Successful emergency management of the animal with difficulty breathing demands that the clinician remain acutely aware of the fragility of the dyspneic patient. In a critically dyspneic animal, even a brief major body system evaluation can prove fatal, especially in cats. Consequently, the risks of any manipulation must be carefully weighed against the potential benefits. The stress of life-threatening disease coupled with transport and the unfamiliar surroundings of a noisy emergency clinic should never be underestimated. Dyspneic animals are often as their most fragile immediately following presentation and gentle restraint can prove life threatening. Apart from the most severe upper airway obstructions, most animals will benefit from a period in 100% oxygen in an oxygen cage prior to a complete major body system evaluation. Once an animal has suffered a respiratory arrest, the odds are hugely stacked against you—prevention is inordinately better than cure!
Respiratory assessment
Initial evaluation of the respiratory system comprises respiratory rate, effort and respiratory auscultation. A normal animal should have a respiratory rate of 15–30 breaths per minute and, because the majority of a resting inspiration is due to diaphragmatic contraction, there should be very little apparent chest movement. During normal inspiration, diaphragmatic contraction displaces abdominal viscera caudally and the abdominal wall moves out passively (i.e., the chest and abdomen move out together). It should therefore be intuitive that contraction of the abdominal muscles (abdominal effort) can only assist with expiration. This should not be confused with paradoxical abdominal movement, which is a manifestation of severe dyspnea. Much information can be gleaned from simply observing the breathing pattern of the patient while in 100% oxygen. One should look for the postural manifestations of dyspnea such as an extended neck, abducted elbows, open mouth breathing, an anxious facial expression, increased abdominal movement, and paradoxical abdominal movement. Straightening of the neck and open mouth breathing occur in both dogs and cats, however, some other postural manifestations of more severe dyspnea vary between species. Dogs prefer to stand with abducted elbows, while cats tend to sit in sternal recumbency. Constantly changing body position in cats implies a much worse degree of dyspnea than it does in dogs. Lateral recumbency due to dyspnea is a serious sign in a dog; however, it often means impending respiratory arrest in a cat. Another flag to pull out the endotracheal tubes is the marked mydriasis that cats will develop immediately prior to respiratory arrest. Remember that deciding to actively take control of the airway (which often only requires very small doses of sedative in severely dyspneic cats) is vastly superior to tubing them following a respiratory arrest.
Paradoxical abdominal movement occurs when increased intercostal contraction draws the diaphragm and abdominal viscera cranially on inspiration and the abdominal wall moves in (i.e., the chest and abdomen move in opposite directions). This can occur due to decreased lung compliance, upper airway obstruction, diaphragmatic rupture or paralysis, and occasionally, in cats with severe pleural effusion. The radiograph to the left is from a cat with diffuse interstitial metastasis and extremely non-compliant lungs. In addition to paradoxical abdominal movement, the intercostal muscles were actually being sucked in on inspiration.
The respiratory system can be divided into five divisions: the upper airway, small airways, pulmonary parenchyma, pleural space and the chest wall, and diaphragm. In a dyspneic animal, the respiratory pattern can sometimes help localize the level of the respiratory tract affected. Dynamic upper airway obstruction is usually associated with prolonged inspiration with inspiratory stridor or stertor, followed by a short expiration. An inspiratory dyspnea without stridor in a cat can occasionally occur with severe, chronic pleural effusion. Small airway disease, such as feline asthma, classically presents with a mixed inspiratory and expiratory dyspnea but with a longer expiratory phase and increased abdominal effort. Most other causes of dyspnea are associated with mixed respiratory patterns. Although it has been suggested that pleural space disease is associated with short shallow respirations, this pattern in not specific for pleural space disease, nor do all animals with pleural space disease present with short shallow respirations. One clinical scenario that is often associated with this respiratory pattern is pneumothorax, and in dogs with spontaneous, rather than traumatically induced pneumothorax, the degree of chest movement can be surprisingly mild for the volume of pneumothorax.
Pulmonary Auscultation
Pulmonary auscultation in the dyspneic patient is one of the true arts of veterinary medicine. It requires a good stethoscope and diligent practice. Basically, you have to make a serious effort; lackadaisical auscultations are tantamount to useless. With dedication, many respiratory abnormalities can be differentiated on physical examination alone, especially in cats. The easiest way to ensure a complete auscultation is to divide the chest into a tic-tac-toe board, then auscult each square. This enables comparison of dorsal, middle, and ventral aspects of the cranial, middle, and caudal lung fields. In a more stable patient, each individual stethoscope field can be ausculted. Lung sounds should be compared in different areas on one side of the chest and in the same area on opposite sides. Lung sounds are normally slightly louder and coarser in the cranioventral lung fields compared to the dorsocaudal fields. Indeed, in some large breed dogs and in animals taking very shallow breaths, it can be difficult to hear lung sounds in the caudodorsal chest. Lung sounds are symmetrical when the same area is compared on both sides of the chest except for the area of cardiac dullness in the cranial portion of the left ventral chest. This means that, regardless of whether one can determine which is the louder or quieter side, any asymmetry is abnormal.
