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208
C. V. Pollack, Jr. et al.
Special Populations
Age
• Incidence of AF increases with advancing age.
• “Lone AF” more common below age 50.
Co-morbidities
• As under “Pathophysiology and Etiology,” a host of other cardiac and meta-
bolic disorders are frequent co-morbidities in patients with AF.
• Binge alcohol consumption predisposes to “holiday heart.”
Pitfalls inDiagnosis
Critical Steps Not toMiss
• Complications such as blood clot formation, strokes, and heart failure may arise,
but rhythm conversion reduces the chances that such complications will develop.
Mimics
• Atrial utter
• Multifocal atrial tachycardia
• Supraventricular tachycardia
Time-Dependent Interventions
• Patients may have potentially life-threatening symptoms that need immediate
intervention with electrical cardioversion, including decompensated congestive heart failure, hypotension, angina, or cardiac ischemia.
12 Atr ial Fibrillation
Overall Principles ofTreatment
• The initial focus of AF management is rate control to minimize any perfusion
stress on the ventricles.
• The usual approach is with titrated doses of calcium channel blockers or
beta-blockers.
• Once rate is controlled (or if patient presents with a controlled ventricular
rate), consideration is given to converting the rhythm out of AF back into a
sinus rhythm.
• This may be approached pharmacologically with a variety of potential
drugs, such as ibutilide or procainamide, or electrically via synchronized
cardioversion.
• If the patient has been in AF for 24 to 48 hours or longer, anticoagulation
therapy should be provided before attempting cardioversion, as clots that may
have formed in the brillating atria or atrial appendage may dislodge and
embolize when normal atrial electrical activity is restored. Therapy may be
provided acutely with parenteral agents such as unfractionated or low-molecular weight heparin or with fast-acting non-warfarin oral anticoagulants (dabigatran, rivaroxaban, apixaban, edoxaban)
• Alternatively, cardioversion may be attempted after transesophageal echo-
cardiography that excludes atrial clots
• Likelihood of stroke or systemic embolization may be assessed with
CHA2DS2-VASc score
209
CHADS2VASC score points for prediction of stroke in atrial brillation. (Data from
Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ.Validation
of Clinical Classication Schemes for Predicting Stroke: Results From the National
Registry of Atrial Fibrillation. JAMA.2001;285(22):2864-2870. https://doi.org/10.1001/
jama.285.22.2864.) [Table from Verheugt FWA. The new oral anticoagulants.
Netherlands Heart Journal. 2010 Jun;18(6):314–8.] Caption adapted from original
• Patients whose AF is resistant to cardioversion or recurs after initially successful cardioversion may be referred to electrophysiology, where the possibility of catheter ablation of the electrical source of the AF can be addressed
denitively and specically.
• Success rates usually exceed 65–75 %
210
C. V. Pollack, Jr. et al.
Disease Course
• The most feared complication of AF is thromboembolism to a critical vascular bed—especially stroke.
• The palpitations of AF may have a very adverse effect on quality of life. They
may be symptomatic even in patients with controlled ventricular response.
• Patients with diminished pump function are particularly sensitive to the
absence of consistent ventricular lling (the missing “atrial kick”) and may
experience persistent easy fatigability and even angina.
• Longstanding AF increases mortality.
Related Evidence
Papers of particular importance have been highlighted as:
** Of key importance
Practice Guideline
January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, Conti JB,
Ellinor PT, Ezekowitz MD, Field ME, Murray KT, Sacco RL, Stevenson WG,
Tchou PJ, Tracy CM, Yancy CW; American College of Cardiology/American
Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC/HRS
guideline for the management of patients with atrial brillation: a report of the
American College of Cardiology/American Heart Association Task Force on
Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2014 Dec
2;64(21):e1-76. https://doi.org/10.1016/j.jacc.2014.03.022. PMID: 24685669.
http://www.ncbi.nlm.nih.gov/pubmed/24685669 **
Verma A, Cairns JA, Mitchell LB, Macle L, Stiell IG, Gladstone D, McMurtry MS,
Connolly S, Cox JL, Dorian P, Ivers N, Leblanc K, Nattel S, Healey JS; CCS
Atrial Fibrillation Guidelines Committee. 2014 focused update of the Canadian
Cardiovascular Society Guidelines for the management of atrial brillation. Can
J Cardiol. 2014 Oct;30(10):1114-30.
PMID: 25262857. http://www.ncbi.nlm.nih.gov/pubmed/25262857 **
Steinberg BA, Beckley PD, Deering TF, Clark CL, Amin AN, Bauer KA, Cryer B,
Mansour M, Scheiman JM, Zenati MA, Newby LK, Peacock WF, Bhatt DL;
Society of Cardiovascular Patient Care. Evaluation and management of the atrial
brillation patient: a report from the Society of Cardiovascular Patient Care. Crit
Pathw Cardiol. 2013 Sep;12(3):107-15.
