolic pattern by significant secondary alteration of ventricular repolarization in antero-lateral and inferior wall.

Figure 10

Approximately 90% of carriers present altered ECGs, and in follow-up, no ARVC/D presents normal ECG at six years. The following are major criteria: presence of epsilon waves, inverted T waves in right precordial leads >14 years in absence of RBBB and recording of monomorphic VT with pattern of CLBBB and superior axis; duration V1+ V2+ V3 / V4+ V5+ V6 . ≥ 1.2, QRS duration from V1 to V2 >110 ms in absence of RBBB and prolongation of ascending ramp of S from V1 through V3 in absence of RBBB(9). Figure 11

In the diagnosis of arrhythmogenic RV cardiomyopathy/dysplasia

Sinus rhythm, complete RBBB, terminal notch located in the J point J (EPSILON wave). EPSILON wave would be the result of delayed activation in the RV, and visible from V1 through V3 and in the frontal plane leads. T wave inversion is observed in V1 through V3 characteristic of ARVC/D.

Typical example of ECG of ARVC/D Figure 11

In the clinical and epidemiological screening of chronic chagasic myocarditisIn all of Latin America, the electrocardiographic pattern characterized by association of CRBBB + LAFB and polymorphic premature ventricular contractions in patients from endemic area, should raise the suspicion of American trypanosomiasis.The next example presents the mentioned characteristics. Figure 12.

Figure 12

Tumultuous, brief, RV impulse with wide fixed split second heart sound, no murmurs 3/6 + in pulmonary focus in the 2nd intercostal space, and ECG with pattern of IRBBB or CRBBB, suggesting ASD-OS. Figure 13.

In congenital heart diseases

Figure 13

Child with Down syndrome, fremitus and systolic murmur of mitral valve insufficiency, ejection mumur in pulmonary focus and wide and fixed split second sound, with ECG pattern of RBBB + LAFB + BVE is very suggestive of ASD-OP or endocardial cushion defect. (10). Figure 14.

DI DII DIII aVR aVL aVF

V1 V2 V3 V4 V5 V6V4R

First degree AV block, biventricular enlargement, right bundle branch block and left anterior fascicular block. First degree AV block + BVE + CRBBB + LAFB

Figure 14

Cyanotic, hypoxic infant, with possible non-circular pupil, associated to RAE, P of Gamboa pattern + diastolic LVE + extreme axis shift to the left, strongly suggesting tricuspid atresia. Figure 15.

RAE: Visible in V2 and with notch in the ascending ramp of P wave.LVE: Deep S in V1 and R of increased voltage in V5. In V6, it resembles ILBBB.LAFB: AQRS with extreme shift in the left upper quadrant and counterclockwise rotation in the FP.qR in DI and aVL. rS in inferior leads.

Figure 15

Giant P wave + bizarre RBBB of low voltage or WPW, suggesting Ebstein’s anomaly.(11)Systolic murmur in the mesocardium associated to wide isodiphasism in intermediate precordial leads: (Katz-Wachtel sign) of BVE suggesting VSD(12). Figure 16.

Katz-Walchtel ECG sign or phenomenon

Isodiphasic wide QRS in intermediate precordial leads. It indicates biventricular enlargement/hypertrophy

Figure 16

Q wave >40 ms in children in the apical or lateral wall, suggesting anomalous origin of the coronary artery; one of the important causes of sudden cardiac death in young athletes.

Negative P wave in I and positive in aVR, deep Q wave in I and aVL, progressively smaller QRS complexes from V1 through V6 indicating Dextrocardia. Figure 17.

Clinical diagnosis: True simple dextrocardia: mirror image. Total atrio-visceral situs inversus without heart disease. ECG diagnosis: SAP to the right and below, pointing at around +1200 ( DIII). Negative P wave in aVL and DI, positive in DIII. Reverse progression of r wave in precordial leads. V2 through V5 (decreasing).

