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ECG - Electrocardiogram

This document discusses the electrocardiogram (ECG) and its components. It begins by describing the myocardial action potential and its phases. It then discusses the pacemaker action potential and ECG waves including the P, QRS, T, and U waves. It explains ECG intervals such as the PR, QT, and ST segments. The document also covers ECG leads, normal values, procedures for recording an ECG, interpreting ECG findings, and clinical applications of the ECG.

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THE ELECTROCARDIOGRAM By Dr. Prajwal
ECG machine
Myocardial action potential Phase 0 = rapid upstroke and depolarization—voltage- gated Na+ channels open. Phase 1 = initial repolarization—inactivation of voltage- gated Na+ channels. Voltage-gated K+ channels begin to open. Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction. Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Phase 4 = resting potential—high K+ permeability through K+ channels.
Top, Monophasic action potential from a ventricular muscle fiber Bottom, Electrocardiogram recorded simultaneously.
Pacemaker action potential Occurs in the SA and AV nodes. Key differences from the ventricular action potential include: Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles. Phases 1 and 2 are absent. Phase 3 = inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑K+ efflux. Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR.
Recording the depolarization wave (A and B) and the repolarization wave (C and D) from a cardiac muscle fiber.
Transmission of the cardiac impulse through the heart, showing the time of appearance
P wave. Commonly called the “atrial complex”, represents the start of depolarization at the SA node (the first part of the heart to be depolarized), and depolarization of atria. Normally, it is upwards except in lead aVR where it is inverted. Duration = 0.11 sec; Amplitude = usually less than 2.5 mm. QRS complex (Ventricular complex). The QRS complex represents ventricular depolarization. Duration = less than 0.08 sec (maximum=0.12 sec), i.e. 2 small squares. Amplitude = 1.5 – 2 mV The Q wave is the first negative wave after P wave and represents excitation of upper interventricular septum. It is often inconspicuous. The R wave is the first prominent positive wave after P wave. It represents excitation of major part of myocardium. The S wave, the negative wave after R, represents activation of posterior basal part of ventricles. (These three waves represent three instantaneous vectors ). If the entire QRS complex is negative, it is called QS complex. T wave. This wave is due to ventricular repolarization. Normally, it is in the same direction as the QRS complex because repolarization follows a path that is opposite to that of depolarization, i.e. it occurs from epicardium to endocardium. (One of the reasons for this is that the endocardial areas have a longer period of contraction and are thus slow to repolarize). U wave. The U wave is seen just after the T wave in some individuals. It is due possibly to slow repolarization of the intraventricular contracting system (papillary muscles).
P-R segment. It extends from the end of P wave to the start of QRS complex and is usually isoelectric. J point. The J point occurs at the end of QRS complex. At this point, the entire ventricular muscle is depolarized. Normally, the J point is on the isoelectric line but it is displaced up or down by the current of injury resulting from myocardial ischemia or infarction. ST Segment. This segment extends from the J point to the onset of T wave. Normally it is isoelectric but may vary from + 0.5 to + 2.0 mm in chest leads. Elevation or depression of ST segment (due to current of injury), indicates myocardial damage. (Since the current of injury continues to flow during diastole of the heart (TP interval), it shifts the zero potential line (drawn through the J point) up or down, giving the impression of elevation or depression of the ST segment. During the ST segment interval, the entire ventricular myocardium is depolarized.
PR or PQ Interval if Q wave is present. It is the interval between the beginning of P wave to the start of QRS complex It is a measure of atriovenrtricular (AV) conduction time, ie, the time taken by the excitatory wave to pass from the atria to the ventricles, including the delay at the AV node. Thus it indicates the conduction time of the bundle of HIS which connects the atria and the ventricles. The AV node is activated at the top of P wave. Normal duration = 0.12–0.2 sec. depending on the heart rate. The PR interval is prolonged in various types of heart block.
ST interval. It is measured from the end of S wave to the end of T wave. It represents the ventricular repolarization. Duration = 0.32 sec. TP segment. It is measured from the end of T wave to beginning of the next P wave. Duration = 0.2 sec (depending inversely on heart rate. PP interval. It is the interval between beginning or peaks of two successive P waves. RR interval. This is the interval between the peaks of two successive R waves. It is measured for calculating heart rate (ventricular rate).
QT interval. It is measured from the beginning of Q (or R wave) to the end of T wave. Duration = 0.40 to 0.43 sec. It represents ventricular depolarization and repolarization. It corresponds to the duration of electrical systole. QT interval varies with Heart Rate Therefore corrected QT interval (QTc) is measured by using Bazett’s formula QTc = 𝑄𝑇 𝑅𝑅
Electrocardiographic Leads The term lead is used for the specific points of electrical contacts, as well as the actual record obtained from any two points. Two types of leads can be employed: Direct leads. they are applied directly to the exposed heart, as during heart surgery, or during an experiment. Indirect leads. These are applied away from the heart, ie, on the skin surface They are limb leads, chest leads, and esophageal lead. These leads are used in routine ECG procedures.
Electrode Positions The ECG leads (electrodes) are of two types: bipolar and unipolar. In bipolar leads, the potential difference is recorded between two active electrodes. In unipolar leads, one electrode is kept at zero potential while the other is the exploring electrode.
