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31 G oiter
• Goiters with associated hyperthyroidism: These are usually associated
with Graves’ disease. These patients need to have their primary disease
process treated. Goiters associated with Graves’ will often become smaller
owing to treatment of the Graves’.
• Any goiter or thyroid nodule that has features or ndings concerning for
malignancy should have a ne needle aspiration (FNA) biopsy performed.
• Radioiodine ablation works best in large, hyperfunctioning (hyperthyroid),
multinodular goiters. In this setting there can be a 30–40% reduction in the
size of the goiter.
Disease Course
• Goiters usually grow slowly.
• Most will continue to increase in size over time, but a minority may remain
stable in size.
Related Evidence
467
Papers of particular interest have been highlighted as:
** Of key importance
Practice Guideline
Chen AY, Bernet VJ, Carty SE, Davies TF, Ganly I, Inabnet WB 3rd, Shaha AR;
Surgical Affairs Committee of the American Thyroid Association. American
Thyroid Association statement on optimal surgical management of goiter. Thyroid.
2014 Feb;24(2):181-9. https://doi.org/10.1089/thy.2013.0291. Epub 2014 Jan 20.
PubMed PMID: 24295043. http://www.ncbi.nlm.nih.gov/pubmed/24295043 **
Gharib H, Papini E, Paschke R, Duick DS, Valcavi R, Hegedüs L, Vitti P; AACE/
AME/ETA Task Force on Thyroid Nodules. American Association of Clinical
Endocrinologists, Associazione Medici Endocrinologi, and EuropeanThyroid
Association Medical Guidelines for Clinical Practice for the Diagnosis and
Management of Thyroid Nodules. Endocr Pract. 2010 May-Jun;16 Suppl 1:1-43.
https://doi.org/10.4158/10024.GL. PubMed PMID: 20497938. http://www.ncbi.
nlm.nih.gov/pubmed/20497938 **
468
C. J. Rees et al.
Meta-Analysis
Malboosbaf R, Hosseinpanah F, Mojarrad M, Jambarsang S, Azizi F.Relationship
between goiter and gender: a systematic review and meta-analysis. Endocrine.
2013 Jun;43(3):539-47. https://doi.org/10.1007/s12020-012-9831-8. Epub
2012 Dec 14. Review. PubMed PMID: 23238875. http://www.ncbi.nlm.nih.
gov/pubmed/23238875
Review
Carlé A, Krejbjerg A, Laurberg P. Epidemiology of nodular goitre. Inuence of
iodine intake. Best Pract Res Clin Endocrinol Metab. 2014 Aug;28(4):465-79.
https://doi.org/10.1016/j.beem.2014.01.001. Epub 2014 Jan 10. Review. PubMed
PMID: 25047199. http://www.ncbi.nlm.nih.gov/pubmed/25047199 **
Fiore E, Tonacchera M, Vitti P.Inuence of iodization programmes on the epidemi-
ology of nodular goitre. Best Pract Res Clin Endocrinol Metab. 2014
Aug;28(4):577-88. https://doi.org/10.1016/j.beem.2014.04.002. Epub 2014 May
14. Review. PubMed PMID: 25047207. http://www.ncbi.nlm.nih.gov/
pubmed/25047207
Rago T, Vitti P.Diagnostic role of ultrasound and elastosonography in nodular goi-
ter. Best Pract Res Clin Endocrinol Metab. 2014 Aug;28(4):519-29. https://doi.
org/10.1016/j.beem.2014.02.003. Epub 2014 Mar 20. Review. PubMed PMID:
25047203. http://www.ncbi.nlm.nih.gov/pubmed/25047203
Watt T, Cramon P, Frendl DM, Ware JE Jr; ThyQoL Group. Assessing health- related
quality of life in patients with benign non-toxic goitre. Best Pract Res Clin
Endocrinol Metab. 2014 Aug;28(4):559-75. https://doi.org/10.1016/j.
beem.2014.01.009. Epub 2014 Jan 28. Review. PubMed PMID: 25047206.
