More than that, the entire right ventricle is lacking in the model. It would not be difficult to implement one, but little is known about the shape of right-ventricular APs, let alone about how to assign them to the various cell assemblies. The ratio of the activation velocities of the Purkinje system to that between the myocardial cells is set at 6 and is kept constant throughout the slice. Variations of this ratio within reason were found not to produce essentially different results.
We postulated the body as homogeneous and infinite. To take into account inhomogeneity and non-infinity would mean to pretentiously stretch the limits of a simple model. With greater computing effort the model can be expanded to an entire three-dimensional representation with more or less realistic estimates of tissue inhomogeneities and boundaries [27] and with P anywhere in space.
A first simple three-dimensional model showed some variations in T- and U-wave configuration but not essentially different results. In the model the mid-myocardium consisted exclusively of M cells.
U waves are an integral component of ventricular repolarization and can be expected to occur in every ECG, perhaps modulated by wall stress. In our own material, through the use of a special measurement program [28] , we found them present in every lead ECG, in agreement with unpublished observations by Surawicz [6].
The measurement of QT duration has received increasing attention over the past decade. Recent requirements for drug safety testing [29,30] impose submission of data on possible drug-induced QT prolongation. And not only that: the differential lead vector model as presented here gives a different meaning to the definition of the end of the T wave. In our opinion T and U form a continuum without a sharp separation between the two.
What is generally regarded as the end of T coincides more or less with the AP 90 of endocardial repolarization. The repolarization of the myocardium in its totality is only completed at the end of the U wave. T and U together are the resultant of the same process, i. This means that our ideas about QT duration and prolongation, whether drug-induced or congenital, must perhaps be viewed in a somewhat different perspective and that regulatory authorities should exert caution in imposing rules on drug testing based on measurement of QT duration.
Einthoven W. Google Scholar. The different forms of the human electrocardiogram and their signification Lancet 30 Hoffman B. Cranefield P. Antzelevitch C.
Sicouri S. Clinical relevance of cardiac arrhythmias generated by afterdepolarisations. Role of M cells in the generation of U waves, triggered activity and torsades de pointes J Am Coll Cardiol 23 Di Bernardo D. Murray A. Origin on the electrocardiogram of U-waves and abnormal U-wave inversion Cardiovasc Res 53 Surawicz B. U wave: facts, hypotheses, misconceptions, and misnomers J Cardiovasc Electrophysiol 9 Zipes D.
Early afterdepolarisations, U waves, and torsade de pointes Circulation Wohlfart B. Drouin E. Charpentier F. Gauthier C. Laurent K. Le Marec H. Electrophysiological characteristics of cells spanning the left ventricular wall of human heart: evidence for the presence of M cells J Am Coll Cardiol 26 Lab M. Mechanically dependent changes in action potentials recorded from intact frog ventricle Circ Res 42 Zabel M.
Koller B. Sachs F. Franz M. Stretch-induced voltage changes in the isolated beating heart: importance of the timing of stretch and implications for stretch-activated ion channels Cardiovasc Res 32 Taggart P. Sutton P. Opthof T. Coronel R. Trimlett R. Pugsley W. Inhomogeneous transmural conduction during early ischaemia in patients with coronary artery disease J Mol Cell Cardiol 32 Plonsey R.
Burger H. Van Milaan J. Heart-vector and leads Br Heart J 8 Watanabe Y. Purkinje repolarization as a possible cause of the U wave in the electrocardiogram Circulation 51 Lepeschkin E. Physiologic basis of the U wave Schlant R. Hurst J. Nesterenko V. Simulation of the electrocardiographic U wave in heterogeneous myocardium: effect of local junctional resistance.
Yan G. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome Circulation 98 Burkhoff D.
Yue D. Sagawa K. Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts Cardiovasc Res 23 Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia Cardiovasc Res 50 Conrath C. Wilders R. De Bakker J. De Groot J. Intercellular coupling through gap junctions masks M cells in the human heart Cardiovasc Res 62 Abildskov J. The sequence of normal recovery of excitability in the dog heart Circulation 52 Anyukhovsky E.
Sosunov E. Rosen M. Regional differences in electrophysiological properties of epicardium, midmyocardium, and endocardium Circulation 94 El-Sherif N. Caref E. Yin H. Restivo M. The electrophysiological mechanism of ventricular arrhythmias in the long QT syndrome Circ Res 79 Ritsema van Eck HJ.