Bipolar limb leads (Standard leads or “classical” limb leads) These were the earliest leads to be used (Wilhelm Einthoven of Leyden, 1860–1927). These leads measure the potential using two active electrodes placed on any two limbs and represent the algebraic sum of the potentials of two constituent active (electrodes) leads. There are three bipolar limb leads: a. Lead I. It records the potential at the left arm (LA) minus the potential at the right arm (RA), or LA–RA (left arm positive) . b. Lead II. is the potential at the left leg (LL) minus the potential at right arm (RA), or LL–RA (left leg positive). c. Lead III. This leads records the potential at the left leg (LL) minus the potential at the left arm (LA), or LL–LA (left leg positive).
Einthoven triangle
Einthoven’s Law. Einthoven’s law states that if the ECGs are recorded simultaneously with the three limb leads, the sum of the potentials recorded in leads I and III will equal the potential in lead II. Lead I potential Lead III potential + = Lead II potential Einthoven Triangle the two shoulders and the left leg (left foot) form the apices of an equilateral triangle – the Einthoven triangle – that surrounds the heart. The heart is thus placed approximately in the center of a volume conductor. Lines that bisect each side of the triangle (i.e. at the zero axis of each side, where the potential is zero at all times), meet the center of the triangle at the heart.
Unipolar leads These leads record the potential from a single region of the body (limbs or chest). One electrode, the indifferent electrode, is kept at zero potential by connecting the three limb leads to a common central terminal in the machine where the currents from the limbs neutralize each other. The other electrode can be on a limb or on the chest. Thus, there are three such limb leads and a number of chest leads.
Unipolar limb leads Any of the limb electrodes can be used to record cardiac potentials in comparison to the indifferent electrode kept at zero potential. Thus, there are three limb leads, each denoted by the letter V (vector)—VR, VL, VF (left foot). Augmented limb leads. Since the recorded voltages are small. indifferent electrode is connected through high resistance to other two electrodes, Thus, the augmented limb leads are : aVR= between RA and (LA+LL); aVL = between LA and (RA+LL); and aVF = between LL and (RA+LA). V=IxR
Unipolar chest leads (also called unipolar precordial leads). These leads record the potentials from the anterior surface of the heart, from the right side to the left side of the chest, in relation to the indifferent electrode (RA + LA + LL). Esophageal leads E18, E20
The mean frontal axis is the sum of all the ventricular depolarization forces. The average direction of the flow of current is called the electrical axis of the heart (the mean QRS axis) lies between –30° and +90°, though most believe it to be + 50. This is generally calculated from leads I and III. There is right axis deviation when the QRS waves in these leads point towards each other, while left axis deviation is when they point in opposite direction. If QRS complex is primarily positive in these two leads, the axis is normal. Normal RAD LAD Lead I ↑ ↓ ↑ Lead II ↑ ↑/↓ ↓ Lead III ↑/↓ ↑ ↓
The standardized sites for the unipolar chest leads are as follows: V1 is in the 4th intercostal space (ICS), just to the right of the sternum V2 is in the 4th ICS, just to the left of the sternum V3 is halfway between V2 and V4 V4 is at the midclavicular line in the 5th ICS V5 is in the anterior axillary line at the same level as V4 V6 is in the mid-axillary line in the same level as V4 (5th ICS) V7 is in the posterior axillary line in the 5th ICS V8 is on the infrascapular line, just below the angle of the scapula.
QTc prolongation (ms) Men Women Normal ≤ 430 ≤ 450 Borderline 431-450 451-470 Abnormal > 450 > 470 QTcB = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) Bazett's formula QTcF = 𝑄𝑇(𝑠) 3 𝑅𝑅(𝑠) Fridericia's formula
Normal values for waves and intervals are as follows:  RR interval: 0.6-1.2 seconds  P wave: 80 milliseconds  PR interval: 120-200 milliseconds  PR segment: 50-120 milliseconds  QRS complex: 80-100 milliseconds  J-point: N/A  ST segment: 80-120 milliseconds  T wave: 160 milliseconds  ST interval: 320 milliseconds  QT interval: 420 milliseconds or less if heart rate is 60 beats per minute (bpm) References Schlant RC, Adolph RJ, DiMarco JP, Dreifus LS, Dunn MI, Fisch C, et al. Guidelines for electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography). Circulation.
PROCEDURE 1. Ask the subject to lie down supine on the bed and be comfortable and relaxed, no electronic gadgets with the subject. 2. Check that the ECG machine is properly earthed. Rub small amounts of electrolyte jelly on the fronts of wrists and just above the ankles. 3. Apply the limb electrodes firmly on these points and fix them in place with rubber straps. Fix the lead wires, identified with the letters- RA, LA, LL, and RL electrodes. Connect the connector cable to the machine. 4. Switch on the machine and “center” the stylus (pen); run the paper and, using the CAL (calibration) push the button 2–3 times and adjust the pen deflection to 10 mm. 5. Using the lead selector switch, record 4–6 ECG complexes in the standard order—leads I, II, III, aVR, aVL, aVF—in this order. (Figure 2-18) 6. Stop the machine and apply the electrode jelly on the chest positions for V1 to V6. Using the chest electrode, record the ECG from these positions one after the other. 7. Tear off the paper from the machine and label the various leads. Note down the name of the person and date.