HPC.0b013e31829834ed. PMID: 23892939. http://www.ncbi.nlm.nih.gov/
pubmed/23892939
**
https://doi.org/10.1016/j.cjca.2014.08.001.
https://doi.org/10.1097/
12 Atr ial Fibrillation
211
Frendl G, Sodickson AC, Chung MK, Waldo AL, Gersh BJ, Tisdale JE, Calkins H,
Aranki S, Kaneko T, Cassivi S, Smith SC Jr, Darbar D, Wee JO, Waddell TK,
Amar D, Adler D; American Association for Thoracic Surgery. 2014 AATS
guidelines for the prevention and management of perioperative atrial brillation
and utter for thoracic surgical procedures. J Thorac Cardiovasc Surg. 2014
Sep;148(3):e153-93.
https://doi.org/10.1016/j.jtcvs.2014.06.036. PMID:
25129609. http://www.ncbi.nlm.nih.gov/pubmed/25129609**
Review
Zoni-Berisso M, Lercari F, Carazza T, Domenicucci S.Epidemiology of atrial bril-
lation: European perspective. Clin Epidemiol. 2014 Jun 16;6:213-20. https://doi.
org/10.2147/CLEP.S47385. PMID: 24966695. http://www.ncbi.nlm.nih.gov/
pubmed/24966695
Ball J, Carrington MJ, McMurray JJ, Stewart S.Atrial brillation: prole and burden
of an evolving epidemic in the 21st century. Int J Cardiol. 2013 Sep 1;
167(5):1807-24. https://doi.org/10.1016/j.ijcard.2012.12.093. PMID: 23380698.
http://www.ncbi.nlm.nih.gov/pubmed/23380698
Hu YF, Chen YJ, Lin YJ, Chen SA. Inammation and the pathogenesis of atrial
brillation. Nat Rev Cardiol. 2015 Jan 27. https://doi.org/10.1038/nrcar-
dio.2015.2. PMID: 25622848. http://www.ncbi.nlm.nih.gov/pubmed/25622848**
Mohmand-Borkowski A, Tang WH.Atrial brillation as manifestation and conse-
quence of underlying cardiomyopathies: from common conditions to genetic
diseases. Heart Fail Rev. 2014 May;19(3):295-304. https://doi.org/10.1007/
s10741-014-9424-0. PMID: 24531802. http://www.ncbi.nlm.nih.gov/
pubmed/24531802**
Longobardo L, Todaro MC, Zito C, Piccione MC, Di Bella G, Oreto L, Khandheria
BK, Carerj S.Role of imaging in assessment of atrial brosis in patients with
atrial brillation: state-of-the-art review. Eur Heart J Cardiovasc Imaging. 2014
Jan;15(1):1-5.
www.ncbi.nlm.nih.gov/pubmed/23798579**
Chapa DW, Akintade B, Thomas SA, Friedmann E.Gender differences in stroke,
mortality, and hospitalization among patients with atrial brillation: A systematic review. Heart Lung. 2015 Feb 19. pii: S0147-9563(15)00009-6. https://doi.
org/10.1016/j.hrtlng.2015.01.008. PMID: 25703992. http://www.ncbi.nlm.nih.
gov/pubmed/25703992**
Vergara P, Della Bella P.Management of atrial brillation. F1000Prime Rep. 2014
Apr 1;6:22. https://doi.org/10.12703/P6-22. PMID: 24765527. http://www.ncbi.
nlm.nih.gov/pubmed/24765527**
**
https://doi.org/10.1093/ehjci/jet116. PMID: 23798579. http://
Use PubMed Clinical Queries to nd the most recent evidence. Use this search strategy:
“Atrial Fibrillation”[Mesh] OR “Atrial Fibrillation”
Chapter 13
Bradyarrhythmias
ChristopherJ.Rees, RichardM.Cantor, CharlesV.Pollack,Jr.,
andVictoriaG.Riese
Name andSynonyms
Bradyarrhythmias
• Bradycardia
Incidence/Epidemiology
• The bradyarrhythmias encompass a broad range of disorders; therefore, their
incidence varies widely.
• Sinus bradycardia may be normal in up to 35 % of people younger than 25 years.
It also may be normal in well-conditioned athletes at most ages.
• Sick sinus syndrome becomes more common as people age, with more than
50 % of cases occurring in people over 50, but it may occur at any age.