Digital computer simulation of cardiac excitation and repolarization in man. Dalhousie: Dalhousie University; [Thesis]. Ritsema van Eck H. Fiducial segment averaging to improve cardiac interval estimates J Electrocardiol 35 Suppl. Fenichel R, Koerner J. Washington; Oxford University Press is a department of the University of Oxford.
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Sign In. Advanced Search. Search Menu. Article Navigation. Close mobile search navigation Article Navigation. Volume Article Contents Abstract. The U wave in the electrocardiogram: A solution for a year-old riddle. Ritsema van Eck , Henk J. Email address: h. Oxford Academic. Jan A. Gerard van Herpen. Time for primary review 14 days. Revision received:. Cite Cite Henk J. Select Format Select format. Permissions Icon Permissions. Abstract Objective : In the electrocardiogram ECG the U wave follows the T, which is considered to reflect the repolarization of the cardiac ventricles.
Open in new tab Download slide. A potential will be generated at a given point P in or on the body by each dipole source D. This potential is a function of the magnitude of the dipole vector D and the so-called lead vector. This lead vector L of P is determined by the geometrical position of P relative to the location of D and by the electrical properties of the interposed tissues [14—16]. The potential at point P is then given by:. Considering that the potential field generated by the different sources is linear, by superposition the potential V P at point P is obtained as the sum of the weighted contributions of all N source vectors.
Since the dipole sources are time-varying and consequently also V P , we write:. For the infinitesimal case, Eq. In the string model each dipole is determined by only 2 neighboring cells Fig. Then, all dipoles are directed along the axis of the cell string. The different forms of the human electrocardiogram and their signification.
Google Scholar Crossref. Search ADS. Role of M cells in the generation of U waves, triggered activity and torsades de pointes. Google Scholar PubMed. Electrophysiological characteristics of cells spanning the left ventricular wall of human heart: evidence for the presence of M cells. Mechanically dependent changes in action potentials recorded from intact frog ventricle.
Stretch-induced voltage changes in the isolated beating heart: importance of the timing of stretch and implications for stretch-activated ion channels.
Inhomogeneous transmural conduction during early ischaemia in patients with coronary artery disease. Purkinje repolarization as a possible cause of the U wave in the electrocardiogram. Proc computers in cardiology. Cellular basis for the normal T wave and the electrocardiographic manifestations of the long-QT syndrome.
Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts. Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia. Intercellular coupling through gap junctions masks M cells in the human heart.
Regional differences in electrophysiological properties of epicardium, midmyocardium, and endocardium. The electrophysiological mechanism of ventricular arrhythmias in the long QT syndrome. Points to consider: the assessment of the potential for QT interval prolongation by non-cardiovascular medicinal products.
Issue Section:. Download all slides. Note the P wave immediately before the Q as seen on lead II. This P wave is common for all junctional rhythms as the depolarization pacing point are in the AV node, and the depolarization wave must travel upwards into the atria simultaneously, or the closest thing to concurrent, as the same aberrant firing wave heads to the His bundle and ventricles Knapp, Junctional rhythms will have a regular RR interval, and as a signature sign, one of the following P wave variations:.
A sign that the AV node is sending depolarization impulses simultaneously to the atria and ventricles. Before we leave the top of the heart, we need to discuss a few fine fast arrhythmias that can lead to a lot of mischief, the atrial tachycardias. They are, nevertheless, supraventricular tachycardias, even though a goodly percentage of cardiologists harumph at that designation.
The name says it all. Multifocal, yes. There must be at least three different P wave morphologies to qualify. Each differing P reflects an alternate or aberrant depolarization origin within the atrium. Atrial, yes. The depolarizations are initiating from within the heart atria. Whether from areas of inflammation, irritation, scaring, or from medication or chemical toxicities.
Tachycardia, yes. Faster than bpm. In lead, II notice the arrows, which each point out distinctly different P wave morphologies. P-P waves will be largely irregular. Not fibrillation, not flutter, but irregular from the multiplicity of electrical stimulation points. MAT is not in itself life-threatening. However, the comorbidities frequently associated with it are severe. A rapid irregular pulse may be the only indication of the presence of MAT. Complaints that might cause a client to possess this arrhythmia include increased shortness of breath, chest pain, palpitations, lightheadedness, or feelings of syncope.
Multifocal atrial arrhythmias can lead to some direct complications. These include myocardial infarction from unsteady oxygen supply and demand, pulmonary emboli, or atrial thrombi, especially stroke Tandon, Atrial Fibrillation AFib or AF is considered the most common type of treated cardiac arrhythmia, affecting between 2. When irritation, inflammation, or any other disorganizing factor gets in the way of the orderly metronome of the SA node, the chaotic firing of random atrial depolarization impulses leads to fibrillation, e.
