Chronic Obstructive Pulmonary
Disease (COPD)

by Dr. Melissa M. Norton

Chronic obstructive pulmonary disease (COPD) affects a significant number of Pugs and is a leading cause of death in the breed. The condition often goes untreated because its symptoms may not be recognized by owners and veterinarians. Understanding COPD, its causes, complications, signs and treatment options may help you prolong your Pug's life.

The respiratory system of all mammals is a delicate balance between a ventilation system for moving air and circulatory system for exchanging oxygen and the waste gas carbon dioxide. The ventilation system is composed of airways (nasal passages, larynx, trachea, bronchi and bronchioli) that end in a microscopic sponge like network of elastic air sacs called alveoli inside the lungs. The layout of mammalian lungs can be visualized like a bunch of grapes, substituting grape stems for airways, and grapes for clusters of alveoli. Another important component of the ventilation system are the muscles that move the ribs and diaphragm to control respiration.

The circulatory system involved in respiration begins with the right side of the heart. The right side of the heart receives oxygen-poor and carbon dioxide-rich blood from the rest of the body. It then pumps this blood to the lungs through the pulmonary artery. Blood then is filtered through the large pulmonary capillary network that surrounds the alveoli. During respiration, oxygen is exchanged for carbon dioxide across the thin alveolar and capillary walls. The actual surface area for this gas exchange to take place in the lungs is enormous. If it were possible to lay out a normal adult human's alveoli side by side, they would easily cover a tennis court. A Pug's lung surface area would cover approximately a third of a tennis court. Oxygen-rich blood filters out of the vast capillary bed and into the pulmonary veins and is returned to the left side of the heart. The left side of the heart pumps oxygen-rich blood out the aorta to the rest of the body.

Normal respiration in all mammals is accomplished by a process called negative pressure ventilation. Lungs operate much like a balloon in a vacuum. There is no physical attachment between the lungs and the chest wall or diaphragm. In the normal mammalian chest there is a vacuum between the lungs and the chest wall. As the muscles of respiration pull the diaphragm downward, and ribs up and outward, the lungs are pulled along and expanded by the vacuum. As the lungs expand, a negative pressure is created inside the lungs. Air rushes in through the airways to equalize the pressure in the alveoli with the atmosphere.

Exhalation in a normal individual is a passive process. As the respiratory muscles relax, the diaphragm relaxes upward and the ribs fall inward. The lungs are now compressed, creating a higher pressure gradient inside the lungs. Air moves back outside to again equalize the pressure in the lungs with the atmosphere.

In an animal with a normal unobstructed airway there is very little turbulence and only a small amount of respiratory noise at rest. In an animal with an airway obstruction there is increased turbulence and increased respiratory sounds such as wheezing, gurgling, or coughing.

Despite being composed largely of very thin alveolar walls and capillaries, mammalian lungs are designed to last a very long time. With no disease process, mechanical or chemical irritation, to interfere, a normal set of lungs would last approximately 200 years! Despite their potential longevity, lungs do not have much capacity to heal.

Environmental factors that shorten pulmonary longevity include first and secondhand smoke, pollution and dust irritation, infection and trauma. These insults can damage lung tissue directly or cause irritation and constriction of the airways, leading to chronic obstructive pulmonary disease.

Pulmonary tissue reacts to insults by creating scar tissue in an attempt to toughen the fragile alveolar walls, or by having these thin alveolar walls rupture. When alveoli rupture, they can collapse into small areas of scarred lung tissue, or they can form larger chambers (emphysema) in the lung. In addition to reducing the effective surface area for gas exchange, collapsed and emphysematous alveoli cause the lung to lose elasticity and make respiration more difficult. More effort must go into inhalation.

Severely diseased lungs require effort for exhalation. Instead of allowing the diaphragm and ribs to return in their normal resting position to accomplish exhalation, an individual with COPD must actively use their muscles of respiration to compress the chest and force more air out. COPD can be a vicious cycle, the disease process makes an individual breath harder, and the increased respiratory effort in turn can cause more lung damage.

