wandering pacemaker irregular

Ectopic Supraventricular Arrhythmias

Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment.

(See also Overview of Arrhythmias .)

Ectopic supraventricular rhythms include

Atrial premature beats

Atrial tachycardia, multifocal atrial tachycardia, nonparoxysmal junctional tachycardia, wandering atrial pacemaker.

Atrial premature beats (APB), or premature atrial contractions (PAC), are common episodic impulses. They may occur in normal hearts with or without precipitating factors (eg, coffee, tea, alcohol, pseudoephedrine ) or may be a sign of a cardiopulmonary disorder. They are common in patients with chronic obstructive pulmonary disease (COPD). They occasionally cause palpitations.

Diagnosis is by electrocardiography (ECG—see figure Atrial premature beat ).

Atrial premature beat (APB)

Image courtesy of L. Brent Mitchell, MD.

APBs may be normally, aberrantly, or not conducted and are usually followed by a noncompensatory pause. Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.

Atrial escape beats are ectopic atrial beats that emerge after long sinus pauses or sinus arrest. They may be single or multiple; escape beats from a single focus may produce a continuous rhythm (called ectopic atrial rhythm). Heart rate is typically slower, P wave morphology is typically different, and PR interval is slightly shorter than in sinus rhythm.

Atrial tachycardia is a regular rhythm caused by the consistent, rapid atrial activation from a single atrial focus. Heart rate is usually 150 to 200 beats/minute; however, with a very rapid atrial rate, nodal dysfunction, and/or digitalis toxicity, atrioventricular (AV) block may be present, and ventricular rate may be slower. Mechanisms include enhanced atrial automaticity and intra-atrial reentry.

Atrial tachycardia is the least common form (5%) of paroxysmal supraventricular tachycardia and usually occurs in patients with a structural heart disorder. Other causes include atrial irritation (eg, pericarditis

Symptoms are those of other tachycardias (eg, light-headedness, dizziness, palpitations, and rarely syncope).

Diagnosis is by electrocardiography (ECG); P waves, which differ in morphology from normal sinus P waves, precede QRS complexes but may be hidden within the preceding T wave (see figure True atrial tachycardia ).

True atrial tachycardia

Vagal maneuvers may be used to slow the heart rate, allowing visualization of P waves when they are hidden, but these maneuvers do not usually terminate the arrhythmia (demonstrating that the AV node is not an obligate part of the arrhythmia circuit).

Treatment involves managing causes and slowing ventricular response rate using a beta-blocker or calcium channel blocker. An episode may be terminated by direct current cardioversion . Pharmacologic approaches to termination and prevention of atrial tachycardia include antiarrhythmic drugs in class Ia, Ic, or III. If these noninvasive measures are ineffective, alternatives include overdrive pacing and ablation .

Multifocal atrial tachycardia (chaotic atrial tachycardia) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is > 100 beats/minute. On ECG, P-wave morphology differs from beat to beat, and there are ≥ 3 distinct P-wave morphologies. The presence of P waves distinguishes multifocal atrial tachycardia from atrial fibrillation . Except for the rate, features are the same as those of wandering atrial pacemaker. Symptoms, when they occur, are those of rapid tachycardia. Multifocal atrial tachycardia can be due to an underlying pulmonary disorder such as chronic obstructive pulmonary disease coronary artery disease , and electrolyte abnormalities such as hypokalemia . Treatment is directed at the underlying disorder.

Nonparoxysmal junctional tachycardia is caused by abnormal automaticity in the AV node or adjacent tissue, which typically follows open heart surgery, acute inferior myocardial infarction, myocarditis, or digitalis toxicity. Heart rate is 60 to 120 beats/minute; thus, symptoms are usually absent. ECG shows regular, normal-appearing QRS complexes without identifiable P waves or with retrograde P waves (inverted in the inferior leads) that occur shortly before ( < 0.1 second) or after the QRS complex. The rhythm is distinguished from paroxysmal supraventricular tachycardia by the lower heart rate and gradual onset and offset. Treatment is directed at causes.

Wandering atrial pacemaker (multifocal atrial rhythm) is an irregularly irregular rhythm caused by the random discharge of multiple ectopic atrial foci. By definition, heart rate is ≤ 100 beats/minute. Except for the rate, features are the same as those of multifocal atrial tachycardia. Treatment is directed at causes.

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Wandering Atrial Pacemaker

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ESSENTIALS OF DIAGNOSIS

Progressive cyclic variation in P-wave morphology

Heart rate 60–100 bpm

Variation of P-wave morphology, P-P interval, and P-R interval

GENERAL CONSIDERATIONS

This rhythm is benign

This rhythm and multifocal atrial tachycardia are similar except for heart rate

The other possible explanation is that there is significant respiratory sinus arrhythmia, with uncovering of latent foci of pacemaker activity

Usually, it is associated with underlying lung disease

In the elderly, it may be a manifestation of sick sinus syndrome

In the young and athletic heart, it may represent enhanced vagal tone

SYMPTOMS AND SIGNS

Usually causes no symptoms and is incidentally discovered

Occasional patient may feel skipped beats

PHYSICAL EXAM FINDINGS

Variable S 1

DIFFERENTIAL DIAGNOSIS

Multifocal atrial tachycardia (heart rate > 100 bpm)

Frequent premature atrial complexes and atrial bigeminy

LABORATORY TESTS

None specific

ELECTROCARDIOGRAPHY

ECG to document rhythm

CARDIOLOGY REFERRAL

Not required

MEDICATIONS

No specific treatment

Monitor and treat the underlying cause, such as sick sinus syndrome or lung disease

DIET AND ACTIVITY

No restrictions

General healthy lifestyle

Once a year if sinus node abnormality is suspected; otherwise when symptoms arise

COMPLICATIONS

May progress to sick sinus syndrome

This condition by itself is benign

PRACTICE GUIDELINES

Indications for pacemaker:

– If part of sick sinus syndrome

– If associated with documented symptomatic bradycardia

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The Wandering Atrial Pacemaker

What’s in a name, boring bundle branch block, non-physiologic atrial pacing, exotic ventricular ectopy part two.

Today, it is unusual to see an electrocardiograph (ECG) with the diagnosis of Wandering Atrial Pacemaker , but when we do, it is often incorrect. The last one I saw was a marked sinus arrhythmia with unifocal atrial ectopics and it is important to differentiate these two diagnoses as the treatment and prognosis are very different.

Wandering atrial pacemaker, as the name implies, is an irregular ECG rhythm which wanders from sinus to at least two other different atrial ectopic foci resulting in P waves with three different morphologies.

Here is an example:

The rate is slow and there are two atrial ectopic foci: crista terminalis (looks like the sinus P wave), low atrial (inverted P waves), and not surprisingly, atrial fusion beats with maybe more than one P wave morphology. Clearly, the atrium is very irritable, and therefore the rhythm is a precursor to atrial fibrillation. The term chaotic atrial mechanism is also used. Most examples of this rhythm are difficult to diagnose because the rhythm is faster than 100 bpm and hence is called multifocal atrial tachycardia .

It is easy to see how this rhythm can be confused with atrial fibrillation with an uncontrolled ventricular response. Indeed, an ECG performed soon after this Holter monitor recording showed atrial fibrillation, confirming the transient appearance and thus rarity of this rhythm.

In the past this ECG was seen with severe cor pulmonale, cyanosis and right heart disease. The uncontrolled atrial fibrillation in such a sick patient was often a terminal event.

Dr Harry Mond

About Assoc Prof Harry Mond

In 49+ years as a practicing cardiologist, Dr Harry Mond has published 260+ published manuscripts & books. A co-founder of CardioScan, he remains Medical Director and oversees 500K+ heart studies each year.

Download his full profile here.

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Thursday, March 4, 2021

Blog #200 — wandering pacemaker (vs mat).

There is no clinical information is available for the ECG and 2-lead rhythm strip shown below in  Figure-1 .

• HOW would you interpret this tracing?
• What treatment is likely to be needed? 

====================================

Editorial  Comment:

It is always challenging to interpret tracings without the benefit of clinical information. That said — this situation is common in clinical practice. My experience in this area derives from the 30 years during which I was charged with interpreting  all  ECGs ordered by 35 medical providers at a primary care clinic — as well periodic stints during which I interpreted hospital tracings without the benefit of any history. 

• The challenge lies with having to decide  which  tracings in the  “pile of ECGs to be interpreted”  were those for which I needed to pull the medical chart ( or call the provider ) because of ECG findings of immediate potential concern.
• Obvious time constraints made it impossible to pull the chart for each ECG that I was given to read ( I’d never get anything else done if I did so ).
• I therefore became well versed in the skill of limiting the charts that I would pull to those patients whose ECGs showed findings I thought were important  and  potentially indicative of an acute situation that may have been overlooked.

=====================================

MY Thoughts  on the ECG in Figure-1:

As always — systematic interpretation of  any  ECG should begin with assessing the cardiac rhythm. In general —  lead II  and  lead V1  are the 2  best  leads on a 12-lead tracing for assessing atrial activity — and we have the advantage in  Figure-1  of a  simultaneously-recorded  2-lead rhythm strip of both of these leads.  By the  Ps ,  Qs and  3R Approach:

• The rhythm in  Figure-1  is  clearly   irregular .
• The  QRS  complex is  narrow ( ie,  not  more than half a large box in duration = ≤0.10 second ) . 
• The rate  varies  from  50 /minute — to just under  100 /minute.
• More than 1 P wave morphology is present . That said — P waves  do  appear to be related to neighboring QRS complexes, because the PR interval for the P wave shapes that we see remains constant  ( See   Figure-2 ) .

MY Thoughts  on Figure-2:

There are 2 different P wave shapes in  Figure-2 .