http://www.ncbi.nlm.nih.gov/pubmed/25047206
Sørensen JR, Hegedüs L, Kruse-Andersen S, Godballe C, Bonnema SJ.The impact
of goitre and its treatment on the trachea, airow, oesophagus and swallowing
function. A systematic review. Best Pract Res Clin Endocrinol Metab. 2014
Aug;28(4):481-94. https://doi.org/10.1016/j.beem.2014.03.002. Epub 2014 Apr
4. Review. PubMed PMID: 25047200.
pubmed/25047200 **
Medeiros-Neto G, Camargo RY, Tomimori EK.Approach to and treatment of goi-
ters. Med Clin North Am. 2012 Mar;96(2):351-68. https://doi.org/10.1016/j.
mcna.2012.01.010. Review. PubMed PMID: 22443980. http://www.ncbi.nlm.
nih.gov/pubmed/22443980
Bahn RS, Castro MR.Approach to the patient with nontoxic multinodular goiter. J
Clin Endocrinol Metab. 2011 May;96(5):1202-12.
jc.2010-2583. Review. PubMed PMID: 21543434. http://www.ncbi.nlm.nih.
gov/pubmed/21543434
http://www.ncbi.nlm.nih.gov/
https://doi.org/10.1210/
31 G oiter
469
Luster M, Verburg FA, Scheidhauer K.Diagnostic imaging work up in multi- nodular
goiter. Minerva Endocrinol. 2010 Sep;35(3):153-9. Review. PubMed PMID:
20938418. http://www.ncbi.nlm.nih.gov/pubmed/20938418
Tonacchera M, Pinchera A, Vitti P. Assessment of nodular goitre. Best Pract Res
Clin Endocrinol Metab. 2010 Feb;24(1):51-61. https://doi.org/10.1016/j.
beem.2009.08.008. Review. PubMed PMID: 20172470. http://www.ncbi.nlm.
nih.gov/pubmed/20172470 **
Moalem J, Suh I, Duh QY.Treatment and prevention of recurrence of multinodular
goiter: an evidence-based review of the literature. World J Surg. 2008
Jul;32(7):1301-12. https://doi.org/10.1007/s00268-008-9477-0. Review.
PubMed PMID: 18305998. http://www.ncbi.nlm.nih.gov/pubmed/18305998
Portereld JR Jr, Thompson GB, Farley DR, Grant CS, Richards ML. Evidence-
based management of toxic multinodular goiter (Plummer's Disease). World J
Surg. 2008 Jul;32(7):1278-84.
https://doi.org/10.1007/s00268-008-9566-0.
Review. PubMed PMID: 18357484. http://www.ncbi.nlm.nih.gov/pubmed
White ML, Doherty GM, Gauger PG.Evidence-based surgical management of sub-
sternal goiter. World J Surg. 2008 Jul;32(7):1285-300. https://doi.org/10.1007/
s00268-008-9466-3. PubMed PMID: 18266028. http://www.ncbi.nlm.nih.gov/
pubmed/18266028
Kotwal A, Priya R, Qadeer I.Goiter and other iodine deciency disorders: A sys-
tematic review of epidemiological studies to deconstruct the complex web. Arch
Med Res. 2007 Jan;38(1):1-14. Review. Erratum in: Arch Med Res. 2007
Apr;38(3):366. PubMed PMID: 17174717. http://www.ncbi.nlm.nih.gov/
pubmed/17174717
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy: “Goiter”[Mh] OR “goiter”[tiab] OR “goiters”[tiab]
Chapter 32
Heart Failure
CharlesV.Pollack,Jr. andVictoriaG.Riese
Name andSynonyms
Heart Failure; Congestive Heart Failure
Incidence/Epidemiology
• Heart failure is a clinical state in which perfusion of tissues and/or venous
return to the heart is impaired because of inadequate pumping functionality of
the cardiac muscle, or when perfusion can only be maintained from an abnormally high diastolic volume.
• There are multiple ways to characterize heart failure:
• Systolic vs diastolic
• In systolic failure, the ventricles are unable to contract normally.
• In diastolic failure, the ventricles fail to relax and ll properly.
• Patients who have both dilated and hypertrophic ventricles may have
both systolic and diastolic failure
• Right-sided vs left-sided
• Left-sided heart failure leaves blood in the lungs and therefore usually
presents as pulmonary edema.
C.V. Pollack,Jr. ()
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_32
471© Springer Nature Switzerland AG 2019
472
• Right-sided heart failure leaves blood in the periphery and therefore
usually presents with edema and liver congestion.
