| Electrocardiography | |
|---|---|
 ECG of a heart in normalsinus rhythm | |
| ICD-10-PCS | R94.31 |
| ICD-9-CM | 89.52 |
| MeSH | D004562 |
| MedlinePlus | 003868 |
Electrocardiography is the process of producing anelectrocardiogram (ECG orEKG[a]), a recording of the heart's electrical activity through repeatedcardiac cycles.[4] It is anelectrogram of theheart which is a graph ofvoltage versus time of the electrical activity of the heart[5] usingelectrodes placed on the skin. These electrodes detect the small electrical changes that are a consequence ofcardiac muscledepolarization followed byrepolarization during eachcardiac cycle (heartbeat). Changes in the normal ECG pattern occur in numerous cardiac abnormalities, including:
Traditionally, "ECG" usually means a12-lead ECG taken while lying down as discussed below.However, other devices can record the electrical activity of the heart such as aHolter monitor but also some models ofsmartwatch are capable of recording an ECG.ECG signals can be recorded in other contexts with other devices.
In a conventional 12-lead ECG, ten electrodes are placed on the patient's limbs and on the surface of the chest. The overallmagnitude of the heart'selectrical potential is then measured from twelve different angles ("leads") and is recorded over a period of time (usually ten seconds). In this way, the overall magnitude and direction of the heart's electrical depolarization is captured at each moment throughout thecardiac cycle.[11]
There are three main components to an ECG:[12]
During each heartbeat, a healthy heart has an orderly progression of depolarization that starts withpacemaker cells in thesinoatrial node, spreads throughout theatrium, and passes through theatrioventricular node down into thebundle of His and into thePurkinje fibers, spreading down and to the left throughout theventricles.[12] This orderly pattern of depolarization gives rise to the characteristic ECG tracing. To the trainedclinician, an ECG conveys a large amount of information about the structure of the heart and the function of its electrical conduction system.[13] Among other things, an ECG can be used to measure the rate and rhythm of heartbeats, the size and position of theheart chambers, the presence of any damage to the heart's muscle cells or conduction system, the effects of heart drugs, and the function of implantedpacemakers.[14]
The overall goal of performing an ECG is to obtain information about the electrical functioning of the heart. Medical uses for this information are varied and often need to be combined with knowledge of the structure of the heart and physical examination signs to be interpreted. Someindications for performing an ECG include the following:
ECGs can be recorded as short intermittent tracings orcontinuous ECG monitoring. Continuous monitoring is used for critically ill patients, patients undergoing general anesthesia,[18][17] and patients who have an infrequently occurring cardiac arrhythmia that would unlikely be seen on a conventional ten-second ECG. Continuous monitoring can be conducted by usingHolter monitors, internal and externaldefibrillators andpacemakers, and/orbiotelemetry.[19]
For adults, evidence does not support the use of ECGs among those without symptoms or at low risk ofcardiovascular disease as an effort for prevention.[20][21][22] This is because an ECG may falsely indicate the existence of a problem, leading tomisdiagnosis, the recommendation of invasive procedures, andovertreatment. However, persons employed in certain critical occupations, such as aircraft pilots,[23] may be required to have an ECG as part of their routine health evaluations.Hypertrophic cardiomyopathy screening may also be considered in adolescents as part of asports physical out of concern forsudden cardiac death.[24]
Electrocardiograms are recorded by machines that consist of a set of electrodes connected to a central unit.[25] Early ECG machines were constructed withanalog electronics, where the signal drove a motor to print out the signal onto paper. Today, electrocardiographs useanalog-to-digital converters to convert the electrical activity of the heart to adigital signal. Many ECG machines are now portable and commonly include a screen, keyboard, and printer on a small wheeled cart. Recent advancements in electrocardiography include developing even smaller devices for inclusion in fitness trackers andsmart watches.[26] These smaller devices often rely on only two electrodes to deliver a single lead I.[27] Portable twelve-lead devices powered by batteries are also available.
