Respiratory distress is a common presenting complaint in the emergency clinic. It represents a life threatening condition that warrants immediate medical or surgical attention to restore tissue oxygenation. Tissue oxygen delivery is determined by two variables: cardiac output and blood oxygen content. Blood oxygen is most dependent on hemoglobin concentration and oxygen saturation of hemoglobin (SaO₂). Although the amount of oxygen dissolved in the plasma (PaO₂) is small when compared to the amount of oxygen carried on hemoglobin, understanding the relationship between PaO₂ and SaO₂ has important clinical ramifications. PaO₂ and SaO₂ are related by the oxygen dissociation curve. As hypoxia develops (secondary to hypoventilation, diffusion impairment, shunt, or V/Q mismatching) and PaO₂ drops from 100, the SaO₂ does not decrease markedly for some time because of the flat nature of the curve for PaO₂ values from 80 to 100. Clinically, this means that: i) Animals with some degree of respiratory compromise can compensate and maintain a reasonable level of tissue oxygenation; and ii) A pulse oximeter reading (measuring SaO₂) may not reflect the severity of the respiratory compromise. As the PaO₂ falls further, the slope of the oxygen dissociation curve becomes steeper. This means that small decreases in the PaO₂ result in progressively greater hemoglobin desaturation, decreased tissue oxygen delivery, and subsequent death. Clinically, many animals present on this "threshold of disaster". They have used up all their compensatory mechanisms. Any further decrease in ventilation or increase in oxygen demand will cause complete decompensation.

Practically, this means that animals with respiratory difficulty should be handled with minimal restraint to prevent or to minimize struggling, which increases oxygen consumption. Procedures such as jugular venipuncture often result in struggling and breath holding, further compromising oxygenation. However, intravenous access is mandatory in the dyspneic patient. A catheter is placed using minimal restraint and blood collected for an emergency database. Immediate oxygen supplementation should be provided, using a mask, oxygen cage or tent. Although nasal and transtracheal oxygen supplementation methods are described, they are probably not applicable to a severely dyspneic animal. If the airway is not patent at presentation, it should be cleared and if necessary, the animal intubated. If an obstruction prevents intubation, then emergency tracheostomy should be performed.

The animal is examined during or after stabilization, depending on its condition. It is important to rule out cardiac disease as a cause of respiratory distress. In dogs and cats, cardiac disease often is associated with heart murmurs, gallop rhythms, muffled heart sounds (pericardial effusions), or cardiac arrhythmias. If no cardiac abnormalities are detected on the initial physical examination and ECG, consideration should be directed at pulmonary or extrapulmonary causes of respiratory distress. A great deal of information can be gained by careful observation of the breathing pattern before beginning a physical examination. An animal with a long inspiratory phase and an associated stridor on inspiration most likely has an upper airway obstruction. If respiratory distress occurs mainly during expiration, the animal may have a dynamic obstruction within the chest cavity. Severely irregular respiratory rhythms are almost invariably associated with central nervous system abnormalities. Poor airway compliance due to pulmonary parenchymal disease or restricted lung expansion often results in rapid and shallow respirations. Airway narrowing or fixed obstruction may be manifested as very slow and prolonged respirations.

Upper airway disease may involve the pharynx, larynx, or trachea. Differential diagnoses for disease processes affecting the upper airway include edema, infection, foreign bodies, neoplasia, and neuromuscular and degenerative diseases. The most common upper airway diseases seen in non-brachycephalic dogs are laryngeal paralysis (large breeds) and collapsing trachea (small breeds). One of the hallmarks of upper airway disease is respiratory noise on inspiration. Animals with dynamic extra-thoracic airway obstruction (eg, laryngeal paralysis) will have severe inspiratory difficulty. Collapsing trachea patients may have both inspiratory or expiratory difficulty depending upon the location of the collapsing segments of the trachea. Often these animals respond well to sedation. Sedation with acepromazine (30 - 50 ug/kg iv or im) is indicated in animals with adequate perfusion. The work associated with breathing often generates a great deal of heat, and monitoring the temperature is important in these animal. Cooling is best achieved by cool intravenous fluids. Some of these animals with laryngeal or tracheal edema can benefit from anti-inflammatory doses of corticosteroids.

