ECG Made Easy® Atul Luthra
INDEX
Page numbers followed by f refer to figure, and t refer to table.
A
Aberrant ventricular conduction 77, 130, 185, 267t
Acidosis 126, 136, 188, 200, 201
metabolic 245
Addison's disease 245
Adrenaline 254
Adrenergic drugs 160
Alcohol intoxication 177, 178, 272
Alkalosis, metabolic 242
Amiodarone 77, 88, 126, 126f, 163, 180, 191, 210, 249, 250
effects of 83f, 88f
Amitryptyline 250
Amlodipine 236
Anemia 159
Aneurysm 188
left ventricular 38
ventricular 112, 137, 256
Angina 178, 189, 253
pectoris 108f, 149
Angiotensin converting enzyme inhibitors 246
Antiangiotensin drugs 245
Antiarrhythmic drugs 77, 126, 171, 179, 249
Anticoagulants 180
Anxiety 87, 106, 159
neurosis 137
Aortic incompetence 235
Aortic valve 66
disease 80, 224, 238
stenosis 235, 238
Arrhythmias 52t, 114, 201
ventricular 282
Atenolol 236, 271
Athlete's heart 116, 256
Atrial activity 176
Atrial contraction, ineffectual 178
Atrial contribution, loss of 178, 189
Atrial depolarization 25f
Atrial enlargement 104
causes of 57t
Atrial fibrillation 50f, 53, 82, 83, 174, 175f, 176, 176f, 177, 179, 201, 217, 269, 271, 271t, 281, 283
causes of 272t
treatment of 273
Atrial flutter 53, 157, 157f, 158, 158t, 165, 167, 173, 176, 176t, 271t
Atrial infarction 104
Atrial natriuretic peptide 268
Atrial pacing 228, 229f
Atrial premature
beat 130f, 148, 129
complex 129, 136, 208, 211
Atrial rate 52, 158, 176
Atrial repolarization 11f
Atrial rhythm 47, 47f
fast 170
Atrial septal
defect 57, 80
repair 224
Atrial tachycardia 47, 153, 155, 155t, 158, 158t, 160, 161, 166, 170, 172, 176, 267
ectopic 173
Atrial thrombus 179
Atrioventricular block 141, 144, 204
advanced 253, 254
complete 52, 219, 224
first-degree 119, 145f, 280, 282
second-degree 123, 144, 146f, 150, 215
third-degree 147f, 148f, 220f, 221f
Atrioventricular dissociation 51f
Atrioventricular nodal reentrant tachycardia 264, 265
Atrioventricular node 273, 277
Atrioventricular relationship 43, 51
Atrioventricular valve disease 57
Atropine 149, 159, 254
resistant bradyarrhythmias 149
Augmented limb leads 16, 18, 21
Automatic implantable cardioverter defibrillator 261
Autosomal dominant
inheritance 81
without deafness 126, 249
B
Beta-agonists 159, 242
Beta-blocker 119, 149, 150, 209, 210
administration 119
Biatrial chamber 6f
Bigeminal rhythm 211
Biventricular chamber 6f
Blocked atrial ectopic beats 204, 208
Body fluid loss 242
Body mass index 233, 255
Bradyarrhythmias 127, 249
Bradycardia 43, 44, 149, 206f
Brain hemorrhage 249
Breath, shortness of 236
Brugada syndrome 81, 81f, 250, 256, 258, 259, 259t, 260
features of 259f
Bundle branch block 77, 78, 80, 87, 93f, 106, 112, 186, 223, 237, 282
complete 195
Bundle of His 122
Bundle of Kent 121, 161, 262f
Burns 245
Bypass tract 54
C
Caffeine 159
Calcification 66
Calcium 126, 249
channel blockers 119
Cannon waves 186
Cardiac decompensation
absence of 190
presence of 190
Cardiac enzymes, normal 116
Cardiac pacing 38
Cardiac rhythm 45f, 197
irregular 212
origin of 47f
regular 152, 166, 193, 219
Cardiac surgery 136, 160, 165, 170, 178, 195, 224, 272
Cardiac trauma 80, 178, 188, 272
Cardiomyopathy 57, 80, 87, 106, 137, 188, 238
chronic dilated 66
dilated 140, 238, 272, 282
hypertrophic 75, 235, 281, 282
apical 94f
obstructive 140
idiopathic 178
ischemic 62
severe 201
Cardiovascular drugs 88
Carditis, rheumatic 136, 170, 195, 217
Carotid massage 267
Carotid sinus
hypersensitivity 225, 253, 254
massage 186
pressure 156, 225
effects of 158
Catecholamine excess 200
Catecholaminergic ventricular tachycardia 81, 250, 260
Catheterization 137
Cerebrovascular accident 87, 88, 106
Chaotic atrial activation 270f
Chest
leads 19
wall
effects of 4f
trauma 104
Cholecystitis 87, 106
Cholesterol lowering drug 127
Chronic obstructive pulmonary disease 82, 238
Chronotropic incompetence 229
Cisapride 127, 249, 250
Coarctation of aorta 75, 235, 281
