Clinical Electrocardiography (ECG) Interpretation

Clinical ECG Interpretation

From cell to reperfusion

The section on Clinical Electrocardiography offers an in-depth exploration of the fundamental principles and practical applications of ECG in cardiovascular medicine. This section provides a clear, step-by-step guide to understanding and interpreting ECGs, blending theoretical knowledge with real-world cases to equip clinicians with the skills necessary to enhance patient outcomes. Authored by Dr. Araz Rawshani, it is one of the world’s most-read resources on ECG interpretation. This comprehensive section guides users from basic concepts to advanced levels of understanding, incorporating the latest guideline recommendations. Additionally, self-assessment tests are available for each topic covered.

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Figure 1. The cardiac cycle starts when cells in the sinoatrial node discharges an action potential that spreads as an electrical impulse through the atria and – via the atrioventricular node – to the ventricles. As the impulse spreads through the myocardium, it activates the cells which respond by contracting. The action potential generates electrical currents which gives rise to the classical ECG waveforms presented here. Activation of the atria is reflected as the P-wave and activation of the ventricles results in the QRS complex. The T-wave reflects the recovery (repolarization) of the ventricles. Note that the ECG rarely shows atrial recovery (repolarization) since it coincides with ventricular depolarization (i.e QRS complex), which has much stronger electrical potentials.

Cardiac electrophysiology and ECG interpretation

Principles of cardiac electrophysiology and electrocardiography (ECG) To ensure effective cardiac

Figure 7. The action potential in the sinoatrial node and in contractile myocardial cells. Phase 4 of the action potential in the sinoatrial node is called 'pacemaker potential', because it is responsible for the spontaneous repetitive depolarization.

Cardiac electrophysiology: Action potential, automaticity and vectors

Cardiac electrophysiology: Membrane potential, action potential, automaticity and electrical vectors

Figure 18. The organization of the limb leads. Note that the electrode on the right leg is not included in any lead, but serves as a ground wire. Leads I, II and III are Einthoven's original leads, and they can be presented with Einthoven's triangle (lower panel). Leads aVR, aVL and aVF were constructed by Goldberger; their reference point is the average of two electrodes. Lead aVR can be inverted into lead –aVR which is recommended as it may facilitate interpretation. All modern ECG machines are capable of presenting both aVR and -aVR.

The ECG leads: Electrodes, limb leads, chest (precordial) leads and the 12-Lead ECG

The ECG leads Before discussing the ECG leads and various lead

Figure 19. The Cabrera format and inverted aVR.

The Cabrera format of the 12-lead ECG & lead –aVR instead of aVR

2016

The normal electrocardiogram (ECG) waves. ECG interpretation.

ECG interpretation: Characteristics of the normal ECG (P-wave, QRS complex, ST segment, T-wave)

ECG Interpretation: definitions, criteria, and characteristics of the normal ECG

How to interpret the ECG: A systematic approach

A systematic approach to ECG interpretation: an efficient and safe

Mechanisms of cardiac arrhythmias: from automaticity to re-entry (reentry)

Mechanisms of cardiac arrhythmias: from automaticity to re-entry This chapter

$Figure 1. Aberrant conduction. The figure shows a supraventriclar extrasystole (an extra atrial impulse, discharged by an ectopic focus outside of the sinoatrial node). The supraventricular extrasystole arrives into the ventricles while the right bundle branch is still refractory, which is why it blocks the impulse. The resulting QRS-complex has a right bundle branch block pattern.$

Aberrant ventricular conduction (aberrancy, aberration)

Aberrant ventricular conduction (aberrancy, aberration) Aberrant conduction is not a

Figure 1. Premature ventricular contraction (complex/beat). Typical appearance. Note the paper speed 50 mm/s (1 large box equals 100 ms).

Premature ventricular contractions (premature ventricular complex, premature ventricular beats)

Premature ventricular contractions (premature ventricular complex, premature ventricular beats): ECG &

Figure 4. Premature atrial beat with incomplete compensatory pause.

Premature atrial contraction (premature atrial beat / complex): ECG & clinical implications

Premature atrial contraction (premature atrial beat / complex) It is caused by

Figure 1. Sinus rhythm. Paper speed 25 mm/s.

Sinus rhythm: physiology, ECG criteria & clinical implications

Sinus rhythm: the normal rhythm of the heart A rhythm

Sinus arrhythmia (respiratory sinus arrhythmia)

Definition of sinus arrhythmia (respiratory sinus arrhythmia) Sinus arrhythmia and

Figure 1. Sinus bradycardia. Paper speed 25 mm/s. Calculate the rate by dividing 300 by the number of large boxes between two cycles (e.g between two R waves). As seen in the figure, there are approximately 6.5 large boxes between two R waves. 300/6.5 equals 46 beats/min.