Animals that stabilize with medical treatment can have a more detailed physical examination performed. The clinician should keep a broad range of differential diagnoses in mind. The airway should be palpated externally for laryngeal, perilaryngeal, or tracheal masses. Radiographs of the larynx, trachea and thorax should be made, provided the animal does not become stressed in lateral recumbency. In many instances, a final diagnosis of many pharyngeal and laryngeal conditions cannot be made until the pharynx and larynx are inspected under light general anesthesia. Recommended anesthetic agents include propofol, barbiturates, and perhaps narcotics. When assessing laryngeal function, the anesthetic should be titrated so the animal is still gagging during the examination.

Some animals with upper airway obstruction remain extremely dyspneic and require intubation. Endotracheal tubes with a variety of diameters, lengths and stiffnesses should be available. Anesthesia is titrated to effect allowing laryngeal function to be evaluated quickly, and the animal is intubated. Definitive surgical treatment or tracheostomy is then performed.

Tracheotomy is performed with the animal in dorsal recumbency, with the neck clipped and prepared for aseptic surgery. The cricoid cartilage is palpated and a midline incision is made caudal to it for approximately 4-5 cm. The sternohyoid muscles are split and retracted. A transverse incision is made in the annular ligament between two tracheal rings, at least two rings caudal to the cricoid cartilage. A monofilament suture is placed around a tracheal cartilage immediately caudal to the tracheotomy. This suture will allow the incision to be raised into the incision to facilitate replacement of the tracheostomy tube if necessary. The tracheostomy tube should be no larger than 75% of the tracheal diameter. It should be cuffed if positive pressure ventilation is required, and should have an inner cannula to facilitate cleaning. The tube is secured with sutures to the skin of the neck and with an umbilical tape encircling the neck. In some brachycephalic dogs, it is necessary to loosely suture the tube to the trachea to prevent displacement.

Air passing through the tracheostomy tube bypasses the upper airway, and is not warmed, humidified, or filtered. Postoperative care of a patient with a tracheostomy tube should include intravenous fluids to ensure adequate hydration, nebulization at the tracheostomy site, and frequent removal and cleaning of the inner cannula to prevent obstruction of the tube with mucus. Suctioning of the trachea should be avoided if possible, as it can significantly decrease arterial PaO₂ and irritate the tracheal mucosa.

Diseases of the pleural space, thoracic wall, and diaphragm may cause severe respiratory distress. Thoracic wall abnormalities such as rib fractures or flail chest are relatively easy to diagnose. Rib fractures are often associated with lung contusion or lacerations of intercostal blood vessels. Although pain, pneumo/hemothorax, and inadequate movement of the affected segment of the chest wall all contribute to decreased ventilation, often it is the pulmonary contusions which impair adequate ventilation to the greatest degree. Non-displaced rib fractures are managed conservatively. Intercostal nerve blocks reduce pain and may improve ventilatory efforts. Displaced rib fracture fragments often require surgery, and may be removed or repaired by internal fixation. Flail chest, a condition where ribs are fractured both dorsally and ventrally, is clinically impressive as the flail segment moves paradoxically to the chest wall during respiration. Much attention has been given to surgical stabilization of the flail segment, but experimentally, large flail segments do not significantly compromise respiration. It is, therefore, important to look beyond the rib fractures and consider the pain associated with the fractures and underlying pulmonary contusions as major causes of impaired ventilation and gas exchange. The pain can be treated by intercostal nerve blocks or intrapleural bupivicaine. Systemic analgesia with narcotics should be administered cautiously as the narcotics may cause respiratory depression. Most patients are treated by external splinting to eliminate paradoxical motion. The flail chest segment is secured to a polyvinyl-orthoplast mold using large circumcostal sutures of non-absorbable material (0 or #1 nylon or Prolene). Sternal luxations are rare and require crossed IM pin and wire internal fixation if there is much pain or respiratory compromise. Most cases are sternal subluxations which are managed conservatively.

Open pneumothorax is a true life threatening emergency. Animals present with a wound that sucks air when the skin obstructing the thoracic penetration is moved. Some animals will present in respiratory arrest. They should be intubated and ventilated immediately, and a chest tube inserted into the "sucking" chest wound. The area around the wound and tube is covered with a water soluble gel and an occlusive dressing to provide an airtight seal. The pleural space can then be evacuated and the animal stabilized for definitive treatment.

