Successful emergency management of the animal with difficulty breathing demands that the clinician remains acutely aware of the fragility of the dyspnoeic patient. In a critically dyspnoeic 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. Dyspnoeic 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!
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 dyspnoea. 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 dyspnoea 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 dyspnoea 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 dyspnoea than it does in dogs. Lateral recumbency due to dyspnoea 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 dyspnoeic animals) is vastly superior to tubing them following a respiratory arrest.
Paradoxical abdominal movement occurs when increased intercostal muscle 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 respiratory system can be divided into 5 divisions: the upper airway, small airways, pulmonary parenchyma, pleural space and the chest wall and diaphragm. In a dyspnoeic 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 dyspnoea 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 dyspnoea but with a longer expiratory phase and increased abdominal effort. Most other causes of dyspnoea 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 in the dyspnoeic 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 noughts and crosses 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.
In human medicine, adventitious lung sounds are subdivided into rales (crackles) and rhonchi (wheezes) and subclassifying rhonchi has diagnostic relevance. In veterinary patients subclassification of rhonchi is of questionable use and in this author's opinion, abnormal lung sounds should be classified as crackles or harsh lung sounds (i.e., louder and coarser than normal). The term "wheeze" is rather vague and confusing. Occasionally, asthmatic cats and animals with other processes which 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 tachypnoeic following exercise will have harsh lung sounds. Therefore, one must determine whether the lung sounds are harsher than expected for the degree of tachypnoea. This is especially important in dogs following motor vehicle trauma. Many are tachypnoeic from fear or pain and the increase in lung sounds from the tachypnoea per se must be differentiated from that of pulmonary contusions. Harsh lung sounds can be caused by 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 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 (which is often localized to these lung fields in mild to moderate cases). Cardiogenic edema may be associated with harsh lung sounds or crackles loudest over the heart base.
Pleural effusion allows the lungs to float into 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 may not be 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 which can complicate auscultation. The pneumothorax dampens lung sounds, whereas the pulmonary contusion make 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 dyspnoea in such a patient with normal volume lung sounds should point towards concurrent pulmonary contusions and pneumothorax.
The ability to establish a working diagnosis and treat on the basis of history and physical examination without additional diagnostics, such as chest radiographs, can mean the difference between life and death in some dyspnoeic animals. An immense amount of information can be obtained by simply watching the animal breathe in the oxygen cage and by assessing the animal's body condition, in conjunction with the history along with 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 dyspnoea 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 of asthma in most situations. When empirical treatment must be instituted prior to a definitive diagnosis, good clinical reasoning and maintaining perspective as to the likely differential diagnoses is tantamount. The vast majority of cats that present for dyspnoea have either pleural effusion, heart disease, or asthma. The clinical findings in each of these conditions are often distinct. A severely dyspnoeic 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 frusemide 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 which are harsh in all fields and a concurrent history of coughing (and hopefully not an incidental heart murmur!). Some cats may be so dyspneic that virtually any handling outside of 100% oxygen proves fatal. In these cases it is not unreasonable to treat for potential pulmonary edema and asthma with frusemide and an injectable, fast acting corticosteroid such as dexamethasone prior to establishing a definitive diagnosis. Another example of maintaining perspective as to the most likely diagnoses is in the puppy with dyspnoea. The majority of 2-6 month old puppies which present to our emergency service have either 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 dyspnoeic patient with prudently obtaining diagnostic information.
Oxygen delivery to the tissues is the product of the amount of blood flow (proportional to cardiac output) and the total oxygen content of the blood. Oxygen is carried in two ways in the bloodstream: bound to haemoglobin and dissolved in plasma. The vast majority of oxygen (approximately 98.5%) is carried by haemoglobin.
