Electrocardiogram (ECG) - 12 lead
Introduction
Learning objectivesKey
Rationale behind ECG recording
An ECG is a method of graphic tracing of the electric current generated by the heart muscle during a heartbeat. The tracing is recorded with an electrocardiograph. Electrocardiography is an important diagnostic tool for heart disease. It can be used to monitor a patient's heart rate, assess the effects of injury or disease on cardiac function, assess pacemaker function, determine response to medication, or to obtain a baseline measure of cardiac function.
An ECG recording can provide information about the orientation of the heart in the chest, electrical effects of medications, conduction disturbances, cardiac muscle mass, and the presence of ischemic changes.
Physiology of the heart
Blood flow
The right atrium of the heart receives deoxygenated blood from the body, via the inferior and superior vena cavae, and also from the coronary sinus (draining the heart muscle). Contraction of the right atrium causes the blood to flow through the tricuspid valve into the right ventricle(atrial kick). Contraction of the right ventricle closes the tricuspid valve and the blood is expelled through the pulmonary valve and into the pulmonary trunk. The pulmonary trunk divides into the right and left pulmonary arteries, to supply the right and left lungs respectively, where the blood becomes oxygenated.
Oxygenated blood flows from the lungs into the left atrium, via the four pulmonary veins (two veins from each lung). Contraction of the left atrium pushes blood into the left ventricle (atrial kick) through the mitral (bicuspid) valve. Contraction of the left ventricle closes the mitral valve and the blood is directed through the aortic valve and into the aorta. The blood passes through the divisions of the aorta and is distributed throughout the body. The coronary arteries lie just beyond the aortic valve cusps, and supply oxygenated blood to the heart muscle. Blood enters the coronary arteries when the ventricles are relaxed.
Normal heart
Cardiac cycle
"Cardiac cycle" is the term used to describe the repeated pumping process of the heart, and includes all the events associated with flow of blood through the heart. The cardiac cycle consists of two phases:
Systole - the period during which a heart chamber contracts and blood is forced out. Systole includes contraction of both the atria and the ventricles
Diastole - the period during which a heart chamber relaxes and fills with blood. The atria and the ventricles both have a diastolic phase. The myocardiumreceives oxygenated blood during diastole
The cardiac cycle depends on the ability of the cardiac muscle to contract. The efficiency of the heart as a pump may be affected by the state of the cardiac muscle, the valves, or the conduction system.
The pressure within each chamber increases during systole and decreases during diastole. The valves of the heart operate to ensure that blood travels in the correct direction through the heart. Blood flows from one chamber to the next if the pressure in the first chamber is greater than the pressure in the second chamber.
Heart rate
Heart rate is a measurement of the number of heart beats per minute. The heart rate is influenced by both the sympathetic and parasympathetic divisions of the autonomic nervous system.
Baroreceptors and chemoreceptors
Baroreceptors and chemoreceptors are specialized nerve tissues found in the internal carotid arteries and in the aortic arch.
Baroreceptors are responsible for detecting changes in arterial blood pressure. When stimulated by a change in pressure, the baroreceptors generate a reflex response in the autonomic nervous system.
Chemoreceptors detect changes in the concentration of oxygen and carbon dioxide, and variations in the pH of the blood. The chemoreceptors also feed back to the autonomic nervous system to alter heart and respiratory (breathing) rates.
The heart as a pump
Venous return
"Venous return" is the term used to describe the return of blood to the heart from the systemic circulation via the inferior and superior vena cavae (and the coronary sinus). Venous return is the most significant factor determining the amount of blood pumped out of the heart.
Cardiac output
Cardiac output is the amount of blood pumped out of the heart each minute. It is calculated by multiplying the heart rate by the stroke volume(the amount of blood expelled from the ventricles with each heart beat). The cardiac output of an average adult ranges from 4 to 8 L/minute; at rest, the cardiac output is approximately 5 L/minute.
Blood pressure
Blood pressure is the force exerted on the arterial walls by the circulating blood volume. Blood pressure is maintained by the contraction of the heart, the resistance of the blood vessels, the elasticity of the vessel walls, and the volume and viscosity of the blood. The degree of resistance to the flow of blood in the peripheral blood vessels (peripheral vascular resistance) depends on the tone of the musculature in the vessels and the diameter of the vessels. Blood pressure can be calculated by multiplying the cardiac output by the peripheral vascular resistance.
Stroke volume
Stroke volume is the amount of blood ejected from the ventricle with each heart beat. It is determined by three factors: the amount of blood that fills the ventricle when the heart is relaxed (preload); the pressure against which the ventricle must pump (afterload); and the myocardium's contractile state (ie, relaxed or contracted).
Preload is defined as the force exerted on the ventricular walls at the end of diastole(relaxation). The volume of blood returning to the heart influences preload; a higher venous returnincreases preload, and a lower venous return decreases preload
The Frank-Starling law of the heart states that, to a degree, the greater the volume of blood in the heart during diastole (end diastolic volume), the greater the volume of blood ejected during systole (stroke volume). This allows the heart to alter its pumping capacity in response to a change in venous return (eg, exercise)
Afterload is the resistance against which the ventricles must pump to eject blood. Afterload is determined by arterial blood pressure, arterial resistance, and the ability of the arteries to stretch (arterial distensibility)
Electrophysiology of the heart
Cardiac cells
Cardiac cells have either a mechanical (contractile) or electrical (pacemaker) function. Myocardial cells contain contractile filaments which, when stimulated, cause the cells to contract and shorten. These cells form the muscular layers of the atrial and ventricular walls (myocardium). The myocardial cells rely on pacemaker cells to generate an electrical impulse to stimulate them to contract. Pacemaker cells are specialized cardiac cells that spontaneously generate and conduct electrical impulses.
Cardiac action potential
Body fluids that contain electrolytesare capable of conducting an electric current. The main electrolytes that affect the function of the heart are sodium (Na+), potassium (K+), calcium (Ca2+), and chloride (Cl-). A cardiac action potential is a five-phase cycle (numbered 0 to 4) that reflects the difference in the concentration of electrolytes across the cell membrane at a given time.
Monophasic action potential
Polarization
Cell membranes contain channels through which specific electrolytes and other water-soluble molecules can pass into the cell from outside it. When a cell is at rest, the inside of the cell is more negatively charged than the outside of the cell (ie, it is polarized). The difference in electrical charges (voltage) across the membrane is known as the "membrane potential".
Depolarization
A pacemaker cell is able to produce an electrical impulse only when there is a flow of electrolytes across the cell membrane. When stimulated, the cell membrane becomes permeable to Na+ and K+ ions. The influx of Na+ions into the cell causes the cell to become more positive, a process known as depolarization. An upwards spike is recorded on the ECG. The stimulus that alters the electrical charge across the cell may be chemical, electrical, or mechanical. Depolarization of a cell membrane results in the generation of an impulse that causes channels to open in the neighboring cell membrane and then the next. Under normal circumstances, the impulse begins in pacemaker cells found in the SA node. A chain reaction, known as a wave of depolarization, occurs from cell to cell, until all cells in the heart's electrical conduction system have been depolarized. The impulse eventually spreads from the pacemaker cell to the myocardial cells, which contract when they are stimulated.
Repolarization
After depolarization, the cell rapidly begins to restore its normal electrical charge. The process of electrolytes moving across a cell membrane to restore the negative charge of the inside of the cell is known as "repolarization". The cell stops the influx of Na+ ions into the cell and allows K+ cells to leave; the negatively charged particles remaining inside the cell restore the cell to its resting state. Repolarization of the myocardial cells causes them to relax. Repolarization begins in the epicardium and spreads towards the endocardium.
Phases of the cardiac action potential
Refractory periods
The refractory period is the amount of time required for a cell membrane to be ready for the next stimulus after it has been excited. In the myocardium, the refractory period is longer than the contraction itself.
Conduction system of the heart
ECG paper
The ECG is recorded on special standardized ECG paper at a constant speed of 25 mm/second. The horizontal axis measures duration of time and the vertical axis measures voltage amplitude (in a correctly calibrated machine). The ECG paper is divided into a number of large and small squares. Each small 1 mm square is equivalent to 0.04 seconds duration and 0.1 mV amplitude. Five small squares make up one large square, equivalent to 0.5 mV and 0.2 seconds duration (so there are five large blocks per second).
ECG waveform
ECG waveform
Click to see animation of ECG complex formation.
Artifact
An artifact is a distortion of the ECG tracing that occurs due to interference by electrical activity that does not come from the heart. An ECG artifact on a tracing may look like a cardiac arrhythmia. Thorough patient evaluation is important.
Artifacts may be caused by several factors: loose electrodes, patient movement/muscle activity, 60-cycle interference, broken ECG cables/wires, and external chest compressions.
1. Preparation
This procedure should be done under clinical supervision of a clinically competent supervisor until you are clinically competent to do it on your own.
1.1 Tray preparation
Before beginning this procedure, set up the tray with the necessary equipment.
Attach an electrode to each of the ECG leads. Ensure the terminal cable is correctly plugged into the ECG monitor.
Check that the ECG monitor has adequate paper to record the ECG.
ECG monitor
1.2 Patient preparation
Explain the procedure to the patient and obtain verbal consent to proceed.
Position the patient semi-recumbent, with upper body clothing removed (maintaining privacy where possible).
