Respiratory Emergencies PDF

R e s p i r a t o r y Em e r g e n c i e s Carissa W. Tong, BVM&S, MRCVS a , Anthony L. Gonzalez, DVM b,c, * KEYWORDS  Respiratory distress  Hypoxemia  Oxygen  Ventilation KEY POINTS  Respiratory distress has a wide spectrum of severity in initial presentation.  The method of oxygen sup...

R e s p i r a t o r y Em e r g e n c i e s Carissa W. Tong, BVM&S, MRCVS a , Anthony L. Gonzalez, DVM b,c, * KEYWORDS  Respiratory distress  Hypoxemia  Oxygen  Ventilation KEY POINTS  Respiratory distress has a wide spectrum of severity in initial presentation.  The method of oxygen supplementation selected should provide the highest fraction of inspired oxygen while minimizing patient stress.  Rapid identification of respiratory distress and localization of respiratory disease play a vital role in stabilization efforts and subsequent diagnostics performed. INTRODUCTION Disorders of the respiratory system are a common cause for seeking emergency care in small animals. Presenting clinical signs can have a wide spectrum of severity, with some patients presenting with a mild cough whereas others present in fulminant respiratory distress with imminent fatigue and respiratory or cardiac arrest. Prompt recognition of respiratory distress and the ability to localize upper versus lower respiratory tract dysfunction are important in order to initiate appropriate management in a timely manner. As such, the emergency clinician needs to have an understanding of general respiratory physiology and the pathophysiology and management techniques as they relate to common respiratory diseases seen. This article reviews the basic anatomy of the respiratory tract, physiology relating to gas exchange and development of hypoxemia, and a stepwise approach when faced with a patient in respiratory distress, including localization within the respiratory tract, stabilization and initial diagnostic testing. ANATOMY OF THE RESPIRATORY SYSTEM The respiratory system can be divided anatomically into the upper and lower airways, pulmonary parenchyma, pleural space, and thoracic wall. Collectively, the respiratory system functions to move air in and out of the patient (ventilation) and to perform gas a Emergency and Critical Care, Cornell University Veterinary Specialists, 880 Canal Street, Stamford, CT 06902, USA; b Cornell University Veterinary Specialists, 880 Canal Street, Stamford, CT 06902, USA; c Emergency and Critical Care, Cornell University College of Veterinary Medicine, Ithaca, NY, USA * Corresponding author. Cornell University Veterinary Specialists, 880 Canal Street, Stamford, CT 06902. E-mail address: [email protected] Vet Clin Small Anim 50 (2020) 1237–1259 https://doi.org/10.1016/j.cvsm.2020.07.002 0195-5616/20/Published by Elsevier Inc. vetsmall.theclinics.com 1238 Tong & Gonzalez exchange at the level of the alveoli (oxygenation).1 Upon inspiration, air enters through the upper airways, which consists of the nasal cavity, nasal sinuses, nasopharynx, larynx, and trachea. This is known as the conducting zone and is where air encounters the most resistance as it is filtered, warmed, and humidified.1 Air then travels into the lower airways, which consist of bronchi, bronchioles, and the components of the respiratory zone, which includes respiratory bronchioles, alveolar ducts, alveolar sacs, and alveoli.1 The respiratory zone is where gas exchange occurs in the pulmonary parenchyma via diffusion between the alveoli and capillary blood at the level of the alveoli.1 Gas exchange occurs along a concentration gradient, allowing oxygen to enter the capillary to then be delivered to tissues and carbon dioxide (CO2) to enter the alveoli for expiration. The lower airways and pulmonary parenchyma are contained within the pleural space of the chest cavity, which is outlined laterally by the thoracic wall and caudally by the diaphragm. The thoracic wall, diaphragm, and pulmonary parenchyma work together to create negative pressure within the pleural space, ensuring ventilation and oxygenation occur appropriately.1 The respiratory system is equipped with several built-in defenses against invading pathogens that include nasal hairs, turbinates, the mucociliary apparatus, cough and sneeze reflex, and alveolar macrophages.1 CAUSES OF HYPOXEMIA Hypoxemia is defined as a partial pressure of oxygen in arterial blood (PaO2) less than 80 mm Hg, with severe hypoxemia defined as a PaO2 less than 60 mm Hg. Hypoxemia develops when the process of ventilation or oxygenation does not occur appropriately.2 The 5 causes of hypoxemia include low fraction of inspired oxygen (FiO2), global hypoventilation, right-to-left shunt, diffusion impairment, and ventilation-perfusion (V/ Q) mismatch. In clinical practice, V/Q mismatch is the most common cause of hypoxemia, with a variety of diseases as the potential underlying cause, such as moderate to severe pulmonary parenchymal diseases (eg, pneumonia and pulmonary hemorrhage) and pulmonary thromboembolism (PTE).2 ANATOMIC LOCALIZATION Most respiratory diseases can be localized to a specific region of the respiratory system. The ability of the clinician to correctly and rapidly identify the affected region is crucial, because it ensures that the most effective stabilization efforts take place in a timely manner. Numerous studies have shown that a patient’s respiratory pattern and breathing sounds can be utilized to identify the source of respiratory distress.3–5 Localization allows clinicians to create a focused differential diagnosis list and pursue subsequent diagnostics and therapeutics as indicated (Table 1). It is equally important for the clinician to be able to recognize patients who are not in true respiratory distress, despite similar appearance. Nonrespiratory look-alikes describe diseases that can result in increased respiratory effort and tachypnea. These can occur secondary to causes unrelated to the respiratory system, such as electrolyte disturbances, metabolic changes, and secondary to pharmacologic interventions. Upper Airway Patients with upper airway disease present with increased effort and prolongation during inspiration. Diseases that involve the more rostral portion of the upper airway (eg, nasopharynx) commonly produce stertorous breathing, described as a snoring noise.4 Diseases in the more caudal portion of upper airway (eg, larynx) tend to produce stridorous breathing, described as a