AFib is a cardiac output disaster, especially in the elderly or those with comorbid medical conditions, as the billows-like effect from organized contractions can no longer push adequate quantities of blood into the ventricles.
Despite this lack of compression, many people are asymptomatic with AFib. Those who do feel sudden fatigue, shortness of breath, dizziness, or chest pain tend to be surprised at how irregular their heart has become Vaidya, Fast, then slower, then well, chaotic.
So unpredictable that there are, in some viewpoints, three different types of atrial fibrillation. Runs of fibrillation, when they occur, that tend to last longer than one week or until delivery of a small electric cardioversion shock or medications, reset the heart back to a normal sinus rhythm.
In unstable clients, emergent, electrical cardioversion back to an NSR is needed. In clients whose condition allows more time, the consideration of rather to control the rhythm or control the heart rate must be explored. Generally, medication therapies must be individualized, and some surgical options are available.
Oh, and anticipate that the client will be put on anticoagulants to minimize the occurrence of clot formation. Atrial flutter is the quintessential atrial tachyarrhythmia. The distinctive saw-tooth pattern of the atrial flutter waves is characteristic of multiple P waves successfully constricting the atria, yet only penetrating to the ventricle myocardium every second, third, or more atrial depolarizations.
Atrial rates will typically run bpm. While ventricular rates will range around bpm, with the most common ventricular rate in atrial flutter being bpm, due to a phenomenon known as atrioventricular block, which we will cover later. Here is a blowup of V1 from above. Note the choppy ocean waves of P in relation to the QRS complex. Most are , three P waves to each QRS. However, there is a variable ratio of P: QRS as we examine more of this lead. Atrial flutter tends to go hand in hand with an atrioventricular block AV block.
AV blocks are depolarization conduction delays, or at times complete barriers, to electrical conduction from the atria to the ventricles. Something as innocuous as increased vagal tone occurring during sleep, exercise, pain, or even stimulation of the carotid sinus. An AV block may also be related to cardiac fibrosis or sclerosis, ischemic heart disease, changes to the myocardial tissue, medications, or elevated plasma potassium Medzcool, The absent or slowed conduction from atria to ventricles, an atrioventricular block, is described by degrees.
The seriousness of the conduction problem ranges from one to three. Regular PR intervals greater than ms milliseconds with no interruption in atrial to ventricular conduction are the signature indication of a first-degree AV block Medzcool, It is remarkable in that there are no skipped beats.
QRS complexes follow all P waves. In well-trained athletes or healthy younger clients with a high level of vagal tone, a first-degree AV presentation may be non-pathologic and found only by chance. Further study is warranted for the rest of us to determine if an underlying cardiac condition may be developing, or most likely, some drug effect is manifesting Mitchell, This sequential lengthening until a QRS complex is dropped and the AV node conduction picked back up with the next beat is often referred to as the Wenckebach phenomenon, described by Karel Frederik Wenckebach in Second-degree AV block Mobitz type I is generally considered to be a harmless point of interest.
Little risk of complete heart block exists with this arrhythmia. When it does cause, hemodynamic issues implantation of a cardiac pacemaker is the treatment by consensus. Mobitz type II second-degree AV block is about the His-Purkinje system, sometimes referred to as the distal conduction system.
When a block occurs at the level of the His bundle, or even slightly below at the Purkinje branches, no normal conduction will pass. The P: QRS ratio can vary. However, each client should remain consistent. That is, you as a health professional may see across a spectrum of clients P: QRS ratios of , , , etc. However, in any one individual, the ratio P: QRS should remain consistent. Type II Mobitz blocks can readily progress into a complete heart block where ventricular escape beats are too slow to maintain adequate perfusion or sudden cardiac death SUD.
Go ahead and do diagnostics, even a twenty-four-hour wearable cardiac monitor, sometimes referred to as a Holter monitor. Yet keep in mind the preferred treatment is an implanted cardiac pacemaker Mitchell, Complete heart block, the lack of any conduction impulses making it through to the ventricles, is another way of saying third-degree AV block.
P wave rate should always be faster than the QRS ventricular firing rate due to inherent escape rates in the atria and ventricles. The escape pacing below the atria originating from above the His bundle bifurcation e. Escape pacing coming from below the bifurcation e. Junctional escape rhythms are a sequence of electrical depolarizations that originate at, or near, the level of the AV node in the absence of a quicker, atrial, electrical depolarization event. Notice in this monitor strip the atrial rate is fast, bpm, and regular.
