42 PART ONE — Approach to Problems in Respiratory Medicine
44. Venker-van Haagen AJ, Engelse EJJ, van den Ingh TSGAM:
Congenital subglottic stenosis in a dog. J Am Anim Hosp Assoc
17:223, 1981.
45. Peterson J, Streeter V: Laryngeal obstruction secondary to brodifa-
coum toxicosis in a dog, J Am Vet Med Assoc 208:352, 1996.
46. Saik JE, Toll SL, Diters RW et al: Canine and feline laryngeal neo-
plasia: A 10-year survey, J Am Anim Hosp Assoc 22:359, 1986.
47. Ogilvie GK: Tumors of the endocrine system. In Withrow SJ,
MacEwan EG, editors: Small animal clinical oncology, ed 2,
Philadelphia, 1996, WB Saunders.
48. Hardie EM, Spodnick GJ, Gilson SD et al: Tracheal rupture in cats:
16 cases, J Am Vet Med Assoc 214:508, 1999.
49. Mitchell SL, McCarthy R, Rudloff E et al: Tracheal rupture associ-
ated with intubation in cats: 20 cases (1996-1998), J Am Vet Med
Assoc 216:1592, 2000.
50. Lotti U, Niebauer GW: Tracheobronchial foreign bodies of plant
origin in 153 hunting dogs, Comp Cont Ed Pract Vet 14:7, 1992.
51. Carlisle CH, Biery DN, Thrall DE: Tracheal and laryngeal tumors of
the dog and cat: Literature review and 13 additional patients, Vet
Radiol 32:229, 1991.
52. Brovida C, Castagnaro M: Tracheal obstruction due to an
eosinophilic granuloma in a dog: Surgical treatment and clinico-
pathological observations, J Am Anim Hosp Assoc 28:8, 1992.
53. Metcalfe SS: Filaroides osleri in a dog, Aust Vet Pract 27:65, 1997.
54. Cobb MA, Fischer MA: Crenosoma vulpis infection in a dog, Vet
Rec 130:452, 1992.
55. Blocker TL, Roberts BK: Acute tracheal obstruction associated with
anticoagulant rodenticide intoxication in a dog, J Small Anim Pract
40:577, 1999.
56. Sheaffer KA, Dillon AR: Obstructive tracheal mass due to an in-
flammatory polyp in a cat, J Am Anim Hosp Assoc 32:431, 1996.
CHAPTER 6
Acute and Chronic Cough
Elizabeth A. Rozanski • John E. Rush
C ough is a common presenting complaint for dogs
and, to a lesser extent, cats. Cough is a sign of an un-
derlying disorder, not a disease in itself. Therefore, the
cause of the cough should be identified and the under-
lying disease, not just the cough, should be treated. The
cause of cough may be simple to identify and easy to
correct in many cases. In other animals, the etiology can
be obscure, diagnostic testing unrewarding, and the
cough may remain unresponsive to therapeutic manipu-
lation. It is therefore important to have a strong grasp of
the underlying pathophysiology and as well as the com-
mon and uncommon causes of cough.
Definition and Clinical Signs
Cough is defined as a sudden expiratory effort, initially
against a closed glottis, producing a noisy expulsion of
57. Fitzgerald SD, Johnson CA, Peck EJ: A fatal case of intrathoracic
cuterebriasis in a cat, J Am Anim Hosp Assoc 32:353, 1996.
58. Harvey CE, Goldschmidt MH: Healing following short duration
transverse incision tracheotomy in the dog, Vet Surg 11:77, 1982.
59. Smith MM, Saunders GK, Leib MS et al: Evaluation of horizontal
and vertical tracheotomy healing following short duration tra-
cheostomy in dogs, Vet Surg 23:416, 1994.
60. Macintire DK, Henderson RA, Wilson ER et al: Transverse flap tra-
cheostomy: A technique for temporary tracheostomy of intermedi-
ate duration, J Vet Emerg Crit Care 5:25, 1995.
61. Tsuda T, Noguchi H, Takumi Y et al: Optimum humidification of
air administered to a tracheostomy in dogs: Scanning electron mi-
croscopy and surfactant studies, J Anaesth 49:965, 1977.