1. Heart rate. It can be determined by any of the following method: a. By dividing 1500 by the number of small squares between 2 successive R waves. (1500 small squares represent 1 minute) For example, number of small squares between 2 R waves = 21 Heart rate = 1500/21 = 70 per min. 2. Rhythm. In normal sinus rhythm, P waves precede each QRS complex. Atrial, junctional and ventricular arrhythmias are detected by in-hospital and ambulatory ECG monitoring. 3. Mean cardiac vector. Evaluation of the frontal plane QRS axis provides the information. 4. Morphology of various waves, intervals, and segments are carefully studied.
P-R segment S-T segment T-P segment PR or PQ Interval QT Interval RR Interval PP Interval ST Interval 50-120 ms80-120 ms200 ms0.6-1.2 sec120-200 ms320 ms<420 ms80 ms80-100 ms160 ms J-point J-point N/A
1. Heart rate: Atrial and Ventricular Rate
2. Rhythm
3. QRS axis
3. Mean cardiac vector
4. Morphology of various waves, intervals, and segments
Clinical Applications of ECG ECG provides useful information in: 1. Diagnosis and prognostic information in ischemic heart disease (coronary artery disease, CAD), such as angina, heart attack (acute CAD). 2. Detection of cardiac arrhythmias—both atrial and ventricular. 3. Different types of heart block. For example, in complete heart block, diseases of AV node or bundle of HIS, which is the only pathway from atria to ventricles, there is complete dissociation between atria and ventricles. The heart rate may be 15–20/min. and serious emergency may arise, with prolonged periods of asystole. Due to cerebral cortical ischemia (Stokes- Adams syndrome), there is dizziness or ‘faints’. It is in such cases that artificial pacemakers are implanted. 4. Hypertrophy of atria and ventricles. 5. Electrical activity resulting from general metabolic and electrolyte changes.
Special Uses of ECG 1. In-hospital ECG monitoring. Cardiac arrest or severe arrhythmia patients who are shifted to the hospital need special care. 2. Ambulatory ECG monitoring (Holter). Patients with episodic palpitation and dizziness or unstable angina, are given a Holter monitor to wear for 24 hours. Analysis of the recorded tape often identifies the cause of the condition. 3. Exercise ECG. The ECG recorded during exercise (Treadmill test, TMT), as per Bruce protocol in otherwise normal. Arrhythmias and ST segment changes are more likely to be detected during TMT
Causes of ST Segment Elevation 1. Coronary vasospasm (Prinzmetal’s angina) 2. Organic stenosis of coronary arteries (MI) 3. LV aneurysm 4. Pericarditis (elevated concave upwards S-T segment associated with tall, peaked T-waves and no reciprocal changes in the opposite leads) 5. Early repolarisation.
Causes of S-T Segment Depression 1. In coronary insufficiency 2. Hypokalaemia 3. Hypothermia 4. Tachycardia 5. Hyperventilation 6. Anxiety 7. Post-prandial, cold drinks 8. MVP 9. CVA 10. Smoking 11. Pheochromocytoma 12. Digoxin therapy 13. RBBB and LBBB.
Causes of Low Voltage Complexes Obesity Global ischaemia Thick chest wall Cardiomyopathy Hypothyroidism Amyloid heart disease Hypopituitarism Pericardial effusion Hypothermia Incorrect standardisation Emphysema.
Causes of Tall Symmetrical T-waves 1. Acute subendocardial ischaemia, injury or infarct 2. Recovering inferior wall MI 3. Hyperacute anterior wall MI 4. Prinzmetal angina 5. True posterior wall MI 6. Hyperkalaemia. Absent P-waves 1. Atrial fibrillation 2. Sinoatrial arrest or block 3. Nodal rhythm 4. Hyperkalaemia.
Causes of Pathological Q-wave 1. Transmural MI 2. HOCM 3. WPW syndrome 4. Cardiac contusion and myocarditis 5. Amyloid heart 6. Anomalous origin of coronary arteries 7. Racial.
Causes of Prolonged QTc Interval (Normally, QT interval is less than 50% of RR interval) 1. During sleep 2. Hypocalcaemia 3. Acute myocarditis 4. Acute MI 5. Quinidine effect 6. Procainamide effect 7. Tricyclic and tetracyclic antidepressant drugs, phenothiazines 8. Cerebral injury 9. Hypothermia 10. HOCM 11. Advanced or complete block, with torsades de pointes 12. The Jervell-Lange-Nielsen syndrome (congenital deafness, syncopal attacks and sudden death) 13. The Romano-Ward syndrome (no deafness) 14. Hypothyroidism 15. MVP 16. Pulmonary embolism 17. Increased ICT.
