The presence of respiratory distress indicates either a problems with obstruction (e.g. laryngeal paralysis) or the lungs or pleural space.
Respiratory distress is a common emergency. The presence of respiratory distress indicates either a problems with obstruction (eg. Laryngeal paralysis) or the lungs or pleural space. When the blood oxygen levels fall, increased respiratory rates and efforts are observed. Hypoxemia is defined as a low blood oxygen level and may result in significant morbidity and even mortality. It is very important to determine the cause of the distress, and at the same time minimize the stress to the patient. By the time respiratory distress is evident, there may be minimal reserves left. On the other hand, specific therapy based upon a known disease process (CHF versus asthma) is more likely to be successful than simple supportive measures.
There are five general causes of hypoxemia:
1. Hypoventilation (eg. intracranial disease or anesthetics suppressing respiratory center)
2. Decreased inspired oxygen concentration (eg. high altitude, general anesthesia mishaps)
3. Diffusion impairment (eg. pneumonia, pulmonary fibrosis)
4. V/Q mismatch (eg. COPD, PTE, interstitial lung disease)
5. Right to left shunt (eg. reverse PDA, tetralogy of fallot)
*Tip: The first four causes of hypoxemia respond to oxygen supplementation, while true right to left shunts do not.
In the initial evaluation of the patient with respiratory distress you want to achieve a brief but accurate (limited stress goes a long way for the patient in respiratory distress) as possible physical examination and history. For the history, the client should be questioned regarding pertinent medical history of the pet and the development/progression of the current clinical signs of the pet. Have the technical and emergency staff trained to inform/ask permission from the client at triage to place catheter, do blood work, radiographs, or simply we are going to put "Fluffy" in oxygen and as soon as she is stable the doctor will be out to talk to you and discuss findings/additional tests. Supplemental oxygen is warranted in patients with respiratory distress. Animals with signs of upper airway obstruction may be benefit more from sedation or even intubation, as in their case the hypoxemia is a result of inadequate air flow.
The initial physical examination may be limited if moderate to severe respiratory distress is present. However, it should include the three major body systems, heart, brain, lungs (auscultation with heart rate, assessment of perfusion/mental status, assessment of breathing pattern and rate), and temperature and weight (if possible).
Observation of the breathing pattern often provides valuable information to the origin of the respiratory distress/disease. Prolonged inspiratory time/stridor may be the result of upper airway obstructions. Upper airway obstructions typically produce loud sounds, including stridor (high pitched wheezing sound) and referred upper airway sounds during the inhalation phase of the respiratory cycle. The obstruction acts to block inspiratory flow through the airway and the sound that you hear results from turbulent flow. The sounds become louder with increased effort, because of greater flow and pressure changes (resistance) across the airway. Common examples of upper airway obstructions include laryngeal paralysis, cervical tracheal collapse, and components of the brachycephalic airway syndrome (breeds:Pugs, English Bulldogs). Upper airway obstructions are much less common in cats, but may occur with nasopharyngeal polyps, or other laryngeal masses (lymphoma, squamous cell carcinoma). Prolonged expiration/expiratory wheezes are typically seen in lower airway diseases such as feline asthma or chronic bronchitis. The expiratory cycle is affected, because the lower airway disease are associated with airway inflammation, mucous, smooth muscle hypertrophy. These changes can have a dramatic effect on exhalation. Rapid shallow breathing is typical seen in animals with pleural space diseases. Pleural effusions may result from congestive heart failure, neoplasia, pneumothorax, chylothorax, pyothorax, and others. Pleural effusions may also result from neoplasia (lymphoma), or diaphragmatic hernias (congenital or traumatic). Due to compression of lung tissue by the effusion, the lung capacity is subsequently reduced. Compensation causes an increase in respiratory rate, in order to make up for decreased tidal volume (minute ventilation = tidal volume X RR). Mixed inspiratory and expiratory effort, typically is associated with pulmonary parenchymal diseases (eg. pulmonary edema, pneumonia, pulmonary contusions, neoplasia or PTE).