62. Mebius C: A comparative evaluation of disposable humidifiers,
Acta Anaesthesiol Scand 27:403, 1983.
63. John E, Ermocilla R, Golden J et al: Effects of gas temperature and
particulate water on rabbit lungs during ventilation, Pediatr Res 14:
1186, 1980.
64. Sackner MA, Lander J, Greenletch N et al: Pathogenesis and pre-
vention of tracheobronchial damage with suction procedures,
Chest 64:284, 1973.
65. Plum F, Dunning MF: Techniques for minimizing trauma to the tra-
cheobronchial tree after tracheotomy, N Eng J Med 254:193, 1956.
66. Naigow D, Powaser MM: The effect of different endotracheal suc-
tion procedures on arterial blood gases in a controlled experimen-
tal model, Heart Lung 6:808, 1977.
67. Shim C, Fernandez R, Fine N et al: Cardiac arrhythmias resulting
from tracheal suctioning, Am International Med 71:1149, 1969.
68. Vaughan RS, Menke JA, Giacoia GP: Pneumothorax: A complica-
tion of endotracheal tube suctioning, J Pediatr 92:633, 1978.
69. Young CS: Recommended guidelines for suction, Physiotherapy
70:106, 1984.
air from the lungs. A cough usually signals an effort to
clear the lungs or upper airway of real or perceived for-
eign material. Cough is therefore not a final diagnosis,
but rather a clinical sign noted with a variety of under-
lying causes. A cough can be classified as acute or
chronic. Coughing is considered chronic if it persists for
2 months or longer.
Historical information and a description of the cough
may help to pinpoint the etiology. Cough may also be de-
scribed as moist, dry, productive, or honking. A moist
cough suggests the presence of airway secretions.
Animals may be observed to either swallow or produce
sputum after a bout of coughing, and in these cases the
cough is considered productive. Cough may also be clas-
sified regarding the time of day that it occurs (e.g., night
or morning) or coupled with an event such as drinking,
eating, running, or pulling on a leash. In cats, cough
may be confused with retching or attempts to vomit

Figure 6-1. A cat demonstrating the characteristic posture of
cough. Note the extended head and neck.
(Figure 6-1). In a variety of diseases, cough is often the
primary presenting complaint, particularly when cough
is a new clinical sign. However, in some dogs with
chronic or multisystemic signs, cough may not be specif-
ically identified as a complaint unless the client is pre-
cisely questioned.
Pathophysiology
Coughing can be both a voluntary and an involuntary
act, although in animals it is difficult to determine the
immediate trigger. Most coughing in animals is pre-
sumed to be an involuntary response. Stimuli to cough
include pressure on the outside of the airway or the pres-
ence of foreign material, excessive secretions, or noxious
gases in the airway. Cough serves as an important func-
tion both by aiding in the clearance of foreign debris and
by enhancing the actions of the mucociliary escalator.1
The cough reflex is the primary defense mechanism of
the pulmonary system.1,2
The cough pathway has been extensively investigated
in animals.3-7 It includes the cough receptors and sensory
nerves in the airway, the vagus nerve, the central cough
center (brainstem, pons) and the effectors including the
glottis and expiratory muscles (Figure 6-2).1,3 Innervation
for these receptors and the sites for triggering cough is
supplied exclusively by the vagus nerve.1,3,8 Therefore,
some structures that are not usually considered to be part
of the respiratory tract (e.g., the external auditory meatus
and the tympanic membrane) may also be involved in
the cough reflex.8
The first step in creation of a cough is stimulation of
the cough receptors, which are made up of sensory
nerves. Species differences exist in sensory nerves; how-
ever, much of the research on cough receptors has been
performed in animals.1,3-7,9,10 At least three different re-
ceptors are involved in stimulation of a cough response:
the rapidly adapting stretch receptors, the pulmonary C-
fibers and the bronchial C-fibers.2,3 The rapidly adapting
stretch receptors (or “irritant” receptors) are located
within the mucosa of the tracheobronchial tree. During
normal breathing, these myelinated receptors discharge
sporadically, and they respond to light mechanical stim-
ulus.2,3 These are the receptors that are most likely to be
stimulated by foreign debris.
