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CARDIOVASCULAR SYSTEM
ELECTROCARDIOGRAM (ECG)

AP DR SWE SWE WIN Physiology Unit Division of Basic Sciences Faculty of Medicine Cyberjaya University Cyberjaya Medical College No. 3410, Jalan Teknokrat 3, Cyber 4, 63000 Cyberjaya Selangor, Malaysia

ELECTROCARDIOGRAPHY (ECG)
Topic I BASIC THEORY ON ECG I.1 Functional Anatomy and Histology of the Heart I.2 The Electrical Activity of the Heart I.2.1 Characteristics of a Resting Ventricular Muscle I.2.2 Production of Pacemaker Potential and Action Potential By the SA Node I.2.3 Action Potential of a ventricular fibre (Fast Response) I.3 Functional Organisation of the Conducting System Page 3 4 4 4 6

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1.4 Background of ECG II HISTORICAL BACKGROUND OF ECG II. 1 Nature of ECG II.2 Uses of ECG III HOW TO PERFORM ECG The Steps in Setting Up Basic ECG Measurement IV INTERPRETING BASIC ECG Approach for reading ECG Determination of IV.1 Heart rate IV.2 Rhythm IV.3 Cardiac Axis/Vectors IV.4 Waves IV.5 Intervals IV. 6 Segments

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ELECTROCARDIOGRAPHY (ECG)
I. BASIC THEORY ON ECG Electrocardiogram (ECG) It is a standard clinical tool used to study the electrical activity of the heart. It works by picking up and amplifying very small electrical potential changes between different points on the surface of the body caused by cyclical depolarisation and repolarisation of the heart cells (cardiac myocytes). The location of the electrodes and the conventional ways in which they are connected enable the ECG to look at the heart from a series of different designated directions. The cycle of electrical changes during a single heart beat is termed an ECG complex. Different component of ECG complex reflect the activation of different parts of the heart.

Functional Anatomy of the Heart


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I.1 FUNCTIONAL ANATOMY AND HISTOLOGY OF THE HEART

The heart lies mainly in the lower part of left side of the chest It is normally oriented so that the ventricles point diagonally downwards away from the atria which lie close to the midline.

I.2 THE ELECTRICAL ACTIVITY OF THE HEART


I.2.1 CHARACTERISTICS OF A RESTING VENTRICULAR MUSCLE CELL (Concentrations in mEq/L) ECF ion IC ion Equilibrium Permeability concentration concentration potential 4 135 -94 mV high 145 10 +70 mV low 2 10-4 +132 mV low

K+ Na+ Ca2+

MEMBRANE CHANNELS Ungated Potassium Channels Always open and unless the membrane potential reaches the potassium equilibrium potential (-94 mV), a potassium flux (efflux) continues through these channels.

Voltage-gated (- Dependent) Sodium Channels Closed under resting conditions. Membrane depolarisation is the signal that causes these channels to quickly open and then close.
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Because they open and close quickly, they are sometimes referred to as the fast channels. These channels have the same characteristics as the voltage-gated (VG) sodium channels in the neuron axon. Once closed, they will not respond to a second stimulus until the cell repolarises.

Voltage-gated(VG) Calcium Channels Closed under resting conditions. Depolarisation is the signal that causes these channels to open, but they open more slowly than the sodium channels. Consequently, they are sometimes called the slow channels, because they allow sodium as well as calcium to pass, the slow calcium-sodium channel (as an appropriate terminology). The calcium entering the cell through these channels will participate in contraction and will also be involved in the release of additional calcium from the sarcoplasmic reticulum. If the fast Ca2+channels fail to open, depolarisation occurs via the entrance of calcium through these channels.

Voltage-Gated Potassium Channels Open under resting conditions. Depolarisation is the signal to close these channels. They will be closing during the depolarisation phase and will be closed during the main part of the plateau phase. They begin to reopen during the latter part of the plateau phase and continue to reopen during repolarisation. Thus, potassium conductance o is exceptionally high under resting conditions, o decreases during depolarisation, o is at a minimum during the plateau phase, and o increases back toward the high resting level during repolarisation.

I.2.2 PRODUCTION OF PACEMAKER POTENTIAL AND ACTION POTENTIAL BY THE SA NODE PACEMAKER POTENTIALS

I.2.3 ACTION POTENTIAL OF A VENTRICULAR FIBRE (FAST RESPONSE)

Electrical Versus Mechanical Events (Excitation-contraction Coupling in Cardiac Muscle)

I.3 FUNCTIONAL ORGANISATION OF THE CONDUCTING SYSTEM

The intrinsic rate of AP generation is fastest in SA node & slowest in BOH. Conduction velocity is fastest in Purkinje system & slowest in AV node.

The Heart and Its Electrical Conducting System


Time Taken for Impulse Through Different Tissue

SA node 0.03 sec AV node 0.16 sec Bundle branches 0.19 sec Purkinje fibers 0.22sec Endocardial and epicardial surface of ventricles

Ventricular Depolarisation Proceeds from endocardium to epicardium. The duration of the action potential of myocytes near the endocardium is longer than that of outer myocytes. As a result, the outermost cells repolarise1st and EC current flow towards V3-V6, which thus record a positive deflection (T wave). Ventricular Repolarisation Proceeds from epicardium to endocardium. When cardiac cycle is completed, no myocytes are depolarised and ECG returns to baseline (isoelectric line).
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Sequence of Cardiac Excitation

Conduction Pathways and Velocity of Conduction Pathway Sequential spread of action potential from SA node (delay) Purkinje fibres ventricular muscle

atrial muscle

AV node

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I.4 BACKGROUND OF ECG Normally, the chambers of the heart beat in an ordered sequence. The heartbeat occurs in response to electrical excitation of muscle fibres by propagated action potentials. The origin of propagated action potentials is the dominant pacemaker of the heartnormally the SA node of the right atrium. These electrical waves are transmitted via the conducting system of the heart to contracting muscle fibres. Excitation, then, contraction, of the atria (atrial systole) is followed by excitation, then contraction, of the ventricles (ventricular systole). Between these electrical events, and during diastole, all 4 chambers are relaxed. Because our body fluids are good electrical conductors, the algebraic sum of action currents from excited cardiac muscle fibres can be recorded as voltage signals on the surface of the body. In a volume conductor of these small currents, voltage difference may be derived by electronically subtracting voltage signals from 2, strategically positioned, electrodes on the body surface and, therefore, displaying these differences as an ECG. When voltage signals are recorded from arms and leg, the limb act as linear conductor connected to volume conductor.

Normal spread of electrical activity in the heart

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II. HISTORICAL BACKGROUND OF ECG British physiologist, Augustus D. Waller was the pioneer of Electrocardiography and in 1887 published the first human Electrocardiogram. In 1942, the Noble prize in Physiology / Medicine was awarded to a Dutch physiologist, William Einthoven, who transformed the electrocardiogram into clinical recording device that is still used today.

II.1 NATURE OF ECG The record of the potential fluctuations during the cardiac cycle is called electrocardiography.
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The machine used to record these potential fluctuations is called Electrocardiograph (sensitive galvanometer). It has electrical filters that reduce the electrical noise. The recording produced by this non-invasive procedure is termed an electrocardiogram (also ECG or EKG- German word = Elektro-kardiographie). Moving limbs, breathing, coughing, shivering, and faulty contact between the skin and the electrode produce artifacts on the recorded ECG.

ECG is a transthoracic (across the thorax or chest) interpretation of the electrical activity of the heart over a period of time, as detected by electrodes attached to the surface of the skin and recorded by a device external to the body (Not a direct recording of actual electrical activity of heart). ECG recording represent overall spread of activity throughout heart during depolarisation & repolarisation. (Not a recording of a single action potential in a single cell at a single point of time). ECG refers to extracellular recording of the summed-up electrical events of all the cardiac muscle fibres generated with each heart beat. ECG is the surface recording of the potential difference (algebraic sum of electrical currents and potential) detected by electrodes placed on the body surface (called leads). It requires special amplifiers. Such detection is possible because body fluids contain electrolytes and therefore, are good conductors of electricity (i.e. the body acts are a volume conductor). ECG recording represents comparison in voltage detected by electrodes at different points on the body (Not the action potential). Because the movement of charge (i.e. the spreading wave of electrical activity of the heart) has both a three- dimensional direction and magnitude, the signal measured on the ECG is a vector. The system that clinicians use to measure the hearts 3-dimensional, time-dependent electrical vector is simple to understand and easy to implement, but it can be challenging to interpret. The continuous electrical in the heart alternating between depolarisation and repolarisation in all parts of the heart following transmission of impulses. Electrically heart behaves as a dipole, i.e. two terminal batteries in which the excited part (depolarised segment) forms a negative and non-excited forms the positive pole.

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++++++++++++++++++++++ + + + + + + + + + + + + + + ++ + + + + - - - -- - -- - - + + + + + + + + + + + ++ + + + + + + + + + + ++ + + + + + + + + + + ++ + + + ++ + + + + ++++++++++++ + + + + + + + + + + + ++ + + + + + + + + + + +

Depolarised segment

Non-excited segment

The Heart as a Dipole

Current flowing towards an electrode gives a positive deflection


++

Current flowing at right angles to an electrode gives no deflection

---

Current flowing away from an electrode gives negative deflection

II. 2 USES OF ECG Electrocardiography (ECG or EKG) is used for detection, monitoring, confirmation of heart rate (both atrial & ventricular) heart rhythm (regularity of heartbeats) site of origin and conduction of cardiac impulses (sinus, atrial, junctional / ventricular, accelerated, delayed or blocked; site of defect) changes in myocardial perfusion (ischemia), structure (infarction, hypertrophy) or function (ventricular fibrillation, cardiac arrest). changes in plasma electrolytes (K+, Ca2+) (K+ changes influences repolarisation, producing very tall slender peaked T waves in hyperkalaemia, and ST segment depression and prominent U waves in hypokalaemia). other systemic disorders the effects of drugs or devices used to regulate the heart, such as a pacemaker.
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III. HOW TO PERFORM ECG (RECORDING OF ECG)

The 4th electrode, connected to the right leg, is used for electrical grounding. RECORDING OF ECG ECG is constructed as a system of leads in two planes that are perpendicular to each other. 1. 6 limb leads (I, II, III, aVR, aVL, aVF) view the heart in vertical plane. 2. 6 precordial/chest leads (V1- V6) view the heart in horizontal plane. 3. Anatomical relationships: o leads II, III, and aVF view the inferior surface of the heart; o leads V1 to V4 view the anterior surface; o leads I, aVL, V5, and V6 view the lateral surface; and o leads V1 and aVR look through the right atrium directly into the cavity of the left ventricle. Each lead is an axis in one of the two planes, onto which the heart projects its electrical activity. ECG recording from a single lead shows how that lead views the time-dependent changes in voltage of the heart. ECG Recording Electrodes (LEADS) ECG leads have different viewpoints of the hearts electrical activity. ECG leads refer to the 2 electrodes which are placed on the body surface and connected to ECG machine for measuring the potential fluctuations between only 2 points. In a lead one electrode is treated as the positive side of a voltmeter and the other one or more electrodes as the negative side. Therefore, a lead records the fluctuation in voltage difference between positive and negative electrodes. By variation of which electrodes are positive and which are negative, a standard 12lead ECG is recorded.
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Each lead looks from a unique angle and plane, i. e. from what is essentially its own unique point of view. ECG is recorded using 2 types of leads (12-lead ECG) o The bipolar leads o Unipolar leads ECG leads record the fluctuation in difference between positive & negative electrodes. Purpose Record electrical difference between 2 electrodes One electrodeactive/exploring/+ve terminal Next electrodeindifferent/zero/negative terminal connecting two other limbs. Recording Electrodes Negative & positive (Both active) aVR
+ve = Right arm -ve = LA + LF

ECG Leads Bipolar

Unipolar

Type of Leads Standard limb leads LI, II, III Limb leads aVR (cavity
of ventricles, 150),

View/ Plane Vertical / Frontal Vertical / Frontal

aVL
+ve = Left arm -ve = RA + LF

aVL (lateral
surface of ventricles, 30),

aVF
+ve = Left foot -ve = LA + RA

aVF (inferior
surface of ventricles, +90)

+ve to one of the 6 different location on chest wall. -ve to o middle of chest o average of 3 limb electrodes

Chest leads V1 V6 ( V7 V9 in special cases)

Transverse/ Horizontal

Normal ECG waves P wave = 0 - + 75 QRS complex = -30 - + 90 T wave = Tangle < 45 Frontal < 60 Precordial 1.BIPOLAR LEADS These record the potential difference between 2 active electrodes. In each bipolar recording, both the electrodes are activeo one of the active electrode is connected to negative terminal of the ECG
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machine and o the other active electrode is connective to the positive terminal. Current flowing towards the positive electrode produces an upward deflection on the ECG. Clinically, 3 bipolar leads are used. Standard limb Leads (3 limb leads) Limb leads look at the heart in a vertical plane. Three standard limb leads used in bipolar recording are based on Einthovens hypothesis that the body is like an electrically homogenous plate in which the right and left shoulders and the pubic region form the corners of an equilateral triangle with heart in its centre (EINTHOVENS TRIANGLE)

Einthoven law states that: The sum of the potentials at the points of an equilateral triangle (LA, RA, and LF) with a current source (heart) in the centre is zero at all times. If the electrical potentials of any two of the three bipolar limb ECG leads are known at any given instant, the third one can be determined mathematically from the first two by simply summation the first two. (Note: the positive and negative signs of different leads must be observed when making this summation= Voltage lead I + voltage lead III = voltage lead II) That 2 active electrodes need to be placed at 2 corners of this triangle. But for conveniences the electrodes are connected to the left are (LA), right arm (RA) and left foot (LF) instead of the shoulders and the pubic region (Figures below). Practically, it does not make any difference whether the electrodes are placed in proximal or distal part of the extremities; because the current flows in the body fluids and so the records obtained are similar. These record the potential difference between 2 limbs. If these electrodes are connected to a common terminal, an indifferent electrode that stays near zero potential is obtained. This is because in a volume conductor, the sum of the potentials at the points of an equilateral triangle (LA, RA, and LA) with a current source (the heart) in the centre is zero at all times (Einthovens triangle). In 3 standard limb leads, the 2 active electrodes are connected as Lead + ve electrode -ve electrode RA= LA RA RA = LF RA LA= LF LA Defines an axis in the frontal plane at 0 (degree) + 60 (degrees) + 120 (degrees)

I II III

Left arm (LA) Left foot (LF) left Leg (LL) Left leg (LL) (LF)

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Normal Left axis deviation

30 to Normal 90

Normal

Left axis deviation is considered 30 to May indicate left anterior fascicular normal in pregnant women and 90 block or Q waves from inferior MI. those with emphysema. May indicate left posterior Right deviation is considered Right axis +90 to fascicular block, Q waves from normal in children and is a deviation +180 high lateral MI, or a right standard effect of dextrocardia. ventricular strain pattern Extreme right +180 Is rare, and considered an electrical axis deviation to 90 no-mans land

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Right leg (usually black) = earth lead

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2. UNIPOLAR LEADS In unipolar recording, 1 electrode is active (exploring electrode)- placed on a chosen site linked with and the other electrode- called indifferent electrodeat zero potential. One being zero, the potential difference between the two represents the actual local potential (potential flutuations occuring at the site of exploring electrode). In a volume conductor, the sum potentials at the points of an equilateral triangle with a current source at the center is zero at all times. Therefore, if the 3 electrodes (placed on left arm, right arm and on the left leg) are connected to a common terminal, through a resistance, an indifferent electrode that stays near zero potential is obtained. In clinical ECG, 2 types of unipolar leads are used. 2.1 Unipolar limb Leads 2.2 Unipolar chest Leads They (aVR, aVL, aVK, V1-V6) are called V leads because record values approching meaningful voltages.

