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PUBLISHED FEBRUARY 20, 2013

CARDIOVASCULAR March 2023
In This Issue
Cardiac Asthma: Not Your Typical
Digital Magazine
Asthma Archives
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Mark H. J. Litzinger, BSc, BSc Pharm, RPh
Clinical Instructor of Pharmacy Practice
School of Pharmacy
Philadelphia College of Osteopathic Medicine–Georgia Related CE
Suwanee, Georgia
$6.97 Per CE Exam or $59 for 12 Lessons
Julia K. N. Aluyen, PharmD
Clinical Approaches to the Management
Ramon Cereceres, Jr., PharmD of Obesity

Ashley N. Feik, PharmD Candidate

Medication-Focused Overview of the
Katherine E. Iltis, PharmD 2022 AHA/ACC/HFSA Heart Failure
Management
Criselle R. Perez, PharmD
University of the Incarnate Word View More CE
Feik School of Pharmacy
San Antonio, Texas
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Triple Therapy for a Cardiac Indication in
Monica Litzinger BSc, BSc Pharm, RPh a Veteran Population
Outpatient Pharmacist
Suwanee, Georgia An Update on Smoking Cessation

Age Affects Gender-Related Heart

Attack
US Pharm. 2013;38(2):HS-12-HS-18.
ABSTRACT: Cardiac asthma is a condition secondary to heart
failure that is marked by dyspnea, wheezing, cough, frothy or
bloody sputum, and rales.1 These symptoms usually occur at
night and are more prevalent in the elderly population. Because
its symptoms are similar to those of bronchial asthma, cardiac
asthma is often misdiagnosed. However, an accurate
diagnosis is imperative because treatments for the two
conditions differ, and incorrect treatment can exacerbate
cardiac asthma.2 IV furosemide, nitroglycerin, and morphine
are used for the acute treatment of cardiac asthma.3 If the
patient is hypoxic, supplemental oxygen also may be used.3
Outpatient medication regimens focus on treating heart failure.

In 1833, the physician James Hope coined the term cardiac

asthma to describe the inadequate oxygenation of blood and
the sensation of wanting breath resulting from it.1,4 Since
then, cardiac asthma has been better deHned, but there is still
much confusion surrounding its diagnosis. In fact, cardiac
asthma is commonly mistaken for bronchial asthma since
both conditions have similar symptoms and timing.5
However, the primary mechanisms that cause these
symptoms are dissimilar.5 By focusing on the subtle
differences in symptoms and test results, providers can more
easily differentiate the disorders.

Cardiac asthma involves paroxysms of dyspnea

(breathlessness) and wheezing that often occur during the
night as a result of congestion in the lungs secondary to heart
failure (HF).4-6 In bronchial asthma, symptoms are due to an
inOammatory process, rather than a cardiac process. It is
important to correctly identify the etiology of the patient’s
symptoms because treatment differs for these disorders, and
incorrect treatment of cardiac asthma may exacerbate the
condition.

Epidemiology
Since cardiac asthma and bronchial asthma have differing
etiologies, it is pertinent to discuss epidemiological
differences because the disease processes dictate the
populations most affected. It makes sense that HF would be
more prevalent in the elderly, given the disease progression.
The American Heart Association’s 2011 update reported that
HF has an incidence of 10 per 1,000 population in people
older than 65 years, and the incidence of new HF events is at
least 15 per 1,000.7 The incidence of new HF events can
exceed 65 per 1,000 population in people older than 85 years,
supporting a direct relationship between HF and age.7
Prevalence rates of HF in patients aged 20 to 30 years and
those aged 80 years and older (0.3% and 11.5%, respectively)
also support this relationship.7

The incidence and prevalence of cardiac asthma are unclear,

owing to insuWcient data from published studies. In a 2007
study, the incidence of cardiac asthma in elderly patients was
35%, versus the 10% to 15% incidence seen in younger
patients in earlier studies.8 Trends noted in the cardiac
asthma group (in the 2007 study) were increased use of
tobacco products and diagnosis of chronic obstructive
pulmonary disease.8 One factor not considered in this study
was whether the wheezing was cardiac or pulmonary in
origin, a distinction that could affect incidence results.8

Asthma is more prevalent in children than in adults.