• The tracing begins with  3  sinus  beats ( ie,  RED arrows highlight 3 similar-looking upright-in-lead-II P waves — all with the same PR interval ) .
• P wave shape then changes  for beats #4, 5 and 6  ( ie,  BLUE arrows highlighting an almost isoelectric, if not negative P wave with fixed PR interval ) .
• The atrial focus then shifts back , with return to sinus P waves for beats #7, 8, 9 and 10 (ie,  return of RED arrows highlighting similar-looking, upright P waves in lead II — albeit with variability in the R-R interval ).
• The rhythm in  Figure-2  concludes with a  slowing-down  of the ventricular rate, as  the 2nd atrial focus returns , in which the P wave is almost isoelectric (ie,  BLUE arrows for beats #11 and 12 ).

BOTTOM LINE  regarding  Figure-1:  The rhythm in  Figure-2  is most consistent with a  Wandering  Atrial  Pacemaker . This is because the change from one atrial site to the next occurs gradually over a period of several beats.

• PEARL:  The reason it is uncommon ( if not rare ) in clinical practice to see a wandering atrial pacemaker — is that most providers do not pay  long enough  attention to  beat-to-beat  change in P wave morphology needed to identify  gradual  shift between  at least  3 different atrial sites.

SUMMARY:  Review of the  KEY  features of wandering atrial pacemaker is the theme below for our  ECG  Media  Pearl #17 ( a 3:30 minute audio recording ).

• Written review of wandering pacemaker appears below in  Figure-3 .
• Review of  MAT  is covered in our  ECG Blog #199 .

Today’s   E CG  M edia   P EARL  # 17 ( 3:30 minutes   Audio )  —   What is a  Wandering  Atrial Pacemaker ( as opposed to MAT )?

A DDENDUM   ( 3/4/2021 ) :

I received the following note from  David Richley  regarding today’s tracing: “I think I would use different terminology to describe this because to me the atrial pacemaker doesn’t so much ‘wander’ as ‘jump’. I would describe this as sinus arrhythmia with junctional escape rhythm at 60-65/minute every time the sinus node discharge rate slows to below that rate. I interpret the escape beats as junctional rather than atrial, because athough the P waves, ( which are initially negative in II, aVF and V4-V6 — and positive in aVR ) precede the QRS — the PR segment is very short, suggesting an AV nodal origin. However, we describe this phenomenon — I do agree that it’s likely to be completely benign.

MY Thoughts:  Dave’s comment is one of the reasons why:  i )  The diagnosis of wandering pacemaker requires clear demonstration of shift in the atrial pacemaker in  at least  3 different sites. We  only  see 2 different sites here;  and ,  ii )  The diagnosis of wandering atrial pacemaker is  not  common. 

• It’s impossible to rule out Dave’s theory from the single tracing we have.
• That said — the BLUE arrow P wave site may or may not be of AV nodal origin ( you can see a similar, near-isoelectric P wave with short PR interval from a low atrial site ).
• I also considered the possibility of the BLUE arrow P waves representing junctional escape — but decided against it because the difference in R-R interval from what we see between beats #9-10  vs  what we see between beats #10-11 is  more  than what I’d expect based on the cadence of rate variation I see from beats #7-10.
• Bottom Line:  We both agree there is a shift in the pacemaker site in a rhythm that is likely to be benign. And, we both agree that additional monitoring would be needed for a definitive response.  THANK YOU Dave!

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WikEM mobile app access is moving to Eolas! Our website will remain the same, but for mobile app users, this transition will offer an improved user interface, as well as additional in-app content such as MDCalc and a host of published guidelines.  Download the free Eolas app now to ensure uninterrupted mobile app access.

• Wandering atrial pacemaker
• 2 Clinical Features
• 3.1 Palpitations
• 4.2 Diagnosis
• 5 Management
• 6 Disposition
• 8 External Links
• 9 References
• Three or more ectopic foci within the atrial myocardium serve as the pacemaker
• Rate is less than 100bpm (in contrast to MAT )
• Is irregularly irregular therefore sometimes confused with atrial fibrillation and sinus arrhythmia
• Intrinsic cardiac or pulmonary disease
• Metabolic derangements
• Drug toxicity (including Digoxin )

Clinical Features

• Often seen in the extremes of age and in athletes
• Rarely causes symptoms

Differential Diagnosis

Palpitations.

• Narrow-complex tachycardias
• Wide-complex tachycardias
• Second Degree AV Block Type I (Wenckeback)
• Second Degree AV Block Type II
• Third Degree AV Block
• Premature atrial contraction
• Premature junctional contraction
• Premature ventricular contraction
• Sick sinus syndrome
• Acute coronary syndrome
• Cardiomyopathy
• Congenital heart disease
• Congestive heart failure (CHF)
• Mitral valve prolapse
• Pacemaker complication
• Pericarditis
• Myocarditis
• Valvular disease
• Panic attack
• Somatic Symptom Disorder
• Drugs of abuse (e.g. cocaine )
• Medications (e.g. digoxin , theophylline )
• Thyroid storm
• Pulmonary embolism
• Dehydration
• Pheochromocytoma

• ECG should show three distinct P wave morphologies with a ventricular rate <100bpm
• Rarely requires treatment

Disposition

• Outpatient management
• Multifocal atrial tachycardia
• Dysrhythmia

External Links

• Richard Cunningham
• fardis tavangary
• Ross Donaldson
• Privacy policy
• Disclaimers

Multifocal Atrial Tachycardia (MAT)

• Ed Burns and Robert Buttner
• Jun 4, 2021

Multifocal Atrial Tachycardia (MAT) Overview

• A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.
• Most commonly seen in patients with severe COPD  or congestive heart failure.
• It is typically a transitional rhythm between frequent premature atrial complexes (PACs) and atrial flutter / fibrillation.

AKA “Chaotic atrial tachycardia”

Electrocardiographic Features

• Heart rate > 100 bpm (usually 100-150 bpm; may be as high as 250 bpm).
• Irregularly irregular rhythm with varying PP, PR and RR intervals.
• At least 3 distinct P-wave morphologies in the same lead.
• Isoelectric baseline between P-waves (i.e. no flutter waves).
• Absence of a single dominant atrial pacemaker (i.e. not just sinus rhythm with frequent PACs).
• Some P waves may be nonconducted; others may be aberrantly conducted to the ventricles.

There may be additional electrocardiographic features suggestive of COPD.

Clinical Relevance

• Usually occurs in seriously ill elderly patients with respiratory failure (e.g. exacerbation of COPD / CHF).
• Tends to resolve following treatment of the underlying disorder.
• The development of MAT during an acute illness is a poor prognostic sign, associated with a 60% in-hospital mortality and mean survival of just over a year. Death occurs due to the underlying illness; not the arrhythmia itself.

Arises due to a combination of factors that are present in hospitalised patients with acute-on-chronic respiratory failure:

• Right atrial dilatation (from cor pulmonale )
• Increased sympathetic drive
• Hypoxia and hypercarbia
• Beta-agonists
• Theophylline
• Electrolyte abnormalities: Hypokalaemia and hypomagnesaemia  (e.g. secondary to diuretics / beta-agonists)

The net result is increased atrial automaticity.

ECG Examples

Multifocal atrial tachycardia:

• Rapid irregular rhythm > 100 bpm.
• At least 3 distinctive P-wave morphologies (arrows).

MAT with additional features of COPD :

• Rapid, irregular rhythm with multiple P-wave morphologies (best seen in the rhythm strip).
• Right axis deviation, dominant R wave in V1 and deep S wave in V6 suggest right ventricular hypertrophy due to cor pulmonale. 

Related Topics

• The ECG in COPD
• Right atrial enlargement (P pulmonale)
• Right ventricular hypertrophy

Advanced Reading

• Wiesbauer F, Kühn P. ECG Mastery: Yellow Belt online course. Understand ECG basics. Medmastery
• Wiesbauer F, Kühn P. ECG Mastery: Blue Belt online course : Become an ECG expert. Medmastery
• Kühn P, Houghton A. ECG Mastery: Black Belt Workshop . Advanced ECG interpretation. Medmastery
• Rawshani A. Clinical ECG Interpretation ECG Waves
• Smith SW. Dr Smith’s ECG blog .
• Zimmerman FH. ECG Core Curriculum . 2023
• Mattu A, Berberian J, Brady WJ. Emergency ECGs: Case-Based Review and Interpretations , 2022
• Straus DG, Schocken DD. Marriott’s Practical Electrocardiography 13e, 2021
• Brady WJ, Lipinski MJ et al. Electrocardiogram in Clinical Medicine . 1e, 2020
• Mattu A, Tabas JA, Brady WJ. Electrocardiography in Emergency, Acute, and Critical Care . 2e, 2019
• Hampton J, Adlam D. The ECG Made Practical 7e, 2019
• Kühn P, Lang C, Wiesbauer F. ECG Mastery: The Simplest Way to Learn the ECG . 2015
• Grauer K. ECG Pocket Brain (Expanded) 6e, 2014
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric 6e, 2008
• Chan TC. ECG in Emergency Medicine and Acute Care 1e, 2004

LITFL Further Reading

• ECG Library Basics – Waves, Intervals, Segments and Clinical Interpretation
• ECG A to Z by diagnosis – ECG interpretation in clinical context
• ECG Exigency and Cardiovascular Curveball – ECG Clinical Cases
• 100 ECG Quiz – Self-assessment tool for examination practice
• ECG Reference SITES and BOOKS – the best of the rest

ECG LIBRARY

Emergency Physician in Prehospital and Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education | ECG Library |

Robert Buttner

MBBS (UWA) CCPU (RCE, Biliary, DVT, E-FAST, AAA) Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Editor-in-chief of the LITFL ECG Library . Twitter: @rob_buttner

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Atrial Rhythms ECG Interpretation

This page provides an introduction to atrial rhythms and links to training materials on this website.

