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Day 6:  Ectopic Arrhythmias and Triggered Activity

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Day 6: ectopic arrhythmias and triggered activity.

• Interpretations of Sample Tracings
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Ectopy—a disorder of impulse formation

Mechanisms of ectopic arrhythmias

Ectopic arrhythmias require:

Default—slowing of the normal dominant sinus pacemaker which allows a slower focus to take control, or

Usurpation—an acceleration of a lower pacemaker which takes control by virtue of being faster than the sinus rate

Disorders of the sinus node, such as SA arrest, SA exit block, or excessive vagal tone may allow a lower focus to take control by default

A variety of factors, including digitalis toxicity, hypoxia, electrolyte disturbances, ischemia, or chronic lung disease may stimulate an ectopic focus to accelerate and usurp control from the SA node

Properties of ectopic arrhythmias

Ectopic arrhythmias usually start and stop gradually ( non-paroxysmally )

They are not usually initiated by a premature beat

They may be somewhat irregular

They are not terminated by vagal maneuvers, although AV block may be increased

AV block of varying degrees is frequently present (particularly if digitalis toxicity is the cause)

These arrhythmias are usually quite resistant to treatment with standard class I or III agents

Catheter ablation may be effective if a causative agent cannot be identified or treated

The major ectopic arrhythmias

Wandering atrial pacemaker

Mechanisms and causes

There are three or more ectopic atrial pacemakers

This arrhythmia is typically seen in young healthy persons, particularly athletes

The etiology is uncertain

Heart rate—the heart rate is 60–100 and is usually irregular

ECG morphology ( Day 6-01 )

There are at least three P wave morphologies with varying PR intervals

There is usually moderate variation in the heart rate

Multifocal atrial tachycardia

Caused by multiple ectopic atrial foci

Chronic lung disease is typically the underlying clinical abnormality, although it can also occur in the setting of hypoxia, electrolyte abnormalities, acid-base disturbances, and ischemia (i.e., frequently in the intensive care setting)

ECG morphology ( Day 6-02 )

The rate is 100–140

There is typically 1:1 AV conduction

This arrhythmia is frequently confused with atrial fibrillation; the distinction is an important one since management is usually very different

Ectopic atrial rhythms

A single ectopic atrial focus accelerates and usurps control from the sinus node, or the sinus node slows down and allows an ectopic focus to appear

Digitalis toxicity, electrolyte abnormalities, ischemia, hypoxia, and chronic lung disease are typical causes

ECG morphology ( Day 6-03 ) ( Day 6-04 )

The P waves are of the same morphology but have an abnormal axis, indicating their ectopic origin

The atrial rate may be slightly irregular

AV block of varying degrees is sometimes present (particularly if digitalis toxicity is the cause)

Atrial tachycardia with AV block should be considered a manifestation of digitalis toxicity until proven otherwise ( Day 6-05 )

The atrial rate in atrial tachycardia is usually 140–200

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14 Things You Can't Do With a Pacemaker

Take a few simple precautions, and life should be virtually normal

• Getting a Pacemaker
• Precautions
• Daily Activities

Frequently Asked Questions

A pacemaker is a small electronic device that is implanted under the skin to help regulate the heart rhythm. Most pacemakers are implanted to treat symptoms resulting from bradycardia (slow heart rate) caused by  sick sinus syndrome  or  heart block .

Having a pacemaker is supposed to eliminate or prevent problems, not cause them. That's generally the case, but there are things to avoid with a pacemaker once you begin living with one.

This article presents a few simple precautions to consider as you follow your healthcare provider's guidance and a routine schedule for periodic follow-up care.

After Pacemaker Implantation

Pacemaker implantation is a minimally invasive surgery. The typical recovery period is not lengthy or difficult. You may experience pain at the incision site for a few days.

Your healthcare provider may ask you to restrict vigorous activity or lifting heavy objects for a week or two. The  incision site  is usually completely healed after two or three weeks, and you should have no further restrictions.

During this initial period, you should watch for signs of bleeding or infection, such as:

• Increased redness
• Worsening pain

Let your healthcare provider know if any of these signs occur. Fortunately, these complications are infrequent.

You will need to have your pacemaker checked periodically to make sure it is functioning normally and its battery has plenty of energy. Usually, these pacemaker checks can be done from home, wirelessly, using a special device your healthcare provider will give you for remote follow-up.

You will also be checked in your healthcare provider's office once or twice a year.

When the battery begins to run out, usually after five to 10 years, your healthcare provider will schedule an elective pacemaker replacement. This is a relatively simple procedure, carried out under local anesthesia, in which your old pacemaker generator is detached from its leads and thrown away.

A new generator is then attached and the incision is sewn up. Generally, the pacemaker leads never need to be replaced unless they develop a problem.

Precautions to Take with a Pacemaker

Contrary to popular belief, modern home appliances, including microwave ovens, do not interfere with pacemakers and should not cause any concern whatsoever. With certain other devices, there are only a few special precautions you will need to take to avoid problems like electromagnetic interference (EMI).

Airport Security Metal Detectors

Your pacemaker may set off the walk-through metal detector commonly used in airport security. The metal detector will not affect your pacemaker.

But a potential problem is the hand-held scanner the security agent may use on you after you set off the metal detector. The hand-held scanner contains a magnet that may interfere with your pacemaker when it is brought near.