The ventricular rate is regular but slow, 47 bpm. Neither atrial nor ventricular rates relate to the other. Most clients experiencing complete heart block will require an implanted cardiac pacemaker, as their heart system is no longer able to supply this function adequately. The Wandering Pacemaker. A wandering atrial pacemaker is an arrhythmia originating in the atria where the pacemaker cells shift between the SA node, odd source spots within the atria themselves, and the AV node.
These shifting, skipping about stimuli sites are generally best seen from lead II by looking for morphologic changes in the P waveform.
It is most often seen in the young, the old, or in fit athletes. It tends not to be symptomatic and rarely requires treatment though the presence of the medication digoxin, or sometimes COPD, has been associated with it. At least three different sources of atrial stimulation are present. QRS should be consistent and narrow. If this heart rate were faster, the arrhythmia would be considered multifocal atrial tachycardia.
Wolff-Parkinson-White WPW displays intervals of abnormally fast heartbeats intruding on what otherwise would be a normally functioning heart rate. This rate is due to an additional abnormal electrical conduction pathway in the heart, which occasionally activates, leading to an extremely fast supraventricular tachycardia. The accessory pathways APs or bypass tracts connect the atrium to the ipsilateral on the same side ventricle allowing the ventricles a depolarization charge that pre-excites them, urging them to fire fast and often Calkins, This accessory pathway phenomenon, sometimes referred to as the Kent pathway, is shown by a short PR interval.
By bypassing the AV node, the PR interval shortens. A delta wave becomes visible and represents early activation of the ventricles from the bypass tract. A form of fusion QRS results from two activation sequences, one from the bypass tract and one from the AV node. ST-T changes occur secondary to changes in the ventricular activation sequence.
Short PR intervals and delta waves are best seen in leads V These pathways predispose the patient to atrial tachycardia since there is no blocking of impulses at the AV node. PRI: If this interval is short, the sinus impulse partially avoids its normal delay in the AV node by traveling rapidly down the accessory pathway.
QRS: Often greater than 0. Subsequent activation of the ventricles depends upon intra-atrial conduction time from the sinus node to the accessory pathway plus conduction time down the accessory pathway, compared with sinus node conduction time to ventricles via orthodoxy conduction pathways.
Secondary T wave changes: Because ventricular depolarization is abnormal, repolarization will also be abnormal, causing ST and T wave changes secondary to the degree and area of pre-excitation. Such Q waves are often seen in the presence of an accessory AV pathway and may be misdiagnosed as Myocardial infarction. These are negative delta waves, not Q waves, and they reflect pre-excitation and not myocardial necrosis. Ventricular impulses come from the ventricles.
The large muscular chambers of the lower heart push a pulsing stream of blood out into the body. When a command to contract signals fails to arrive from the primary pacemaker, the sinus node, escape cells within the ventricles step up to emit electrical depolarization waves that contract the ventricular myocardium.
Any early, untimely cardiac contraction arising from the ventricles is a premature ventricular complex PVC. Many, if not most people who have the occasional PVC are completely unaware of them. Those who do perceive them tend to describe the sensation as a skipped beat or pounding heart. Both are accurate descriptions of what is brought about by the hemodynamic changes of sudden, early ventricular contractions.
Rhythm: Irregular due to PVC. If PVC is sandwiched between two normal beats, it is called interpolated, and the overall rhythm will be regular. T wave frequently in the opposite direction of the QRS complex. The PVC may produce a weak pulse, and it is the client who should be treated, not the monitor.
Paired PVCs are referred to as couplets. PVCs occurring from more than one ventricular escape source during a sixty-second cycle are called multifocal PVCs. Image PVCs coming fast upon the QRS complex directly before, especially during the T wave myocardial recovery cycle, are a red alert for triggering a ventricular depolarization loop leading into ventricular tachycardia or straight into ventricular fibrillation. When considering abnormal ventricular beats, the top considerations are where the source originates and the speed.
So, let us talk speed. Without irritation from comorbid or causation factors, a ventricular escape rhythm rate will be limited to bpm. Three or more ventricular origin beats in a row constitute IVR. Typically, IVR is transient, with a brisk return to a heartbeat of atrial derivation. Syncope, dizziness, and all that accompanies the rapid hemodynamic slowing which accompanies this rhythm.
It may be due to: MI, metabolic imbalances, or severe hypoxia. Treatment includes activation of emergency code, CPR if a client is pulseless. Lidocaine is contraindicated since it may knock out the last available pacemaker. Faster than a ventricular escape rhythm, yet not fast enough to meet the blood pressure dropping ventricular tachycardia criteria.