high-pitched whistle.4 Both stertor and stridor reflect Respiratory Emergencies Table 1 Anatomic localization of the respiratory system with associated diseases and clinical signs Anatomic Location Common Diseases Clinical Signs Upper airway      Prolonged inspiration  Stertor  Stridor Lower airway  Chronic bronchitis  Feline asthma  Prolonged expiration  Wheezing  Coughing Pulmonary parenchyma  Cardiogenic pulmonary edema  Noncardiogenic pulmonary edema  Pneumonia  Contusions  Variable thoracic auscultation  May have an impact on both inspiration and exhalation  Signs of systemic illness Vascular  PTE  Acute respiratory distress  Severe respiratory effort with unremarkable parenchymal auscultation Pleural space      Restrictive breathing pattern  Decreased heart and lung sounds on auscultation Thoracic wall  Flail chest Brachycephalic airway syndrome Tracheal collapse Laryngeal paralysis Nasopharyngeal polyps Pleural effusion Pneumothorax Diaphragmatic hernia Mediastinal/pleural masses  Paradoxic breathing pattern  Lack of chest wall movement increased resistance to airflow encountered in the upper airways. Patients begin to open-mouth breathe as a way to bypass this resistance to air intake and subsequently can become hyperthermic. Obstruction to air movement in the upper airway can be static or dynamic in nature. Static obstructions can be caused by extraluminal or intraluminal masses (eg, neoplasm in dogs and polyps or neoplasms in cats), trauma, or foreign bodies. Dynamic obstructions are seen more commonly in dogs, with the most common underlying diseases including laryngeal paralysis, brachycephalic obstructive airway syndrome, and tracheal collapse.4 With severe obstruction and increased respiratory effort, airway mucosal edema can develop, which exacerbates the already increased resistance to airflow. A portion of these patients may present as orthopneic, where emergent intubation is necessary to reestablish a patent airway. Lower Airway With lower airway disease, increased effort and prolongation are seen during exhalation, because there is an increased resistance secondary to airway narrowing or collapse. An expiratory push can be seen in patients in attempts to overcome this resistance. Patients often have a chronic history of a combination of coughing, wheezing, and respiratory distress.4,6 The most common lower airway disease seen in cats is feline asthma.6 Recently, potassium bromide has been reported to cause neutrophilic-eosinophilic lower airway disease in cats.7 In dogs, lower airway disease may include chronic bronchitis, eosinophilic bronchopneumopathy, or neoplasia. Pulmonary Parenchyma Patients with pulmonary parenchymal disease can have increases in both inspiratory and expiratory effort, with accompanying increases in chest and abdominal wall 1239 1240 Tong & Gonzalez excursions.5 Abnormalities in lung sounds, such as crackles, wheezes, or absence of lung sounds, can be noted on auscultation.5 These patients also can exhibit signs of systemic illness. The pulmonary parenchyma can be affected by a variety of diseases, including pulmonary edema (cardiogenic or noncardiogenic), bronchopneumonia, contusions, hemorrhage, and interstitial diseases. Cardiogenic pulmonary edema should be suspected in patients presenting in respiratory distress with pulmonary crackles and a concurrent heart murmur. In cats, the concurrent presence of a gallop rhythm, hypothermia, tachycardia, and tachypnea is strongly suggestive of underlying cardiac disease causing distress.3 The absence of a heart murmur does not rule out a cardiac cause for respiratory cause of respiratory distress in cats. In addition to murmurs, dysrhythmias also should be made note of because dogs with arrhythmogenic right ventricular cardiomyopathy and dilated cardiomyopathy do not often develop a murmur but may have dysrhythmias present. Noncardiogenic pulmonary edema can be caused by head trauma, prolonged seizures, and acute upper airway obstruction, such as strangulation or sharp pull of a neck lead.8 The edema formation is thought to occur secondary to massive sympathetic activity that leads to increased hydrostatic pressure and permeability in the lungs.9 Numerous types of pneumonia exist in dogs and cats, including aspiration, lipid, hematogenous, infectious, and parasitic pneumonia.10 Clinical signs may be mild earlier in the disease, with patients exhibiting an intermittent soft cough.10 As the disease progresses, patients can develop a productive, moist cough with development of increased respiratory effort, exercise intolerance, fever, and often systemic signs, such as anorexia and severe lethargy.10 Vascular PTE is a potentially life-threatening condition where an obstruction of a pulmonary vessel or vessels by a thrombus occurs secondary to an underlying disease that causes hypercoagulability.11 The pulmonary artery is affected most commonly. An acute PTE can cause significant hypoxemia such that the patient can develop respiratory distress in the face of unremarkable thoracic auscultation or radiographs.11 Pleural Space Abnormal accumulation of fluid, air, or soft tissue (eg, mediastinal mass or diaphragmatic hernia) can occupy the pleural space and result in a reduction of functional residual capacity,12 the volume of gas that is left behind in the lungs at the end of expiration after a normal tidal breath.1 This volume maintains a gas reserve between breaths and prevents small airways from collapsing.1 As such, patients classically present with a rapid, shallow restrictive breathing pattern. A dyssynchronous (or paradoxic) breathing pattern also has been shown to be associated with pleural space disease.4 On auscultation, patients with pleural effusion or soft tissue accumulation often have decreased lung sounds ventrally, whereas patients with air accumulation tend to have decreased lung sounds dorsally. Fluid accumulation in the pleural space (pleural effusion) can occur secondary to various disease processes, including right-sided heart failure, neoplasia, infection (pyothorax), hemorrhage (hemothorax), and chylothorax.12 Dogs presenting with hemothorax should be evaluated for concurrent pericardial effusion and pulmonary hemorrhage, because anticoagulant rodenticide toxicity can lead to diffuse hemorrhage. A pneumothorax can develop secondary to blunt or penetrating trauma, esophageal perforation, rupture of pulmonary lesions (eg, neoplasia