Atrial rhythms originate in the atria, not from the SA node. The P wave's shape can be different from a normal sinus rhythm as the electrical impulse follows a different path. For a complete discussion of atrial rhythm ECG, use our atrial rhythms training module and our practice strips. Atrial rhythms categories:

• Atrial Fibrillation (afib)
• Atrial Flutter

Premature Atrial Complex

Multifocal atrial tachycardia, supraventricular tachycardia.

• Wandering Atrial Pacemaker

Wolff-Parkinson-White Syndrome

Atrial rhythm categories.

• Atrial Fibrillation

Sites in the atria are firing very rapidly, between 400-600 bpm. These rapid pacemaking signals cause the atria to quiver. The ventricles beat at a slower rate because the AV node blocks some of the atrial impulses.

There are two types of atrial flutter. Type I (also called classical or typical) has a rate of 250-350 bpm. Type II (also called non-typical) are faster, ranging from 350-450 bpm. ECG tracings will show tightly spaced waves or saw-tooth shaped waveforms (F-waves).

During multifocal atrial tachycardia, several (non-SA) sites are creating impulses. The P waves will vary in shape and at least three different shapes can be observed. The PR Interval varies. Ventricular rhythm is irregular.

Premature atrial complex occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node. If the ectopic site is near the SA node, the P wave will often have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.

This term covers three types of tachycardia that originate in the atria, AV junction or SA node.

Wandering atrial pacemaker is an irregular rhythm. In is similar to multifocal atrial tachycardia but the heart rate is under 100 bpm. P waves are present but will vary in shape.

Wolff-Parkinson-White Syndrome occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent. The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely. ECG characteristics include a shorter PR Interval, longer QRS complex and a delta wave.

Training Resources

Atrial rhythm training.

After a brief review of cardiac rhythm analysis, this module explains morphologic features and qualifying criteria of atrial rhythms.

Atrial Rhythms Course

ECG Rhythm Tests

Hundreds heart rhythms in this practice test. Test can be tailored for specific learning needs.

ECG Monitor Challenge

A quiz using a simulated patient monitor. Evaluate a scrolling waveform rather than a paper tracing.

Lesson #1: Rhythm Analysis Method - 312

The five steps of rhythm analysis will be followed when analyzing any rhythm strip.

• Analyze each step in the following order.

Rhythm Regularity

• P wave morphology
• P R interval or PRi
• QRS complex duration and morphology
• Carefully measure from the tip of one R wave to the next, from the beginning to the end of the tracing.
• A rhythm is considered “regular or constant” when the distance apart is either the same or varies by 1 ½ small boxes or less from one R wave to the next R wave.

Heart Rate Regular (Constant) Rhythms

• The heart rate determination technique used will be the 1500 technique.
• Starting at the beginning of the tracing through the end, measure from one R wave to the next R wave (ventricular assessment), then P wave to P wave (atrial assessment), then count the number of small boxes between each and divide that number into 1500. This technique will give you the most accurate heart rate when analyzing regular heart rhythms. You may include ½ of a small box i.e. 1500/37.5 = 40 bpm (don’t forget to round up or down if a portion of a beat is included in the answer).

Step 2 (Cont)

Heart rate - irregular rhythms.

• If the rhythm varies by two small boxes or more, the rhythm is considered “irregular”.
• The heart rate determination technique used for irregular rhythms will be the “six-second technique”.
• Simply count the number of cardiac complexes in six seconds and multiply by ten.

P wave Morphology (shape)

• Lead II is most commonly referenced in cardiac monitoring
• In this training module, lead two will specifically be referenced unless otherwise specified.
• The P wave in lead II in a normal heart is typically rounded and upright in appearance.
• Changes in shape must be reported. This can be an indicator that the locus of stimulation is changing or the pathway taken is changing.
• P waves may come in a variety of morphologies i.e. rounded and upright, peaked, flattened, notched, biphasic(pictured), inverted and even buried or absent!
• Remember to describe the shape. This can be very important to the physician when diagnosing the patient.

PR interval (PRi)

• Measurement of the PR interval reflects the amount of time from the beginning of atrial depolarization to the beginning of ventricular depolarization.
• Plainly stated, this measurement is from the beginning of the P wave to the beginning of the QRS complex.
• The normal range for PR interval is: 0.12 – 0.20 seconds (3 to 5 small boxes)
• It is important that you measure each PR interval on the rhythm strip.
• Some tracings do not have the same PRi measurement from one cardiac complex to the next. Sometimes there is a prolonging pattern, sometimes not.
• If the PR intervals are variable, report them as variable, but note if a pattern is present or not.

QRS complex

• QRS represents ventricular depolarization.
• It is very important to analyze each QRS complex on the tracing and report the duration measurement and describe the shape (including any changes in shape).
• As discussed in step 3, when referring to P waves, remember changes in the shape of the waveform can indicate the locus of stimulation has changed or a different conduction pathway was followed. It is no different when analyzing the QRS complex. The difference is that in step 3, we were looking at atrial activity. Now we are looking at ventricular activity.
• Measure from the beginning to the end of ventricular depolarization.
• The normal duration of the QRS complex is: 0.06 – 0.10 second

Lesson #2: Interpretation - 312

Introduction.

• The previous slides presented the five-steps of rhythm analysis. These five steps must be followed regardless of how simple of complex the tracing is you are reviewing.
• The information gathered in these steps are telling a story.
• The title of that story is the interpretation.

Atrial Dysrhythmias Types

The dysrhythmias in this category occur as a result of problems in the atria. These atrial dysrhythmias primarily affect the P wave. We will be discussing the following complexes and rhythms:

• Premature Atrial Complexes (PAC’s)

Lesson #3: Premature Atrial Complex

Intro to pac.

• PAC's can occur for a number of different reasons i.e., diet, fatigue, stress, disease, ischemia to name a few.
• Premature complexes frequently occur in bradycardic rhythms, but may occur almost any time.
• PAC's occur when an early electrical impulse occurs from a location in the atria other than the SA node.

Intro to PAC 2

• This early impulse causes an early cardiac complex which disrupts the underlying rhythm.
• The locus of stimulation being different, results in a change in the morphology of the P wave.
• PAC's can occur occasionally or frequently.
• PAC's can be observed with or without a pattern
• The P wave with PAC's will always be upright

ECG Analysis

Notice the following: the R to R interval is irregular, the fifth complex is early and the P wave on the early complex is a different shape.

ECG Practice Strip

Analyze this tracing using the five steps of rhythm analysis.

• Rhythm: Irregular
• P wave: Upright & uniform (except early complexes - biphasic)
• PR interval: 0.16 second
• Interpretation: Sinus Bradycardia with PAC's

Lesson #4: Wandering Atrial Pacemaker

Description.

• Rhythms are often named according to the origin of the electrical activity in the heart or the structure where the problem is occurring.
• Wandering Atrial Pacemaker is aptly named due to the electrical impulses causing the atrial activity are moving or wandering.
• These changes in the locus of stimulation affect the morphology of the P waves.
• In Wandering Atrial Pacemaker, you must observe at least three different shaped P waves. No other changes in the tracing may be observed. The rhythm may or may not be regular.
• The PR interval is often affected, but does not have to be.
• The bottom line, is you must observe at least three different shaped P waves.

Practice Strip

• P wave: Changing Shapes (3 or more)
• PR interval: Variable
• Interpretation: Wandering Atrial Pacemaker

Lesson #5: Multifocal Atrial Tachycardia

• Multifocal Atrial Tachycardia is just a faster version of Wandering Atrial Pacemaker. The criteria is the same as Wandering Atrial Pacemaker with the only difference being the heart rate exceeds 100 bpm.
• These changes in the locus of stimulation within the atria affect the morphology of the P waves.
• Remember, you must observe at least three different shaped P waves.
• Due to the presence of irregular R to R intervals coupled with the changing P wave morphology, some people have confused this rhythm with Atrial Fibrillation.

Lesson #6: Atrial Flutter

• Atrial Flutter occurs when there is an obstruction within the atrial electrical conduction system.
• Due to this impediment a series of rapid depolarizations occur.
• These depolarizations may occur two, three, four or more times per QRS complex.
• The AV node functions like a “gatekeeper” blocking the extra impulses until the ventricular conduction system is able to accept the impulse.
• The impulse that is accepted will cause the QRS complex to occur.
• Each flutter wave represents atrial depolarization. This will be noted next to the P wave step in rhythm analysis. Instead of P waves, this tracing has “F” waves. No P waves mean there is no PR interval measurement.
• When the tracing is interpreted, the ratio of F waves to each QRS complex will be documented along with the rhythm i.e. Atrial Flutter 4:1 (indicates 4 “F” waves to each QRS complex). Not all Atrial Flutter will have a regular rhythm. In that case just document and report your observations.
• Compare your answers with the answers on the next slide.

Practice Strip Answers

• Rhythm: Regular
• Rate: Ventricles - 80, Atria - 320
• P wave: "F" waves
• PR interval: absent
• Interpretation: Atrial Flutter 4:1

Lesson #7: Atrial Fibrillation

• Atrial Fibrillation occurs when multiple electrical impulses occur within the atria. This chaotic electrical activity results in a chaotic wave form between the QRS complexes. P waves are absent. They are replaced by lower case "f" waves. No P waves means there is no PR interval measurement.
• This rapid electrical activity overwhelms the AV node causing impulses to enter the ventricular conduction system at irregular points. This results in irregular R to R intervals.
• Not all fibrillatory waves are created equal. The "f" waves can be coarse (majority measure 3 mm or more) or can be fine (majority of waveforms measure less than 3 mm) to almost absent. Regardless always report your observations. Many times when a patient has "new onset" Atrial Fibrillation the patient will report with a heart rate of 160 bpm or more.
• When a patient experiences A-fib, the atria are not contracting as they normally would. They are just quivering. This absence of contraction of the atria can result in a loss of cardiac output anywhere from 15 - 30% due to the absence of "atrial kick". This is why the heart rate is so high. The body is trying to maintain homeostasis.
• It will be impossible to determine the atrial rate. You will only be able to analyze and report the ventricular rate.
• Atrial Fibrillation with a ventricular response in excess of 100 bpm is commonly referred to as Atrial Fibrillation with “rapid ventricular response” or "uncontrolled A-fib".
• Rate: Ventricles - 90, Atria - Unable to determine (UTD)
• P wave: "f" waves
• Interpretation: Atrial Fibrillation

Lesson #8: Quiz: Test Questions - 312

Authors and reviewers.