ELECTROCARDIOGRAPHY (ECG) Normal Values
Name: Age: Sex: Date: Time: ELECTROCARDIOGRAPHY (ECG)
1. Heart Rate Atrial Rate: 1500 𝑃𝑃 𝐼𝑛𝑡𝑒𝑟𝑣𝑎𝑙 (𝑆𝑚𝑎𝑙𝑙 𝑏𝑜𝑥) Ventricular Rate: 1500 𝑅𝑅 𝐼𝑛𝑡𝑒𝑟𝑣𝑎𝑙 (𝑆𝑚𝑎𝑙𝑙 𝑏𝑜𝑥) 2. Rhythm: 3. Axis: Regular Normal
4. Waves, Segments & Intervals Waves Duration(s) Amplitude(mV) Comment P Wave ? ? Normal QRS Complex ? ? Normal T Wave ? ? Normal U Wave ? ? Normal Segment Duration(s) Comment PR segment ? Normal ST segment ? Isoelectric
Interval Duration(s) Comment PR interval ? Normal ST interval ? Normal RR interval ? Normal QT interval ? Normal QTc = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) ? Normal Report: ECG of the given subject appears Normal
QTc prolongation (ms) Men Women Normal ≤ 430 ≤ 450 Borderline 431-450 451-470 Abnormal > 450 > 470 QTcB = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) Bazett's formula QTcF = 𝑄𝑇(𝑠) 3 𝑅𝑅(𝑠) Fridericia's formula
Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
Normal values for waves and intervals are as follows:  RR interval: 0.6-1.2 seconds  P wave: 80 milliseconds  PR interval: 120-200 milliseconds  PR segment: 50-120 milliseconds  QRS complex: 80-100 milliseconds  J-point: N/A  ST segment: 80-120 milliseconds  T wave: 160 milliseconds  ST interval: 320 milliseconds  QT interval: 420 milliseconds or less if heart rate is 60 beats per minute (bpm) References Schlant RC, Adolph RJ, DiMarco JP, Dreifus LS, Dunn MI, Fisch C, et al. Guidelines for electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography). Circulation.
Myocardial action potential Phase 0 = rapid upstroke and depolarization—voltage- gated Na+ channels open. Phase 1 = initial repolarization—inactivation of voltage- gated Na+ channels. Voltage-gated K+ channels begin to open. Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction. Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Phase 4 = resting potential—high K+ permeability through K+ channels.
HIS BUNDLE ELECTROGRAM The record of the electrical activity obtained with the catheter is the His bundle electrogram (HBE). It normally shows an A deflection when the AV node is activated, an H spike during transmission through the His bundle, and a V deflection during ventricular depolarization. With the HBE and the standard electrocardiographic leads, it is possible to time three intervals accurately: (1) the PA interval, the time from the first appearance of atrial depolarization to the A wave in the HBE, which represents conduction time from the SA node to the AV node; (2) the AH interval, from the A wave to the start of the H spike, which represents the AV nodal conduction time; and (3) the HV interval, the time from the start of the H spike to the start of the QRS deflection in the ECG, which represents conduction in the bundle of His and the bundle branches. The approximate normal values for these intervals in adults are PA, 27 ms; AH, 92 ms; and HV, 43 ms. These values illustrate the relative slowness of conduction in the AV node.
Delta waves seen in a) Brugada syndrome b) Hypothermia c) Torsades de pointes d) WPW Syndrome
ECG - Electrocardiogram
ECG - Electrocardiogram
ECG - Electrocardiogram
ECG - Electrocardiogram
ECG - Electrocardiogram

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ECG - Electrocardiogram

  • 1.
  • 2.
  • 3.
    Myocardial action potential Phase0 = rapid upstroke and depolarization—voltage- gated Na+ channels open. Phase 1 = initial repolarization—inactivation of voltage- gated Na+ channels. Voltage-gated K+ channels begin to open. Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction. Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Phase 4 = resting potential—high K+ permeability through K+ channels.
  • 5.
    Top, Monophasic actionpotential from a ventricular muscle fiber Bottom, Electrocardiogram recorded simultaneously.
  • 6.
    Pacemaker action potential Occursin the SA and AV nodes. Key differences from the ventricular action potential include: Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles. Phases 1 and 2 are absent. Phase 3 = inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑K+ efflux. Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR.
  • 9.
    Recording the depolarizationwave (A and B) and the repolarization wave (C and D) from a cardiac muscle fiber.
  • 11.
    Transmission of thecardiac impulse through the heart, showing the time of appearance
  • 13.
    P wave. Commonlycalled the “atrial complex”, represents the start of depolarization at the SA node (the first part of the heart to be depolarized), and depolarization of atria. Normally, it is upwards except in lead aVR where it is inverted. Duration = 0.11 sec; Amplitude = usually less than 2.5 mm. QRS complex (Ventricular complex). The QRS complex represents ventricular depolarization. Duration = less than 0.08 sec (maximum=0.12 sec), i.e. 2 small squares. Amplitude = 1.5 – 2 mV The Q wave is the first negative wave after P wave and represents excitation of upper interventricular septum. It is often inconspicuous. The R wave is the first prominent positive wave after P wave. It represents excitation of major part of myocardium. The S wave, the negative wave after R, represents activation of posterior basal part of ventricles. (These three waves represent three instantaneous vectors ). If the entire QRS complex is negative, it is called QS complex. T wave. This wave is due to ventricular repolarization. Normally, it is in the same direction as the QRS complex because repolarization follows a path that is opposite to that of depolarization, i.e. it occurs from epicardium to endocardium. (One of the reasons for this is that the endocardial areas have a longer period of contraction and are thus slow to repolarize). U wave. The U wave is seen just after the T wave in some individuals. It is due possibly to slow repolarization of the intraventricular contracting system (papillary muscles).