Before you go through airport security, you should tell the agent that you have a pacemaker and that they should not use the hand-held scanner near your pacemaker.

Airport Security Full-Body Scanners

The full-body scanners at airports (the devices that make an image of your body) apparently will not affect your pacemaker, but there is surprisingly little objective evidence available on this issue. 

Magnetic Resonance Imaging (MRI)

Magnetic resonance imaging , or MRI, uses strong magnetic fields and pulses of radiofrequency to generate detailed images of your inner body. These mechanisms can cause the pacemaker to overheat, or interfere with its pacing.

MRI-safe pacemakers were approved by the FDA in 2011, and have since become the standard pacemaker in many parts of the world. For those with an older pacemaker who need an MRI, there are several protocols healthcare providers can take to minimize the risk of MRI interference, such as setting the pacemaker to safe-mode before the scan then reprogramming the pacemaker afterwards.

Diathermy is a type of therapy often used in physical therapy for pain relief. The therapy works by using high-frequency electromagnetic currents to generate heat within body tissues. This can effectively relieve pain, relax muscles, and expedite healing.

The electromagnetic fields produced via diathermy can interfere with the pacemaker's pulse generator, and can result in permanent damage. Diathermy is thus not recommended for most people with pacemakers.

Being Around Large Motors

Large motors, including those in cars and trucks, boats, aircraft, bulldozers, and cranes can temporarily interfere with your pacemaker's function. As such, you will need to make sure these motors are completely powered off when you are in close contact with or working on them.

To minimize this risk, it's important to keep motorized items at least six inches away from the body, especially when the item is powered on.

Arc Welders and Construction

Welding and construction equipment often involve powerful electric and/or magnetic fields that can interfere with a pacemaker's ability to regulate heart rhythm, particularly when those items get close to the body.

If you have a pacemaker, stay at least two feet away from the following:

• Arc welders
• Electric drills (including cordless drills)
• Power saws, routers, and sanders
• Stud finders
• Laser levels
• Soldering irons and other light metalworking tools

Magnetic fields in magnets can interfere with pulse generators in pacemakers. To avoid this risk, you will need to avoid prolonged contact with devices or machinery that contain magnets. If you have to be in contact with them, stay at least inches away at all times.

Items that contain magnets include:

• CPAP masks with magnetic clips used to secure the headgear
• Fitbit and Apple Watch
• Apple AirPods Pro charging case
• Microsoft Surface Pen

Take care to avoid carrying portable electronic devices with magnets in your shirt or jacket pocket, or resting them on your chest while lying down.

Anti-Theft Detectors

The walk-through anti-theft detectors in stores work by generating electromagnetic waves, which can momentarily interfere with the function of a pacemaker. However, as long as you walk through the detector normally, without stopping or pausing, you should not experience any problems. Just keep moving.

Cellular Telephones

Cellular phones, if held close to the pacemaker (which may happen if the phone is kept in a breast pocket) can potentially affect the function of a pacemaker. But as long as the phone is kept 6 inches or more away from the pacemaker there should not be a problem.

Most headphones contain magnets that can interfere with pacemakers. This includes earbud and clip-on headphones. If you use headphones, keep them at least six inches away from your pacemaker, and don't store them in your jacket or shirt pocket, or drape them around your neck when not in use.

Lithotripsy

Extracorporeal shock-wave lithotripsy (ESWL) is a treatment that uses hydraulic shocks to dissolve gallstones or kidney stones. The treatment can also interfere with pacemaker functioning. If you must get ESWL, your pacemaker will need to be reprogrammed after the treatment. You may also need follow ups with your healthcare provider in the months after ESWL treatment to ensure your pacemaker is functioning properly.

Transcutaneous electrical nerve/muscle stimulators ( TENS ) are medical devices that transmit electrical currents through the skin to activate nerves, blocking or changing your perception of pain. TENS utilize a pulse generator that can briefly interfere with your pacemaker.

Radiation Therapy

The powerful radiation used in radiation therapy for cancer can damage the circuits of a pacemaker. If you need radiation therapy, your pacemaker will need to be specially shielded to protect it from the radiation field.

Electrocautery

Electrocautery is a procedure used during surgery to control bleeding. While it is generally regarded as safe in people with pacemakers, there have been some reports of it interfering with pacemaker functioning.

In general, it makes good sense to remind any of your healthcare providers that you have a pacemaker before they do any medical procedure.

Can I Return to My Daily Activities With a Pacemaker?

Despite what may seem a long list of things to avoid with a pacemaker, there are minimal lifestyle changes you'll need to make in the day-to-day.

When you have a pacemaker, you are free to return to these activities:

• Doing yard work
• Driving a car, provided that you do not have any symptoms, such as fainting

If you want to return to exercise and playing sports, be sure to do so only on the advice of your healthcare provider.

There aren't really specific foods to avoid with a pacemaker itself. But if you have one it's because you have a heart condition, and that diagnosis means you need to adopt a heart-healthy diet. These diet changes focus on limiting red meat, many dairy products, and unhealthy fats, while adding whole grains, fresh fruits, and vegetables.

Can I Drink Alcohol if I Have a Pacemaker?

