ttp://www.bsava.

com REVIEW

Coughing in dogs: what is the evidence

for and against a cardiac cough?
L. Ferasin1,* and C. Linney†

*Lumbry Park Veterinary Specialists, Alton, Hampshire, GU34 3HL, UK

†
Willows Veterinary Referral Service, Solihull, West Midlands B90 4NH, UK
1
Corresponding author email: luca.ferasin@cvsvets.com

Cough has been historically reported as a major clinical sign of cardiogenic pulmonary oedema in
dogs. However, recent evidence appears to contradict the traditional dogmatic approach that linked
cough to congestive heart failure in dogs. Here we use a question-based format to introduce and
discuss the modern evidence regarding “cardiac cough” and the interpretation of this important but
often misleading clinical sign.

Journal of Small Animal Practice (2019)

DOI: 10.1111/jsap.12976
Accepted: 5 December 2018

WHAT IS COUGHING? The typical coughing reflex (CR) is characterised by an initial

Luca Ferasin: Cough is a vital defensive physiological func-
tion frequently observed both in people and small animals. The
cough reflex prevents aspiration of foreign or noxious material
and preserves the health of the respiratory system by inducing a
rapid and forceful removal of harmful substances, such as inhaled
foreign particles, pathogens or excessive bronchial secretions
from the upper airways. However, cough is not always a gentle
defensive mechanism. Excessive and inappropriate coughing can
emerge as a primary presenting sign of many airway diseases. It
can also represent an important sign of an underlying disease
that is not strictly associated with the airways, like postnasal drip
syndrome (PNDS) or gastro-oesophageal reflux, and can even
potentially become a harmful sign when it becomes persistent
(Chung 2003). Indeed, once initiated, the cough reflex cannot
be easily interrupted and, due to its typical loud sound during
the explosive expiratory phase, cough is inevitably observed.
When persistent, cough can also affect quality of life by inter-
fering with sleeping, breathing, exercise, eating and drinking.
Approximately one in three people are woken up by a bout of
coughing every year (Janson et al. 2001) and, similarly, many
coughing dogs can keep their owners awake at night, prompt-
ing a visit to the veterinarian. This is especially true of dogs
that might sleep in owners’ bedrooms. Occasionally, cough can
cause syncope, urinary and faecal incontinence, muscle pain and
exhaustion (Ferasin 2013a). The frequent and noticeable pre-
sentation of coughing makes this sign a very common complaint
reported to physicians (Altman & Irwin 2010) and veterinarians
worldwide.
deep inspiration, followed by a rapid and powerful expiratory act
against the closed glottis and finally opening of the glottis, closing
of the nasopharynx and forceful expiration through the mouth,
accompanied by a typical vocalisation caused by the vibration of
the vocal cords. Cough is more frequently evoked by stimulation
of cough receptors in the larynx, trachea and bronchi, whereas
irritation of smaller bronchi, bronchioles and alveoli does not
elicit coughing (Widdicombe 1996, 2001, Chang 1999) (Fig. 1).
A second important defensive mechanism, similar to cough, is
the expiratory reflex (ER). This is induced by stimulation of the
vocal cords or trachea and consists of a forced expiratory effort
against a closed glottis which it is not preceded by a deep inspira-
tion (Widdicombe & Fontana 2006). ER is often observed in
dogs with laryngotracheitis (“kennel cough”) and it sounds like
a “huff ” sound, often described by dog owners as “a bone stuck
in the throat” or “clearing the throat”. The distinction between
CR and ER is important since their physiological functions are
different. True cough will draw air into the lungs to augment the
force of the subsequent expulsive phase, thereby promoting clear-
ance of mucus and foreign material from trachea and bronchi, as
frequently observed in dogs with lower airway disease character-
ised by excessive bronchial secretions which tend to accumulate
in the bronchial lumen (i.e. chronic bronchitis). Conversely, the
ER observed after upper airway irritation will be characterised
by absence of a deep inspiration. The two reflexes may also have
different sensory pathways since one starts with an inspiratory act
and the other with an expiratory effort. Furthermore, the phar-
macological inhibition of the two reflexes is also different since
codeine, at the antitussive dose, has minimal action on the ER
(Widdicombe & Fontana 2006).

Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 1
 L. Ferasin and C. Linney
FIG 1. Anatomical distribution of coughing receptors in the respiratory
system. Cough can be mechanically or chemically stimulated, both
endogenously (e.g. airway secretions, inflammatory mediators), and
exogenously (e.g. aspiration of foreign bodies, smoke, etc). Mechanical
laryngeal stimulation causes an immediate ER (cough without prior
inspiration), whereas stimulation of the respiratory tract distal to the
larynx produces the most typical cough, which is preceded by a deep
inspiration. The more proximal airways (larynx to trachea) are extremely
sensitive to mechanical stimulation, while distal airways are more chemo-
sensitive and less mechano-sensitive. Stimulation of smaller bronchi,
bronchioles and alveoli does not cause cough (Chang 1999, Widdicombe
2001)
CAN YOU BRIEFLY EXPLAIN THE MECHANISM
OF COUGHING?
Luca Ferasin: Cough can be mechanically or chemically stimu-
lated endogenously (bronchial secretions during airway inflam-
mation and inflammatory mediators) or exogenously (inhalation
of foreign body or irritants, such as smoke, dust, etc). However,
it is important to reiterate that there is evidence that irritation
of the smaller airways (small bronchi, bronchioles and alveoli)
does not cause coughing. Furthermore, the luminal flow in the
lower tract of the respiratory tree would be too low to generate
sufficient shear forces to clear airway mucus and debris from such
sites (Widdicombe 2001, Ferasin 2013a). Cough sensitivity and
cough patterns depend on the site and type of stimulation. For
example, stimulation of the larynx causes an immediate expira-
tory effort not preceded by deep inspiration, whereas stimula-
tion of the lower airways produces a more prominent inspiratory
phase. The upper airways are extremely sensitive to mechanical
stimulations, while lower airways are more chemo-sensitive. In
the lung periphery, at the bronchiolar and alveolar level, there
are no reported cough receptors, except for C-fibres – similar to
unmyelinated nociceptors of the somatic nervous system. How-
ever, the role of bronchopulmonary C-fibres in the cough reflex
is controversial and there is considerable evidence to indicate that
these fibres do not evoke cough and may actually inhibit the CR
and ER evoked by other receptors, as demonstrated in anaesthe-
tised animal models (Ferasin 2013a).
2 Journal of Small Animal Practice
In healthy individuals, cough reflex is naturally evoked during
the day without this being even noticed. However, during the
clinical course of a disease, two main mechanisms are responsible
for producing coughing. Firstly, stimulation of sensory recep-
tors directly by airway secretions, foreign bodies and mechanical
compression (e.g. thoracic masses, chest trauma, pleural effu-
sion). Secondly, abnormal increase in cough receptor sensitivity
or reduction of coughing threshold, leads to persistent coughing.
The latter is also referred to as enhanced “cough sensitivity” and
it reflects the complexity of the plasticity of the cough reflex,
which is due to changes in the sensitivity of the neural pathways
regulating cough (Mazzone 2005, Korpas et al. 2007). Cough
disorders are often characterised by a reduction in the thresh-
old for reflex initiation and, as a consequence, the occurrence of
cough in response to stimuli that are normally innocuous. This
explains why coughing often represents a challenging medical
diagnosis and why current therapeutic strategies for the treat-
ment of cough disorders are only moderately effective (Mazzone
2005, Ferasin 2013b).
WHAT IS “CARDIAC COUGH”?
Chris Linney: “Cardiac cough” is defined as a cough that is
associated with cardiac disease, but not necessarily congestive
heart failure. It is important to emphasise that while cough and
heart disease often occur at the same time, they are not neces-
sarily linked and cough may be secondary to another disease
process. Another commonly used definition of cardiac cough
is “cough as the direct result of congestive heart failure (CHF),
in the form of pulmonary oedema”. As a result of two differing
definitions, the following discussion is separated into cardiac
cough without pulmonary oedema and cardiac cough with pul-
monary oedema.
CARDIAC COUGH WITHOUT PULMONARY
OEDEMA
Cardiomegaly with marked left atrial (LA) dilation and main
stem bronchus compression is often cited as a possible cause of