An accelerated idioventricular rhythm might, rarely, be considered a benign or asymptomatic arrhythmia. However, do not get complacent with the lack of symptoms as AIVR is most common during cardiac tissue recovery from a myocardial injury. A time when any additional stress on the heart can tip recovery into adversity. It may be due to Heart disease e. Ventricular tachycardia V-Tach, VT is a regular fast heart rate originating from an area of ventricular irritation. Short bursts of rapid ventricular contractions may not endanger a person.
However, the less efficient circulation of blood from prolonged bouts can be life-endangering. VT can be monomorphic, originating from one electrical excitation where all QRS complexes look alike. Or polymorphic, where multiple spots of electric stimulation are firing within the ventricles. Bursts of VT lasting under 30 seconds are referred to as non-sustained V-Tach, while stretches longer than 30 seconds are referred to as sustained V-Tach.
Symptoms of ventricular tachycardia fall along the lines of reduced cardiac output and include hypotension, dizziness, syncope, cardiogenic shock, cardiac arrest. P Waves: May or may not be present. If present, they have no set relationship to the QRS complexes. Often difficult to differentiate between QRS and T wave. There may be a long or a short run.
A client may or may not have a pulse. It may be due to: An early or a late complication of a heart attack, or during cardiomyopathy, alveolar heart disease, myocarditis, electrolyte imbalance, or following heart surgery.
The characteristic that makes TdP distinctive is how the QRS complexes twist around the isoelectric baseline during self-limiting bursts. For example, as a PVC, stomps on the tail of an extended T wave torsades de pointes or polymorphic VT may be triggered.
This occurrence magnifies the need for a thorough review of client medications as drug-induced long QT syndrome is, unfortunately, common Cohagan, QRS Complex: Each differs from its neighbor. There will be an overall effect of tall QRSs, which shorten then regain height.
QT Interval: Prolonged QT intervals may be congenital, or more commonly, an unwanted effect of some prescription and over-the-counter medications. Other Components: TdP is a significant adverse arrhythmia. However, the great concern when present increases in rate and degenerates into an even deadlier arrhythmia, ventricular fibrillation. It may be due to: R on T trigger, antiarrhythmics, antipsychotics, antiemetics, antifungals, antimicrobials, basically any pharmaceutical with the adverse effect of prolonging the cardiac QT interval.
Also, beware of substances that slow the hepatic metabolism. Slower liver breakdown of complex chemicals can turn a previously tolerated QT-prolonging substance into a landmine trigger, just waiting for an early R wave to activate the torsades effect Cohagan, Ventricular fibrillation V-fib or VF is where the lower heart chambers quiver rather than constrict.
Too many electrical polarization signals, arriving much too rapidly, reduce the strong rhythmic myocardial contractions to chaotic spasms. V-fib is a lethal arrhythmia resulting in rapid loss of consciousness, no pulse, and cardiac death in the absence of treatment. Without treatment, clinical death comes within minutes when V-fib is the prominent rhythm. Even when rescue efforts succeed, residual damage from the anoxic brain and neurologic damage requires follow-up and perhaps long-term treatment Ludhwani, V-Fib tends to accompany damage to the structure of the heart.
Anything that can irritate or inflame the Purkinje cells of the ventricles has the potential to initiate the fast and multiple stimuli sites leading toward VF. Many common conditions are associated with the chaotic irritability of V-Fib, including electrolyte abnormalities hypokalemia, hyperkalemia, hypomagnesemia , acidosis, hypothermia, hypoxia, cardiomyopathies, family history of sudden cardiac death, congenital QT abnormalities, and alcohol use Ludhwani, Other Components: Coarse VF is where most waveforms are 3mm or wider.
Fine VF is where most waveforms are less than 3mm. Asystole is synonymous with Ventricular Standstill and death. Asystole is usually associated with prolonged circulatory insufficiency and cardiogenic shock. It could also be drug-related, hypothermia-related, and at times reversible. The natural electrical sources produce heart rhythms within the heart. When those natural pacemaker sites fail by producing too fast, too slow, or an absence of depolarization signals, another source of control is warranted.
Enter the artificial cardiac pacemaker. An implantable cardiac pacemaker is the most common type used. There are also external pacemakers that introduce a rhythmic electronic pulse that is used mostly during emergencies. Internal pacemakers are used in cases requiring long-term availability to override a dangerous heart rhythm or replace an absence of functional heart rhythm.
Implantable pacemakers can pace on-demand or continuously. They tend to stimulate just one heart chamber, or sometimes two. The small pacemaker unit is implanted under the skin with output leads connected directly to the heart muscle. Small batteries provide power to recognize the heart's electrical activity and provide needed electrical pulses to the heart muscle.