2.1 Unipolar limb Leads (3 leads) These include VR (Right arm), VL (Left arm), VF (Left leg).

Lead Exploring electrode VR Right arm VL Left arm VF Left foot The exploring electrode is connected to the positive terminal of ECG. The indifferent electrode is placed over a limb and is connected to the negative terminal of ECG. These leads are not used and have been replaced by augmented limb leads aVR, aVL, aVF When the amplitude of deflection in increased (a= augmented) Augmented Unipolar limb Leads Generally the augmented unipolar limb leads designated as aVR, aVL, aVF are used. In augmented leads, the size of the potential is increased by 50% without any change in configuration from the non-augmented record. The active electrode is from one of the limbs, and the indifferent electrode is obtained by connecting the other 2 limbs. (Recordings between one limb and the other two limbs). Lead Leads aVR aVL aVF Exploring electrode Indifferent electrode (+ve electrode)* Right arm (usually red) LA + LF Left arm (usually yellow) Left foot (usually green) RA + LF RA + LA Defines axis in Frontal plane - 150 - 30 + 90

*(Negative electrode connection is electrotonically defined in the middle of the heart)


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Direction of augmented limb leads in vertical plane, and their orientation to the heart and the cardiac vector in the centre of the triangle; aVR- Lead reflects the activity of the cavity of the ventricles,irrespective of the position of the heart. - P wave, QRS complex, T wave are negative deflection. aVL Lead reflects the electrical activity of left lateral surface of the heart- (formed by the left ventricle) - Like that of V6, QRS is predominately positive aVF Lead reflects the electrical activity of the inferior surface of the heart (formed by left ventricles and interventricular septum) - Like that of V3 & V4, QRS complex is predominantly biphasic.

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2.2 Unipolar Chest Leads (Precordial Leads) They lie in the transverse plane, perpendicular to the plane of frontal leads (look at the heart in a horizontal plane). o The positive connection is one of the six different locations on the chest wall, o The negative connection is electrotonically defined in the middle of the heart by averaging of the 3 limb electrodes. The resultant leads are named V1 to V6

V1 V2 V3 V4 V5 V6 (V7

4th intercostals space (ICS), right sterna border/margin 4th intercostals space (ICS), left sterna border/margin Equidistant between V2 and V3 5th ICS, mid clavicular line 5th ICS, anterior axillary line 5th ICS, midaxillary line 5th ICS, posterior axillary line so forth up to V9) for posterior MI
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A Standard 12-lead ECG V1 & V2 Reflects right ventricular activity: The main QRS complex is negative V3 & V4 Reflects activity of Interventricular septum and anterior wall of the left ventricle: The main QRS complex is biphasic V5 & V6 Reflects avtivity of Anterior and lateral walls of the left ventricle: The main QRS complex is positive R wave Gradually increases in size from V1 to V6 leads. in V1- R wave represents activity of right ventricle V6- R wave represents activity of left ventricle S wave- Gradually decreases in size from lead V1 to V6. in V1- S wave represents activity of left ventricle V6- S wave represents activity of right ventricle
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Red - 4th intercostals space (ICS), right sterna margin (V1) Yellow- 4th (ICS), left sterna margin (V2) Green - Between yellow & brown (V3) Brown Anatomical position apex of the heart- 5th ICS (V4) Black - 5th ICS, anterior axillary line (V5) Purple - 5th ICS, mid axillary line (V6)

CARDIAC AXIS (VECTOR) of a wave Cardiac axis refers to mean direction of the wave of ventricular depolarization in the vertical plane, measured from zero reference point. The zero reference = same viewpoint as lead I. An axis above line is negative number, and axis below line is positive number. The normal range for cardiac axis is between 30 and 90. An axis <-30 is termed left axis deviation, whereas an axis >90 is termed right axis deviation. It is the determination of magnitude & direction (arrow) of current flow (potential generated) through the heart. By convention, the arrow head points towards the direction & length of the arrow is drawn proportional to the voltage of the potential. During most of the cycle of ventricular depolarisation direction of electrical potential (negative to positive) is from the base of the ventricles towards the apex. This preponderant direction of potential during depolarisation is called the mean QRS vector (mean electrical axis of the heart) and is drawn through the centre of the ventricles in a direction from the base of the heart toward the apex. The instant vector represents the magnitude and direction of potential at a particular instant during the cardiac cycle. The instantaneous vector of 5 different instants during the process (sequence) of ventricular depolarisation is shown below.
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It refers to the overall direction of the wave of ventricular depolarisation in the vertical plane measured from a zero reference point. The normal range of axis of ventricular depolarisation in the frontal plane (cardiac axis) is between -30 and + 90.

Lead Axis () The electrode lies in plane I 0 Horizontal direction II 60 Horizontal III aVF 120 90

Positive electrode

Negative electrode

Algebraic sum

Left arm Left leg

Right arm Right arm Left arm Indifferent electrode RA + LA LA + LF RA + LF

Q (-3), R (+13),S (-5) = -3+13 -5 = 5 mV Q (-1), R (+15), S (-0) = -1 +15 0 = + 14 mV

Horizontal Left leg Vertical Left leg

aVR aVL

210 -30

Vertical Vertical

Right arm Left arm

Sequence of ventricular depolarisation

QRS Axis
There are many ways to determine QRS axis. The one described below combines simplicity and efficiency.

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The limits of normal and abnormal QRS axis are summarized in the diagram to the right.

QRS axis is the direction in which the mean QRS current flows. The normal axis points mostly downward and to the left because the more muscular left ventricle generates a stronger depolarizing current that overwhelms that generated by the less bulky right. Although both right axis deviation (RAD) and left axis deviation (LAD) are not necessarily associated with organic heart disease, they are seen in a number of settings and their presence can provide added evidence to support a clinical diagnosis. RAD is seen in right ventricular (RV) hypertrophy and in infarction involving the left ventricle (LV). Right ventricular muscle bulk is relatively larger than that of the left in both conditions and generates a stronger depolarizing current in its direction.

LAD is seen, but not always, in patients with left ventricular hypertrophy. More commonly the QRS axis is horizontal in this condition.

It is only necessary to examine the QRS complexes in leads I and II to determine whether the QRS axis in normal or deviated to the left or the right; a precise calculation of the QRS axis is not required in clinical interpretation of the ECG. It has been explained in a previous section that a current flowing in the direction of a recording electrode (an ECG lead) registers a positive deflection and a current flowing away registers a negative deflection.

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Therefore, the QRS in lead I would be positive if the QRS current flows in the direction of lead I and negative if away. Similarly the QRS in lead II would be positive if the QRS axis points in the direction of lead II and negative if away. By overlapping the two circles representing leads I and II, it can be seen that the QRS axis is between +90o and -30o and normal if the QRS is positive both in lead I and lead II.

QRS axis is between -30o and -90o or deviated to the left (left axis deviation or LAD) if the QRS is positive in lead I but negative in lead II.

QRS axis is between +90o and +150o or deviated to the right (right axis deviation or RAD) if the QRS is negative in lead I but positive in lead II.

On occasions the QRS complexes in all 6 limb leads are biphasic, neither positive nor negative. In these instances the QRS axis is said to be indeterminate.

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In summary:

Normal QRS axis.

Left axis deviation

Right axis deviation

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TO CALCULATE CARDIAC AXIS, The simplest method is inspection of leads I, II, and III.

Conditions for which determination of the axis is helpful in diagnosis


Conduction defects for example, left anterior hemiblock Ventricular enlargement for example, right ventricular hypertrophy Broad complex tachycardia for example, bizarre axis suggestive of ventricular origin Congenital heart disease for example, atrial septal defects Pre-excited conductionfor example, Wolff-Parkinson-White syndrome

Pulmonary embolus A more accurate estimate of axis achieved if all six limb leads examined. The direction of current flow is towards leads with a positive deflection, away from leads with a negative deflection, and at 90 to a lead with an equiphasic QRS complex. The axis is determined as follows: Choose the limb lead closest to being equiphasic. The axis lies about 90 to right or left of this lead Inspect QRS complexes in leads adjacent to equiphasic lead. If lead to the left is positive, then axis is 90 to the equiphasic lead towards the left. If the lead to the right side is positive, then the axis is 90 to the equiphasic lead towards the right. Schematic diagram used to determine the direction of electrical changes in the six limb leads on an ECG However, this axis can change in a number of pathological situations, including o hypertrophy of one or both ventricular walls (a common sequel of prolonged hypertension) o conducting blocks in one or several of the ventricular conducting pathways. Mean Electrical Axis o The mean electrical axis of the ventricles describes the net direction of current movement during ventricular depolarisation. o It is affected by a number of factors, including the position of the heart, heart mass, and conduction time. o It can be calculated by summing the depolarisation during the QRS complex in any two leads. The axis is normal if leads I and II are positive. A simple method to calculate the axis is by inspection of the QRS complex in leads I, II, III. An axis more negative than -30 is termed left axis deviation. An axis more positive than +90 is termed right axis deviation.

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DETERMINATION OF QRS COMPLEX FROM ECG QRS complex

Direction of depolarization (vector) of the QRS complex 1. The left ventricle is thicker so the mean QRS vector is down and to the left. (The origin of the vector is the AV node with the left ventricle being down and to the left of this). 2. The vector will point toward hypertrophy (thickened wall) and away from the infarct (electrically dead area).

Figure: Axis nomenclature. Normal axis Left axis deviation Right axis deviation -30 to +90 degrees -30 to -90 degrees +90 to +/-180 degrees

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Indeterminate (extreme) axis deviation -90 to +/-180 degrees Since lead I and aVF are perpendicular to each other, you can use those two leads to quickly determine axis. Lead I runs from right to left across a patient's body, positive at the left hand:

If the QRS in lead I is positive (mainly above the baseline), the direction of depolarization will be in the positive half (right half) of the circle above.

Lead aVF runs from top to bottom across a patient's body, positive at the feet:

If the QRS in lead aVF is positive (mainly above the baseline), the direction of depolarization will be in the positive half (lower half) of the circle above.

To find the axis overlap the two circles. The common shaded area is the quadrant in which the axis lies. In this example, the axis lies in the normal quadrant, which on a patient, points down and to the left.

You can repeat this process for any two leads, but I and aVF are the classic places to look. If you realize that there are two leads to consider and a positive (+) or (-) orientation for each lead, there would be four possible combinations. Memorize the following axis guidelines.

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Lead I 1. Normal axis (0 to +90 degrees)

Lead aVF

Positive Positive

2. Left axis deviation (-30 to -90) Also check lead II. To be true left axis deviation, it should also be Positive Negative down in lead II. If the QRS is upright in II, the axis is still normal (0 to -30). 3. Right axis deviation (+90 to +180) 4. Indeterminate axis (-90 to -180) Negative Positive Negative Negative

Figure: Normal axis

Figure: Left axis deviation

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Figure: Right axis deviation. The bottom line is, if the axis is shifted out of the normal quadrant, evaluate the reasons for this. Differential Diagnosis Left axis deviation LVH, left anterior fascicular block, inferior wall MI Right axis deviation RVH, left posterior fascicular block, lateral wall MI

The electrical axis represents the average direction of the total force produced by the right and left ventricular depolarization. A three step process can be used when determining axis: 1. Out of leads I, II, III, aVF, AVL, AVR, determine which lead is has roughly equal amplitude of positive and negative deflections. This is the "isoelectric" lead. 2. Find the lead that is perpendicular to this isoelectric lead. 3. Identify the direction of the QRS axis in the lead identified in step 2. If the QRS deflection is positive, then the axis is the same as the positive pole of that lead. If negative, then the axis is the same as the negative pole.

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The normal axis is generally between -30 and +90 degrees. Right axis deviation is defined as axis located between 90 degrees and 180 degrees. Left axis deviation is defined as the axis located between -30 degrees and -90 degrees. Indeterminate (or extreme) axis deviation is defined as an axis in the arc between 180 to -90 degrees.

Another quick way to approximate the axis is to look first at leads I and aVF. The following table can be used to determine the axis rapidly although this method is not as rigorous as above.

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Right Axis Deviation

Right Axis Deviation

Definition
QRS axis between + 90 and + 180 degrees

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Right axis deviation: +90 to +180 degrees

How to recognise right axis deviation (RAD)


QRS is positive (dominant R wave) in leads III and aVF QRS is negative (dominant S wave) in leads I and aVL

Right axis deviation: leads III and aVF are positive; leads I and aVL are negative

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Causes of RAD

Left posterior fascicular block Lateral myocardial infarction Right ventricular hypertrophy Acute lung disease (e.g. PE) Chronic lung disease (e.g. COPD) Ventricular ectopy Hyperkalaemia Sodium-channel blocker toxicity WPW syndrome Normal in children or thin adults with a horizontally positioned heart

Left Axis Deviation

Left ventricular hypertrophy

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Left Axis Deviation


Definition

QRS axis between -30 and -90 degrees

Left axis deviation: -30 to -90 degrees

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How to recognise left axis deviation (LAD)


QRS is positive (dominant R wave) in leads I and aVL QRS is negative (dominant S wave) in leads II and aVF

Left Axis Deviation: leads I and aVL are positive; leads II and aVF are negative

Causes of left axis deviation (LAD)


Left anterior fascicular block Left bundle branch block Left ventricular hypertrophy Inferior MI Ventricular ectopy Paced rhythm Wolff-Parkinson White syndrome

LEFT AXIS DEVIATION (LAD) is said to be present when the MEA lies between -30 and - 90 (or 2 and 12 Oclock). Lead I is positive and lead II and III negative.