“cardiac cough” but it has been shown that LA dilation and LA
pressure alone may not be sufficient to cause cough secondary to
bronchial compression without concurrent underlying tracheo-
bronchial disease (Ferasin et al. 2013, Ferasin 2017). Indeed,
small dogs commonly develop airway diseases such as tracheal
collapse, chronic bronchitis and bronchomalacia, which will
trigger coughing more frequently if there is also cardiomegaly
(Johnson & Pollard 2010, Ferasin et al. 2013). The mechanism
of “cardiac cough without pulmonary oedema” in medium-to-
large dogs may differ from that observed in small dogs, because
the former rarely develop bronchomalacia and their “cardiac
cough without pulmonary oedema” may most likely be second-
ary to chronic bronchitis, which is also more commonly observed
in older large dogs with concurrent heart disease. It could also
be attributable to any other disease that can stimulate cough-
• © 2019 British Small Animal Veterinary Association
 Coughing in dogs: evidence for cardiac cough
ing receptors such as gastro-oesophageal reflux disease (GORD),
PNDS, neoplasia, laryngeal disorders, etc.
CARDIAC COUGH WITH PULMONARY OEDEMA
There is a division in the literature regarding cough as a con-
sistent feature of CHF. In human medicine, the most current
guidelines for the diagnosis and treatment of acute and chronic
heart failure of the European Society of Cardiology list cough as
a “less typical” sign of CHF (Ponikowski et al. 2016). Part of the
controversy in “cardiac cough” is the difficulty in determining
the true origin of cough; there is dispute over cardiomegaly as
an isolated cause of coughing versus concurrent bronchomalacia
as the main inciting cause in smaller dogs with mitral valve dis-
ease. Cardiac cough secondary to fulminant pulmonary oedema
remains a possible cause, but only in association with peracute
CHF due to flooding of airways and subsequent stimulation of
coughing receptors.
Nevertheless, there are studies reporting cough as an impor-
tant sign of CHF in dogs. A retrospective case series of 369 dogs
with dilated cardiomyopathy (DCM) and CHF reported 64%
of subjects presented with cough, with approximately 90% of
these being medium-to-large dogs (Martin et al. 2009). Further-
more, an investigation of CHF secondary to mitral valve disease
demonstrated 85% of the 366 dogs, with median body weight
7.5 kg, presented with coughing, with approximately half experi-
encing frequent or very frequent episodes of cough at the onset of
CHF (Chetboul et al. 2017). However, there are other plausible,
and perhaps more likely, explanations for the cause of coughing
in these patients than pulmonary oedema alone. Small dogs are
susceptible to concurrent airway disease and this was not actively
excluded as a cause of coughing in these studies. Large dogs with
DCM can present with fulminant oedema or biventricular failure
with associated pleural effusion, which can mechanically stimu-
late coughing receptors.
Historically, and still in some current veterinary textbooks,
“cardiac cough” is considered to be one of the hallmarks of CHF,
but this concept was disputed in a study involving 206 dogs with
mitral valve disease (Ferasin et al. 2013). The historical assump-
tion was also superseded by another study documenting respira-
tory rate as one of the best non-radiographic indicators of CHF
(Schober et al. 2010). While respiratory rate was one of the most
sensitive and specific markers of CHF, this same study also dem-
onstrated a significant increase in coughing in dogs that develop
CHF compared to those that do not, in association with both
mitral valve disease and DCM.
Of interest from human medicine is the low positive predic-
tive value (PPV) of a cough (Morrison et al. 2002). PPV, in this
context, assesses the accuracy of cough as a predictor of CHF
(for instance, cough would be a completely accurate predictor of
CHF if the PPV was 100%). The reported PPV of cough in this
study was only 43%, with a specificity of 61%, highlighting the
frequency of false positives (type 1 error) for CHF as a cause of
cough in humans. As a result, it would seem prudent not to use
cough as the sole indicator for CHF when other features, such as
Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 3
loss of sinus arrhythmia and tachypnoea, are shown to be much
stronger indicators of significant underlying heart disease.