Coarse fibrillation 176, 271
Conduction defects 114
Confusion 253
Congestion, pulmonary 178
Conn's syndrome 242
Conventional 12-lead electrocardiogram 16f
Cor pulmonale 57, 72, 165
Coronary artery 98
disease 112, 119, 137, 150, 177, 249, 256, 272, 282
spasm 98t, 115t
Coronary disease 126, 224
Coronary filling time, shortened 178, 189
Coronary insufficiency 87, 91, 92f, 106
chronic 66
Cushing's disease 242
D
Deep Q waves 280, 282
Deep S waves 76
Deep sleep 209
Deep T wave inversion 283
Deflection, magnitude of 4f
Delta wave 85
Demand-mode pacing 230
Dementia 253
Depolarization 7f
Depression 105
Dextrocardia, mirror-image 71, 74
Diarrhea 242
Digitalis 87, 88, 106, 119, 149, 150, 177, 188, 201, 225
effects of 88f, 94, 125
toxicity 94, 136, 160, 170, 195
management of 217
Digoxin 163, 210
Diltiazem 149, 150, 163, 210, 225, 271
Diphtheria 119, 150
Diuresis 242
Dizziness 149, 253
spells of 233
Dressler's syndrome 112, 116, 256
Drug
intoxication 188, 201
therapy 150, 225
Dual-chamber
atrioventricular sequential pacing 231f
concept 6f
pacing 230
Dyspnea 149, 178, 189, 253
E
Early repolarization syndrome 116, 117f, 255, 255f, 256, 256t
Ebstein's anomaly 80
ECG
changes, serial evolution of 114
deflections
magnitude of 4f
nomenclature of 1
normal 9f
significance of 10
intervals, normal 12f, 30f
leads 113t
report 279
segments, normal 13f, 31f
values, normal 25
Ectopy, degree of 138
Edema, pulmonary 179, 189
Einthoven triangle 20, 21
Eisenmenger's syndrome 281
Electrical alternans 61f, 283
Electrical axis 33
determination of 33
Electrical cardioversion 191
Electrical defibrillation 181
Electrocardiogram 1
signal averaged 189
Electrocardiographic leads 15
Electrocardiography 23
grid 23
paper 24f
Electrolyte
deficiency 126, 249
imbalance 77, 177
Electrophysiological studies 164, 253, 268
Electrophysiology 5
Endocrine 87
Enzymes, cardiac 109
Erythromycin 250
Excessive beta-blocker sensitivity 149
Exercise 159
Extracardiac disorders 87, 106
Extrasystolic ventricular
bigeminy 134f
trigeminy 135f
Extreme right axis deviation 38
F
Fainting attacks 149
Fallot's tetralogy 72, 281
Fascicular block 64, 119
Fast irregular
bizarre QRS rhythm, clinical relevance of 200
narrow QRS rhythm, clinical relevance of 176
rhythm 152, 172, 182, 197
Fast regular
narrow QRS rhythm, clinical relevance of 158
wide QRS rhythm, clinical relevance of 187
Fast rhythm
irregular 172
regular 152
Fatigue 90, 149, 178, 253
Febrile illness, acute 150
Fever 116, 159
acute rheumatic 119, 282
Fibrocalcerous degeneration 66, 224, 238
Fibrocalcerous disease 80
Flutter-fibrillation 176, 271
Framingham criteria 234
Free fatty acids, accumulation of 200
G
Gatifloxacin 250
Glaucoma 209
Grave's disease 261
clinical sign of 261
H
Haloperidol 250
Head injury 127, 249
Headaches 233
Heart
disease
absence of 190, 280
congenital 38, 72, 177, 224, 272, 280
hypertensive 178, 272
ischemic 100, 165
organic 186, 267
presence of 190
rheumatic 165, 177, 188
severity of 178
valvular 272, 281
electrical wiring network of 8f
failure 149, 159
congestive 137
rate 40, 41f, 42t, 43, 44, 44f, 154156, 205f, 213f
calculation of 41f
determination of 40
fast 178, 189
normal 44
variation of 43f
rhythm 43
sounds 179, 186
Heavy meals 87
Hemiblock 64
Hemodynamics 186, 267
Hemolysis 245
Hemorrhage 87, 106, 127, 159
Hexaxial system 24f, 33, 35f
His bundle 7
rhythm 224
Hyperaldosteronism 242
Hypercalcemia 125
Hypercapnia 177
Hyperglycemia 245
Hyperkalemia 54, 77, 84, 95, 95f, 125, 125f, 126, 128, 200, 244f, 246
causes of 245t
effects of 84f, 95f
features of 243
progressive 245t
severe 246
treatment of 96
Hyperkalemic periodic paralysis 245, 246
Hypertension 57, 66, 137
pulmonary 57, 72
systemic 57, 74, 80, 235, 238
Hyperthermia 126
Hypertrophy 3
biventricular 281
right atrial 280
ventricular 87, 93f, 101f, 106, 112f
Hyperventilation 87, 106
Hypoaldosteronism 245
Hypocalcemia 100, 127, 159, 200
