Primary Survey (Triage) and Resuscitation

Animals with complete large airway obstruction are unconscious and apneic. Partial large airway obstruction causes noisy breathing (stridor or stertor), heard without the aid of a stethoscope. Cyanosis and anxiety are often present with loud referred airway sounds heard throughout the thorax on auscultation. Compromise of the extrathoracic airway (nasal passages, pharynx, larynx, or cervical trachea) causes inspiratory stridor; compromise of the intrathoracic trachea or bronchi causes expiratory stridor. Stertor is most common with pharyngeal disease. Possible causes of large airway pathology include foreign bodies, edema, laryngeal paralysis or paresis, tracheal collapse, elongated soft palate, aspiration of stomach contents, neoplasia, and pharyngeal hematomas. Animals with severe small airway obstruction have labored breathing with an expiratory push of the diaphragm, cyanosis, and anxiety. Auscultation reveals high-pitched wheezes throughout the lung field. In severe life-threatening situations, the animal is cyanotic, open-mouth breathing, collapsed, and asphyxiating. Common causes include anaphylactic reactions; asthma (cats); and bronchial obstruction from edema, mucus, exudates, or foreign material.

Unconscious, apneic animals require immediate tracheal intubation. The clinician should be practiced in orotracheal intubation of animals in dorsal, lateral, and sternal recumbency. If an obstruction is present, it must be immediately relieved (with suction, manual removal, or the Heimlich maneuver) or bypassed via emergency tracheotomy. Once an airway is established, confirmed, and secured, ventilation is initiated with 100% oxygen via a bag-valve-mask. Should auscultation during ventilation detect absent or muffled lung sounds indicative of pleural fluid or air, immediate thoracocentesis is warranted. Heart sounds and pulses are checked and, when absent, cardiopulmonary resuscitation (see Cardiopulmonary Resuscitation) is initiated.

With partial large airway obstruction, flow-by oxygen is delivered through oxygen tubing at a high flow rate aimed at the open, panting mouth until an airway is secured or, if appropriate, a transtracheal or nasotracheal oxygen line is placed. Heavy sedation using a narcotic/tranquilizer (eg, butorphanol 0.2–0.4 mg/kg with or without acepromazine 0.01–0.05 mg/kg) combination may be used to relieve anxiety and struggling, to allow a cursory examination of the pharynx and larynx, and to remove pharyngeal foreign bodies. When tracheal intubation is necessary, general anesthesia should be induced using rapid-acting IV anesthetics such as etomidate (0.5–3 mg/kg), ketamine/diazepam combination (5–20 mg/kg and 0.1–0.4 mg/kg), or propofol (6–8 mg/kg to effect). The ability of the laryngeal cartilages to abduct during inspiration should be assessed during intubation and a full oropharyngeal examination performed when time allows. A tracheotomy is necessary when pharyngeal, laryngeal, or tracheal pathology prevents orotracheal intubation or when prolonged intubation is anticipated. A transtracheal catheter can be used to provide oxygen support during stabilization. When the airway pathology lies within the thoracic cavity, airway patency must be established down to the bifurcation of the trachea. Once the airway is established, it should be secured with a tie and inflation of the cuff mechanism, as well as confirmed with at least two of the following methods: palpation of the tube within trachea in the cervical region, ausculation of the lungs and visualization of chest wall movement when a breath is administered, visualization of the tube entering the airway, placement of an end-tidal CO₂ monitor, or radiographs.

Cyanosis from small airway obstructive disease is treated by providing oxygen by flow-by, hood, or nasal cannula and sedation with a narcotic/tranquilizer combination. Epinephrine is given for its bronchodilatory effects both in anaphylaxis (0.01–0.02 mg/kg, IV) and in life-threatening asthma (0.02 mg/kg, IM). Corticosteroids (prednisone sodium succinate, 15 mg/kg, IV, or dexamethasone, 2–4 mg/kg, IM or IV) are given for allergic bronchitis, asthma, or severe swelling of the larynx or pharyngeal tissues. Other bronchodilators, such as aminophylline or terbutaline, are given IM, or albuterol can be given by nebulization in the case of an animal in crisis. Also see the calculator on this page for various emergency drug doses for dogs and cats.

Compromised breathing in both dogs and cats manifests with an increased respiratory rate and effort, immediately followed by a change in the respiratory pattern. Postural changes (orthopnea) follow; dogs stand with the elbows abducted and the back arched or high on the rear haunches with the head and neck extended, whereas cats may sit crouched on all four limbs with the sternum slightly elevated. Obvious labored, open-mouth breathing, and changes in mucous membrane color (gray and/or blue [cyanosis]) develop last and indicate significant loss of pulmonary function and impending pulmonary arrest.