According to the 2009 CDC National Health Statistics report,
9.6% of children and 7.7% of adults had asthma.9 Boys were
found to have a higher prevalence than girls, whereas in
adulthood the opposite was true.9 In patients aged 85 years,
asthma prevalence was approximately 5% in both men and
women.9

The epidemiological differences between cardiac asthma and

bronchial asthma reveal that cardiac asthma is more likely to
occur in an older adult population, whereas bronchial asthma
is more likely in children. Nevertheless, more research is
necessary to clarify the incidence and prevalence of cardiac
asthma.

Pathophysiology
In congestive heart failure (CHF), the heart’s inability to pump
blood out of the left ventricle results in excess Ouid in the
pulmonary circulation.10 Pulmonary congestion is the
consequence of Ouid being pushed into the alveolar lumen.
Cardiac asthma may be associated with bronchiolar
pathology, rather than simply the accumulation of alveolar
Ouid.

Not only does the presence of Ouid in the lungs make

breathing diWcult, it can cause asthmalike symptoms as well.
The wheezing experienced by CHF patients may be due to a
narrowing or obstruction of the bronchioles rather than
simply to pulmonary congestion. Various studies have
identiHed bronchial hyperreactivity as the mechanism behind
cardiac asthma.11-13 Patients in these studies inhaled either
acetylcholine or methacholine (cholinergic agonists).
Compared with patients without cardiac asthma symptoms,
those with symptoms demonstrated greater airway narrowing
in response to the inhaled drug. The mechanism by which this
narrowing occurs is not fully understood. Another study
suggested that downregulation of beta2 receptors resulting
from excessive adrenergic stimulation might cause
bronchoconstriction in HF patients.14 Either mechanism is
detrimental and undesirable in patients already experiencing
pulmonary congestion.

Cardiac asthma may be better attributed to bronchial

anatomy. The bronchial blood supply involves a separate
vascular system from that which supplies the alveoli. Similar
to the mechanism of Ouid buildup in the alveoli, the blood
supply to the bronchioles may exhibit Ouid buildup. Two
hypotheses exist regarding the pathophysiology behind this:
theory A and theory B (FIGURE 1).10 Theory A hypothesizes
that an increase in blood Oow to the bronchial circulation may
produce edema in the interstitial space, thereby squeezing
the bronchiolar lumen.10 Conversely, theory B posits that
certain pathological changes in HF, including pulmonary
edema (PE), may compete for interthoracic space,
compressing the entire airway structure and the bronchiole
wall.10

The pathologic cause of cardiac asthma is not deHnitively

explained. ReOex bronchoconstriction involving the vagus
nerve has been suggested. Increased pulmonary vascular
pressure may stimulate afferent nerve endings, causing reOex
narrowing of large and small airways.15 ReOex
bronchoconstriction, in addition to edema and hyperreactivity,
can exponentially reduce breathing capability in CHF patients.
The pathophysiology of cardiac asthma may incorporate a
combination of mechanisms, creating a number of treatment
challenges. The absence of inOammation is the major
difference between cardiac asthma and bronchial asthma,
even though the symptoms are similar.

Clinical Presentation and Differential Diagnosis

As noted earlier, cardiac asthma involves symptoms of
airOow obstruction that are due to HF.16 In most cases, the
clinical presentation includes severe dyspnea, cough, frothy
or watery sputum, and rales, but the most signiHcant
symptom indicative of cardiac asthma is wheezing.4,6 These
symptoms are more prevalent in elderly patients.4

Cardiac asthma often is characterized by abrupt waking from

sleep caused by sudden, severe episodes of dyspnea.4 In a
typical attack, the symptoms generally subside after the
patient sits upright for 20 to 30 minutes, after which he or she
may be able to return to bed without needing medication.6 In
severe cases, the patient may experience recurrent episodes
in a single night and have cyanosis (blue or purple
discoloration of the skin), cold sweats, blood-tinged sputum,
and Ouid buildup in the lungs.4,6 Cardiac asthma is diWcult to
diagnose because its symptoms are similar to those of
bronchial asthma. TABLE 1 compares symptoms and
diagnosing strategies for asthma, HF, and cardiac asthma.6,16-
22