Recording an ECG is a safe and painless procedure.[28] The machines are powered bymains power but they are designed with several safety features including an earthed (ground) lead.Other features include:
Most modern ECG machines includeautomated interpretationalgorithms. This analysis calculates features such as thePR interval,QT interval,corrected QT (QTc) interval, PR axis, QRS axis, rhythm and more. The results from these automated algorithms are considered "preliminary" until verified and/or modified by expert interpretation. Despite recent advances, computer misinterpretation remains a significant problem and can result in clinical mismanagement.[29]
Besides the standard electrocardiograph machine, there are other devices capable of recording ECG signals. Portable devices have existed since theHolter monitor was introduced in 1962.Traditionally, these monitors have used electrodes with patches on the skin to record the ECG, but new devices can stick to the chest as a single patch without need for wires, developed by Zio (Zio XT), TZ Medical (Trident),Philips (BioTel) and BardyDx (CAM) among many others.Implantable devices such as theartificial cardiac pacemaker andimplantable cardioverter-defibrillator are capable of measuring a "far field" signal between the leads in the heart and the implanted battery/generator that resembles an ECG signal (technically, the signal recorded in the heart is called anelectrogram, which is interpreted differently).Advancement of the Holter monitor became theimplantable loop recorder that performs the same function but in an implantable device with batteries that last on the order of years.
Additionally, there are available variousArduino kits with ECG sensor modules andsmartwatch devices that are capable of recording an ECG signal as well, such as with the 4th generationApple Watch,Samsung Galaxy Watch 4 and newer devices.
Electrodes are the actual conductive pads attached to the body surface.[31] Any pair of electrodes can measure theelectrical potential difference between the two corresponding locations of attachment. Such a pair formsa lead. However, "leads" can also be formed between a physical electrode and avirtual electrode, which is the average of numerous leads. All clinical ECGs useWilson's central terminal (WCT) as the virtual electrode from which the precordial leads are measured, whose potential is defined as the average potential measured by the three standard limb leads.[32]
Commonly, 10 electrodes attached to the body are used to form 12 ECG leads, with each lead measuring a specific electrical potential difference.[33]
Leads are broken down into three types: limb; augmented limb; and precordial or chest. The 12-lead ECG has a total of threelimb leads and threeaugmented limb leads arranged like spokes of a wheel in thecoronal plane (vertical), and sixprecordial leads orchest leads that lie on the perpendiculartransverse plane (horizontal).[34]
Electrodes should be placed in standard positions, with 'left' or 'right' referring toanatomical directions, being the patient's left or right. Exceptions due to emergency or other issues should be recorded to avoid erroneous analysis.[35]
The 12 standard ECG leads and electrodes are listed below.[36] All leads are effectively bipolar, with one positive and one negative electrode; the term "unipolar" is not true, nor useful.[32]
| Type | Name (AHA) | Color (AHA) | Placement | Name (IEC) | Color (IEC) |
|---|---|---|---|---|---|
| Limb | RA (Right Arm) | White | On the right arm, below the shoulders, avoiding thickmuscle. | R (Right) | Red |
| LA (Left Arm) | Black | Symmetrical to the placement of the RA. | L (Left) | Yellow | |
| RL (Right Leg) | Green | On the right leg, below the hips. | N (Neutral) | Black | |
| LL (Left Leg) | Red | Symmetrical to the placement of the RL. | F (Foot) | Green | |
| Precordial | V1 | Brown & Red | Fourthintercostal space on the rightsternal border. | C1 | White & Red |
| V2 | Brown & Yellow | Fourth intercostal space on the left sternal border (symmetrical to V1). | C2 | White & Yellow | |
| V3 | Brown & Green | Halfway between electrodes V2 and V4 (in a straight line). | C3 | White & Green | |
| V4 | Brown & Blue | Fifth intercostal space on themidclavicular line. | C4 | White & Brown | |
| V5 | Brown & Orange | Leftanterior axillary line on the same horizontal plane as V4. If the anterior axillary line is ambiguous, place halfway between V4 and V6. | C5 | White & Black | |
| V6 | Brown & Purple | Leftmidaxillary line on the same horizontal plane as V4. | C6 | White & Purple. |
| Type | Name | Lead view |
|---|---|---|
| Limb | I | From the RA to the LA. Along the frontal and horizontal planes at 0° (directly to the left). |
| II | From the RA to the LL. Along the frontal plane at 60° clockwise from I. | |
| III | From the LA to the LL. Along the frontal plane at 120° clockwise from I. | |
| Augmented Limb | aVL | From WCT to the LA. Along the frontal plane at -30° (which is 330° clockwise from I). |
| aVR | From WCT to the RA. Along the frontal plane at -150° (which is 210° from I). | |
| aVF | From WCT to the LL. Along the front plane at 90°. | |
| Precordial | V1 | In the fourthintercostal space (between ribs 4 and 5) just to the right of thesternum (breastbone) |
| V2 | In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum. | |
| V3 | Between leads V2 and V4. | |
| V4 | In the fifth intercostal space (between ribs 5 and 6) in themid-clavicular line. | |
| V5 | Along the same horizontal line as V4, in the leftanterior axillary line. | |
| V6 | Along the same horizontal line as V4 and V5 in themid-axillary line. |
Two types of electrodes in common use are a flat paper-thin sticker and a self-adhesive circular pad.The former are typically used in a single ECG recording while the latter are for continuous recordings as they stick longer.Each electrode consists of anelectrically conductive electrolyte gel and asilver/silver chloride conductor.[37]The gel typically containspotassium chloride – sometimessilver chloride as well – to permitelectron conduction from the skin to the wire and to the electrocardiogram.[38]
The virtual electrode is used to obtain useful measurements from the precordial leads, and also allows the creation of the augmented limb leads.