Prepare the region where the electrodes will be placed:
Clean the skin with gauze or alcohol wipes (to remove oil, sweat, or dead skin)
Shave (where necessary) any excess hair
1.3 Operator preparation
Take universal precautions.
2. Place electrodes
Ten electrodes are placed in defined positions on the body, and twelve "leads" are derived from the electrical signals the electrodes obtain. A "lead" gives a representation of the electrical activity that occurs between two electrodes.
2.1 Place the limb electrodes
Attach the limb electrodes in the appropriate positions.
NameLocationColorRARight armWhiteLALeft armBlackRLRight legGreenLLLeft legRed
Placement of limb
electrodes
Note:
Avoid placing over burnt or damaged skin. If necessary the electrode can be placed on the same limb, as near to the correct site as possible, but this will result in decreased voltage in the ECG reading.
Each lead records the electrical activity in a specific place in the heart, and each lead "views" the heart from a different angle.
Views of the heart
When no electrical activity is recorded between electrodes, a straight line (isoelectric line) is recorded on the ECG trace. Movement away from the baseline generates a waveform. If the electrical impulse is travelling towards the positive electrode, the waveform will be upward (positive); an electrical impulse travelling away from the positive electrode will cause a downward (negative) waveform. When the electrical impulse is travelling perpendicularly to the positive electrode a biphasic waveform is recorded.
Recording electrical
activity
All leads have a positive electrode. A bipolar lead has both a positive and a negative electrode.
2.1.1 Bipolar limb leads
Leads I, II, and III are the standard limb leads. The limb leads are bipolar, as each has a positive and a negative electrode. The positive electrode is located at the wrist in lead I, while the positive electrode is located at the left foot in leads II and III.
Einthoven's triangle
Einthoven's triangle is an imaginary equilateral triangle with corners that lie at the left and right shoulders and the pubic region. The sides of the triangle are represented by the axes of ECG limb leads I, II, and III.
Einthoven's triangleLeadPosition of positive electrodePosition of negative electrodeView of heartILeft armRight armLateral surfaceIILeft legRight armInferior surfaceIIILeft legLeft armInferior surface
2.1.2 Unipolar limb leads: augmented leads
The ECG machine increases the amplitude of a further three limb leads by approximately 50%, as the electrical potential produced by these leads is normally small. Leads aVR, aVL, and aVF are the augmented limb leads (aV = augmented voltage). The positive electrodes for these leads are those located at the right arm, left arm, and left foot, respectively. The augmented limb leads are considered unipolar as they do not have a specific negative electrode. The center of the heart is considered as the theoretical negative electrode.
LeadPosition of positive electrodeView of heartaVRRight armBase of heartaVLLeft armLateral surfaceaVFLeft legInferior surface
Unipolar limb leads
2.2 Place the chest electrodes
The chest leads are labeled V1 - V6. Attach the electrodes to the chest in the appropriate positions:
NameLocationV1Fourth intercostal space at the right sternal borderV2Fourth intercostal space at the left sternal borderV3Midway between V2 and V4V4Fifth intercostal space in the midclavicular lineV5Anterior axilliary line at the same horizontal level as V4V6Mid-axillary line at the same horizontal level as V4 and V5
Placement of chest leads
2.2.1 Unipolar leads: Chest leads
The six chest leads view the heart from a horizontal perspective. The chest leads are unipolar, where the positive electrode is the electrode placed on the chest while the negative electrode is a theoretical electrode at the center of the heart.
LeadPosition of positive electrodeView of heartV1Fourth intercostal space at the right sternumSeptumV2Fourth intercostal space at the left sternumSeptumV3Midway between V2 and V4Anterior surfaceV4Fifth intercostal space in the left midclavicular lineAnterior surfaceV5Left anterior axillary line at the same horizontal level as V4Lateral surfaceV6Left mid-axillary line at the same horizontal level as V4 and V5Lateral surface
3. Record the ECG
3.1 Enter the patient's details into the machine
3.2 Check the machine is calibrated
A 12-lead ECG is calibrated at 10 mm/mV; a standard signal of 1 mV must move the stylus vertically by 10 mm. Traditionally, measurements of ECG waveforms are quoted in millimeters rather than millivolts.
ECG machine
collaboration
3.3 Record the ECG
Press the start (or run) button to begin analyzing and recording the ECG.
3.4 Annotate the presence of symptoms on the ECG tracing
Make a record of any symptoms the patient experiences while the ECG is being recorded (eg, chest pain, dizziness, palpitations, etc).
Postprocedure considerations
Clearly write the date, time, and patient's name on the ECG recording (if not already printed by the ECG machine).
Remove (and dispose of) all ECG electrodes, unless repeat ECG recording is likely.
Document the indication and the procedure in the patient's records.
4. Analyze the rhythm strip (2 lead)
4.1 Assess the rate
There are four methods used to determine heart rate.
4.1.1 The 6-second ECG count
This is the simplest and the most common method to determine heart rate, particularly if the rhythm is irregular. Count the number of QRS complexes in a 6-second period and multiply by 10 to obtain the average number of contractions per minute.
The 6-second
ECG count
4.1.2 Count large squares
If the rhythm is regular (R-R intervalremains constant), counting the number of large squares occurring between the ECG complexes can determine the rate. If the rhythm is irregular, a rate range can be determined. This method can be used to determine both the ventricular rate (R-R interval) and the atrial rate (P-P interval).
R-R interval
Count the number of large squares occurring between QRS complexes (or P waves) and divide 300 by that number to calculate the rate per minute. The figure below shows an ECG tracing with a rate of 75 per minute (300/4 squares = 75).
4.1.3 Count small squares
A similar but more accurate method of determining the rate is to count the number of small squares between QRS complexes (or P waves) and divide that number into 1500. The figure above can now be accurately calculated as 71/minute (1500/21 squares = 71.4).
4.1.4 Sequence method
Select an R wave that falls on a dark vertical line, then number the next six dark vertical lines as follows: 300, 150, 100, 75, 60, and 50. Where the next R wave falls in relation to the six vertical lines is the heart rate.
Note:
Do not confuse heart rate with pulse rate. In some circumstances (such as premature ventricular contraction, or pulseless electrical activity) the electrical activity of the heart may not produce sufficient contraction of the heart to result in a palpable pulse.
4.2 Assess the rhythm
Measure several points on the rhythm strip to determine whether the rhythm is regular or irregular. If it is irregular, decide if the rhythm is regularly irregular (ie, a pattern) or irregularly irregular.
4.2.1 Ventricular rhythm
Measure the R-R interval (distance between R waves on two successive QRS complexes). Compare with other R-R intervals on the ECG strip.
4.2.2 Atrial rhythm
Measure the P-P interval (distance between P waves on two successive P waves). Compare with other P-P intervals on the ECG strip.
4.2.3 Regularity
If the distance between R waves is consistent (plus or minus 10%), the rhythm is considered regular.
Regular rhythm
If the distance is variable, the rhythm is irregular.
Regularly irregular - a repeating pattern of irregularity
Irregularly irregular - completely irregular rhythm
4.3 Identify and assess the P wave
The P wave represents depolarizationof the right and left atria from the sinoatrial (SA) node. Normally, each P wave is followed by a narrow QRS complex, and each QRS complex is preceded by a P wave.
A normal P wave is usually less than 0.10 seconds in duration and approximately 0.25 mV (2.5 mm high). The wave shape should be even, rounded, and regular. P waves are positive (upright) in leads I, II, aVF, and V2-V6.
A tall P wave indicates right atrial enlargement (P-pulmonale), while a broad and bifid (two bumps) P wave suggests enlargement of the left atrium (P-mitrale).
An absent or inverted P wave indicates the rhythm originates in the atrioventricular (AV) junction or in the ventricles.
4.4 Assess the intervals (conduction)
4.4.1 PR interval
The PR interval is measured from the start of the P wave, to the first deflection of the QRS complex (either a Q or an R wave). It represents the time taken for the electrical impulse to travel from the SA node, via the atria and through the AV node. The PR interval is normally 0.12 to 0.2 seconds (3-5 small squares) in duration.
PR interval
Shortening of the PR interval is often the result of a direct connection between the atria and the ventricles (eg, an accessory pathway).
Lengthening of the PR interval (greater than 0.20 seconds) indicates a delay in the spread of the impulse through the atria or an AV nodal block (interruption of the signal through the AV node by a pathological process such as ischemia, fibrosis, or toxicity).
4.4.2 QRS duration
The QRS complex represents depolarization of the ventricles (and buried atrial repolarization). The larger amplitude (seen as greater height) of the QRS relative to the P wave indicates the comparatively larger muscle mass of the ventricles. Large deflections are depicted using upper case (capital) letters, while small deflections (less than half the total amplitude) use lower case; however, it is always referred to as the QRS complex.
Q wave: The Q (q) wave is the first negative wave occurring after the P wave, and notpreceded by an R wave. It reflects the depolarization of the interventricular septum. A normal Q wave is less than 0.04 seconds long (1 small square wide) and less than 2 mV deep. A deep Q wave (more than 1/3 the height of the QRS complex) is considered as pathological and is often the result of myocardial ischemia or infarction; these changes may be new or may exist from a previous myocardial infarction.