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Left axis deviation

Causes of left axis deviation:


A block of the anterior bundle of the main left bundle conducting system. Normal variation (physiologic, often with age) Mechanical shifts, such as expiration, high diaphragm (pregnancy, ascites, abdominal tumour) Left ventricular hypertrophy
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Left bundle branch block Left anterior fascicular block Wolff-Parkinson-White syndrome Congenital heart disease (e.g. atrial septal defect) Emphysema Hyperkalaemia Ventricular ectopic rhythms Preexcitation syndromes Anterolateral myocardial infarction Inferior myocardial infarction Obesity Pacemaker rhythm

Left Atrial Enlargement AKA: Left atrial hypertrophy, left atrial abnormality. Background Left atrial enlargement (LAE) is due to pressure or volume overload of the left atrium. It is often a precursor to atrial fibrillation. Electrocardiographic Criteria LAE produces a broad, bifid P wave in lead II (P mitrale) and enlarges the terminal negative portion of the P wave in V1. Diagnostic criteria are as follows: In lead II Bifid P wave with > 40 ms between the two peaks Total P wave duration > 110 ms In V1 Biphasic P wave with terminal negative portion > 40 ms duration Biphasic P wave with terminal negative portion > 1mm deep Causes In isolation: Classically seen with mitral stenosis In association with left ventricular hypertrophy: Systemic hypertension Aortic stenosis Mitral incompetence Hypertrophic cardiomyopathy
Examples

Broad (>110ms), bifid P wave in lead II (P mitrale) with > 40ms between the peaks

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P wave terminal portion > 40 ms duration in V1

P waves with terminal portion > 1mm

Right Atrial Enlargement


AKA: Right atrial hypertrophy, right atrial abnormality
Electrocardiographic Criteria

Right atrial enlargement produces a peaked P wave (P pulmonale) with amplitude: > 2.5 mm in the inferior leads (II, III and AVF) > 1.5 mm in V1 and V2 Causes of right atrial enlargement The principal cause is pulmonary hypertension due to: Chronic lung disease (cor pulmonale) Tricuspid stenosis Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot) Primary pulmonary hypertension
Examples

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Right atrial enlargement: P wave amplitude > 2.5mm in leads II, III and aVF

Right atrial enlargement: P wave amplitude > 1.5 mm in V2

RIGHT AXIS DEVIATION (RAD) is said to be present when the mean electrical axis (MEA) lies between +120 and + 180 (7 & 9 Oclock position). Lead 1 is negative and lead III positive.

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Right axis deviation

Causes of right axis deviation:

Normal variation (vertical heart with an axis of 90)


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Mechanical shifts, such as inspiration and emphysema Right ventricular hypertrophy secondary to chronic lung disease or pulmonary valve stenosis. Right bundle branch block causing delayed activation of the right ventricle Left posterior fascicular block Dextrocardia Ventricular ectopic rhythms Wolff-Parkinson-White syndrome Preexcitation syndromes Posterior (or inferior) myocardial infarction Lateral wall myocardial infarction Right ventricular load, for example Pulmonary Embolism or Cor Pulmonale (as in COPD

Biatrial Enlargement
Definition Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG. The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement is summarised in the following diagram:

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Reproduced from Wagner et al. (2007)


Electrocardiographic Criteria

The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads. In lead II Bifid P wave with: Amplitude 2.5mm and Duration 120 ms In V1 Biphasic P waves with: Initial positive deflection 1.5mm tall and Terminal negative deflection 1mm deep and Terminal negative deflection 40 ms duration Combination criteria P wave positive deflection 1.5 mm in leads V1 or V2 and Notched P waves with duration >120 ms in limb leads, V5 or V6 Causes Combination of both left and right atrial enlargement. Right atrial enlargement Pulmonary hypertension due to: Chronic lung disease (cor pulmonale)
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Tricuspid stenosis Congenital heart disease (pulmonary stenosis, Tetralogy of Fallot) Primary pulmonary hypertension Left Atrial Enlargement Mitral valve disease Aortic valve disease Hypertension Aortic stenosis Mitral incompetence Hypertrophic cardiomyopathy (HOCM) Example ECGs Example 1

Biatrial enlargement due to idiopathic cardiomyopathy: Biphasic P waves in V1 with a very tall positive deflection (almost 3 mm in height!) and a negative deflection that is both deep (> 1 mm) and wide (> 40 ms). Example 2

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Biatrial enlargement: P waves in lead II are tall (> 2.5mm) and wide (> 120 ms). P waves in V2 are tall (> 1.5 mm), while the terminal negative portion of V1 is deep (> 1mm) and wide (> 40 ms).

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ELECTROCARDIOGRAPHIC CONVENTIONS Depolarisation moving towards the active electrode : Upward (positive ) deflection moving away from the active elective electrode : Downward (negative) deflection past a lead produces a +ve then a ve (equipolar) deflection

Vectors and view

Current flowing towards active electrode gives a positive deflection

Current flowing at right angles to active electrode gives no deflection

Current flowing away from an active electrode gives a negative deflection

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Current flowing at right angles to an electrode gives no deflectin Category Inferior leads' Colour on chart Yellow Leads Activity

Leads II, Look at electrical activity from the vantage point of the III and inferior surface (diaphragmatic surface of heart) aVF Look at the electrical activity from the vantage point of the lateral wall of left ventricle

Lateral leads

Green

I, aVL, V5 and V6

The positive electrode for leads I and aVL should be located distally on the left arm and because of which, leads I and aVL are sometimes referred to as the high lateral leads. Because the positive electrodes for leads V5 and V6 are on the patient's chest, they are sometimes referred to as the low lateral leads.

Septal leads Anterior leads

Orange Blue

V1 and V2 V3 and V4

Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum) Look at electrical activity from the vantage point of the anterior wall of the right and left ventricles (sternocostal surface of the heart)
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III. HOW TO PERFORM ECG An ECG can be done in a clinic, doctors office, or hospital It is a painless procedure that takes < 5 minutes. Small, sticky electrodes patches are placed on the patients chest, wrists and ankles. A special machine that records the electrical activity of the heart is connected to the patches by multiple wires. A recording is made and printed on paper for doctor to interpret. THE STEPS IN SETTING UP ECG MEASUREMENT 1. Prepare bed & bring ECG machine, wire, suction-end & electrode. 2. The patient must lie down and relax to avoid muscle tremor. 3. Place the 4 limb leads o Right anterior shoulder, just below the clavicle o Left anterior shoulder, just below the clavicle o Left leg o Right leg 4. Place the 6 precordial/chest electrodes 5. Connect up the electrodes 6. Calibrate the record with 1 mV signal & enter patients details 7. Record ECG 8. Remove the electrodes- clean gel on patient 9. Remove ECG paper & review/ show IV. INTERPRETING BASIC ECG A systematic approach to reading the 12-lead ECG should be practised so as to avoid missing data and making mistakes. The following or similar approach is advised: Check these data (patients name, birthday, and identification number; date and time of tracing)on the ECG to make sure: It belongs to the patient you are reviewing. It was obtained on the day and time you requested the examination. Review the patients medical history, physical and laboratory findings, diagnosis, and indication of the ECG examination. These pieces of information help to focus your attention when reviewing the tracing. However, to focus attention does not mean developing tunnel vision. You still should review all aspects of the ECG before drawing your conclusion. Make old tracings available for comparison. In medical practice, changes in findings over time are as important as the presence or absence of findings at any discrete moment in time. Check heart rate. Check rhythm: Primary rhythm: supraventricular (sinus, atrial, junctional) or ventricular in origin.
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Superimposed abnormalities (escape or premature beats). Check heart blocks. Check QRS axis. Check signs of clinical abnormalities: Right and left atrial abnormalities. Right and left ventricular hypertrophy. Right and left bundle branch block. Acute myocardial infarction. Electrolyte abnormalities. Drug effects. Pulmonary embolism. Correlate the ECG findings with the patients clinical presentation. Treat the patient; not the waveforms.

ELECTROCARDIOGRAPH The electrocardiograph (ECG machine) is essentially a sophisticated string galvanometer. A modern ECG amplifies and records the potential fluctuations on a moving strip of paper. The recording mechanisms used are o Some machines have a writing pen that records directly on the moving sheet of paper. o In other machines- instead of ink pen, special paper is used which turns black on

ECG Paper
ECG paper has a grid of small 1-mm square boxes and larger 5-mm square boxes. The vertical axis is calibrated at 0.1 mV/mm The horizontal (time axis) at 0.04 s/mm(small box) or 0.2 s /5mm (large box) Thus, 5 large boxes correspond to 1.0 second

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COMMON CONVENTIONS Sensitivity adjusted to: 1 mV causes a deflection of 10 mm (= 1 cm) (amplitude/ height/vertical) (y axis) (each mm represents 0.1 mV) Paper speed: 25 mm/s (x axis)

Vertical Horizontal (Amplitude) (Time axis) Each large square (= 5 small squares) (5 mm) 0.5 mV Each small square (1 mm) 0.1 mV 0.2 s (200 ms) 0.04 s (40ms)

A standard signal of 1 mV must move the stylus vertically 1 cm, that is, two large squares on ECG paper. 5 large boxes 1.0 second THE NORMAL ECG (EKG) The fluctuations in extracellular voltage recorded by each lead vary from fractions of a millivolt to several millivolts. These fluctuations are called waves and are named with letter of alphabet. o P wave represents atrial depolarisation of the right & left atrial muscle. o QRS complex represents depolarisation of ventricular muscle o T wave represents repolarisation of both ventricles o U wave (rarely seen) represents repolarisation of the papillary muscle The shape & magnitude of these waves are different in each lead because each lead views the electrical activity of the heart from a unique position in space.

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J POINT- Occurs at the end of QRS complex (S wave) - Represents end of depolarisation & start of repolarisation of ventricles (all parts of ventricles are depolarised).

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INTERVALS & SEGMENTS PR INTERVAL o Onset of P wave to start of QRS complex. o Represents AV conduction time (atrial depolarisation, AV nodal delay, BOH conduction to ventricles. o Duration: 0.12- 0. 21 s (3 5 small squares) depending on heart rate. QT INTERVAL o Start of Q wave to end of T wave. o Represents time taken for ventricular depolarisation & repolarisation (systolic time for ventricles) o Duration: 0.4 0.44 s QRS INTERVAL- Start of Q wave to end of S wave ST INTERVAL- End of S wave to end of T wave PR SEGNMENT End of T wave to start of QRS complex ST SEGMENT o Isoelectric period between end of S wave to beginning of T wave o Represents interval between ventricular depolarisation & ventricular repolarisation. o Duration: 0.32 s RR INTERVAL-Interval between 2 successive R waves (use in calculating atria rate) PP INTERVAL - Interval between 2 successive P waves(use in calculating vent.rate)

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The component of ECG waves was arbitrarily named P, Q, R, S and T in early days of electrophysiology. P and T waves are distinct entities, but the naming of QRS complex follows the following rules: o The 1st deflection of QRS complex id downward, it is called Q wave. o An upward deflection is always called R wave irrespective of whether it is preceded by a Q wave. o A negative deflection immediately following R wave is called S wave.

P wave

It is the positive (upright rounded) deflection. Normally it precedes QRS complex. It represents atrial depolarisation of the right & left atrial muscle (so also called atrial complex) It begins as the impulse spreads from the SA node across the atria. The duration of P wave (0.1 second) indicates the time taken for the impulse to spread throughout the atria (P wave duration indicates how long atrial depolarisation takes). Amplitude is from 0.1 0.12 mV (amplitude of P wave is a guide to the functional activity of atria.
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Because the impulse spreads from right to left and downwards, P wave is o upright in all leads (except in aVR where it is inverted). o Upright P wave in lead II and inverted P wave in aVR indicate sinus rhythm (i.e. SA node is the pacemaker) The magnitude of P wave is some guide to the functional activity of the atria.

Clinical significance: o Broad & notched (>0.12 s, i.e. 3 small squares) in left atrial enlargement (P mitrale e.g. mitral stenosis)

o Tall (0.5 mV)& peaked (> 2.5 mm) with normal duration in right atrial enlargement (P pulmonalee.g. pulmonary hypertension)(tricuspid stenosis)

o In atrial fibrillation p wave disappears and replaced by flutter or fibrillation waves (fine irregular oscillations).

o When the cardiac impulse arises from an ectopic pacemaker, the P wave is altered or even inverted. o Absent in sinoatrial block.
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Atrial fibrillation (AF) It is a complex arrhythmia characterised by both abnormal automatic firing and the presence of multiple interacting re-entry circuits looping around the atria. It is characterised by a totally irregular, rapid rate (350-500 beats/min) It is due to contraction of only small portion of the atrial musculature at one time because large portion of the atria are still in refractory period. Re-entry is more likely to occur in atria that are enlarged, or in which conduction is slow (as in many forms of heart disease). Appearance: ECG shows o normal but irregular QRS complexes and T waves o There is no P wave but the base line may show irregular fibrillation waves. o R-R interval is irregularly irregular Causes of AF (associated with enlargement or dilation of atria) o Coronary heart disease o Valvular heart disease (especially rheumatic mitral valve disease) o Hypertension o Sinoatrial disease o Alcohol excess o Hyperthyroidism o Cardiomyopathy o Congenital heart diseases o Chronic lung diseases o Pulmonary embolism o Pericardial disease o Idiopathic- in normal hearts (lone AF 20% of cases) Complications: Long-term fibrillation are frequently associated with enlarged atria secondary to AV valve disease.

PR interval It is measured from the start of P wave to the start of QRS complex (i.e. to the onset of Q wave if there is one, or to the onset of R wave if there is no Q wave. Actually it is PQ interval but Q wave is frequently absent therefore, it is called PR interval). It measures the AV conduction time (including the AV nodal delay) which measures o atrial depolarisation o AV nodal delay o conduction down the bundle of His to the ventricular myocardium. Duration: 0.12 0.21 s (3-5 small squares)(normal adults with normal heart rates) (depending on heart rate) It indicates how long it takes the action potential to conduct through the AV node before activating the ventricles. Clinical significance: Prolonged PR interval (> 0.22s) indicates AV conduction block. o First degree block PR interval between 0.2 0.3 s o Second degree block- PR interval increased 0.3 0.45 s

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The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad QRS and a slurred upstroke to the QRS complex, the delta wave.

J point It refers to the point on ECG which coincides with the end of depolarisation and start of repolarisation of ventricles, i.e. it occurs at the end of QRS complex. At this point since all parts of the ventricles are depolarised, so, no current is flowing around the heart. Therefore, at J point, the potential of ECG is exactly zero voltage.

QRS Complex QRS complex with

with QRS deflections

with QR deflections

with RS deflections

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with only R wave


with RSR deflections with QS wave

It represents depolarisation of ventricular muscle. R wave is an upward / first positive deflection of QRS. Q wave is a downward deflection preceding an R wave: normal Q waves are small & narrow; deep (> 2 mm), wide (> 1mm) Q wave (except in aVR and V1) indicate myocardial infarction. S wave is a downward/ first negative deflection following an R wave. In the routine 12 lead ECG, the manifestation of atrial repolarisation is submerged in QRS complex. QRS duration: the upper limit of is 0.10 s (normally < 0.08 s) QRS duration reveals how long it takes for the wave of depolarisation to spread throughout the ventricles (intraventricular conduction time). Amplitude of Q wave: is 0.1 0.2 mV R wave: 1.0 mV S wave: 0.4 mV Total QRS: 1.5 1.6 mV Clinical significance: QRS precordial leads are more than limb leads. Deep Q wave (> 0.2 mV) along with other changes is an important sign of myocardial infarction. A wide/ prolonged QRS complex (>0.10 s, 2.5 small squares) occurs if conduction is delayed, e.g. o with RBBB or LBBB o conduction through a pathway other than the right or left bundle branches e.g. impulse generated by abnormal focus of activity in the ventricles (ventricular ectopic) Tall R wave (> 1,3 mV) in ventricular hypertrophy. Low voltage QRS complex (total sum < 1.5 mV) seen in hypothyroidism - pericardial effusion.