or bullae), lung lobe Respiratory Emergencies torsion,12 and has been reported to occur spontaneously in cats with chronic lower airway disease.13 Thoracic Wall Thoracic wall diseases include congenital malformation, trauma-induced injury, cervical spinal disease, and neuromuscular disease.14 Disease of the thoracic wall can be identified by decreased outward movements of the thoracic wall during inspiration, which leads to hypoventilation. Patients with thoracic wall disease often have short and shallow breaths with decreased chest expansion, increased abdominal effort and may exhibit cheek puffing. They do not respond to oxygen because their primary problem is ventilation, not oxygenation, and as such, may require mechanical ventilation. Look-Alikes Acid-base and metabolic disturbances Patients with metabolic acidosis may develop tachypnea as a compensatory mechanism to normalize systemic pH by blowing off CO2.15 Kussmaul breathing, which is described as a deep, slow, labored breathing pattern, can develop in patients with profound metabolic acidosis.15 Electrolyte disturbances (hypokalemia and hypocalcemia) and hypoglycemia also can have an impact on respiratory muscle function.16,17 Cats with hyperthyroidism can exhibit signs such as tacyhpnea, including tachypnea, and in chronic unregulated cats exhibit respiratory weakness and, and reduced respiratory muscle contractions.18 Decreased oxyhemoglobin content A decrease in oxyhemoglobin content adversely affects the ability of oxygen to carry and deliver oxygen, resulting in tissue hypoxia. This can be seen in patients with anemia or dyshemoglobinemias (eg, carboxyhemoglobin and methemoglobinemia).19,20 Tachypnea develops as a compensatory mechanism for the tissue hypoxia. Pain/distress Patients can become severely tachypneic due to sympathetic stimulation secondary to pain or stress causing alteration in their respiratory pattern.21 Pain caused by thoracic wall injuries also can limit expansion of the thoracic wall, leading to shallow breathing and hypoventilation.14 Pharmacologic Various medications also may create abnormalities in the respiratory pattern of a patient. Some opioids can cause central respiratory depression (eg, fentanyl), whereas others (eg, hydromorphone and methadone) cause tachypnea and panting. Agents that induce neuromuscular blockade (eg, atracurium) may cause respiratory paralysis. Propofol is a drug used for induction of anesthesia in small animal patients and frequently causes respiratory depression or apnea. Slow administration of propofol can reduce apneic events. Pretreatment with flow-by oxygen is recommended to avoid propofol-induced hypoventilation and hypoxemia during anesthesia induction. PATIENT HISTORY Obtaining an accurate and detailed history can be extremely informative. A patient’s history prior to the onset of distress can provide either a clear cause for the respiratory clinical signs (eg, traumatic injury) or valuable information for the clinician to pair with the signalment and examination findings when beginning to formulate a list of 1241 1242 Tong & Gonzalez differential diagnoses. For example, a young dog that presents for increased respiratory effort may lead the clinician to consider infectious pneumonia as the top differential diagnosis, whereas the same presentation in an older dog with a history of voice change may lead the clinician to consider laryngeal paralysis with secondary aspiration pneumonia. It also is prudent to ask questions about relevant preexisting medical conditions (eg, cardiac disease, neoplasia, and endocrinopathies) and any current medications the patient is receiving. Depending on the presenting signs, potential exposure to various toxins, such as smoke inhalation or anticoagulant rodenticide, should be asked about. The speed of progression of respiratory distress also should be ascertained as it helps clinicians prioritize diseases on their differential lists. In cats, signs of lethargy and abnormal behavior may precede respiratory distress. Lastly, depending on the region, the patient’s travel history also may help rule in or out other infectious causes of respiratory illness, such as fungal disease. INITIAL STABILIZATION Patients presenting in respiratory distress should be considered critical because many can be on the verge of decompensation and respiratory arrest. Their tolerance of stress from handling and restraint is minimal, creating a very narrow window for evaluation, which requires an organized and strategic approach to an initial assessment. The plan should be shared with the support team to ensure everyone moves in unison with any needed equipment or instruments made readily available and to avoid unnecessary stressors that can further exacerbate respiratory compromise. Oxygen Therapy Oxygen therapy should be provided immediately upon triage for patients presenting in respiratory distress. There are various ways to provide supplemental oxygen in small animals (Table 2). Ideally, the method selected would provide the highest FiO2 with the Table 2 Methods of oxygen supplementation Method of Oxygenation Mean Fraction of Inspired Oxygen Achieved (%) Flow-by oxygen 24–45 Face mask 35–55 Unilateral nasal catheter 30–50 Bilateral nasal catheter 30–70 Oxygen hood 21–60 Oxygen cage 21–60 HFOT 21–100 Positive-pressure ventilation 21–100 Hyperbaric oxygen 100 Adapted from Sumner C, Rozanski E. Management of respiratory emergencies in small animals. Vet Clin North Am Small Anim Pract. 