R wave: The R (r) wave is the first positive deflection in the QRS complex, and represents early depolarization of the ventricles. Additional positive deflections are designated R' (R prime).
S wave: The S (s) wave is the first negative deflection following the R wave, and represents late depolarization of the ventricles. Additional negative deflections after the R wave are designated S' (S prime).
QRS complexes
Height of the QRS complex:
The height (amplitude) of the QRS complex reflects the relative muscle bulk of the ventricles; therefore, an increase in the amplitude of the QRS complex can indicate ventricular hypertrophy.
Duration of the QRS complex:
In normal activation of the ventricles, the QRS duration is 0.06 seconds, and should not exceed 0.11 seconds (3 small squares). Widening of the QRS occurs in a number of situations and generally indicates slowed ventricular conduction. One reason the QRS complex can widen is the presence of an ectopic electrical pacemaker within the bundles or ventricles.
4.4.3 QT interval
The interval from the onset of the QRS complex to the end of the T wave is termed the "QT interval". The QT interval represents the total time for ventricular depolarization (activation) and repolarization(recovery). Normal QT interval ranges from 0.30 to 0.44 seconds (up to 0.45 for women), but the interval varies with heart rate. The QT interval must be corrected for rate (QTc). A rapid method to obtain a QTc is to first measure the QT interval. Then measure the R-R interval (the distance between two consecutive R waves), and divide that number by two. If the QT interval is less than half the R-R interval, then it is likely to be normal. If it is more than half the R-R interval it is considered to be prolonged.
QT interval
A significantly prolonged or shortened QT interval (greater than 0.5 seconds or less than 0.3 seconds respectively) may be associated with congenital cardiac abnormalities (Long QT syndrome, Short QT syndrome), or toxicity from tricyclic antidepressants or a number of other drugs. Both Long QT syndrome and Short QT syndrome can lead to syncope (fainting) or sudden death due to fatal
arrhythmias such as ventricular fibrillation, ventricular tachycardia, or Torsades de Points.
4.5 Evaluate overall appearance
ST segment
The ST segment, measured from the end of the S wave to the beginning of the T wave, is isoelectric as it reflects a period of relative electrical inactivity. The ST segment is compared to the isoelectric linepresent at either the PR segment (between the P wave and QRS complex) or the TP segment (between the end of the T wave and beginning of the P wave). Deviation of the ST segment from the baseline, either above (elevation) or below (depression) the isoelectric line, can be both a normal variant or it may indicate a number of cardiac diseases (eg, pericarditis, myopathy). In the limb leads, ST segment depression of more than 0.5 mm or elevation of more than 1 mm suggests cardiac ischemia (or infarction). ST depression of 0.5 mm or elevation of more than 2 mm in the chest leads suggests myocardial ischemia.
T wave
The T wave represents repolarizationof the ventricles, and is the first wave following the QRS complex. The peak of the T wave indicates the beginning of the relative refractory period, where a higher than normal stimulus may result in a cardiac action potential (and subsequent ventricular arrhythmia). Generally, the T wave deflection is in the same direction as the QRS complex that precedes it, and is positive in most leads, although a negative deflection (inversion) of the T wave is common and often non-specific. Abnormal T waves can indicate a number of different conditions:
Inverted T waves can occur in cardiac ischemia/infarction, tension pneumothorax, digitalis toxicity, or CNS disturbance
T waves in the opposite direction of the preceding QRS complex may indicate an abnormal QRS complex (eg, ventricular premature beat, ventricular arrhythmia, bundle branch block)
Tall and "peaked" T waves are associated with hyperkalemia (elevated blood potassium)
Flattened T waves may be seen with hypokalemia (low blood potassium) and cardiac ischemia
T wave variations
5. Sinus rhythms
A normal heartbeat results from an electrical impulse that begins in the sinoatrial (SA) node. Normally, the pacemaker cells in the SA nodedepolarize more rapidly than other cardiac cells; therefore, the SA node usually dominates areas that may be depolarizing at a slower rate.
5.1 Features of sinus rhythms
Sinus rhythm is the name given to a normal heart rhythm, and reflects normal electrical activity. The rhythm begins in the SA node and continues through the normal conduction pathways, through the atria, atrioventricular (AV) junction, bundle branches, and ventricles. The SA node usually fires at a regular rate of between 60 and 100 beats per minute.
Sinus rhythm refers to when each P wave is followed by a narrow QRS complex (0.12 seconds), and each QRS complex is preceded by a P wave. The PR interval is less than 0.20.
5.2 Sinus bradycardia
Sinus bradycardia occurs when the SA node fires at a rate that is slower than normal. In adults, sinus bradycardia is defined as a heart rate of less than 60 beats per minute. Sinus bradycardia with a rate of less than 40 beats per minute is sometimes called "severe sinus bradycardia".
5.3 Sinus tachycardia
Sinus tachycardia occurs when the SA node fires at a rate that is faster than normal. In adults, sinus tachycardia is defined as a heart rate of greater than 100 beats per minute. Sinus tachycardia begins and ends gradually.
5.4 Sinus arrhythmia
Sinus arrhythmia occurs when the SA node fires irregularly. A sinus arrhythmia that is associated with the phases of respiration is called "respiratory sinus arrhythmia", while a sinus arrhythmia that is not associated with the respiratory cycle is called "non-respiratory sinus arrhythmia" (eg, due to medication or heart disease).
5.5 Sinoatrial block
In sinoatrial block, the electrical impulse initiated by the pacemaker cells in the SA node is blocked as it exits the SA node. Sinoatrial block is a disorder of conductivity, as the SA node fails to conduct the impulse to the surrounding atrium. The blocked impulse appears as a single missed beat on the ECG rhythm strip (where the PQRST complex is missing). The length of the pause is an exact multiple of the P-P interval of the underlying rhythm.
5.6 Sinus arrest
Sinus arrest occurs when the pacemaker cells of the SA node fail to initiate an electrical impulse for one or more beats. When sinus arrest occurs, an escape pacemaker site (AV junction or ventricles) should take over responsibility for pacing the heart. If this does not happen, PQRST complexes will be absent from the ECG. The P-P interval will not be an exact multiple of the underlying rhythm.
Summary of sinus rhythms
RateRhythmP wavesPR intervalQRS durationSinus rhythm60 - 100 bpmRegularPositiveNormal NormalSinus bradycardiaLess than 60 bpmRegularPositive
Normal
Normal
Sinus tachycardia101 - 180 bpmRegularPositive
Normal
Normal
Sinus arrhythmia60 - 100 bpmIrregular
Positive
Normal
Normal
Sinoatrial blockVariableIrregular
Positive
Normal
Normal
Sinus arrestVariableIrregularPositive
Normal
Normal
6. Atrial arrhythmia
6.1 Premature atrial complexes (PACs)
A premature atrial complex (PAC) occurs when an irritable site (ectopic focus) within the atria generates an electrical impulse before the sinoatrial (SA) node is due to fire its next electrical impulse, which interrupts the sinus rhythm. The P wave may look similar to P waves generated by the SA node, particularly if the irritable site is close to the SA node. However, the P wave may be biphasic, flattened, notched, or pointed.
A pause in the ECG is often seen after a premature complex. The pause following a PAC is generally a non-compensatory (incomplete) pause. The pause represents the delay during which the SA node resets its rhythm for the next beat. A compensatory (complete) pause often follows a premature ventricular complex (PVC) as the SA node continues to fire at a regular rate and rhythm.
6.2 Wandering atrial pacemaker
A wandering atrial pacemaker(multiformed atrial rhythm) results from the gradual shifting of the dominant pacemaker between the SA node, atria, and/or the atrioventricular (AV) junction. The shape, size, and direction of the P wave varies, sometimes from beat to beat.
6.3 Multifocal atrial tachycardia
If the ventricular rate associated with a wandering atrial pacemaker is greater than 100 beats per minute, the rhythm is known as multifocal atrial tachycardia. In this condition, multiple ectopic sites are responsible for stimulating the atria.
6.4 Supraventricular tachycardia
Supraventricular arrhythmias arise from above the bundle of His, meaning that they may include rhythms that begin in the atrial tissue, SA node, or the AV junction. Supraventricular tachycardia (SVT) incorporates three main types of abnormally fast rhythm: atrial tachycardia, AV nodal reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT).
6.4.1 Atrial tachycardia
Atrial tachycardia is the result of a series of rapid beats that are generated from an irritable site in the atria, often brought on by a PAC. The rapid rate of firing from the irritable atrial site overrides the SA node and it becomes the dominant pacemaker.
Paroxysmal atrial tachycardia (PAT) is the term used for atrial tachycardia that begins or ends suddenly. With rapid atrial rates, the AV node may filter (block) some of the impulses reaching it, in order to protect the ventricles from excessively rapid rates. The rhythm is then termed "paroxysmal atrial tachycardia with block".
"Focal atrial tachycardia" is the term used to describe an atrial tachycardia that begins in a small area (focus) within the atria.
Automatic atrial tachycardia is a type of atrial tachycardia associated with a "warm up" and "cool down" period. The "warm up" period involves a progressive shortening of the P-P interval throughout the first few beats of the arrhythmia. Automatic atrial tachycardia gradually slows down as it ends, known as a "cool down" period. The atrial rate associated with automatic atrial tachycardia is generally between 100 and 250 beats per minute.