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QT interval

It extends from the start of QRS complex to the end of T wave. It is primarily measure the total time taken for ventricular myocardium depolarization & repolarisation (which is dependent on heart rate- shorter at faster rates) (indicates total systolic time of ventricles) Duration: 0.4 0.44 s (QRS duration + ST segment duration)(QT interval is corrected for heart rate QTc). Prolonged > 0.45 s QTc = QT interval square root of PR interval (in seconds) It indicates how long the ventricles remain depolarized and is thus a rough measure of the duration of the overall ventricular action potential. Clinical significance: When QT interval is prolonged (Long QT syndrome) o may be congenital o may be acquired (hypokalaemia or hypomagnesaemia, drugs e.g. quinidine, sotalol, chlorpromazine) o Ischemia o Any conduction defect o It is associated with ventricular arrhythmias and sudden death
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Hypercalcemia and Hypocalcemia ECG signs of hypercalcemia and hypocalcemia may not be obvious even in patients who have deranged plasma calcium concentrations that are clinically significant. If they are present, hypercalcemia is associated with short QT interval (A) and hypocalcemia with long QT interval (B). Interval shortening or lengthening is mainly in the ST segment. QT segment gets shorter as the heart rate increases, reflecting the shorter action potentials that are observed at high rates.

T wave

represents repolarisation of both ventricles T wave normally is the last positive, dome shaped deflection, since repolarisation takes place in the reverse direction from depolarisation. Duration of T wave: 0.27 s Amplitude of T wave: 0.3 mV Clinical significance: o In old age- T wave is flattened. o Exercise- increases T wave amplitude in healthy hearts. o Hyperkalaemia: tall & peaked T wave o Myocardial ischemia/infarction inverted T wave

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T wave inversion

Some causes of inverted T waves


Smoking Anxiety Tachycardia, Haemorrhage & Shock Hypokalaemia, Pericarditis, MI (new & previous) Bundle branch block WPW syndrome

Changes in T wave

MYOCARDIAL INFARCTION Physiological basis of ECG changes in acute myocardial infarction (MI) Affected part of myocardium gets depolarised partly or completely but does not get repolarised rapidly injury current (from affected to unaffected part of myocardium) In acute MI Decline in resting membrane potential: o The ischemic necrosis of myocardial fibres results in breakdown of cell membrane producing K+ efflux & Na+ influx inside the infracted cells become less negative as compared to the unaffected area. o During ventricular diastole, the current flows into the infract from the unaffected area results in a depression of TQ segment in leads overlying the infracted area (recorded as ST elevation). Delayed depolarisation of infracted cells causes o the infracted area to be positive relative to the unaffected area. o Therefore current flows out of infarcted area into the unaffected area. Rapid repolarisation in infracted cells occurs rapidly as compared to unaffected area due to accelerated opening of K+ channels. o Because of the rapid repolarisation in the infarct, the membrane potential of the affected area becomes greater than that of the unaffected area. o Extracellularly, current therefore flows out of the infracted into the normal unaffected area.
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o This current flow toward electrodes over the injured area, causing increased positivity between the S and T waves of ECG. o Consequently, leads on the opposite side of the heart show ST segment depression. Hall mark of myocardial infarction o is ST segment elevation (> 1 mm above the isoelectric line) in leads overlying the area of early stages of myocardial infarction and with acute pericarditis. o ST segment depression (> 0.5 mm below the isoelectric line) in leads on the opposite side of the heart indicates myocardial ischemia - at a later stage, ST segment elevation becomes less pronounced as T wave inversion develops.

ST segment elevation

ST segment depression

Acute Myocardial Infarction

Acute myocardial infarction (MI) affects both ventricular depolarization (appearance of pathological Q waves) and repolarization (ST-T wave changes). Specific manifestations depend on whether the lesion is subendocardial or transmural in location.

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The ECG sign of subendocardial ischemia is ST segment depression (A). Depression is reversible if ischemia is only transient but depression persists if ischemia is severe enough to produce infarction. T wave inversion with or without ST segment depression (B) is sometimes seen but not ST segment elevation or Q wave. That is why subendocardial infarction is also called non-STelevation myocardial infarction (NSTEMI) and less commonly non-Q wave myocardial infarction. ST segment depression seen in subendocardial ischemia or infarction can take on different patterns: The most typical being horizontal or down-sloping depression. Up-sloping ST depression is less specific. In exercise stress tests, horizontal or down-sloping depression of 1 mm or more (A, B, & C) or up-sloping depression of the same magnitude 80 ms beyond the J point (D) is considered positive signs of ischemia. Up-sloping depression of less than 1 mm at 80 ms beyond the J point (E) is simply J point depression and not ST segment depression.

In transmural MI, ischemia in the subendocardium spreads to the epicardium and involves full thickness of the myocardium. In the acute phase, the ECG signs are ST segment elevation. The elevated ST segment may slope upward or be horizontal or dome-shape. Hyperacute (tall positive) T waves may precede ST segment elevation (A) or seen at the same time with ST elevation (B) during this acute phase.

Hours to days later during the evolving phase, pathological Q waves appear, the elevated ST segments return towards baseline, and the T waves become inverted.

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Q wave is normal if it is shallow and brief (A).

Q wave is pathological if it is wider than 40 ms or deeper than a third of the height of the entire QRS complex (B & C). Significant Q wave usually persists even after recovery.

Localization of myocardial infarction By way of their position, the 12 ECG leads can be used to distinguish myocardial infarction occurring in different regions of the heart. The chest leads cluster around the heart in the horizontal plane and look in from the front (V1 to V4) and from the left (V5 and V6); leads I and aVL also look in from the left while leads II, III, and aVF look in at the under surface.

Signs of anterior MI (grey area), territory supplied by the left anterior descending coronary artery (LAD), are seen in V1 to V4.

Signs of lateral MI (grey area), territory supplied by the left circumflex coronary artery (LC), are seen in leads I, aVL, V5 and V6.

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Signs of inferior MI (grey area), territory supplied by the right coronary artery (RCA), are seen in leads II, III, and aVF.

Signs of posterior MI on a 12-lead ECG are not the characteristic ST elevation and Q waves, which would be the case if there is a lead recording from the patients back. Since V1 and V2 are attached to the patients front, they will record changes reciprocal to changes seen from the back, which are ST depression and tall R waves. These uncharacteristic signs make the diagnosis of posterior MI difficult without heightened vigilance. Suffice it to say, pure posterior wall infarctions are rare. Most extend to involve the inferior wall or lateral wall and leads II, III, and aVF should be examined for characteristic signs of this extension in the former and leads I, aVL, V5 and V6 in the latter. MI in the presence of LBBB The presence of LBBB complicates the ECG diagnosis of acute MI. This is because LBBB alone can produce signs that may be confused with those of infarction: deep QS waves in the right chest leads and ST depression and T wave inversion in the left chest leads. Furthermore, the Q wave of left ventricular MI may be buried within the widened QRS complex. Therefore, the diagnosis of acute myocardial infarction should be made circumspectively in the presence of pre-existing LBBB. On the other hand, the appearance of new LBBB should be regarded as sign of acute MI until proven otherwise.

CHRONIC MI Physiological basis of ECG changes in old cases of myocardial infarction (MI) After days or weeks of infarction, the dead myocardium and scar tissue become electrically silent. Therefore, the affected area becomes negative relative to unaffected normal myocardium during systole, and it fails to contribute its share of positivity to ECG complexes. The occurance of Q wave in some leads (which normally lack) and depending of Q wave in other leads is one of the manifestations of this negativity. Localisation of area of MI 1. Myocardial myocardial infarction (MI) Leads showing changes of MI are lead I, aVL and V3 V5 Leads showing reciprocal changes are lead II, III and aVF 2. Posterior (inferior) MI Leads showing changes of MI are lead II, III, and aVF Leads showing reciprocal changes are lead I, aVR, aVL and V1 to V6
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3. Lateral MI Leads showing changes of MI are lead I, aVL, and V6 Leads showing reciprocal changes are lead II, III, aVF and V1 4. Septal MI Leads showing changes of MI are V1-V3

U wave (rarely seen) Configuration: it is a small/ low voltage round positive wave (after T wave & before P wave). Cause: It represents slow repolarisation of the papillary muscle (or of the intraventricular conducting system) Duration: When present 0.08s Amplitute: 0.2 mV It is most marked in lead V3. Significance: It is rarely seen normally. It because prominent in hypocalcaemia. NOTE: Since atrial repolarisation coincides ventricular depolarisation, so it is merged with QRS complex and thus not recorded as a separate wave. TP or UP interval (reference potential level) It is measured from the end of T wave to the beginning of P wave. It measures the diastolic period of the heart (the whole heart is in the resting polarized state and the record is isoelectric). Clinical significance: Variable TP interval indicates atrioventricular dissociation. P-P interval It is the interval between 2 successive P waves. Equal P-P intervals indicate rhythmic depolarisation of the atria.

ST segment

It is an isoelectric period between the end of QRS complex and beginning of T wave. It represents repolarisation of both ventricles Duration: 0.32 s Clinical significance: o Myocardial infarction- elevated ST segment o Current/ acute myocardial injury- ST segment shift Causes of ST segment elevation

Acute myocardial infarction Coronary vasospasm (Printzmetals angina)


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Pericarditis Benign early repolarisation Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm Brugada syndrome Ventricular paced rhythm

R-R interval The interval between an R wave and the next R wave Duration: 0.6 1.2 s It measures the heart (ventricular) rate (normal- 60- 100 bpm)

APPROACH FOR READING AN ECG 1. 2. 3. 4. 5. 6. 7. 8. Search for P waves Determine the relationship of P waves and QRS complexes. Identify pacemaker Measure the heart rates from different waves (e.g. P-P interval, R-R interval). Characterise QRS shape (i.e. narrow/ wide) Examine features of ST segment Estimate the mean QRS axis (and the axes of the other waves of interest) Examine the cardiac rhythm (e.g. look at a 20-to-30s ECG record from lead II

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IV.1 DETERMINATION OF HEART RATE IN ECG (Rate Interpretation) The usual paper speed is 25mm/sec: 1mm (small square) = 0.04 sec 5mm (big square) = 0.2 sec If a different paper speed is used, calculations will have to be modified appropriately. Calculate atrial and ventricular rates separately if they are different (e.g. complete heart block). There are multiple methods to estimate the rate: For regular rhythms: Rate = 300 / number of large squares in between each consecutive R wave (R-R). For very fast rhythms: Rate = 1500 / number of small squares in between each consecutive R wave (R-R). For slow or irregular rhythms: Rate = number of complexes on the rhythm strip x 6 (this gives the average rate over a ten-second period) DETERMINATION OF HEART RATE FROM THE ECG R-R Interval (Ventricular rate) P-P interval (Atrial rate) (in number of large boxes of 0.2 s) 1 2 3 4 5 6 Heart Rate (beats per minute) 300 150 100 75 60 50

Calculation 300/1 300/2 300/3 300/4 300/5 300/6

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Cardinal features of sinus rhythm


The P wave is upright in leads I and II Each P wave is usually followed by a QRS complex The heart rate is 60-99 beats/min

The machine reading can also be used and is usually correct however, it may occasionally

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be inaccurate in the presence of abnormal QRS/T-wave morphology, e.g. may count peaked T waves as QRS complexes or miss QRS complexes with reduced amplitude.
When irregular rhythm, rate calculated from rhythm strip. One second = 2.5 cm of trace. Heart rate / minute = the number of R waves in 10 seconds (namely, 25 cm of recording paper) and multiplying by 6.

Interpretation (adults)

60100beats/min o Normal >100beats/min o Tachycardia <60beats/min o Bradycardia

Normal Heart Rates in Children


Newborn: 110 150 bpm 2 years: 85 125 bpm 4 years: 75 115 bpm 6 years+: 60 100 bpm

Causes of Sinus Bradycardia (< 60 bpm) 1. MI 2. Structural SA node disease (sick sinus syndrome), or ischemia 3. Hypothermia 4. Increased vagal tone (due to vagal stimulation or drugs) 5. Hypothyroidism 6. Drugs- -blockers, digoxin, verapamil 7. raised intracranial pressure 8. Obstructive jaundice, and even in uremia Causes of Sinus Tachycardia (> 100 bpm) 1. Any cause of adrenergic stimulation (including anxiety, pain) 2. Thyrotoxicosis 3. Hypovolaemia 4. Vagolytic drugs (e.g. atropine) 5. Anaemia, pregnancy 6. Drugs- vasodilator drugs including many hypotensive agents, -agonists (bronchodilators) 7. Fever 8. Myocarditis 9. Heart failure 10. Pheochromocytoma
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IV.2 DETERMINATION OF HEART RHYTHM FROM ECG The determination of rhythm is more complex. When the heart follows the normal conducting pathway at a normal rate and in normal sequence- the rhythm is called normal sinus rhythm. The rhythm is best analysed by looking at a rhythm strip. On a 12 lead ECG this is usually a 0.10 second recording from Lead II. Confirm or corroborate any findings in this lead by checking the other leads. A longer rhythm strip, recorded perhaps recorded at a slower speed, may be helpful.

A useful 7 step approach to rhythm analysis is described. 1. Rate


Tachycardia or bradycardia? Normal rate is 60-100/min.

2. Pattern of QRS complexes


Regular or irregular? If irregular is it regularly irregular or irregularly irregular?

3. QRS morphology

Narrow complex sinus, atrial or junctional origin. Wide complex ventricular origin, or supraventricular with aberrant conduction.

4. P waves

Absent sinus arrest, atrial fibrillation Present morphology and PR interval may suggest sinus, atrial, junctional or even retrograde from the ventricles.

5. Relationship between P waves and QRS complexes


AV association (may be difficult to distinguish from isorhythmic dissociation) AV dissociation o complete atrial and ventricular activity is always independent. o incomplete intermittent capture.

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6. Onset and termination


Abrupt suggests re-entrant process. Gradual suggests increased automaticity.

7. Response to vagal manoeuvres

Vagal maneuvers are methods used to stimulate baroreceptors located in the internal carotid arteries and the aortic arch. Stimulation of these receptors results in reflex stimulation of the vagus nerve and release of acetylcholine. Acetylcholine slows conduction through the AV node, resulting in slowing of the heart rate.

Sinus tachycardia, ectopic atrial tachydysrhythmia gradual slowing during the vagal maneuvers, but resumes on cessation. AVNRT or AVRT abrupt termination or no response. Atrial fibrillation and atrial flutter gradual slowing during the manoeuvre. VT no response.

Differential Diagnosis

Narrow Complex (Supraventricular) Tachycardias Regular Atrial


Irregular

Sinus tachycardia Atrial tachycardia Atrial flutter Inappropriate sinus tachycardia Sinus node re-entrant tachycardia Atrioventricular re-entry tachycardia (AVRT) AV nodal re-entry tachycardia (AVNRT) Automatic junctional tachycardia

Atrial fibrillation Atrial flutter with variable block Multifocal atrial tachycardia

Atrioventricular

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AV nodal reentrant tachycardia Broad Complex Tachycardias Regular


Ventricular tachycardia Antidromic atrioventricular re-entry tachycardia (AVRT). Any regular supraventricular tachycardia with aberrant conduction e.g. due to bundle branch block, rate-related aberrancy.