The virtual electrode is known asWilson's Central Terminal (WCT). For the precordial leads, WCT is formed by averaging the three standard limb leads (I, II, and III):
WCT is therefore a virtual electrode which sits slightlyposteriorly to the heart. It is a useful point, from which the electrical potential of the precordial leads is measured.[32]
WCT used to be used as a reference for the virtual limb leads, however use in this way produced leads with very small amplitudes. Goldberger's modification is now used to produce each augmented limb lead, aVF, aVR, and aVL, which produces 50% larger amplitude leads than the standard WCT. Goldberger's WCT is formed according to the following:[32]
In a 12-lead ECG, all leads except the limb leads are assumed to be unipolar (aVR, aVL, aVF, V1, V2, V3, V4, V5, and V6).The measurement of a voltage requires two contacts and so, electrically, the unipolar leads are measured from the common lead (negative) and the unipolar lead (positive).This averaging for the common lead and the abstract unipolar lead concept makes for a more challenging understanding and is complicated by sloppy usage of "lead" and "electrode".In fact, instead of being a constant reference, VW has a value that fluctuates throughout the heart cycle. It also does not truly represent the center-of-heart potential due to the body parts the signals travel through.[39] Because voltage is by definition a bipolar measurement between two points, describing an electrocardiographic lead as "unipolar" makes little sense electrically and should be avoided. The American Heart Association states "All leads are effectively 'bipolar,' and the term 'unipolar' in description of the augmented limb leads and the precordial leads lacks precision."[40]
Leads I, II and III are called thelimb leads. The electrodes that form these signals are located on the limbs – one on each arm and one on the left leg.[41][42] The limb leads form the points of what is known asEinthoven's triangle.[43]
Leads aVR, aVL, and aVF are theaugmented limb leads. They are derived from the same three electrodes as leads I, II, and III, but they use Goldberger's central terminal as their negative pole. Goldberger's central terminal is a combination of inputs from two limb electrodes, with a different combination for each augmented lead. It is referred to immediately below as "the negative pole".
Together with leads I, II, and III, augmented limb leads aVR, aVL, and aVF form the basis of thehexaxial reference system, which is used to calculate the heart's electrical axis in the frontal plane.[44]
Older versions of the nodes (VR, VL, VF) use Wilson's central terminal as the negative pole, but the amplitude is too small for the thick lines of old ECG machines. The Goldberger terminals scale up (augments) the Wilson results by 50%, at the cost of sacrificing physical correctness by not having the same negative pole for all three.[45]
Theprecordial leads lie in the transverse (horizontal) plane, perpendicular to the other six leads. The six precordial electrodes act as the positive poles for the six corresponding precordial leads: (V1, V2, V3, V4, V5, and V6). Wilson's central terminal is used as the negative pole. Recently, unipolar precordial leads have been used to create bipolar precordial leads that explore the right to left axis in the horizontal plane.[46]
Additional electrodes may rarely be placed to generate other leads for specific diagnostic purposes.Right-sided precordial leads may be used to better study pathology of the right ventricle or fordextrocardia (and are denoted with an R (e.g., V5R).Posterior leads (V7 to V9) may be used to demonstrate the presence of a posterior myocardial infarction. TheLewis lead or S5-lead (requiring an electrode at the right sternal border in the second intercostal space) can be used to better detect atrial activity in relation to that of the ventricles.[47]
Anesophageal lead can be inserted to a part of theesophagus where the distance to the posterior wall of theleft atrium is only approximately 5–6 mm (remaining constant in people of different age and weight).[48] An esophageal lead avails for a more accurate differentiation between certain cardiac arrhythmias, particularlyatrial flutter,AV nodal reentrant tachycardia and orthodromicatrioventricular reentrant tachycardia.[49] It can also evaluate the risk in people withWolff-Parkinson-White syndrome, as well as terminatesupraventricular tachycardia caused byre-entry.[49]