Moderate drinking doesn't appear to be harmful for people with some heart conditions. That said, people with certain heart arrhythmias or a history of heart failure should avoid drinking alcohol. A history of arrhythmia is common in people who have pacemakers, so talk to your healthcare provider about alcohol use.

Pacemakers are sensitive to electric and magnetic fields found in numerous devices and machinery. If you have a pacemaker, you will need to avoid electromagnetic interference by keeping a safe distance from these items. Airport security scanners, MRIs, large motors in cars and boats, electric drills, and cell phones are just a few of them. Avoid placing small, magnetic or electric items in your jacket or shirt pocket, and make sure motorized machines are powered off before you get too close.

Follow your healthcare provider's recommendations about exercise. You'll likely need to limit activity for a few weeks after surgery while your incision heals. Afterwards, if your healthcare provider says it's OK, you should be able to resume your normal level of activity.

A pacemaker can help you to live a normal life span. A 2015 study found that the life expectancy for pacemaker patients is similar to the life expectancy for the general population.

Kotsakou M, Kioumis I, Lazaridis G, et al. Pacemaker insertion . Ann Transl Med . 2015;3(3):42. doi:10.3978/j.issn.2305-5839.2015.02.06

American Heart Association. Devices that may interfere with ICDs and pacemakers .

Gupta S, Ya'qoub L, Wimmer A, Fisher S, Saeed I. Safety and clinical impact of MRI in patients with Non-MRI-conditional cardiac devices . Radiology . 2020 Oct;2(5). doi:10.1148/ryct.2020200086

Harvard Health Publishing. Getting an MRI if you have a pacemaker .

Pollet J, Ranica G, Pedersini P, Lazzarini S, Pancera S, Buraschi R. The efficacy of electromagnetic diathermy for the treatment of musculoskeletal disorders: A systematic review and meta-analysis . J Clin Med . 2023 Jun;12(12):3956. doi:10.3390/jcm12123956

Johns Hopkins Medicine. Living with a pacemaker or ICD .

Stunder D, Seckler T, Joosten S, et al. In vivo study of electromagnetic interference with pacemakers caused by everyday electric and magnetic fields . Circulation . 2017 Feb;135(1):907-909. doi:10.1161/CIRCULATIONAHA.116.024558

Frankel Cardiovascular Center. Devices that may interfere with ICDs and pacemakers .

Harvard Health Publishing. Can my phone and other devices interfere with my pacemaker? .

American Heart Association. Magnets in newer portable electronic devices can interfere with implanted defibrillators .

Qureshi A, Ahmed I, Khan A. Pacemaker failure to capture caused by electrocautery: A rare pacemaker pulse generator change complication . Cureus . 2022 Aug;14(8):e28252. doi:10.7759/cureus.28252

Alberta. Heart rhythm problems and driving .

Johns Hopkins Medicine. Alcohol and Heart Health .

American Heart Association. Living with your pacemaker .

Bradshaw P, Stobie P, Knuiman M, Briffa T, Hobbs M. Life expectancy after implantation of a first cardiac permanent pacemaker (1995–2008): A population-based study .  Int J Cardiol . 2015;190:42-46. doi:10.1016/j.ijcard.2015.04.099

Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons . J Am Coll Cardiol 2008; 51:e1. doi:10.1016/j.jacc.2008.02.032

Hauser RG, Hayes DL, Kallinen LM, Cannom DS, Epstein AE, Almquist AK, Song SL, Tyers GF, Vlay SC, Irwin M. Clinical experience with pacemaker pulse generators and transvenous leads: an 8-year prospective multicenter study . Heart Rhythm . 2007 Feb;4(2):154-60. doi:10.1016/j.hrthm.2006.10.009

By Richard N. Fogoros, MD Richard N. Fogoros, MD, is a retired professor of medicine and board-certified in internal medicine, clinical cardiology, and clinical electrophysiology.

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INTRODUCTION

The sinoatrial (SA) node represents the integrated activity of pacemaker cells, sometimes called P cells, in a compact region at the junction of the high right atrium and the superior vena cava. Perinodal cells, sometimes called transitional or (T) cells, transmit the electrical impulse from the SA node to the right atrium. Each of these cell types has distinct expression profiles of ion channels and gap junctions.

Given the architecture of the SA node, SA nodal dysfunction typically results from either abnormalities in impulse generation by the P cells or abnormalities in conduction across the T cells. SA nodal dysfunction is more commonly an acquired condition, but in some patients it can be inherited, with gene mutations having been described in some forms of inherited SA nodal dysfunction [ 1 ]. Patients with SA nodal dysfunction may be asymptomatic or highly symptomatic as in cases of sinus node dysfunction (SND).

Sinoatrial nodal pauses, arrest, and exit block will be discussed here. Additional details regarding the anatomy and electrophysiology of the SA node, as well as a discussion of the SND, are presented separately. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history" .)

Sinus pause, arrest, and exit block may arise from hyperkalemia; excessive vagal tone; ischemic, inflammatory, or infiltrative or fibrotic disease of the SA node; sleep apnea; certain drugs (eg, digitalis). The causes of SND are discussed in detail elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Sinus node dysfunction: Epidemiology, etiology, and natural history", section on 'Etiology' and "Obstructive sleep apnea and cardiovascular disease in adults", section on 'Other arrhythmias' and "Cardiac arrhythmias due to digoxin toxicity", section on 'Sinus bradycardia, tachycardia, block, and arrest' .)