• ECG heart rhythm modules: Thomas O'Brien.
• ECG monitor simulation developer: Steve Collmann
• 12 Lead Course: Dr. Michael Mazzini, MD .
• Spanish language ECG: Breena R. Taira, MD, MPH
• Medical review: Dr. Jonathan Keroes, MD
• Medical review: Dr. Pedro Azevedo, MD, Cardiology
• Last Update: 11/8/2021
• Electrocardiography for Healthcare Professionals, 6th Edition Kathryn Booth and Thomas O'Brien ISBN10: 1265013470, ISBN13: 9781265013479 McGraw Hill, 2023
• Rapid Interpretation of EKG's, Sixth Edition Dale Dublin Cover Publishing Company
• EKG Reference Guide EKG.Academy
• 12 Lead EKG for Nurses: Simple Steps to Interpret Rhythms, Arrhythmias, Blocks, Hypertrophy, Infarcts, & Cardiac Drugs Aaron Reed Create Space Independent Publishing
• Heart Sounds and Murmurs: A Practical Guide with Audio CD-ROM 3rd Edition Elsevier-Health Sciences Division Barbara A. Erickson, PhD, RN, CCRN
• The Virtual Cardiac Patient: A Multimedia Guide to Heart Sounds, Murmurs, EKG Jonathan Keroes, David Lieberman Publisher: Lippincott Williams & Wilkin) ISBN-10: 0781784425; ISBN-13: 978-0781784429
• Project Semilla, UCLA Emergency Medicine, EKG Training Breena R. Taira, MD, MPH
• ECG Reference Guide PracticalClinicalSkills.com

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INTRODUCTION

Multifocal atrial tachycardia (MAT) is an arrhythmia that can be seen in a variety of clinical disorders [ 1 ]. In addition to a heart rate greater than 100 beats per minute (bpm), the characteristic electrocardiographic (ECG) feature is variability in P-wave morphology. Although this abnormality had been noted for many years during some types of atrial tachycardia, the term MAT became commonplace terminology in the late 1960s [ 2 ]. Patients with multiple P-wave morphologies but a normal heart rate (60 to 100 bpm) are considered to have a wandering atrial pacemaker, since the heart rate does not meet criteria for a tachycardia. (See 'Terminology' below.)

This topic will review the definition, pathogenesis, etiology, and treatment of MAT in adults. Other tachycardias of atrial origin, as well as the discussion of this arrhythmia in children, are reviewed separately. (See "Focal atrial tachycardia" and "Atrial tachyarrhythmias in children" and "Atrioventricular nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" .)

DEFINITION, PATHOGENESIS, AND PREVALENCE

As with any tachycardia, the heart rate in MAT exceeds 100 bpm. To distinguish MAT from other tachyarrhythmias of atrial origin, there should be organized atrial activity yielding P waves with three or more different morphologies. (See 'Clinical manifestations and diagnosis' below.)

Terminology  —  A number of authors have used the term "chaotic" to describe MAT [ 3-5 ]. However, chaos in modern usage in nonlinear dynamics and mathematics implies there is order in what appear to be random events [ 6 ]. A more accurate term for this arrhythmia is probably "multiform" as there is no proof that the arrhythmia is actually multifocal, although multifocal remains the commonly used term [ 1 ].

The tachycardic threshold for multifocal atrial tachycardia (MAT) has traditionally been set at 100 bpm, but a review of 60 patients with multifocal atrial arrhythmias found a stronger association between the incidence of COPD exacerbations and the diagnosis of MAT if a threshold of 90 bpm was used [ 7 ]. The definition of MAT also requires the presence of at least three distinct P-wave morphologies.

A. KESH HEBBAR, M.D., AND WILLIAM J. HUESTON, M.D.

A more recent article on  common types of supraventricular tachycardia  is available.

Am Fam Physician. 2002;65(12):2479-2487

This is part I of a two-part article on common arrhythmias. Part II, “Ventricular Arrhythmias and Arrhythmias in Special Populations,” appears on page 2491 of this issue.

Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option.

Heart palpitations and cardiac arrhythmias are common problems encountered by family physicians. Patients may present with acute cardiac rhythm abnormalities. Although these arrhythmias are usually benign, they can indicate significant underlying heart disease. More often, patients have chronic arrhythmias, such as atrial fibrillation, that may require treatment to reduce the risk of future complications. The challenges for the family physician are to determine which arrhythmias are benign and which indicate probable cardiac malfunction, and to manage recurrent or chronic rhythm abnormalities.

This two-part article reviews common atrial and ventricular arrhythmias, with a focus on initial management decisions. Part I discusses supraventricular arrhythmias. Part II discusses ventricular arrhythmias and the management of rhythm abnormalities in special populations, including pregnant women, athletes, and children.

Atrial Fibrillation

Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter. This rhythm abnormality affects 3 to 5 percent of patients more than 60 years of age 1 and becomes increasingly common with advancing age. The median age of patients with atrial fibrillation is 75 years, and the prevalence of the arrhythmia doubles every 10 years after the age of 55. 2 , 3 In the United States, atrial fibrillation is estimated to affect almost 9 percent of patients more than 75 years of age. 2

Most risk factors for atrial fibrillation are associated with structural or ischemic heart disease. Risk factors include hypertension, left ventricular hypertrophy, dilated and restrictive cardiomyopathies, coronary artery disease, chronic obstructive pulmonary disease, and diabetes in women. 1

The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year. 4 Anticoagulation with warfarin (Coumadin) reduces the risk by about two thirds. 4 The mortality rate for stroke in patients with atrial fibrillation is approximately twice as high as the rate in patients without this rhythm abnormality. 5 Although anticoagulation is contraindicated in some elderly patients, a study in Great Britain 6 found that about 60 percent of patients identified in community screenings as having atrial fibrillation were eligible for, and would benefit from, this treatment.

The first step in managing a patient with atrial fibrillation is to decide whether there is a high likelihood of safe conversion to sinus rhythm or whether the patient should be allowed to remain in atrial fibrillation. A patient with recent onset of atrial fibrillation (within the previous 12 months) and no evidence of enlargement of the left atrium has a greater chance of achieving and maintaining sinus rhythm. If the arrhythmia is long-standing and the patient is not a suitable candidate for rate cardioversion, initial treatment should focus on ventricular rate control, with consideration given to long-term stroke prophylaxis.

Restoration of Sinus Rhythm

Patients who present within 48 hours of the onset of new atrial fibrillation are candidates for cardioversion with a low risk of embolism. Conversion to sinus rhythm can be attempted by electrical shock or with antiarrhythmic drugs. Patients who have been in atrial fibrillation for more than 48 hours or for an undetermined period are more likely to have atrial thrombi and may develop emboli with immediate electrical or medical (pharmacologic) cardioversion.

Atrial thrombi are not evident on transthoracic echocardiograms, but they can been seen on transesophageal echocardiograms. 7 If the transesophageal echocardiogram reveals thrombi, anticoagulation is recommended before cardioversion is attempted. Anticoagulation can be accomplished using warfarin, with the dosage adjusted to achieve an International Normalized Ratio (INR) between 2.0 and 3.0 for a minimum of 21 days. 8

If the transesophageal echocardiogram does not show thrombi on multiplane views, cardioversion can be attempted. Short-term anticoagulation with heparin should be started before the procedure, and warfarin therapy should be initiated after cardioversion. 8

When rhythm conversion is indicated, it can be accomplished using direct-current cardioversion or pharmacologic therapy. Synchronized cardioversion is currently considered the treatment of choice for the restoration of sinus rhythm and, in appropriately selected patients, has a success rate of at least 80 percent. 4 Cardioversion is also indicated in patients with hypotension, angina, heart failure, or other evidence of severe compromise caused by atrial fibrillation. 5

Medical cardioversion of atrial fibrillation may be achieved with class IA drugs (quinidine, disopyramide [Norpace], procainamide [Procanbid]) or with amiodarone (Cordarone). In the past, quinidine was frequently used for both cardioversion and maintenance of sinus rhythm in patients who had undergone electrical cardioversion. However, because of the proarrhythmic action of class IA agents and their detrimental effects on left ventricular function, these drugs are now used less often than amiodarone for primary therapy of atrial fibrillation. 4

Amiodarone therapy is successful in 86 percent of patients who have had atrial fibrillation for less than two years. 4 , 9 Treatment is also effective in 40 to 60 percent of patients with long-standing atrial fibrillation that has been resistant to other agents and to electrical cardioversion. 4 Amiodarone can be given in a dosage of 200 mg a day, which is lower than the dosages that have been associated with thyroid abnormalities and pulmonary fibrosis. Although there is little risk of toxicity when amiodarone is given in a low dosage, it is prudent to monitor patients for the development of thyroid, pulmonary, hepatic, and cardiac side effects.