6.4.2 AVNRT
AV nodal re-entrant tachycardia(AVNRT) is the result of impulse re-entry in the area of the AV node. Patients with this condition have two conduction pathways within the AV node; each with a different conduction rate and different recovery time. The slow pathway conducts impulses more slowly but has a shorter recovery time (refractory period). The fast pathway conducts impulses quickly but has a longer refractory period. Under certain conditions, the slow and fast pathways form an electrical circuit or loop. AVNRT is generally caused by a PAC that is spread via the electrical circuit formed by the slow and fast conduction pathways, allowing the impulse to re-enter the normal electrical pathway with each pass around the circuit. The resulting rhythm is very rapid and regular, and ranges from 150 to 250 beats per minute.
6.4.3 AVRT
AV re-entrant tachycardia (AVRT) is caused by an impulse being conducted along a pathway that lies outside the AV node and bundle of His, generating a rhythm known as "pre-excitation". Because it bypasses the normal impulse delay in the AV node, the supraventricular impulse excites the ventricles sooner than if it had travelled via the normal conduction pathway.
In Wolff-Parkinson-White (WPW) Syndrome, the impulse travels quickly through an accessory pathway, bypassing the usual delay in the AV node, thereby resulting in a shortened PR interval. On ECG, pre-excitation of the ventricles may be observed through the presence of a delta wave in some leads. The QRS appears widened as the impulse is initially conducted through the ventricular muscle cells, although the remainder of the impulse is conducted normally. As a result of the abnormal ventricular activation, there may be associated ST segmentand T wave changes in WPW (in the opposite direction to the QRS complex), due to the abnormal repolarization of the ventricles that follows.
6.5 Atrial flutter
Atrial flutter is divided into two types:
Type I (classical or typical) atrial flutter is the result of re-entry, whereby the impulse circles around a large area of tissue, such as the entire right atrium. In this type of atrial flutter, the atrial rate ranges from 250 to 350 beats per minute
Type II (very rapid or atypical) atrial flutter often develops into atrial fibrillation. The exact cause of this type of atrial flutter is not known. In type II atrial flutter, the atrial rate ranges from 350 to 450 beats per minute
P waves are not visible and consequently the PR interval is not measurable. The flutter wave, which replaces the P wave, has a characteristic "saw tooth" appearance, due to the re-entrant electrical circuit within the atrium. The ventricles are protected from this rapid stimulation by the AV node, which cannot conduct at such a rapid rate. As a result, some of the impulses are blocked by the AV node, producing a slower ventricular rate (than the atrial rate). The ventricular rhythm is determined by the rate at which the AV node blocks incoming impulses and is described as a ratio of the atrial rate (atrial rate:ventricular rate).
The ventricular rhythm is usually even (2:1, 4:1, 6:1) and regular, but variable conduction can occur, resulting in an irregular ventricular response.
6.6 Atrial fibrillation
Atrial fibrillation occurs when one or more irritable sites in the atria begin firing at a rate of 400 to 600 times per minute. The rapid impulses are disorganized and cause the atrial muscles to quiver (fibrillate), leading to less effective atrial contraction, decreased stroke volume, and a subsequent decrease in cardiac output. Most of the atrial impulses are blocked by the AV node and not conducted to the ventricles, but some P waves do cause a ventricular response, which results in an irregularly irregular ventricular rhythm.
There are no discernable P waves (due to the disorganized electrical activity), and the PR interval is not measureable. The QRS complex is narrow, as the impulse is conducted normally after it passes through the AV node.
Atrial fibrillation is associated with a significant increase in the risk of stroke, particularly among patients with pre-existing coronary heart disease or cardiac failure. Stroke may be brought about by pooling of blood within the atria and the formation of blood clots (caused by ineffectual atrial contraction).
Summary of atrial arrhythmia
RateRhythmP wavesPR intervalQRS durationPACs60 - 100 bpmRegular, with premature beatsPositive, prematureNormal or prolongedNormalWandering atrial pacemaker60 - 100 bpmMaybe irregularVariable
Variable
Normal
Atrial tachycardia100 - 250 bpmRegularDifferent from sinus P waves
Variable
Normal
AVNRT150 - 250 bpmVentricular rhythm is regularMay be hidden in QRS complex
Not measurable
Normal
WPW60 - 100 bpmRegularPositive
ShortenedProlonged
Atrial flutter250 - 450 bpmAtrial regular, ventricular variable"Saw-toothed" appearance
Not measurable
Normal
Atrial fibrillation400 - 600 bpmVentricular rhythm irregularly irregularNot identifiableNot measurable
Normal
7. Junctional arrhythmia
The atrioventricular (AV) node is located in the lower part of the right atrium, above the base of the tricuspid valve. The main function of the AV node is to delay conduction of the electrical impulse, to allow the atria to contract and complete filling of the ventricles before the next ventricular contraction. The bundle of His connects the AV node with the two bundle branches, and contains pacemaker cells with an intrinsic firing rate of 40 to 60 beats per minute. The AV junction is composed of the AV node and the non-branching portion of the bundle of His.
The AV junction may assume responsibility for pacing the heart if any of the following occur:
The sinoatrial (SA) node fails to discharge
An impulse from the SA node is blocked as it exits the SA node
The rate of firing from the SA node is slower than the rate of firing from the AV junction
The impulse from the SA node is conducted through the atria but is not conducted to the ventricles
If the AV junction assumes responsibility for pacing the heart, the impulse must travel in a retrograde (backward) direction in order to activate the atria. Therefore, if P waves are seen on the ECG, they will be inverted in leads II, III, and aVF, as the impulse is travelling away from the positive electrode:
An inverted P wave with a shortened PR interval (0.12 seconds or less) will be seen if the atria depolarize before the ventricles
The P wave may be buried (or hidden) within the QRS complexand will therefore not be visible if the atria and ventricles depolarize at the same time
An inverted P wave may be seen after the QRS complex, if the atria depolarize after the ventricles
7.1 Premature junctional complexes (PJCs)
A premature junctional complex (PJC) occurs when an irritable site in the AV junction discharges an electrical impulse before the next SA node impulse is due to discharge, leading to an interruption of the sinus rhythm. The QRS complex looks normal as the electrical impulse is conducted through the ventricles in the normal manner.
A pause in the ECG is often seen after a premature complex. The pause following a PJC is generally a non-compensatory (incomplete) pause. The pause represents the delay during which the SA node resets its rhythm for the next beat. In contrast, a compensatory (complete) pause often follows a premature ventricular complex (PVC) as the SA node continues to fire at a regular rate and rhythm.
If a junctional complex occurs beforethe next expected sinus beat it is called a "premature junctional complex". A junctional complex that occurs after the expected sinus beat is called a "junctional escape beat".
7.2 Junctional escape beats/rhythm
A junctional escape beat begins in the AV junction and appears afterthe next expected sinus beat. They commonly occur when the SA node fails to fire (sinus arrest) and serve as a protective mechanism to maintain cardiac activity. The AV junction temporarily takes over from the SA node as the cardiac pacemaker.
A junctional escape rhythm(junctional rhythm) is the term applied to several sequential junctional escape beats. Junctional rhythms have the characteristic features of a complex originating in the AV junction: absent, inverted, or retrograde P waves, with a normally conducted QRS complex. The intrinsic pacemaker rate of the AV junction is 40 to 60 beats per minute, which dictates the rate of a junctional rhythm. Junctional bradycardia occurs when the AV junction is pacing the heart at a rate that is slower than 40 beats per minute, whereas accelerated junctional rhythm and junctional tachycardia refer to rhythms originating in the AV junction with a rate of more than 60 beats per minute.
7.3 Accelerated junctional rhythm
An accelerated junctional rhythmoccurs when the AV junction is firing at a rate of 61 to 100 beats per minute, resulting from enhanced automaticity of the bundle of His. The only difference between a junctional rhythm and an accelerated junctional rhythm on ECG is the increase in ventricular rate.
7.4 Junctional tachycardia
Junctional tachycardia occurs when three or more sequential junctional complexes occur at a rate of more than 100 beats per minute, resulting from enhanced automaticity of the bundle of His. Junctional tachycardia may be paroxysmal (sudden and transient) or non-paroxysmal (continuous).