4are 16 4patients 4patients

There
Asthma
and
exclusively
disease,
that
heart.
coughing,
to bronchodilators.
symptoms
can Severe
often
be
cardiac
aand
at
seen
fewnight
is
wheezing.
cardiac
tend
subtle
triggered
asthma
upon
when
to asthma
chest
differences
worsen
the
by
Unlike
x-ray,
allergens
patient
typically
atasthma,
night;
usually
whereas
between
is or
lying
involves
cardiac
have
some
however,
asthma
cardiac
in an
bed.
other
asthma
PE,
enlarged
cardiac
asthma
which
Because
precipitating
attacks
causes
heart
asthma
and
have
ofoccur
true
preexisting
(cardiomegaly)
adyspnea,
factor
responds
normal-sized
asthma.
almost
(TABLE
heart
poorly
1),

Another distinction between the two disorders is circulation

time (how long it takes for blood to Oow from one part of the
body to another).16 In the past, circulation time typically was
measured by injecting sodium dehydrocholate into an arm
vein and measuring how long it took to produce a bitter taste
on the tongue (arm-to-tongue circulation).23 However, this
test’s unreliability caused it to be replaced by other
techniques, including radionuclide angiocardiography, CT, and
MRI.23 Circulation time is believed to be prolonged in HF
patients; therefore, measurement may provide crucial
information for differentiating between pulmonary and
cardiac disorders.16,23

Since cardiac asthma stems from a heart problem, it can be

diWcult to distinguish its symptoms from those of HF. The
three cardinal symptoms of HF are dyspnea, fatigue, and Ouid
retention; the presence of wheezing is diagnostic of cardiac
asthma.18 Chronic HF often is associated with decreased
forced expiratory volume in 1 second (FEV1); however, in one
study, cardiac asthma patients (deHned as having CHF and
wheezing) exhibited lower FEV1 values than patients with
CHF alone.8,16 Chest x-ray is useful for conHrming the
presence of pulmonary congestion as well as for identifying
cardiomegaly, which also indicates a heart disorder.4,15
Cardiomegaly often occurs in cardiac asthma patients, but
not to the same degree as in strictly HF patients.8 Physical
examination and lung auscultation may reveal rales, which
are attributable to PE, but the best way to diagnose HF is to
obtain a two-dimensional echocardiogram with Doppler,
which can identify structural abnormalities and reduced
ejection fraction (EF).4,8,19

Treatment
Currently, no well-deHned treatment plans exist for cardiac
asthma in the acute or chronic setting. Discussions of cardiac
asthma management target the pathophysiology of the
underlying condition (i.e., PE and HF). The use and eWcacy of
bronchodilators such as albuterol and ipratropium, which are
used to relieve symptoms of bronchial asthma, have not been
established in cardiac asthma.8

Traditional medications used in the acute treatment of

cardiac asthma include furosemide, morphine, and nitrates
(TABLE 2).3,4,17 Supplemental oxygen, noninvasive ventilation
(NIV), and proper positioning of the patient also are
important.3 Each treatment has a unique beneHt and may
work synergistically with other treatments. Because patients
presenting with an acute episode of cardiac asthma usually
are hypoxic, the initial use of oxygen and/or NIV is
recommended and has been shown to decrease
mortality.24,25 If the patient shows no signs of hypoxia,
oxygen and NIV are not recommended. As mentioned
previously, a patient who awakens at night with dyspnea may
alleviate symptoms by remaining awake for 20 to 30 minutes.
Proper positioning, in which the patient stands erect or sits
upright with feet hanging off the side of the bed, will result in
decreased venous return.26,27 The amount of blood to the
bronchioles is thereby lessened, interstitial-space edema is
reduced, and the squeezing effect of the bronchiolar lumen
described in theory A is diminished.3,4,26,27

Table2.AgentsUsedinAcuteCardiacAsthma
Drug Dosage MOA SideEffects
Furosemide(IV)40mgandtitrate Inhibitssodiumand Hypotension,electrolyte
toeffect chloridereabsorptionindisturbances,gout
ascendingloopofHenleexacerbations,reversible
anddistaltubules hearingloss,worsening
renalfunction

Nitroglycerin(I)5mcg/minand Vasodilatoryeffectsvia Hypotension,headache,

titratetoeffect; NOradicalactivation abdominalpain
max200mcg/minofGC
Morphine(IV) 1-3mgand StimulatesmureceptorsRespiratorydepression
sedation,itching
GC:guanylateeyelase;max:maxmin, МОЛ: mechanionofactionsNOnitricoxide

Source:References25-29.