In patients receiving one or more agents that depress SA node and atrioventricular (AV) node function, a syndrome of bradycardia, renal failure, AV block, shock, and hyperkalemia (BRASH), has been described [ 2,3 ]. Patients with BRASH are generally taking therapeutic doses of SA and AV node blocking medications, and the level of hyperkalemia may be mild. However, the severity of bradycardia (caused by sinus arrest and/or AV block) is generally greater than expected for either the dose/level of SA and AV node blocker or the level of hyperkalemia.

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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MATTHEW KENDALL HAWKS, MD, MADISON L.B. PAUL, MD, AND OMOJO ODIHI MALU, MD, MSc

Am Fam Physician. 2021;104(2):179-185

Author disclosure: No relevant financial affiliations.

Sinus node dysfunction, previously known as sick sinus syndrome, describes disorders related to abnormal conduction and propagation of electrical impulses at the sinoatrial node. An abnormal atrial rate may result in the inability to meet physiologic demands, especially during periods of stress or physical activity. Sinus node dysfunction may occur at any age, but is usually more common in older persons. The causes of sinus node dysfunction are intrinsic (e.g., degenerative idiopathic fibrosis, cardiac remodeling) or extrinsic (e.g., medications, metabolic abnormalities) to the sinoatrial node. Many extrinsic causes are reversible. Electrocardiography findings include sinus bradycardia, sinus pauses or arrest, sinoatrial exit block, chronotropic incompetence, or alternating bradycardia and tachycardia (i.e., bradycardia-tachycardia syndrome). Clinical symptoms result from the hypoperfusion of end organs. About 50% of patients present with cerebral hypoperfusion (e.g., syncope, presyncope, lightheadedness, cerebrovascular accident). Other symptoms include palpitations, decreased physical activity tolerance, angina, muscular fatigue, or oliguria. A diagnosis is made by directly correlating symptoms with a bradyarrhythmia and eliminating potentially reversible extrinsic causes. Heart rate monitoring using electrocardiography or ambulatory cardiac event monitoring is performed based on the frequency of symptoms. An exercise stress test should be performed when symptoms are associated with exertion. The patient's inability to reach a heart rate of at least 80% of their predicted maximum (220 beats per minute – age) may indicate chronotropic incompetence, which is present in 50% of patients with sinus node dysfunction. First-line treatment for patients with confirmed sinus node dysfunction is permanent pacemaker placement with atrial-based pacing and limited ventricular pacing when necessary.

Sinus node dysfunction, previously known as sick sinus syndrome, is characterized by abnormal initiation and propagation of electrical impulses from the sinoatrial node (SAN). The resulting abnormalities include bradycardia (less than 50 beats per minute [bpm]), sinus pause (more than three seconds), sinus arrest, and sinoatrial exit blocks, which are sometimes associated with supraventricular tachyarrhythmias in bradycardia-tachycardia syndrome 1 – 4 ( Table 1 5 – 11 ) . Bradycardia-tachycardia syndrome occurs in approximately 50% of patients with sinus node dysfunction and increases the risk of stroke and death. 5 , 12 Symptoms manifest as end-organ hypoperfusion, including palpitations, decreased physical activity tolerance, easy fatigability, dizziness, and syncope. 2 , 5 , 6 , 13 To diagnose sinus node dysfunction, a combination of symptoms and documented electrical abnormalities must be present. 5 , 7

Epidemiology

Sinus node dysfunction may occur at any age 7 , 14 ; however, increasing age is the most significant risk factor with the highest disease prevalence in patients 70 to 89 years of age. 2 , 7 , 8 , 14 The incidence of sinus node dysfunction is 0.8 per 1,000 person-years and is expected to double by 2060 due to the aging population. 15 Conditions associated with advanced age such as hypertension, chronic kidney disease, diabetes mellitus, and coronary heart disease are overlapping risk factors and potential causes of sinus node dysfunction. 2 , 15 Brugada syndrome, a rare inherited ion channel disorder that results in ventricular tachyarrhythmias and sudden cardiac death, is also associated with sinus node dysfunction. 5 , 16 , 17

Causes of sinus node dysfunction are generally categorized as intrinsic or extrinsic based on their effect on the SAN ( Table 2 2 , 5 – 8 , 18 ) . It is important to note that sinus node dysfunction is usually a progressive condition and most causes are chronic and irreversible. 5

INTRINSIC CAUSES

Intrinsic causes originate from structural or functional changes within the SAN. These changes can occur because of fibrosis, ischemia, cardiac remodeling, infiltrative disease, or ion channel dysfunction. 8 , 18 , 19 Degenerative idiopathic fibrosis of the SAN is the most common cause of sinus node dysfunction. 4 , 5 , 7 , 8 , 15 Elastic fiber and fatty and fibrous tissue buildup at the SAN and surrounding myocardial tissue increases with age and may lead to prolonged SAN refractory time and, therefore, a decreased intrinsic heart rate. 2 , 4 , 8 Ischemic heart disease and embolization of the sinus node artery may cause ischemic necrosis of the node, resulting in sinus node dysfunction. 8 Acute myocardial infarction may induce a transient sinus node dysfunction caused by autonomic disturbance and increased vagal tone. 2 , 12 Cardiac remodeling following myocardial infarction, congestive heart failure, or advanced age can result in structural changes that decrease cardiac tissue voltage transmission and ultimately delay or block the SAN and result in sinus node dysfunction. 3 , 8 , 14

Another result of this remodeling is the formation of bradycardia-tachycardia syndrome. It is unclear if a supraventricular tachycardia or sinus node dysfunction is the primary disorder in bradycardia-tachycardia syndrome. The etiology is further complicated by current contradictory evidence about the role of supraventricular tachycardia and atrial fibrillation as a cause of sinus node dysfunction. 3 At a minimum, it is clear that these diagnoses are associated even if the causal pathway is unclear.