  • 16.
    P-R segment. Itextends from the end of P wave to the start of QRS complex and is usually isoelectric. J point. The J point occurs at the end of QRS complex. At this point, the entire ventricular muscle is depolarized. Normally, the J point is on the isoelectric line but it is displaced up or down by the current of injury resulting from myocardial ischemia or infarction. ST Segment. This segment extends from the J point to the onset of T wave. Normally it is isoelectric but may vary from + 0.5 to + 2.0 mm in chest leads. Elevation or depression of ST segment (due to current of injury), indicates myocardial damage. (Since the current of injury continues to flow during diastole of the heart (TP interval), it shifts the zero potential line (drawn through the J point) up or down, giving the impression of elevation or depression of the ST segment. During the ST segment interval, the entire ventricular myocardium is depolarized.
  • 17.
    PR or PQInterval if Q wave is present. It is the interval between the beginning of P wave to the start of QRS complex It is a measure of atriovenrtricular (AV) conduction time, ie, the time taken by the excitatory wave to pass from the atria to the ventricles, including the delay at the AV node. Thus it indicates the conduction time of the bundle of HIS which connects the atria and the ventricles. The AV node is activated at the top of P wave. Normal duration = 0.12–0.2 sec. depending on the heart rate. The PR interval is prolonged in various types of heart block.
  • 18.
    ST interval. Itis measured from the end of S wave to the end of T wave. It represents the ventricular repolarization. Duration = 0.32 sec. TP segment. It is measured from the end of T wave to beginning of the next P wave. Duration = 0.2 sec (depending inversely on heart rate. PP interval. It is the interval between beginning or peaks of two successive P waves. RR interval. This is the interval between the peaks of two successive R waves. It is measured for calculating heart rate (ventricular rate).
  • 19.
    QT interval. Itis measured from the beginning of Q (or R wave) to the end of T wave. Duration = 0.40 to 0.43 sec. It represents ventricular depolarization and repolarization. It corresponds to the duration of electrical systole. QT interval varies with Heart Rate Therefore corrected QT interval (QTc) is measured by using Bazett’s formula QTc = 𝑄𝑇 𝑅𝑅
  • 20.
    Electrocardiographic Leads The termlead is used for the specific points of electrical contacts, as well as the actual record obtained from any two points. Two types of leads can be employed: Direct leads. they are applied directly to the exposed heart, as during heart surgery, or during an experiment. Indirect leads. These are applied away from the heart, ie, on the skin surface They are limb leads, chest leads, and esophageal lead. These leads are used in routine ECG procedures.
  • 21.
    Electrode Positions The ECGleads (electrodes) are of two types: bipolar and unipolar. In bipolar leads, the potential difference is recorded between two active electrodes. In unipolar leads, one electrode is kept at zero potential while the other is the exploring electrode.
  • 22.
    Bipolar limb leads(Standard leads or “classical” limb leads) These were the earliest leads to be used (Wilhelm Einthoven of Leyden, 1860–1927). These leads measure the potential using two active electrodes placed on any two limbs and represent the algebraic sum of the potentials of two constituent active (electrodes) leads. There are three bipolar limb leads: a. Lead I. It records the potential at the left arm (LA) minus the potential at the right arm (RA), or LA–RA (left arm positive) . b. Lead II. is the potential at the left leg (LL) minus the potential at right arm (RA), or LL–RA (left leg positive). c. Lead III. This leads records the potential at the left leg (LL) minus the potential at the left arm (LA), or LL–LA (left leg positive).
  • 24.
  • 25.
    Einthoven’s Law. Einthoven’slaw states that if the ECGs are recorded simultaneously with the three limb leads, the sum of the potentials recorded in leads I and III will equal the potential in lead II. Lead I potential Lead III potential + = Lead II potential Einthoven Triangle the two shoulders and the left leg (left foot) form the apices of an equilateral triangle – the Einthoven triangle – that surrounds the heart. The heart is thus placed approximately in the center of a volume conductor. Lines that bisect each side of the triangle (i.e. at the zero axis of each side, where the potential is zero at all times), meet the center of the triangle at the heart.
  • 26.
    Unipolar leads These leadsrecord the potential from a single region of the body (limbs or chest). One electrode, the indifferent electrode, is kept at zero potential by connecting the three limb leads to a common central terminal in the machine where the currents from the limbs neutralize each other. The other electrode can be on a limb or on the chest. Thus, there are three such limb leads and a number of chest leads.
  • 27.
    Unipolar limb leads Anyof the limb electrodes can be used to record cardiac potentials in comparison to the indifferent electrode kept at zero potential. Thus, there are three limb leads, each denoted by the letter V (vector)—VR, VL, VF (left foot). Augmented limb leads. Since the recorded voltages are small. indifferent electrode is connected through high resistance to other two electrodes, Thus, the augmented limb leads are : aVR= between RA and (LA+LL); aVL = between LA and (RA+LL); and aVF = between LL and (RA+LA). V=IxR
  • 29.