2013;43(4):799-815; with permission. Respiratory Emergencies least amount of stress imposed on the patient. This ultimately is determined on an individual basis, taking into account patient characteristics, severity of hypoxemia, and clinic resources. Flow-by oxygen Flow-by oxygen is the simplest method to provide supplemental oxygen, is generally well tolerated, and can reach FiO2 levels of 0.25 to 0.4 with flow rates of 2 L/min.22 Drawbacks to this method are that it achieves a low FiO2, requires a handler to hold the oxygen tubing to the patient, and ultimately is a short-term strategy. Oxygenation has been shown to be significantly improved if oxygen is provided with a face mask compared with conventional flow-by techniques, where the oxygen tubing is held near the patient’s nares.23 Flow-by and face mask techniques allow short-term provision of oxygen and are well suited during initial patient assessment for immobilized patients or those recovering from anesthesia. Oxygen hoods Oxygen hoods can be better tolerated than face masks, especially with patients who are mobile. Although available for purchase, an oxygen hood can be made easily by fitting an Elizabethan (E)-collar on the patient with a clear plastic wrap that covers two-thirds of the hood, allowing the remaining space open for ventilation and elimination of heat and CO2. An oxygen tube is secured to the inner aspect of the E-collar.24 An oxygen hood has been shown to achieve an oxygen concentration of 70% within 90 seconds.25 Patients should be closely monitored as the use of an oxygen hood does carry a risk for accumulation of CO2 and condensation with subsequent overheating.24 Oxygen cage Oxygen cages often are utilized to provide a constant rate of oxygen supplementation. Commercially available cages are designed to regulate FiO2, temperature, and humidity with a scavenger system for CO2.24 Cages are a minimally invasive way to provide oxygen supplementation up to a concentration of 60% and allow for continuous visual monitoring of the patient. Use of an oxygen cage is limited by a patient’s size, as larger dogs either do not fit in the cage or tend to overheat. A caretaker’s ability to hear respiratory sounds is muted by the door. In addition, whenever the door or window is opened for monitoring or therapy, there is rapid loss of oxygen concentration within the cage.24 Nasal oxygen Nasal oxygen is a more invasive modality compared with the options discussed previously. This can be provided via placement of a nasal catheter or use of commercially available nasal prongs. Nasopharyngeal catheters can be made from a red rubber atheter or infant feeding tube and generally are easily placed and well tolerated by most patients.24 The placement of nasopharyngeal catheters is outlined in Box 1. Nasal prongs are limited in use as the prongs do not fit every patient, whereas with nasal catheters, the size of the catheter used can be adjusted based on the size of a patient’s nares. Placement of bilateral nasal catheters allows for higher oxygen concentrations, of up to 50% to 60%, to be reached, versus a unilateral nasal catheter, achieving oxygen concentrations of 27% to 40%.26 Both nasal prongs and nasal catheters should be connected to a humidified oxygen source to minimize desiccation of the nasal mucosa.24 Nasal oxygen may prove less effective in patients that are panting excessively. 1243 1244 Tong & Gonzalez Box 1 Nasopharyngeal oxygen catheter placement Equipment required 1. Oxygen flowmeter with attached bubble humidifier 2. Red rubber catheter A. 3.5F to 5F for small dogs and cats B. 5F to 8F for medium dogs C. 8F to 10F for large dogs 3. Sterile lubricating jelly 4. Proparacaine ophthalmic drops or 2% lidocaine gel 5. Nonabsorbable suture material and suturing instruments 6. E-collar 7. With or without Christmas tree adapter Procedure 1. Apply 2 drops of proparacaine ophthalmic drops or topical lidocaine gel into the desired nares. 2. Premeasure the tube from the nose to the lateral canthus of the eye and mark the tube accordingly. This places the tip of the tube into the nasopharynx. 3. Apply a small amount of lubricating jelly onto the distal end of the tube. 4. Insert the tube into the nose and advance until the premarked point. A. Cats: insert the tube in a ventromedial direction. B. Dogs: insert the tube in a dorsomedial direction, then ventromedially. 5. Once the tube is in place, secure the tube as close to the nasal planum as possible using the Chinese finger trap suturing method. A second suture should be placed either on the side of the face or on the forehead. 6. Connect the catheter to the oxygen tubing and turn on flowmeter. 7. Place E-collar to prevent the patient from removing the catheter. Adapted from Boyle J. Oxygen Therapy. In: Burkitt Creedon JM, Davis H eds. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. 1st ed. Chichester, UK: Wiley-Blackwell; 2012:263-273; with permission. High-flow oxygen therapy High-flow oxygen therapy (HFOT) has gained use as a noninvasive method to support the hypoxemic patient when conventional oxygen therapy is not sufficient.27–29 It involves the use of specialized nasal cannulas that allow the administration of heated and humidified oxygen at concentrations up to 100% with flow rates as high as 60 L/min. It is speculated that HFOT provides patients with some degree of positive end-expiratory pressure/continuous positive airway pressure.27 HFOT has been shown to be a successful therapeutic option with minimal complications in a population of dogs with moderate to severe hypoxemia.27 Hyperbaric oxygen therapy Hyperbaric oxygen therapy involves the delivery of 100% oxygen that is pressurized to a value above atmospheric pressure, allowing more oxygen to be made available for diffusion into the pulmonary capillaries.30 It has been reported to be beneficial in patients with carbon monoxide poisoning, severe burns, wounds, and thromboembolic Respiratory Emergencies diease, as well as post-cardiopulmonary resuscitation.30 Hyperbaric oxygen therapy is not a widely available treatment modality in veterinary medicine and thus its use in acute hypoxemia has not been fully validated. Complications of Oxygen Therapy  Oxygen toxicity: prolonged exposure to high oxygen concentrations (eg, 100% oxygen for more than 12 hours) can predispose patients to oxygen toxicity. It is believed that the toxic effects are due to the formation of oxygen-derived free radical species, which induce endothelial and epithelial cell damage, increase endothelial permeability, and ultimately cause inflammation and alveolar damage.22  Absorption atelectasis: high concentrations of oxygen being delivered to the alveoli result in a washout of the nitrogen support skeleton, resulting in alveolar collapse.22  Hypoventilation: hypoventilation is seen in patients where oxygen has replaced CO2 as the main respiratory stimulus, such as patients with chronic obstructive pulmonary disease. Under normal conditions, CO2 is a primary stimulus for breathing. In animals with chronic obstructive pulmonary disease or in some brachycephalic breeds, oxygen replaces CO2 as the stimulus for breathing. Supplementation with oxygen can decrease respiratory drive and result in significant hypoventilation.22 Establishing Intravascular Access Obtaining vascular access is a key