Thoracic radiographs, lung ultrasonography or both may be
useful tools to determine causes of cough in cardiac patients.
Therefore, if cough becomes a feature in a patient with preexist-
ing cardiac disease, further thoracic imaging would be recom-
mended (Ward et al. 2017).
WHAT IS THE CURRENT EVIDENCE ON CARDIAC
COUGH?
Chris Linney: In many veterinary textbooks cough is associated
with cardiogenic pulmonary oedema, especially in dogs. How-
ever, it should also be acknowledged that most dogs that develop
CHF are small geriatric individuals affected by chronic degenera-
tive mitral valve disease (MMVD) and are also predisposed to
concomitant airway disease (Ferasin et al. 2013). Furthermore,
cardiomegaly and, in particular, LA enlargement, can potentially
contribute to inducing coughing in these patients by mechanical
dorsal compression of trachea and main stem bronchi. Although
there seems to be no association between increased LA size and
airway collapse in dogs (Singh et al. 2012), it should be noted
that the high prevalence of bronchomalacia in small older dogs
is likely independent of the high prevalence of MMVD, but the
clinical expression of bronchomalacia, as evidenced by cough-
ing, could be impacted by the underlying cardiac disease and,
more specifically, by the associated cardiomegaly. Cardiomegaly,
interpreted as increased vertebral heart score, has been identi-
fied as a diagnostic indicator for differentiating “cardiac cough”
from “cough of non-cardiac origin” based on thoracic radio-
graphs (Guglielmini et al. 2009). However, the only study spe-
cifically designed to identify a relationship between coughing
and MMVD in dogs did not demonstrate a statistical association
between coughing and CHF identified by radiological evidence
of cardiogenic pulmonary oedema (Ferasin et al. 2013). Indeed,
fluid in the alveolar or interstitial spaces should not trigger cough
in patients with pulmonary oedema unless the amount of fluid
is sufficient to invade the upper airways (i.e. fulminant oedema).
Furthermore, the same study showed that dogs with pulmonary
oedema inevitably presented with dyspnoea/tachypnoea, sup-
porting the concept that isolated coughing (without dyspnoea/
tachypnoea) cannot be a sign of CHF in dogs. Similar obser-
vations have been reported in human heart failure patients, in
which the common signs are lethargy, exercise intolerance, dys-
pnoea and peripheral oedema, while cough is only considered a
minor sign (Watson et al. 2000). Another study that supports
this concept revealed that increased respiratory rate is the most
reliable independent predictor of CHF in dogs (Schober et al.
2010). This same study did show an increase in coughing from
0% of cases in preclinical DCM dogs to 85% of DCM cases with
CHF, and an increase in coughing from 43% of cases in pre-
clinical mitral valve disease to 86% of cases in mitral valve disease
and CHF, potentially supporting the theory that cough and CHF
are intrinsically related. However, the increased occurrence of
cough in this population of dogs could also be explained by more
 L. Ferasin and C. Linney
advanced cardiomegaly in patients with CHF. It should also be
noted that the study published by Ferasin et al. (2013) was a
double-blind controlled study to avoid the bias of the historical
assumption that cough is a major feature of pulmonary oedema.
Conversely, in all other studies, cough as a clinical sign could
have been interpreted as an inclusion criterion for diagnosing
dogs with CHF. Furthermore, some pet owners often interpret
expiratory efforts or gagging reflex as “cough,” which represents
another important misleading factor for the correct evaluation of
this clinical sign.
Moreover, dogs affected by non-cardiogenic pulmonary
oedema resulting from airway obstruction, head trauma, electric
shock or seizures, especially puppies or brachycephalic individu-
als, inevitably present with tachypnoea/dyspnoea, rather than
coughing, thereby providing another line of supporting evidence
that stimulation of lower airways and alveoli is not sufficient to
cause cough (Drobatz et al. 1995, Egenvall et al. 2003). Even
some cardinal studies on prognostic characteristics in dogs with
MMVD do not report coughing as a variable associated with sur-
vival, indicating that coughing, unlike respiratory effort and exer-
cise intolerance, is not an important indicator of CHF severity