Irregular

Ventricular fibrillation Polymorphic VT Torsades de Pointes AF with Wolff-Parkinson-White syndrome Any irregular supraventricular tachycardia with aberrant conduction e.g. due to bundle branch block, rate-related aberrancy.

Bradycardias P waves present Each P wave is followed by a QRS complex (= sinus node dysfunction)

Sinus bradycardia Sinus node exit block Sinus pause / arrest


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Not every P wave is followed by a QRS complex (= AV node dysfunction)


AV block: 2nd degree, Mobitz I (Wenckebachs phenomenon)) AV block: 2nd degree, Mobitz II AV block: 2nd degree, fixed ratio blocks (2:1, 3:1) AV block: 2nd degree, high grade AV block AV block: 3rd degree (complete heart block)

P waves absent Narrow complexes Junctional escape rhythm Broad complexes Ventricular escape rhythm Sinus Rhythm Sinus rhythm implies that the SA node is the pacemaker and normal sinus rhythm (NSR) is simply sinus rhythm with heart rate in the normal range of 60 100 beats/min. The P waves in sinus rhythm have normal axis and are positive in lead II and negative in lead aVR. The QRS width in sinus rhythm is normal because the ventricles are activated rapidly by impulses conducted down the His bundle and bundle branches.

In disease (e.g. sick sinus syndrome) the SA node can fail in its pacing function. If failure is brief and recovery is prompt, the result is only a missed beat (sinus pause). If recovery is delayed and no other focus assumes pacing function, cardiac arrest follows.

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Escape rhythms

An escape beat is a heart beat arising from an ectopic focus in the atria, the AV junction, or the ventricles when the sinus node fails in its role as a pacemaker or when the sinus impulse fails to be conducted to the ventricles as in complete heart block (see section on Heart Blocks below). The ectopic impulse in this instance is always late, appearing only after the next anticipated sinus beat fails to materialize. If the sinus node failure or heart block is only brief, the ectopic focus may generate only a single escape beat; if the sinus node failure or heart block is prolonged, the ectopic focus produces a rhythm of escape beats to assume full pacing function. This escape mechanism offers protection against total cardiac standstill in the event of sinus node failure or complete heart block Atrial escape

Atria escape, either in escape beat or escape rhythm, produces a P wave that has abnormal axis and looks different from the P wave produced by the sinus beat. However, depolarization spreads to the ventricles normally down the AV junction, the His bundle, and bundle branches. Therefore the QRS complex of the atrial escape beats looks exactly like the QRS complex of the sinus beat. The inherent rate of atrial escape rhythm is between 60 and 80 beats/min. Junctional escape

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In junctional (AV junctional) beat or rhythm the atrial depolarization current points cephalad and to the right, away from lead II and toward lead aVR. Therefore the P wave, if seen, would be negative in lead II and positive in lead aVR. However this P wave is usually buried by the QRS complex and not visible. On less common occasions when the P wave is visible, it may be either immediately before or immediately after the QRS complex. Since the impulse is conducted to the ventricles via the His bundle and bundle branches, the QRS complex of junctional beats is narrow and looks exactly like the QRS complex of the sinus beat. The inherent rate of junctional escape rhythm is 40 60 beats/min.

Ventricular escape

If the ventricular escape rhythm is the result of sinus node failure, no P wave of atrial contraction is seen as in the tracing above. If the ventricular escape rhythm is the result of 3rd degree (complete) heart block, the sinus node paces the atria independently and regular P waves unrelated to the ventricular escape beats can be seen. The inherent rate of ventricular escape rhythm is between 20 and 40 beats/min.

Premature Beats A premature beat also arises from an ectopic pacemaker: in the atria, the AV junction, or the ventricles. The non-sinus impulse is early, initiating a heart beat before the next anticipated sinus beat as its name implies. The reason the ectopic focus discharges a pacing impulse early in this instance is because the ectopic focus is irritable and competes with the sinus node.

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Atrial Premature Beat

Atrial premature beat (APB) arises from an irritable focus in one of the atria. It depolarizes the atria prematurely (premature to the next timely sinus beat) and produces a P wave that looks different from a sinus-node generated P wave because the direction in which the atria depolarize is abnormal (abnormal P wave axis). Since the premature atrial impulse is conducted in a normal fashion via the AV node, the His bundle, and the bundle branches to depolarize the ventricles, the QRS complex associated with an APB has normal QRS duration and the same morphology as that of the sinus beat.

Junctional Premature Beat

Junctional premature beat (JPB) arises from an irritable focus at the AV junction. The P wave associated with atrial depolarization in this instance is usually buried inside the QRS complex and not visible (see Junctional Escape above). However, the P wave may appear on occasions either immediately before or immediately after the QRS complex. When it is visible, the P wave is negative in lead II and positive in lead aVR because of retrograde atrial depolarization. Since the premature junctional impulse is conducted in a normal fashion down the His bundle and bundle branches to depolarize the ventricles, the QRS associated with JPB has normal duration and the same morphology as that of the sinus-node generated beat.

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Ventricular Premature Beat

Ventricular premature beat arises from an irritable focus in the ventricles. Ventricular premature impulse is not transmitted to the rest of the ventricles along the His bundle and bundle branches. t is conducted along abnormal pathway in the ventricular myocardium. This slow process produces an abnormally wide QRS and bizarre looking T wave. Being a ventricle-generated beat, there is no P wave activity before the QRS complex.

Tachycardias
If an ectopic focus discharges a premature impulse only occasionally, the result is premature beats superimposed on the basic rhythm; if the irritable focus generates 3 premature beat repeatedly in a continuous sequence, the result is ectopic tachycardia. The run is called non-sustained if it lasts up to 30 seconds and sustained if longer than 30 seconds. Tachycardias, other than sinus tachycardia, can be classified into supraventricular tachycardia (SVT) or ventricular tachycardia (VT), depending on their site of origin.

Supraventricular Tachycardia

Tachycardias arising from an ectopic focus in the atria or AV junction are called supraventricular tachycardias (SVT). Heart rate is faster than 150 per minute and commonly around 180 per minute. At this very fast heart rate, the P waves of atrial contraction are buried within the waves of the beats before irrespective of whether the tachycardia is of atrial or junctional origin. Differentiation of the two is not possible on the surface ECG and they are simply called paroxysmal supraventricular tachycardia (PSVT) because of their paroxysmal (sudden) onset. Since PSVT impulses depolarize the ventricles by passing down the His bundle and bundle branches, the accompanying QRS complexes are of normal width and have the same morphology as that of sinus beats.

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Atrial Flutter

In atrial flutter an atrial focus activates the atria at a rate of around 300 times per minute. The baseline of the ECG becomes all P waves, giving it a saw tooth appearance in one or more leads. Since it is unusual for the AV node to conduct impulses at a rate faster than 200 per minute, AV block occurs: commonly at a 2 to 1, 3 to 1, or 4 to 1 ratio, yielding a ventricular response rate of 150, 100, or 75 per minute respectively. (NB: When the ratio of P waves to QRS complex is 2:1, 3:1, or 4:1 it would be more correct to use the term 2:1, 3:1, or 4:1 conduction rather than block. To avoid confusion, some authors simply use the term 2:1, 3:1, or 4:1 flutter.) Since the atrial flutter impulses depolarize the ventricles by passing down the His bundle and bundle branches, the accompanying QRS complexes are normal in width and have the same morphology as that of sinus beats.

Atrial Fibrillation

Atrial fibrillation is one of the most common arrhythmias in which multiple foci in the atria depolarize rapidly and erratically at a combined rate of 400 times/min or more. Instead of generating well recognized P waves, the atria just quiver and produce fine f waves on the ECG baseline seen in one or more leads. The AV node is constantly bombarded by depolarization impulses but only some of these impulses manage to get through. The ventricular response is totally irregular without discernible pattern (irregularly irregular) generally at a rate between 110 and 180 beats/min. Since impulses that manage to pass through the AV node are conducted down the His Bundle and bundle branches, the ventricles are activated normally and their QRS complexes are normal in width and have the same morphology as that of sinus beats.

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Monomorphic Ventricular Tachycardia

Ventricular tachycardia (VT) arises from an irritable ventricular focus that discharges premature impulses for 3 or more beats without interruption. The rate of depolarization is 150/min or faster. Since these impulses are conducted to the rest of the ventricles via abnormal pathway in the ventricular myocardium and not via the His Bundle and bundle branches, the QRS complexes are broader than normal and without distinguishable T waves. In monomorphic VT, consecutive QRS complexes have the same appearance.

Polymorphic Ventricular Tachycardia


In polymorphic ventricular tachycardia, there is beat-to-beat variation in the QRS morphology. A common example is Torsades de Pointes (twisting of the points) shown below:

Ventricular Fibrillation

Ventricular fibrillation occurs when multiple ventricular foci discharge rapidly and chaotically. The ventricles twitch asynchronously and are not effective as pumps. No organized QRS complexes are seenjust disorganized oscillatory waves which can be coarse (as shown) or fine in appearance.
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Right and Left Atrial Abnormalities


(NB: Atrial abnormality is a term being used increasingly in place of atrial enlargement, atrial dilatation or atrial hypertrophy.) Look for signs of atrial abnormalities in leads in which the P wave is most prominent: usually lead II, but also leads III, aVF, and V1.

In sinus rhythm the right atrial depolarization wave (brown) precedes that of the left atrium (blue) and the combined depolarization waves, the P wave, is less than 120 ms wide and less than 2.5 mm high.

In right atrial abnormality, right atrial depolarization lasts longer than normal and its wave extends to the end of left atrial depolarization. Although the amplitude of the right atrial depolarization current remains unchanged, its peak now falls on top of that of the left atrial depolarization wave. As a result, the combined waves of right and left atrial depolarization, the P wave, is taller than normal (taller than 2.5 mm) but its width remains within 120 ms.

In left atrial abnormality left atrial depolarization lasts longer than normal but its amplitude remains unchanged. Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than120 ms. A notch (broken line) near its peak may or may not be present.

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A biphasic P wave in V1 is another sign suggesting atrial abnormality. In right atrial abnormality, the initial positive portion of the biphasic P wave is larger than the terminal negative portion.

A biphasic P wave in V1, with its terminal negative deflection more than 40 ms wide and more than 1 mm deep is another ECG sign of left atrial abnormality.

Right and Left Ventricular Hypertrophy


Look for signs of right and left ventricular hypertrophy in the right chest leads (V1 and V2) and left chest leads (V5 and V6). When the ventricles are normal, the QRS complexes across the chest leads of an ECG have these configurations: In right chest leads V1 and V2, the QRS complexes are predominantly negative with small R waves and relatively deep S waves because the more muscular left ventricle produces depolarization current flowing away from these leads. In left chest leads V5 and V6, the QRS complexes are predominantly positive with tall R waves because the more muscular left ventricle produces net current flowing towards these leads. The QRS complexes in V3 and V4 reflect a transition between the right and left chest leads. The normal transition zone, where the R wave and S wave are equal, is between V3 and V4. Early transition may appear in V2 while late transition may not appear until V5 or V6.

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In right ventricular hypertrophy (RVH), the configurations of the QRS complexes across the chest leads are changed: In V1 the QRS are positive with tall R waves. This is because increased right ventricular muscle mass causes the net ventricular depolarization current to move towards this right chest lead. R wavesthat are taller than S waves are deep in V1 are highly suggestive of RVH. The S waves are unusually deep in V6 and may be even deeper than the R wave is tall.

Other ECG signs of RVH include: Right axis deviation due to the overpowering current generated by a hypertrophied right ventricle. Ventricular repolarization changes manifest as downward sloping of the ST segment and T wave inversion, the so called ventricular strain pattern, may or may not be present in the right chest leads. (See V1 in above ECG.) P wave > 2.5 mm tall in lead II, III, aVF or biphasic P wave in V1 suggesting the presence of right atrial enlargement. (Right atrial abnormality results from the right atrium having to pump blood into a thick-wall non-compliant hypertrophied right ventricle.) In left ventricular hypertrophy (LVH), the configurations of the QRS complexes across the chest leads are also changed and consist of: Unusually tall R wave in left chest leads V5 and V6 and unusually prominent S wave in right chest leads V1 and V2. These are exaggerations of the normal configurations due to increase in left ventricular muscle mass. The sum of the S wave in V1 and the R wave in V5 or V6 is > 35 mm. (Tall R waves in chest leads is common among young and slender individuals. This finding alone should not be used as the only criteria of LVH.) Additional ECG signs of LVH include: R waves taller than 14 mm in lead I or taller than 11 mm in Lead aVL. However, tall R waves in limb leads and chest leads do not always coexist. Left axis deviation may or may not be present. Repolarization abnormalities of ST segment depression and T wave inversion suggesting
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ventricular strain may be present in the left chest leads with tall R waves. (See leads V5 and V6 in above ECG.) Signs of left atrial enlargement in leads II, III, aVF or V1 may be present. Left atrial abnormality is the result of having to pump blood into a muscular non-compliant left ventricle. Bundle Branch Blocks Look for signs of bundle branch block (BBB) in V1 and V6. In the absence of BBB, passage of the depolarizing impulse down the His bundle and bundle branches is rapid and activation of the right and left ventricles is simultaneous and synchronous. The individual QRS complexes of the right and the left ventricles superimpose on each other and produce a composite QRS complex that is narrow in width (< 120 ms). In BBB, irrespective of whether it is right or left, activation of the ventricles becomes asynchronous: Depolarization of the ventricle on the blocked side is delayed. This delay causes the individual QRS complex of the blocked ventricle to be wider than normal and appear after the individual QRS complex of the notblocked ventricle. As a result, the composite QRS complex is > 120 ms wide and has RSR waves: the R wave belongs to the individual QRS of the not-blocked ventricle and the R wave to the individual QRS of the blocked ventricle. The S wave between the R and R waves may be deep and falls below the baseline; it may not be so deep and causes a notch between the R and R waves only; or it may be hardly visible such that the QRS complex is simply a tall and wide R wave.

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In right bundle branch block (RBBB), the widened RR complex is seen most typically in V1. Secondary T wave inversion can also be seen in this lead because when depolarization is abnormal repolarization can also be expected to be abnormal. Since the late right ventricular depolarization current moves away from left chest leads, it shows up as wide S waves in V6. When there is an RR complex in V1 but it is less than 120 ms wide, the condition is called incomplete right bundle branch block.

In left bundle branch block (LBBB) the widened RR complex is seen most typically in V6. Secondary T wave inversion is present in the left but not right chest leads. Since the late left ventricular depolarization current moves away from the right chest leads, it shows up as deep and broad S waves in V1.

Bundle branch block or ventricular rhythm?


The QRS complexes are wider than normal in both BBB and ventricular rhythm. But the rhythm in BBB is supraventricular in origin. There is a one-to-one P wave to QRS relationship in BBB:

In sinus rhythm with 3rd degree heart block, there are regular P waves that are totally asynchronous with the QRS complexes, which represent escape rhythm from a ventricular focus.

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In ventricular rhythm with sinus arrest, only wide QRS complexes are seen and P waves are absent.