Patients experiencing an acute cardiac asthma episode likely

will require Ouid removal. In such cases, gradual diuresis
using a loop diuretic is warranted. Furosemide, which acts at
the ascending portion of the loop of Henle and at the distal
tubule, inhibits the reabsorption of sodium and chloride and
causes diuresis.25-27 This improves symptoms by reducing
preload in the heart. Symptomatic improvement in patients
with pulmonary congestion is seen with an initial
recommended furosemide dosage of 40 mg IV.25-27 The dose
may be increased based on clinical response but must
remain gradual to avoid hypotension, electrolyte
disturbances, gout exacerbations, hearing loss (reversible),
and worsening renal function.24-27

Some patients may exhibit persistent pulmonary congestion

despite aggressive diuresis. In these instances, an IV nitrate
(e.g., nitroglycerin) may be used adjunctively in both
hypertensive and normotensive patients. Acting as a
venodilator, nitroglycerin will lessen the pressure in the left
ventricle, thereby reducing pulmonary congestion.25,26,28
Nitroglycerin should be started at a dosage of 5 mcg/min; it
may be titrated to 200 mcg/min. Nitroglycerin dosing beyond
200 mcg/min is not recommended, and the patient requiring
it should be considered a nonresponder.25,26,28 Some side
effects associated with nitroglycerin use are hypotension,
headache, and abdominal pain.

IV morphine ameliorates symptoms in patients with

pulmonary congestion.4,24 Morphine used in the setting of
cardiac asthma enables easier breathing and reduces a
patient’s anxiety level during the episode.4,25,26,29 The
mechanism by which easier breathing occurs is believed to
involve venodilation and reduction in preload.4,25,26,29 The
morphine dosage commonly used is 1 to 3 mg IV every 5
minutes until relief occurs without inducing respiratory
depression.24-26,29

Once the acute cardiac asthma episode is resolved, HF

therapy should be initiated or optimized to prevent future
occurrences. The use of ACE inhibitors and beta-blockers in
HF patients is recommended to decrease morbidity and
mortality rates.24,25 The continuance of diuretics postepisode
will help maintain a normal volume status in this patient
population and prevent future cardiac asthma occurrences.
Digoxin, although not shown to reduce mortality, may be used
to improve congestive symptoms in patients with HF.
Additional information about chronic HF management,
including anticoagulation, amiodarone use, alternative
treatments, dosing, and so on, may be found in current HF
practice guidelines.24,25

Conclusion
The incidence of cardiac asthma will likely increase as
knowledge about diagnosis and treatment improves. Current
management of cardiac asthma focuses on controlling the
underlying HF and PE.5 Recognition of cardiac asthma and
recommendations concerning appropriate treatment can
greatly reduce disease occurrence and signiHcantly improve
the patient’s quality of life.4,7 Pharmacists can make a
signiHcant impact on the diagnosis and progression of this
little-known disease. Counseling patients who are at risk for
cardiac asthma and who present with related issues will
enhance proper diagnosis. Pharmacists familiar with
treatment options and optimization of therapy for
concomitant diseases can better manage their patients’
symptoms, improve quality of life, and help slow the
progression of this disorder.

