Approach to the patient in respiratory distress (Proceedings)


Patients presenting with severe respiratory distress have minimal respiratory reserves, so stress during physical evaluation and treatment must be minimized. Quick evaluation of the patient with minimal additional stress (i.e. radiographs, blood draws) is ideal so that accurate therapy can be instituted without delay.

Patients presenting with severe respiratory distress have minimal respiratory reserves, so stress during physical evaluation and treatment must be minimized. Quick evaluation of the patient with minimal additional stress (i.e. radiographs, blood draws) is ideal so that accurate therapy can be instituted without delay. Once the problem is localized, proper emergency treatment can be instituted prior to subjecting the patients to stressful or lengthy diagnostic tests, minimizing the risk of respiratory arrest.

Respiratory anatomy

The main function of the lungs is gas exchange, moving oxygen into the blood and carbon dioxide out. The air passages are made up of conducting airways, whose primary purpose is to move air into and out of the lungs, and the respiratory zone, where gas exchange occurs. Conducting airways are made up of the trachea, right and left main bronchi, lobar bronchi, segmental bronchi, and terminal bronchioles. These airways contain no alveoli and take no part in gas exchange thereby functioning as an anatomic dead space.

The respiratory zone is made up of respiratory bronchioles with occasional budding alveoli, and the alveolar ducts completely lined with alveoli. The respiratory zone makes up most of the volume of the lung.

The physiology of breathing

During inspiration the volume of the thoracic cavity increases, and air is drawn into the lung. Contraction of the diaphragm and intercostals increases the cross sectional area and draws air down to the terminal bronchioles. During expiration elastic recoil passively returns lungs to pre-inspiratory volume. This is a low-pressure system and requires little work in normal patients. Oxygen and CO2 move between air and blood by simple diffusion, as the blood-gas barrier is exceedingly thin with an enormous surface area.

Respiratory pathology

The location of respiratory disease may include the upper airways (laryngeal paralysis, upper airway obstructing foreign body or mass, pharyngeal/laryngeal airway swelling, hemorrhage, brachycephalic airway syndrome, collapsing trachea, nasopharyngeal polyps); lower airways (asthma, bronchopneumonia); lung parenchyma, including the interstitium and alveoli (pneumonia, edema, infiltrative disease, cardiogenic or non-cardiogenic edema, contusions); or may be extra-pulmonary, such as the pleural space (pneumothorax, pleural effusion, pleural space occupying masses, diaphragmatic hernia), thoracic wall, CNS or PNS, or systemic disease.

Respiratory failure may be a failure of ventilation, oxygenation, or both. Ventilation failure manifests as an increase in CO2 tension (hypercapnea). This is always accompanied by hypoxemia unless the patient is receiving supplemental oxygen. Ventilation failure can result from central or peripheral nervous system disease (cervical spinal cord injury, polyradiculoneuritis, central respiratory depressant drugs, etc.), chest wall trauma (flail chest), or pleural space disease (pneumothorax, diaphragmatic hernia, etc.).

Oxygenation failure manifests as hypoxemia. Causes of oxygenation failure can include decreased inspired oxygen (i.e. high altitude), ventilation-perfusion mismatch, a true shunt, hypoventilation, or diffusion impairment.

Ventilation-perfusion mismatch is the most common cause of oxygenation failure and occurs when there is an uncoupling of appropriately matched regional alveolar ventilation and blood flow. Examples of diseases that lead to ventilation-perfusion mismatch include pneumonia, inhalant lung injury, COPD, asthma, and cardiogenic or non-cardiogenic edema.

A true shunt or venous admixture results in the addition of un-oxygenated venous blood to the arterial system. Shunts may be extrapulmonary (congenital cardiac defects—VSD, PDA, and ASD) or intrapulmonary (lung consolidation or complete atelectasis resulting in blood flow to un-ventilated lungs). True shunts are rarely oxygen responsive.

Hypoventilation is always associated with elevated PaCO2 as well as hypoxemia. Addition of oxygen may correct the hypoxemia but will not correct the ventilatory problem.

Diffusion impairment results in a lack of equilibration of oxygen from alveolar gas to the blood. This usually results from a thickened blood-gas barrier with interstitial diseases (pulmonary fibrosis, interstitial neoplasia, severe edema). Oxygen supplementation often overcomes diffusion impairment.

Localization of respiratory pathology can be based on the respiratory rate and pattern of respiration. Two classic breathing patterns can be induced by alterations in the work of breathing. Obstructive diseases obstruct movement of air into or out of the lungs and are usually associated with increases in airway resistance. This typically results in a slower and deeper respiratory pattern than normal. Examples include chronic bronchitis/bronchiolitis, compressive tracheobronchial lesions, extraluminal compression, foreign body, neoplasia, and laryngeal diseases.

Restrictive diseases restrict the expansion of the lungs or chest wall. This is usually associated with decreases in compliance with stiffer lungs or chest wall. Restrictive diseases result in a faster and shallower respiratory pattern. Examples of restrictive diseases include pleural effusion, pneumothorax, diaphragmatic hernia, chest tumors, pulmonary fibrosis, edema, pneumonia, hemorrhage, embolism, severe abdominal distension, and severe obesity. These patient's lungs operate at smaller volumes.