IV.3 DETERMINATION OF AXIS (VECTOR) INTERPRETATION FROM ECG Axis/ Vector Definition the mean direction of electrical forces in the frontal plane ( limb leads) as measured from the zero reference point (lead 1) Normal values o P wave: 0 to 75 degrees o QRS complex: -30 to + 90 degrees o T wave: QRS-T angle <45 degrees frontal or <60 degrees precordial Measurement Quick look tests The simplest method of identifying gross deviations in axis is to look at the QRS complexes in leads I and aVF. Lead I is a left-sided lead, and as aVF is perpendicular to lead I, it can be considered a right-sided lead. o Both leads I and aVF have mainly positive QRS complexes=normal axis. o Lead I is positive and aVF is negative=left axis deviation (LAD). o Lead I is negative and aVF is positive=right axis deviation (RAD). o Both leads negative=extreme RAD or North-West axis Quick look test Limb leads Normal o 0 to 90 degrees Right Axis Deviation (RAD) o > 90 degrees moderate RAD: 90 to 120 degrees marked RAD: 120 to 180 degrees o Differential diagnosis Right Ventricular Hypertrophy (RVH) most common Left Posterior Fascicular Block (LPFB) diagnosis of exclusion
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Lateral and apical MI Acute Right Heart Strain, e.g. acute lung disease such as pulmonary embolus Chronic lung disease, e.g. COPD Dextrocardia Ventricular pre-excitation (WPW) LV free wall accessory pathway Ventricular ectopy Hyperkalaemia Sodium-channel blockade, e.g. tricyclic toxicity Secundum ASD rSR pattern Normal in infants and children Normal young or slender adults with a horizontally positioned heart can also demonstrate a rightward QRS axis on the ECG.

Left Axis Deviation (LAD) o <-30 degrees moderate LAD: -30 to -45 degrees marked LAD: -45 to -90 degrees o Differential diagnosis Left ventricular hypertrophy (LVH) Left Anterior Fascicular Block (LAFB) diagnosis of exclusion LBBB inferior MI ventricular ectopy paced beats Ventricular pre-excitation (WPW) Primum ASD rSR pattern Extreme Axis Deviation o 180 to -90 degrees rare o Differential diagnosis Right Ventricular Hypertrophy (RVH) Apical MI VT Hyperkalemia

Rotation can be thought of as the axis of the heart in the transverse axis (the precordial leads) Normal o isoelectric QRS in V3 and V4, indicating the transition point between the right and left ventricular electric forces Clockwise rotation o isoelectric QRS in V5, V6 Anti-clockwise rotation o isoelectric QRS in V1, V2 Rule of thumb: the heart rotates towards 95epolarizat and away from infarction
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IV.4 DETERMINATION OF ECG WAVES


The P wave The P wave is the first positive deflection on the ECG It represents atrial depolarization Characteristics of the Normal Sinus P Wave Morphology Smooth contour Monophasic in lead II Biphasic in V1 Axis Normal P wave axis is between 0 and +75 P waves should be upright in leads I and II, inverted in aVR Duration < 120 ms Amplitude < 2.5 mm in the limb leads, < 1.5 mm in the precordial leads Atrial abnormalities are most easily seen in the inferior leads (II, III and aVF) and lead V1, as the P waves are most prominent in these leads. The Atrial Waveform Relationship to the P wave

Atrial depolarization proceeds sequentially from right to left, with the right atrium activated before the left atrium. The right and left atrial waveforms summate to form the P wave. The first 1/3 of the P wave corresponds to right atrial activation, the final 1/3 corresponds to left atrial activation; the middle 1/3 is a combination of the two. In most leads (e.g. lead II), the right and left atrial waveforms move in the same direction, forming a monophasic P wave. However, in lead V1 the right and left atrial waveforms move in opposite directions. This produces a biphasic P wave with the initial positive deflection corresponding to right atrial activation and the subsequent negative deflection denoting left atrial activation. This separation of right and left atrial electrical forces in lead V1 means that abnormalities affecting each individual atrial waveform can be discerned in this lead. Elsewhere, the overall shape of the P wave is used to infer the atrial abnormality.

Normal P-wave Morphology Lead II


The right atrial depolarization wave (brown) precedes that of the left atrium (blue). The combined depolarization wave, the P wave, is less than 120 ms wide and less than 2.5 mm high.

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Right Atrial Enlargement Lead II


In right atrial enlargement, right atrial depolarization lasts longer than normal and its waveform extends to the end of left atrial depolarization. Although the amplitude of the right atrial depolarization current remains unchanged, its peak now falls on top of that of the left atrial depolarization wave. The combination of these two waveforms produces a P waves that is taller than normal (> 2.5 mm), although the width remains unchanged (< 120 ms).

Left Atrial Enlargement Lead II


In left atrial enlargement, left atrial depolarization lasts longer than normal but its amplitude remains unchanged. Therefore, the height of the resultant P wave remains within normal limits but its duration is longer than 120 ms. A notch (broken line) near its peak may or may not be present (P mitrale).

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Normal P-wave Morphology Lead V1 The P wave is typically biphasic in V1, with similar sizes of the positive and negative deflections.

Normal P wave in V1 Right Atrial Enlargement Lead V1 Right atrial enlargement causes increased height (> 1.5mm) in V1 of the initial positive deflection of the P wave.

NB. This patient also has evidence of right ventricular hypertrophy. Left Atrial Enlargement Lead V1 Left atrial enlargement causes widening (> 40ms wide) and deepening (> 1mm deep) in V1 of the terminal negative portion of the P wave.

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Biatrial Enlargement Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG. The spectrum of P-wave changes in leads II and V1 with right, left and bi-atrial enlargement

Common P Wave Abnormalities Common P wave abnormalities include: Tall P mitrale (widened bifid P waves), seen with left atrial enlargement.
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P pulmonale ( > 3 large squares) (peaked P waves), seen with right atrial enlargement. Absent P wave AF, sinoatrial block, junctional (AV rhythm). P wave inversion, seen with ectopic atrial and junctional rhythms. Variable P wave morphology, seen in multifocal atrial rhythms. dissociation between P wave and QRS complex indicates complete heart block. P mitrale The presence of broad, notched (bifid) P waves in lead II is a sign of left atrial enlargement, classically due to mitral stenosis.

Bifid P waves (P mitrale) in left atrial enlargement

P Pulmonale The presence of tall, peaked P waves in lead II is a sign of right atrial enlargement, usually due to pulmonary hypertension (e.g. cor pulmonale from chronic respiratory disease).

Peaked P waves (P pulmonale) due to right atrial enlargement Inverted P Waves P-wave inversion in the inferior leads indicates a non-sinus origin of the P waves.

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When the PR interval is < 120 ms, the origin is in the AV junction (e.g. accelerated junctional rhythm):

Accelerated Junctional Rhythm When the PR interval is 120 ms, the origin is within the atria (e.g. ectopic atrial rhythm):

Ectopic Atrial Rhythm Variable P-Wave Morphology The presence of multiple P wave morphologies indicates multiple ectopic pacemakers within the atria and/or AV junction. If 3 different P wave morphologies are seen, then multifocal atrial rhythm is diagnosed:

Multifocal Atrial Rhythm If 3 different P wave morphologies are seen and the rate is 100, then multifocal atrial tachycardia (MAT) is diagnosed:

Multifocal Atrial Tachycardia

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Q Wave A Q wave is any negative deflection that precedes an R wave

Normal Q wave

Normal Q wave in V6 Origin of the Q Wave The Q wave represents the normal left-to-right depolarization of the interventricular septum Small septal Q waves are typically seen in the left-sided leads (I, aVL, V5 and V6) Q waves in different leads Small Q waves are normal in most leads Deeper Q waves (>2 mm) may be seen in leads III and aVR as a normal variant Under normal circumstances, Q waves are not seen in the right-sided leads (V1-3) Pathological Q Waves Q waves are considered pathological if: > 40 ms (1 mm) wide > 2 mm deep > 25% of depth of QRS complex Seen in leads V1-3 Pathological Q waves usually indicate current or prior myocardial infarction. Differential Diagnosis

Myocardial infarction Cardiomyopathies Hypertrophic (HOCM), infiltrative myocardial disease Rotation of the heart Extreme clockwise or counter-clockwise rotation Lead placement errors e.g. upper limb leads placed on lower limbs
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Examples

Inferior Q waves (II, III, aVF) with ST elevation due to acute MI

Lateral Q waves (I, aVL) with ST elevation due to acute MI

Lateral Q waves (V5-6) with T-wave flattening due to previous MI

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Anterior Q waves (V1-4) with ST elevation due to acute MI

Anterior Q waves (V1-4) with T-wave inversion due to recent MI

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Inferior Q waves (II, III, aVF) with T-wave inversion due to previous MI

Loss of normal Q waves


The absence of small septal Q waves in leads V5-6 should be considered abnormal. Absent Q waves in V5-6 is most commonly due to LBBB.

R Wave Abnormalities of the R wave Dominant R wave in V1 Dominant R wave in aVR Poor R wave progression Causes of Dominant R wave in V1

Normal in children and young adults RVH o Pulmonary Embolus o Persistence of infantile pattern o Left to right shunt RBBB Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9) WPW type A (Wolff-Parkinson-White) Incorrect lead placement (e.g. V1 and V3 reversed) Dextrocardia Hypertrophic cardiomyopathy Dystrophy o Myotonic dystrophy o Duchenne Muscular dystrophy

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Normal paediatric ECG (2 yr old)

Paediatric ECG V1 R wave Right Ventricular Hypertrophy (RVH)

RVH

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Right Bundle Branch Block

Right Bundle Branch Block (RBBB) (Dominant R wave in V1)

Causes of RBBB Normal variant RVH or strain e.g. pulmonary embolism Congenital heart disease, e.g. ASD Coronary artery disease

Right Bundle Branch Block MoRRoW (Dominant R wave in V1)

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Posterior MI

Posterior AMI WPW (type A)

WPW Type A

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Leads V1 and V3 reversed Note biphasic P wave (typically seen in only in V1) in lead V3

Leads V1 and V3 reversed Muscular dystrophy

Muscular Dystrophy
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Dominant R wave in aVR


Poisoning with sodium-channel blocking drugs (e.g. TCAs) Dextrocardia Incorrect lead placement (left/right arm leads reversed)

Poisoning with sodium-channel blocking drugs


Causes a characteristic dominant terminal R wave in aVR Poisoning with sodium-channel blocking agents is suggested if: o R wave height > 3mm o R/S ratio > 0.7

Na Channel blockade with dominant aVR R wave Dextrocardia This ECG shows all the classic features of dextrocardia: Positive QRS complexes (with upright P and T waves) in aVR Negative QRS complexes (with inverted P and T waves) in lead I Marked right axis deviation Absent R-wave progression in the chest leads (dominant S waves throughout)

Dextrocardia

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Left arm/right arm lead reversal The most common cause of a dominant R wave in aVR is incorrect limb lead placement, with reversal of the left and right arm electrodes. This produces a similar pattern to dextrocardia in the limb leads but with normal R-wave progression in the chest leads. With LA/RA lead reversal: Lead I becomes inverted Leads aVR and aVL switch places Leads II and III switch places

Lead reversal

Lead reversal reversed

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Poor R wave progression Defined as an R wave 3 mm in V3 Causes Prior anteroseptal MI LVH Inaccurate lead placement May be a normal variant

Poor R wave progression Note that absent R wave progression is characteristically seen in dextrocardia (see previous ECG). QRS duration reflects the time taken that excitation takes to spread through the ventricles. A wide QRS complex (>0.10 s, 2.5 small squares) occurs if conduction is delayed, e.g. with right or left a pathway other than the right and left bundle branches, e.g. an impulse generated by an abnormal focus of activity in the ventricle (ventricular ectopic). T wave The T wave is the positive deflection after each QRS complex. It represents ventricular repolarisation. In general, the direction of T wave is the same as that of QRS complex. Inverted T waves occur in many conditions and, although usually abnormal, they are non-specific finding.

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Characteristics of the normal T wave Upright in all leads except aVR and V1 Amplitude < 5mm in limb leads, < 15mm in precordial leads Duration (see QT interval) T wave abnormalities Hyperacute T waves Inverted T waves Biphasic T waves Camel Hump T waves Flattened T waves Peaked T waves Tall, narrow, symmetrically peaked T-waves are characteristically seen in hyperkalaemia.

Peaked T waves due to hyperkalaemia

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Hyperacute T waves Broad, asymmetrically peaked or hyperacute T-waves are seen in the early stages of STelevation MI (STEMI) and often precede the appearance of ST elevation and Q waves. They are also seen with Prinzmetal angina.

Hyperacute T waves due to anterior STEMI

Loss of precordial T-wave balance Loss of precordial T-wave imbalance occurs when the upright T wave is larger than that in V6. This is a type of hyperacute T wave. The normal T wave in V1 is inverted. An upright T wave in V1 is considered abnormal especially if it is tall (TTV1), and especially if it is new (NTTV1). This finding indicates a high likelihood of coronary artery disease, and when new implies acute ischemia. Inverted T waves Inverted T waves are seen in: Normal finding in children Persistent juvenile T wave pattern Myocardial ischaemia and infarction Bundle branch block Ventricular hypertrophy (strain patterns) Pulmonary embolism Hypertrophic cardiomyopathy Raised intracranial pressure T wave inversion in lead III is a normal variant. New T-wave inversion (compared with prior ECGs) is always abnormal. Pathological T wave inversion is usually symmetrical and deep (>3mm).
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Paediatric T waves Inverted T-waves in the right precordial leads (V1-3) are a normal finding in children, representing the dominance of right ventricular forces.

Normal pattern of T-wave inversions in a 2-year old boy

Persistent Juvenile T-wave Pattern T-wave inversions in the right precordial leads may persist into adulthood and are most commonly seen in young Afro-Caribbean women. Persistent juvenile T-waves are asymmetric, shallow (<3mm) and usually limited to leads V1-3.

Persistent juvenile T-waves in an adult

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Myocardial Ischaemia and Infarction T-wave inversions due to myocardial ischaemia or infarction occur in contiguous leads based on the anatomical location of the area of ischaemia/infarction: Inferior = II, III, aVF Lateral = I, aVL, V5-6 Anterior = V2-6 NOTE: Dynamic T-wave inversions are seen with acute myocardial ischaemia. Fixed T-wave inversions are seen following infarction, usually in association with pathological Q waves.

Inferior T wave inversion due to acute ischaemia

Inferior T wave inversion with Q waves due to prior inferior MI

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T wave inversion in the lateral leads due to acute ischaemia

Anterior T wave inversion with Q waves due to recent anterior MI * Myocardial ischemia in page 116, Inferior STEMI in page 118, Posterior MI in page 119 BUNDLE BRANCH BLOCK Left Bundle Branch Block Left bundle branch block produces T-wave inversion in the lateral leads I, aVL and V5-6.

Lateral T wave inversion due to LBBB


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Right Bundle Branch Block Right bundle branch block produces T-wave inversion in the right precordial leads V1-3.

T-wave inversion in the right precordial leads due to RBBB Causes of RBBB Coronary artery disease Hypertension Aortic valve disease Cardiomyopathy VENTRICULAR HYPERTROPHY Ventricular hypertrophy occurs when the work of the ventricle is increased sufficiently. In ventricular hypertrophy, the number of myocardial cells remain the same, but the diameter of the individual cells increases, raising the diffusion distance for O2 and other metabolites.