They are used primarily on clients with significant or complete heart blocks. The rate is pre-set to a rate such as 70 bpm, though rate changes can be made using external magnetic control most commonly. Only fires when the R-R interval of the client's natural rhythm meets or exceeds a preset limit. When dealing with heart blocks possessing occasional sinus rhythm, the ventricular synchronized demand-type pacemaker, the R wave triggered pacer, looks for the absence of R waves and stimulates the heart ventricles should they not appear after a short delay.
For clients with sinus rhythm and only an occasional heart block, the R wave blocked pacemaker stops firing when it detects a natural R wave produced by the client. When detecting natural atrial depolarization, the pacemaker stimulates the ventricles after a reasonable delay. This pacemaker provides the best cardiac output while following the normal atrial rate fluctuations. Treats most sino-atrial conditions by providing both atrial and ventricular stimulation whenever it is needed.
Firing refers to the pacemaker's generation of electrical stimuli. This impulse is seen as a narrow vertical pacemaker spike on the ECG. Capture refers to the presence of a P, a QRS, or both after a pacemaker spike. This capture indicates that the tissue in the heart chamber being paced has been depolarized.
The term is that the pacemaker has "captured" the chamber being paced. Most pacemakers function in the demand mode and fire when needed. Our heart is an exquisitely crafted pumping machine whose myocardial muscle cells move upwards of six thousand liters of blood every day.
These wonderful engines are controlled by rhythmic electrical pulsations originating from natural pacemaker cells located in the apex of the heart itself. Ironically, this problem is one reason we need a consistent method of examining the heart's electrical activity to see what in our heart is happening. Electrocardiography is the science of recording and examining the activity of the heart.
This depolarization wave creates myocardial muscle contracture of the near atrial chambers and quickly after the large muscular ventricles of the heart, creating a bellows that pushes blood into an eager body.
Each step the electrical conduction wave takes through the heart creates a different waveform on the isoelectric baseline of an ECG monitor strip. The atrial depolarization from the sinus node is the P wave.
The movement of the electric pulse through the atrial tissue to the AV node and the His-Purkinje fibers causes atrial constriction. This constriction is the PR Interval. The short period of recovery occurring between ventricular cell depolarization and repolarization is seen as the ST segment, with the T wave signaling full repolarization.
Always one for a bit of mystery, our heart can throw up a wave we call U, which follows the T and precedes the P. We have no idea why, yet life contains plenty of mysteries to pique our curiosity Amboss, We place the positive and negative cardiac monitor to give us special angles for viewing the hearts' electrical activity.
Twelve special lead placements compose a cardiac lead ECG, the diagnostic standard for electrocardiograms. How we evaluate what is going on in the heart using an ECG strip requires a system. Using a systematic approach, we can determine where the rhythm originates from the atria, junction, or ventricles if it is normal, fast, or slow; If there are unusual beats; If the entire rhythm is unusual and perhaps unwanted, an arrhythmia; if unusual spots of excitement, electrical blockage, chaotic electrical fibrillation, or lack of electrical activity are present.
Not only can we see and diagnosis natural cardiac functions, but we can also look at the functioning of implanted cardiac pacemaker devices to determine if their function is appropriate or failing. A failing artificial pacemaker can show as under sense, failure to capture, or output failure. Alzheimer's and Dementia. How much does CEUfast cost? How soon do I get my certificate? You are not currently logged in. Please log in to CEUfast to enable the course progress and auto resume features.
This peer reviewed course is applicable for the following professions:. This course will be updated or discontinued on or before Friday, September 1, After this course, the participant will be able to: Describe normal cardiac anatomy and normal electrical conduction through the heart.
Identify and relate ECG waveforms to the cardiac cycle. Characterize the different lead placements and the purpose of each lead placement. Utilize a systematic process when approaching the interpretation of the ECG. Differentiate normal and abnormal components on ECG.
Recognize sinus, atrial, junctional, and ventricular dysrhythmia on ECG and relate cause, significance, and symptoms. Identify three pacemaker malfunctions. CEUFast Inc. The Planning Committee and Authors do not have any conflict of interest. Complete Course. Options Back Complete Course Print. Time Remaining:. Nursing Assistants from California, only. You must read the material on this page before you can take the test. The California Department of Public Health, Training Program Review Unit has determined that is the only way to prove that you actually spent the time to read the course.