Sinus bradycardia: definitions, ECG, causes and management

Sinus bradycardia: ECG, causes & management Definition of sinus bradycardia

Chronotropic incompetence (inability to increase heart rate)

Chronotropic incompetence: inability to adequately increase heart rate Chronotropic incompetence

Figure 1. Sinoatrial arrest. Also note the ST-segment elevations (which in this case has no relation to the sinoatrial arrest).

Sinoatrial arrest & sinoatrial pause (sinus pause / arrest)

Sinoatrial arrest & sinoatrial pause (sinus pause/arrest): ECG characteristics &

Sinoatrial block (SA block): ECG criteria, causes and clinical features

Sinoatrial block (SA block): from ECG to clinical management Sinoatrial

Sinus node dysfunction (SND) and sick sinus syndrome (SSS)

Sinus node dysfunction and sick sinus syndrome Sinus node dysfunction

Figure 1. ECG showing sinus tachycardia. Paper speed 25 mm/s. Calculate the heart rate by dividing 300 by the number of large boxes between R-waves. There are approximately 3 large boxes between the R-waves; 300/3 equals 100 beats per minute.

Sinus tachycardia & Inappropriate sinus tachycardia

Sinus tachycardia: causes, ECG, normal variants & pathological variants Sinus

Figure 4. ECG showing Ashman's phenomenon during atrial fibrillation.

Atrial fibrillation: ECG, classification, causes, risk factors & management

Atrial fibrillation: definitions, causes, risk factors, ECG diagnosis and management Atrial

Atrial flutter: classification, causes, ECG diagnosis & management

Atrial flutter: from ECG to clinical management Atrial flutter is

Ectopic atrial rhythm (EAT), atrial tachycardia (AT) & multifocal atrial tachycardia (MAT)

Atrial rhythms: ectopic atrial rhythm, atrial tachycardia and multifocal atrial

Figure 2. Types of atrioventricular nodal reentry tachycardia (AVNRT).

Atrioventricular nodal reentry tachycardia (AVNRT): ECG features & management

Atrioventricular Nodal Reentry (Reentrant) Tachycardia (AVNRT): clinical features, mechanisms, ECG

Figure 1. Hallmarks of pre-excitation on the ECG.

Pre-excitation, Atrioventricular Reentrant (Reentry) Tachycardia (AVRT), Wolff-Parkinson-White (WPW) syndrome

Pre-excitation, Atrioventricular Reentrant (reentry) Tachycardia (AVRT) and Wolff-Parkinson-White (WPW) syndrome:

Figure 1. Two types of junctional (escape) rhythm.

Junctional rhythm (escape rhythm) and junctional tachycardia

Rhythms arising near the atrioventricular node: junctional rhythm (escape rhythm)

Ventricular rhythm and accelerated ventricular rhythm (idioventricular rhythm)

Ventricular rhythm and accelerated ventricular rhythm (idioventricular rhythm) In this

Ventricular tachycardia (VT): ECG criteria, causes, classification, treatment

Ventricular tachycardia (VT): types, causes, ECG features and management This chapter

Figure 1. Ventricular fibrillation and asystole.

Ventricular fibrillation, pulseless electrical activity and sudden cardiac arrest

Ventricular fibrillation, pulseless electrical activity (PEA) and sudden cardiac arrest

ECG showing an episode of sinus rhythm (with multiple ventricular premature beats) spontaneously converting to Torsade de Pointes ventricular tachycardia. Notice how arterial blood pressure (ABP) drops at the onset of TdP. ECG by Nakstad et al (Scand J Trauma Resusc Emerg Med. 2010; 18: 7)

Long QT (QTc) interval, long QT syndrome (LQTS) & torsades de pointes

The QT interval, long QT syndrome (LQTS) & ventricular arrhythmias

Pacemaker mediated tachycardia (PMT): ECG and management

Pacemaker mediated tachycardia (PMT) Pacemaker mediated tachycardia may arise if

Figure 1. Overview of tachyarrhythmia (tachycardia).