component of emergency stabilization of the patient with respiratory distress. It gives the clinician the ability to intravenously (IV) administer rapidly acting drugs for bronchodilation, sedation, or induction of anesthesia if emergent endotracheal intubation is needed (Table 3). A peripheral IV catheter should be placed once the patient is deemed stable enough to endure restraint. Over-the-needle peripheral catheters are used routinely and can be placed readily in the cephalic, accessory cephalic, or lateral saphenous vein. Sedation Sedation and anxiolytics often are used in the emergency setting to reduce the stress associated with respiratory difficulty. This is useful particularly with patients in an upper respiratory crisis. In patients in whom an underlying cardiac cause has not been fully ruled out, the decision to use sedation should be made cautiously as some sedative agents have a degree of cardiovascular depressant effects.31 For a majority of patients, low-dose butorphanol (00.1–0.3 mg/kg; IV, intramuscularly [IM], or subcutaneously [SQ]) and/or acepromazine (0.005–0.02 mg/kg; IV, IM, or orally) can be considered because they have a rapid onset of action and can be administered IM. A disadvantage of butorphanol and acepromazine is that neither of them has direct reversal agents. Benzodiazepines, such as midazolam or diazepam, could be considered as adjunct sedatives, with a 0.1 mg/kg to 0.3 mg/kg dose, IV, IM (midazolam only), or PO. The benzodiazepines may cause excitement, particularly in cats.31 Appropriate monitoring should take place with any use of sedatives, such that any adverse effects can be acted on and immediately reversed, when necessary. Other Pharmacologic Agents Bronchodilators could be considered in patients presenting with lower airway disease, such as feline asthma or bronchitis. Both aminophylline (8–10 mg/kg, IV) and terbutaline (0.01 mg/kg, SQ or IM) are injectable bronchodilators, which should be considered 1245 1246 Tong & Gonzalez Table 3 Common pharmacologic agents used in respiratory emergencies Drug Dose Route Comments Acepromazine 0.005–0.02 mg/kg IV, IM, PO  May cause hypotension Aminophylline 8–10 mg/kg IV  May cause tachycardia, central nervous system stimulation Butorphanol 0.05–0.3 mg/kg IV, IM  May cause respiratory depression Dexamethasone sodium phosphate 0.1–0.15 mg/kg IV, IM, SQ  Anti-inflammatory dose Dexmedetomidine 2–5 mg/kg IV, IM  Reversible  Minimal respiratory depression Diazepam 0.2–0.4 mg/kg IV  PO may cause fulminant hepatic failure in cats  Reversible  May cause excitement or myoclonus if given alone Furosemide 1–4 mg/kg IV, IM, SQ  May cause prerenal azotemia, worsen preexisting nephropathies Midazolam 0.2–0.4 mg/kg IV, IM  Reversible  May cause excitement or myoclonus if given alone Terbutaline 0.01 mg/kg IM, SQ  May cause tachyarrhythmias Data from Plumb DC. Plumb’s Veterinary Drugs. https://www.plumbsveterinarydrugs.com. Updated September 2017. Accessed December 10, 2019. initially due to the ease of administration. Aminophylline causes direct bronchial smooth muscle relaxation, increases the strength of diaphragmatic contraction, has weak chronotropic and inotropic effects, and can lead to centrally mediated respiratory stimulation in some patients.31 Injectable glucocorticoids can be a valuable tool to reduce swelling in patients presenting with an upper airway obstruction, such as in laryngeal paralysis or brachycephalic airway syndrome. Dexamethasone sodium phosphate (0.1–0.15 mg/kg, IV, SQ, or IM) is commonly utilized as it has a quick onset (1–2 h) and an intermediate duration of action (24–36 h).31 Long-acting steroids (eg, methylprednisolone acetate) have mineralocorticoid effects that can lead to acute plasma volume expansion. As such, they are not recommended in the acute setting because they may precipitate congestive heart failure, particularly in cats.32 It also is important that clinicians establish whether a patient recently has been given nonsteroidal anti-inflammatories prior to presentation, because coadministration with glucocorticoids may precipitate adverse gastrointestinal effects, such as ulceration and perforation. In patients where congestive heart failure is suspected or not able to be completely ruled out, a trial dose of injectable furosemide (1–4 mg/kg; IV, IM, or SQ) can be considered. Improvement of clinical signs after furosemide administration may help clinicians further narrow down their differential diagnoses to cardiac causes. Control of Hyperthermia Patients presenting with respiratory distress, in particular brachycephalic breeds or dogs with laryngeal paralysis, often are unable to thermoregulate.33 Active cooling measures should be started immediately when hyperthermia is noted in order to minimize the development of deleterious systemic effects (eg, disseminated intravascular Respiratory Emergencies coagulation).34 Active cooling via a fan, wetting the fur, or even shaving down the fur may be considered to reduce the core body temperature. Cooling efforts should be discontinued once the core body temperature reaches 103.5 F to 104 F (39.7 – 40 C) to prevent rebound hypothermia and shivering.34 Often, sedation and oxygen supplementation prove sufficient. EMERGENCY PROCEDURES Thoracocentesis Thoracocentesis involves entering the thoracic cavity, most commonly to remove fluid or air from the pleural space. A thoracocentesis generally is performed between the seventh and ninth intercostal spaces, with the needle directed dorsally for air and ventrally for fluid. The site of needle insertion can be guided by use of a cage-side ultrasound to visualize accessible pockets of fluid or an area where there is an absent glide sign indicating a pneumothorax.35 Based on patient size, the pleural space can be entered with a butterfly catheter such as in cats and small dogs, or with a needle or over-the-needle IV catheter of various gauges in medium to large dogs. A thoracocentesis can be either of diagnostic value, where the goal is to collect a sample to confirm the presence and/or evaluate the cause of air or fluid accumulation, or of therapeutic value, where the volume removed is sufficient to alleviate clinical signs. Development of respiratory signs in cats and dogs due to pleural effusion occurs once a volume of 20 mL/kg and 30-60 mL/kg is reached within the pleural space, respectively.36 In patients with moderate to severe