Findings on the usefulness of various agents for the conversion of atrial fibrillation, based on the evidence-based practice program of the Agency for Healthcare Research and Quality, are summarized in Table 1 . 10 Although drugs such as digitalis preparations and sotalol (Betapace) are sometimes used for rate control, they are not effective for converting atrial fibrillation to sinus rhythm. 10 , 11

If external electrical cardioversion is unsuccessful and antiarrhythmic drug therapy fails, other measures can be used. However, these approaches are usually reserved for use in patients who cannot tolerate atrial fibrillation and patients who have associated systolic dysfunction. Techniques include internal electrical cardioversion through the application of electrical current to pulmonary veins via a transcatheter cathode 4 and radiofrequency ablation of the atrioventricular node with insertion of a ventricular pacemaker. 12 In addition, an implantable atrial defibrillator can be used to provide rapid cardioversion in patients with atrial fibrillation that cannot be controlled with medications. 13

Rate Control in Chronic Atrial Fibrillation

In patients in whom rhythm conversion is not indicated or those who have new-onset atrial fibrillation with a rapid ventricular response, treatment may be needed to control the ventricular rhythm. Excessive ventricular rates may result in diminished cardiac output because of poor filling time, and in ischemia because of increased myocardial oxygen demand. Medications used for ventricular rate control in patients with atrial fibrillation are listed in Table 2 . 14

Acute management of ventricular rates can usually be achieved with intravenously administered diltiazem (Cardizem), given in an initial bolus of 15 to 20 mg (0.25 mg per kg) over two minutes, or with an intravenously administered beta blocker such as propranolol (Inderal), given in a dose of 0.5 to 1 mg (up to 3 to 5 mg if needed).

A number of medications, including calcium channel blockers, beta blockers, and digoxin (Lanoxin), are effective for maintaining ventricular rates within acceptable ranges. Because calcium channel blockers are associated with better exercise tolerance, they may be preferable to beta blockers. 15 Digoxin is associated with a high degree of exercise intolerance; therefore, it should be reserved for use in patients who are relatively immobile, who cannot tolerate other treatment options, or who have significant ventricular dysfunction.

Paroxysmal Supraventricular Tachycardias

Based on duration, supraventricular tachycardias are usually categorized as paroxysmal, persistent, or chronic. Paroxysmal supraventricular tachycardia (PSVT) is the most common of these arrhythmias and the one that is most often encountered in the primary care setting. Longer-duration supraventricular tachycardias can be treated similarly to PSVT, but cardiology consultation is often required to identify the electrophysiologic mechanism responsible for sustaining the arrhythmia. In contrast to ventricular tachycardias (discussed in part II of this article) and atrial fibrillation, PSVT is usually a narrow-complex tachycardia with a regular rate.

Atrioventricular Nodal Reentry Causing PSVT

Atrioventricular nodal reentry, the most common mechanism of PSVT, occurs when two pathways exist with different conduction rates. A premature atrial complex that is blocked in the fast pathway and redirected through the slow pathway usually triggers the tachycardia ( Figure 1 ) . The electrical signal proceeds down the slow pathway and then reenters the fast pathway in a retrograde direction. By the time the signal has propagated down the slow pathway and back around on the fast pathway, the slow pathway is no longer refractory and is ready to conduct the signal again, completing a continuous circuit.

Reentrant tachycardias usually produce a narrow-complex tachycardia with no discernible P wave. The rate is usually between 160 and 190 beats per minute. In a less common form of atrioventricular nodal reentrant tachycardia, the circulating wavefront proceeds in an antegrade fashion down the fast pathway and in a retrograde fashion up the slow pathway. In this form, inverted P waves ( Figure 2 ) are clearly visible in lead II of the electrocardiogram (ECG).

It is important to note that atrioventricular nodal reentrant tachycardia can result in a wide-complex tachycardia if the patient has preexisting bundle branch block.

Accessory Pathways Causing PSVT

Accessory pathways (Wolff-Parkinson-White syndrome) and other bypass tracts can cause PSVT. In patients with Wolff-Parkinson-White syndrome, a shortened PR interval and a slurred upstrike to the QRS complex “delta wave” on the resting ECG indicate the presence of an accessory pathway ( Figure 3 ) .

It should be noted that the resting ECG may be normal in some patients with Wolff-Parkinson-White syndrome, because of the inability of the accessory pathway to conduct in the antegrade direction. The usual mechanism of PSVT in this setting is antegrade conduction down the normal pathways through the atrioventricular node and retrograde conduction through the accessory pathway.

The ECG in an atrial arrhythmia with an accessory pathway usually shows a narrow-complex tachycardia at rates of 160 to 240 beats per minute. Delta waves are absent because the normal pathways are used for ventricular activation. Inverted P waves may be seen in the inferior leads. In a much less common form of PSVT, antegrade conduction is down the bypass tract and results in a wide-complex tachycardia.

Increased Automaticity Causing PSVT

Increased automaticity usually occurs when the atrium is enlarged, as in patients with chronic lung disease, congestive heart failure, or electrolyte and acid-base disturbances. Usually, the stretched atria fire irregularly, producing multiple premature beats that emanate from different areas of the atria. Because the foci for the ectopic beats are in multiple sites, the P waves vary in morphology, giving rise to the term “multifocal atrial tachycardia.”

The diagnosis of multifocal atrial tachycardia depends on the identification of an irregular rhythm with three or more different P-wave morphologies. The rate is usually between 130 and 180 beats per minute. Treatment is directed at correcting the underlying cause. Antiarrhythmic drugs are usually not helpful.

In most patients, PSVT is benign and self-limited. However, some patients can have angina, hypotension, and intense anxiety. The first step in the management of PSVT is to determine whether the patient is hemodynamically stable. If PSVT is sustained and there is any indication of instability (i.e., angina, shortness of breath, decreased level of consciousness, hypotension, or congestive heart failure), electrical cardioversion should be performed urgently.

If the symptoms are restricted to discomfort (e.g., palpitations and anxiety), conservative measures should be applied. Conservative management of PSVT can include both nonpharmacologic and pharmacologic measures ( Table 3 ) . 16

Vagal maneuvers to increase parasympathetic tone and slow conduction through the atrioventricular node should be the first approach. Patients should be taught some of these maneuvers for use in future episodes. They should also be instructed to avoid inciting factors, such as caffeine, tobacco, alcohol, pseudoephedrine, and stress. Carotid sinus massage can be attempted, but its role hasbecome more limited because of the effectiveness of drug therapy and the risk of embolism from carotid pressure in some patients.

The goal of pharmacologic management is to slow or block atrioventricular nodal conduction. Agents used for this purpose include adenosine (Adenocard), calcium channel blockers (verapamil [Calan] or diltiazem), and beta blockers (e.g., esmolol [Brevibloc]).

Adenosine is an ultra–short-acting agent that is cleared quickly (half-life of 1 to 6 seconds). This agent is given intravenously in an initial dose of 6 mg, which is followed by one or two 12-mg boluses. Adenosine works by reducing conductance along the slow antegrade pathway. Side effects include flushing, dyspnea, and chest pain. Because of the short half-life of adenosine, these effects are usually very brief and do not ordinarily result in complications.

One advantage of adenosine is that it lacks the negative inotropic effects of calcium channel blockers. Adenosine can also decrease the sinus rate transiently and produce a “rebound” sinus tachycardia. Adenosine should not be used in patients with heart transplants, because such patients may be too sensitive to its effects. 17

Calcium channel blockers can also be used to disrupt a reentrant pathway. Verapamil can be given in a 5- to 10-mg bolus over 2 minutes, followed by 10 mg in 15 to 30 minutes if the initial dose does not convert the arrhythmia. 18 Verapamil and other calcium channel blockers should not be used in patients with an undiagnosed wide-complex tachycardia, because of the risk of fatal hypotension or ventricular fibrillation if the arrhythmia is actually ventricular tachycardia and not PSVT. 19

Intravenously administered diltiazem is also effective. 20 Initial treatment consists of a bolus of 0.25 mg per kg administered over two minutes. A repeat bolus of 0.35 mg per kg given over two minutes can be administered 15 minutes later.

Esmolol, a short-acting beta blocker, can be given in an intravenous bolus of 0.5 mg per kg over 1 minute or in an infusion at a rate of 0.5 mg per kg per minute after an initial loading dose of 0.5 mg per kg. An advantage of esmolol over other beta blockers is its short half-life (four to five minutes), compared with the much longer half-lives (three hours or more) of most other beta blockers. Because of a similar depressive effect on left ventricular contractility, esmolol should be used with caution if initial treatment with a calcium channel blocker is not successful.

Other antiarrhythmic drugs, including quinidine, procainamide, flecainide (Tambocor), and amiodarone, may be used in patients who do not respond to initial medications. However, selective radiofrequency ablation is rapidly becoming the treatment of choice in this situation.

Long-term control of recurrent PSVT caused by atrioventricular nodal reentry may be achieved with pharmacologic therapy or radiofrequency ablation. Patients who have infrequent, well-tolerated recurrences may manage these episodes with self-administered physiologic maneuvers.

Radiofrequency ablation is now used early in the management of patients with PSVT caused by an accessory pathway (Wolff-Parkinson-White syndrome), atrioventricular nodal reentrant tachycardia, or atrial tachycardia. 21 The success rate for radiofrequency ablation is 95 percent in patients with an accessory pathway or atrioventricular nodal reentrant tachycardia, and approximately 80 percent in patients with atrial tachycardia. 21

Other Atrial Arrhythmias

Sinus arrhythmia.

Sinus arrhythmia is usually a normal event in young persons and athletes. In fact, it occurs with such high frequency that it may considered a normal variant rather than a true arrhythmia.

There are two forms of sinus arrhythmia. In the “respiratory” form, the RR interval shortens during inspiration and slows during expiration. Breath-holding eliminates the variation. In the “nonrespiratory” form, the same phasic variation is seen in the RR interval but is not related to respirations. This form of sinus arrhythmia occurs in elderly patients, patients with digoxin overdose, and patients with increased intracranial pressure.

Sinus arrhythmia is usually asymptomatic. Sometimes, however, the long pauses can cause dizziness or syncope. Treatment is usually unnecessary.