CONCLUSION: True Dextrocardia.

Figure 17

Independence of P and QRS, narrow QRS with low HR, suggesting congenital complete AV block. Figure 18.

Figure 18

Electrical interference: baseline with oscillations. Cause: poor ground connection; inappropriate cleaning of the skin; baseline oscillations; limbs movement: sudden irregularities of the baseline: children or neurological patients with involuntary movements, Parkinson’s tremor. It may resemble VT (3) or atrial flutter. The placement of electrodes in the origin of the limbs decreases the interference caused by myopotentials.Exchange of limb electrodes resembling dextrocardia; however, precordial progression is normal. Exchange of precordial electrodes; incorrect placement. In case of a daltonic technician, he/she may exchange V1 (red) by V3 (green) or placement at an upper or lower level. And the great precordial electrode: by using conductive gel in the band: tracing recording equal from V1 through V6(13). Figure 19.

In the identification of artifacts

Parkinson’s tremor that resembles ventricular tachycardia

Figure 19

1. It may be dangerous if we trust too much in a normal ECG and ignore the clinical context;2. The presence of normal ECG does not rule out the presence of severe CAD3. There are infarctions without the presence of Q wave and without ventricular repolarization alterations;4. It presents a low sensibility in the diagnosis of ventricular enlargement;5. Normal ECG does not mean “life is guaranteed”;6. It is extremely important to bear in mind the existence of false positives and false negatives;7. In the release for the practice of sports, a normal ECG does not mean absence of risk. A release without

another more accurate test, such as ergometer test or echocardiogram will depend on the clinical context;

8. The presence of factors that may influence the ECG should always be considered, such as: gender, weight, ethnical group, body type, chest deformities (pectus excavatus, mastectomized straight back), competitive practice of sports, hypothermia, hyperventilation, injection of glucose, ingestion of alcohol, etc;

9. Presence of artifacts: tremor, Parkinson, young children, accidental electrode exchange, poor standardization (damping), inappropriate paper speed.

Limitations

In all cases, the interpretation of ECG should take into account the clinical context, as any other supplementary method and it should be interpreted by an experienced physician.The method is still decisive in several clinical scenarios, when making a diagnosis or in management.

Conclusions

Patients with known cardiovascular disease or dysfunction

Class I As initial evaluation; Patients in whom the pharmacological treatment may produce electrocardiographic alterations

correlated with therapeutic response or progression of the disease; Patients in whom the pharmacological treatment may produce adverse effects that may be predicted or

detected by alterations in ECG. Patients with changes in symptoms, signs or relevant lab findings; Patients with permanent pacemaker or cardioverter defibrillator; As pre-operative evaluation; Patients with syncope or pre-syncope; Patients with changes in pattern of chest pain; Precordial pain; Initial dyspnea or worsening of NYHA functional class; Extreme unexplained fatigue, weakness or prostration; Presence of murmur; Presence of friction; Complaint of palpitations; Appearance of new signs of CHF; Signs that suggest pulmonary hypertension; Poorly controlled or accelerated hypertension; Evidence of recent stroke; New episode of arrhythmia or abnormal ventricular rate; Acquired or chronic congenital cardiovascular disease.

Rest ECG. Levels of evidence to indicate it.

Patients with known cardiovascular disease or dysfunction

Class II Pre-operative period of hemodynamically stable patients with non-significant heart disease, mild

hypertension and infrequent PVCs.

Class III Patient with benign heart condition as mitral valve prolapse and mild hypertension; Adult patients with stable chronic heart disease, seen at intervals of 4 months or less, and with no new or

unexplained findings.

Patients in risk of developing cardiovascular disease or dysfunction

Class I Users of cocaine, amphetamines or any other illicit drug; Excessive dose of drugs with effects on the heart; Use of antineoplastic agents, lithium, AIDS drugs, and antidepressants.