in these patients (Borgarelli et al. 2008, Haggstrom et al. 2008).
Lopez-Alvarez et al. (2015) reported that coughing appeared
independently associated with higher hazard of cardiac-related
death. However, in this study, dogs developed cough during the
clinical progress of their disease at a much earlier stage than they
developed overt signs of CHF. Therefore, the explanation that
cough is caused by cardiomegaly and concomitant airway abnor-
malities, rather than pulmonary oedema, appeared to be sup-
ported also by these results (Lopez-Alvarez et al. 2015).
Concomitant LA enlargement and airway disease represents
the higher risk factor for coughing in dogs affected by MMVD
because of the anatomical localisation of airway disease that
is expected to stimulate cough receptors (Fig. 2). Similar co-
morbidities are also reported in humans with CHF (Janssen et
al. 2011, Ferasin et al. 2013). Concomitant cardiomegaly and
airway disease represents the most important morbidity factors
leading to coughing in dogs with MMVD and, since airway dis-
ease is more commonly observed in small geriatric dogs, it can be
FIG 2. Interaction between respiratory disease and increased LA size for
the risk of coughing in dogs with naturally-acquired mitral valve disease
(from Ferasin et al. 2013, modified)
4 Journal of Small Animal Practice
speculated that cardiomegaly is more likely a cause of cough in
patients with preexisting airway disease than in young individu-
als with a healthy respiratory system (Ferasin et al. 2013). Finally
administration of ACE inhibitors in dogs with CHF could
potentially increase the frequency of coughing as is commonly
reported in human patients (Poulose et al. 2016). In conclusion,
the term “cardiac cough” should be considered a misnomer, since
cough always originates from stimulation of coughing receptors
in the airways, both in cardiac and non-cardiac patients.
BASED ON THE ABOVE EVIDENCE HOW CAN
CARDIAC DISEASE CAUSE COUGHING?
Chris Linney: With the mechanisms for cough described above,
it is challenging to describe exactly how cardiac disease might
evoke a cough. Based on pathophysiology, pulmonary oedema
needs to be severe and fulminant to cause coughing and there-
fore should not be considered a definite cause in the majority
of CHF cases with mitral valve disease. For these individuals,
cardiomegaly with mechanical dorsal compression of the trachea
and/or main stem bronchi, possibly in combination with under-
lying airway disease, should be considered. In conditions, such
as DCM, particularly in large dogs such as the Dobermann, ful-
minant pulmonary oedema may be so extensive as to trigger the
cough receptors in the mid-to-higher level bronchial tree. These
patients will often present acutely de-compensated with severe
dyspnoea/tachypnoea and expiratory effort that could be misin-
terpreted as a “soft cough.” Indeed, in the retrospective study by
Martin et al. (2009) the boxer, Dobermann and great Dane con-
stituted 40% of all dogs and these are not commonly reported
breeds for primary airway disease, yet were 64% of all subjects
presented with cough as a clinical feature, similar to results shown
by Schober et al. (2010). For smaller dogs, in which mitral valve
disease is more prevalent, there is also an increased risk of lower
airway disease, and the combination of these together is consid-
ered a likely cause of “cardiac cough.” In contrast, progressive car-
diomegaly may eventually lead to mechanical compression of the
bronchial tree and trachea, either because of global cardiomegaly
or isolated LA dilation, causing activation of cough receptors and
therefore coughing. In this particular situation, it is important
to consider that the mechanism may be unrelated to pulmonary
oedema (Figs. 3 and 4).
SO, IF COUGH IS NOT CAUSED BY PULMONARY
OEDEMA, WHY DOES COUGH IMPROVE ON
CARDIAC MEDICATIONS?
Luca Ferasin: In one study (Ferasin et al. 2013) cough was pres-
ent in approximately 50% of dogs with MMVD, although less
than a third of dogs with pulmonary oedema presented with
cough, while 100% of dogs with radiographic evidence of CHF
presented with tachypnoea/dyspnoea. In another study (Schober
et al. 2010), cough was observed in a higher percentage of cases,
both in dogs with CHF (84%) and without CHF (43%) but even
• © 2019 British Small Animal Veterinary Association
 Coughing in dogs: evidence for cardiac cough