CHAPTER 6 — Acute and Chronic Cough 43
Cough stimulus Cortex
(Mechanical, chemical,
inflammatory)
Central cough center
(Brainstem/Pons)
Cough receptors Vagus nerve
(Rapid-adapting receptors,
C-fibers)
Cough
Mediators
(Tachykinins, substance P)
Figure 6-2. Flow chart demonstrating the cough pathway. Note
the involvement of the stimulus, cough receptors, mediators, and
efferent pathways.
C-fibers are unmyelinated receptors located close to
blood vessels. They respond to lung hyperinflation as well
as to endogenous and exogenous stimulants. The pul-
monary C-fibers are located within peripheral airways and
are supplied by blood from the pulmonary circulation. The
bronchial C-fibers are located within larger airways and
are supplied by the bronchial circulation. Both of these
C-fiber receptors are more sensitive to chemical stimula-
tion than mechanical stimulus.11,12 Not all C-fibers are in-
volved in the generation of cough, and substantial species
differences exist. C-fibers are also important in bron-
choconstriction and in the neural control of respiration.
The cough pathway may be stimulated by mechanical
or chemical factors.2,3 Endogenous triggers of coughing
include the presence of airway secretions and airway in-
flammation. Exogenous agents include smoke and aspi-
rated foreign materials such as food or water. Certain
diseases can magnify the response to a specific agent,
resulting in increased cough. For example, dogs with ex-
perimentally induced Bordetella bronchiseptica infection
have a marked increase in the response of the rapidly
adapting stretch receptor.7 Anatomical differences also
affect the resulting cough response because airways dif-
fer in their reactions to various stimuli. The more proxi-
mal airways (i.e., larynx and trachea) are very sensitive
to mechanical stimuli, but are less sensitive to chemical
stimulation. The more distal airways (e.g., the bronchi
and bronchioles) are more sensitive to chemical stimu-
lus and less responsive to mechanical stimulation. This
is largely a reflection of the type of receptors present in
each location. Direct stimulation of the larynx results in
the expiratory reflex, which is a cough without prior in-
spiration. This reflex may be appreciated in the initial
cough triggered during attempts at endotracheal intuba-
tion in cats. Stimulation of receptors from distal airways
typically results in an inspiratory phase prior to the
cough. The prior inspiration serves to maximize the sub-
sequent expiratory airflow rate.
Chemical mediators, released by receptors in re-
sponse to stimulation, serve to modulate the cough re-
44 PART ONE — Approach to Problems in Respiratory Medicine
sponse. These mediators include substance P, calcitonin
gene-related peptide (CGRP), neurokinin A (NKA), and
other tachykinins.9 The relative roles of these neu-
ropeptides in modification or stimulation of cough is
still under investigation. Substance P (SP) has been ex-
tensively investigated. It is a potent proinflammatory
agent in the airways that causes increased vascular per-
meability, vasodilation, and submucosal gland secre-
tion.9 Research to date suggests that the neuropeptides
(including SP) are the final mediators of many abnor-
malities in the inflamed airways, including cough.
Neuropeptides are degraded by neutral endopeptidase
(NEP), angiotensin converting enzyme (ACE), and other
enzymes. Modification of neuropeptide degradation
may ultimately be useful in management of cough.
Practically, in human medicine, cough that is linked to
ACE inhibitor use (e.g., benazepril or enalapril) is
thought to reflect either delayed degradation of SP or lo-
cal increases in bradykinin that stimulate the C-fibers.