An intracardiac electrogram (ICEG) is essentially an ECG with some addedintracardiac leads (that is, inside the heart). The standard ECG leads (external leads) are I, II, III, aVL, V1, and V6. Two to four intracardiac leads are added via cardiac catheterization. The word "electrogram" (EGM) without further specification usually means an intracardiac electrogram.[50]
A standard 12-lead ECG report (an electrocardiograph) shows a 2.5 second tracing of each of the twelve leads. The tracings are most commonly arranged in a grid of four columns and three rows. The first column is the limb leads (I, II, and III), the second column is the augmented limb leads (aVR, aVL, and aVF), and the last two columns are the precordial leads (V1 to V6).Additionally, a rhythm strip may be included as a fourth or fifth row.[44]
The timing across the page is continuous and notes tracings of the 12 leads for the same time period.In other words, if the output were traced by needles on paper, each row would switch which leads as the paper is pulled under the needle.For example, the top row would first trace lead I, then switch to lead aVR, then switch to V1, and then switch to V4, and so none of these four tracings of the leads are from the same time period as they are traced in sequence through time.[51]
Each of the 12 ECG leads records the electrical activity of the heart from a different angle, and therefore align with different anatomical areas of the heart. Two leads that look at neighboring anatomical areas are said to becontiguous.[44]
| Category | Leads | Activity |
|---|---|---|
| Inferior leads | Leads II, III and aVF | Look at electrical activity from the vantage point of theinferior surface (diaphragmatic surface of heart) |
| Lateral leads | I, aVL, V5 and V6 | Look at the electrical activity from the vantage point of thelateral wall of leftventricle |
| Septal leads | V1 and V2 | Look at electrical activity from the vantage point of theseptal surface of the heart (interventricular septum) |
| Anterior leads | V3 and V4 | Look at electrical activity from the vantage point of theanterior wall of the right and left ventricles (Sternocostal surface of heart) |
In addition, any two precordial leads next to one another are considered to be contiguous. For example, though V4 is an anterior lead and V5 is a lateral lead, they are contiguous because they are next to one another.
The study of the conduction system of the heart is calledcardiac electrophysiology (EP). An EP study is performed via a right-sidedcardiac catheterization: a wire with an electrode at its tip is inserted into the right heart chambers from a peripheral vein, and placed in various positions in close proximity to the conduction system so that the electrical activity of that system can be recorded.[citation needed]
Standard catheter positions for an EP study include "high right atrium" or hRA near thesinus node, a "His" across the septal wall of the tricuspid valve to measurebundle of His, a "coronary sinus" into thecoronary sinus, and a "right ventricle" in the apex of the right ventricle.[52]
Interpretation of the ECG is fundamentally about understanding theelectrical conduction system of the heart.Normal conduction starts and propagates in a predictable pattern, and deviation from this pattern can be a normal variation or bepathological.An ECG does not equate with mechanical pumping activity of the heart; for example,pulseless electrical activity produces an ECG that should pump blood but no pulses are felt (and constitutes amedical emergency andCPR should be performed).Ventricular fibrillation produces an ECG but is too dysfunctional to produce a life-sustaining cardiac output. Certain rhythms are known to have good cardiac output and some are known to have bad cardiac output.Ultimately, anechocardiogram or other anatomical imaging modality is useful in assessing the mechanical function of the heart.[53]
Like all medical tests, what constitutes "normal" is based onpopulation studies. The heartrate range of between 60 and 100 beats per minute (bpm) is considered normal since data shows this to be the usual resting heart rate.[54]
Interpretation of the ECG is ultimately that of pattern recognition.In order to understand the patterns found, it is helpful to understand the theory of what ECGs represent.The theory is rooted inelectromagnetics and boils down to the four following points:[55]
Thus, the overall direction of depolarization and repolarization produces positive or negative deflection on each lead's trace.For example, depolarizing from right to left would produce a positive deflection in lead I because the two vectors point in the same direction.In contrast, that same depolarization would produce minimal deflection in V1 and V2 because the vectors are perpendicular, and this phenomenon is called isoelectric.