Diaphragmatic rupture and pleural space abnormalities are not as obvious as rib fractures. Clinical findings include diminished respiratory sounds either unilaterally or bilaterally, and rapid, shallow respirations. Definitive diagnosis of diaphragmatic rupture requires thoracic radiographs, ultrasound, or contrast radiography. A contrast upper gastrointestinal study has been recommended for the diagnosis of diaphragmatic rupture. This will be diagnostic if a portion of the intestinal tract is present within the thorax. However, this is not always the case. In such cases, an intraperitoneal contrast study may be helpful. Two milliliters/kg body weight of 25% iodinated contrast material (not barium) may be injected into the peritoneal space. Abdominal and thoracic radiographs taken five to fifteen minutes post injection may reveal contrast material in the thoracic space confirming the diagnosis of a diaphragmatic rupture. Definitive repair of the diaphragmatic rupture requires surgery. Definitive repair may be delayed until the next day if the patient is stable, and can be observed throughout the night. Immediate surgical repair should be done if the patient cannot be stabilized due to respiratory compromise secondary to the tear. The presence of the stomach within the thorax warrants immediate surgery because little can be done to relieve gastric distention if it occurs. General anesthesia is induced rapidly and without any stress. Controlled respiration should be instituted immediately with care taken not to exceed 15 to 20 cm H₂O airway pressure during positive pressure ventilation. Higher airway pressure has been associated with uncontrollable pneumothorax after surgery in cases of chronic diaphragmatic hernia. In addition, some animals in which lungs were forcefully re-inflated at surgery developed substantial and sometimes fatal postoperative pulmonary edema. This appears to be a manifestation of reperfusion injury, with oxygen radicals causing massive increases in pulmonary capillary permeability. A cranial ventral midline laparotomy is used for repair of most diaphragmatic hernias. The incision may be continued cranially through the sternum if viscera are adhered in the thorax. The abdominal organs are gently returned to the abdomen. The hernial opening may be enlarged if necessary. The edges of the diaphragm are sutured and a chest tube is placed prior to closure. The lungs are not forcibly inflated. Chronically atelectic lung lobes are left alone and will usually reinflate several weeks after surgery.

Pleural effusions may be due to a variety of causes including congestive heart failure, neoplasia, infection, lung lobe torsion, vasculitis, hepatic disorders, coagulopathy, pulmonary thrombosis, diaphragmatic hernia, and chylothorax. Respiratory signs are usually a result of restriction of expansion of the lungs resulting in small, rapid respirations. Effusions may be unilateral or bilateral. Diminished ventral respiratory sounds are detected during auscultation of the chest. If pleural effusion is suspected in an animal with severe respiratory distress, thoracocentesis is often diagnostic and therapeutic. The area over the lateral chest wall is clipped and prepared. A butterfly needle can be used to tap the pleural cavity in cats and nearly all non-obese dogs under 35 kg. The fluid should be analyzed.

Some cases of severe pneumothorax, pyothorax, and chylothorax require chest tube drainage as an emergency procedure. Although chest tubes can be placed using local anesthetic, chest tubes are best placed with the animal intubated under general anesthesia. The animal is rapidly clipped and prepared before induction of anesthesia. Small doses of narcotics or rapidly acting barbiturate are titrated to allow intubation in dogs. Barbiturate or ketamine/valium are used in cats. In cases of tension pneumothorax, more air will accumulate in the pleural space with each positive pressure ventilation; it is, therefore, imperative that a small incision is rapidly made into the pleural cavity. The skin over the thorax is grasped firmly and pulled from the 12^th intercostal space cranially to the 8^th intercostal space. An incision is made at the 8^th intercostal space and a hemostat used to dissect down to and then gently through the tough parietal pleura. The chest tube is inserted into the pleural space directly through this incision. The surgeon must check to ensure that all fenestrations in the tube are in the pleural cavity. The skin is released, creating a subcutaneous tunnel that prevents atmospheric air from leaking around the tube into the pleural space. The tube is secured to the skin with a Chinese fingertrap suture. The surgeon must insure that all connections to the tube are secure and leakproof.