distress, a thoracocentesis should be performed prior to any additional testing, such as venipuncture or thoracic radiographs. Risks associated with thoracocentesis include hemorrhage, infection, iatrogenic lung or cardiac puncture, and pneumothorax.35 As a rule of thumb, any pleural fluid collected should be analyzed as it may help reveal the causative etiology (Table 4). Thoracostomy Tube In some patients, air can continue to accumulate within the pleural space until a tension pneumothorax forms, which can be seen when thoracic or pulmonary injury acts as a 1-way valve, allowing air into the pleural space during inspiration but prevents expulsion during expiration. In these cases, when negative pressure cannot be obtained in the pleural space following repeat thoracocentesis due to the reaccumulation of air, unilateral or bilateral placement of a thoracostomy tube should be considered.35 The most common type of thoracostomy tube used is an Argyle tube, which utilizes a trocar for entry into the thoracic cavity. Use of the trocarized tube is advantageous in that the tubes come in various lengths and sizes (8–32 French [F]); however, placement generally requires general anesthesia. As an alternative, commercially available over-the-wire thoracic drainage cathetersa are now available, that utilize the modified Seldinger technique for placement (Box 2). These are usually well tolerated by most patients with use of sedation or local anesthesia, and have been shown to be effective with minimal complications.35 Despite being available in only 12-gauge and 14-gauge sizes, the over-the-wire thoracic drainage catheters have demonstrated comparable efficacy to large-bore catheters when aspirating thick fluid, such has that observed in cases of pyothorax.37 Temporary Tracheostomy A temporary tracheostomy may be required to alleviate a life-threatening upper airway obstruction, which can be secondary to severe laryngeal swelling or hemorrhage, foreign body, or neoplasia.38 Ideally, a tracheostomy is performed under controlled 1247 1248 Tong & Gonzalez Table 4 In-house evaluation of pleural effusion Gross examination and physical characteristics Includes transparency or turbidity, color, odor, clots, and fibrin TP Transudate: TP <2.5 g/dL, TNCC <3000/uL TNC Modified transudate: TP >2.5 g/dL, TNCC <3000/uL Exudate: TNCC >3000/uL PCV Evaluate for hemorrhagic effusion Triglyceride and cholesterol Evaluates for chylous effusion  Fluid cholesterol-triglyceride ratio <1  Fluid triglyceride, >100 mg/dL Cytologic examination Performed on spun-down sample Evaluates for bacteria, fungal, or plant materials Abbreviations: PCV, packed cell volume, TNCC, total nucleated cell count; TP, total protein concentration. Adapted from Bohn AA. Analysis of canine peritoneal fluid analysis. Vet Clin North Am Small Anim Pract. 2017;47(1):123-133; with permission. settings with the patient under general anesthesia with a cuffed endotracheal tube in place. If endotracheal intubation is unsuccessful or a complete occlusion cannot be relieved, an emergent slash tracheostomy may be required.39 Contraindications to performing a tracheostomy include coagulopathies, obstruction (eg, mass, foreign body, and tracheal collapse) distal to the site of tracheostomy, and previous tracheal stent placement.38 Readers are referred to additional sources regarding the details of tracheostomy tube placement.38 Mechanical Ventilation Mechanical ventilation is indicated when a patient is failing conventional oxygen therapy or has impending signs of respiratory fatigue. Generally speaking, the rule of 60s can be applied as criteria for when to consider mechanical ventilation:  Severe hypoxemia (PaO2 <60 mm Hg) on FiO2 0.6  Hypoventilation with severe hypercapnia (PaCO2 >60 mm Hg)  Excessive respiratory effort with impending fatigue or failure Mechanical ventilation relieves the patient’s work of breathing and provides relief from distress. Prognosis for a patient’s ability to be weaned from the ventilator highly depends on the underlying disease process. Dogs and cats that require mechanical ventilation due to traumatic pulmonary contusions and congestive heart failure have 30% and 62.5% survival rates, respectively.40,41 Those requiring ventilation due to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), however, have a poor prognosis, with one-twelfth of dogs and one-quarter cats surviving to discharge.42 DIAGNOSTICS Once anatomic localization of the cause of respiratory difficulty is complete and stabilization efforts are under way, the clinician can be begin formulating a differential list and diagnostic plan. The importance of having a systematic and strategic diagnostic plan cannot be underplayed, because it allows the clinician to perform diagnostics in a stepwise fashion that provides the greatest amount of information without further jeopardizing a patient’s stability. Respiratory Emergencies Box 2 Thoracostomy tube placement Equipment required 1. Clippers 2. Surgical scrub (eg, chlorhexidine gluconate, 4%) 3. Sterile gloves 4. Sterile drape and supplies 5. Sterile instruments: needle holder, nonabsorbable suture, #11 blade 6. MILA guide wire style thoracostomy tube set (includes 18-g over-the-needle, guide wire, dilator, and thoracostomy tube) 7. Local anesthetic Procedure 1. Depending on stability, patients can be placed into either sternal or lateral recumbency for placement. 2. Shave the thoracic wall between rib spaces 5 to 11 and surgically prepare the site using chlorhexidine scrub and alcohol. 3. Don sterile gloves and drape the site. 4. Local anesthetic (lidocaine, bupivacaine) can be injected into the SQ space and the intercostal muscles at the planned site of insertion. Intercostal nerve block also can be performed. 5. The skin is pulled cranially and a small full thickness stab incision is made into the skin at the insertion site, usually over seventh–eighth intercostal space. 6. An 18-g over-the-needle catheter is inserted through the stab incision into the thoracic cavity. 