Normal rhythm produces four entities – aP wave, aQRS complex, aT wave, and aU wave – that each have a fairly unique pattern.
Changes in the structure of the heart and its surroundings (including blood composition) change the patterns of these four entities.
The U wave is not typically seen and its absence is generally ignored. Atrial repolarization is typically hidden in the much more prominent QRS complex and normally cannot be seen without additional, specialized electrodes.
ECGs are normally printed on a grid.The horizontal axis represents time and the vertical axis represents voltage.The standard values on this grid are shown in the adjacent image at 25mm/sec (or 40ms per mm):[56]
The "large" box is represented by a heavierline weight than the small boxes.
The standard printing speed in the United States is 25 mm per sec (5 big boxes per second), but in other countries it can be 50 mm per sec.Faster speeds such as 100 and 200 mm per sec are used during electrophysiology studies.
Not all aspects of an ECG rely on precise recordings or having a known scaling of amplitude or time.For example, determining if the tracing is a sinus rhythm only requires feature recognition and matching, and not measurement of amplitudes or times (i.e., the scale of the grids are irrelevant).An example to the contrary, the voltage requirements ofleft ventricular hypertrophy require knowing the grid scale.
In a normal heart, the heart rate is the rate at which thesinoatrial node depolarizes since it is the source of depolarization of the heart.Heart rate, like othervital signs such as blood pressure and respiratory rate, change with age.In adults, a normal heart rate is between 60 and 100 bpm (normocardic), whereas it is higher in children.[57]A heart rate below normal is called "bradycardia" (<60 in adults) and above normal is called "tachycardia" (>100 in adults).A complication of this is when the atria and ventricles are not in synchrony and the "heart rate" must be specified as atrial or ventricular (e.g., the ventricular rate inventricular fibrillation is 300–600 bpm, whereas the atrial rate can be normal [60–100] or faster [100–150]).[citation needed]
In normal resting hearts, the physiologic rhythm of the heart isnormal sinus rhythm (NSR).Normal sinus rhythm produces the prototypical pattern of P wave, QRS complex, and T wave.Generally, deviation from normal sinus rhythm is considered acardiac arrhythmia.Thus, the first question in interpreting an ECG is whether or not there is a sinus rhythm.A criterion for sinus rhythm is that P waves and QRS complexes appear 1-to-1, thus implying that the P wave causes the QRS complex.[51]
Once sinus rhythm is established, or not, the second question is the rate.For a sinus rhythm, this is either the rate of P waves or QRS complexes since they are 1-to-1.If the rate is too fast, then it issinus tachycardia, and if it is too slow, then it issinus bradycardia.
If it is not a sinus rhythm, then determining the rhythm is necessary before proceeding with further interpretation.Some arrhythmias with characteristic findings:
Determination of rate and rhythm is necessary in order to make sense of further interpretation.
The heart has several axes, but the most common by far is the axis of the QRS complex (references to "the axis" imply the QRS axis).Each axis can be computationally determined to result in a number representing degrees of deviation from zero, or it can be categorized into a few types.[58]
The QRS axis is the general direction of the ventricular depolarization wavefront (or mean electrical vector) in the frontal plane.It is often sufficient to classify the axis as one of three types: normal, left deviated, or right deviated.Population data shows that a normal QRS axis is from −30° to 105°, with 0° being along lead I and positive being inferior and negative being superior (best understood graphically as thehexaxial reference system).[59]Beyond +105° isright axis deviation and beyond −30° isleft axis deviation (the third quadrant of −90° to −180° is very rare and is an indeterminate axis).A shortcut for determining if the QRS axis is normal is if the QRS complex is mostly positive in lead I and lead II (or lead I and aVF if +90° is the upper limit of normal).[60]
The normal QRS axis is generallydown and to the left, following the anatomical orientation of the heart within the chest. An abnormal axis suggests a change in the physical shape and orientation of the heart or a defect in its conduction system that causes the ventricles to depolarize in an abnormal way.[51]
| Classification | Angle | Notes |
|---|---|---|
| Normal | −30° to 105° | Normal |
| Left axis deviation | −30° to −90° | May indicateleft ventricular hypertrophy,left anterior fascicular block, or an old inferior STEMI |
| Right axis deviation | +105° to +180° | May indicateright ventricular hypertrophy,left posterior fascicular block, or an old lateral STEMI |
| Indeterminate axis | +180° to −90° | Rarely seen; considered an 'electrical no-man's land' |
The extent of a normal axis can be +90° or 105° depending on the source.