• Long-standing heart failure usually manifests ndings of both left- and
right-sided failure
• Acute vs chronic
• Acute heart failure usually develops immediately after a large myocardial infarction or rupture of a heart valve.
• Chronic heart failure develops more slowly and is often due to systemic
hypertension, dilated cardiomyopathy, or multivalvular disease.
Chronic heart failure
Acute heart failure
Heart failure with reduced
LVEF (also referred to as
systolic heart failure or heart
failure with reduced systolic
function)
Heart failure with preserved
LVEF (also referred to as
diastolic heart failure or heart
failure with preserved systolic
function)
C. V. Pollack, Jr. and V. G. Riese
Chronic heart failure is a clinical syndrome characterized by complex and
variable symptoms and signs. The cardinal manifestations of heart failure
are dyspnea and fatigue, which may limit exercise tolerance, and fluid
retention, which may lead to pulmonary congestion and peripheral edema.
Chronic heart failure is often punctuated by acute decompensation.
New onset of decompensated heart failure or decompensation of chronic,
established heart failure with symptoms sufficient to warrant hospitalization.
Cardiac dysfunction can be related to systolic or diastolic dysfunction, to
abnormalities in cardiac rhythm, or to preload and after-load mismatch.
A clinical syndrome characterized by signs and symptoms of heart failure
and reduced LVEF. Most commonly associated with left ventricular
chamber dilation.
A clinical syndrome characterized by signs and symptoms of heart failure
with preserved LVEF. Most commonly associated with a nondilated left
ventricle. May be the result of valvular disease or other causes.
Classication of the heart failure syndrome. Heart failure is often classied as heart
failure with abnormal systolic function versus heart failure with preserved systolic
function. These classications often consider normal systolic function and normal
ejection fraction to be the same. Heart failure with preserved left ventricular ejection fraction (LVEF) is variably dened as an LVEF greater than 40%, greater than
45%, or greater than 50%. Heart failure with preserved LVEF is not a distinct condition, but rather a syndrome with numerous possible causative or comorbid conditions, including hypertension, diabetes mellitus, vascular stiffness, renal impairment,
and atrial brillation. There is no current consensus about nomenclature for heart
failure with preserved systolic function. The clinical classication of patients with
acute decompensated heart failure continues to evolve and reects ongoing changes
in the understanding of the pathophysiology of this syndrome. Worsening renal
function, persistent neurohormonal activation, and progressive deterioration in
myocardial function all seem to play a role. Decompensation also commonly occurs
without a fundamental worsening of underlying cardiac structure or function.
Failure to adhere to prescribed medications or an inadequate medical regimen may
32 Heart Failure
473
lead to hospitalization without a worsening of underlying circulatory function.
Other descriptive terms used for heart failure include right- and left-sided heart
failure referring to syndromes presenting predominately with congestion of the
systemic or pulmonary vascular beds. Mild, moderate, and severe heart failure are
used as clinical symptomatic descriptions instead of or in addition to NewYork
Heart Association functional classication. [Kittleson MM, Fonarow GC.Clinical
Syndromes of Acute and Chronic Heart Failure. In: Colucci WS, editor. Atlas of
heart failure, 5th ed. Philadelphia: Current Medicine Group; 2008. 344 p. ISBN:
1-57340-261-3] Caption adapted from original
• Black males have the highest incidence of heart failure per capita.
US heart failure deaths by age, sex, and race. Among all age groups, black men
experienced the highest rates of heart failure death. In all age groups except ages 75
to 84 years, black women experienced the next highest rates of heart failure death
followed by white men. In the age group of 75 to 84 years, white men had higher
rates of heart failure–‐related death than black women. In all age groups, white
women experienced the least heart failure–related mortality (American Heart
Association: Heart Disease and Stroke Statistics —2007 Update.. Dallas: American
Heart Association; 2007). [Parikh NI, Vasan RS.The Epidemiology of Heart Failure.