Non-paroxysmal junctional tachycardia
Usually begins as an accelerated junctional rhythm, with the heart rate gradually increasing to greater than 100 beats per minute
The ventricular rate usually ranges from 101 to 140 beats per minute
Paroxysmal junctional tachycardia
Begins and ends suddenly
May be precipitated by a PJC
The ventricular rate is usually greater than 140 beats per minute
Summary of junctional arrhythmia
RateRhythmP wavesPR intervalQRS durationPJCs60 - 100 bpmRegularVariable, inverted in leads II, III, and aVFNormal if P wave occurs before QRSNormalJunctional escape beat60 - 100 bpmRegularVariable, inverted in leads II, III, and aVF
Normal if P wave occurs before QRS
Normal
Junctional escape rhythm40 - 60 bpmRegularVariable, inverted in leads II, III, and aVF
Normal if P wave occurs before QRS
Normal
Accelerated junctional rhythm60 - 100 bpmRegularVariable, inverted in leads II, III, and aVF
Normal if P wave occurs before QRS
Normal
Junctional tachycardia100 - 180 bpmRegularVariable, inverted in leads II, III, and aVF
Normal if P wave occurs before QRS
Normal
8. Ventricular arrhythmia
The ventricles may assume responsibility for pacing the heart if any of the following occur:
The sinoatrial (SA) node fails to discharge
An impulse from the SA node is blocked as it exits the SA node
The rate of firing from the SA node is slower than the rate of firing from the atrioventricular (AV) junction
An irritable site in either ventricle produces an early beat or rapid rhythm
The intrinsic (natural) pacemaker rate of the ventricles is 20 to 40 beats per minute, which sets the rate of a ventricular rhythm. Ventricular beats and rhythms can occur as the result of re-entry, triggered activity, or enhanced automaticity. They can begin in any part of the ventricle. If an ectopic site in the ventricle assumes responsibility for pacing the heart, the electrical impulse bypasses the normal conduction pathway in the ventricles, resulting in QRS complexes that are abnormally shaped and longer than the usual 0.12 seconds. As a result of the abnormal activation of the ventricle, there may be associated ST segmentand T wave changes (in the opposite direction to the QRS complex), due to the subsequent abnormal repolarization of the ventricles. P waves are usually absent, or if visible, have no consistent relationship to the QRS complex.
8.1 Premature ventricular complexes
A premature ventricular complex(PVC) is caused by an irritable ventricular focus, and occurs before the next expected sinus beat. The QRS associated with a PVC is generally greater than or equal to 0.12 seconds as the ventricles fire in an abnormal way. The T wave is generally in the opposite direction of the QRS complex. A full compensatory (complete) pause often follows a premature ventricular complex (PVC) as the SA node timing is not interrupted and continues to fire at a regular rate and rhythm.
8.1.1 Types of PVC
Uniform PVCs are beats that are identical in the same lead. These originate from the same anatomic site (focus)
Uniform premature
ventricular complexes
Multiform PVCs are beats that look different in the same lead. Usually, but not always, these arise from different ectopic sites
Multiform premature
ventricular complexes
Sequences of PVCs
Ventricular bigeminy is an arrhythmia that consists of the repeated sequence of one PVC followed by one normal beat
Ventricular trigeminy is an arrhythmia that is comprised of a repeated sequence of one PVC followed by two normal beats
Ventricular quadrigeminy is an arrhythmia that consists of a repeated sequence of one PVC followed by three normal beats
Multiple PVCs
A pair of PVCs occurring sequentially is called a PVC couplet
A repeated sequence of three or more PVCs in a row, at a rate of greater than 100 beats per minute, is defined as a "run" or "burst" of ventricular tachycardia (covered later in the section)
The PVC occurs so early that the R wave falls on the T wave of the preceding beat
The PVC occurs during the relative refractory period of the ventricles, when the ventricles are vulnerable to electrical stimulation, which may precipitate a ventricular dysrhythmia
Occurs when a PVC occurs at the same time as an impulse from another site
If a PVC arises at the same time as a sinus impulse, a P wave will be associated with the fusion beat
Appearance is a combination of a PVC and a normally conducted impulse
8.2 Ventricular escape beats
A ventricular escape beat occurs after a pause in which the supraventricular pacemaker has not fired; the escape beat is late as it appears after the next expected sinus beat. A ventricular escape beat is a protective mechanism as it prevents the heart from extreme slowing or from asystole (no cardiac electrical activity).
8.3 Idioventricular rhythm
An idioventricular rhythm (IVR) is the term given to describe the situation when three or more ventricular escape beats occur in a row at a rate of 20 to 40 beats per minute (also known as a ventricular escape rhythm). The rate reflects the intrinsic (natural) pacemaker rate of the ventricles. The impulse begins in the ventricles and bypasses the normal conduction pathway, resulting in a wide and bizarre QRS complex. This rhythm may be associated with low cardiac output due to the slow heart rate. An IVR at a rate of less than 20 beats per minute is termed an "agonal rhythm", which is often a terminal event (occurring immediately prior to death).
8.4 Accelerated idioventricular rhythm (AIVR)
Accelerated idioventricular rhythm(AIVR) is the term used to denote the presence of three or more ventricular escape beats that occur in a row at a rate of between 41 and 100 beats per minute. Generally considered a benign escape rhythm, it appears when the sinus rate slows down, and then disappears when the sinus rate speeds up. Episodes of AIVR generally last from a few seconds to one minute, and fusion beats are often seen at the beginning and end of the rhythm.
8.5 Ventricular tachycardia (VT)
Ventricular tachycardia (VT) occurs when three or more PVCs occur in a row at a rate of greater than 100 beats per minute. Ventricular tachycardia can occur for a short "run" of less than 30 seconds duration, known as "non-sustained" VT, but if it persists for more than 30 seconds it is termed "sustained" VT.
Note:
VT can be difficult to distinguish from SVT with an interventricular conduction delay. A 12-lead ECG recording may help to differentiate the two. Confirm the presence or absence of a pulse when VT is encountered, as all types of VT can either be perfusing or non-perfusing (with or without peripheral pulses).
8.5.1 Types of VT
Monomorphic VT
The QRS complexes of the VT are all of the same amplitudeand shape. In some cases, a patient with monomorphic VT remains stable, but often the patient becomes hemodynamically unstable (eg, shock, chest pain, hypotension, shortness of breath) as a result of the tachycardia. Monomorphic VT can occur either with or without a pulse, and may degenerate into polymorphic VT or ventricular fibrillation.
Polymorphic VT
A sustained VT where the QRS complexes vary in amplitude and shape from beat to beat, and appear to twist around the isoelectric line (alternating from upright to negative and vice versa), resembling a spindle.
Polymorphic VT is classified in two distinctive forms, based on its association with a normal or prolonged QT interval:
Normal QT interval (referred to as polymorphic VT or polymorphic VT resembling Torsades de Pointes (Tdp))
Long QT syndrome
Long QT syndrome (LQTS) is the result of an abnormality of the electrical system of the heart, while the mechanical function of the heart remains normal. The electrical abnormality results in a prolonged QT interval, which predisposes the affected person to TdP
LQTS may be acquired (as a result of medications, electrolyte imbalance, toxic substances) or congenital (inherited)
When polymorphic VT occurs in the presence of long QT intervals, the condition is known as Torsades de Pointes (TdP), a life threatening arrhythmia which means "twisting of the points". TdP is usually not sustained, but may deteriorate into sustained VT, ventricular fibrillation or asystole
Long QT syndrome should be considered with recurrent syncope (fainting) and unexpected cardiac arrest (particularly in young people)
8.6 Ventricular fibrillation (VF)
Ventricular fibrillation (VF) is a chaotic rhythm in which there is no organized depolarization of the ventricles. Consequently, myocardial contraction is not effective and as a result there is no cardiac output and no pulse. There are no normal waveforms visible in the ECG.
The amplitude and frequency of the fibrillatory waves is used to further define the VF as either "coarse" VFwhere the waves are greater than 3mm high, or "fine" VF where the undulations are of low amplitude (less than 3 mm).
8.7 Asystole
Asystole is the complete absence of any ventricular activity; there are no QRS complexes, no ventricular rate or rhythm, no cardiac output, and no pulse. There may be evidence of atrial electrical activity and, if so, the rhythm is known as "P wave asystole"(or ventricular standstill).
8.8 Pulseless electrical activity
Pulseless electrical activity (PEA) is a clinical condition rather than a specific dysrhythmia. It occurs when organized electrical activity (other than VT) is evident on the cardiac monitor, but the patient is unresponsive, does not have a pulse, and is not breathing. Unless the cause of PEA can be rapidly determined and treated, it is associated with a poor prognosis.
Summary of ventricular arrhytmia
RateRhythmP wavesPR intervalQRS durationPVCs60 - 100 bpmRegularUsually absentNot presentProlongedVentricular escape beats60 - 100 bpmRegularUsually absentNot presentProlongedIdioventricular rhythm20 - 40 bpmRegularUsually absentNot presentProlongedAIVR40 - 100 bpmRegularUsually absentNot presentProlongedVentricular tachycardia100 - 250 bpmRegularVariableNot presentProlongedVentricular fibrillationNot measurableRapid and chaoticNot measurableNot measurableNot measurableAsystoleNot measurableNot measurableUsually absentNot measurableAbsent
9. AV blocks
An atrioventricular (AV) block occurs when there is a delay or interruption to the electrical impulse within the AV node, bundle of His, or the His-Purkinje system. AV blockade may be due to a pathological process such as ischemia, fibrosis, or toxicity.
9.1 First-degree AV block
In first-degree AV block, all parts of the ECG are within normal ranges, except for a prolonged PR interval. Electrical impulses travel normally through the atria from the sinoatrial (SA) node, but there is a delay in impulse conduction, usually at the AV node. The sinus impulse is not blocked as all the beats are conducted, but there is a simple slowing of conduction, reflected by a prolonged PR interval (more than 0.2 seconds).
9.2 Second-degree AV block
Second-degree AV blocks occur when the conduction delay from atria to ventricles is intermittently complete so that some, but not all, of the atrial impulses are blocked from reaching the ventricles. Each P waveoccurs at regular intervals across the rhythm strip, but not all P waves are followed by a QRS complex. Second-degree AV block is classified as either type I or type II according to the location of the block.