All of the waves on an ECG tracing and the intervals between them have a predictable time duration, a range of acceptable amplitudes (voltages), and a typical morphology. Any deviation from the normal tracing is potentially pathological and therefore of clinical significance.[61]
For ease of measuring the amplitudes and intervals, an ECG is printed on graph paper at a standard scale: each 1 mm (one small box on the standard 25mm/s ECG paper) represents 40 milliseconds of time on the x-axis, and 0.1 millivolts on the y-axis.[62]
| Feature | Description | Pathology | Duration |
|---|---|---|---|
| P wave | The P wave represents depolarization of the atria. Atrial depolarization spreads from the SA node towards the AV node, and from the rightatrium to the leftatrium. | The P wave is typically upright in most leads except for aVR; an unusual P wave axis (inverted in other leads) can indicate anectopic atrial pacemaker. If the P wave is of unusually long duration, it may represent atrial enlargement. Typically a largeright atrium gives a tall, peaked P wave while a largeleft atrium gives a two-humped bifid P wave. | <80 ms |
| PR interval | The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. This interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node. | A PR interval shorter than 120 ms suggests that the electrical impulse is bypassing the AV node, as inWolff-Parkinson-White syndrome. A PR interval consistently longer than 200 ms diagnosesfirst degree atrioventricular block. The PR segment (the portion of the tracing after the P wave and before the QRS complex) is typically completely flat, but may be depressed inpericarditis. | 120 to 200 ms |
| QRS complex | The QRS complex represents the rapid depolarization of the right and left ventricles. The ventricles have a greater muscle mass proportion compared to the atria, hence the QRS complex usually has a much larger amplitude than the P wave. | If the QRS complex is wide (longer than 120 ms) it suggests disruption of the heart's conduction system, such as inLBBB,RBBB, or ventricular rhythms such asventricular tachycardia. Metabolic issues such as severehyperkalemia, ortricyclic antidepressant overdose can also widen the QRS complex. An unusually tall QRS complex may representleft ventricular hypertrophy while a very low-amplitude QRS complex may represent apericardial effusion orinfiltrative myocardial disease. | 80 to 100 ms |
| J-point | The J-point is the point at which the QRS complex finishes and the ST segment begins. | The J-point may be elevated as a normal variant. The appearance of a separateJ wave orOsborn wave at the J-point ispathognomonic ofhypothermia orhypercalcemia.[63] | |
| ST segment | The ST segment connects the QRS complex and the T wave; it represents the period when the ventricles are depolarized. | It is usually isoelectric, but may be depressed or elevated withmyocardial infarction or ischemia.ST depression can also be caused byLVH ordigoxin.ST elevation can also be caused bypericarditis,Brugada syndrome, or can be a normal variant (J-point elevation). | |
| T wave | The T wave represents the repolarization of the ventricles. It is generally upright in all leads except aVR and lead V1. | Inverted T waves can be a sign of myocardial ischemia,left ventricular hypertrophy, highintracranial pressure, or metabolic abnormalities. Peaked T waves can be a sign ofhyperkalemia or very earlymyocardial infarction. | 160 ms |
| Corrected QT interval (QTc) | The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Acceptable ranges vary with heart rate, so it must becorrected to the QTc by dividing by the square root of the RR interval. | A prolonged QTc interval is a risk factor for ventricular tachyarrhythmias and sudden death. Long QT can arise as agenetic syndrome, or as a side effect of certain medications. An unusually short QTc can be seen in severe hypercalcemia. | <440 ms |
| U wave | The U wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent. | A very prominent U wave can be a sign of hypokalemia, hypercalcemia or hyperthyroidism.[64] |
In electrocardiogram (ECG) signal processing, Time-Frequency Analysis (TFA) is an important technique used to reveal how the frequency characteristics of ECG signals change over time, especially in non-stationary signals such as arrhythmias or transient cardiac events.