7. Thoracostomy tube is placed via the modified Seldinger technique. A. The needle stylet of the catheter is removed and the guide wire is fed through the catheter cranially until two-thirds of the wire is passed into the thoracic cavity. B. The catheter is withdrawn over the guide wire, leaving the guide wire in the thoracic cavity. It is prudent that the clinician does not let go of the guide wire at any time. C. The small-bore thoracostomy tube is fed into the thorax over the guide wire. D. The guide wire is removed from the distal end of the thoracostomy tube and the tube is clamped as soon as the guide wire is removed. E. A luer lock cap is placed onto the proximal end of the thoracostomy tube. 8. Once the tracheostomy tube is inserted into the thorax, the skin is released, creating an SQ tunnel for the thoracostomy tube. 9. The tube is secured to the patient at the 2 wings and base with sutures. 10. A sterile adherent dressing is placed over the insertion site. 11. A radiograph should be taken to confirm appropriate placement in the pleural space. Adapted from Lombardi R, Savino E, Waddell LS. Pleural Space Drainage. In: Burkitt Creedon JM, Davis H eds, Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. 1st ed. Chichester, UK: Wiley-Blackwell; 2012:378-392; with permission. 1249 1250 Tong & Gonzalez Pulse Oximetry Pulse oximetry is a noninvasive measurement that provides a crude estimate of PaO2, utilizing spectrophotometric technology to estimate the oxygen saturation of hemoglobin in arterial blood.43 Oxygen saturation, as measured by pulse oximetry (SpO2) measurements are correlated to PaO2 via the oxygen-hemoglobin dissociation curve.2,43 An SpO2 of greater than 97% is considered normal as it correlates to a PaO2 of 80 mm Hg to 100 mm Hg, while SpO2 readings of 95% and 90% are considered abnormal, as they correlate to PaO2 of 80 mm Hg and 60 mm Hg, respectively.2 The accuracy of each measurement should be verified by matching the patient’s heart rate to the calculated heart rate displayed and by the signal strength of the reading. SpO2 readings should also be evaluated in conjunction with a patient’s respiratory effort and any interference (eg, supplemental oxygen). Limitations with use of pulse oximetry include the inability to differentiate oxyhemoglobin from dyshemoglobinemia and numerous factors that could produce erroneous results, including severe anemia, hypoperfusion, excessive fluorescent light, and motion artifact.43 Arterial Blood Gas An arterial blood gas (ABG) is considered the gold standard for evaluating oxygenation. The ABG also concurrently evaluates a patient’s overall acid-base status, with some panels containing additional parameters (eg, blood glucose, lactate, and electrolytes). Normal parameters of ABG samples and expected acid-base compensations are outlined in Table 5. Arterial samples can be drawn from the dorsal metatarsal, coccygeal, sublingual, femoral, or aural arteries into preheparinized syringes and then analyzed by benchtop machines.44 A PaO2 of less than 80 mm Hg indicates hypoxemia, with less than 60 mm Hg indicative of severe hypoxemia. The PaO2, along with calculation of the maximal expected partial pressure of oxygen within the alveolus (PAO2), is used in calculating the alveolar to arterial (A-a) gradient. The PaO2 is obtained from the blood gas and the PAO2 is derived from the alveolar gas equation: PAO2 5 [(PB – PH20)  FiO2] – [PaCO2/RQ], where PB is barometric pressure (mm Hg), PH2O is water vapor pressure (mm Hg), and RQ is respiratory quotient, commonly 0.8.44 Assuming atmospheric pressure of 760 mm Hg, a water vapor of 47 mm Hg, and FiO2 0.21, the equation can be rearranged as PAO2 5 150 – PaCO2/0.8. Once the PAO2 is calculated, the A-a gradient is calculated by subtracting PaO2 from PAO2. Normally, the A-a gradient is approximately less than 10 mm Hg and indicates normal pulmonary function.44 Values greater than 15 to 20 are considered abnormal and indicate some form of diffusion impairment.44 Older dogs are more likely to have a higher PaCO2 and a lower PaO2, which could imply their A-a gradient is higher. One exception to this rule is that brachycephalic breeds tend to have a higher A-a gradient than mesocephalic or dolichocephalic breeds.45 At higher altitudes, where the barometric pressure is considerably lower than that of sea level, the actual barometric pressure obtained at the time of blood sample collection should be used for calculation. The A-a gradient can be calculated only when the ABG is obtained from a patient breathing room air with no oxygen supplementation. A normal PaO2 is generally 5 times the FiO2. For patients on supplemental oxygen, a PaO2/FiO2 (PF) ratio can be calculated. In veterinary patients, a PF ratio of greater than or equal to 450 to 500 is considered normal, whereas a PF ratio less than 300 indicates ALI and a PF ratio less than 200 indicates ARDS.46 An SpO2/ FiO2 ratio has been investigated as a surrogate for PF ratio, showing good correlation in healthy dogs.47 No current studies are available investigating correlation and its use in patients with respiratory disease. Respiratory Emergencies Table 5 Normal arterial blood gas parameters and guidelines for compensation Value Dog Cat pH 7.31–7.46 7.21–7.41 PaO2 92 mm Hg (80–105) 105 mm Hg (95–115) PaCO2 37 mm Hg (32–43) 31 mm Hg (26–36) SaO2 >95% >95% Disturbances Guideline for Compensation Metabolic acidosis Each 1 mEq/L decrease in HCO3 decreases PCO2 by 0.7 mm Hg Metabolic alkalosis Each 1 mEq/L decrease in HCO3 increases PCO2 by 0.7 mm Hg Respiratory acidosis Acute Each 1 mm Hg increase in PCO2 increases HCO3 by 0.15 mEq/L Chronic Each 1 mm Hg increase in PCO2 increases HCO3 by 0.35 mEq/L Respiratory alkalosis Acute Each 1 mm Hg decrease in PCO2 increases HCO3 by 0.25 mEq/L Chronic Each 1 mm Hg decrease in PCO2 increases HCO3 by 0.55 mEq/L Abbreviations: HCO3, bicarbonate; SaO2, oxygen saturation Adapted from de Morais HSA, DiBartola, SP. Ventilatory and metabolic compensation in dogs with acid-base disturbances. J Vet Emerg Crit Care. 1991;1(2):39–49; with permission. Ventilation also can be assessed by measuring PaCO2. Aside from a true airway obstruction, it is rare for small animal patients to present with hypercarbia. A venous blood gas also can be used to evaluate ventilation in a patient and tends to require less technical expertise than obtaining an arterial sample. In patients with normal perfusion, the venous partial pressure of carbon dioxide usually is 5 mm Hg higher than the PaCO2.44 A low PCO2 is reflective of hyperventilation and the patient’s increased breathing effort. In intubated patients, capnometry/capnography also can be used to determine the efficiency of ventilation. Radiographs Radiographs are one of the most commonly utilized diagnostic