Infiltrative diseases such as sarcoidosis, amyloidosis, hemochromatosis, and connective tissue diseases can disrupt the cardiac tissue and result in abnormal SAN function. 2 , 5 Similarly, sinus node dysfunction has been associated with cardiomyopathy from infection with Chagas disease, with which the arrhythmia may be permanent. 6 , 8 Rhythm abnormalities associated with myocarditis from infections such as diphtheria and typhoid and immune-mediated disorders such as rheumatic fever may cause sinus node dysfunction temporarily. 6 , 8

About 80% of patients younger than 21 years with sinus node dysfunction have a history of congenital heart malformations (e.g., atrial septal defect, transposition of the great arteries) that required surgical intervention. 18 , 20 Genetic mutations in genes responsible for coding ion channels, such as HCN4 and SCN5A , have also been identified as a cause of intrinsic sinus node dysfunction. 18

EXTRINSIC CAUSES

Extrinsic causes are related to external factors causing abnormal conduction at the SAN. These causes include medications, metabolic abnormalities, autonomic imbalances, toxins, and endocrine disorders ( Table 2 2 , 5 – 8 , 18 ) . Extrinsic causes may be reversible, such as electrolyte abnormalities, hypothyroidism, metabolic abnormalities, and certain medications. 2 , 8 Anesthesia (e.g., sympatholytic drugs) has been shown to induce autonomic imbalances that may mimic sinus node dysfunction or may reveal the underlying dysfunction in previously asymptomatic patients. 8 , 21 Other pharmacotherapies known to cause sinus node dysfunction include beta blockers, nondihydropyridine calcium channel blockers, digoxin, lithium, and antiarrhythmics. 5 , 7 , 8 Toxins such as nicotine and marijuana have also been implicated in sinus node dysfunction. 7 , 8 , 22

Patients with sinus node dysfunction typically present with end-organ hypoperfusion symptoms from decreased cardiac output caused by the underlying arrhythmia ( Table 1 5 – 11 ) . The most common symptoms of cerebral hypoperfusion are syncope, presyncope, lightheadedness, and cerebrovascular accidents, with syncope occurring in 50% of patients with sinus node dysfunction. 2 , 5 , 7 , 23 Cardiovascular hypoperfusion can present with palpitations, decreased physical activity tolerance, angina, or, less commonly, heart failure. Musculoskeletal hypoperfusion can present with muscle fatigue. Renal hypoperfusion can present as oliguria. 2 , 5 , 6 , 13 , 23 Correlation between symptoms and arrhythmias is considered the diagnostic standard (on electrocardiography [ECG] or other cardiac monitoring). 2 , 5 , 6

A definitive diagnosis of sinus node dysfunction is established when symptoms are directly associated with cardiac monitoring that demonstrates a bradyarrhythmia 2 , 6 ( Table 1 5 – 11 ) . The initial assessment should begin with a history and physical examination ( Figure 1 2 – 4 , 8 , 14 , 17 , 21 , 24 ) . Clinicians should focus their history by investigating the intrinsic and extrinsic causes of sinus node dysfunction ( Table 2 2 , 5 – 8 , 18 ) . It should include a medication review to assess for a potential extrinsic cause. Initial diagnostic evaluation should include 12-lead ECG, a basic chemical panel to assess for metabolic abnormalities, and any additional laboratory tests needed to rule out other extrinsic causes that were not excluded by the history or physical examination (i.e., thyroid-stimulating hormone to rule out hypothyroidism or A1C to rule out diabetic atrial myopathy). 5 , 6

Initial evaluation of sinus node dysfunction can be performed in an outpatient setting; patients with hemodynamic instability (i.e., systolic blood pressure less than 90 mm Hg, ventricular arrhythmias) or severe symptoms (i.e., recurrent syncope, anginal symptoms) should be hospitalized because these patients need urgent evaluation and may require temporary transcutaneous pacing for stabilization. 2 When a potential extrinsic factor is identified during the workup, further evaluation should focus on confirming the diagnosis followed by a trial of therapy. With successful treatment of the extrinsic factor (e.g., continuous positive airway pressure for confirmed sleep apnea or thyroid supplementation for hypothyroidism) and subsequent resolution of sinus node dysfunction, no further workup is indicated.