The location of the pathology—pleural space or parenchymal disease—can be determined at presentation by careful observation of the breathing pattern and auscultation of the thorax. This will direct resuscitative efforts. Taking radiographs or performing stressful diagnostic procedures before the animal has been stabilized can lead to rapid decompensation.

Pleural space disease causes asynchronous breathing. The chest expands on inspiration as the abdomen is pulled inward, then the chest moves inward on expiration as the abdomen expands. In cats, breathing is slower and more deliberate than in dogs. The respiratory pattern is the same whether air, fluid, or abdominal contents are in the pleural space. Thoracic auscultation reveals muffled lung sounds over the affected regions.

Lung parenchymal disease causes quiet, smooth breathing, with the chest and abdominal wall moving in the same direction. Inspiration and expiration are equally labored unless concurrent small airway edema or constriction adds an expiratory push. Cats demonstrate rapid, shallow synchronous breathing, often with movement of the cupula. Thoracic auscultation reveals louder than normal lung sounds in early phases. As disease progresses, harsh lung sounds with moist crackles and rales are heard over the affected lungs. Pulmonary edema may be cardiogenic, often accompanied by a murmur, gallop, or arrhythmia noted on auscultation and mild hypothermia. Other differential diagnoses include CNS disease, pneumonia (viral, parasitic, fungal, or bacterial), aspiration, pulmonary contusions, or hemoglobin abnormalities. Noncardiogenic pulmonary edema may be caused by seizures, electrocution, after an acute airway obstruction (such as after choking or near-drowning) and acute lung injury, or respiratory distress syndrome.

Thoracic radiography should be performed only when the animal is able to tolerate the procedure. Radiographs can help differentiate many of these diseases; however, imaging should not delay therapy. Some animals may be more tolerant of ultrasonography. The thoracic focused assessment with sonography (TFAST) technique may be used to identify pleural fluid and air, examining both hemithoraces between the fifth and sixth ribs ventrally and between the seventh and ninth ribs dorsally. A pneumothorax may be present when the "slide sign" is absent; this is a linear movement noted between the visceral and parietal pleura and requires practice to identify.

Oxygen is administered immediately via flow-by, mask, hood, or oxygen cage techniques. Sedation with a narcotic/tranquilizer combination (butorphanol 0.2–0.4 mg/kg, IV or IM, with or without acepromazine, 0.05 mg/kg, IV or IM) can relieve struggling and anxiety. Longterm continuous supplemental oxygen is best provided by a nasal oxygen catheter. The intranasal oxygen catheter is placed after topical anesthetic has been instilled into the nostril where the tube is to be inserted. Humidified nasal oxygen flow rates of 50–100 mL/kg/min deliver 40%–60% inspired oxygen while allowing the animal to be examined and the underlying disease treated. Nasopharyngeal or nasotracheal catheters or bilateral nasal cannulas may provide higher percentages of inspired oxygen. If cyanosis and decompensation persist or work of breathing is profound, intubation and positive-pressure manual ventilation or mechanical ventilation with 100% oxygen is necessary.

Catastrophic pleural space disease with rapid cardiovascular decompensation, absent lung sounds throughout the thorax, and a barrel-shaped chest suggests tension pneumothorax. A routine thoracocentesis is often inadequate for these animals, so an intercostal incision or placement of a large-bore catheter is necessary: lidocaine is injected for local anesthesia, a small skin incision is made between ribs (at the seventh to eighth intercostal space), and hemostats are used to enter the pleural space, relieving the tension within the thorax. This allows cardiovascular filling and lung reexpansion. The open pneumothorax is then managed by placing a chest tube and surgically closing the intercostal incision.

When breathing is severely compromised by pleural air or fluid without tension pneumothorax, the pleural space should be drained by thoracocentesis. The intended site is clipped and aseptically prepared (when time permits). If fluid is expected, the needle is inserted ventrally between the sternum and costochondral junction. When air is to be recovered, the needle is inserted into the dorsal half of the thorax, above the costochondral junction. A local anesthetic is placed into the skin, subcutaneous tissue, and intercostal muscle at the site to be tapped. After the needle is inserted just through the skin, a drop of saline is placed in the hub of the needle. The needle is then gradually inserted straight into the thorax (with the needle perpendicular to the chest wall) until the saline in the needle hub moves. The movement of the saline in the hub indicates that the pleural space has been entered, although this may not always occur. The needle is immediately directed so that it lies against the parietal pleura. This prevents laceration of the lung by the needle as the lung reexpands. As soon as the pleural space is entered, the evacuation apparatus (an IV extension set, 3-way stopcock, and syringe) is attached and aspiration begins. In animals in which the pleural space cannot be emptied (eg, tension pneumothorax, ongoing hemorrhage) or when repeated chest taps are required within minutes to hours, an indwelling chest tube should be placed for continuous closed suction until the problem resolves or futher therapy is performed.