ACE inhibitor–associated cough has rarely been re-
ported in veterinary medicine and, in fact, most studies
show substantial improvement in cough following the
addition of an ACE-inhibitor due to better control of
congestive heart failure.13
Sensory and neuropeptide activity is altered in human
asthmatics when compared to healthy controls. Whereas
cough and bronchoconstriction are triggered by closely
related stimuli, these phenomena are clinical signs actu-
ally initiated by separate sensory pathways.11 For exam-
ple, cough suppressants such as codeine have no effect
on bronchoconstriction. The mast cell stabilizer cromo-
glycate blocks bronchoconstriction but has no effect on
cough.1,11 This concept appears to be significant in un-
BOX 6-1
Causes of Cough in Small Animals
Allergic/Inflammatory
Feline asthma
Chronic bronchitis
Chronic obstructive pulmonary disease (COPD)
Pulmonary infiltrates with eosinophilia (PIE)
Eosinophilic pneumonitis
Cardiovascular
Pulmonary edema
Left atrial enlargement
Pulmonary embolism (uncommon)
Infectious
Tracheobronchitis
Pneumonia
Bacterial
Viral
Fungal
Protozoal
Neoplastic
Primary
Lung
derstanding the pathophysiology of cough and bron-
choconstriction. This distinction has not been described
in spontaneously-occurring animal disease such as feline
asthma, although laboratory evidence with experimental
animal models suggests that similar physiology may ex-
ist in many species.1,3-5
The cough reflex has been objectively tested in people
and experimental animals. In this test, an agent known
to trigger cough (e.g., capsaicin, a red pepper extract) is
nebulized at increasing concentrations until two or more
coughs occur.14 Individuals who cough at lower concen-
trations are regarded as having an increased cough reflex.
This test is thought to be useful to provide more objec-
tive data about the symptom of cough, but it has not
found clinical utility in clinical veterinary medicine.
Differential Diagnosis
Many underlying diseases are recognized to cause cough
(Box 6-1). Cough can be seen in animals with disease in
the nasal passages, larynx, trachea, bronchi, alveoli,
pleural space; and in animals with cardiac disease.
Broad categories or etiologic agents include allergic/
inflammatory, cardiac, infectious, neoplastic, parasitic,
trauma, and physical factors. Multiple causes of cough
exist in some animals (e.g., the aged dog with heart dis-
ease and collapsing trachea), and in these cases the
cough may be triggered by more than one disease. It is
usually helpful to consider species, age, breed or body
conformation, history, and physical examination find-
ings when considering differential diagnoses, in order to
develop a diagnostic plan.
Primary, cont’d
Trachea
Larynx
Metastatic
Heart-base tumor
Compression due to enlarged lymph nodes
Parasites
Filaroides
Aelurostrongylus
Paragonimus
Capillaria
Dirofiliaria
Others
Trauma and Physical Abnormalities
Foreign body
Collapsing trachea
Tracheal hypoplasia
Tracheal stenosis
Smoke inhalation

Diagnostic Testing
Diagnostic testing for acute and chronic cough is usu-
ally based, at least in part, on the signalment, history,
and physical examination findings. In some cases (e.g.,
mild infectious tracheobronchitis with typical historical
and physical examination findings) no further testing
may be required. However, in almost all pets with
cough, a thoracic radiograph is an essential initial di-
agnostic test. Thoracic radiography provides useful in-
formation about the lung parenchyma, the pleural
space, and the cardiovascular system. Further diagnos-
tic testing is often based upon the result of the thoracic
radiographs. For example, if pleural effusion is evident,
then thoracocentesis is appropriate; whereas if alveolar
infiltrates are noted in a cranioventral location, then
tracheal aspiration with cytology and culture should be
performed.
Routine laboratory testing such as a complete blood
count, chemistry profile, urinalysis, and fecal examina-
tion are helpful to complete the minimum database and
to exclude some systemic and parasitic causes of cough.
Fluoroscopy may be indicated if dynamic airway ob-
struction is suspected, and direct visualization of the air-
ways (i.e., laryngoscopy and bronchoscopy) with subse-
quent sample collection for cytology and bacterial culture
may be useful in infectious or inflammatory causes of
cough. Echocardiography and electrocardiography are
very useful in evaluating the patient with suspected left-
sided heart failure or the patient with cor pulmonale due
to chronic bronchitis. Ultrasonographic evaluation of
noncardiac structures is often useful for suspected mass
lesions and pleural effusion of unknown etiology.
Heartworm (serology) and lungworm (Baermann fecal)
testing is recommended in animals from endemic areas.
Pulmonary function tests may or may not be abnor-
mal in animals with cough. Arterial blood gases may
document hypoxemia or hypercarbia but do not provide
information about the underlying etiology. More special-
ized pulmonary function testing (e.g., plethysomogra-
phy) may help to clarify the type of impairment present
and can also be used as a tool to judge the response to
therapy.