Hypokalemia 87, 89, 89f, 90, 100, 100f, 106, 108f, 127f, 188, 241, 241f
causes of 90, 242t
effects of 89f
features of 239
management of 242
progressive 241t
treatment of 90
Hypokalemic periodic paralysis 242
Hypopituitarism 60, 209
Hypotension 159
Hypothermia 87, 106, 201, 206f, 209
Hypothyroidism 60, 60f, 87, 209
Hypoxemia 159
Hypoxia 136, 177, 188, 200, 201
I
Idiojunctional rhythm 47
Idioventricular rhythm 47, 52
accelerated 193, 194, 194f, 195
Imipramine 250
Implantable cardioverter defibrillator 81, 82, 192, 251
Impulse
origin, rate of 43
spread of 7f
Impure flutter 176, 271
Infarction 137, 188, 190
anterolateral 63
anteroseptal 94, 224
area of 70
hyperacute 95
lateral wall 38, 94
location of 113, 113t
Inferior wall
infarction 38, 64, 66, 94, 150, 170
ischemia 94
Insulin therapy 242
Intensive coronary care unit 195, 202
Interpolated ventricular premature complex 134f
Intracardiac shunt 57, 72
Intracranial event 127, 249
Intracranial tension 209
Intraventricular conduction defect 77, 83, 186, 195, 223
Inverted correction sign 107f
Irregular rhythm 49, 175f
slow 212
Ischemia 103f, 137, 187
anteroseptal 94
management of 137
regional 179
J
Jaundice, obstructive 209
Jervell-Lange-Neilsen syndrome 126, 249
Junctional escape rhythm 47, 149, 205, 222f, 252
Junctional pacemaker 204
rhythm 123
Junctional premature
beats 129, 131f
complex 131, 136
Junctional rhythm 47, 47f, 54, 121f, 169t, 206, 207f, 210, 277, 280
accelerated 168f, 169
Junctional tachycardia, extrasystolic 169
K
Ketanserin 250
Ketoconazole 250
Kidney disease, chronic 128
L
Lactates 200
Lead orientation 20
Left anterior
fascicular block 65f
hemiblock 38, 64, 66, 281, 282
Left atrial enlargement 57, 58f
Left axis deviation 38, 63, 64, 65f
Left bundle branch 7
block 68, 71, 7678, 79f, 94, 236, 237, 237f, 238, 281
causes of 238t
Left circumflex disease 114
Left posterior
fascicular block 65f
hemiblock 38, 63, 66
Left ventricle, region of 20t
Left ventricular
activation 3f
apex, aneurysm of 64
diastolic overload 76, 100, 281
dysfunction 179
hypertrophy 38, 64, 66, 68, 71, 74, 75f, 93f, 94, 140, 233, 234t, 235, 281, 282
causes of 235, 235t
voltage criteria of 117
strain pattern 281
Leg cramps 90
Lev's disease 224
Lidocaine 191
Limb leads 15
Einthoven triangle of 21f
Lone atrial fibrillation 178, 272
Long QT syndrome 81, 250, 260
Low cardiac output state 179, 189
Low voltage graph 60
Lown's classification 138, 138t
Lown-Ganong-Levine syndrome 77, 122, 122f
Lung disease, chronic 38, 63, 68
M
Macrolide antibiotic 127
Magnetic resonance imaging 82
Malignant ventricular arrhythmias 253
Marrow QRS complexes 153f
Massive pulmonary embolism 159
Memory defects 149
Mental confusion 149
Metabolic disorder 188
Metoprolol 180
Minor axis deviation 280
Mitral incompetence 75
Mitral regurgitation 57, 235, 281
Mitral stenosis 57, 281
Mitral valve
disease 72
prolapse 188, 281
syndrome 94, 137
Mobitz atrioventricular block 150
Monomorphic ventricular tachycardia 183f, 275f
Multifocal atrial tachycardia 55, 83, 123, 130, 173, 174, 174f, 175, 177, 214
Multifocal ventricular premature complex 133f
Muscle, atrial 5f
Myocardial activation
direction of 5f
during fibrillation 50f
Myocardial depolarization 50
Myocardial disease 57, 77, 188, 282
diffuse 68
Myocardial infarction 80, 91, 112, 136, 201, 238, 249, 256, 282
acute 112, 113f, 126, 225
extensive anterior wall 91f
inferior 97f, 110f
non-Q anterior wall 92f, 109f
anterior wall 236
zones of 69f
Myocardial injury 95
Myocardial ischemia 92, 95, 109f, 160, 190, 282
Myocardial oxygen demand 178
Myocardial scar 188
Myocarditis 77, 87, 106, 137, 159, 165, 188, 190, 249
acute 80, 126, 160, 282
diffuse 62
viral 126, 249
Myocardium 52
hibernating 114
N
Narrow QRS
complexes 221f
tachycardia, abrupt onset of 265f
Neuromuscular paralysis 90
Nicotine 159
Noncoronary disease 256
Nonsteroidal anti-inflammatory drugs 245, 246