Introduction Electrocardiograms are used in the ambulance, emergency room, surgery, intensive and critical care, or any other hospital room to diagnose a suspected heart attack, syncope, abnormal vital signs, or pulse. Anatomy and Physiology The heart is a hollow, chambered, muscular organ located in the middle of the thoracic cavity, cradled in a cage of bone, cartilage, and muscle. Function Activities of the right side of the heart and the left side of the heart occur simultaneously.
Coronary Arteries Our heart supplies or pushes oxygenated blood to the cells throughout the body. Electrical Activity of the Heart The human heart is a remarkable piece of engineering. If the SA node falters, a hierarchy of backup pacemakers can take over. Atrial, AV node, and ventricular escape pacemakers can function as subsidiary pacemakers. However, they generated impulses at a much slower rate.
The AV node generates rates between 40 to 60 bpm and the Purkinje fibers at 20 to 40 bpm. Electrical impulse does not always equal the contraction of the heart. Accessory pathways play a role in re-entry tachydysrhythmias, providing a detour for unwanted electrical impulses to circle through the heart.
Components of the Electrical System There are two basic cardiac cell types. Electrophysiological Properties of a Cardiac Cell Cardiac cells are surrounded by and filled with a solution that contains ions. Electrical Events of Depolarization and Repolarization Cardiac cells that are resting have a negative polarization. Phase 0. Slowly repolarization continues Calcium continues to flow into the cell through slow calcium channels Phase 3.
Rapidly the cell completes repolarization Calcium channels close Potassium rapidly flows out of the cell Active transport via the potassium-sodium pump begins restoring potassium to the inside of the cell and sodium to the outside of the cell Cell now in the negative state due to the outflow of potassium Gradually the cell becomes extremely sensitive to external stimuli until its original sensitivity has been restored, called the relative refractory period.
Phase 4. Corresponds to diastole Calcium and sodium remain outside the cell Potassium remains inside the cell During this phase, the heart is "polarized" and getting ready for discharge Once another stimulus occurs, the cell will reactivate Image Properties of the Heart. Automaticity The heart can initiate an electrical impulse. Excitability The heart can respond to an electrical impulse.
Conductivity The heart can conduct an electrical impulse. The velocity of the impulse conduction transfer varies in the different cardiac tissues: 0. Doctor, Conduction System The heart is all about electricity. The first wave is called the P wave.
It records the electrical activity of the atria. The second and largest wave, the QRS wave, records the electrical activity of the ventricles. The third wave is the T wave. It records the heart's return to the resting state. Rate and Rhythm Utilize a Systematic Approach. Is it a Regular rhythm?
Are there P waves? What is the QRS width? Does each QRS have a P wave in front? What is the Heart Rate? Analyzing a Rhythm Strip Using the Eight Step Approach The eight-step system is a good starter system, and you will quickly learn what to look for in any suspect monitor stip. Step One: Determine the Rate To determine the atrial rate, measure the distance between P-P and determine the rate by one of the methods listed earlier.
What is the ventricular rate? To determine the ventricular rate, measure the distance between R-R. To determine if the atrial rate is regular or irregular, measure the distance between two consecutive P-P intervals. Use a point from one P wave to the same point on the next P wave. Then compare this with another P-P interval. If the atrial rate is regular, the P-P interval will measure the same. Determine if the ventricular rate is regular or irregular, measure the distance between two consecutive R-R intervals.
Use a point from one R wave to the same point on the next R wave. Then compare this with another R-R interval. If the ventricular rate is regular, the R-R interval will measure the same. Is the rhythm regular?
Regularly irregular? Irregularly irregular? Are P waves upright positive in Lead II? Do P waves appear regularly before each QRS complex? Is there more than one P wave before a QRS complex? If irregular, is there an associated QRS? The normal P-R interval is 0. Is the P-R interval consistent? If the QRS measures. If the QRS complex is greater than.
The QRS normally measures 0. Determine if they are married to the P waves. Are T waves smooth and rounded? Do they have a normal amplitude of 0. Is the deflection the same as the preceding QRS? Is there a relationship between any ectopy to the T wave? Sloping or scooped? Are U waves present? Are there other funny little beats FLB's detected? Origin of the impulse. Is it sinus, atrial, junctional, or ventricular? For example, sinus bradycardia, sinus tachycardia, junctional, or ventricular tachycardia.
Reentry This ventricular pacemaker occurs when an electrical impulse is delayed, blocked, or both in one or more portions of the conduction system.
Image Standard Electrocardiogram Waveform Diagram. ECG Augmented Leads Using the same placement of three-electrode pads and a little fancy math, we can get different views of the electrical activity in the heart. Lead aVR : The augmented unipolar right arm lead is oriented toward the cavity of the heart.