9.2.1 Second-degree AV block type I (Wenckebach, or Mobitz type I)
In second-degree AV block type I, the conduction delay normally occurs at the level of the AV node. The conduction delay (and thus the PR interval) becomes progressively longer on consecutive complexes, until the signal is completely blocked and the QRS is dropped. After a pause, the AV node recovers and the cycle is repeated. The QRS is usually narrow as the block occurs above the level of the bundle branches.
9.2.2 Second-degree AV block type II (Mobitz type II)
In second-degree AV block type II, the conduction delay occurs below the level of the AV node, at either the bundle of His or at the level of the bundle branches. This type of block commonly progresses to third-degree AV block. The atrial rate is regular, but conduction through the AV node is intermittently completely blocked. The blockade occurs at the level of the His-Purkinje system, reflected by the widening of the QRS complex.
9.2.3 Second-degree AV block, 2:1 conduction (2:1 AV block)
In 2:1 AV block, two P waves occur for each QRS complex (2:1 conduction). Generally, a 2:1 AV block with a narrow QRS complex is representative of a second-degree AV block type I, whereas a 2:1 AV block with wide QRS complexes is usually associated with a type II block.
9.3 Third-degree/complete AV block
In third-degree/complete AV block, the impulses generated in the SA node are blocked before reaching the ventricles, so no P waves are conducted (complete heart block). As a consequence, the atria and ventricles beat independently of each other (known as AV dissociation). P waves are often regular and have a normal appearance, but there is no relationship with the QRS complex. The conduction block can occur at the AV node, at the bundle of His, or at the bundle branches. A secondary pacemaker is then responsible for pacing the ventricles with an escape rhythm, and thus the QRS complex may be wide or narrow, depending on the location of the pacemaker site (wide, if located in the ventricles or narrow if located in the AV junction) and on the condition of the interventricular conduction pathways.
Third degree AV block is often associated with ischemia involving the left coronary arteries:
Third-degree AV block that is associated with an inferior MI(usually the right coronary artery ) is considered to be the result of a block above the bundle of His. The resulting rhythm is usually stable as the escape pacemaker is usually junctional (narrow QRS complexes), with a ventricular rate of greater than 40 beats per minute
Third-degree AV block that is associated with an anterior MI(left anterior descending coronary artery) usually results in an unstable rhythm because the escape pacemaker is usually ventricular (wide QRS complexes), with a resulting ventricular rate of less than 40 beats per minute
Summary of AV blocks
RateRhythmP wavesPR intervalQRS durationFirst-degree block60 - 100 bpmRegularNormalProlongedNormalSecond-degree block; type IAtrial rate greater than ventricular rateAtrial regular; ventricular irregularNormalIncreasingly prolonged until a P wave appears without a QRSNormalSecond-degree block; type IIAtrial rate greater than ventricular rate
Atrial regular; ventricular irregular
NormalNormal or prolongedProlongedSecond-degree block; 2:1 conductionAtrial rate double the ventricular rateRegularNormal; every second P wave followed by a QRSConstantNormal or prolongedThird-degree blockAtrial rate greater than ventricular rateRegular; no relationship between atrial and ventricular rhythmNormalNot presentVariable
10. Pacemaker rhythms
10.1 Pacemaker terminology
10.2 Pacemaker systems
A pacemaker is a device used to stimulate the heart with an electrical current, in place of the heart's natural pacemaker. A pacemaker system comprises a pulse generator (power source), which sends and receives electrical signals along one or more pacing leads (each with an electrode implanted in the heart). The pacemaker can analyze the intrinsic activity of the heart and can be programmed to stimulate the heart either continuously or intermittently.
Permanent pacemakers
Permanent pacemakers are surgically implanted in the body (usually under local anesthesia). The circuitry of the pacemaker is contained within a titanium case that is airtight and impermeable to fluid. The entire pacemaker must be replaced when the battery gets low. Permanent pacemakers use sensing and pacing device leads. Permanent pacemakers are indicated in atrioventricular (AV) block, sinus arrest, and symptomatic bradycardia with syncope.
Temporary pacemakers
Temporary pacing of the heart is often used in an emergency. Pacing of the heart is achieved through epicardial, transvenous, or transcutaneous routes, but the pulse generator is externally located. Emergency temporary pacing is indicated for hemodynamically unstable bradycardia, overdrive pacing of tachycardia, bradycardia that is unresponsive to treatment with medication, or in brady-asystolic arrest.
10.2.1 Single-chamber pacemakers
One lead is placed in the heart, which paces a single heart chamber (either the atrium or the ventricle).
Achieved by placing the electrode in the right atrium
Stimulation of the atrium results in a pacemaker spike on the ECG, followed by a P wave
Used when the sinoatrial (SA) node is dysfunctional but conduction through the AV node and ventricles is normal
Achieved by placing the electrode in the right ventricle
When the ventricle is stimulated a pacemaker spike appears on the ECG followed by a wide QRS complex; the QRS complex is wide because the impulse does not follow the normal ventricular conduction pathway
Ventricular demand pacing is rarely used when the SA node is intact, as the intrinsic pacemaker (and thus atrial contraction) would not function synchronously (in time) with the ventricular contraction (AV asynchrony)
10.2.2 Dual-chamber pacemakers
Dual-chamber pacemakers use a two-lead system to pace both the atrium and the ventricle. One lead is placed in the right atrium and the other in the right ventricle. The AV sequential pacemaker stimulates the right atrium followed by the right ventricle. This is similar to normal cardiac physiology and thus preserves the atrial contribution to ventricular filling (atrial kick).
10.2.3 Transcutaneous pacing
Transcutaneous pacing is a recommended means of pacing in the heart in an emergency. It is safe, effective, quick, and less invasive than other pacing techniques. It is commonly used for symptomatic bradycardia that does not respond to treatment with drugs (atropine).
Transcutaneous pacing is achieved by placing two electrodes on the skin of the patient's outer chest wall. Normally, the negative chest electrode is placed on the left lower anterior chest (to the left of the sternum) and the positive electrode is positioned posteriorly on the left lower thorax, directly behind the negative electrode (anterior-posterior positioning).
Alternatively, the negative electrode can be placed on the left lower anterior chest and the positive electrode on the right upper chest in the subclavicular area.
The pads are then connected to a cardiac defibrillator, and a rhythm strip obtained. A heart rate is selected (60-80 beats per minute in the presence of a pulse, or 80-100 beats per minute for asystole). The current is gradually increased until electrical capture is achieved, characterized by a wide QRS complex and a tall, broad T wave. Sedation or analgesia may be required to prevent patient discomfort.
If defibrillation is necessary, the paddles should be placed 3/4 to 1 inch (2-3 cm) away from the pacemaker electrodes, in order to prevent arcing.
10.3 Pacemaker malfunction and complications
Failure to pace
Failure to pace occurs when the pacemaker does not deliver an electrical stimulus or when it does not deliver the correct number of electrical stimuli per minute. Failure to pace can be seen on the ECG as an absence of pacemaker spikes, with a return to the underlying pathological rhythm. It may be caused by failure of the battery, a disruption in the connecting wires, or incorrect programming.
Failure to capture
"Failure to capture" is the term used to describe the failure of the pacemaker stimulus to properly depolarize the myocardium. Pacemaker spikes are present on the ECG but they are not followed by P waves (if the atrium is stimulated) or QRS complexes (if the ventricle is stimulated).
Failure to sense
Failure to sense occurs when the pacemaker fails to recognize spontaneous cardiac depolarization. It can be seen on the ECG as pacemaker spikes that follow too closely after the QRS complexes. This type of malfunction may lead to pacemaker spikes occurring during T waves (R-on-T phenomenon) and/or competition between the patient's own cardiac rhythm and the pacemaker.
Oversensing
Oversensing occurs when the pacemaker is too sensitive and detects extraneous electrical signals:
Muscle movement
External electrical interference
Atrial pacemakers may detect ventricular electrical activity
Ventricular pacemakers may interpret a tall, peaked T wave as being a QRS complex.
Oversensing is shown on the ECG as pacemaker spikes that are at a slower rate than the pacemaker's preset rate, or an absence of paced beats despite the pacemaker's preset rate being greater than the intrinsic rate.
10.4 Analyzing pacemaker function with an ECG
Identify the intrinsic rate and rhythm
Are P waves present and, if so, at what rate?
Are QRS complexes present and, if so, at what rate?
Is there evidence of paced activity?
Evaluate the paced interval if paced atrial activity is present in the ECG
Measure the distance between consecutively paced atrial beats
Assess the rate and regularity of the paced interval
Evaluate the paced interval of ventricular activity, if it is present
Measure the distance between consecutively paced ventricular beats
Assess the rate and regularity of the paced interval
Evaluate the escape interval
Compare the escape interval to the paced interval; they should be similar
Analyze the rhythm strip
Analyze the strip for failure to pace, failure to capture, failure to sense, and oversensing
11. Interpret the 12-lead ECG
11.1 Normal 12-lead ECG
A 12-lead ECG provides a view of the heart in the frontal and horizontal planes, and views the surface of the left ventricle from 12 different angles. The 12-lead ECG consists of six limb leads ( I, II, III, aVR, aVL, and aVF) and six chest leads (V1, V2, V3, V4, V5, and V6). The limb leads view the heart in the frontal (coronal) plane, whereas the chest leads view the heart in the horizontal (transverse) plane.