WANDERING ATRIAL PACEMAKER

Patients with wandering atrial pacemaker are usually not symptomatic. The condition is most often an isolated finding on the ECG and requires no treatment. Sometimes it is noted on physical examination as an irregularly irregular rhythm.

With wandering atrial pacemaker, the ECG shows variable P-wave morphology and PR intervals. The atrial impulses conduct in a 1:1 fashion and usually control the rhythm for several beats before shifting to another focus. The normal heart rate in wandering atrial pacemaker differentiates this condition from multifocal atrial tachycardia.

PREMATURE ATRIAL COMPLEXES

A premature atrial complex is generated from an ectopic focus in the atria. Therefore, the P wave is usually different in morphology from the usual sinus P wave. The impulse conducts along the normal pathways, generating a narrow QRS complex followed by a pause. Sometimes the premature atrial complex is not conducted and can mimic heart block ( Figure 4 ) .

Premature atrial complexes are found in a variety of settings, including the excessive consumption of caffeine or alcohol and the use of sympathomimetic drugs. These complexes can also be present in patients with structural heart disease.

Patients with premature atrial complexes are usually asymptomatic and require no treatment. A beta blocker given in a low dosage can be tried in patients with uncomfortable symptoms, but no studies of efficacy have been reported. Patients should be counseled to decrease their intake of caffeine, tobacco, and alcohol, and their use of over-the-counter sympathomimetic substances, which are often present in cold medicines and weight-loss preparations.

It is important to note that premature atrial complexes sometimes precipitate supraventricular tachycardia, atrial flutter, or atrial fibrillation.

Sinus Nodal Arrhythmias

Sinus pause and sinoatrial exit block.

Sinus pause or arrest occurs when the sinoatrial node fails to discharge. The ECG shows a pause in the sinus rhythm, with no preceding P wave. Patients usually have no symptoms, but if the pause is prolonged, they may have lightheadedness, palpitations, syncope, and falls. In sinus arrest, the length of the pause has no relationship to the PP interval. Sinoatrial exit block is recognized by the pauses being multiples of PP intervals.

Sinus node dysfunction is usually caused by drugs such as digoxin, quinidine, or procainamide. It can also be caused by ischemia, myocarditis, or fibrosis.

From a therapeutic standpoint, it is probably not important to distinguish between sinus arrest and sino-atrial exit block. Both can occur in well-trained athletes 22 and can be a factor in sick sinus syndrome. 23

SICK SINUS SYNDROME

The term “sick sinus syndrome” encompasses a number of abnormalities, including sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances, and atrial tachyarrhythmias. More than one of these arrhythmias may be recorded in the same patient (bradycardia-tachycardia syndrome).

The abnormalities in sick sinus syndrome are usually due to ischemia, fibrosis, or drug-induced or autonomic dysfunction. Signs and symptoms are related to cerebral hypoperfusion and reduced cardiac output.

Treatment of recurrent symptomatic bradycardia or prolonged pauses requires implantation of a permanent pacemaker. 24

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Management of new onset atrial fibrillation. Summary, evidence report/technology assessment: no. 12. Rockville, Md.: Agency for Healthcare Research and Quality, May 2000; AHRQ publication no. 00-E006. Retrieved April 23, 2002, from www.ahcpr.gov/clinic/epcsums/atrialsum.htm .

Falk RH, Knowlton AA, Bernard SA, Gotlieb NE, Battinelli NJ. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm. A randomized, double-blinded trial. Ann Intern Med. 1987;106:503-6.

Pappone C, Rosanio S, Oreto G, Tocchi M, Gugliotta F, Vicedo-mini G, et al. Circumferential radiofrequency ablation of pulmonary vein ostia: a new anatomic approach for curing atrial fibrillation. Circulation. 2000;102:2619-28.

Swerdlow CD, Schsls W, Dijkman B, Jung W, Sheth NV, Olson WH, et al. Detection of atrial fibrillation and flutter by a dual-chamber implantable cardioverter-defibrillator. For the Worldwide Jewel AF Investigators. Circulation. 2000;101:878-85.

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Segal JB, McNamara RL, Miller MR, Kim N, Goodman SN, Powe NR, et al. The evidence regarding the drugs used for ventricular rate control. J Fam Pract. 2000;49:47-59.

Myerburg RJ, Kessler KM, Castellanos A. Recognition, clinical assessment, and management of arrhythmias and conduction disturbances. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst's The heart, arteries and veins. 9th ed. New York: McGraw-Hill, Health Professions Division, 1998:873–942.

O'Nunain S, Jennison S, Bashir Y, Garratt C, McKenna W, Camm AJ. Effects of adenosine on atrial repolarization in the transplanted human heart. Am J Cardiol. 1993;71:248-51.

Rinkenberger RL, Prystowsky EN, Heger JJ, Troup PJ, Jackman WM, Zipes DP. Effects of intravenous and chronic oral verapamil administration in patients with supraventricular tachyarrhyth-mias. Circulation. 1980;62:996-1010.

Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and outcome after emergent therapy. Ann Intern Med. 1986;104:766-71.

Betriu A, Chaitman BR, Bourassa MG, Brevers G, Scholl JM, Bruneau P, et al. Beneficial effect of intravenous diltiazem in the acute management of paroxysmal supraventricular tach-yarrhythmias. Circulation. 1983;67:88-94.

Morady F. Radio-frequency ablation as treatment for cardiac arrhythmias. N Engl J Med. 1999;340:534-44.

Bjornstad H, Storstein L, Meen HD, Hals O. Ambulatory electrocardiographic findings in top athletes, athletic students and control subjects. Cardiology. 1994;84:42-50.

Wu DL, Yeh SJ, Lin FC, Wang CC, Cherng WJ. Sinus automaticity and sinoatrial conduction in severe symptomatic sick sinus syndrome. J Am Coll Cardiol. 1992;19:355-64.

Haywood GA, Katritsis D, Ward J, Leigh-Jones M, Ward DE, Camm AJ. Atrial adaptive rate pacing in sick sinus syndrome: effects on exercise capacity and arrhythmias. Br Heart J. 1993;69:174-8.

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Wandering Pacemaker

When several pacemakers are competing, p-waves with different origins and thus configurations occur. The rhythm is slightly different from beat to beat.

note If the heart rate increases to above 100bpm, it is called Multifocal Atrial Tachycardia . Possible causes are hypoxia, COPD and medication such as digoxin.

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• v.13(9); 2021 Sep

Electrical Injury and Wandering Atrial Pacemaker

Ranjan k singh.

1 Internal Medicine, Anti-Retroviral Therapy Centre, District Hospital, Khagaria, IND

The supply of household electricity remains a low-voltage (110-220 V) energy source, and its effects on the human body depend on several factors, including the type of contact and duration of contact, among other things. In a significant number of cases, direct contact with household electricity causes reversible cardiac arrhythmia-ventricular fibrillation, ventricular premature beats, atrial tachycardia, and atrial fibrillation.

Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia observed in elderly patients suffering from obstructive pulmonary diseases that result from an ischemic heart. This report discusses WAP as observed in a patient who suffered an electrical injury.

Introduction

The effects of electrical injury vary from skin burn to internal organ damage directed especially at the cardiovascular and nervous systems. The extent of electrical injury depends on the type of electricity source, i.e., direct current (DC) or alternating current (AC), the duration of contact with the source of electricity, the state of the body whether wet or dry, the presence of calluses over the palm, the route of electrical flow, and the level of voltage [ 1 ]. The severity of an electric shock depends on the current flow (I) measured in ampere (A). It is linked to the resistance of the conductor (R, unit: ohm ‘W’) and the potential difference between the two ends of a conductor (Volt; unit V), and is derived by applying the formula based on Ohm’s law: i.e., I = V/R. The severity of an electrical burn, by contrast, depends on the energy (Watt) and is derived from Joule’s formula W=I2 x R x T (duration of exposure with the source of current).

Household electrical supply is a low-voltage (220 V) AC at 60 Hz frequency. The physiological effects of contact with a low-frequency AC (60 Hz) current vary at different amperes. For example, 1mA (1/1000 A) is barely perceptible as numbness, whereas 20 mA can cause respiratory muscle paralysis, while 100 mA reaches a threshold for ventricular fibrillation [ 1 , 2 ]. The resulting cardiac arrhythmia may take the form of ventricular fibrillation, ventricular tachycardia, ventricular premature beats, atrial premature beats, atrial arrhythmia, and/or heart block [ 2 ].

Case presentation

A 40-year-old male patient was brought into the emergency ward after suffering an accidental electrical injury that involved an entry wound in the middle of his left hand and an exit wound in the back of his chest. He was holding the hanging rod for a ceiling fan when the connection was plugged in, resulting in electric shock. He lost consciousness and fell to the ground with the rod clenched in his hand for a minute and a half. The electricity source was disconnected and cardiopulmonary resuscitation was administered to the patient by his neighbors. The patient regained consciousness and complained of aching all over the body along with general weakness. 

He had a black hole in the middle of his left palm (Figure ​ (Figure1A) 1A ) and a linear burn on the back of his chest (Figure ​ (Figure1B 1B ).

His pulse was irregularly irregular at 78/minute, and his blood pressure was 110/78 mm Hg. His total leucocyte count was 8600/cmm with neutrophils at 64%, and his hemoglobin was 13 gm/dL. Urinalysis did not show myoglobin. Serum sodium and potassium were 134 mEq/L and 4.2 mEq/L, respectively. Electrocardiography (ECG) showed occasional ventricular premature beat with wandering atrial pacemaker (Figures ​ (Figures2A 2A - ​ -2B). 2B ). Of note, the patient did not have any kind of cardiac ailment previously. The patient was hydrated with intravenous fluids and his wounds were treated with antiseptic dressings and antibiotics. He remained under observation for 48 hours and the ECG showed sinus rhythm (Figure ​ (Figure2C 2C ).