Electrical current from the heart is traveling towards the right arm. Lead aVL : The augmented unipolar left arm lead oriented toward the heart facing the anterolateral aspect of the left ventricle. Electrical current from the heart is traveling towards the left arm.
Lead aVF : The augmented unipolar left leg lead feet. It is oriented toward the inferior surface of the heart. Electrical current from the heart is traveling toward the feet. Image Augmented Leads. Precordial Leads The precordial, or chest leads, view the heart's electrical conduction from the straight face-to-face view. Modified Chest Leads MCL, or modified chest leads, are different placements of electrodes used to focus on premature beats, bundle branch blocks, or supraventricular rhythms.
MCL1 : It is a variation of V1, where the negative electrode is situated below the left clavicle close to the left shoulder. Positive electrode in the fourth intercostal space to the right of the sternum and ground just below the right clavicle.
Useful in assessing the anterior wall of the left ventricle and conduction through the ventricles. QRS appears mostly as negative deflections. MCL6 : This variation is a deviation of chest lead V6. The negative electrode is placed just below the left clavicle. Positive electrode is placed in the fifth intercostal space at the left midaxillary line like lead V6 while the ground is placed below the right shoulder.
This lead may be used as an alternative to MCL1 for the same purposes and views the low lateral wall of the left ventricle while monitoring ventricular conduction changes. Got Rhythm? Normal Sinus Rhythm We consider normal a regular contracting heartbeat stemming from an electrical stimulus originating from the sinoatrial node SA located in the upper right atrium of our heart.
Sinus Bradycardia. Sinus Tachycardia. Sinus Arrhythmia Have you ever heard that there is a healthy arrhythmia? Sinus Arrest or Sinus Pause A sinus pause is not your friendly neighborhood sinus arrhythmia.
Sinus Exit Block Sinoatrial Block Sinus exit blocks are when a depolarization wave leaves the SA node yet fails to be conducted to the atria and therefore fails to stimulate the ventricles.
Supraventricular Tachycardia Tachycardia means fast. Hahn, Regular SVT Supraventricular tachycardias come in two basic types, regular or irregular. Definition: Accessory Pathway An accessory pathway is an abnormal electrical connection between the atrium and ventricle that is usually congenital.
Amboss, Atrioventricular Nodal Reentrant Tachycardia. Atrioventricular Reentry Tachycardia. Antidromic Atrioventricular Reentry Tachycardia. Image Junctional Tachycardia. Atrial Tachycardias Before we leave the top of the heart, we need to discuss a few fine fast arrhythmias that can lead to a lot of mischief, the atrial tachycardias.
Multifocal Atrial Tachycardia The name says it all. Image Multifocal Atrial Tachycardia. Atrial Fibrillation. Atrial Flutter Atrial flutter is the quintessential atrial tachyarrhythmia. Image Atrial Flutter. Atrioventricular Block Atrial flutter tends to go hand in hand with an atrioventricular block AV block. First Degree AV Blocks Regular PR intervals greater than ms milliseconds with no interruption in atrial to ventricular conduction are the signature indication of a first-degree AV block Medzcool, Third Degree AV Block Complete heart block, the lack of any conduction impulses making it through to the ventricles, is another way of saying third-degree AV block.
Junctional Escape Rhythm Junctional escape rhythms are a sequence of electrical depolarizations that originate at, or near, the level of the AV node in the absence of a quicker, atrial, electrical depolarization event. Heart rate will be bpm. Narrow QRS complexes. Ventricular Escape Rhythm A rhythmic electrical depolarization that originates at, or near, the bundle of His Heart rate bpm.
Wide QRS. Image Wandering Atrial Pacemaker. Ventricular Rhythms Ventricular impulses come from the ventricles. Premature Ventricular Complexes. Rate: Intrinsic rate is beats per minute. Rhythm: Atrial not discernible, ventricular essentially regular. P waves: Absent. PRI: None. Image Accelerated Idioventricular Rhythm.
Accelerated Idioventricular Rhythm AIVR Faster than a ventricular escape rhythm, yet not fast enough to meet the blood pressure dropping ventricular tachycardia criteria.
Rhythm: Ventricular rate regular, an atrial rate not discernable. PR Interval: None. QT Interval: Regular. Image Ventricular Tachycardia. Image Torsades de Pointes. Ventricular Fibrillation VF. Ventricular Asystole Asystole is synonymous with Ventricular Standstill and death. Artificial Cardiac Pacemakers The natural electrical sources produce heart rhythms within the heart.
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