Evaluation of the patient in respiratory distress

Initial evaluation comprises determination of the respiratory rate and effort, and thoracic auscultation. The normal respiratory rate is15-30 breaths per minute, and there should be minimal apparent chest movement. Non-respiratory causes of tachypnea should be ruled out and can include hyperthermia, acidosis, exercise, anxiety, anemia or RBC disorder, metabolic or endocrine disease (Cushing's, hyperthyroidism), and narcotic or other drug administration.

Observation of the animal can give some clues as to the severity of respiratory compromise. Extended neck, abducted elbows, open mouth breathing, anxious facial expression, increased abdominal movement, paradoxical abdominal movement, and straightening of the neck are all physical indications of respiratory distress. Other indications may include activation of accessory muscles for respiration (flaring of nostrils, intercostal rib retraction, movement of the cupula). Dogs have a tendency to stand and may abduct their elbows. Cats tend to sit in sternal recumbency with the chest elevated from the ground on close observation. Constant changing body position implies much worse degree of dyspnea in cats than it does in dogs.

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). Paradoxical abdominal movement occurs when excess 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 is often seen with pleural space disease (diaphragmatic hernia, chylothorax, other pleural effusion, pneumomediastinum, pneumothorax), but can also be seen with decreased lung compliance and upper airway obstruction.

Determination of the respiratory pattern can aid in diagnosis of the respiratory pathology. Animals that take shallow, rapid breaths with a small tidal volume often have a restrictive disorder such as disease leading to stiff lungs, pleural space disease or thoracic wall disease. Prolonged, deep breaths often indicate airway narrowing. This pattern of breathing helps to avoid airway collapse caused by rapid pressure changes. Cheyne-Stokes or apneustic pattern breathing usually indicate CNS disorders.

Animals should be evaluated to determine if the respiratory effort is worse on inspiration or on expiration. Increased inspiratory effort indicates an upper airway obstruction or disorder. These patients may have a gasping type inspiratory effort with minimal air movement, pronounced inspiratory stridor or whispering type sounds, or paradoxical abdominal movement during inspiration. These patients may be anxious or panicked. Diseases of the pleural space or chest wall, or diseases leading to severe loss of lung compliance can also lead to an increased inspiratory effort, as the patient is unable to expand its lungs with each inspiration.

Increased expiratory effort can result from lower airway obstruction or disorder (asthma, COPD, infectious bronchitis). This is often accompanied by an expiratory push.

An increase in both inspiratory and expiratory effort often results from diseases of the lung parenchyma leading to both lower airway obstruction as well as loss of compliance.

Noise of breathing should also be evaluated on respiratory patients. Upper airway noises can include stertor, which is a loud, sonorous noise like a snore, from the nose or nasopharynx; and stridor, which is a harsh, high pitched sound typically heard on inspiration and originating in the laryngeal area.

Lower airway noises may manifest as crackles, wheezes, or diminished sounds. Crackles are discontinuous tiny popping sounds. Fine crackles may be heard at the end of inspiration, due to opening of collapsed small airways and can be normal in older dogs. Coarse crackles are usually associated with parenchymal disease, but occasionally airway diseases can cause these.

Location of the crackles should be determined to help determine location of the lung disease. Wheezes (musical noises) occur from air moving through narrowed or collapsed airways. Pleural space diseases often lead to diminished lung sounds ventrally with effusion, and dorsally with pneumothorax. Heart sounds are usually not diminished with pleural disease.

Localizing disease based on other clinical symptoms

Coughing can result from airway disease (asthma, COPD, or pulmonary parasites such as filaroides or heartworm); or cardiac disease (secondary to pulmonary edema or compression of the mainstem bronchus). Character of the cough should be ascertained. A productive cough suggests excess mucus or edema, or pneumonia. A hacking cough that is harsh and forceful is often indicative of tracheobronchial disease. A soft cough may indicate pneumonia or pleuritis, as these can be painful diseases. A dry cough may come from cardiac mainstem bronchus compression, tracheobronchitis, or neoplasia. If a click is heard with the cough, consider tracheal collapse. Nocturnal coughs are most often associated with cardiac causes. A stimulated cough may indicate tracheal inflammation or collapse, and a honking cough is the classic sound of collapsing trachea.

Nasal discharge should also be evaluated for its character. Serous or watery discharge can come from a healthy animal, an animal with a viral infection, or may indicate early bacterial infection. A mucopurulent (white, greenish, or yellow mucus) discharge can indicate infection, oral disease, a foreign body, neoplasia, nasopharyngeal polyps, or inflammatory disease. A hemorrhagic discharge (epistaxis) can be from trauma, neoplasia, fungal infection, an acute foreign body, or a bleeding disorder. The discharge should also be assessed as a unilateral or bilateral process.


With respiratory emergencies, timing is everything. The ability to localize a disease without stressful diagnostic tests may be vital in helping to narrow our differentials as early as possible. This will allow the clinician to choose an accurate and appropriate treatment plan in order to relieve the patient's respiratory distress without further endangering the patient's life.

References available by request.

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