Low voltage currents cause severe electrical burns to the skin as a result of high energy output from the current flow. Dry skin with callouses over palm (resistance of 500 W) and a long contact of palm with the source of electricity attribute to severe burn in this patient (Joule formula). Thereby, the electrical energy output is dissipated and there is less internal injury [ 3 , 4 ].

Low voltage currents travel through the body along low-resistance pathway nerves and blood vessels to cause severe cardiac injury. Also, the distance between the entry and exit wounds can determine the severity of the cardiac injury. The heart remains in the central location of the electrical current’s pathway between the left palm and back of the chest. Current spikes occur in the palm and fingers of an individual holding a metal rod that is suddenly connected to an electric source [ 5 ]. The electric shock causes depolarisation of cardiac muscles and increases membrane pores of the cells resulting in arrhythmias; sinus tachycardia, ventricular premature beats, ventricular tachycardia, and atrial fibrillation are common [ 6 , 7 ]. Wandering atrial pacemaker (WAP) is a benign atrial arrhythmia that has been observed in this case study. WAP and multifocal atrial tachycardia (MAT) differ only with the heart rate - WAP has a heart rate less than 100 bpm whereas MAT has a heart rate greater than 100 bpm. In the WAP rhythm, the pacemaker wanders with the impulses originating from the sinoatrial node to the atrium, and to the atrioventricular junction with a changing focus. Hence, the P waves on an ECG are presented in different configurations. WAP is differentiated from sinus arrhythmia by the fact that heart rate variability occurs from beat-to-beat, and is not phasic. Also, in sinus arrhythmia, the P-wave morphology and the P-R interval are constant [ 7 ]. Most of the arrhythmias occur soon after electric shock and are short-lived. However, delayed arrhythmias occurring 12 hours after electric shock have been reported, too [ 8 ].

Conclusions

Household electric supply is low voltage AC of 60 Hz. It is the electric current that determines the pathophysiological effects in the body but the voltage does determine the outcome of electric shock. Even a low-voltage shock can cause ventricular fibrillation if resistance is low and current flow reaches a threshold of 100 mA. The severity of burn lesion is determined by the resistance of skin and duration of exposure with the source of current. Most cardiac arrhythmias are short-lived and do not require treatment.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

Human Ethics

Consent was obtained or waived by all participants in this study. NA issued approval NA. This is a case report.

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Table of contents.

• Alternative/Holistic Medicine
• Anesthesia & Pain Management
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Benefits and Limitations

The electrocardiogram (ECG or EKG) provides a graphic representation of the electrical depolarization and repolarization processes of the cardiac muscle, as "viewed" from the body surface. The amplitude of these electrical potential differences between various points on the body is measured in millivolts (mV) and their duration in seconds. The ECG can provide information on heart rate, rhythm, and intracardiac conduction; it may also reveal evidence of specific chamber enlargement, myocardial disease or ischemia, pericardial disease, certain electrolyte imbalances, and some drug toxicities. But note that although the ECG is a valuable part of the cardiac evaluation, it cannot determine if congestive heart failure is present, or (in itself) predict whether an animal will survive procedures requiring anesthesia, nor can it provide much information on the strength (or even presence) of cardiac contractions.

Sinus rhythm is the normal cardiac rhythm, described above. The P waves are positive in the caudal leads (II and aVF), the P-Q intervals are consistent and the R-R intervals occur regularly, with less than 10% variation in timing. Normally, the QRS complexes are narrow and upright in leads II and aVF; however, if an intraventricular conduction disturbance or ventricular enlargement pattern is present, they may be wide and abnormally shaped.

Sinus bradycardia is a rhythm that originates in the sinus node and is conducted normally but has too slow a rate, while sinus tachycardia also originates in the sinus node and is conducted normally but is too rapid.

Sinus arrhythmia is characterized by a cyclical slowing and speeding of the sinus rate, most commonly associated with respiration. The rate tends to increase on inspiration and decrease with expiration because of changes in vagal tone. Often, there is an accompanying change in P wave configuration (wandering pacemaker) with the P waves becoming taller and spiked during inspiration and flatter in expiration. Marked sinus arrhythmia occurs in some animals with chronic pulmonary disease. Sinus arrhythmia is a normal rhythm variation . It is commonly seen in dogs, but not often in the clinical setting in normal cats. However, cats frequently have sinus arrhythmia when relaxed or sleeping.

Sinus arrest is a cessation of sinus node activity lasting at least twice as long as the patient's longest expected R-R interval. The resulting pause in heart rate is interrupted by either an escape beat or resumption of sinus activity. Fainting or weakness may result during these pauses.

Conduction blocks in the major ventricular conduction system also disturb the normal activation process and result in altered QRS configurations. The portion of the ventricles served by the diseased bundle branch is activated late and slowly, resulting in widening of the QRS with the terminal forces oriented toward the area of delayed activation.

Rhythm Disturbances

Impulses originating from outside the sinus node are abnormal and create an arrhythmia (dysrhythmia). Abnormal or ectopic impulses are described based on their site of origin (atrial, junctional, supraventricular, ventricular). They are also characterized by timing , that is, whether they occur earlier than the next expected sinus impulse ( premature ) or whether they occur late ( escape ), as a rescue mechanism. Abnormal premature impulses (complexes) may occur singly or in multiples. Groups of three or more comprise an episode of tachycardia ; bouts of tachycardia may be brief (paroxysmal tachycardia) or quite prolonged (sustained tachycardia). A bigeminal pattern occurs when each normal QRS is followed by a premature complex; the origin of the premature complexes determines whether the rhythm is atrial or ventricular bigeminy.

Supraventricular (atrial, junctional) premature complexes originate above the AV node, in either the atrium or the AV junctional (near the AV node) area; however, since they are conducted through the ventricles in the normal manner, their QRS configuration is normal (unless an intraventricular conduction disturbance is also present). Atrial premature complexes are preceded by an abnormal P wave (either positive, negative or biphasic).

Ventricular premature complexes (VPCs or PVCs) originate below the AV node and do not activate the ventricles by the normal pathway; therefore, they have an abnormal ECG configuration. Ventricular ectopic complexes are also wider than the normal QRS complexes because of their slower conduction through ventricular muscle. When the configuration of VPCs or tachycardia in a patient is consistent, the complexes are described as being uniform or unifocal. When the VPCs occurring in an individual have differing configurations, they are said to be multiform. Increased electrical instability of the heart is thought to accompany multiform VPCs or tachycardia. Ventricular tachycardia defines a rapid series of VPCs (greater than 100 beats/minute in the dog, for example). The R-R interval is usually regular, although some variation is not uncommon. Sinus P waves may be seen superimposed on or between the ventricular complexes; they are unrelated to the VPCs because the AV node and/or ventricles are in the refractory period (physiologic AV dissociation).

Atrial fibrillation ("delirium cordis") is a common arrhythmia characterized by rapid, chaotic electrical activation of the atria. There are no P waves on the ECG; rather, the baseline usually shows irregular undulations (fibrillation waves). Since there is no organized electrical activity, meaningful atrial contraction is absent. The AV node, being constantly bombarded with these disorganized electrical impulses, conducts as many as possible to the ventricles. The (ventricular) heart rate is, therefore, determined by how many impulses the AV node can conduct. Atrial fibrillation results in an irregular heart rhythm, which is usually quite rapid. Most often, the QRS complexes appear normal in configuration, since the normal intraventricular conduction pathway is used. Atrial fibrillation tends to be a consequence of significant atrial disease and enlargement in small animals.

Atrio - ventricular (AV) conduction blocks may result from therapy with certain drugs, high vagal tone, and organic disease of the AV node and/or ventricular conduction system. AV blocks are also called "Heart Blocks."

Matthew W. Miller, DVM, MS, DACVIM (Cardiology) College of Veterinary Medicine and Biomedical Sciences Texas A&M University College Station, TX, USA

Introduction to Atrial Rhythms

This page provides an introduction to atrial rhythms and links to our EKG interpretation courses and drills.

Atrial rhythms originate in the atria rather than in the SA node. The P wave will be positive, but its shape can be different from a normal sinus rhythm because the electrical impulse follows a different path to the AV (atrioventricular) node. These EKG differences are covered on our atrial rhythms training module as well as in practice strips which are available via a link in the right column. Atrial rhythms are classified as:

• Atrial Fibrillation (afib)
• Atrial Flutter

Multifocal Atrial Tachycardia

Premature atrial complex, supraventricular tachycardia.

• Wandering Atrial Pacemaker

Wolff-Parkinson-White Syndrome

Atrial rhythm categories.

• Atrial Fibrillation

Irritable sites in the atria fire very rapidly, between 400-600 bpm. This very rapid pacemaking causes the atria to quiver. The ventricles beat at a slower rate due to the AV node's blocking some of the atrial impulses.

There are two types of atrial flutter. Type I (also called classical or typical) has a rate of 250-350 bpm. Type II (also called non-typical) are faster, ranging from 350-450 bpm. EKG tracings will show tightly spaced waves or saw-tooth waveforms (F-waves).

When multifocal atrial tachycardia occurs, multiple (non-SA) sites are firing impulses. The P waves will vary in shape and at least three different shapes can be observed. The PR Interval varies. Ventricular rhythm is irregular.

This occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node. If the ectopic site is near the SA node, the P wave will likely have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.

This term covers three types of tachycardia that originate in the atria, AV junction or SA node.

Wandering atrial pacemaker is an irregular rhythm. In is similar to multifocal atrial tachycardia but the heart rate is under 100 bpm. P waves are present but will vary in shape.

This occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent. The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely. EKG characteristics include a shorter PR Interval, longer QRS complex and a delta wave.

Training Resources

Atrial rhythm training.