    Unipolar chest leads(also called unipolar precordial leads). These leads record the potentials from the anterior surface of the heart, from the right side to the left side of the chest, in relation to the indifferent electrode (RA + LA + LL). Esophageal leads E18, E20
  • 31.
    The mean frontalaxis is the sum of all the ventricular depolarization forces. The average direction of the flow of current is called the electrical axis of the heart (the mean QRS axis) lies between –30° and +90°, though most believe it to be + 50. This is generally calculated from leads I and III. There is right axis deviation when the QRS waves in these leads point towards each other, while left axis deviation is when they point in opposite direction. If QRS complex is primarily positive in these two leads, the axis is normal. Normal RAD LAD Lead I ↑ ↓ ↑ Lead II ↑ ↑/↓ ↓ Lead III ↑/↓ ↑ ↓
  • 37.
    The standardized sitesfor the unipolar chest leads are as follows: V1 is in the 4th intercostal space (ICS), just to the right of the sternum V2 is in the 4th ICS, just to the left of the sternum V3 is halfway between V2 and V4 V4 is at the midclavicular line in the 5th ICS V5 is in the anterior axillary line at the same level as V4 V6 is in the mid-axillary line in the same level as V4 (5th ICS) V7 is in the posterior axillary line in the 5th ICS V8 is on the infrascapular line, just below the angle of the scapula.
  • 43.
    QTc prolongation (ms)Men Women Normal ≤ 430 ≤ 450 Borderline 431-450 451-470 Abnormal > 450 > 470 QTcB = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) Bazett's formula QTcF = 𝑄𝑇(𝑠) 3 𝑅𝑅(𝑠) Fridericia's formula
  • 44.
    Normal values forwaves and intervals are as follows:  RR interval: 0.6-1.2 seconds  P wave: 80 milliseconds  PR interval: 120-200 milliseconds  PR segment: 50-120 milliseconds  QRS complex: 80-100 milliseconds  J-point: N/A  ST segment: 80-120 milliseconds  T wave: 160 milliseconds  ST interval: 320 milliseconds  QT interval: 420 milliseconds or less if heart rate is 60 beats per minute (bpm) References Schlant RC, Adolph RJ, DiMarco JP, Dreifus LS, Dunn MI, Fisch C, et al. Guidelines for electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography). Circulation.
  • 45.
    PROCEDURE 1. Ask thesubject to lie down supine on the bed and be comfortable and relaxed, no electronic gadgets with the subject. 2. Check that the ECG machine is properly earthed. Rub small amounts of electrolyte jelly on the fronts of wrists and just above the ankles. 3. Apply the limb electrodes firmly on these points and fix them in place with rubber straps. Fix the lead wires, identified with the letters- RA, LA, LL, and RL electrodes. Connect the connector cable to the machine. 4. Switch on the machine and “center” the stylus (pen); run the paper and, using the CAL (calibration) push the button 2–3 times and adjust the pen deflection to 10 mm. 5. Using the lead selector switch, record 4–6 ECG complexes in the standard order—leads I, II, III, aVR, aVL, aVF—in this order. (Figure 2-18) 6. Stop the machine and apply the electrode jelly on the chest positions for V1 to V6. Using the chest electrode, record the ECG from these positions one after the other. 7. Tear off the paper from the machine and label the various leads. Note down the name of the person and date.
  • 46.
    1. Heart rate.It can be determined by any of the following method: a. By dividing 1500 by the number of small squares between 2 successive R waves. (1500 small squares represent 1 minute) For example, number of small squares between 2 R waves = 21 Heart rate = 1500/21 = 70 per min. 2. Rhythm. In normal sinus rhythm, P waves precede each QRS complex. Atrial, junctional and ventricular arrhythmias are detected by in-hospital and ambulatory ECG monitoring. 3. Mean cardiac vector. Evaluation of the frontal plane QRS axis provides the information. 4. Morphology of various waves, intervals, and segments are carefully studied.
  • 48.
    P-R segment S-Tsegment T-P segment PR or PQ Interval QT Interval RR Interval PP Interval ST Interval 50-120 ms80-120 ms200 ms0.6-1.2 sec120-200 ms320 ms<420 ms80 ms80-100 ms160 ms J-point J-point N/A
  • 50.
    1. Heart rate:Atrial and Ventricular Rate
  • 51.
  • 52.
  • 54.
  • 55.
    4. Morphology ofvarious waves, intervals, and segments
  • 57.
    Clinical Applications ofECG ECG provides useful information in: 1. Diagnosis and prognostic information in ischemic heart disease (coronary artery disease, CAD), such as angina, heart attack (acute CAD). 2. Detection of cardiac arrhythmias—both atrial and ventricular. 3. Different types of heart block. For example, in complete heart block, diseases of AV node or bundle of HIS, which is the only pathway from atria to ventricles, there is complete dissociation between atria and ventricles. The heart rate may be 15–20/min. and serious emergency may arise, with prolonged periods of asystole. Due to cerebral cortical ischemia (Stokes- Adams syndrome), there is dizziness or ‘faints’. It is in such cases that artificial pacemakers are implanted. 4. Hypertrophy of atria and ventricles. 5. Electrical activity resulting from general metabolic and electrolyte changes.