Northwest QRS axis 38
O
Olanzapine 249
Old anteroseptal infarction 68
Oral diltiazem 180
Ostium
primum 80
ASD 38, 64
secundum ASD 38, 64, 80
Oxygen demand 189
P
P wave 53, 156, 267
abnormalities of 53
inverted 54
normal 25, 25f, 53
Pacemaker
implantation 228
rhythm, external 222, 223f, 226
Palpitations 149, 178, 189, 253
Pancreatitis 87, 106
Paroxysmal atrial
fibrillation 178, 272
tachycardia 154, 160, 266
Paroxysmal reentrant atrial tachycardia 266
Paroxysmal supraventricular tachycardia 264, 265
Patent ductus arteriosus 75, 235, 281
Pericardial disease 283
Pericardial effusion 87, 283
Pericarditis 87, 136, 159, 165
acute 103f, 104, 112, 115f, 256, 283
constrictive 60, 178, 272
Permanent pacemaker implantation 254
Persistent atrial fibrillation 272
Persistent juvenile pattern 71, 73, 94, 117
Pharmacological therapy 190
Physical exercise 136, 137
Pleuropericardial rub, appearance of 116
Polymorphic ventricular tachycardia 184f, 250f, 276, 276f
Posterior wall infarction 68, 73
Potassium 126, 249
gain 245
sparing diuretics 245, 246
P-QRS relationship 186, 267
PR interval 11
abnormalities of 118
normal 29, 118
prolonged 119
shortened 119, 120, 121f
variable 119, 123
PR segment 13
abnormalities of 102
depression 102, 283
normal 31
Precordial leads 15
Precordial pain 116
Pregnancy 159
Premature beats 49, 129, 141, 281
Premature complexes, clinical relevance of 136
Prinzmetal's angina 95, 97, 112, 256
Procainamide 249, 250
Propranolol 225, 271
Pseudo-prolonged QT interval 127f
Psychiatry drugs 250
Psychotropic drugs 127
Pulmonary disease 283
chronic 72, 80, 82, 283
Pulmonary embolism 38, 64, 87, 106, 256, 283
acute 71, 80, 82, 94, 260
Pulse 179
Purkinje fiber 139
Purkinje system repolarization 29f
Q
Q wave
abnormal 68
appearance of 114
location of 70
normal 26f
QRS axis 34
abnormal 62
determination of 35
indeterminate 38
normal 38
QRS complex
abnormalities of 59
configurations of 10f
low voltage 60, 83
normal 26, 28f, 59
right axis deviation of 72
QRS electrical alternans 282
QRS voltage
alternating 61
low 283
QRS width 156, 186, 267
QT interval 12
abnormalities of 124
normal 30, 124
prolonged 126, 282, 283
shortened 125
QT syndromes
acquired 126
congenital 126
prolonged 247
Quinidine 87, 106, 126, 188, 201, 249, 250
R
R wave
height, low 282
nonprogression of 66, 283
Radiofrequency ablation 164, 181, 269, 274
Ramipril 236
Rapid impulse discharge 153
Reentrant tachycardia 153, 156, 156t, 160
Regular narrow QRS rhythm, clinical relevance of 170
Regular rhythm 49, 129, 157f
normal 166, 193
slow 204, 219
Regular wide QRS rhythm, clinical relevance of 195
Regurgitation 72
aortic 75, 281
Renal failure, acute 245
Renal tubular acidosis 241, 242, 245, 246
Reperfusion 137, 187
Repolarization 7f
Respiratory failure, acute 165
Respiratory sinus arrhythmia 213, 216
Respiratory tract infection 177
Resuscitation, cardiopulmonary 202
Rhabdomyolysis 245
Rheumatic fever 126, 150, 160, 249
treatment of 137
Rhythm
clock-like regularity of 156
regularity of 186, 267
Right atrial enlargement 57, 58f, 72, 83
Right axis deviation 38, 63, 65f, 72, 283
Right branch block 259
Right bundle branch 7
block 66, 67, 7173, 78, 79f, 82, 94, 237, 238, 283
causes of 80
Right coronary artery spasm 150
Right ventricular
dysplasia 188
arrhythmogenic 82, 94, 140, 190, 260
hypertrophy 38, 63, 67, 71, 72f, 83, 94, 281, 283
severe 64
infarction 260
Right ward QRS axis 82
deviation 83
Romano-ward syndrome 126, 249
S
Salbutamol 136
Secondary ST depression, causes of 112f
Secondary T wave inversion, causes of 93f
Septal activation 3f
Septal defect 224
Septal depolarization 26f
Shock 87, 106
electrical 201
Short PR interval 85, 121f, 122f
Sick sinus syndrome 149, 178, 209, 210, 225, 251, 252, 252t, 254, 272
symptoms of 253t
treatment of 149
Sinoatrial block 141, 142, 149, 204, 207f, 222f
complete 221, 224, 225
second-degree 149, 206, 215