Auscultation may help localize the obstruction to the upper airway (listen over the area of the trachea), or referred sound may be present on thoracic auscultation when evaluating the heart and lungs. The presence of abnormal heart sounds or rhythm (murmur/gallop/arrhythmia) is strong evidence for cardiac disease. Most animals that are dyspneic from heart failure are also tachycardiac, and cats tend to be hypothermic and may be relatively bradycardic. Crackles tend to indicate fluid in alveolar spaces, and are due to alveoli opening and closing. This may occur with congestive heart failure or any other cause of fluid accumulation. Cats with asthma often have wheezes and/or crackles. Wheezes are suggestive of the narrowing of small airways. Diminished heart and/or airway sounds, may suggest the presence of a pleural space disease (fluid, air, or space occupying lesions). Careful evaluation of the perfusion parameters (heart rate, pulse quality/rate, mm color and capillary refill time), as well as mental status (normal, depressed, obtunded, coma) can provide significant clues to the underlying etiology.
Tubing containing oxygen is held near the mouth and nose, either directly or with cone attached to concentrate near the face. This tends to be very easy, but labor-intensive and may stress the patient by blowing oxygen on their face. This requires a dedicated individual to stand near the patient and hold the tube. If patient is struggling it is not terribly effective and may not increase inspired oxygen concentration. It is mostly useful during initial presentation and stabilization.
Supplemental oxygen is connected to a clear plastic face mask. The mask is placed over the patient's mouth and nose. This method works well for weak or debilitated patients and may result in higher oxygen concentrations than flow-by. Better for small dogs and cats, where you maybe able to place their face in the mask itself.
Humidified oxygen may be administered via a soft flexible tube (usually red rubber or argyle tube) placed within the nostril. The tube is placed to the level of the medial canthus of the eye and then sutured in place. Nasal oxygen is particular useful in larger dogs. Some dogs require e-collars to prevent premature removal. Nasal oxygen is particularly easy to place as dogs are recovering from anesthesia, especially if suspected to require longer term oxygen supplementation past the anesthetic event. A good starting point is 50-100 ml/kg/min on the flow meter.
Supplemental oxygen may be delivered via an enclosed oxygen cage. Oxygen cages may be purchased as entire units (Snyder manufacturing) or occasionally converted from standard cages or human baby incubators. Oxygen cages are usually very well-tolerated but allow limited access to the patient. Also, depending on the unit specifications and size may cause larger dogs to overheat.
Positive pressure ventilation
Artificial ventilation may be used in patients not responding to more conservative methods of oxygen supplementation. Mechanical ventilators may deliver 21-100% oxygen and help to overcome the work of breathing in some patients with marked respiratory diseases. In the short term, and anesthesia ventilator may be used, but with long term use (>12 hrs) can cause oxygen toxicity. Long term ventilation requires the access to a critical care ventilator, educated staff, and intensive monitoring.
Therapeutic approach to the patient with severe dyspnea, includes giving oxygen, minimize stress (ie. no IV catheter, no radiographs until stable), and administer medications for specific known or suspected etiologies (eg. lasix for patients with pulmonary edema). If you are not sure the case of respiratory distress, consider lasix, ± glucocorticoids, ± thoracocentesis. Response to therapy may help reveal the accurate diagnosis. Mild-Moderate distress (more common) is treated as above, but with expand physical examination and historical questions. Additionally, consider radiography, advanced imaging (echocardiography), evaluating oxygenation/ventilation relationships with arterial blood gases or pulse oximetry.
Cats with dyspnea can be more challenging to manage over dogs with dyspnea. Common causes of feline respiratory distress are cardiogenic pulmonary edema (CHF), pleural effusion, asthma, upper respiratory infection and neoplasia. It is important to distinguish respiratory distress that is a presenting complaint from respiratory distress that develops during hospitalization.
Cats have a lower incidence of traumatic pulmonary contusion or pneumothorax than dogs, access to the outdoors may support a traumatic etiology. Physical examination findings are often helpful in determining the cause of feline respiratory distress. The body temperature is frequently subnormal in cats with heart disease, but is generally normal or even elevated with pulmonary disease. The presence of a heart murmur, gallop rhythm or arrhythmias is strong evidence for cardiac disease. Jugular venous distension may be present with heart disease, although some evidence suggests that jugular distension may accompany pleural effusion of any etiology. Crackles may be present with both pulmonary edema and asthma. Diminished respiratory sounds, particularly ventrally, often signifies pleural effusion as does a significant abdominal component to respiration.