  • 58.
    Special Uses ofECG 1. In-hospital ECG monitoring. Cardiac arrest or severe arrhythmia patients who are shifted to the hospital need special care. 2. Ambulatory ECG monitoring (Holter). Patients with episodic palpitation and dizziness or unstable angina, are given a Holter monitor to wear for 24 hours. Analysis of the recorded tape often identifies the cause of the condition. 3. Exercise ECG. The ECG recorded during exercise (Treadmill test, TMT), as per Bruce protocol in otherwise normal. Arrhythmias and ST segment changes are more likely to be detected during TMT
  • 59.
    Causes of STSegment Elevation 1. Coronary vasospasm (Prinzmetal’s angina) 2. Organic stenosis of coronary arteries (MI) 3. LV aneurysm 4. Pericarditis (elevated concave upwards S-T segment associated with tall, peaked T-waves and no reciprocal changes in the opposite leads) 5. Early repolarisation.
  • 60.
    Causes of S-TSegment Depression 1. In coronary insufficiency 2. Hypokalaemia 3. Hypothermia 4. Tachycardia 5. Hyperventilation 6. Anxiety 7. Post-prandial, cold drinks 8. MVP 9. CVA 10. Smoking 11. Pheochromocytoma 12. Digoxin therapy 13. RBBB and LBBB.
  • 61.
    Causes of LowVoltage Complexes Obesity Global ischaemia Thick chest wall Cardiomyopathy Hypothyroidism Amyloid heart disease Hypopituitarism Pericardial effusion Hypothermia Incorrect standardisation Emphysema.
  • 62.
    Causes of TallSymmetrical T-waves 1. Acute subendocardial ischaemia, injury or infarct 2. Recovering inferior wall MI 3. Hyperacute anterior wall MI 4. Prinzmetal angina 5. True posterior wall MI 6. Hyperkalaemia. Absent P-waves 1. Atrial fibrillation 2. Sinoatrial arrest or block 3. Nodal rhythm 4. Hyperkalaemia.
  • 63.
    Causes of PathologicalQ-wave 1. Transmural MI 2. HOCM 3. WPW syndrome 4. Cardiac contusion and myocarditis 5. Amyloid heart 6. Anomalous origin of coronary arteries 7. Racial.
  • 64.
    Causes of ProlongedQTc Interval (Normally, QT interval is less than 50% of RR interval) 1. During sleep 2. Hypocalcaemia 3. Acute myocarditis 4. Acute MI 5. Quinidine effect 6. Procainamide effect 7. Tricyclic and tetracyclic antidepressant drugs, phenothiazines 8. Cerebral injury 9. Hypothermia 10. HOCM 11. Advanced or complete block, with torsades de pointes 12. The Jervell-Lange-Nielsen syndrome (congenital deafness, syncopal attacks and sudden death) 13. The Romano-Ward syndrome (no deafness) 14. Hypothyroidism 15. MVP 16. Pulmonary embolism 17. Increased ICT.
  • 65.
  • 66.
  • 67.
    1. Heart Rate AtrialRate: 1500 𝑃𝑃 𝐼𝑛𝑡𝑒𝑟𝑣𝑎𝑙 (𝑆𝑚𝑎𝑙𝑙 𝑏𝑜𝑥) Ventricular Rate: 1500 𝑅𝑅 𝐼𝑛𝑡𝑒𝑟𝑣𝑎𝑙 (𝑆𝑚𝑎𝑙𝑙 𝑏𝑜𝑥) 2. Rhythm: 3. Axis: Regular Normal
  • 68.
    4. Waves, Segments& Intervals Waves Duration(s) Amplitude(mV) Comment P Wave ? ? Normal QRS Complex ? ? Normal T Wave ? ? Normal U Wave ? ? Normal Segment Duration(s) Comment PR segment ? Normal ST segment ? Isoelectric
  • 69.
    Interval Duration(s) Comment PRinterval ? Normal ST interval ? Normal RR interval ? Normal QT interval ? Normal QTc = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) ? Normal Report: ECG of the given subject appears Normal
  • 70.
    QTc prolongation (ms)Men Women Normal ≤ 430 ≤ 450 Borderline 431-450 451-470 Abnormal > 450 > 470 QTcB = 𝑄𝑇(𝑠) 𝑅𝑅(𝑠) Bazett's formula QTcF = 𝑄𝑇(𝑠) 3 𝑅𝑅(𝑠) Fridericia's formula
  • 72.
    Diagrammatic illustration ofserial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
  • 73.
    Diagrammatic illustration ofserial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
  • 74.
    Diagrammatic illustration ofserial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction). C) Later pattern (many hours to a few days D) Late established pattern (many days to weeks E) Very late pattern: This may occur many months to years after the infarction.
  • 78.