Sinoatrial conduction time 253
Sinoatrial exit block 252
Sinoatrial node 46, 204
Sinus 155t
arrhythmia 117, 213f, 216, 280
absence of 216
nonrespiratory 213, 216
bradycardia 46, 117, 127, 149, 204, 205f, 209, 249, 252, 252f, 280
symptomatic 209
node
dysfunction 149, 225
recovery time 253
rhythm 47, 47f, 195, 206, 208, 210, 215, 217
normal 166, 170
tachycardia 82, 104, 152, 153f, 155, 158, 281283
Causes of 159
Slow atrial fibrillation 149, 217, 252
Slow irregular narrow QRS rhythm, clinical relevance of 216
Slow regular narrow QRS rhythm, clinical relevance of 209
Slow rhythm 223, 227
irregular 212
regular 204
Sokolow and Lyon criteria 234
ST depression
degree of 110
duration of 111
nature of 111
timing of 111
upsloping 280
ST elevation
location of 115t
myocardial infarction 112
without reciprocal depression 116
ST segment 14
abnormalities of 105
depression 105, 108, 282
types of 109f
elevation 112, 282
causes of 256t, 260t
saddle-shaped 115f
upsloping 280
normal 32
Stable hemodynamic parameters 156
Standard limb leads 16
Stenosis 72
aortic 57, 74, 281
calcific 80, 224
pulmonary 57, 72, 281
Steroid therapy 116
Stokes-Adams attacks 225
causes of 253, 254t
Stress
emotional 136, 137
test 103f
Subclavian steal syndrome 225, 253, 254
Sudden cardiac death 81, 192, 250, 260
Supraventricular extrasystole 280
Supraventricular premature complexes 136
Supraventricular rhythm 49f
Symmetrical T wave 280
inversion 114
Sympathomimetics 137, 187
drugs 149
Syncope 149, 189, 247, 253
recurrent 274
vasovagal 209
Systemic embolization 179
Systolic left ventricular overload 74
T
T inversion, nonspecific 283
T wave
abnormalities of 86
flattening 282
inversion 82, 108, 280282
inverted 86
normal 28, 86
Tachyarrhythmias, ventricular 282
Tachy-brady syndrome 149, 252
Tachycardia 43f, 44, 87, 106, 116
antidromic 155
ectopic 156, 156t
inadequate 149
junctional 47, 52, 167, 168, 169t, 170, 171
nonparoxysmal junctional 168
recurrent episodes of 156
sudden onset of 156
supraventricular 161, 185, 186, 264, 265, 267t
termination of 161
ventricular 47, 54, 64, 85, 179, 182, 183, 186, 186t, 187, 201, 267t, 274
Tall P wave 55, 71, 82, 280
Tall T wave 95, 280
Terfenadine 127, 249, 250
Theophylline 136, 137, 177, 187
Thiazide 236
Three standard limb leads 17f
Three unipolar limb leads 18f
Thromboembolism 180
pulmonary 272
Thyrotoxicosis 136, 137, 159, 160, 165, 170, 178, 272
control of 137
Torsade de pointes 128, 201, 250, 276
Triaxial reference system 21f, 22f, 34f
Tricuspid
regurgitation 57
stenosis 57
Tricyclic antidepressant 127
drugs 100
True posterior wall infarction 71
Tumor lysis 245
U
U wave
abnormalities of 99
inverted 100
normal 28, 99
prominent 99
Uremia 209
V
Vagal dominance in athletes 119
Vagal maneuvers 156, 163
Vagal stimulation 225
Valvular abnormality 188
Ventricular activation pattern 49f
Ventricular arrhythmia, serious 224, 254
Ventricular depolarization 28f
Ventricular ectopic beats
couplet of 135f
triplet of 135f
Ventricular ectopy
Lown's classification of 138t
severity of 138
Ventricular escape rhythm 47
Ventricular fibrillation 50f, 198, 199, 199f, 200
Ventricular filling 178, 189, 197, 198f, 200
Ventricular mass repolarization 29f
Ventricular pacing 229, 229f, 230f
Ventricular pre-excitation 77, 84
syndrome 195
Ventricular premature
beats 129, 132f, 282
complex 131, 137, 139, 187
Ventricular rate 52, 158, 176, 178
Ventricular reentrant circuit 275f
Ventricular rhythm 47, 47f, 49f, 51f, 220
Ventricular septal defect 57, 75, 235, 281
Verapamil 209, 271
Voltage criteria 75, 117
Volume depletion 159
Vomiting 242
W
Wandering pacemaker 280
rhythm 55, 123, 213, 214, 214f, 216
Wenckebach phenomenon 146f
Wide QRS
arrhythmias 77
complex 77, 84, 220f, 237f, 282
pre-existing 223
rhythm
irregular 197
normal 193
slow 219
Wolff-Parkinson-White syndrome 38, 54, 64, 68, 71, 74, 77, 84, 85, 85f, 87, 93f, 94, 106, 112f, 121, 121f, 160, 161, 178, 179, 186, 193, 223, 261, 262, 272
