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The-ECG-in-Practice

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The paper discusses the critical interpretation of electrocardiograms (ECGs) in clinical practice, highlighting common ECG abnormalities and their clinical correlations. It emphasizes that a normal ECG does not necessarily rule out heart disease, and conversely, abnormal ECG patterns can appear in healthy individuals. The paper details various conditions associated with specific ECG findings, serving as a comprehensive guide for practitioners in accurately diagnosing and distinguishing cardiac conditions.

Figures (608)
Fig. 1.1 The wiring diagram of the heart The P wave of the ECG represents depolarization (remember: depolarization, not contraction) of the atria. The PR interval represents conduction through the AV node and the His bundle, and measures the time taken for the depolarization wave to spread from the atria to the interventricular septum, which is the first part of the ventricles to depolarize. The QRS complex represents depolarization of the ventricles, and the T wave represents ventricular muscle repolarization (Fig. 1.2). Normally each heartbeat involves one P wave per QRS comple and a QRS complex can have only one associated T wave. If there are maro P wavee than ORS comnloevec there mict he 4 dienrder
Fig. 1.1 The wiring diagram of the heart The P wave of the ECG represents depolarization (remember: depolarization, not contraction) of the atria. The PR interval represents conduction through the AV node and the His bundle, and measures the time taken for the depolarization wave to spread from the atria to the interventricular septum, which is the first part of the ventricles to depolarize. The QRS complex represents depolarization of the ventricles, and the T wave represents ventricular muscle repolarization (Fig. 1.2). Normally each heartbeat involves one P wave per QRS comple and a QRS complex can have only one associated T wave. If there are maro P wavee than ORS comnloevec there mict he 4 dienrder
Fig. 1.4 The chest leads. Note that the rib spaces are numbered
Fig. 1.4 The chest leads. Note that the rib spaces are numbered
Fig. 1.7 Sinoatrial block
Fig. 1.7 Sinoatrial block
Fig. 1.11 Second degree block (Mobitz type 2)
Fig. 1.11 Second degree block (Mobitz type 2)
Fig. 1.12 Second degree block (Wenckebach)
Fig. 1.12 Second degree block (Wenckebach)
Fig. 1.15 Complete (third degree) block
Fig. 1.15 Complete (third degree) block
Fig 1.16 Complete (third Degree) block
Fig 1.16 Complete (third Degree) block
e Sinus rhythm with a normal PR interval e Left axis deviation « RSR' pattern in V, and a wide S wave in V, indicate RBBB
e Sinus rhythm with a normal PR interval e Left axis deviation « RSR' pattern in V, and a wide S wave in V, indicate RBBB
Fig. 1.24 Sinus arrhythmia
Fig. 1.24 Sinus arrhythmia
Fig. 1.25 Sinus arrest
Fig. 1.25 Sinus arrest
Fig. 1.27 Supraventricular and ventricular rhythms
Fig. 1.27 Supraventricular and ventricular rhythms
Fig. 1.28 Atrial extrasystole
Fig. 1.28 Atrial extrasystole
Fig. 1.29 Junctional (AV nodal) extrasystole
Fig. 1.29 Junctional (AV nodal) extrasystole
Fig. 1.32 Ventricular extrasystoles
Fig. 1.32 Ventricular extrasystoles
Fig. 1.35 Junctional escape beat
Fig. 1.35 Junctional escape beat
Fig. 1.36 Junctional (escape) rhythm
Fig. 1.36 Junctional (escape) rhythm
Fig. 1.37 Junctional (escape) rhythm
Fig. 1.37 Junctional (escape) rhythm
Fig. 1.38 Ventricular escape beat
Fig. 1.38 Ventricular escape beat
Fig. 1.39 Accelerated idioventricular rhythm
Fig. 1.39 Accelerated idioventricular rhythm
Fig. 1.40 Accelerated idionodal rhythm
Fig. 1.40 Accelerated idionodal rhythm
Fig. 1.42 Wolff—Parkinson—White syndrome
Fig. 1.42 Wolff—Parkinson—White syndrome
Fig. 1.46 Atrial fibrillation
Fig. 1.46 Atrial fibrillation
Fig. 1.47 AV nodal re-entry (junctional) tachycardia
Fig. 1.47 AV nodal re-entry (junctional) tachycardia
Fig. 1.49 Ventricular tachycardia (torsade de pointes)
Fig. 1.49 Ventricular tachycardia (torsade de pointes)
Fig. 1.48 Ventricular tachycardia
Fig. 1.48 Ventricular tachycardia
Fig. 1.51 Junctional tachycardia
Fig. 1.51 Junctional tachycardia
Fig. 1.50 Atrial tachycardia
Fig. 1.50 Atrial tachycardia
The possible causes of sinus rhythm with a fast heart rate are:
The possible causes of sinus rhythm with a fast heart rate are:
Fig. 2.9 Normal ECG
Fig. 2.9 Normal ECG
Fig. 2.19 Normal ECG
Fig. 2.19 Normal ECG
A small Q wave is also common in lead III in normal people: it is then always narrow but can be more than 3 mm deep. Occasionally there will be a similar Q wave in lead VF (Fig. 2.25). These ‘normal’ Q waves become much less deep, and may disappear altogether, on deep inspiration.