Initial Management Pending
Results of Diagnostic Testing
The most successful management of cough involves
treatment and resolution of the underlying cause.
Specific disease-oriented therapy often results in near
complete resolution of coughing. When cough is accom-
panied by dyspnea or respiratory distress, oxygen ther-
apy is indicated while diagnostic testing is proceeding.
In most cases, cough does not require immediate treat-
ment prior to completion of a complete history, physical
examination, and thoracic radiograph.
If cough is associated with bronchoconstriction, bron-
chodilator therapy can result in partial resolution of the
CHAPTER 6 — Acute and Chronic Cough 45
cough. For animals with infectious etiologies and pro-
ductive cough, nebulization and coupage can improve
clearance of airway secretions and debris and thereby
improve the effectiveness of the cough reflex.
Unfortunately, in some animals coughing persists de-
spite therapy for the underlying etiology. This is espe-
cially true for animals with chronic nonproductive
cough. In these cases, cough suppressants may be indi-
cated. Excessive or frequent coughing, to the point of ex-
haustion for the patient or insomnia on the part of the
patient or the client, is often the reason for use of cough
suppressant therapy. Some dogs experience syncopal
episodes precipitated by paroxysms of coughing, and in
many cases cough suppression can reduce the frequency
of syncope. Even in these cases, it is important to iden-
tify the underlying disease and the reason(s) to suppress
coughing. Cough suppression is contraindicated (or rel-
atively contraindicated) in dogs with infectious disease
and productive cough.
Medications that suppress cough include drugs that
directly inhibit the cough receptors including the nar-
cotics (e.g., butorphanol, hydrocodone), antiinflamma-
tory agents (specifically glucocorticoids), and bron-
chodilators (e.g., the methylxanthines and ␤2-agonists).
The most appropriate choice of cough suppressant de-
pends upon the underlying disease.
In most small animals with cough, a specific disease
or disorder can be identified as the etiology. Airway in-
flammation is a common denominator for many diseases
causing cough, and modulating the inflammatory re-
sponse may be appropriate in many cases. Treatment of
the primary process, when possible, will result in the
most effective long-term control of clinical signs.
REFERENCES
1. Chang AB: Cough, cough receptors, and asthma in children,
Pediatric Pulmonology 8:59-70, 1999.
2. Fuller RW, Jackson DM: Physiology and treatment of cough,
Thorax 45:425-430, 1990.
3. Widdicombe JG: Neurophysiology of the cough reflex, Eur Respir J
8:1193-1202, 1995.
4. Dixon M, Jackson DM, Richards IM: A study of the afferent and ef-
ferent nerve distribution to the lungs of dogs, Respiration 39:144-
149, 1980.
5. Davies A, Dixon M, Callahan D et al: Lung reflexes in rabbits dur-
ing pulmonary stretch receptor block by sulphur dioxide, Respir
Physiol 34:83-101, 1978.
6. Widdicombe JG: Afferent receptors in the airways and cough,
Respir Physiol 114:5-15, 1998.
7. Dixon M, Jackson DM, Richards IM: The effect of respiratory tract
infection on histamine-induced changes in lung mechanics and ir-
ritant receptor discharge in dogs, Am Rev Respir Dis 120: 843-848,
1979.
8. Karlsson J, Sant’Ambrogio G, Widdicombe J: Afferent neural path-
ways in cough and reflex bronchoconstriction, J Appl Physiol
65:1007-1023,1988.
9. Sekizawa K, Jia YX, Ebihara T et al: Role of substance P in cough,
Pulmonary Pharmacology 9: 323-328, 1996.
10. Ujiie Y, Sekizawa K, Aikawa T et al: Evidence for substance P as
an endogenous substance causing cough in guinea pigs, Am Rev
Respir Dis 148:1628-1632, 1993.
11. Choudry NB, Fuller RW, Anderson N et al: Separation of cough and
reflex bronchoconstriction by inhaled local anaesthetics, Eur Resp
J 3:579-583, 1990.