Class II To evaluate the response to the administration of a drug that may knowingly cause electrolytic

alteration;

Class III To evaluate the response to administration of a drug known not to affect cardiac function.

Rest ECG: Levels of evidence to perform it

Rest ECG: Level of evidence to perform it

Patients without suspected heart disease or dysfunction

Class I

• People older than 40 that undergo medical examination;

• Before the administration of antineoplastic drugs (high incidence of adverse effects); Criteria to confirm or classify a preliminary diagnosis of cardiac dysfunction

• People of any age, whose job requires an optimal cardiovascular state: Policemen, pilots, drivers, firemen, air traffic controller, elite athletes;

• People with more than 40 years, as pre-operative evaluation;

• People evaluated as heart transplant donor or receptor of non-cardiac transplant.

I) Cardiomyopathy characterized by LVEF decrease, global or more severe in the septum

II) Symptoms associated to HF.

III) Signs associated to HF, such as S3 gallop, tachycardia, or both

IV) Reduction of LVEF of at least 5 for less than 55% with signs or symptoms of HF, or drop of LVEF of at least 10 for less than 55%, without sings of symptoms.

1. Huff JS, Decker WW, Quinn JV, et al. Clinical policy: critical issues in the evaluation and management of adult patients presenting to the emergency department with syncope. Ann Emerg. Med. Apr 2007; 49: 431-444.

2. Rodrigues de Oliveira Neto N et al Correlação entre eletrocardiograma e função sistólica na presença de bloqueio de ramo esquerdo. Relampa 2012; 25: 91-98.

3. Galeotti L,et al. Evaluating strict and conventional left bundle branch block criteria using electrocardiographic simulations. Europace. 2013  Dec;15(12):1816-21)

4. Bax JJ et al. Echocardiography and non invasive imaging in cardiac resyncrhornization therapy;results of the PROSPECT(Predictors of Response to Cardiac Resynchronization Therapy) Study on perspective J Am Coll Cardiol 2009; 53: 1933-43.

5. Zayas Molina R et al Terapia de resincornización con marcapasos biventriculares. Evaluación a los 5 años de seguimiento. Relampa 2012; 25: 99-106)

6. Van Bommel RJ et al Characteristics of heart failure patients associated with good and poor response to cardiac resynchronization theraphy: a PROSPECT( Predictor of Response to CRT) sub-analysis. Eur Heart J 2009; 30: 2470-2477.)

7. Yusuf J et al Fragmented narrow QRS complex: Predictor of left ventricular dyssynchrony in non-ischemic dilated cardiomyopathy.Indian Heart J. 2013 Mar-Apr;65:172-179.

8. Pérez-Riera AR, de Lucca AA, Barbosa-Barros R,Yanowitz FG de Cano SF, Cano MN, Palandri-Chagas AC. Value of electro-vectorcardiogram in hypertrophic cardiomyopathy. Ann Noninvasive Electrocardiol. 2013 Jul;18(4):311-26

9. Nasir K, Bomma C, Tandri H, Roguin A, Dalal D, Prakasa K, Tichnell C, James C, Spevak PJ, Marcus F, Calkins H. Electrocardiographic features of arrhythmogenic right ventricular dysplasia/cardiomyopathy according to disease severity: a need to broaden diagnostic criteria. Circulation. 2004; 110:1527-1534.

References

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11. Muñoz-Castellanos L, Espinola-Zavaleta N, Kuri-Nivón M, Keirns C. Ebstein's Anomaly: anatomo-echocardiographic correlation. Cardiovasc Ultrasound. Nov 23 2007;5:43.

12. Katz LN and Wachtel H. The diphasic QRS type of electrocardiogram in congenital heart disease. Am Heart J; 1937, 13: 202-206

13. Barake W, Baranchuk A, Pinter A. Pseudo-Ventricular Tachycardia Mimicking Malignant Arrhythmia in a Patient with Rapid Atrial Fibrillation Am J Crit Care. 2014 May;23(3):270-272.