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13 Bradya rrhythmias
• Sick sinus syndrome: this is an indication for a permanent pacemaker.
• Junctional bradycardia: usually does not require treatment and is transient.
If the patient is symptomatic or unstable, atropine and/or pacing may be used;
however, it also is important to search for the underlying cause.
• SA block: often requires no treatment; however, the underlying cause should
be evaluated.
• First-degree AV block: usually requires no treatment.
• Second-degree AV block, Mobitz type I (Wenckebach): usually does not
require treatment unless the patient has symptoms. It usually is transient, and
when the underlying cause is identied and treated, the block usually resolves.
If treatment is necessary, most patients will respond to atropine.
• Second-degree AV block, Mobitz type II: these patients are unstable, with a
high risk of progression to complete heart block. They should have pacemaker
pads placed and attached for use if necessary. Atropine may be used as a temporizing measure (about 60 % of patients respond), but in most circumstances,
pacing will be necessary. Because this type of block usually is associated with
permanent damage to the conduction system, most patients will require a
permanent pacemaker at some point in their care.
• Third-degree heart block (complete heart block): this is an inherently unstable
block and usually is symptomatic and hemodynamically signicant. It usually
indicates permanent damage to the conduction system and requires either
transcutaneous or transvenous pacing as a bridge to a permanent pacemaker.
Some patients may respond to atropine if the block is higher within the
His–Purkinje system.
229
Disease Course
• As detailed earlier, many of these rhythms/conduction problems are either
normal variants or transient and can be resolved with identication and treatment of the underlying disorders.
• Higher-grade AV blocks almost always indicate some permanent damage to
the conducting system and require placement of a permanent pacemaker.
Related Evidence
Papers of particular interest have been highlighted as:
** Of key importance
230
C. J. Rees et al.
Practice Guideline
European Society of Cardiology (ESC); European Heart Rhythm Association
(EHRA), Brignole M, Auricchio A, Baron-Esquivias G, Bordachar P, Boriani G,
Breithardt OA, Cleland J, Deharo JC, Delgado V, Elliott PM, Gorenek B, Israel
CW, Leclercq C, Linde C, Mont L, Padeletti L, Sutton R, Vardas PE. 2013 ESC
guidelines on cardiac pacing and cardiac resynchronization therapy: the task
force on cardiac pacing and resynchronization therapy of the European Society
of Cardiology (ESC). Developed in collaboration with the European Heart
Rhythm Association (EHRA). Europace. 2013 Aug;15(8):1070-118. https://doi.
org/10.1093/europace/eut206. PMID: 23801827. http://www.ncbi.nlm.nih.gov/
pubmed/23801827 **
Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA 3rd, Freedman RA, Gettes LS,
Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK,
Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM,
Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA 3rd, Ferguson TB Jr,
Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ,
Silka MJ, Stevenson LW, Stevenson WG, Varosy PD; American College of
Cardiology Foundation; American Heart Association Task Force on Practice
Guidelines; Heart Rhythm Society. 2012 ACCF/AHA/HRS focused update
incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based
therapy of cardiac rhythm abnormalities: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice
Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2013 Jan
22;61(3):e6-75. https://doi.org/10.1016/j.jacc.2012.11.007. PMID: 23265327.
http://www.ncbi.nlm.nih.gov/pubmed/23265327 **
Review
Tadros R, Ton AT, Fiset C, Nattel S. Sex differences in cardiac electrophysiology
and clinical arrhythmias: epidemiology, therapeutics, and mechanisms. Can J
Cardiol. 2014 Jul;30(7):783-92. https://doi.org/10.1016/j.cjca.2014.03.032.
PMID: 24970790.
Sohinki D, Obel OA.Newer algorithms in bradycardia management. Cardiol Clin.
2014 May;32(2):283-92. https://doi.org/10.1016/j.ccl.2014.01.004. PMID:
24793803. http://www.ncbi.nlm.nih.gov/pubmed/24793803 **
Deal N. Evaluation and management of bradydysrhythmias in the emergency
department. Emerg Med Pract. 2013 Sep;15(9):1-15; quiz 15-6. PMID:
24044868. http://www.ncbi.nlm.nih.gov/pubmed/24044868 **
Semelka M, Gera J, Usman S.Sick sinus syndrome: a review. Am Fam Physician.
2013 May 15;87(10):691-6. PMID: 23939447.
pubmed/23939447
http://www.ncbi.nlm.nih.gov/pubmed/24970790 **
http://www.ncbi.nlm.nih.gov/
**
13 Bradya rrhythmias
231
Vogler J, Breithardt G, Eckardt L.Bradyarrhythmias and conduction blocks. Rev
Esp Cardiol (Engl Ed). 2012 Jul;65(7):656-67. https://doi.org/10.1016/j.