46 PART ONE — Approach to Problems in Respiratory Medicine
12. Coleridge HM, Coleridge JCG, Baker DG et al: Comparison of the
effects of histamine and prostaglandin on afferent C-fibre endings
and irritant receptors in intrapulmonary airways, Adv in Exp Med
Biol 99:291-305, 1978.
13. Kitagawa H, Wakamiya H, Kitoh K et al: Efficacy of monotherapy
with benazepril, an angiotensin converting enzyme inhibitor, in
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Sci 59:513-520, 1997.
CHAPTER 7
Panting
Susan G. Hackner
P anting is defined as rapid, shallow respiration, with a
respiratory frequency of 200 to 400 breaths per minute and
a decreased tidal volume, such that alveolar ventilation re-
mains relatively unchanged.1-4 It is a normal thermoregu-
latory mechanism in many species, including the dog and
cat.2,4,5 Panting is seldom a primary complaint but is com-
monly observed on presentation or during hospitalization.
Because of the usually innocuous causes of panting, it is
often overlooked. It may, however, be an indicator of more
serious underlying disease or drug therapy.
Physiology
Panting is the major method of thermoregulation in
small animals exposed to heat or exercise.2,4,6 By rapidly
replacing moist air over the evaporative surfaces of the
nasal passages and the mouth with fresh, dry air, pant-
ing increases evaporative heat loss.2,5,7 During panting,
the mechanical capabilities of the respiratory system are
devoted to efficient air flow through the upper airway to
maximize evaporative cooling.5,8 Evaporative loss is en-
hanced by a concurrent rise in lingual and nasal blood
flow (up to sevenfold).7,9,10 Secretions from the lateral
nasal glands increase up to fortyfold,2,11 and it has been
suggested that the role of these glands is analogous to
that of sweat glands in humans.
Additional heat generated by muscular work is
avoided by panting with a rhythmic motion that ap-
proaches the resonant frequency of the respiratory sys-
tem5,8: that is, the elastic properties of the lungs and tho-
rax allow expansion and contraction at this rate with a
minimum of external work.8 The oxygen consumption of
respiratory muscles during thermal panting is minimally
increased, and is less than that observed for a compara-
ble level of ventilation produced by hypercapnia.8,12
14. Fuller RW, Karlsson J, Choudry NB et al: Effect of inhaled and sys-
temic opiates on responses to inhaled capsaicin in humans, J Appl
Physiol 65:1125-1130, 1988.
Panting is characterized by a high respiratory fre-
quency and a low tidal volume.3,4,13 Dead space ventila-
tion is proportionally increased relative to alveolar ven-
tilation and minute ventilation.14,15 Although the
magnitude of tidal volume is decreased, it remains
slightly greater than dead space such that, over a wide
range of heat stress and relative humidity, gas exchange
is adequate and arterial blood gases and intracellular pH
are well defended.8,16 This pattern of ventilation and gas
exchange is analogous to contemporary methods of
high frequency positive pressure ventilation.14 Only af-
ter prolonged exposure to extreme heat stress do some
animals exhibit deterioration of their blood gases, and
heat exhaustion is finally associated with severe respi-
ratory alkalosis.1,8,16
Panting is controlled by the thermoregulatory centers
of the brain.1,13 When the blood becomes overheated, the
hypothalamus initiates neurogenic signals to decrease
the body temperature, resulting in vasodilation and
panting. The actual panting process is controlled by the
panting center, associated with the pneumotaxic respira-
tory center located in the pons.13
Temperature detection occurs both centrally and pe-
ripherally. The anterior hypothalamic-preoptic area con-
tains large numbers of heat-sensitive neurons.13 These
function as heat sensors, the neurons increasing their fir-
ing rate twofold to tenfold in response to an increase in
body temperature of 1° C.13 Peripheral temperature re-
ceptors are found in the skin, the spinal cord, the ab-
dominal viscera, and around the great veins of the cra-
nial abdomen and thorax. These receptors, however,
mainly detect cold rather than heat, and play a lesser
role in protection from overheating than do the central
receptors.13 Sensory signals from both central and pe-
ripheral receptors are transmitted to the posterior hypo-
thalamus, where temperature-controlling effector mech-