After a brief review of cardiac rhythm analysis, this module explains morphologic features and qualifying criteria of atrial rhythms.

Atrial Rhythms

EKG Rhythm Tests

Hundreds heart rhythms in this practice test. Test can be tailored for specific learning needs.

EKG Monitor Challenge

A quiz using a simulated patient monitor. Evaluate a scrolling waveform rather than a paper tracing.

Lesson #1: Rhythm Analysis Method 312

The five steps of rhythm analysis will be followed when analyzing any rhythm strip.

• Analyze each step in the following order.

Rhythm Regularity

• P wave morphology
• P R interval or PRi
• QRS complex duration and morphology
• Carefully measure from the tip of one R wave to the next, from the beginning to the end of the tracing.
• A rhythm is considered “regular or constant” when the distance apart is either the same or varies by 1 ½ small boxes or less from one R wave to the next R wave.

Heart Rate Regular (Constant) Rhythms

• The heart rate determination technique used will be the 1500 technique.
• Starting at the beginning of the tracing through the end, measure from one R wave to the next R wave (ventricular assessment), then P wave to P wave (atrial assessment), then count the number of small boxes between each and divide that number into 1500. This technique will give you the most accurate heart rate when analyzing regular heart rhythms. You may include ½ of a small box i.e. 1500/37.5 = 40 bpm (don’t forget to round up or down if a portion of a beat is included in the answer).

Step 2 (Cont)

Heart rate - irregular rhythms.

• If the rhythm varies by two small boxes or more, the rhythm is considered “irregular”.
• The heart rate determination technique used for irregular rhythms will be the “six-second technique”.
• Simply count the number of cardiac complexes in six seconds and multiply by ten.

P wave Morphology (shape)

• Lead II is most commonly referenced in cardiac monitoring
• In this training module, lead two will specifically be referenced unless otherwise specified.
• The P wave in lead II in a normal heart is typically rounded and upright in appearance.
• Changes in shape must be reported. This can be an indicator that the locus of stimulation is changing or the pathway taken is changing.
• P waves may come in a variety of morphologies i.e. rounded and upright, peaked, flattened, notched, biphasic(pictured), inverted and even buried or absent!
• Remember to describe the shape. This can be very important to the physician when diagnosing the patient.

PR interval (PRi)

• Measurement of the PR interval reflects the amount of time from the beginning of atrial depolarization to the beginning of ventricular depolarization.
• Plainly stated, this measurement is from the beginning of the P wave to the beginning of the QRS complex.
• The normal range for PR interval is: 0.12 – 0.20 seconds (3 to 5 small boxes)
• It is important that you measure each PR interval on the rhythm strip.
• Some tracings do not have the same PRi measurement from one cardiac complex to the next. Sometimes there is a prolonging pattern, sometimes not.
• If the PR intervals are variable, report them as variable, but note if a pattern is present or not.

QRS complex

• QRS represents ventricular depolarization.
• It is very important to analyze each QRS complex on the tracing and report the duration measurement and describe the shape (including any changes in shape).
• As discussed in step 3, when referring to P waves, remember changes in the shape of the waveform can indicate the locus of stimulation has changed or a different conduction pathway was followed. It is no different when analyzing the QRS complex. The difference is that in step 3, we were looking at atrial activity. Now we are looking at ventricular activity.
• Measure from the beginning to the end of ventricular depolarization.
• The normal duration of the QRS complex is: 0.06 – 0.10 second

Lesson #2: Interpretation 312

Introduction.

• The previous slides presented the five-steps of rhythm analysis. These five steps must be followed regardless of how simple of complex the tracing is you are reviewing.
• The information gathered in these steps are telling a story.
• The title of that story is the interpretation.

Atrial Dysrhythmias Types

The dysrhythmias in this category occur as a result of problems in the atria. These atrial dysrhythmias primarily affect the P wave. We will be discussing the following complexes and rhythms:

• Premature Atrial Complexes (PAC’s)

Lesson #3: Premature Atrial Complex

Intro to pacs.

• PACs can occur for a number of different reasons i.e., diet, fatigue, stress, disease, ischemia to name a few.
• Premature complexes frequently occur in bradycardic rhythms, but may occur almost any time.
• PACs occur when an early electrical impulse occurs from a location in the atria other than the SA node.

Intro to PACs 2

• This early impulse causes an early cardiac complex which disrupts the underlying rhythm.
• The locus of stimulation being different, results in a change in the morphology of the P wave.
• PACs can occur occasionally or frequently.
• PACs ECG can be observed with or without a pattern
• The P wave with PAC's will always be upright

EKG Analysis

Notice the following: the R to R interval is irregular, the fifth complex is early and the P wave on the early complex is a different shape.

EKG Practice Strip

Analyze this tracing using the five steps of rhythm analysis.

• Rhythm: Irregular
• P wave: Upright & uniform (except early complexes - biphasic)
• PR interval: 0.16 second
• Interpretation: Sinus Bradycardia with PACs

Lesson #4: Wandering Atrial Pacemaker

Description.

• Rhythms are often named according to the origin of the electrical activity in the heart or the structure where the problem is occurring.
• Wandering Atrial Pacemaker is aptly named due to the electrical impulses causing the atrial activity are moving or wandering.
• These changes in the locus of stimulation affect the morphology of the P waves.
• In Wandering Atrial Pacemaker ECG, you must observe at least three different shaped P waves. No other changes in the tracing may be observed. The rhythm may or may not be regular.
• The PR interval is often affected, but does not have to be.
• The bottom line, is you must observe at least three different shaped P waves.

Practice Strip

• P wave: Changing Shapes (3 or more)
• PR interval: Variable
• Interpretation: Wandering Atrial Pacemaker

Lesson #5: Multifocal Atrial Tachycardia

• Multifocal Atrial Tachycardia is just a faster version of Wandering Atrial Pacemaker. The criteria is the same as Wandering Atrial Pacemaker with the only difference being the heart rate exceeds 100 bpm.
• These changes in the locus of stimulation within the atria affect the morphology of the P waves.
• Remember, you must observe at least three different shaped P waves.
• Due to the presence of irregular R to R intervals coupled with the changing P wave morphology, some people have confused this rhythm with Atrial Fibrillation.

Lesson #6: Atrial Flutter

• Atrial Flutter (sometimes called a flutter) occurs when there is an obstruction within the atrial electrical conduction system.
• Due to this impediment a series of rapid depolarizations occur.
• These depolarizations may occur two, three, four or more times per QRS complex.
• The AV node functions like a “gatekeeper” blocking the extra impulses until the ventricular conduction system is able to accept the impulse.
• The impulse that is accepted will cause the QRS complex to occur.
• Each atrial flutter ECG wave represents atrial depolarization. This will be noted next to the P wave step in rhythm analysis. Instead of P waves, this tracing has “F” waves. No P waves mean there is no PR interval measurement.
• When the tracing is interpreted, the ratio of F waves to each QRS complex will be documented along with the rhythm i.e. Atrial Flutter 4:1 (indicates 4 “F” waves to each QRS complex). Not all Atrial Flutter rhythm strips will have a regular rhythm. In that case just document and report your observations.
• Compare your answers with the answers on the next slide.

Practice Strip Answers

• Rhythm: Regular
• Rate: Ventricles - 80, Atria - 320
• P wave: "F" waves
• PR interval: absent
• Interpretation: Atrial Flutter 4:1

Lesson #7: Atrial Fibrillation

• Atrial Fibrillation (afeb) occurs when multiple electrical impulses occur within the atria. This chaotic electrical activity results in a chaotic wave form between the QRS complexes. P waves are absent. They are replaced by lower case "f" waves. No P waves means there is no PR interval measurement.
• This rapid electrical activity overwhelms the AV node causing impulses to enter the ventricular conduction system at irregular points. This results in irregular R to R intervals.
• Not all fibrillatory waves are created equal. The "f" waves can be coarse (majority measure 3 mm or more) or can be fine (majority of waveforms measure less than 3 mm) to almost absent. Regardless always report your observations. Many times when a patient has "new onset" Atrial Fibrillation the patient will report with a heart rate of 160 bpm or more.
• When a patient experiences A-fib, the atria are not contracting as they normally would. They are just quivering. This absence of contraction of the atria can result in a loss of cardiac output anywhere from 15 - 30% due to the absence of "atrial kick". This is why the heart rate is so high. The body is trying to maintain homeostasis.
• It will be impossible to determine the atrial rate. You will only be able to analyze and report the ventricular rate.
• Atrial Fibrillation with a ventricular response in excess of 100 bpm is commonly referred to as Atrial Fibrillation with “rapid ventricular response” or "uncontrolled A-fib".
• Rate: Ventricles - 90, Atria - Unable to determine (UTD)
• P wave: "f" waves
• Interpretation: Atrial Fibrillation

Lesson #8: Quiz Test Questions 312

Authors and reviewers.

• EKG heart rhythm modules: Thomas O'Brien
• Medical review: Dr. Jonathan Keroes, MD
• Medical review: Dr. Pedro Azevedo, MD, Cardiology
• Last Update: 11/8/2021
• Electrocardiography for Healthcare Professionals, 5th Edition Kathryn Booth and Thomas O'Brien ISBN10: 1260064778, ISBN13: 9781260064773 McGraw Hill, 2019
• Rapid Interpretation of EKG's, Sixth Edition Dale Dublin Cover Publishing Company
• 12 Lead EKG for Nurses: Simple Steps to Interpret Rhythms, Arrhythmias, Blocks, Hypertrophy, Infarcts, & Cardiac Drugs Aaron Reed Create Space Independent Publishing
• The Virtual Cardiac Patient: A Multimedia Guide to Heart Sounds, Murmurs, EKG Jonathan Keroes, David Lieberman Publisher: Lippincott Williams & Wilkin) ISBN-10: 0781784425; ISBN-13: 978-0781784429

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