Patients with history or physical examination findings for underlying structural defects such as a history of valvular disease, new cardiac murmur, bibasilar crackles, lower extremity edema, or concerning ECG findings (e.g., left bundle branch block, second-degree Mobitz type II block, third-degree atrioventricular block) should have transthoracic echocardiography. 2 If the results suggest a specific pathology, further workup and treatment should be initiated based on the suspected etiology. Abnormal results may be because of complications from sinus node dysfunction or an alternative diagnosis, and will require further workup and potential specialty referral for evaluation and treatment.

Chronotropic incompetence is associated with sinus node dysfunction, with 50% of patients diagnosed with sinus node dysfunction also meeting chronotropic incompetence criteria. 25 , 26 It is a separate diagnosis associated with an array of diseases, including sinus node dysfunction. Chronotropic incompetence is defined as the sinus node's inability to mount a heart rate high enough to meet physiologic demands during exertion, resulting in symptoms of central nervous system hypoperfusion similar to those found in sinus node dysfunction. 5 , 25 When symptoms are associated with exertion, the patient should have an exercise ECG test to assess chronotropic incompetence. A diagnosis of chronotropic incompetence is made if the patient is unable to meet 80% of the maximum heart rate (220 bpm – age) during exertion. 2 , 25 It is important to distinguish that chronotropic incompetence is a separate disease process and alone is not enough to diagnose sinus node dysfunction. Sinus node dysfunction and chronotropic incompetence follow the same treatment algorithm ( Figure 1 2 – 4 , 8 , 14 , 17 , 21 , 24 ) .

When initial 12-lead ECG is unable to confirm sinus node dysfunction by correlating symptoms with a definitive bradyarrhythmia ( Table 1 5 – 11 ) , further electrical monitoring is indicated. 2 , 5 , 9 There are multiple types of ambulatory monitoring available. These devices include continuous monitoring (e.g., Holter monitor, external patch recorder, ambulatory telemetry) and patient- or event-activated devices (e.g., event monitor, external loop recorder, implantable loop recorder). First-line devices include the original Holter monitor or the external patch recorder. 8 , 9 , 27 – 32 The external patch recorder is a smaller second-generation monitor that is water-resistant and can be worn for seven to 14 days. The external patch recorder detected more arrhythmias and was better tolerated by patients compared with the Holter monitor. 31 , 33 The frequency of symptoms, the patient's ability to use the device, and the need for continuous vs. intermittent monitoring should be considered when deciding the best form of monitoring for a patient. 9 Table 3 lists cardiac monitoring options with associated indications and pros and cons of use. 9 , 27 – 31 If sinus node dysfunction cannot be definitively established after ambulatory monitoring is completed, further evaluation for an alternative diagnosis and expert consultation should be considered.

Permanent pacemaker placement is the first-line treatment for patients with confirmed sinus node dysfunction , 2 , 5 , 34 – 36 accounting for 50% of pacemakers implanted in the United States. 5 , 7 , 12 Pacemaker therapy has been found to provide symptom relief and improve quality of life, but it is unclear if it provides a mortality benefit. 5 , 36 This treatment includes patients with chronotropic incompetence and patients with pharmacologically induced sinus node dysfunction where continued treatment is clinically necessary. Atrial-based pacing has been established as superior because right ventricular pacing has been associated with an increased risk of arrhythmias and decreased cardiac function. 2 , 37 , 38 A well-powered randomized controlled trial demonstrated no difference in mortality, stroke, heart failure, or atrial fibrillation hospitalizations when comparing single-chamber atrial pacing with dual-chamber atrial pacing. 21 However, over five years of follow-up, 3% to 35% of patients will transition from a single-chamber atrial device to a dual-chamber device with minimized ventricular pacing. 2 , 6 To minimize the risk of these additional procedures, patients with evidence of atrioventricular nodal or bundle branch conduction dysfunction should be considered for initial dual-chamber device placement. 2 It is common in the United States for patients to receive a dual-chamber device with right atrial pacing unless otherwise indicated. Overall, permanent pacemaker placement is relatively safe, with complications estimated at less than 1% to 6%. Most common complications include lead dislodgment (5.7% in left ventricular leads), hematomas (3.5%), venous thrombus/obstruction (2%), infections (1%), and pneumothorax (1%). 34

Medication control of sinus node dysfunction is a secondary option for patients who decline permanent pacemaker placement. Phosphodiesterase inhibitors (e.g., theophylline, cilostazol [Pletal]) have a positive chronotropic effect, resulting in symptom control for patients with sinus node dysfunction. However, the long-term impact of medication control on disease progression and mortality is unclear. 2 , 35 Other pharmaceuticals (e.g., atropine, dopamine, epinephrine, glucagon) used in advanced cardiac life support protocols for acutely unstable bradycardic patients are effective for short-term control of unstable patients but are not appropriate for long-term management of sinus node dysfunction because of significant adverse effect profiles. 2 , 35

The role of oral anticoagulation in patients with sinus node dysfunction is unclear. There is limited evidence to support its use in patients with sinus node dysfunction who do not have another indication for anticoagulation therapy. 2 , 37 , 39 Anticoagulation is currently not routinely recommended for the treatment of sinus node dysfunction.

This article updates previous articles on this topic by Semelka, et al. , 5 and by Adán and Crown . 7

Data Sources: We searched Essential Evidence, PubMed, and Google Scholar. Key words included sinus node dysfunction, sick sinus syndrome, causes, bradyarrhythmia, permanent pacemaker indications, chronotropic incompetence, loop recorders, ambulator cardiac monitoring. The search included practice guidelines, randomized controlled trials, a retrospective case control study, and review articles. Search dates: December 2019 to October 2020.