C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, USA
R. M. Cantor
Department of Emergency Medicine and Pediatrics, State University of NewYork Upstate
Medical University, Syracuse, NY, USA
C. V. Pollack,
Department of Emergency Medicine, Thomas Jefferson University,
Philadelphia, PA, USA
V. G. Riese
Librarian Consultant, Eldersburg, MD, USA
C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_13
Jr. ()
213© Springer Nature Switzerland AG 2019
214
C. J. Rees et al.
Differential Diagnosis
• Clinically signicant bradycardias may cause a wide range of symptoms, the most
common of which are syncope, presyncope, chest pain, general fatigue, dyspnea
on exertion, and dyspnea at rest. As such, the differential is broad and far ranging.
• Bradycardias also have a broad range of causes; therefore, the differential
diagnosis of the bradycardia itself also is extensive.
Pathophysiology andEtiology
• Bradycardia is dened as a heart rate below 60 bpm.
• Bradycardia generally is caused by two different mechanisms:
• Slowing, blocking, or failure of impulse generation in the sinus node
• Block in the conduction system from the atrioventricular (AV) node down
through the His–Purkinje system.
• Many different processes may lead to these mechanisms, including intrinsic
conduction system disease, other heart diseases, other systemic diseases, and
drugs, to name a few.
• When these blocks occur, alternative pacemakers within the heart take over
the pacemaker function. Other conduction tissue, or even myocytes, may act
as alternative pacemakers. In general, the higher within the conduction system the impulse originates, the faster the rate; if the impulse is generated
within or above the bundle of His, the rate generally is enough to maintain
adequate cardiac output. This association also may be used as a clue to the
location of the block based on the escape rate.
• Although slow heart rates can occur with junctional or ventricular pacemakers,
the bradyarrhythmias usually are classied according to the location of the
block: either sinoatrial (SA) node dysfunction or AV node dysfunction.
• Sinus node dysfunction:
• Sinus bradycardia: dened as a sinus node rate less than 60 impulses per
minute.
• An ECG will show normal sinus P waves and a xed P-P interval that is
equal to the R-R interval, with 1:1 AV conduction.
• It may be physiologic and normal in well-conditioned athletes, in young
people, and during sleep.
• It may be secondary to excess vagal stimulation, which may even occur
as a result of a necktie that is too tight.
• Medications are a common cause, especially beta-blockers, calcium
channel blockers, digoxin, and opioids.
• It also (although less commonly) may be pathologic. Sinus bradycardia
may be seen in the setting of acute inferior myocardial infarction (MI),
increased intracranial pressure, carotid sinus hypersensitivity, and profound hypothyroidism.
13 Bradya rrhythmias
215
Sinus bradycardia. No other abnormalities noted here except for sinus bradycardia
at 50 bpm. [Almasry IO. Evidenced-based approach to bradyarrhythmias. In:
Stergiopoulos K, Brown DL, editors. Evidence-based cardiology consult [Internet].
London: Springer; 2014 [cited 2015 May 22]. p.105–18. Available from:
http://link.
springer.com/10.1007/978-1-4471-4441-0_9] Caption adapted from original
• Sinus arrhythmia (sinus dysrhythmia): similar to sinus bradycardia except for
the presence of a variable P-P interval, leading to a slightly irregular rhythm.
This is a normal variant and not pathologic. It is common in children and
young adults. In the most common situation, the sinus node rate increases
with inspiration and decreases during expiration because of the changes in
vagal tone with breathing.
Sinus arrhythmia. Rhythmic variation in the sinus rate is noted across the rhythm
strip. P-wave morphology and PR intervals remain essentially unchanged. [Foreman
B. Common atrial and ventricular arrhythmias. In: Toth PP, Cannon CP, editors.
Comprehensive cardiovascular medicine in the primary care setting [Internet].
Totowa, NJ: Humana Press; 2011 [cited 2015 May 22]. p.459–96. Available from:
http://link.springer.com/10.1007/978-1-60327-963-5_24] Caption from original
• Sinus arrest (sinus pause). In sinus arrest, the SA node fails to generate an
impulse. It is recognized as a pause in the sinus rhythm. During the pause/
arrest, no P waves are seen on the ECG.The P-P interval of the two complexes surrounding the pause will not be a multiple of the usual P-P interval,
as would be the case if the pause were from an SA exit block. If the pause lasts
long enough, there may be an escape beat from somewhere else along the
conduction system or the ventricles. This may be a normal variant, but it also
occurs in acute MI, intrinsic SA node disease, digitalis toxicity, stroke, and
excessive vagal stimulation. Notably, frequent and prolonged sinus pauses
may be seen in up to 30 % of patients with obstructive sleep apnea.
Sinus arrest. Note sudden cessation of sinus impulse for 3 s prior to resumption of
normal sinus rhythm. [Almasry IO.Evidenced-based approach to bradyarrhythmias.
In: Stergiopoulos K, Brown DL, editors. Evidence-based cardiology consult [Internet].