Ruptured alveoli can also make respiration difficult by breaking the vacuum seal between the lungs and the chest wall. Ruptured alveoli can act as a one-way valve allowing air to pass through the lungs. If enough emphysematous alveoli rupture at once, a large volume of air may leak into the chest cavity, leading to lung collapse and death by asphyxiation.

Heart disease secondary to lung disease (Cor Pulmonale) is caused by pulmonary hypertension. Blood pressure rises significantly in diseased lung tissue because it is harder for blood to flow through scar tissues Additionally, the increased pressure within the chest cavity from the greater respiratory effort can cause compression and periodic collapse of small pulmonary blood vessels. Very rarely, chest pressure can be large enough to cause collapse of large veins in the chest and shut of blood return to the heart, which can induce fainting episodes. Working against a large pressure gradient increases the workload of the heart, causing cardiac muscle fatigue and damage. The right side of the heart fails first, but the left side will eventually follow suit if the disease process is not slowed.

Pugs with COPD face an even more difficult respiratory gradient than their human counterparts. While everyone has to contend with environmental insults to their respiratory system, many Pugs also have to contend with internal airway obstructions in the form of poor anatomy. Air turbulence caused by airway obstruction not only leads to increased lung damage, it also causes swelling of the obstruction, leading to further constriction of the airway and even more difficulty breathing.

Pugs, like all brachycephalic breeds, are prone to a variety of airway obstructions which can lead to COPD. Airway obstructions observed in Pugs include stenotic nares, tonsillitis, elongated soft palate, everted laryngeal saccules, laryngeal paralysis, hypoplastic trachea, collapsing trachea and asthma. These components of the Brachycephalic Syndrome can be a vicious cycle. These anatomical problems may be congenital, but they tend to worsen with every inhalation if left untreated.

Stenotic nares are narrow nostrils that tend to collapse inward as the affected Pug inhales. The harder the Pug breathes, the more the nostrils collapse, so that just when the Pug is trying to pull in more oxygen, it can't. You can mimic this effect by inhaling sharply and noting how much your own nostrils constrict and how much less air you move than while breathing quietly. A Pug with stenotic nares is easily diagnosed simply by watching his nose as it breathes. A normal Pug will have its nostrils dilate slightly as it inhales. A Pug with stenotic nares will have his nostrils collapse.

Fortunately, this condition is rare in Pugs. (Beware that it is sometimes over diagnosed!) Stenotic nares can be corrected surgically. Occasionally, a young puppy with stenotic nares will have the condition improve with age and avoid the need for surgical correction.

The tonsils are located in the back of the mouth. Enlarged tonsils in and of themselves rarely impair respiration. However, the tonsils are part of the immune system. They contain a large number of white blood cells that in turn produce chemical factors that stimulate the immune system to combat infection. These factors also cause generalized tissue inflammation and swelling. It is this secondary swelling effect that contributes to airway constriction. Tonsillectomy may be helpful in reducing generalized upper airway inflammation in affected individuals.

Elongated soft palates are the most common airway obstruction in Pugs. The soft palate is an extension of the hard palate which forms the roof of the mouth. The soft palate is supposed to act as a mobile flap to prevent food and water entering the nasal passages during swallowing. An elongated soft palate hangs in front of the airway or falls into the larynx during inhalation.

Affected Pugs will breathe rather noisily when exited. Pugs with elongated soft palates often sound like someone slurping the last of their soda through a straw. They frequently gag in an attempt to clear their airway, bringing up foamy saliva while eating, drinking, or excited. Dogs with elongated soft palates may have "reverse sneeze" attacks where they appear to be in a great deal of distress caught in a spasm of breathing very rapidly and noisily during inhalation. A Pug can often be broken out of a "reverse sneeze" attack by rubbing its throat or blowing sharply on the nose to cause it to swallow and displace the soft palate. The harder the affected Pug breathes, the more turbulence causes the palate to swell and elongate even more over time.