Diagnosis and management of narrow and wide complex tachycardia

Diagnosis and management of supraventricular and ventricular tachyarrhythmias: Narrow complex

Cardiac electrophysiology: action potentials and electrical vectors

Video lecture: Cardiac electrophysiology, action potentials, ECG leads & vectors

Introduction to Electrocardiology and ECG Interpretation

Video lecture: Introduction to ECG interpretation

Basic Cardiac Anatomy (Anatomy of the Heart)

Video lecture: Cardiac Anatomy

The QT and QTc Interval

Video lecture: Assessment of the QT interval (QTc interval)

The T-wave: T-wave inversions, hyperacute T-waves, large T-waves, flat T-waves

Video lecture: The T-wave: normal, inverted (negative) hyperacute and flat

The ST segment: J-point, J-60 point, ST depression, ST elevation

Video lecture: The ST segment: J point, J 60 point,

The Electrical Axis of the Heart

Video lecture: Assessment of the electrical axis of the heart

The QRS Complex: Q-wave, R-wave, S-wave, R-wave progression

Video lecture: The QRS complex: Q-wave, R-wave & S-wave

The PR Interval & PR segment

Video lecture: The PR interval & PR segment This video

Approach to ECG Interpretation, Assessment of Rhythm and the P-wave

Video lecture: Assessment of rhythm & P-wave

Figure 1. Atherosclerotic plaque which has ruptured and lead to atherothrombosis.

Introduction to Coronary Artery Disease (Ischemic Heart Disease) & Use of ECG

Coronary artery disease (ischemic heart disease) Coronary artery disease, which

Figure 1. Flow-chart showing the natural course of coronary artery disease and classification of acute coronary syndromes into STEMI, NSTEMI and unstable angina using ECG criteria.

Classification of Acute Coronary Syndromes (ACS) & Acute Myocardial Infarction (AMI)

Classification, diagnosis and definitions of acute coronary syndromes (ACS) and

Figure 2. This figure illustrates ST elevations, ST depressions and T-wave inversions. Patients with STEMI (STE-ACS) always display ST elevations but they may also display ST depressions and/or T-wave inversions. Patients with NSTE-ACS (NSTEMI, unstable angina), on the other hand, may only display ST depressions and/or T-wave inversions.

Clinical application of ECG in chest pain & acute myocardial infarction

Use of ECG in acute coronary syndromes & chest pain

Figure 1. Acute myocardial infarction is usually initiated by rupture or erosion of a vulnerable (unstable) atherosclerotic coronary plaque.

Diagnostic Criteria for Acute Myocardial Infarction: Cardiac troponins, ECG & Symptoms

Acute Myocardial Infarction: Definition & Criteria Acute myocardial infarction is

Cardiac troponin I (TnI) and T (TnT): Interpretation and evaluation in acute coronary syndromes

Troponin is a protein complex expressed in cardiac and skeletal

Figure 1. Myocardial cells require continues oxygen supply in order to maintain normal metabolism. If oxygen supply is less than oxygen demand, ischemia developes. Myocardial cells can switch to anaerobic metabolism and discontinue contractions in order to alleviate the ischemia. This enables the cell to endure up to 30 minutes of severe ischemia. If blood flow is not restored before 30 minutes, the cell will die. Death of myocardial cells is referred to as myocardial infarction.

Myocardial Ischemia & infarction: Reactions, ECG Changes & Symptoms

Myocardial ischemia: reactions, ECG and development of infarction As all

The right ventricle is supplied by the right marginal artery (r. marginalis dx), which originates from the right coronary artery (RCA). The RCA also supplies the inferior left ventricular wall in over 90% of all individuals. Hence, a proximal occlusion (in the RCA) which cuts off blood flow to the right ventricle, will also affect the inferior wall of the left ventricle in 90% of the cases.

The left ventricle in myocardial ischemia and infarction

Acute myocardial infarction (AMI) always affects the left ventricle Myocardial

Figure 3. STE-ACS (STEMI) is caused by a complete occlusion, which means that there is no flow in the artery. The ischemia will affect all layers of the myocardium, from the endocardium to the epicardium (in the region supplied by the occluded artery). This type of ischemia, which affects all myocardial layers, is referred to as transmural ischemia.

Factors that modify the natural course in acute myocardial infarction (AMI)

Factors that modify infarct size and the natural course in

Figure 1. (A) The relation between the action potential and the ECG curve. Myocardial ischemia primarily affects the repolarization, which is reflected on ST-T changes on the ECG. (B) Note that the reference level for measuring deviation (elevation or depression) of the ST segment is the PR segment (the terminal portion of the PR interval). (C) and (D) Shows how to measure the magnitude of ST segment elevation and ST segment depression. The J 60 point is located 60 ms after the J point.

ECG in myocardial ischemia: ischemic changes in the ST segment & T-wave

ECG in acute myocardial ischemia: ischemic ST segment & T-wave

Figure 1. Characteristics of ischemic ST segment depressions on ECG.

ST segment depression in myocardial ischemia and differential diagnoses

ST segment depression due to acute myocardial ischemia ST segment

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Clinical ECG Interpretation

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