11.1.1 Leads
Standard limb leads
Leads I, II, and III are the standard limb leads. Each of these leads is bipolar as they have a distinct negative pole and a distinct positive pole. Lead I views the lateral surface of the left ventricle, while leads II and III view the inferior surface of the left ventricle.
In a normal 12-lead ECG, the P wave, QRS complex, and T wave are all upright in leads I, II, and III.
Leads I, II, and III
Augmented limb leads
Leads aVR, aVL, and aVF are the augmented limb leads. These leads are unipolar. Lead aVR views the heart from the right shoulder and views the base of the heart. Lead aVL views the heart from the left shoulder and views the lateral wall of the left ventricle. Lead aVF views the heart from the left foot and views the inferior surface of the left ventricle.
In a normal 12-lead ECG, the P wave, QRS complex, and T wave are all upright in leads aVL and aVF, whereas in aVR, the P wave, QRS complex, and T wave are all inverted.
Leads aVR, aVL,
and aVF
Chest leads: V1, V2, V3, V4, V5, V6
Leads V1 and V2 view the interventricular septum of the heart, V3 and V4 view the anterior surface of the left ventricle, and V5 and V6 view the lateral surface of the left ventricle.
Chest leads
In the chest leads, the P wave and T wave are upright; the QRS complex changes as the impulse moves from left to right (known as R wave progression).
R wave progression
The interventricular septum depolarizes from left to right, and from posterior to anterior. The wave of depolarization in the major portions of the ventricles normally occurs from right to left, and from anterior to posterior. In a normal patient, when viewing the chest leads, the R wave becomes progressively taller and the S wave smaller as the electrode is moved from right to left, a pattern known as "R wave progression".
"Poor R wave progression" is the term used to describe R waves that decrease in size from V1 to V4. It is often seen in anteroseptal infarction, but can also be a normal variant, particularly in young women. Other causes of poor R wave progression include: left bundle branch block, severe chronic obstructive pulmonary disease, left ventricular hypertrophy, and old anteroseptal and anterior infarctions.
11.1.2 Layout of the 12-lead ECG
Most 12-lead ECG monitors record all 12 leads simultaneously, but display them in a standard format of three rows and four columns.
The standard limb leads are recorded in the first column, the augmented limb leads in the second column, and the chest leads in the third and fourth columns. In each row, the QRS complexes are consecutive, while QRS complexes that are lined up vertically are a simultaneous recording of the same beat.
The 12-lead ECG gives a 2.5 second view of each lead, but a continuous rhythm strip of 10 seconds duration is usually provided at the bottom of the tracing.
Each lead on the 12-lead ECG corresponds to a different surface of the heart so that changes on the recording can be localized to different areas of the heart. Leads I, aVL, V5, and V6 relate to the lateral surface of the heart. Leads II, III, and aVF are the inferior leads. The electrical activity at the septum is recorded by leads V1 and V2, while the anterior heart activity is seen by leads V3 and V4.
Clinical lead
groupings
11.2 Axis
The electrical axis of the heart refers to the general direction of the depolarization wavefront (electromotive forces) within the heart, in the frontal plane, at any one time. It is the main vector of depolarization, and generally refers to the axis of the QRS wavefront.
11.2.1 Vectors
The ECG does not directly measure the heart's electrical activity. Instead, the ECG records the net result of the numerous individual electrical currents in both the left and right ventricles. Since the left ventricle has a much greater mass than the right ventricle, the electrical signal from the left ventricle overpowers that coming from the right ventricle. Therefore, in a normally conducted beat, the QRS complex represents the electrical activity occurring in the left ventricle. A vector (arrow) is used to represent this electrical force.
A mean vector represents the average of depolarization waves in one area of the heart. The mean P vector shows the average magnitude and direction of the left and right atrial depolarization, while the mean QRS vector represents the average of both left and right ventricular depolarization. The mean axis represents the average direction of a mean vector, and is only identified in the frontal plane. The electrical axis is the direction in which the main vector of depolarization is pointing.
11.2.2 Einthoven's triangle/Hexaxial reference system
The electrical axes of leads I, II, and III form an equilateral triangle, known as Einthoven's triangle, with the heart at the centre of the triangle.
The hexaxial reference system includes all of the frontal limb leads with the heart at the center, and is used to express the electrical activity of the heart, in the frontal plane.
Hexaxial reference
system
The reference system forms a 360-degree circle around the heart, with the positive end of lead I designated as zero degrees. The six frontal plane leads divide the circle into 30-degree segments. All degrees above the horizontal line are labeled as negative degrees, while those below the horizontal line are labeled as positive degrees. The normal electrical axis lies between 0 and +90 degrees. When current is flowing to the right of normal it is termed "right axis deviation" (+91 to +180 degrees). When current is flowing to the left of normal it is termed "left axis deviation" (-1 to -90 degrees). If the current is flowing in the direction opposite to that of normal, it is termed "indeterminate" or "extreme right axis deviation" (-91 and -179 degrees).
Note:
According to some authors, the figures for normal electrical axis (0 to +90 degrees) can vary to include a range between -30 and +120 degrees. Anything outside this range is definitely abnormal.
11.2.3 Two-lead method of axis determination
Leads I and aVF can be used to quickly determine the electrical axis of the heart as they divide the heart into four quadrants. Normally, the QRS complex is positive in both of these leads. If the QRS complex in either, or both, of these leads is negative, it is an indication that the axis deviates from normal (axis deviation).
Right axis deviation may be a normal variant, or seen with inspiration, especially in thin or young people. Other causes of right axis deviation include right ventricular hypertrophy, chronic obstructive pulmonary disease, Wolf-Parkinson-White syndrome, and pulmonary embolism.
Left axis deviation may be a normal variant, or seen with expiration, especially in older or obese patients. Other causes of left axis deviation include hyperkalemia, emphysema, left atrial hypertrophy, or a high diaphragm (caused by pregnancy, ascites, or abdominal tumors).
11.3 Myocardial ischemia
Myocardial ischemia is the result of an imbalance between the amount of oxygenated blood required by the myocardium and the flow of oxygenated blood to the myocardium. Ischemia can result from an increase in demand for oxygen by the myocardium, reduced supply of oxygen to the myocardium, or both. Myocardial ischemia may be experienced by the patient as angina (chest pain or discomfort radiating to the arms, neck, or shoulders), shortness of breath, fatigue, sweating, or nausea.
Myocardial ischemia affects the cells in the heart that are responsible for the generation and conduction of electrical impulses, as well as the cells responsible for contraction. The delay in depolarization and repolarizationare reflected by changes in the ST segment and T wave.
11.3.1 ST segment changes
ST segment depression
The presence of ST segment depression on an ECG is suggestive of ischemia, and is considered particularly significant when the depression is greater than 0.5 mm (1 small square) below the baseline, at a point 0.04 seconds to the right of the J point (the point where the QRS ends and the ST segment begins).
ST segment depression
11.3.2 T wave changes
If ischemia extends throughout the full thickness of the myocardium, the T waves will be inverted in the leads that face the ischemic areas of the ventricle. If ischemia affects only the subendocardial layer, the T wave is usually positive, though it may be abnormally tall.
11.4 Myocardial infarction
Myocardial infarction occurs when blood flow to the myocardium stops or is decreased long enough to cause cell death (infarction). Infarcted cells do not function properly or respond to electrical stimuli.
11.4.1 ST changes
ST elevation
ST segment elevation occurs because injured cardiac cells do not depolarize normally, remaining more positive than the surrounding unaffected tissue. The presence of ST elevation provides the primary evidence of myocardial infarction in progress. ST elevation is considered significant if the ST segment is elevated more than 1 mm from the isoelectric line at the J pointin the limb leads and 2mm in the chest leads.
ST elevation
ST depression
During myocardial injury, ST depression can be seen in the leads opposite the affected area, as a "mirror" or reciprocal change.
ST depression
11.4.2 T wave changes
The development of tall T waves is an early indication that myocardial infarction is occurring. These changes may occur within the first few minutes of infarction, and are often not recorded as they may have resolved or become inverted by the time the patient receives medical attention. T-wave inversion may precede ST-segment elevation, indicating the presence of ischemia.
11.4.3 Q waves
An abnormal Q wave (more than 0.04 seconds wide, and more than 1/3 the height of the QRS complex) indicates the presence of dead myocardial tissue and loss of electrical activity. Q waves commonly appear several hours or days after the onset of signs and symptoms of infarction. The combination of abnormal Q waves with ST-segment changes or T-wave changes suggests an acute myocardial infarction.
Over time, the ST segment returns to the isoelectric line and the T wave regains its normal appearance. However, the Q wave may remain abnormal due to scar formation, providing evidence that a myocardial infarction has occurred.
11.5 Pericarditis
Pericarditis is inflammation of the pericardium (the sac that surrounds the heart). The pericardium's normal function is to reduce friction between the heart and surrounding organs and to protect the heart. Acute pericarditis can arise from complications associated with infections, myocardial infarction, or immunologic conditions.
Typical ECG changes associated with acute pericarditis include diffuse concave-upward ST-segment elevation (except aVR, which may show ST depression), in association with PR-segment depression.