Abnormal lung sounds can be classified as crackles or harsh lung sounds (i.e., louder and coarser than normal). The term “wheeze” is rather vague and often serves to confuse rather than clarify. In human medicine, subclassifying wheezes (rhonchi) has diagnostic relevance but in veterinary patients, subclassification of rhonchi is of questionable use. Occasionally, asthmatic cats and animals with other processes that narrow the conducting airways generate true wheezes, but many exhibit only harsh lung sounds. In deciding whether lung sounds are harsher than normal, one has to take into account the respiratory rate and effort and any referred upper airway sounds. A normal dog that is tachypneic following exercise will have harsh lung sounds. Therefore, one must determine whether the lung sounds are harsher than expected for the degree of tachypnea. This is especially important in dogs following motor vehicle trauma. Many are tachypneic from fear or pain and the increase in lung sounds from the tachypnea per se must be differentiated from that of pulmonary contusions. Harsh lung sounds can be due to parenchymal or airway disease. Somewhat surprisingly, many dogs with pneumonia or pulmonary contusions exhibit harsh lung sounds but not crackles. Pulmonary crackles can be either fine or coarse. Fine crackles are usually heard at the very end of inspiration and are probably generated by the opening of collapsed small airways. These are the ones you hear in sixteen-year-old Poodles with no parenchymal disease! Coarse crackles are usually associated with parenchymal disease but occasionally can be due to airway disease. In the author’s experience, the most severe airway crackles occur with eosinophilic bronchitis in dogs.
The distribution of abnormal lung sounds is very useful in differentiating respiratory disease. For example, most dogs with aspiration pneumonia often have harsh lung sounds or crackles in the cranioventral lung fields. The dorsocaudal distribution of harsh lung sounds or crackles can sometimes be appreciated in puppies with neurogenic edema. Mild to moderate cardiogenic edema is often associated with harsh lung sounds or crackles loudest over the heart base.
Pleural effusion allows the lungs to float in the dorsal aspect of the chest cavity so there is an absence of ventral lung sounds and the dorsal sounds are often harsh. Don’t be fooled by the heart sounds in cats with pleural effusion: they are not usually muffled and occasionally can radiate over a larger area of the chest than normal. In contrast to pleural effusion, pneumothorax results in muffling of the lung sounds in the dorsal pleural space as air accumulates in this area. Most people find pleural effusion easier to detect by auscultation than pneumothorax because the distribution of lung sounds is the opposite of normal (quiet ventrally and harsh dorsally). Many dogs with pneumothorax after being hit by a car also have pulmonary contusions that can complicate auscultation. The pneumothorax dampens lung sounds whereas the pulmonary contusion makes them louder and coarser. This can sometimes result in an absolute volume close to normal. With practice, one can appreciate that the lung sounds are both harsh and muffled, however, the severe dyspnea in such a patient with normal volume lung sounds should point towards concurrent pulmonary contusions and pneumothorax.
Putting it all together
The ability to establish a working diagnosis based on history and physical examination without additional diagnostics, such as chest radiographs, can mean the difference between life and death in some dyspneic animals. An immense amount of information can be obtained by simply watching the animal breathe in the oxygen cage and by assessing the animals body condition, in conjunction with the history and the degree of distress the animal is experiencing relative to the degree of chest movement. For example, a young cat in good body condition with a history of coughing and a mixed dyspnea with increased abdominal effort on expiration is more likely to have feline asthma. Although chest radiographs would be necessary to be sure, harsh lung sounds in all fields and the absence of a heart murmur or gallop, would just about clinch the diagnosis in most situations.
When empirical treatment must be instituted prior to a definitive diagnosis, good clinical reasoning and maintaining perspective as to the likely differentials is tantamount. The vast majority of cats that present for dyspnea have pleural effusion, heart disease, or asthma. The clinical findings in each of these conditions are often distinct. A severely dyspneic cat with a heart murmur or gallop rhythm and diffuse bilateral crackles will usually have cardiomyopathy or endomyocarditis and the benefits of intravenous or intramuscular furosemide almost always outweigh the potential risks. As previously mentioned, pleural effusion results in quiet ventral lung sounds and harsh dorsal sounds, whereas most asthmatic cats have lung sounds that are harsh in all fields (and hopefully not an incidental heart murmur!) and a concurrent history of coughing. Another example of maintaining perspective is in the puppy with dyspnea. The majority of two- to six-month-old puppies that present to our emergency service have neurogenic edema, rodenticide intoxication, or occasionally, pneumonia following kennel cough or distemper virus infection.
Although there is no replacement for following the problem-oriented approach with a complete problem list and all diagnostic differentials, the emergency clinical must always maintain perspective as to what are the most likely probable diagnoses. Respiratory distress is one of the most challenging situations facing the emergency clinician. Successfully managing these cases requires excellent physical examination skills, sound clinical reasoning and the ability to balance the fragility of the dyspneic patient with prudently obtaining diagnostic information.