In: Colucci WS, editor. Atlas of heart failure, 5th ed. Philadelphia: Current Medicine
Group; 2008. 344 p. ISBN: 1-57340-261-3] Caption from original
• There is a “heart failure belt” across middle America
474
C. V. Pollack, Jr. and V. G. Riese
Geographic heterogeneity in US heart failure death rates. Numbers reect state‐spe-
cic, age-adjusted death rates per 100,000 persons for men and women > 65 years
of age for the period from 1990 to 1996. The 13 highlighted states have the highest
heart failure death rates. Possible explanations for the apparent “heart failure belt”
across middle‐America are 1) higher prevalence of hypertension and myocardial
infarction in the belt, 2) varying access to early diagnosis, 3) regional differences in
congestive heart failure treatment, or 4) differing practices of diagnostic coding for
heart failure in death certicates (Changes in mortality from heart failure: United
States, 1980‐1995. MMWR Morb Mortal Wkly Rep. 1998; 47:633 -637). [Parikh
NI, Vasan RS.The Epidemiology of Heart Failure. In: Colucci WS, editor. Atlas of
heart failure, 5th ed. Philadelphia: Current Medicine Group; 2008. 344 p. ISBN:
1-57340-261-3] Caption from original
• Heart failure is classied by multiple scales, but the most commonly used is
from the NewYork Heart Association (NHYA) and is symptom-driven.
Class I No limitation of daily physical activity.
Slight limitation of activity. Comfortable at rest but ordinary physical activity produces fatigue and
Class II
dyspnea.
Class
Marked limitation of physical activity. Fatigue and dyspnea results from minimal physical activity.
III
Class IVSevere physical limitation. Dyspnea at rest and unable to carry on physical activity without severe
symptoms.
New York Heart Association classication of heart failure. The functional classication of patients with congestive heart failure developed by the New York Heart
Association is based on the amount of activity tolerated by patients before the onset
of symptoms. Despite the limitations of this subjective classication, it is a useful
32 Heart Failure
475
descriptive system and remains the standard by which patients with heart failure are
compared (Boston: Little, Brown; 1964; 114). [O'Connor C, Tuman K.Chapter 7.
In: Miller RD, Reves JG, editors. Atlas of Anesthesia: Cardiothoracic Anesthesia,
Volume 8, 1e. Philadelphia: Current Medicine Group; 1999. 256 p. ISBN: 0-44307974-9] Caption from original
Differential Diagnosis
• The differential diagnosis of heart failure is to some extent dependent upon
the type of failure being manifest. In general, the differential includes:
• Acute exacerbation of COPD
Differential diagnosis between new onset heart failure and acute exacerbation of
chronic heart failure with timing of imaging and consideration of precipitating
pathophysiology. [Wild D, Herzog E, Aziz E, Kukin M.Pathway for the Management
of Heart Failure Complicating Acute Coronary Syndrome. In: Herzog E, Chaudhry
F, editors. Echocardiography in Acute Coronary Syndrome [Internet]. London:
Springer London; 2009 [cited 2015 Jun 4]. p.365–76. Available from: http://link.
springer.com/10.1007/978-1-84882-027-2_25] Caption from original
476
• Pulmonary embolism
• Pneumonia
• Acute renal failure
• Noncardiogenic pulmonary edema
• Myocardial infarction
• Respiratory failure
Pathophysiology andEtiology
C. V. Pollack, Jr. and V. G. Riese
Pathophysiology of heart failure. [Khan MG.Heart Failure. Cardiac Drug Therapy,
8e [Internet]. Totowa, NJ: Humana Press; 2015 [cited 2015 Jun 4]. p. 369–421.
Available from: http://link.springer.com/10.1007/978-1-61779-962-4_12] Caption
from original
32 Heart Failure
477
Etiologies of heart failure. [Marín-García J.Diagnosis of Heart Failure: EvidenceBased Perspective. Heart Failure [Internet]. Totowa, NJ: Humana Press; 2010 [cited
2015 Jun 4]. p. 353–63. Available from: http://link.springer.com/10.1007/978-1-
60761-147-9_18] Caption from original
• There are many contributing factors to the development of heart failure,
including:
• Increased metabolic demand on the heart, such as:
• Infection
• Anemia
• Other demand for increased cardiac output, such as:
• Pregnancy
• Thyrotoxicosis
• Sepsis
• Hypovolemia
• Physical demand on the heart, such as:
• Hypertension
• Endocarditis
• Pulmonary embolism
• Salt and volume retention