It is important to realize the difference between the partial pressure of oxygen, haemoglobin (Hb) saturation and oxygen content. The partial pressure of oxygen is the figure measured by blood gas analysis. The normal partial pressure of oxygen in arterial blood (PaO2) is 85-100 mmHg. Haemoglobin saturation is the percentage of Hb carrying oxygen. Oxygen content is the amount of oxygen carried by Hb plus the amount dissolved in plasma and can be calculated as follows:
Oxygen content = (1.34 x [Hb] x % saturation) + (0.003 x PaO2)
At a normal PaO2, Hb is almost completely saturated with oxygen. However, when Hb is exposed to the lower oxygen concentrations in the tissues it readily releases its oxygen. Haemoglobin can therefore be viewed as an oxygen reservoir for the tissues. As the PO2 falls from normal to 60 mmHg the saturation of Hb only falls from 97% to 90%. This means that even in hypoxaemic conditions, Hb can still carry adequate amounts of oxygen to the tissues. As can be seen in the oxygen Hb dissociation curve, as the pO2 falls below 60 mmHg the amount of oxygen carried by Hb falls rapidly and there is a risk of serious tissue hypoxia.
It is vitally important not to confuse the PO2 with the oxygen saturation (usually measured with a pulse oximeter). Any pulse oximeter reading less than 95% indicates low blood oxygen levels and a Hb saturation of less than 90% may be life threatening.
A patient with respiratory distress may need support of ventilation or oxygenation. Reduced ability to ventilate occurs with upper airway obstruction, reduced respiratory drive (respiratory muscle fatigue or paralysis) pleural space disease or abnormalities of the chest wall and diaphragm. Reduced ability to oxygenate occurs with the above conditions and also due to small airway disease (feline asthma) and pulmonary parenchymal disease. The 50:50 rule can be used to remember when blood gas abnormalities become life threatening, that is at a PaO2 < 50 mmHg or PaCO2 > 50 mmHg.
Arterial blood gas analysis
Measurement of arterial blood gases yields the most information regarding ventilation and oxygenation and also allows acid base assessment. Positioning and restraining a patient to obtain an arterial blood sample can be very stressful and even life threatening. In addition, patients with bleeding tendencies can have serious bleeding following arterial puncture. Obviously, measurement of blood gases requires that the practice have a blood gas machine, however, prices have fallen and portable, hand held devices can now be purchased for around £2000.
A pulse oximeter measures the saturation of Hb not the partial pressure of oxygen. It works by transmitting light through the tissues and detecting how much is absorbed during arterial pulsations. It does not measure ventilation and, as mentioned earlier, is relatively insensitive to early hypoxia. Pulse oximeter readings can also be inaccurate due to factors such as poor probe positioning, small patient size, patient movement, low pulse pressure and in dogs with pigmented skin.
Methods of OXYGEN supplementation
The simplest method is via an oxygen mask, however, some dyspnoeic animals become extremely distressed when their face is covered. In these patients it is best to hold the oxygen tubing next to the mouth and nose with no mask attached. This method is easy, cheap and readily available, and useful when performing the initial assessment of the animals but in many cases relatively low inspired oxygen concentrations are achieved. Another relatively simple and cheap method is a nasal catheter or human oxygen prongs in animals which will tolerate them. Local anaesthetic is instilled into the nostril and ten minutes later the tube is inserted. To determine the correct depth of placement the catheter is measured to the medial canthus of the eye. It should be anchored as close to nose as possible using either tape butterflies and suture or super glue. The inspired oxygen concentration attained using the intranasal method is variable depending upon the flow rate administered, the size of the animal, and whether it is open mouth breathing. A personal oxygen tent can be rigged using a Buster and cling film or the like. The oxygen tubing is then attached inside the collar. A space must be left so that the animal does not overheat or build up high levels of carbon dioxide. The best method of oxygen administration is using a special oxygen cage. These range from Perspex or polythene fronts for normal cages to temperature and humidity controlled microenvironment systems. The latter allow any oxygen concentration from room air to 100% and can keep large dogs cool which is difficult with other methods. They can also be used to deliver nebulised medication. Oxygen cages also provide a quiet stress free environment. The down side is that they are expensive and once a patient is inside the cage access is limited without letting oxygen out of the cage. The highest level of respiratory support is endotracheal intubation and artificial ventilation. This allows an inspired oxygen concentration of 100% and full control of ventilation and oxygenation, however, the major drawback is that the patient must be under general anaesthesia. Ventilation is also very expensive and labour intensive and for patients with lung disease, survival rates are poor. On the other hand, patients with certain causes of respiratory paralysis, such as cervical spinal cord disease, can have a very good prognosis with artificial ventilation.