features of 262f
×
Chapter Notes

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Nomenclature of ECG DeflectionsChapter 1

 
ELECTROCARDIOGRAM
The electrocardiogram (ECG) provides a graphic depiction of the electrical forces generated by the heart. The ECG graph appears as a series of deflections and waves produced by each cardiac cycle.
Before going on to the genesis of individual deflections and their terminology, it would be worthwhile mentioning certain important facts about the direction and magnitude of ECG waves and the activation pattern of myocardium.
 
Direction
  • By convention, a deflection above the baseline or isoelectric (neutral) line is a positive deflection while one below the isoelectric line is a negative deflection (Fig. 1.1A)
  • The direction of a deflection depends upon two factors namely, the direction of spread of the electrical force and the location of the recording electrode
  • In other words, an electrical impulse moving towards an electrode creates a positive deflection while an impulse moving away from an electrode creates a negative deflection (Fig. 1.1B). Let us see this example.
We know that the sequence of electrical activation is such that the interventricular septum is first activated from left to right followed by activation of the left ventricular free wall from the endocardial to epicardial surface.2
zoom view
Fig. 1.1A: Direction of the deflection on ECG. (A) Above the baseline—positive deflection; (B) Below the baseline—negative deflection
zoom view
Fig. 1.1B: Effect of current direction on polarity of deflection. (A) Towards the electrode—upright deflection; (B) Away from electrode—inverted deflection
If an electrode is placed over the right ventricle, it records an initial positive deflection representing septal activation towards it, followed by a major negative deflection that denotes free wall activation away from it (Fig. 1.2).
If, however, the electrode is placed over the left ventricle, it records an initial negative deflection representing septal activation away from it, followed by a major positive deflection that denotes free wall activation towards it (Fig. 1.2).3
zoom view
Fig. 1.2: Septal (1) and left ventricular (2) activation. As seen from lead V1 (rS pattern); As seen from lead V6 (qR pattern)
 
Magnitude
  • The height of a positive deflection and the depth of a negative deflection are measured vertically from the baseline. This vertical amplitude of the deflection is a measure of its voltage in millimeters (Fig. 1.3A)
  • The magnitude of a deflection depends upon the quantum of the electrical forces generated by the heart and the extent to which they are transmitted to the recording electrode on the body surface. Let us see these examples:
    • ▸ Since the ventricle has a far greater muscle mass than the atrium, ventricular complexes are larger than atrial complexes
    • ▸ When the ventricular wall undergoes thickening (hypertrophy), the ventricular complexes are larger than normal
    • ▸ If the chest wall is thick, the ventricular complexes are smaller than normal since the fat or muscle intervenes between the myocardium and the recording electrode (Fig. 1.3B).4
zoom view
Fig. 1.3A: Magnitude of the ECG deflection. (A) Positive deflection—height; (B) Negative deflection—depth
zoom view
Fig. 1.3B: Effect of chest wall on magnitude of deflection. (A) Thin chest—tall deflection; (B) Thick chest—small deflection
 
Activation
  • Activation of the atria occurs longitudinally by contiguous spread of electrical forces from one myocyte to the other. On the other hand, activation of the ventricles occurs transversely by spread of electrical forces from the endocardial surface (surface facing ventricular cavity) to the epicardial surface (outer surface) (Fig. 1.4).