The opinions and assertions contained herein are those of the authors and are not to be construed as official or as reflecting the views of the Uniformed Services University, the U.S. Air Force Medical Department, the Air Force at large, the U.S. Army Medical Department, the Army at large, or the U.S. Department of Defense.

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Sanders P, Kistler PM, Morton JB, et al. Remodeling of sinus node function in patients with congestive heart failure: reduction in sinus node reserve. Circulation. 2004;110(8):897-903.

Csepe TA, Kalyanasundaram A, Hansen BJ, et al. Fibrosis: a structural modulator of sinoatrial node physiology and dysfunction. Front Physiol. 2015;6:37.

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Bagliani G, Leonelli F, Padeletti L. P wave and the substrates of arrhythmias originating in the atria. Card Electrophysiol Clin. 2017;9(3):365-382.

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Go AS, Mozaffarian D, Roger VL, et al.; American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Executive summary: heart disease and stroke statistics—2013 update: a report from the American Heart Association. Circulation. 2013;127(1):143-152.

Alonso A, Jensen PN, Lopez FL, et al. Association of sick sinus syndrome with incident cardiovascular disease and mortality: the Atherosclerosis Risk in Communities study and Cardiovascular Health Study. PLoS One. 2014;9(10):e109662.

Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: promoting understanding of sick sinus syndrome. Circulation. 2007;115(14):1921-1932.

Jensen PN, Gronroos NN, Chen LY, et al. Incidence of and risk factors for sick sinus syndrome in the general population. J Am Coll Cardiol. 2014;64(6):531-538.

Sarquella-Brugada G, Campuzano O, Arbelo E, et al. Brugada syndrome: clinical and genetic findings. Genet Med. 2016;18(1):3-12.

Mizusawa Y, Wilde AAM. Brugada syndrome. Circ Arrhythm Electrophysiol. 2012;5(3):606-616.

Benson DW, Wang DW, Dyment M, et al. Congenital sick sinus syndrome caused by recessive mutations in the cardiac sodium channel gene (SCN5A). J Clin Invest. 2003;112(7):1019-1028.

Bashour TT. Classification of sinus node dysfunction. Am Heart J. 1985;110(6):1251-1256.

Yabek SM, Swensson RE, Jarmakani JM. Electrocardiographic recognition of sinus node dysfunction in children and young adults. Circulation. 1977;56(2):235-239.

Khanna S, Sreedharan R, Trombetta C, et al. Sick sinus syndrome: sinus node dysfunction in the elderly. Anesthesiology. 2020;132(2):377-378.

Iqbal AM, Mubarik A, Cheetirala VG, et al. Marijuana induced sick sinus syndrome: a case report. Am J Case Rep. 2019;20:882-885.

Nielsen JC, Thomsen PEB, Højberg S, et al.; DANPACE Investigators. A comparison of single-lead atrial pacing with dual-chamber pacing in sick sinus syndrome. Eur Heart J. 2011;32(6):686-696.

John RM, Kumar S. Sinus node and atrial arrhythmias. Circulation. 2016;133(19):1892-1900.

Melzer C, Witte J, Reibis R, et al. Predictors of chronotropic incompetence in the pacemaker patient population. Europace. 2006;8(1):70-75.

Lukl J, Doupal V, Sovová E, et al. Incidence and significance of chronotropic incompetence in patients with indications for primary pacemaker implantation or pacemaker replacement. Pacing Clin Electrophysiol. 1999;22(9):1284-1291.

Sivakumaran S, Krahn AD, Klein GJ, et al. A prospective randomized comparison of loop recorders versus Holter monitors in patients with syncope or presyncope. Am J Med. 2003;115(1):1-5.

Gula LJ, Krahn AD, Massel D, et al. External loop recorders: determinants of diagnostic yield in patients with syncope. Am Heart J. 2004;147(4):644-648.

Olson JA, Fouts AM, Padanilam BJ, et al. Utility of mobile cardiac outpatient telemetry for the diagnosis of palpitations, presyncope, syncope, and the assessment of therapy efficacy. J Cardiovasc Electrophysiol. 2007;18(5):473-477.

Krahn AD, Klein GJ, Skanes AC, et al. Insertable loop recorder use for detection of intermittent arrhythmias. Pacing Clin Electrophysiol. 2004;27(5):657-664.

Steinberg JS, Varma N, Cygankiewicz I, et al. 2017 ISHNE-HRS expert consensus statement on ambulatory ECG and external cardiac monitoring/telemetry [published corrections appear in Heart Rhythm . 2018; 15(5):789, and Heart Rhythm . 2018;15(8):1276]. Heart Rhythm. 2017;14(7):e55-e96.

Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS Guideline for the evaluation and management of patients with syncope: a report of the American College of Cardiology/American Heart Association Task Force on clinical practice guidelines and the Heart Rhythm Society [published correction appears in Circulation . 2017;136(16):e271–e272]. Circulation. 2017;136(5):e60-e122.

Barrett PM, Komatireddy R, Haaser S, et al. Comparison of 24-hour Holter monitoring with 14-day novel adhesive patch electrocardiographic monitoring. Am J Med. 2014;127(1):95.e11-95.e17.