Thoracic radiography is quite useful in determining the etiology of respiratory distress. It is very important to remember that radiographs are not therapeutic, and should not be performed prior to stabilization. The radiographic distribution of cardiogenic pulmonary edema in cats is variable compared with dogs. If a moderate to large volume of pleural effusion is present, it should be removed in order to improve the stability of the cat as well as to help aid in reaching the final diagnosis. Thoracocentesis is performed by first clipping a small amount of fur at the 7-9th intercostal space at the costochondral junction. The skin should be sterilely prepared and then thoracocentesis performed by carefully advancing a butterfly catheter (21gauge) through the skin and into the chest cavity. The intercostal vessels, which run on the caudal aspect of the rib, should ideally be avoided, but in practice this may be hard to appreciate in an average-sized cat. All the available fluid should be withdrawn. An aliquot of fluid should be retained in a serum tube and EDTA tube for culture (if indicated) and cytology respectively. As cats do not have an intact mediastinum, it is rare for fluid to pocket on only one side of the chest but they still usually require to have both sides taped for best results. Cytologic analysis of thoracic fluid may be diagnostic of heart disease, pyothorax, chylothorax or neoplasia. Pleural effusion from a cat with congestive heart failure is typically a modified transudate. Pyothorax may often be identified grossly due to the purulent nature and strong odor. Cytologically, pyothorax appears as degenerative neutrophils with a mixed bacterial population of intra and extracellular organisms. Chylothorax is distinctive for a white appearance of the fluid grossly and microscopically a predominance of lymphocytes. The triglyceride level will be markedly elevated and may if needed, be compared with the serum levels. Neoplastic effusions will vary depending on the tumor type. Lymphoma tends to exfoliate well. In dogs, anticoagulant rodenticide intoxication is a common cause for a hemorrhagic pleural effusion; however, in cats this is very rare.
Thoracic radiographs may also document bronchial infiltrates compatible with allergic airway disease. Occasionally, mild right-sided cardiomegaly (cor pulmonale) is also appreciated. After stabilization with oxygen and glucocorticoids, a transoral tracheal wash may be performed to evaluate the cat for signs of airway inflammation, infection or respiratory parasites. A transoral tracheal wash is performed by first pre-oxygenating the cat, then inducing a moderate place of anesthesia with propofol (2-10 mg/kg iv SLOWLY). A sterile tracheal tube should be placed and then 3-5 ml aliquots of sterile saline should be infused and the aspirated back through the tube. Frequently, better yields are obtained if the tube is also allowed to drain into a sterile specimen cup. Cytological evaluation typically documents an eosinophilic or neutrophilic inflammation. In some cases, a secondary bacterial infection is also present. Heartworm (antibody and antigen) and lung worm testing is warranted in cats from endemic areas.
Finally, in some cats with respiratory distress, echocardiography is required to document the presence or absence of heart disease. Heart disease can be present without auscultable abnormalities, and not all murmurs (even in dyspneic cats!) are associated with heart disease. Echocardiography in particular is useful to document cardiac function and to assess for signs of left atrial enlargement. Echocardiography should not be performed if a patient has marked respiratory distress. Thoracic ultrasonography may be particularly useful in cases of suspected mediastinal masses, for biopsy to determine tumor type. Mediastinal lymphoma often responds well to chemotherapy and thymomas may be cured with surgical excision.
Occasionally, a hospitalized cat will develop moderate to severe respiratory distress while being treated for some other unrelated disease. While in dogs a differential list of aspiration pneumonia, pulmonary thromboembolism, acute respiratory distress syndrome (ARDS) or fluid overload/heart failure may exist, in cats, almost all new on set respiratory distress is volume overload. Cats have a smaller intravascular space that dogs, and several days of three times maintenance fluids will trigger volume overload in many cats. Echocardiograpy or radiography may document previously occult heart disease and appropriate therapy involves decreasing or stopping the fluids and thoracocentesis (if pleural effusion is present).
Bay JD, Johnson LR. Feline Bronchial Disease/Asthma. In: Respiratory Diseases of Dogs and Cats. King LG, editor. WB Saunders Company, Phil Pa, 2004, pp 388-396.
Payne JD, Mehler SJ, Weisse C. Tracheal Collapse. Compendium. May 2006, pp 373-382.
Lee JA, Drobatz KJ. Respiratory Distress and cyanosis in Dogs. In: Respiratory Diseases of Dogs and Cats. King LG, editor. WB Saunders Company, Phil Pa, 2004, pp 1-11.
Mandell DC. Respiratory Distress in Cats. In: Respiratory Diseases of Dogs and Cats. King LG, editor. WB Saunders Company, Phil Pa, 2004, pp 12-16.