An elongated soft palate is almost impossible to positively confirm in a conscious Pug. It can sometimes be visualized on a radiograph but is best diagnosed by direct examination under anesthesia. It is usually surgically corrected at the same time. Care must be taken while shortening a soft palate not to remove too much, as an overly short palate can lead to difficult swallowing.

Everted laryngical saccules are the second most common airway obstruction in Pugs. They are usually secondary to an elongated soft palate or stenotic nares. The increased turbulence in the larynx leads to swelling of the tissue lining the larynx, known as the laryngeal ventricles. As the tissue swells, it is pulled into the airway and causes further constriction. Early surgical correction of an elongated soft palate or stenotic nares may prevent the laryngeal saccules from everting. Everted laryngeal saccules must also be diagnosed under anesthesia.

Laryngeal paralysis is an uncommon finding in Pugs. It can obstruct the airway in two ways. First the vocal cords fail to retract and partially block the airway. Second, the arythenoid cartilages that form part of a framework of the larynx cannot be retracted and so fall across the opening of the larynx. Laryngeal paralysis can be congenital or acquired. The acquired form is often secondary to hypothyroidism and may respond to thyroid supplementation.

A frequent sign of laryngeal paralysis is a change in the dog's bark. Laryngeal paralysis is best diagnosed by observation of the larynx during respiration under anesthesia. Medical therapy with cough suppressants and bronchodilators is the preferred treatment of laryngeal paralysis. Surgical correction may involve removing the vocal folds, performing a tieback procedure of the arythenoid cartilages, or performing a permanent tracheotomy. Unfortunately, these procedures are usually less than satisfactory at relieving the obstruction and tend to make the affected dog prone to inhalation pneumonia.

Collapsing and hypoplastic (small, narrow) tracheas are usually congenital in Pugs. Affected dogs usually suffer from a chronic "honking" cough or dyspnea (difficulty breathing) during exercise. These conditions are usually diagnosed on radiograph. Narrowed or collapsed tracheas are very difficult to surgically correct and are usually treated medically with cough suppressants and bronchodilators.

Asthma is occasionally seen in Pugs. Affected individuals have overdeveloped and overactive smooth muscles in their bronchi, causing these airways to constrict inappropriately when exposed to irritants. Occasionally there is an allergic component to asthma, resulting in a seasonal cough or dyspnea. Dogs with asthma usually have a chronic unproductive cough that is responsive to bronchodilator and/or anti-allergy treatment. Diagnosis is usually made by ruling out other possible causes and observing response to therapy.

Recognizing the signs of a Pug with airway obstruction or COPD is the first important step in obtaining treatment. Pugs with airway obstruction breathe much more noisily while excited or exercising than their normal counterparts. If you can hear your Pug coming from two rooms away, or you can tell he's right beside you on your walks without glancing down, he most likely has an airway obstruction. These Pugs tend to be very exercise intolerant and overheat easily. Coughing, gagging up phlegm, or vomiting during exercise can also be a sign of airway disease.

Dogs that suffer from COPD or Brachycephalic Syndrome tend to be very gassy. The extra effort they put into breathing also causes them to swallow large amounts of air. They may appear bloated or potbellied from excessive air in their gastrointestinal tract. (One of the cardinal rules for distinguishing primary lung from primary heart disease on a radiograph is air in the stomach.)

Pugs that have obstructions that can completely block their airways, or whose lung disease is far enough progressed to change blood flow dynamics in their chest, can suffer fainting episodes. A bluish or grayish cast to the gums or tongue is also a sign of lung disease. Pugs with more advanced COPD tend to develop a barrel shape to their chest and to stand with their forelegs further apart to give their ribs more room to expand. These dogs may exert as much, if not more, effort exhaling as they do inhaling.