Lung parenchymal disease is primarily treated using oxygen supplementation, sedation to relieve anxiety, and therapy directed at the underlying cause. Cardiogenic edema is usually associated with a gallop, murmur (determined by auscultation), arrhythmia, and/or mild hypothermia and responds well to furosemide administration (1–4 mg/kg, IV, every 1–2 hr) in all but the most severe of cases. Furosemide is more effective when delivered as a constant-rate infusion (1–2 mg/kg/hr). Cardiogenic edema can benefit from venodilation from nitroglycerin ointment (¼ in. for cats and ½ in. for larger dogs) applied topically to a shaved area of the abdomen, inguinal region, or directly to a mucous membrane; severely affected animals with normal blood pressure may benefit from a balanced vasodilator (nitroprusside, 0.5–10 mcg/kg/min), tapered up slowly and monitoring blood pressure continuously to keep the mean arterial pressure >85 mmHg. After initial stabilization, further diagnostic procedures (eg, thoracic radiography and echocardiography) aid in determining the cause and specific therapy. Animals with proteinaceous fluid (such as occurs with noncardiogenic pulmonary edema, respiratory distress syndrome, pneumonia, etc) will not respond to simple diuretic therapy. If oxygen supplementation does not maintain PaO₂ >60 mmHg (pulse oximetry or SpO₂ >90%), or if PaCO₂ ≥60 mmHg, or if there is moderate to severe increases in work of breathing despite oxygen therapy, then manual or mechanical positive-pressure ventilation is required.

If respiratory failure is imminent with pulmonary fluid visible in mouth or nares, then intubation, airway suctioning, and manual bag-valve-mask ventilation with 100% oxygen are required. Elevated or postural pulmonary parenchymal evacuation (EPPE) can be performed with two or more people elevating the pet vertically, head down, while guarding the endotracheal tube. The thoracic cavity is manually compressed to assist airway and lung fluid drainage. Manual ventilation with 100% oxygen and suction of the airway should be performed between EPPE efforts.

Animals with circulatory compromise have alterations in their physical perfusion parameters (ie, heart rate, mucous membrane color, capillary refill time [CRT], rectal temperature, pulse quality, and level of consciousness). Careful auscultation of the heart for a murmur, gallop, arrhythmia, or muffled heart sounds and of the lungs for evidence of fluid is important to help identify heart failure as a cause of poor perfusion. Measurement of arterial blood pressure, central venous pressure, central venous PaO₂, and serum lactate provide objective data for reaching resuscitation endpoints and monitoring trends of change after resuscitation.

In the early compensatory stages of hypovolemic shock in dogs, there is a rapid heart rate, pink to red mucous membranes, rapid CRT, and bounding pulses; the animal is most often alert and responsive. Animals with a significant amount of pain or anxiety may appear to be in compensatory shock; pain medications are warranted, and time for the animal to acclimate to the environment is helpful. This stage is rarely identified in cats. Tachycardia is often the first and only sign, so persistent tachycardia must be considered a sign of decreased perfusion and addressed as such. As the pathology progresses, dogs begin to have pale mucous membranes, prolonged CRT, weak pulses, tachycardia, and a decreased level of responsiveness—the classic signs of the middle or early decompensatory stage of shock. Cats have gray mucous membranes, slow CRT, weak or absent pulses, hypothermia, and a normal or low heart rate. As shock approaches the terminal stages, the heart rate slows in both dogs and cats, and animals begin to lose consciousness. Clinical signs in this terminal stage include heart failure, pulmonary edema, severe hypotension, oliguria, and abnormal respiratory patterns. Cardiopulmonary arrest is a common sequela.

The therapeutic goal is to deliver oxygen and substrate to the tissues. This requires a heart that effectively pumps blood and adequate hemoglobin, intravascular volume, vascular tone and patency, as well as sufficient oxygen and substrate for cellular metabolism. General guidelines for treatment of hypovolemic and distributive shock are described below, but modifications may be needed for specific animals or disease processes.