Therefore, atrial activation can reflect atrial enlargement (and not atrial hypertrophy) while ventricular activation can reflect ventricular hypertrophy (and not ventricular enlargement).5
zoom view
Fig. 1.4: Direction of myocardial activation in atrium and ventricle. (A) Atrial muscle—longitudinal, from one myocyte to other; (B) Ventricular—transverse, endocardium to epicardium
 
ELECTROPHYSIOLOGY
The ECG graph consists of a series of deflections or waves. The distances between sequential waves on the time axis are termed as intervals. Portions of the isoelectric line (baseline) between successive waves are termed as segments.
In order to understand the genesis of deflections and the significance of intervals and segments, it would be worthwhile understanding certain basic electrophysiological principles.
  • Anatomically speaking, the heart is a four-chambered organ. But in the electrophysiological sense, it is actually two-chambered. As per the “dual-chamber” concept, the chambers of the heart are the biatrial chamber and the biventricular chamber (Fig. 1.5). This is because the atria are activated together and the ventricles too contact synchronously. Therefore, on the ECG, atrial activation is represented by a single wave and ventricular activation by a single wave-complex
  • In the resting state, the myocyte membrane bears a negative charge on the inner side. When stimulated by an electrical impulse, the charge is altered by an influx of calcium ions across the cell membrane.6
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    Fig. 1.5: The “dual-chamber” concept. (A) Biatrial chamber; (B) Biventricular chamber
    This results in coupling of actin and myosin filaments and muscle contraction. The spread of electrical impulse through the myocardium is known as depolarization (Fig. 1.6)
  • Once the muscle contraction is completed, there is efflux of potassium ions, in order to restore the resting state of the cell membrane. This results in uncoupling of actin and myosin filaments and muscle relaxation. The return of the myocardium to its resting electrical state is known as repolarization (Fig. 1.6)
  • Depolarization and repolarization occur in the atrial muscle as well as in the ventricular myocardium. The wave of excitation is synchronized so that the atria and the ventricles contract and relax in a rhythmic sequence
  • Atrial depolarization is followed by atrial repolarization which is nearly synchronous with ventricular depolarization and finally ventricular repolarization occurs
  • We must appreciate that depolarization and repolarization of the heart muscle are electrical events, while cardiac contraction (systole) and relaxation (diastole) constitute mechanical events7
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    Fig. 1.6: The spread of impulse. (A) Depolarization; (B) Repolarization
  • However, it is true that depolarization just precedes systole and repolarization is immediately followed by diastole.
  • The electrical impulse that initiates myocardial depolarization and contraction originates from a group of cells that comprise the pacemaker of the heart
  • The normal pacemaker is the sinoatrial (SA) node, situated in the upper portion of the right atrium (Fig. 1.7)
  • From the SA node, the electrical impulse spreads to the right atrium through three intra-atrial pathways while the Bachmann's bundle carries the impulse to the left atrium
  • Having activated the atria, the impulse enters the atrioventricular (AV) node situated at the AV junction on the lower part of the interatrial septum. The brief delay of the impulse at the AV node allows time for the atria to empty the blood they contain into their respective ventricles.
After the AV nodal delay, the impulse travels to the ventricles through a specialized conduction system called the bundle of His. The His bundle primarily divides into two bundle branches, a right bundle branch (RBB) which traverses the right ventricle and a left bundle branch (LBB) that traverses the left ventricle (Fig. 1.7).8
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Fig. 1.7: The electrical ‘wiring’ network of the heart
A small septal branch originates from the left bundle branch to activate the interventricular septum from left to right. The left bundle branch further divides into a left posterior fascicle and a left anterior fascicle.
The posterior fascicle is a broad band of fibers which spreads over the posterior and inferior surfaces of the left ventricle. The anterior fascicle is a narrow band of fibers, which spreads over the anterior and superior surfaces of the left ventricle (Fig. 1.7).
Having traversed the bundle branches, the impulse finally passes into their terminal ramifications called Purkinje fibers. These Purkinje fibers traverse the thickness of the myocardium to activate the entire myocardial mass from the endocardial surface to the epicardial surface.
 
DEFLECTIONS
The ECG graph consists of a series of deflections or waves. Each electrocardiographic deflection has been arbitrarily assigned a letter of the alphabet. Accordingly, a sequence of wave that represents a single cardiac cycle is sequentially termed as P Q R S T and U (Fig. 1.8A).9
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Fig. 1.8A: The normal ECG deflections
By convention, P, T and U waves are always denoted by capital letters while the Q, R and S waves can be represented by either a capital letter or a small letter depending upon their relative or absolute magnitude. Large waves (over 5 mm) are assigned capital letters Q, R and S while small waves (under 5 mm) are assigned small letters q, r and s.
The entire QRS complex is viewed as one unit, since it represents ventricular depolarization. The positive deflection is always called the R wave. The negative deflection before the R wave is the Q wave while the negative deflection after the R wave is the S wave (Fig. 1.8B).