216
C. J. Rees et al.
London: Springer; 2014 [cited 2015 May 22]. p.105–18. Available from: http://link.
springer.com/10.1007/978-1-4471-4441-0_9] Caption adapted from original
• SA exit block: recognized as a pause in the usual rhythm resulting from the
absence of a normally expected P wave, usually because of blocked or slowed
impulse generation within the SA node. The P-P interval of the two complexes surrounding the pause will have a P-P interval that is a multiple of the
usual P-P interval. SA exit block may be subclassied as rst degree; second
degree, types I and II; and third degree. These usually are difcult, if not
impossible, to see on a surface ECG and require electrophysiologic mapping
of the sinus node discharge. These blocks may be seen following acute MI,
acute rheumatic fever, and myocarditis, and secondary to drugs such as betablockers, calcium channel blockers, digoxin, quinidine, and salicylates. They
also may be seen in well- conditioned athletes or secondary to excessive vagal
stimulation. They usually are transient and not clinically signicant.
Top panel: Type I second-degree sinoatrial exit block. Note the pause that is less than
two times the PP interval. Also note the group beating consistent with Wenckebach
periodicity. Bottom panel: Type II second-degree sinoatrial exit block. The pause here
is two times the PP interval, with the occurrence of a junctional beat prior to the return
of a sinus P wave which is followed by unperturbed sinus mechanism before there is
another recurrence. [Almasry IO.Evidenced-based approach to bradyarrhythmias. In:
Stergiopoulos K, Brown DL, editors. Evidence-based cardiology consult [Internet].
London: Springer; 2014 [cited 2015 May 22]. p.105–18. Available from: http://link.
springer.com/10.1007/978-1-4471-4441-0_9] Caption from original
• Sick sinus syndrome (tachycardia–bradycardia syndrome/tachy–brady syndrome):
a mixed group of disorders marked by abnormalities of supraventricular impulse
formation and conduction that are associated with both tachy- and bradyarrhythmias. It usually is the result of intrinsic disease of the sinus node or the surrounding
tissue, sometimes with associated AV nodal disease. The tachyarrhythmias usually
are either atrial brillation or atrial utter, and the bradyarrhythmias usually are
marked sinus bradycardia, prolonged sinus arrest, and SA block associated with
abnormal AV conduction leading to inadequate escape rhythms. On prolonged
rhythm monitoring, it is typical to see long periods of tachycardia followed by profound bradycardia upon the spontaneous termination of the tachycardia. It is most
13 Bradya rrhythmias
common in the elderly as a result of brotic degeneration of conduction tissue. It
also may be seen in cardiomyopathies, in connective tissue diseases, and with the
use of some medications. It usually is suspected in elderly patients who present with
syncope and is an indication for a permanent pacemaker.
217
(a) Twelve-lead electrocardiogram of an 84-year-old female who presented with
altered mental status. Atrial utter with 2:1 A:V conduction is seen. (b) 12-lead
218
C. J. Rees et al.
electrocardiogram showing utter termination. A 4.9-s period of asystole is noted
before ventricular activity resumes. The patient had multiple sinus pauses during
sinus rhythm. These rhythms are typical of Tachy–Brady syndrome and are
characteristic of sick sinus syndrome [El Hage L, Badhwar N, Goldschlager N.Top
ten electrocardiographic (ECG) abnormalities not to miss. In: Stergiopoulos K,
Brown DL, editors. Evidence-based cardiology consult [Internet]. London: Springer;
2014 [cited 2015 May 22]. p. 133–48. Available from:
http://link.springer.
com/10.1007/978-1-4471-4441-0_11] Caption from original
• Chronotropic incompetence: failure of the heart rate to increase appropriately
with exercise
• Junctional rhythms. Under typical conditions, the sinus node impulses sup-
press (by nature of being faster) impulse generation distally along the conduction tree. If the sinus impulse is suppressed or blocked, the AV node may take
over the pacemaker function. This is termed a junctional or junctional escape
rhythm. The AV node naturally discharges at a rate of 40–60 bpm, which usually is enough to maintain cardiac output and blood pressure. As the impulse
is generated in the AV node, the QRS complex will be narrow, but because the
sinus impulses are blocked, there will be no P waves. Junctional rhythms may
be seen after acute inferior MI and in congestive heart failure, myocarditis,
hypokalemia, and digoxin toxicity.
ECG shows transient sinus arrest with escape junctional rhythm. Arrow indicates
escape junctional rhythm [Bhaskar EM, Moorthy S, Ganeshwala G, Abraham
G.Cardiac conduction disturbance due to prallethrin (pyrethroid) poisoning. J Med
Toxicol. 2010 Mar;6(1):27–30.] Caption from original
• AV node dysfunction
• AV block is caused by either delayed or blocked conduction of impulses
between the atria and the ventricles.