Mulpuru SK, Madhavan M, McLeod CJ, et al. Cardiac pacemakers: function, troubleshooting, and management: part 1 of a 2-part series. J Am Coll Cardiol. 2017;69(2):189-210.

Sonoura T, Kodera S, Shakya S, et al. Efficacy of cilostazol for sick sinus syndrome to avoid permanent pacemaker implantation: a retrospective case-control study. J Cardiol. 2019;74(4):328-332.

Vardas PE, Auricchio A, Blanc JJ, et al.; European Society of Cardiology; European Heart Rhythm Association. Guidelines for cardiac pacing and cardiac resynchronization therapy. Europace. 2007;9(10):959-998.

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• 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

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, caffeine , 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 ( 1 ). Aberrantly conducted APBs (usually with right bundle branch block morphology) must be distinguished from premature beats of ventricular origin.

Occasional APBs in apparently healthy people are generally considered benign, and nearly everyone has some. Frequent APBs have been shown to be associated with an increased risk of stroke, of all-cause mortality, of cardiovascular mortality, and atrial fibrillation ( 2, 3 ). It is not known if these associations are the consequence of APBs, of unidentified structural heart disorders, of unidentified atrial fibrillation, or simply that they all share the same risk factors (such as aging).

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 or escape atrial rhythm). Heart rate is typically 40 to 60 beats/minute, P wave morphology is typically different, and PR interval is slightly shorter than in sinus rhythm. Accelerated atrial rhythm (also called a nonsinus atrial rhythm) may occur at a rate higher than the sinus rate due to either enhanced normal automaticity or abnormal automaticity. Accelerated atrial rhythm is distinguished from atrial tachycardia by being slower with an arbitrary rate cut-off (usually 100 or 120 beats/minute).

Junctional escape beats are ectopic beats that emerge after long sinus pauses or sinus arrest when not terminated by an atrial escape beat. The "junction" includes the atrioventricular (AV) node, His bundle, and adjacent atrial tissue that produce escape beats that cannot be more specifically localized by the ECG. They may be single or multiple; escape beats from a single junctional focus may produce a continuous rhythm (called ectopic or escape junctional rhythm). Heart rate is typically slow (35 to 50 beats/minute), P wave morphology typically shows low to high atrial activation (negative P waves in leads II, III, aVF), and P waves are located immediately before (

Focal atrial tachycardia

Focal atrial tachycardia is a regular rhythm caused by 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, AV block may be present, and ventricular rate may be slower. Mechanisms include abnormal automaticity, triggered activity, and micro-reentry.

Focal atrial tachycardia is the least common (5 to 10%) form of paroxysmal supraventricular tachycardia ( 4 ) 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). When focal atrial tachycardia is incessant, it may lead to a tachycardic cardiomyopathy and heart failure.

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 Focal Atrial Tachycardia ).

Focal 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 (because the AV node is not an obligate part of the arrhythmia circuit).

adenosine 5 direct current cardioversion .

Pharmacologic approaches to prevention of focal atrial tachycardia include beta-blockers, non-dihydropyridine calcium channel blockers, and/or antiarrhythmic medications in class Ia, Ic, or III ( 5 ). Transcatheter ablation of focal atrial tachycardia, which is effective and reasonably safe, is the preferred approach for chronic prophylaxis.

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 , especially when accompanied by hypoxia, acidosis, theophylline -intoxication, or a combination. Less commonly, it is caused by underlying cardiac disease such as coronary artery disease , and electrolyte abnormalities such as hypokalemia 5 5 ).

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, which tend to be the same as the causes of atrial premature beats.

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 the underlying heart disorder.

Junctional ectopic tachycardia

6 5 ). Transcatheter ablation is less successful than in other supraventricular tachycardias and has a higher risk of inadvertent creation of AV block.

1.  Mond HG, Haqqani HM : The Electrocardiographic Footprints of Atrial Ectopy. Heart Lung Circ 28(10):1463–1471, 2019. doi: 10.1016/j.hlc.2019.03.005

2. Durmaz E, Ikitimur B, Kilickiran Avci B, et al : The clinical significance of premature atrial contractions: How frequent should they become predictive of new-onset atrial fibrillation.  Ann Noninvasive Electrocardiol 25(3):e12718, 2020. doi:10.1111/anec.12718

3. Huang BT, Huang FY, Peng Y, et al : Relation of premature atrial complexes with stroke and death: Systematic review and meta-analysis.  Clin Cardiol 40(11):962–969, 2017. doi:10.1002/clc.22780

4. Porter MJ, Morton JB, Denman R, et al : Influence of age and gender on the mechanism of supraventricular tachycardia. Heart Rhythm  1(4):393–396, 2004. doi: 10.1016/j.hrthm.2004.05.007

5. Brugada J, Katritsis DG, Arbelo E, et al : 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J 41(5):655–720, 2020. doi: 10.1093/eurheartj/ehz467

6. Alasti M, Mirzaee S, Machado C, et al : Junctional ectopic tachycardia (JET). J Arrhythm 36(5):837–844, 2020. doi: 10.1002/joa3.12410

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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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• Wandering atrial pacemaker

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• C R O G V Wandering atrial pacemaker

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