FIG 3. Bronchoscopy images of an anaesthetised 8-year-old female cavalier King Charles spaniel with chronic cough and mitral valve disease with well-
controlled congestive heart failure. At the level of the carina (A) the right main-stem bronchus is readily observed with a normal lumen diameter during
inspiration and expiration. The left main-stem bronchus (B) can be seen with severe dynamic collapse with dorsal compression of the ventral wall of
the bronchus associated with marked cardiomegaly (*). The dynamic change in airway lumen size is appreciated on inspiration (C). Proliferation of the
mucosal surface with a “kissing lesion” (#) is evident following chronic bronchial compression (D)

in this study tachypnoea/dyspnoea were not observed in cough-
ing dogs with MMVD without CHF. Therefore, we can assume
that cough in the absence of tachypnoea/dyspnoea is unlikely to
be related to pulmonary oedema.
It is true that cough improves in some dogs after adminis-
tration of diuretics. However, many dogs still cough even after
radiographic or clinical resolution of pulmonary oedema sug-
gesting, once again, that their cough is not originating from the
bronchiolar or alveolar region. The positive clinical response
observed in some patients after administration of furosemide
can be explained by a number of different mechanisms. Beside
the diuretic properties, furosemide can also provide anti-inflam-
matory and antitussive effects which may result in a satisfactory
inhibition of coughing in patients with cardiac disease, regard-
less of the possible presence (or absence) of pulmonary oedema
(Sudo et al. 2000, Prandota 2002). Additionally, the typical self-
improvement of dogs with infectious tracheo-bronchitis may
lead one to erroneously believe that the administration of furose-
mide was the explanation for clinical improvement (Ferasin et al.
2013). Finally, it is not unrealistic to believe that the plasma vol-
ume contraction that follows pharmacological diuresis causes a
reduction in LA pressure, which may in turn reduce the mechani-
cal stimulation of the cough receptors of the contiguous airways.
Pimobendan may also reduce frequency of coughing through
an indirect mechanism, because previous studies evaluating dogs
with preclinical DCM (Summerfield et al. 2012) and dogs with
symptomatic MMVD (Woolley et al. 2007) demonstrated that
the administration of pimobendan is associated with a reduction
in heart size.
WHY DOES COUGH NOT ALWAYS IMPROVE ON
CARDIAC MEDICATIONS?
Chris Linney: Given the previously described cough mecha-
nisms, it is now readily apparent that coughing as a main sign of
pulmonary oedema differs from historical perceptions. In cases
in which introduction of cardiac medications fails to improve
cough, clinicians must be prepared to revisit their original diag-
nosis: “was cough secondary to heart disease in the first place”?
More frequently cough in isolation, without tachypnoea or
dyspnoea, is a key feature of primary respiratory disease rather
than cardiac disease. Cases of concurrent respiratory disease and
cardiac disease may benefit from advanced imaging such as CT,
bronchoscopy or fluoroscopy. The latter can be very useful for
diagnosis but is not widely available in primary care practice. If
there is fixed or dynamic airway compression, either as a result
of bronchomalacia, tracheal collapse or chronic bronchitis, furo-
semide may be of limited value despite its weak bronchodilatory
effects (Abbott & Kovacic 2008). For airway disease, there are
more suitable medications and surgical treatment options avail-
able, although these are outside the remits of this manuscript.

Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association 5
 L. Ferasin and C. Linney

FIG 4. Thoracic CT images. A dorsoventral multi-planar reconstruction (A) shows the association of the position of the left atrium (*) with the
bifurcation of the trachea into the right and left mainstem bronchi. The transverse section at the level of the mainstem bronchi demonstrates the
normal position taken by the mainstem bronchi as they pass around the heart (B). The left mainstem bronchus (arrow) passes over the roof of the left
atrium (#) and their relationship is shown on the sagittal multi-planar reconstruction (C). (D) There is marked cardiomegaly secondary to mitral valve
disease causing displacement of the normal course of the left main stem bronchus along with severe bronchial collapse with compression (arrow)

Airway compression may also be a feature of extra-luminal disease
such as tracheobronchial lymphadenopathy, mediastinal masses,
as well as other types of thoracic neoplasia. Finally, in inflam-
matory airway disease, cardiac medications may elicit a partial
and temporary effect or no effect at all. In these situations, the
clinician should be confident to consider further investigations,
such as thoracic imaging (radiography, CT) and airway endos-
copy with bronchoalveolar lavage to assess for primary respira-
tory conditions.
SHOULD COUGH STILL BE LISTED AS THE MAIN
CLINICAL SIGN OF CHF IN DOGS?
Luca Ferasin: Cough should no longer be considered a major
clinical sign attributable to pulmonary oedema, since lethargy,
exercise intolerance and tachypnoea/dyspnoea are much more
specific signs of left-sided CHF. The obsolete concept of cough
caused by pulmonary oedema has been handed down for decades
without any solid scientific evidence but merely based on the
observation that dogs with cardiac disease often cough. The
mechanism of cough is complex and the concept that fluid in the
lungs can s­imply trigger the cough reflex is not supported by a
known physiological mechanism. Conversely, we need to accept
that a geriatric dog with cardiac disease is very likely affected by
other co-morbidities which may cause a cumulative stimula-
tion of sensory receptors. Furthermore, we must acknowledge the
complexity of events causing plasticity in peripheral and central
mechanisms of cough. Increased afferent nerve fibre excitability
or changes in afferent nerve fibre anatomy or facilitatory interac-
tions between sensory nerve fibre subtypes are just some of the
important factors that can cause enhanced cough sensitivity in
these patients.
Chris Linney: Based on clinical experience and scientific pub-
lications, coughing should continue to remain listed as a clinical
sign of CHF but in isolation it has a low specificity for heart

6 Journal of Small Animal Practice • © 2019 British Small Animal Veterinary Association
 Coughing in dogs: evidence for cardiac cough
disease and clinicians should not rely on this clinical sign to diag-
nose heart disease or heart failure. Dogs with CHF may cough,
but the cause may not always be pulmonary oedema, and other
features of the cardiac disease or concurrent lower airway disease
are likely to play a part in the “cardiac cough.”
The best clinical sign to predict CHF is increased resting
and sleeping respiratory rates above the reference range, which
occur frequently without concomitant cough. More research into
the frequency of concurrent cardiac and respiratory disease are
required but in patients with unstable CHF, respiratory investi-
gations may be delayed or altogether avoided after CHF is diag-
nosed, likely leading to under reporting of concurrent cardiac
and respiratory disease and their association with coughing. Tho-
racic radiography and/or assessment of B-lines on lung ultraso-
nography by skilled operators should always be undertaken to
confirm pulmonary oedema.
In conclusion, cough in the absence of tachypnoea and/or
dyspnoea should lead the clinician to consider that it is most
likely a feature of primary respiratory disease rather than a cardiac
disease.
Acknowledgements
The authors would like to thank Dr Heidi Ferasin for her kind
assistance in editing and proof reading this manuscript.
Conflict of interest
Authors disclose no conflict of interest.
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