Common Methods for Time-Frequency Analysis
| Method | Advantage | Disadvantage | Example |
|---|---|---|---|
| Short-time Fourier transform | Simple to implement, suitable for analyzing steady or near-steady heart rhythms and easy to perform using Fast Fourier Transform (FFT). | Time and frequency resolution are affected by window length, making it difficult to efficiently capture both short-term and long-term variations simultaneously. | Monitoring short-term heart rate variability. |
| Wavelet transform | Provides multi-resolution analysis, making it suitable for processing non-stationary signals. | Computationally intensive. | Local feature extraction of P-wave or T-wave and frequency analysis of atrial fibrillation signals. |
| Hilbert–Huang transform | Suitable for fully non-stationary and nonlinear signals. Provides instantaneous frequency distribution. | Susceptible to mode mixing issues. | Detection of transient heart rate variability. |
Steps for Time-Frequency Analysis
Step1: Preprocessing
Step2: Select an Appropriate TFA Method
Step3: Compute the Time-Frequency Spectrum
Step4: Feature Extraction
Step5: Pattern Recognition or Diagnosis
Application Scenarios
Heart Rate Variability Analysis (HRV):
Atrial Fibrillation Detection:
Ventricular Fibrillation Analysis:
The animation shown to the right illustrates how the path of electrical conduction gives rise to the ECG waves in the limb leads. What is green zone ?Recall that a positive current (as created by depolarization of cardiac cells) traveling towards the positive electrode and away from the negative electrode creates a positive deflection on the ECG. Likewise, a positive current traveling away from the positive electrode and towards the negative electrode creates a negative deflection on the ECG.[65][66] The red arrow represents the overall direction of travel of the depolarization. The magnitude of the red arrow is proportional to the amount of tissue being depolarized at that instance. The red arrow is simultaneously shown on the axis of each of the 3 limb leads. Both the direction and the magnitude of the red arrow's projection onto the axis of each limb lead is shown with blue arrows. Then, the direction and magnitude of the blue arrows are what theoretically determine the deflections on the ECG. For example, as a blue arrow on the axis for Lead I moves from the negative electrode, to the right, towards the positive electrode, the ECG line rises, creating an upward wave. As the blue arrow on the axis for Lead I moves to the left, a downward wave is created. The greater the magnitude of the blue arrow, the greater the deflection on the ECG for that particular limb lead.[67]
Frames 1–3 depict the depolarization being generated in and spreading through thesinoatrial node. The SA node is too small for its depolarization to be detected on most ECGs. Frames 4–10 depict the depolarization traveling through the atria, towards theatrioventricular node. During frame 7, the depolarization is traveling through the largest amount of tissue in the atria, which creates the highest point in the P wave. Frames 11–12 depict the depolarization traveling through the AV node. Like the SA node, the AV node is too small for the depolarization of its tissue to be detected on most ECGs. This creates the flat PR segment.[68]
Frame 13 depicts an interesting phenomenon in an over-simplified fashion. It depicts the depolarization as it starts to travel down the interventricular septum, through thebundle of His andbundle branches. After the Bundle of His, the conduction system splits into the left bundle branch and the right bundle branch. Both branches conduct action potentials at about 1 m/s. However, the action potential starts traveling down the left bundle branch about 5 milliseconds before it starts traveling down the right bundle branch, as depicted by frame 13. This causes the depolarization of the interventricular septum tissue to spread from left to right, as depicted by the red arrow in frame 14. In some cases, this gives rise to a negative deflection after the PR interval, creating a Q wave such as the one seen in lead I in the animation to the right. Depending on the mean electrical axis of the heart, this phenomenon can result in a Q wave in lead II as well.[69][70]
Following depolarization of the interventricular septum, the depolarization travels towards the apex of the heart. This is depicted by frames 15–17 and results in a positive deflection on all three limb leads, which creates the R wave. Frames 18–21 then depict the depolarization as it travels throughout both ventricles from the apex of the heart, following the action potential in thePurkinje fibers. This phenomenon creates a negative deflection in all three limb leads, forming the S wave on the ECG. Repolarization of the atria occurs at the same time as the generation of the QRS complex, but it is not detected by the ECG since the tissue mass of the ventricles is so much larger than that of the atria. Ventricular contraction occurs between ventricular depolarization and repolarization. During this time, there is no movement of charge, so no deflection is created on the ECG. This results in the flat ST segment after the S wave.[71]
Frames 24–28 in the animation depict repolarization of the ventricles. The epicardium is the first layer of the ventricles to repolarize, followed by the myocardium. The endocardium is the last layer to repolarize. The plateau phase of depolarization has been shown to last longer in endocardial cells than in epicardial cells. This causes repolarization to start from the apex of the heart and move upwards. Since repolarization is the spread of negative current as membrane potentials decrease back down to the resting membrane potential, the red arrow in the animation is pointing in the direction opposite of the repolarization. This therefore creates a positive deflection in the ECG, and creates the T wave.[72]
Ischemia ornon-ST elevation myocardial infarctions (non-STEMIs) may manifest asST depression or inversion ofT waves. It may also affect thehigh frequency band of the QRS.