recesp.2012.01.025. PMID: 22627074. http://www.ncbi.nlm.nih.gov/
pubmed/22627074
**
Barnes BJ, Hollands JM.Drug-induced arrhythmias. Crit Care Med. 2010 Jun;38(6
Suppl):S188-97. https://doi.org/10.1097/CCM.0b013e3181de112a. PMID:
20502173. http://www.ncbi.nlm.nih.gov/pubmed/20502173 **
Lampert R, Ezekowitz MD.Management of arrythmias. Clin Geriatr Med. 2000
Aug;16(3):593-618. PMID: 10918649. http://www.ncbi.nlm.nih.gov/pubmed/
10918649 **
Spodick DH.Normal sinus heart rate: appropriate rate thresholds for sinus tachy-
cardia and bradycardia. South Med J. 1996 Jul;89(7):666-7. PMID: 8685750.
http://www.ncbi.nlm.nih.gov/pubmed/8685750 **
Cohort Study
Udo EO, van Hemel NM, Zuithoff NP, Doevendans PA, Moons KG. Prognosis of
the bradycardia pacemaker recipient assessed at rst implantation: a nationwide
cohort study. Heart. 2013 Nov;99(21):1573-8. https://doi.org/10.1136/
heartjnl-2013-304445. PMID: 23969476. http://www.ncbi.nlm.nih.gov/
pubmed/23969476
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy:
“Bradycardia”[Mesh] OR “Sick Sinus Syndrome”[Mesh] OR “Bradycardia” OR
“Bradyarrhythmia”
Chapter 14
Bronchiectasis
ChristopherJ.Rees, CharlesV.Pollack,Jr., andVictoriaG.Riese
Name andSynonyms
Bronchiectasis
Incidence/Epidemiology
• It is estimated that between 100,000 and 125,000 people in the United States
have bronchiectasis.
• The prevalence increases with age.
• It is more common in women than in men.
• The incidence of bronchiectasis has been decreasing in developed nations.
• The incidence of bronchiectasis may be up to three times higher in developing
nations. This is likely due to a combination of environmental and genetic
factors that lead to a higher incidence of recurrent pulmonary infections, especially among children and young adults.
C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, 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_14
Jr. ()
233© Springer Nature Switzerland AG 2019
234
C. J. Rees et al.
Differential Diagnosis
• The differential diagnosis includes all the causes of chronic cough, sputum
production, and dyspnea.
• This includes chronic bronchitis, asthma, chronic obstructive pulmonary disease, chronic sinusitis, and idiopathic pulmonary brosis, among others.
Pathophysiology andEtiology
• Bronchiectasis refers to lung disease dominated clinically by chronic cough
with sputum production. Symptoms are often present for months to years
prior to diagnosis.
• The major pathophysiologic change is irreversible airway dilatation with wall
thickening and scarring.
https://www.youtube.com/watch?v=uNeprw1rsgE
Video animation of the pathophysiology of bronchiectasis.
Close inspection of the cut surface of this lung in a case of mild bronchiectasis
shows somewhat brotic-walled airways, which are dilated and congested. In addition, there is local, patchy emphysema and some cystic change and interstitial scarring. Many cases of lung disease do not show a single, pure format [Suvarna
SK.Thorax: Heart, Lungs, Mediastinum, and Pleura. In: Suvarna SK, editor. Atlas
of Adult Autopsy [Internet]. Cham: Springer International Publishing; 2016 [cited
2016 Nov 7]. p.65–160. Available from: http://link.springer.com/10.1007/978-3-
319-27022-7_4] Caption from original
14 Bronchiectasis
235
Bronchiectasis. There is dilatation of the airways with inammation and increased
mucous production [Ruggeri G, Gobbi D, Libri M, Lima M.Pediatric Bronchiectasis.
In: Lima M, editor. Pediatric Thoracic Surgery [Internet]. Springer Milan; 2013
[cited 2015 May 11]. p. 351–62. Available from: http://link.springer.com/
chapter/10.1007/978-88-470-5202-4_30]
• The lung changes can be focal or diffuse.
Focal bronchiectasis (circled area of upper panel) may be seen in patients with
recurrent aspiration or pneumonias. Bilateral and diffuse bronchiectasis (arrows in
lower panel) is typically the result of diffuse necrotizing infections in childhood,
cystic brosis, immotile cilia syndromes, or immunoglobulinopathies, among
236
C. J. Rees et al.
others. [Callister T, Budoff M, Braunwald E. Atlas of Cardiovascular Computed
Tomography, Volume 01, Chapter 18. In: Budoff M, Narula J, Achenbach SS,
editors. Atlas of Cardiovascular Computed Tomography. Philadelphia: Current
Medicine; 2007 [cited 2015 May 11]. Book DOI 978-1-57340-267-5] Caption
adapted from original.
• These changes lead to airways that easily collapse and obstruct airow.
• The initiation of bronchiectasis requires many factors. It is felt that there
needs to be an inciting infectious insult, often in the setting of some impaired
host defenses, that leads to airway obstruction that impairs drainage of inammatory and purulent material and sets up a chronic airway inammatory
response. This leads to chronic inammation, with permanent scarring, dilatation, and destruction of the airways (both large and small).
• The chronic inammation leads to recurrent infections, which then lead to
continued inammation, setting up a vicious cycle.
• Many diseases and environmental issues can incite and/or worsen
bronchiectasis.
• The pattern of involvement in the lungs may be a helpful clue as to etiology.