Relatively speaking, a small q followed by a tall R is labeled as qR complex while a large Q followed by a small r is labeled as Qr complex. Similarly, a small r followed by a deep S is termed as rS complex, while a tall R followed by a small s is termed as Rs complex (Fig. 1.9).
Two other situations are worth mentioning. If a QRS deflection is totally negative without an ensuing positivity, it is termed as a QS complex.
Secondly, if the QRS complex reflects two positive waves, the second positive wave is termed as R’ and accordingly, the complex is termed as rSR’ or RsR’ depending upon magnitude of the positive (r or R) wave and the negative (s or S) wave (Fig. 1.9).10
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Fig. 1.8B: The QRS complex is one unit. Q wave—before R wave; S wave—after R wave
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Fig. 1.9: Various configurations of the QRS complexCourtesy: Wang K. Proper Labeling of the Component Waves of the Ventricular Depolarization. In: Atlas of Electrocardiography. 1st ed. Jaypee Brothers Medical Publishers (P) Ltd. 2013.P.6.
 
Significance of ECG Deflections
• P wave:
Produced by atrial depolarization.
• QRS complex:
Produced by ventricular depolarization.
It consists of:
  • Q wave:
  • R wave:
  • S wave:
First negative deflection before R wave.
First positive deflection after Q wave.
First negative deflection after R wave.
• T wave:
Produced by ventricular repolarization.
• U wave:
Produced by Purkinje repolarization (Fig. 1.10).
11
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Fig. 1.10: Depolarization and repolarization depicted as deflections (Note: Atrial repolarization is buried in the QRS complex)
Within ventricular repolarization, the ST segment is the plateau phase and the T wave is the rapid phase.
You would be wondering where is atrial repolarization. Well, it is represented by the Ta wave which occurs just after the P wave. The Ta wave is generally not seen on the ECG as it coincides with (lies buried in) the larger QRS complex.
 
INTERVALS
During analysis of an ECG graph, the distances between certain waves are relevant in order to establish a temporal relationship between sequential events during a cardiac cycle. Since the distance between waves is expressed on a time axis, these distances are termed as ECG intervals. The following ECG intervals are clinically important.
 
PR Interval
The PR interval is measured from the onset of the P wave to the beginning of the QRS complex (Fig. 1.11). Although the term PR interval is in vogue, actually, PQ interval would be more appropriate. Note that the duration of the P wave is included in the measurement.12
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Fig. 1.11: The normal ECG intervals
We know that the P wave represents atrial depolarization while the QRS complex represents ventricular depolarization. Therefore, it is easy to comprehend that the PR interval is an expression of atrioventricular conduction time.
This includes the time for atrial depolarization, conduction delay in the AV node and the time required for the impulse to traverse the ventricular conduction system before ventricular depolarization ensues.
 
QT Interval
The QT interval is measured from the onset of the Q wave to the end of the T wave (Fig. 1.11). If it is measured to the end of the U wave, it is termed QU interval. Note that the duration of the QRS complex, the length of the ST segment and the duration of the T wave are included in the measurement.
We know that the QRS complex represents ventricular depolarization while the T wave represents ventricular repolarization. Therefore, it is easy to comprehend that the QT interval is an expression of total duration of ventricular systole.13
Since the U wave represents Purkinje system repolarization, the QU interval in addition takes into account the time taken for the ventricular Purkinje system to repolarize.
 
SEGMENTS
The magnitude and direction of an ECG deflection is expressed in relation to a baseline, which is referred to as the isoelectric line. The main isoelectric line is the period of electrical inactivity that intervenes between successive cardiac cycles during which no deflections are observed.
It lies between the termination of the T wave (or U wave, if seen) of one cardiac cycle and onset of the P wave of the next cardiac cycle. However, two other segments of the isoelectric line that occur between the waves of a single cardiac cycle, are clinically important.
 
PR Segment
The PR segment is that portion of the isoelectric line which intervenes between the termination of the P wave and the onset of the QRS complex (Fig. 1.12). It represents conduction delay in the atrioventricular node.
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Fig. 1.12: The normal ECG segments
14
Note carefully that the length of the PR segment does not include the width of the P wave, while the duration of the PR interval does include the P wave width.
 
ST Segment
The ST segment is that portion of the isoelectric line which intervenes between the termination of the S wave and the onset of the T wave (Fig. 1.12). It represents the plateau phase of ventricular repolarization. The point at which the QRS complex ends and the ST segment begins is termed the junction point or J point. The ECG waves, intervals and segments are depicted in Figure 1.13.
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Fig. 1.13: The ECG waves, intervals and segmentsCourtesy: Wang K. ECG Waves, Intervals and Segments. In: Atlas of Electrocardiography. 1st ed. Jaypee Brothers Medical Publishers (P) Ltd. 2013. P.4.