11.6 Pericardial effusion
Pericardial effusion is the buildup of fluid in the pericardial cavity. The accumulation of fluid can lead to an increase in intrapericardial pressure, which can have an adverse effect on heart function (cardiac tamponade). Pericardial effusion is usually the result of an abnormal balance between the production and reabsorption of pericardial fluid, or from an abnormality that allows fluid to enter the pericardial cavity.
The ECG changes associated with acute pericarditis and pericardial effusion evolve through four stages. In stage I, the ECG typically shows diffuse ST-segment elevation, in association with PR depression. In stage II of the condition, ST and PR segments normalize. In stage III, widespread T-wave inversions develop, and in stage IV the T waves return to normal.
11.7 Electrolyte imbalance
The main ions involved in the conduction of impulses from cell to cell are calcium, potassium, and sodium.
There are two types of action potential in the heart: fast and slow.
Fast-response action potentials
Occur in the cells of the atria, ventricles, and Purkinje fibers
Are due to the presence of numerous voltage-sensitive sodium channels, which allow a rapid influx of sodium when the channels are open
Slow-response action potentials occur in cells such as the SA and AV nodes
They are due to the presence of slow calcium and slow sodium channels, instead of the fast sodium channels, resulting in a slower rate of depolarization
Slow-response action potentials may occur anywhere in the heart as a result of injury, ischemia, or electrolyte imbalance
11.7.1 Imbalance of sodium ions
Hypernatremia
An excess of sodium ions in the blood
Not associated with any significant changes to the ECG
Hyponatremia
A deficiency of sodium ions in the blood
Not associated with any significant changes to the ECG
11.7.2 Imbalance of calcium ions
Hypercalcemia
An excess of calcium ions in the blood
ECG changes include a prolonged PR interval, shortened QT interval, and a prolonged QRS complex
Hypocalcemia
A deficiency of calcium ions in the blood
ECG changes include a long, flattened ST segment, and a prolonged QT interval
11.7.3 Imbalance of magnesium ions
Hypermagnesemia
An excess of magnesium ions in the blood
ECG changes include a prolonged PR interval, prolonged QRS complex, and a prolonged QT interval
Hypomagnesemia
A deficiency of magnesium ions in the blood
ECG changes include a diminished height of P waves and QRS complexes, slightly widened QRS complexes, flattened T waves, and prominent U waves
11.7.4 Imbalance of potassium ions
Hyperkalemia
An excess of potassium ions in the blood
The ECG changes include tall, peaked T waves, widened QRS complexes, flattened ST segments, prolonged PR intervals, and flattened or absent P waves
If not reversed, hyperkalemia may result in ventricular dysrhythmias or asystole
Hypokalemia
A deficiency of potassium ions in the blood
The ECG changes associated with hypokalemia include ST-segment depression, flattened T waves, and prominent U waves
11.8 Conduction abnormalities
Normally, during ventricular depolarization, the left side of the interventricular septum is stimulated first, by the posterior fascicle (group of fibers) of the left bundle branch (LBB). The electrical stimulus then travels across the septum to stimulate the right side via the right bundle branch (RBB); the right and left ventricles then depolarize simultaneously.
Delays or blocks in conduction can occur in any part of the interventricular conduction system:
Monofascicular block: The block occurs in only one fascicle of the bundle branches
Bifascicular block: The block occurs in any two divisions of the bundle branches
Trifascicular block: A block that occurs in the three primary divisions of the bundle branches
Hemiblock: A block in either fascicle of the LBB
When a block occurs in one of the bundle branches, the ventricles will be depolarized at different times. The stimulus will first travel down the unblocked branch and cause that ventricle to depolarize. Because of the block, the impulse must then travel from cell to cell through the myocardium, in order to stimulate the other ventricle. This results in a slower rate of conduction than normal and, subsequently, the QRS complex is widened on the ECG.
A QRS complex that measures between 0.10 and 0.12 seconds is known as an incomplete right or left bundle branch block. A QRS complex that measures more than 0.12 seconds is known as a complete right or left bundle branch block. The ST-segment and T wave may be in the opposite direction to the QRS complex.
The ECG criteria for diagnosis of a bundle branch block (BBB) are:
QRS duration of greater than 0.12 seconds (if a complete BBB)
QRS complexes must be produced by supraventricular activity (ie, not paced or ventricular in origin)
11.8.1 Right bundle branch block
A right bundle branch block (RBBB) commonly occurs in patients who have underlying organic heart disease, such as coronary artery disease. However, it can occur in patients who do not have pre-existing heart disease. Complete RBBB is evident in between 3% and 7% of patients with acute myocardial infarction and in such cases may require pacemaker intervention. RBBB may progress to complete AV block, especially when it is associated with a fascicular block.
Once BBB is suspected, evaluating lead V1 can help determine whether the right or left bundle branch has been affected by the block.
The RSR' pattern is characteristic of RBBB. RBBB should be suspected whenever the two criteria for BBB are met (wide QRS from a supraventricular origin) and lead V1 displays the RSR' pattern. There may be a qRS pattern in leads V5 and V6.
11.8.2 Left bundle branch block
Left bundle branch block (LBBB) may be acute (as a result of myocardial infarction, pericarditis, or congestive heart failure) or chronic (due to coronary artery disease, hypertensive heart disease, or dilated cardiomyopathy).
Evaluating lead V1 can help determine whether a block is affecting the right or left bundle branch.
The QS pattern is characteristic of LBBB. LBBB should be suspected whenever the two criteria for BBB are met (wide QRS from a supraventricular origin), and lead V1 displays the QS pattern. In addition, the ST segment and T wave are normally in the opposite direction to the QRS complex.
QS pattern in
lead V1
11.9 Analyzing an ECG
It is important to use a systematic method when analyzing an ECG. Findings that suggest an acute MI are considered significant if viewed in two or more leads that look at the same area of the heart (contiguous leads). If these findings are viewed in leads that look directly at the affected area of the heart they are called indicative changes; if the findings are in leads that are opposite to the affected area they are known as reciprocal changes.
11.9.1 Systematic method
Assess the quality of the tracing. Make a note of baseline wander or artifact (if they are present to a significant degree). If the presence of either of these conditions makes assessment of any lead difficult, use a qualifier such as "possible" or "apparent" to describe any findings
Identify the rate and underlying rhythm
Evaluate the intervals: PR interval, QRS duration, QT interval
Evaluate waveforms: P waves, Q waves, R waves (R wave progression), T waves, U waves. If a Q wave is present, note the duration in milliseconds
Evaluate each lead for the presence of ST-segment elevation or depression. If ST-segment elevation is present, express it in millimeters. Assess the areas of ischemia or injury by assessing lead groupings. Evaluate the T waves for any changes in orientation, shape, and size
Determine the axis
Look for evidence of hypertrophy/chamber enlargement
Look for effects of medications and electrolyte imbalances
Interpret your findings
12. Stress testing and Holter monitoring
Stress testing
A cardiac stress test indirectly evaluates arterial blood flow to the heart during exercise. When compared with blood flow during rest, the test highlights imbalances of blood flow to the myocardium of the left ventricle.
The patient usually walks on a treadmill while connected to a 12-lead ECG which is continuously monitored for ischemic changes. The intensity of exercise is gradually increased in 3-minute stages of increased incline and speed. The patient's blood pressure and any symptoms are also assessed regularly throughout the test.
Stress testing
Patients who have abnormal resting ECGs, or those who are unable to walk safely, may be given pharmacological agents that mimic the effects of exercise on the body. A radiotracer is injected into the patient during the simulated exercise, and images of the patient's coronary arteries are taken, to be compared with images of the arteries while at rest.
Stress testing is recommended for patients who have a medium risk of coronary heart disease, based on factors such as smoking, family history of coronary stenosis, diabetes, hypertension, and high cholesterol levels.
Holter monitoring
A Holter monitor, or ambulatory electrocardiography device, is a portable device used for recording the electrical activity of the heart for 24 hours or more. The ability to record an ECG for an extended period of time is useful for observing occasional cardiac arrhythmias that are difficult to identify over a shorter period of time. A cardiac event monitor can be worn for a month or more by patients who have more transient symptoms.
The Holter monitor records the electrical signals from the heart by using electrodes placed on the chest, in a similar manner to a standard ECG. The number and position of electrodes varies by model.
Holter monitor
In addition to wearing the monitor, patients are asked to record a diary of activities such as running, sleeping, symptoms, and the time that their symptoms occur. This information can be used by doctors and technicians to identify problem areas in the vast amount of data that is recorded during the monitoring period.
Bibliography
Abdelhamid T. Illustrated ECG: A Step by Step Approach to Learn ECG. 1st ed. Paper Back Auckland, New Zealand: Medical Education Development Company Ltd; 2014.
Aehlert B. ECGs Made Easy. 5th ed. St. Louis, MO: Elsevier Mosby; 2013.
Petersen Ole H. Lecture Notes; Human Physiology. 5th ed. Oxford: Blackwell Science; 2006.
Dubin D. Rapid Interpretation of EKG's. 6th ed. Tampa, Fla: Cover Pub. Co.; 2000.
Jenkins D, Gerred S. Electrocardiogram (ECG, EKG) library.
http://www.ecglibrary.com/ecghome.html. Updated January 10, 2009.
Accessed December 21, 2016.
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