Focal bronchiectasis points to foreign body aspiration or intrinsic or extrinsic
airway compression as the cause.
• Causes/etiologies of bronchiectasis include:
• Obstruction. Bronchiectasis can result from an aspirated foreign body,
intrinsic compression/blockage from an endobronchial lesion or mass, or
extrinsic compression from a mass.
• Infection. Can be bacterial pneumonia, atypical pneumonia such as viral or
Mycoplasma, tuberculous, and non-tuberculous mycobacteria. Mycobacterium
avium-intracellulare complex (MAC) is the most common non- tuberculous
mycobacteria causing bronchiectasis, classically occurring in nonsmoking
women over age 50.
• Immunodeciency. Hypogammaglobulinemias, such as severe, combined
immunodeciency. These patients often have recurrent infections starting in
childhood. Immunodeciency also includes HIV infection and bronchiolitis
obliterans after lung transplantation.
• Autoimmune/rheumatologic disorders. Rheumatoid arthritis, Sjogren’s syndrome, inammatory bowel disease.
• Immune-mediated diseases such as allergic bronchopulmonary aspergillosis.
• Genetic causes such as cystic brosis, ciliary dyskinesia (by decreasing secretion clearance), alpha-one anti-trypsin deciency (usually causes early-onset
emphysema, but bronchiectatic changes are also common).
• Recurrent aspiration.
• Idiopathic. Often represents from 25– 50% of cases.
• Cigarette smoking.
14 Bronchiectasis
237
Bronchiectasis showing signet ring sign in a 44-year-old man. (a) Lung window image
of CT scan (2.5-mm section thickness) obtained at level of the right upper lobar bronchus shows dilated bronchi showing signet ring sign (arrows) in right upper lobe. Also
note mucus plugging (arrowhead) in dilated bronchi. (b) Gross pathologic specimen
obtained with right upper lobectomy discloses cylindrical bronchiectasis and distal
cystic changes (arrows, cystic bronchiectasis). Also note thickened bronchial wall
(arrowheads) with active inammation [Lee KS, Han J, Chung MP, Jeong YJ.Signet
Ring Sign. Radiology Illustrated: Chest Radiology [Internet]. Berlin, Heidelberg:
Springer Berlin Heidelberg; 2014 [cited 2015 Nov 19]. p.139–42. Available from:
http://link.springer.com/10.1007/978-3-642-37096-0_15] Caption from original.
Presentation
Typical/“Classic”
• The typical presentation of bronchiectasis is one of prolonged (months) cough
that produces thick sputum. Usually there is an absence of acute infectious
symptoms such as fever. Patients may also complain of dyspnea, especially on
exertion. They may also exhibit wheezing.
238
C. J. Rees et al.
Atypical
• Patients may present with symptoms more consistent with chronic obstructive
pulmonary disease or asthma, with wheezing and shortness of breath being
more prominent.
• Patients may also present with a more acutely infectious appearance with
fever, associated with productive cough. This is especially common if they
have been undiagnosed and are suffering from an acute infectious exacerbation from their undiagnosed bronchiectasis.
Primary Differential Considerations
• Asthma
• Acute and chronic bronchitis
• Cystic brosis
• GERD
• Pneumonia
• Alpha-1-antitrypsin deciency
History andPhysical Exam
Findings That Conrm Diagnosis
• A typical presentation with prolonged cough productive of thick sputum will
strongly suggest the diagnosis, but the diagnosis is usually only conrmed by
typical ndings on CT scan of the chest.
Factors That Suggest Diagnosis
• Again, the typical symptoms should strongly suggest the diagnosis.
• This is especially true if the patient has any of the known predisposing
conditions.
Factors That Exclude Diagnosis
• There are no historical or physical examination ndings that can reliably
exclude the diagnosis.
• Bronchiectasis may coexist with many other diseases, especially COPD.
14 Bronchiectasis
Ancillary Studies
Laboratory
• Although there are no laboratory tests specically needed for the diagnosis,
patients will usually require a CBC with differential and basic chemistries in
the evaluation. They may also require tests specic for the disorder if they
need to be evaluated for any of the etiologies of bronchiectasis, such as tests
for RA, SS, and alpha-one antitrypsin.
• Sputum culture may be necessary when trying to evaluate for MAC or
other mycobacterial causes of bronchiectasis. Sputum culture may also be
helpful for management of acute infectious exacerbations of
bronchiectasis.
Imaging
• Chest CT is the diagnostic imaging study of choice for conrming the diagnosis of bronchiectasis.
• Plain chest x-ray may show ndings consistent with bronchiectasis (such as
dilated bronchioles), but CT is necessary to conrm the diagnosis.
239
A Chest X-ray revealed clear lung elds. b High-resolution CT image through the
lungs at the level of bronchus shows right lower lobe and lingular bronchiectasis.
[Toyoda M, Yokomori H, Kaneko F, Yoshida H, Takahashi A, Hoshi K, Takeuchi H,
Tahara K, Kondo H, Motoori T. Hepatic granulomas as primary presentation of
Mycobacterium avium infection in an HIV-negative, nonimmunosuppressed patient.
original.