REFERENCES
1. Hope J. A Treatise on the Diseases of the Heart and Great Vessels. Philadelphia,
PA: Haswell and Johnson; 1842:346-365.
2. Ray P, Birolleau S, Lefort Y, et al. Acute respiratory failure in the elderly: etiology,
emergency diagnosis and prognosis. Crit Care. 2006;10:R82.
3. Sabatine M. Pocket Medicine: The Massachusetts General Hospital Handbook of
Internal Medicine. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:15.
4. Lombardo TA, Harrison TR. Cardiac asthma. Circulation. 1951;4:920-929.
5. Perlman F. Asthma and cardiac dyspnea; a differential diagnosis. Calif Med.
1951;75:199-201.
6. Hamilton JG. Cardiac asthma. Br Med J. 1955;1:39-41.
7. Roger VL, Go AS, Lloyd-Jones DL, et al. Heart disease and stroke statistics—2011
update: a report from the American Heart Association. Circulation. 2011;123:e18-
e209.
8. Jorge S, Becquemin MH, Delerme S, et al. Cardiac asthma in elderly patients:
incidence, clinical presentation and outcome. BMC Cardiovasc Disord. 2007;7:16.
9. Akinbami LJ, Moorman JE, Liu X. Asthma prevalence, health care use, and
mortality: United States, 2005-2009. Natl Health Stat Report. 2011;Jan 12:1-14.
10. Ceridon M, Wanner A, Johnson BD. Does the bronchial circulation contribute to
congestion in heart failure? Med Hypotheses. 2009;73:414-419.
11. Brunnée T, Graf K, Kastens B, et al. Bronchial hyperreactivity in patients with
moderate pulmonary circulation overload. Chest. 1993;103:1477-1481.
12. Nishimura Y, Maeda H, Hashimoto A, et al. Relationship between bronchial
hyperreactivity and symptoms of cardiac asthma in patients with non-valvular left
ventricular failure. Jpn Circ J. 1996;60:933-939.
13. Nishimura Y, Yu Y, Kotani Y, et al. Bronchial hyperresponsiveness and exhaled
nitric oxide in patients with cardiac disease. Respiration. 2001;68:41-45.
14. Borst M, Beuthien W, Schwencke C, et al. Desensitization of the pulmonary
adenylyl cyclase system: a cause of airway hyperresponsiveness in congestive
heart failure? J Am Coll Cardiol. 1999;34:848-856.
15. Snashall PD, Chung KF. Airway obstruction and bronchial hyperresponsiveness
in left ventricular failure and mitral stenosis. Am Rev Respir Dis. 1991;144:945-956.
16. Tanabe T, Kanoh S, Moskowitz WB, Rubin BK. Cardiac asthma: transforming
growth factor-ß from the failing heart leads to squamous metaplasia in human
airway cells and in the murine lung. Chest. 2012;142:1274-1283.
17. National Asthma Education and Prevention Program. Expert Panel Report 3:
Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National
Heart, Lung, and Blood Institute; 2007. NIH Publication No. 08-5846.
18. Hunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into
the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure
in Adults: a report of the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines: developed in collaboration
with the International Society for Heart and Lung Transplantation. Circulation.
2009;119:e391-e479.
19. Jessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/AHA
Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of
the American College of Cardiology Foundation/American Heart Association Task
Force on Practice Guidelines: developed in collaboration with the International
Society for Heart and Lung Transplantation. Circulation. 2009;119:1977-2016.
20. Moore TD, Anderson JR. Heart failure. In: Linn WD, Wofford MR, O’Keeffe ME,
Posey LM, eds. Pharmacotherapy in Primary Care. New York, NY: McGraw-Hill
Medical; 2009.
21. Kusumoto FM.Cardiovascular disorders: heart disease. In: McPhee SJ, Hammer
GD, eds. Pathophysiology of Disease: An Introduction to Clinical Medicine. 6th ed.
New York, NY: McGraw-Hill Medical; 2010.
22. American Heart Association. Ejection fraction heart failure measurement.
www.heart.org/HEARTORG/Conditions/HeartFailure/SymptomsDiagnosisofHeartFa
ilure/Ejection-Fraction-Heart-Failure-Measurement_UCM_306339_Article.jsp.
Accessed January 23, 2013.
23. Shors SM, Cotts WG, Pavlovic-Surjancev B, et al. Heart failure: evaluation of
cardiopulmonary transit times with time-resolved MR angiography. Radiology.
2003;229:743-748.
24. Nieminen MS, Böhm M, Cowie MR, et al. Executive summary of the guidelines
on the diagnosis and treatment of acute heart failure. Eur Heart J. 2005;26:384-416.
25. Lindenfeld J, Albert NM, Boehmer JP, et al. HFSA 2010 Comprehensive Heart
Failure Practice Guideline. J Card Fail. 2010;16:e1-194.
26. Lexi-Comp Online [database]. Hudson, OH: Lexi-Comp, Inc; 2012.
27. Furosemide. Clinical Pharmacology [database]. www.clinicalpharmacology.com.
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28. Nitroglycerin. Clinical Pharmacology [database].
www.clinicalpharmacology.com. Accessed February 3, 2012.
29. Morphine. Clinical Pharmacology [database]. www.clinicalpharmacology.com.
Accessed February 3, 2012.

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