Left Ventricular Hypertrophy (LVH) Occurs in patients with systemic hypertension or aortic valve stenosis. Left ventricular hypertrophy produces T-wave inversion in the lateral leads I, aVL, V5-6 (left ventricular strain pattern), with a similar morphology to that seen in LBBB.

Lateral T wave inversion due to LVH


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LVH Tall R waves (>25 mm) over left ventricle leads aVL, V5-6) Deep S waves (> 30 mm) in the right ventricle leads (V1-2) The sum of the R wave in the left ventricular leads and S wave in the right ventricular leads exceeds 20 mm. ST depression and asymmetrical flattening/inversion of T wave in left ventricular leads- I, aVL and V4-V6 QRS duration slightly increased MEA shows left axis deviation Right Ventricular Hypertrophy (RVH) (e.g in pulmonary hypertension, pulmonary valve stenosis & some congenital heart disease) Right ventricular hypertrophy produces T-wave inversion in the right precordial leads V1-3 (right ventricular strain pattern) and also the inferior leads (II, III, aVF).

T wave inversion in the inferior and right precordial leads due to RVH

Tall R wave in right ventricular lead- V1 Deep S wave in V6 Right axis deviation (RAD)

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PULMONARY EMBOLISM Acute right heart strain (e.g. secondary to massive pulmonary embolism) produces a similar pattern to RVH, with T-wave inversions in the right precordial (V1-3) and inferior (II, III, aVF) leads.

T wave inversion in the inferior and right precordial leads in a patient with bilateral PEs

Deep T wave inversion in V1-3 with RBBB in a patient with massive PE

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Pulmonary embolism may also produce T-wave inversion in lead III as part of the SI QIII TIII pattern (S wave in lead I, Q wave in lead III, T-wave inversion in lead III).

SI QIII TIII pattern in acute PE Pulmonary Embolism The classical ECG signs of acute pulmonary embolism are SIQIIITIII, which are mnemonics representing deep S wave in lead I, pathological Q wave in lead III, and inverted T wave in lead III:

Other nonspecific signs include (see ECG above):


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Sinus tachycardia and atrial and ventricular ectopic beats. Right axis deviation. Right ventricular strain pattern with inverted T waves in right chest leads. Incomplete or complete right bundle branch block pattern. Slow R wave progression in chest leads But all these ECG signs may not be present even in frank pulmonary embolism.

HYPERTROPHIC CARDIOMYOPATHY (HOCM) HOCM is associated with deep T wave inversions in all the precordial leads.

T wave inversion in V1-6 due to HOCM RAISED INTRACRANIAL PRESSURE Events causing a sudden rise in ICP (e.g. subarachnoid haemorrhage) produce widespread deep T-wave inversions with a bizarre morphology.

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Widespread deep T wave inversion due to SAH Biphasic T waves There are two main causes of biphasic T waves: Myocardial ischaemia Hypokalaemia The two waves go in opposite directions: Ischaemic T waves go up then down Hypokalaemic T waves go down then up

Ischaemia

Biphasic T waves Due to Ischaemia PLASMA LEVELS OF POTASSIUM 1. With normal plasma levels of potassium (4-5.5 meq/L): Normal ECG tracings are produced with o PR interval= 0.16 s o QRS interval = 0.06 s o QT interval = 0.4 s 2. Electrolyte Abnormalities Hyperkalemia Serum potassium is the major intracellular ion that participates in the depolarization and repolarization of myocardial cells. Hence its serum concentration has a profound effect on the QRS and ST-T complex. Hyperkalaemia Increase in plasma K+ is very dangerous and potentially lethal condition because of its effects on the heart. Hyperkalaemia with plasma K+ 7.0 mEq/L o PR and QRs intervals are within normal limits. o T wave become tall & peaked Hyperkalaemia with plasma K+ 8.5 mEq/L o Broad and slurred QPS complex with a QRS interval of 0.2 s occurs due to paralysis of atria. o Very tall & slender T wave II,III, V2, V3, V4 Followed by o shortening of QT intervals
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o o o o

Widening of QRS interval ST segment depression Flattening of P wave PR interval prolongation

Narrow and tall peaked T wave (A) is an early sign of hyperkalemia. It is unusual for T waves to be taller than 5 mm in limb leads and taller than 10 mm in chest leads. Hyperkalemia should be suspect if these limits are exceeded in more than one lead. As serum potassium concentration continues to rise, the PR interval becomes longer, the P wave loses its amplitude and may disappear, and the QRS complex widens (B). When hyperkalemia is very severe, the widened QRS complexes merge with their corresponding T waves and the resultant ECG looks like a series of sine waves (C). If the rise in serum potassium continues unabated, the heart arrests in asystole. (NB: The narrow and tall peaked T wave of hyperkalemia may be confused with the hyper-acute T wave occasionally seen in transmural myocardial infarction. The patients presenting history and physical findings would help to differentiate the two.) A further increase in plasma K+ levels may result in ventricular tachycardia& ventricular fibrillation. As the extracellular K+ concentration increases, the resting membrane potential of the muscle fibres decreases & be unable to repolarise. Eventually the fibers become unexcitable because the activation gate of voltage-gated Na+ channels are still closed and action potential production become impossible, and the heart stops in diastole death.

Hypokalaemia Decrease in the plasma level levels of potassium is serious condition but it is not as rapidly fatal as hyperkalaemia.
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With hypokalemia, the T wave becomes flattened together with appearance of a prominent U wave. The ST segment may become depressed and the T wave inverted. Unlike hyperkalemia, these additional changes are not related to the degree of hypokalemia.

Biphasic T waves Due to Hypokalaemia PR interval is prolonged ST segment depression Late T wave inversion in precordial leads Prominent U waves Note generalised T-wave flattening with prominent U waves in the anterior leads (V2 and V3). If T wave & U wave merge, the apparent QT interval is often prolonged. But if T & U waves are separated, QT interval is of normal duration.

T wave flattening due to hypokalaemia

Wellens Syndrome

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Wellens syndrome is a pattern of inverted or biphasic T waves in V2-3 (in patients presenting with ischaemic chest pain) that is highly specific for critical stenosis of the left anterior descending artery. There are two patterns of T-wave abnormality in Wellens syndrome: Type 1 Wellens T-waves are deeply and symmetrically inverted Type 2 Wellens T-waves are biphasic, with the initial deflection positive and the terminal deflection negative

Wellens Type 1

Deeply & symmetrically inverted T wave Wellens Type 2

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Biphasic T wave- Initial positive deflection & terminal negative deflection Camel hump T waves This is a term used by the great ECG lecturer and Emergency Physician Amal Mattu to describe T-waves that have a double peak or camel hump appearance. There are two causes for camel hump T waves: Prominent U waves fused to the end of the T wave, as seen in severe hypokalaemia Hidden P waves embedded in the T wave, as seen in sinus tachycardia and various types of heart block

Prominent U waves due to severe hypokalaemia

Hidden P waves in sinus tachycardia

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Hidden P waves in marked 1st degree heart block

Hidden P waves in 2nd degree heart block with 2:1 conduction Flattened T waves Flattened T waves are a non-specific finding, but may represent ischaemia (if dynamic or in contiguous leads) or electrolyte abnormality, e.g. hypokalaemia (if generalised). Ischaemia Dynamic T-wave flattening due to anterior ischaemia (above). T waves return to normal once the ischaemia resolves (below).

Dynamic T wave flattening due to anterior ischaemia

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T waves return to normal as ischaemia resolves

IV.5 DETERMINATION OF INTERVALS FROM ECG PR Interval The PR interval is the time from the onset of the P wave to the start of the QRS complex. It reflects conduction through the AV node.

PR interval

The normal PR interval is between 120 200 ms duration (three to five small squares). If the PR interval is > 200 ms, first degree heart block is said to be present. PR interval < 120 ms suggests pre-excitation (the presence of an accessory pathway between the atria and ventricles) or AV nodal (junctional) rhythm.

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Heart Blocks
Heart block refers to a pathological delay in AV conduction, either at the AV node or beyond. Signs of heart block lie in the PR interval and P to QRS relationship.

First Degree Heart Block

In first degree heart block the cardiac rhythm is sinus in origin but the time from the initial depolarization of the atria to the initial depolarization of the ventricles is abnormally delayed. This pathologic delay is reflected in a PR interval longer than its upper limit of 200 ms. Nevertheless, each P wave of atrial contraction is followed by a QRS complex of ventricular contraction. First degree AV nodal block (PR >200ms= 0.22 s) Characterised by delayed conduction through the AV node Though all the atrial impulses reach the ventricles but PR interval is abnormally prolonged(> 0.21s) May occur in isolation or co-exist with other blocks (e.g., second-degree AV block, trifascicular block) First degree AV block

Sinus rhythm with marked 1st degree heart block (PR interval 340ms)

Second Degree Heart Block


When transmission of the depolarizing impulse from the sinus node through the AV conduction system of the heart is interrupted intermittently, P wave of atrial contraction is no longer followed by a QRS complex of ventricular contraction in the interrupted beat. This is second degree heart block. There are 2 types of second degree heart block: Mobitz type I & Mobitz type II. In Mobitz type I block there is progressive prolongation of the PR interval, indicating increasing delay in AV conduction, before it fails altogether.
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When failure in AV conduction occurs, the P wave of atrial contraction is not followed by a QRS complex. After this missed ventricular beat, the PR interval returns to its shorter duration and the cycle of progressive PR prolongation and missed ventricular beat repeats itself. Second degree AV nodal block (Mobitz I) with prolonged PR interval

Second degree heart block, Mobitz type I (Wenckeback phenomenon). Note how the baseline PR interval is prolonged, and then further prolongs with each successive beat, until a QRS complex is dropped. The PR interval before the dropped beat is the longest (340ms), while the PR interval after the dropped beat is the shortest (280ms). In Second degree heart block, not all atrial impulses are conducted to the ventricles. It is associated with organic heart disease. Consequently, there may be 1 ventricular contraction after every 2, 3 or 4 atrial contraction producing so-called 2:1, 3:1 or 4:1 (constant block). In Mobitz Type II block, a non-conducted P wave not followed by a QRS complex occurs suddenly without progressive prolongation of the PR interval. That is, the PR interval, which can be normal or prolonged, is constant before the non-conducted beat materializes.

Mobitz type II second degree heart block indicates more serious disease of the conduction system in regions below the AV node and can progress to total failure of AV conduction (third degree heart block) without warning.

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Third Degree Heart Block


In third degree (complete) heart block, all the SA node impulses are blocked and not conducted to the ventricles. In the absence of an alternative pacemaker, ventricular contraction comes to a standstill and the patient dies. But most probably an ectopic pacemaker below the block takes over ventricular pacing and the patient survives. Since the SA node and the ectopic pacemaker pace the atria and ventricles independently, the P waves bear no relationship to the QRS complexes. Two types of QRS complexes can be seen in third degree heart block: If the block is high in the AV node and the ventricular pacemaker is located lower in the AV junction, the QRS complex is normal in width because ventricular activation is via the bundle branches.

If the block is low in the AV junction, the ventricles are paced by an idioventricular pacemaker and the QRS complexes will be widerthan normal because the ventricles are no longer activated via the bundle branches.

Third degree (complete) AV nodal block No impulse from atria can pass to the ventricles. Therefore, ventricles start beating at their own rhythm (about 40 bpm) called idioventricular rhythm. The atria, however, continue to beat at the normal sinus rhythm about 72 bpm. thus, ECG shows that there is complete dissociation between P waves & QRS complex called atrioventricular dissociation.

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The above EKG shows an example of complete heart block. This rhythm is an idioventricular rhythm. The distinguishing characteristic is that no P waves from the atria are conducted to the ventricles. A careful examination will show that the PR interval is random as a result of there being no relationship between the P wave and the QRS complex. This is also referred to as AV dissociation. The QRS complex in this rhythm actually originates in the ventricles (Because there is no relationship between the P wave and the QRS and because the QRS complex is wide, nearly 0.36 seconds) and the effective heart rate is 33 beats per minute. Third degree AV nodal block is caused by o o o organic heart diseases septal myocardial infarction damage to bundle of His during surgical repair of congenital interventricular sepatal defects.

Third degree heart block may be associated with o prolonged ventricular standstill (asystole) until a ventricular focus begins firing. o The asystole, lasting a minute may result in cerebral iachemia producing dizziness and fainting (syncope) termed Stroke-Adams syndrome. o Even death may occur due to prolonged cerebral ischemia.

Short PR interval (<120ms) A short PR interval is seen with: Preexcitation syndromes. AV nodal (junctional) rhythm. Pre-excitation syndromes

Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL) syndromes. These involve the presence of an accessory pathway connecting the atria and ventricles.
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The accessory pathway conducts impulses faster than normal, producing a short PR interval. The accessory pathway also acts as an anatomical re-entry circuit, making patients susceptible to re-entry tachycardia. Patients present with episodes of paroxysmal supraventricular tachycardia (SVT), specifically atrioventricular re-entry tachycardia (AVRT), and characteristic features on the resting 12-lead ECG. Wolff-Parkinson-White syndrome (Acclerated AV conduction) It refers to occurrence of repeated attacks of nodal paroxysmal tachycardia due to presence of bundle of Kent (aberrant musculature or nodal tissue which connects the atria & ventricles directly- congenital/ present from birth). This bundle conducts more rapidly than the slow conducting AV node 7 one ventricle is excited early.

The characteristic features of Wolff-Parkinson-White syndrome are a short PR interval, broad QRS and a slurred upstroke to the QRS complex, the delta wave.

Short PR (<120ms), broad QRS and delta waves in WPW syndrome the presence of bundle of Kent rapidly establishes re-entry phenomenon (circus movement) in prone patients.

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Lown-Ganong-Levine syndrome It is characterized by attacks of paroxysmal supraventicular tachycardia, usual nodal tachycardia in individuals with short PR intervals and normal QRS complexes. In this condition, depolarization presumably passes from the atria to the ventricles via an aberrant bundle that bypasses the AV node but enters the intraventrcular conducting system distal to node. The features of LGL syndrome are a very short PR interval with normal P waves and QRS complexes and absent delta waves.

Short PR interval with normal QRS complexes in LGL syndrome AV nodal (junctional) rhythm

Junctional rhythms are narrow complex, regular rhythms arising from the AV node. P waves are either absent or abnormal (e.g. inverted) with a short PR interval (=retrograde P waves).

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Accelerated junctional rhythm demonstrating inverted P waves with a short PR interval (retrograde P waves)

QT Interval The QT interval is the time from the start of the Q wave to the end of the T wave. It represents the time taken for ventricular depolarisation and repolarisation.