A small Q wave is also common in lead III in normal people: it is then always narrow but can be more than 3 mm deep. Occasionally there will be a similar Q wave in lead VF (Fig. 2.25). These ‘normal’ Q waves become much less deep, and may disappear altogether, on deep inspiration.
Fig. 2.33 Normal ECG during inspiration
Fig. 2.33 Normal ECG during inspiration
Acute myocardial infarction Ischaemic heart disease Cardiomyopathy (hypertrophic or dilated) Long QT syndrome Myocarditis Drugs Apparently normal heart: idiopathi: Ventricular tachycardia
Acute myocardial infarction Ischaemic heart disease Cardiomyopathy (hypertrophic or dilated) Long QT syndrome Myocarditis Drugs Apparently normal heart: idiopathi: Ventricular tachycardia
Fig. 3.9 Tachycardias in Wolff-Parkinson—White syndrome
Fig. 3.9 Tachycardias in Wolff-Parkinson—White syndrome
Variation of PR interval
Variation of PR interval
Fig. 3.20 Second degree block (2:1)
Fig. 3.20 Second degree block (2:1)
Dominant S waves and broad QRS complexes in leads I! and II!
Dominant S waves and broad QRS complexes in leads I! and II!
Dominant S waves in leads {I and III
Dominant S waves in leads {I and III
Long PR interval in leads II and III
Long PR interval in leads II and III
Identical P waves and irregular R—R interval
Identical P waves and irregular R—R interval
Fig. 3.34 R on T phenomenon
Fig. 3.34 R on T phenomenon
Fig. 3.50 Ventricular tachycardia
Fig. 3.50 Ventricular tachycardia
Small Q waves and inverted T waves in lead III
Small Q waves and inverted T waves in lead III
Fig. 3.61 Ventricular tachycardia
Fig. 3.61 Ventricular tachycardia
Fig. 3.66 Wolff—Parkinson—White syndrome
Fig. 3.66 Wolff—Parkinson—White syndrome
Fig. 3.68 Ventricular fibrillation
Fig. 3.68 Ventricular fibrillation
Fig. 3.71 Sinus pauses
Fig. 3.71 Sinus pauses
Fig. 3.73 Sick sinus syndrome: bradycardia—tachycardia syndrome
Fig. 3.73 Sick sinus syndrome: bradycardia—tachycardia syndrome
Fig. 3.78 Atrial fibrillation and complete block
Fig. 3.78 Atrial fibrillation and complete block
P waves in lead V,
P waves in lead V,
P waves in lead VL
P waves in lead VL
Fig. 3.84 Ventricular standstill
Fig. 3.84 Ventricular standstill
Fig. 3.85 Sudden death due to ventricular fibrillation
Fig. 3.85 Sudden death due to ventricular fibrillation
« Pacing spike precedes P waves e Narrow QRS complexes e The third beat shows atrial and ventricular pacing
« Pacing spike precedes P waves e Narrow QRS complexes e The third beat shows atrial and ventricular pacing
Fig. 3.88 Ventricular pacing
Fig. 3.88 Ventricular pacing
Fig. 3.91 Exercise-induced ventricular tachycardia
Fig. 3.91 Exercise-induced ventricular tachycardia
Fig. 3.92 Carotid sinus hypersensitivity
Fig. 3.92 Carotid sinus hypersensitivity
Fig. 3.93 DC conversion of ventricular fibrillation
Fig. 3.93 DC conversion of ventricular fibrillation
Fig. 3.95 CSP in atrial flutter
Fig. 3.95 CSP in atrial flutter
Fig. 3.94 CSP and sinus rhythm
Fig. 3.94 CSP and sinus rhythm
Raised ST segments in leads Ill and VF
Raised ST segments in leads Ill and VF
S waves in jeads J] and Ill: left axis deviation
S waves in jeads J] and Ill: left axis deviation
Fig. 4.10 Old anterior infarction
Fig. 4.10 Old anterior infarction
Raised ST segment in lead V3
Raised ST segment in lead V3
Fig. 4.11 Posterior infarction
Fig. 4.11 Posterior infarction
Fig. 4.16 Acute anterior and old inferior infarctions
Fig. 4.16 Acute anterior and old inferior infarctions
Fig. 4.20 Right bundle branch block and anterior infarction
Fig. 4.20 Right bundle branch block and anterior infarction
Fig. 4.28 Junctional tachycardia with anterior ischaemia
Fig. 4.28 Junctional tachycardia with anterior ischaemia
Fig. 4.29 Prinzmetal’s variant angina
Fig. 4.29 Prinzmetal’s variant angina
Fig. 4.40 Exercise-induced ventricular fibrillation
Fig. 4.40 Exercise-induced ventricular fibrillation
Fig. 4.44 Pulmonary embolus
Fig. 4.44 Pulmonary embolus
Fig. 5.2 Atrial fibrillation with coupled ventricular extrasystoles
Fig. 5.2 Atrial fibrillation with coupled ventricular extrasystoles
Fig. 5.5 Probably normal ECG
Fig. 5.5 Probably normal ECG
Fig. 5.9 ?Left ventricular hypertrophy with severe aortic stenosis
Fig. 5.9 ?Left ventricular hypertrophy with severe aortic stenosis
Fig. 5.21 ?Pulmonary embolus Right bundle branch block
Fig. 5.21 ?Pulmonary embolus Right bundle branch block
Fig. 5.26 Right bundle branch block with atrial septal defect
Fig. 5.26 Right bundle branch block with atrial septal defect
Fig. 6.7 Malignant pericardial effusion
Fig. 6.7 Malignant pericardial effusion
Fig. 6.14 Digoxin toxicity Drugs that prolong the QT interval
Fig. 6.14 Digoxin toxicity Drugs that prolong the QT interval
Changes in leads V, and V; suggesting an anterior infarction
Changes in leads V, and V; suggesting an anterior infarction

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