    Normal values forwaves and intervals are as follows:  RR interval: 0.6-1.2 seconds  P wave: 80 milliseconds  PR interval: 120-200 milliseconds  PR segment: 50-120 milliseconds  QRS complex: 80-100 milliseconds  J-point: N/A  ST segment: 80-120 milliseconds  T wave: 160 milliseconds  ST interval: 320 milliseconds  QT interval: 420 milliseconds or less if heart rate is 60 beats per minute (bpm) References Schlant RC, Adolph RJ, DiMarco JP, Dreifus LS, Dunn MI, Fisch C, et al. Guidelines for electrocardiography. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography). Circulation.
  • 90.
    Myocardial action potential Phase0 = rapid upstroke and depolarization—voltage- gated Na+ channels open. Phase 1 = initial repolarization—inactivation of voltage- gated Na+ channels. Voltage-gated K+ channels begin to open. Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction. Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Phase 4 = resting potential—high K+ permeability through K+ channels.
  • 116.
    HIS BUNDLE ELECTROGRAM Therecord of the electrical activity obtained with the catheter is the His bundle electrogram (HBE). It normally shows an A deflection when the AV node is activated, an H spike during transmission through the His bundle, and a V deflection during ventricular depolarization. With the HBE and the standard electrocardiographic leads, it is possible to time three intervals accurately: (1) the PA interval, the time from the first appearance of atrial depolarization to the A wave in the HBE, which represents conduction time from the SA node to the AV node; (2) the AH interval, from the A wave to the start of the H spike, which represents the AV nodal conduction time; and (3) the HV interval, the time from the start of the H spike to the start of the QRS deflection in the ECG, which represents conduction in the bundle of His and the bundle branches. The approximate normal values for these intervals in adults are PA, 27 ms; AH, 92 ms; and HV, 43 ms. These values illustrate the relative slowness of conduction in the AV node.
  • 118.
    Delta waves seenin a) Brugada syndrome b) Hypothermia c) Torsades de pointes d) WPW Syndrome

Editor's Notes

  • #73  Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction): ST segment elevation in I, aVL, and V3–6; reciprocal ST depression in II, III, and aVF. C) Later pattern (many hours to a few days): Q waves have appeared in I, aVL, and V5–6. QS complexes are present in V3–4. This indicates that the major transmural infarction is underlying the area recorded by V3–4; ST segment changes persist but are of lesser degree, and the T waves are beginning to invert in the leads in which the ST segments are elevated. D) Late established pattern (many days to weeks): The Q waves and QS complexes persist, the ST segments are isoelectric, and the T waves are symmetric and deeply inverted in leads that had ST elevation and tall in leads that had ST depression. This pattern may persist for the remainder of the patient’s life. E) Very late pattern: This may occur many months to years after the infarction. The abnormal Q waves and QS complexes persist. The T waves have gradually returned to normal.
  • #74  Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction): ST segment elevation in I, aVL, and V3–6; reciprocal ST depression in II, III, and aVF. C) Later pattern (many hours to a few days): Q waves have appeared in I, aVL, and V5–6. QS complexes are present in V3–4. This indicates that the major transmural infarction is underlying the area recorded by V3–4; ST segment changes persist but are of lesser degree, and the T waves are beginning to invert in the leads in which the ST segments are elevated. D) Late established pattern (many days to weeks): The Q waves and QS complexes persist, the ST segments are isoelectric, and the T waves are symmetric and deeply inverted in leads that had ST elevation and tall in leads that had ST depression. This pattern may persist for the remainder of the patient’s life. E) Very late pattern: This may occur many months to years after the infarction. The abnormal Q waves and QS complexes persist. The T waves have gradually returned to normal.
  • #75  Diagrammatic illustration of serial electrocardiographic patterns in anterior infarction. A) Normal tracing. B) Very early pattern (hours after infarction): ST segment elevation in I, aVL, and V3–6; reciprocal ST depression in II, III, and aVF. C) Later pattern (many hours to a few days): Q waves have appeared in I, aVL, and V5–6. QS complexes are present in V3–4. This indicates that the major transmural infarction is underlying the area recorded by V3–4; ST segment changes persist but are of lesser degree, and the T waves are beginning to invert in the leads in which the ST segments are elevated. D) Late established pattern (many days to weeks): The Q waves and QS complexes persist, the ST segments are isoelectric, and the T waves are symmetric and deeply inverted in leads that had ST elevation and tall in leads that had ST depression. This pattern may persist for the remainder of the patient’s life. E) Very late pattern: This may occur many months to years after the infarction. The abnormal Q waves and QS complexes persist. The T waves have gradually returned to normal.
  • #76 Lateral wall mi
  • #77 Calculate Heart rate
  • #78 Acute pericarditis with diffuse ST elevations in I, II, III, aVF, V3–V6, without T-wave inversions. Also note concomitant PR-segment elevation in aVR and PR depression in the inferolateral leads.
  • #117 In patients with heart block, the electrical events in the AV node, bundle of His, and Purkinje system are frequently studied with a catheter containing an electrode at its tip that is passed through a vein to the right side of the heart and manipulated into a position close to the tricuspid valve. Three or more standard electrocardiographic leads are recorded simultaneously.
  • #119 Hypothermia [J (Osborn) waves]