The QT interval is inversely proportional to heart rate: The QT shortens at faster heart rates The QT lengthens at slower heart rates An abnormally prolonged QT is associated with an increased risk of ventricular arrhythmias, especially Torsades de Pointes. The recently described congenital short QT syndrome has been found to be associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death. How to measure QT

The QT interval should be measured in either lead II or V5-6 Several successive beats should be measured, with the maximum interval taken Large U waves (> 1mm) that are fused to the T wave should be included in the measurement Smaller U waves and those that are separate from the T wave should be excluded The maximum slope intercept method is used to define the end of the T wave (see below)

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The QT interval is defined from the beginning of the QRS complex to the end of the T wave. The maximum slope intercept method defines the end of the T wave as the intercept between the isoelectric line with the tangent drawn through the maximum down slope of the T wave (left). When notched T waves are present (right), the QT interval is measured from the beginning of the QRS complex extending to the intersection point between the isoelectric line and the tangent drawn from the maximum down slope of the second notch, T2 Corrected QT The corrected QT interval (QTc) estimates the QT interval at a heart rate of 60 bpm. This allows comparison of QT values over time at different heart rates and improves detection of patients at increased risk of arrhythmias. There are multiple formulas used to estimate QTc (see below). It is not clear which formula is the most useful. Bazetts formula: QTC = QT / RR Fredericias formula: QTC = QT / RR 1/3 Framingham formula: QTC = QT + 0.154 (1 RR) Hodges formula: QTC = QT + 1.75 (heart rate 60) NB. The RR interval is given in seconds (RR interval = 60 / heart rate). Bazetts formula is the most commonly used due to its simplicity. It over -corrects at heart rates > 100 bpm and under-corrects at heart rates < 60 bpm, but provides an adequate correction for heart rates ranging from 60 100 bpm. At heart rates outside of the 60 100 bpm range, the Fredericia or Framingham corrections are more accurate and should be used instead. If an ECG is fortuitously captured while the patients heart rate is 60 bpm, the absolute QT interval should be used instead! There are now multiple i-phone apps that will calculate QTc for you (e.g. MedCalc), and the website MDCalc.com has a quick and easy QTc calculator that is free to use. Normal QTc values QTc is prolonged if > 440ms in men or > 460ms in women QTc > 500 is associated with increased risk of torsades de pointes QTc is abnormally short if < 350ms A useful rule of thumb is that a normal QT is less than half the preceding RR interval Causes of a prolonged QTc (>440ms)

Hypokalaemia Hypomagnesaemia Hypocalcaemia Hypothermia Myocardial ischemia Post-cardiac arrest Raised intracranial pressure
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Congenital long QT syndrome DRUGS Hypokalaemia Hypokalaemia causes apparent QTc prolongation in the limb leads (due to T-U fusion) with prominent U waves in the precordial leads.

Apparent QTc 500 ms with prominent U waves in the precordial leads due to hypokalaemia (K 1.9) Hypomagnesaemia

QTc 510 ms secondary to hypomagnesaemia Hypocalcaemia Caused by plasma ionized calcium levels in alkalosis or hyperventilation or in hypoparathyroiism.

Hypocalcaemia typically prolongs the ST segment, leaving the T wave unchanged.

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QTc 510ms due to hypocalcaemia Hypothermia Severe hypothermia can cause marked QTc prolongation, often in association with bradyarrhythmias (especially slow AF), Osborne waves and shivering artifact.

QTc 620 ms due to severe hypothermia Myocardial Ischaemia Myocardial ischemia tends to produce a modest increase in the QTc, in the 450-500 ms range. This may be useful in distinguishing hyperacute MI from benign early repolarization (both may produce similar hyperacute T waves, but BER will usually have a normal QTc).

QTc 495 ms due to hyperacute MI

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Raised ICP A sudden rise in intracranial pressure (e.g. due to subarachnoid haemorrhage) may produce characteristic T wave changes (cerebral T waves): widespread, deep T wave inversions with a prolonged QTc.

QTc 630ms with widespread T wave inversion due to subarachnoid haemorrhage

Congenital Long QT Syndrome There are several congenital disorders of ion channels that produce a long QT syndrome and are associated with increased risk of torsades de pointes and sudden cardiac death.

QTc 550ms due to congenital long QT syndrome

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Causes of a short QTc (<350ms)


Hypercalcaemia Congenital short QT syndrome Digoxin effect

Hypercalcaemia Hypercalcaemia leads to shortening of the ST segment and may be associated with the appearance of Osborne waves.

Marked shortening of the QTc (260ms) due to hypercalcaemia

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Congenital short QT syndrome

Congenital short QT syndrome (SQTS) is an autosomal-dominant inherited disorder of potassium channels associated with an increased risk of paroxysmal atrial and ventricular fibrillation and sudden cardiac death. The main ECG changes are very short QTc (<300-350ms) with tall, peaked T waves.

Very short QTc (280ms) with tall, peaked T waves due to congenital short QT syndrome Short QT syndrome may be suggested by the presence of: Lone atrial fibrillation in young adults Family member with a short QT interval Family history of sudden cardiac death ECG showing QTc < 350 ms with tall, peaked T waves Failure of the QT interval to increase as the heart rate slows

Very short QT (< 300ms) with peaked T waves in two patients with SQTS
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Digoxin Digoxin produces a relative shortening of the QT interval, along with downward sloping ST segment depression in the lateral leads (reverse tick appearance), widespread T-wave flattening and inversion, and a multitude of arrhythmias (ventricular ectopy, atrial tachycardia with block, sinus bradycardia, regularized AF, any type of AV block).

Short QT interval due to digoxin (QT 260 ms, QTc 320ms approx) QT interval scale Viskin (2009) proposes the use of a QT interval scale to aid diagnosis of patients with short and long QT syndromes (once reversible causes have been excluded):

QT interval scale
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Drug-induced QT-Prolongation and Torsades de pointes (ventricular tachycardia)


In the context of acute poisoning with QT-prolonging agents, the risk of TdP is better described by the absolute rather than corrected QT. More precisely, the risk of TdP is determined by considering both the absolute QT interval and the simultaneous heart rate (i.e. on the same ECG tracing). These values are then plotted on the QT nomogram (below) to determine whether the patient is at risk of TdP. A QT interval-heart rate pair that plots above the line indicates that the patient is at risk of TdP. From the nomogram, you can see that QTc-prolonging drugs that are associated with a relative tachycardia (e.g. quetiapine) are much less likely to cause TdP than those that are associated with a relative bradycardia (e.g. amisulpride).

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IV. 6 DETERMINATION OF SEGMENTS FROM ECG PR segment The PR segment is the flat, usually isoelectric segment between the end of the P wave and the start of the QRS complex.

PR segment abnormalities occur in two main conditions: Pericarditis Atrial ischaemia Pericarditis The characteristic changes of acute pericarditis are: PR segment depression. Widespread concave (saddle-shaped) ST elevation. Reciprocal ST depression and PR elevation in aVR and V1 Absence of reciprocal ST depression elsewhere. NB. PR segment changes are relative to the baseline formed by the T-P segment.

Typical ECG of acute pericarditis.


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PR segment depression in V5 due to acute pericarditis (note there is also some concave ST elevation)

PR elevation in aVR due to acute pericarditis (note the reciprocal ST depression) Atrial ischaemia PR segment elevation or depression in patients with myocardial infarction indicates concomitant atrial ischaemia or infarction. This finding has been associated with poor outcomes following MI, increased risk for the development of atrioventricular block, supraventricular arrhythmias and cardiac free-wall rupture. Lius criteria for diagnosing atrial ischaemia / infarction include: PR elevation >0.5 mm in V5 & V6 with reciprocal PR depression in V1 & V2 PR elevation >0.5 mm in lead I with reciprocal PR depression in leads II & III PR depression >1.5 mm in the precordial leads PR depression >1.2 mm in leads I, II, & III Abnormal P wave morphology: M-shaped,W-shaped,irregular,or notched (minor criteria) PR depression in inferior STEMI indicating concomitant atrial infarction

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Profound PR-segment depression in inferior leads with (A) and without (B) clear-cut TP segment in acute inferior myocardial infarction. Note also ST-segment elevation in inferior leads. (Reproduced from Jim et al.)

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Measurement of PR depression

Measurement of PR-segment depression with (A) and with- out (B) clear-cut TP segment. (Reproduced from Jim et al.)

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ST Segment The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. It represents the interval between ventricular depolarisation and repolarisation. The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia / infarction.

Causes of ST segment elevation Acute myocardial infarction Coronary vasospasm (Printzmetals angina) Pericarditis Benign early repolarisation (BER) Left bundle branch block (LBBB) Left ventricular hypertrophy Ventricular aneurysm Brugada syndrome Ventricular paced rhythm Raised intracranial pressure Morphology of the Elevated ST segment Myocardial infarction Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.

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ST segment morphology in other conditions

Pericarditis

BER

LBBB

LV aneurysm

Brugada

Patterns of ST elevation Acute ST elevation myocardial infarction (STEMI) Causes ST segment elevation and Q-wave formation in contiguous leads, either: Septal (V1-2) Anterior (V3-4) Lateral (I + aVL, V5-6) Inferior (II, III, aVF) Right ventricular (V1, V4R) Posterior (V7-9) There is usually reciprocal ST depression in the electrically opposite leads.

Anterolateral STEMI Coronary Vasospasm (Prinzmetals angina) This causes a pattern of ST elevation that is very similar to acute STEMI i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. They may be impossible to differentiate on the ECG.

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Prinzmetal's angina Pericarditis Pericarditis causes widespread concave ST segment elevation with PR segment depression in multiple leads typically I, II, III, aVF, aVL and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1.

Pericarditis Concave saddleback ST elevation in leads I, II, aVL, V4-6 with depressed PR segments. There is reciprocal ST depression and PR elevation in aVR.

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Benign Early Repolarisation Causes mild ST elevation with tall T-waves mainly in the precordial leads. Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point the fish-hook pattern.

Benign Early Repolarisation There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the fish-hook pattern)

Bundle Branch Block (BBB)

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Normal QRS 0.08 0.12 s (4-6 large squares) in length. BBB > 0.12 s (> 6 large squares) This means that there may be a block in one of the bundle branches, or the electrical impulses was conducted through an abnormal conduction pathway. The septum is normally depolarized from left to right. The left ventricles, having the greater muscle mass, exert more influence on the ECG than the right ventricle. Excitation spreading towards a lead causes an upward deflection of the ECG.

Principles of BBB

Left Bundle Branch Block (LBBB) In left bundle branch block, the ST segments and T waves show appropriate discordance i.e. they are directed opposite to the main vector of the QRS complex. This produces ST elevation with upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).

Left Bundle Branch Block Note the ST elevation in leads with deep S waves most apparent in V1-3. Also note the ST depression in leads with tall R waves most apparent in I and aVL.

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Left Ventricular Hypertrophy LVH causes a similar pattern of repolarisation abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).

Left Ventricular Hypertrophy Severe LVH with extremely deep S waves in V1-3 producing associated ST elevation (not due to myocardial ischaemia). Also note the ST depression and T-wave inversion in the lateral leads I, aVL and V6 .

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Ventricular Aneurysm This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.

Ventricular Aneurysm There is ST elevation with deep Q waves and inverted T waves in V1-3. This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.

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Brugada Syndrome This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the Brugada sign ST elevation and partial RBBB in V1-2 with a coved morphology.

Brugada syndrome There is ST elevation and partial RBBB in V1-2 with a coved morphology the Brugada sign.

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Ventricular Paced Rhythm Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.

Sequential atrial and ventricular pacing

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Raised intracranial pressure Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave inversions (cerebral T waves).

ST elevation due to traumatic brain injury Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury. Less common causes of ST segment elevation

Pulmonary embolism and acute cor pulmonale (usually in lead III) Acute aortic dissection (classically causes inferior STEMI due to RCA dissection) J-waves (hypothermia, hypercalcaemia) Hyperkalaemia Sodium-channel blocking drugs (secondary to QRS widening) Following electrical cardioversion Cardiac tumour Mitral valvuloplasty Pancreatitis / gallbladder disease Myocarditis Septic shock Anaphylaxis

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Transient ST elevation after DC cardioversion from VF

J waves in hypothermia simulating ST elevation

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Causes of ST depression Myocardial ischaemia / NSTEMI Reciprocal change in STEMI Posterior MI Digoxin effect Hypokalaemia Supraventricular tachycardia Right bundle branch block Right ventricular hypertrophy Left bundle branch block (see above) Left ventricular hypertrophy (see above) Ventricular paced rhythm (see above) Morphology of ST depression

ST depression can be either upsloping, downsloping, or horizontal. Horizontal or downsloping ST depression 0.5 mm at the J-point in 2 contiguous leads indicates myocardial ischaemia (according to the 2007 Task Force Criteria). Upsloping ST depression is non-specific for myocardial ischaemia. Reciprocal change has a morphology that resembles upside down ST elevation. ST depression in posterior MI occurs in V1-3 and is associated with dominant R waves and upright T waves.

ST depression: upsloping (A), downsloping (B), horizontal (C) ST segment morphology in myocardial ischaemia

Reciprocal change

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ST elevation in III ST segment morphology in posterior MI

Reciprocal change in aVL

Patterns of ST depression Myocardial Ischaemia ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion. NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.

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Widespread subendocardial ischaemia due to LMCA occlusion Reciprocal Change ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads: Inferior STEMI produces reciprocal ST depression in aVL ( lead I). Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF ( lead II). Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).

Reciprocal ST depression in aVL with inferior STEMI

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Reciprocal ST depression in III and aVF with high lateral STEMI Posterior Myocardial Infarction Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (Q-wave equivalent) and upright T waves. There is ST elevation in the posterior leads V7-9.

Posterior MI

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Drug Effects Digoxin Digoxin is a potent pro-arrhythmic drug. At therapeutic plasma level, it causes nonspecific ST segment depression that has a scooping appearance (A) or looks like a reversed (B). (See Case 067: Abnormal ECG at http://www.medicineon-line.com.) At toxic levels, digoxin can cause virtually all kinds of arrhythmia but particularly sinus bradycardia, SA and AV blocks, atrial and junctional tachycardias, and VPB and ventricular tachycardia.

Digoxin Effect Treatment with digoxin causes downsloping ST depression with a sagging morphology, reminiscent of Salvador Dalis moustache.

Anti-arrhythmic Drugs Quinidine, procainamide, and disopyramide (Class IA agents) prolong the QRS duration and the QT interval with or without the appearance of U wave and have the propensity to cause polymorphic ventricular tachycardia (torsade de pointes). Sotalol and amiodarone (Class III agents) can increase PR, QRS, and QT intervals, leading to similar risks of torsade de pointes. They also have significant beta-blocking properties, causing bradyarrhythmias Hypokalaemia Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.

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Hypokalaemia Right ventricular hypertrophy RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.

Right ventricular hypertrophy Right Bundle Branch Block (RBBB) RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.
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Right bundle branch block Causes of RBBB Normal variant (isolated RBBB) pulmonary embolism Cor pulmonale

Supraventricular tachycardia Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia provided that it resolves with treatment.

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AV-nodal re-entry tachycardi Hypercalcemia, some drugs, certain genetic abnormalities, Shortened QT interval hyperkalemia Prolonged QT interval Hypocalcemia, some drugs, certain genetic abnormalities Flattened or inverted T Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs waves Possibly the first manifestation of acute myocardial infarction, where T waves become more prominent, symmetrical, and Hyperacute T waves pointed Peaked T wave, QRS wide, Hyperkalemia, treat with calcium chloride, glucose and insulin prolonged PR, QT short or dialysis Hypokalemia Prominent U waves

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