ST elevation myocardial infarctions (STEMIs) have different characteristic ECG findings based on the amount of time elapsed since the MI first occurred. The earliest sign ishyperacute T waves, peaked T waves due to localhyperkalemia in ischemic myocardium. This then progresses over a period of minutes to elevations of theST segment by at least 1 mm. Over a period of hours, a pathologicQ wave may appear and the T wave will invert. Over a period of days the ST elevation will resolve. Pathologic Q waves generally will remain permanently.[73]
Thecoronary artery that has been occluded can be identified in an STEMI based on the location of ST elevation. Theleft anterior descending (LAD) artery supplies the anterior wall of the heart, and therefore causes ST elevations in anterior leads (V1 and V2). TheLCx supplies the lateral aspect of the heart and therefore causes ST elevations in lateral leads (I, aVL and V6). Theright coronary artery (RCA) usually supplies the inferior aspect of the heart, and therefore causes ST elevations in inferior leads (II, III and aVF).[74]
An ECG tracing is affected by patient motion. Some rhythmic motions (such as shivering ortremors) can create the illusion of cardiac arrhythmia.[75] Artifacts are distorted signals caused by a secondary internal or external sources, such as muscle movement or interference from an electrical device.[76][77]
Distortion poses significant challenges to healthcare providers,[76] who employ various techniques[78] and strategies to safely recognize[79] these false signals.[medical citation needed] Accurately separating the ECG artifact from the true ECG signal can have a significant impact on patient outcomes andlegal liabilities.[80][unreliable medical source?]
Improper lead placement (for example, reversing two of the limb leads) has been estimated to occur in 0.4% to 4% of all ECG recordings,[81] and has resulted in improper diagnosis and treatment including unnecessary use ofthrombolytic therapy.[82][83]
Whitbread, consultant nurse and paramedic, suggests ten rules of the normal ECG, deviation from which is likely to indicate pathology.[84] These have been added to, creating the 15 rules for 12-lead (and 15- or 18-lead) interpretation.[85]
Rule 1: All waves in aVR are negative.
Rule 2: The ST segment (J point) starts on the isoelectric line (except in V1 & V2 where it may be elevated by not greater than 1 mm).
Rule 3: The PR interval should be 0.12–0.2 seconds long.
Rule 4: The QRS complex should not exceed 0.11–0.12 seconds.
Rule 5: The QRS and T waves tend to have the same general direction in the limb leads.
Rule 6: The R wave in the precordial (chest) leads grows from V1 to at least V4 where it may or may not decline again.
Rule 7: The QRS is mainly upright in I and II.
Rule 8: The P wave is upright in I II and V2 to V6.
Rule 9: There is no Q wave or only a small q (<0.04 seconds in width) in I, II and V2 to V6.
Rule 10: The T wave is upright in I II and V2 to V6. The end of the T wave should not drop below the isoelectric baseline.
Rule 11: Does the deepest S wave in V1 plus the tallest R wave in V5 or V6 equal >35 mm?
Rule 12: Is there anEpsilon wave?
Rule 13: Is there an J wave?
Rule 14: Is there aDelta wave?
Rule 15: Are there any patterns representing anocclusive myocardial infarction (OMI)?
Numerous diagnoses and findings can be made based upon electrocardiography, and many are discussed above. Overall, the diagnoses are made based on the patterns. For example, an "irregularly irregular" QRS complex without P waves is the hallmark ofatrial fibrillation; however, other findings can be present as well, such as abundle branch block that alters the shape of the QRS complexes. ECGs can be interpreted in isolation but should be applied – like alldiagnostic tests – in the context of the patient. For example, an observation of peaked T waves is not sufficient to diagnose hyperkalemia; such a diagnosis should be verified by measuring the blood potassium level. Conversely, a discovery of hyperkalemia should be followed by an ECG for manifestations such as peaked T waves, widened QRS complexes, and loss of P waves. The following is an organized list of possible ECG-based diagnoses.[86]
Rhythm disturbances or arrhythmias:[87]
Heart block and conduction problems:
Electrolytes disturbances and intoxication:
Ischemia and infarction:
Structural:
Other phenomena:
The word is derived from theGreekelectro, meaning related to electrical activity;kardia, meaning heart; andgraph, meaning "to write".[100]
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