A veterinary workup for COPD will include a complete history to determine if any of the signs mentioned above are present. When an animal presents with exercise intolerance, difficulty breathing, or a cough, they must also be evaluated for primary heart disease. A careful physical exam and auscultation of the chest, radiographs and even an ECG may be required to distinguish between primary cardiac, or primary respiratory disease. It is important to determine which is the primary system that is affected because the treatment of the two conditions can be very different. If no obstructions are visible on radiology or physical exam, it may be necessary to examine the airway under anesthesia.

Treatment of chronic obstructive pulmonary disease is best accomplished by prevention. Early surgical correction of airway obstructions can prevent a lot of secondary damage to lung and heart tissue. Even if significant pulmonary or cardiac damage has occurred, surgical correction of airway obstruction is warranted to help halt the cycle of injury.

Medical treatment of COPD is aimed ad maximizing lung and cardiac function and minimizing the ongoing damage. Oral brochodilators such as Theophyline or Aminophyline, to expand the airways, are the mainstay of the COPD therapy. Unfortunately, it is virtually impossible to teach a Pug to use inhaler systems or portable oxygen tanks as are used in human therapy. Simethicone antigas preparations, such as Gas-X, are useful in reducing the amount of swallowed air in the stomach. A stomach distended with gas puts pressure on the diaphragm and restricts the amount lungs can expand.

Another drug which is useful at improving respiratory efficiency is Digoxin, a cardiac glycoside. In addition to improving the contractility of the heart muscle, Digoxin appears to improve the function of the diaphragmatic and intercostal muscles. Digoxyn should only be used in Pugs that have had a thorough cardiac workup, since the drug can worsen some cardiac arrhytmias if they are present.

Good dental hygiene in individuals with COPD is a valuable means of reducing low grade bacterial contamination of the lungs through inhalation. Pugs with COPD should have their teeth professionally scaled and polished on a regular basis. Maintaining clean teeth by brushing or using special mouth rinses containing chlorhexidine or zinc sulfate will reduce oral bacteria.

Periodic antibiotic therapy has been found to be useful in both humans and dogs with COPD to minimize bacterial populations in the alveoli. Even low grade bacterial contamination of the lungs will cause pulmonary white blood cells to release chemical factors that cause direct tissue damage. For this reason, periodic use of anti-inflammatory and even immunosuppressant therapy has also been advocated in COPD.

Treatment of secondary cardiac disease must be undertaken with care. Diuretics, such as Lasix, should be avoided in patients with lung disease. Individuals with COPD tend to breathe rapidly to compensate for their reduced lung capacity; as a result their lungs are usually slightly deshydrated from increased air movement. Dehydrating their lungs will only reduce their respiratory efficiency.

Fluid buildup in animal with both lung and heart failure is usually best handled through the use of vasodilating agents, such as nitroglycerine or Enalopril, to increase the fluid holding capacity of the circulatory system, rather than excreting excess fluid through the kidneys. Vasodilators have the added benefit of reducing the heart's workload by lowering the blood pressure it must pump against.

Prevention of chronic obstructive pulmonary disease through selective breeding should be of importance to all Pug breeders. In addition to attempting to improve and lengthen the lives of Pugs that suffer COPD, we have a responsibility as breeders to try to avoid producing affected animals.

The anatomical defects that contribute to COPD should be considered serious structural faults in any breeding program. The tendency to stenotic nares, elongated soft palates, and other problems seems to be hereditary. Please note, however, that external anatomy, such as muzzle length, does not necessarily correlates with the tendency to internal airway obstructions. There are many Pugs of excellent breed type with very flat faces and no respiratory problems. There are also Pugs with moderate length of nose that have significant airway trouble.

Before a Pug that does have an airway obstruction or COPD is bred, it should have its possible positive contributions to the breed weighed against the serious risk of perpetuating a problem.


© 1993 Melissa M. Norton, DVM. First published in The Pug Annual, 1993. Reprinted with permission from the author. Dr. Norton is the breeder of Timeliss Pugs as well as a veterinarian.