imaging techniques. They are readily available and allow assessment of the airways and cardiopulmonary structures.48 Radiographs should not be attempted until a patient is deemed stable, as the stress of positioning may result in respiratory or cardiac arrest. This is important particularly in feline patients that have a high sympathetic drive. Sedation often is required and can provide great relief. Although common practice is to take 2 orthogonal views, it is recommended to perform 3-view studies when possible, to maximize detection of lesions and minimize superimposition of structures.48 Imaging the cervical region also may be of use in certain patients, such as those with a cough, or if an upper airway obstruction is suspected. Any opacities in the pulmonary parenchyma and pattern of distribution, cardiac and pulmonary vessel size, and mainstem airways all should be evaluated. A vertebral heart scale (VHS) can be calculated from a right lateral thoracic radiograph to assess cardiac size. To do this, a long axis measurement of the heart is taken from the ventral aspect of the mainstem bronchus to the apex of the heart, and a short axis measurement is taken perpendicular to the long axis, at the level of the caudal vena cava. These measurements then are aligned with the vertebral column at the cranial edge of the fourth vertebrae, and vertebral bodies wtihin each measurement are 1251 1252 Tong & Gonzalez quantified to give the VHS.49 A VHS of greater than 9.3 was found to be highly specific for the presence of heart disease in cats presenting with acute respiratory distress.49 In dogs and cats, noncardiogenic pulmonary edema is most likely to have a bilaterally symmetric distribution in the caudodorsal lung field.50 When caused by airway obstruction, it often is asymmetric and unilateral (right-sided) with dorsal distribution.50 Dynamic diseases, such as tracheal collapse and mainstem bronchial collapse, may not be seen or may be underestimated on radiography. Macready and colleagues51 showed that even with paired inspiratory and expiratory thoracic radiographs, radiography misdiagnosed the location of tracheal collapse and failed to diagnose tracheal collapse entirely in 44% and 8% of dogs, respectively. In patients with dynamic disease, fluoroscopy and/or bronchoscopy may be necessary to determine diagnosis. Lung Ultrasonography Point-of-care lung ultrasonography (LUS) has gained use as a diagnostic tool and is more commonly used in the emergency setting due to its ease in performance and requirement of minimal equipment.52 The 2 widely used techniques to evaluate the thoracic cavity include the focused assessment with sonography for trauma scan and the veterinary bedside lung ultrasound examination protocol.52,53 Although serving as a quick way to detect the presence of fluid, both can also be used to detect pulmonary edema via the presence of ultrasound artifacts, known as B lines (commonly referred to as lung rockets).52,53 B lines have been shown to be diagnostic for alveolar-interstitial diseases and can be a sensitive test for differentiating cardiac versus noncardiac causes of pulmonary edema.54–56 Compared with traditional radiography, LUS is able to detect a higher incidence of alveolar-interstitial syndrome.55 Besides evaluating for the presence of B-lines, ultrasonographic measurement of the left atrium (LA) compared to the measurement of the aortic root (Ao), known as the LA:Ao ratio, may aid clinicians in distinguishing between cardiac versus noncardiac causes of respiratory abnormalities. The LA:Ao ratio normally is 1:1. LA enlargement resulting in an La:Ao ratio >1.5 was found to be 97% sensitive and 100% specific for detecting congestive heart failure in cats.56 Several other artifacts can be noted on LUS that have diagnostic value. The absence of a glide sign, created by the parietal and visceral pleural surfaces gliding over each other during respiration, indicates the presence of a pneumothorax.57 Recent evaluation of pneumothorax in dogs revealed that an abnormal subpleural sign, known as a curtain sign, also may indicate a pneumothorax.58 Several other subpleural signs, including the shred sign, tissue sign, and nodule sign, have also been described.54,59 For additional information, readers are referred to the Gregory R. Lisciandro’s article, “Cageside Ultrasound in the ER and ICU,” elsewhere in this issue. Advanced Imaging Use of advanced imaging, such as fluoroscopy, tracheobronchoscopy, and computed tomography (CT), may be indicated in certain cases. Awake fluoroscopy allows dynamic assessment of the larger airways (trachea and mainstem bronchi) during both phases of respiration, providing a more global assessment of airway collapse.51 Tracheobronchoscopy is the best modality to evaluate upper and lower airway collapse, allowing visualization of any macroscopic changes to the airways and for the presence of foreign bodies or masses in the airway that may be contributing to the patient’s clinical signs.60 CT has shown superior sensitivity in detecting pulmonary parenchymal changes in both veterinary and human medicine.61–64 The use of CT is limited by the need for sedation or anesthesia; imaging capabilities also are restricted largely Respiratory Emergencies to veterinary referral centers. CT pulmonary angiography is the gold standard for the diagnosis of PTE in humans and has been shown to be a reliable modality in dogs.65,66 A CT pulmonary angiography can be performed under sedation whilst simultaneously administering a bolus of contrast media. The thorax is scanned for complete or partial intraluminal arterial filling defects, which are diagnostic for a PTE.66 Airway Sampling Airway samples can be obtained via a transtracheal wash (TTW), endotracheal wash (ETW), or bronchoalveolar lavage (BAL). The samples collected can be submitted for cytologic evaluation, fluid analysis, and aerobic, anerobic, or fungal cultures, where indicated. The TTW is a minimally invasive procedure that can be performed with/ without mild sedation and is usually reserved for medium to large dogs. For small dogs (<10 kg) and cats, an ETW is recommended. ETW is more invasive than TTW because it requires placement of a sterile endotracheal tube under brief general anesthesia.67 A guide to performing an ETW is outlined in Box 3. A BAL, performed under general anesthesia, allows for visualization of airways and sampling via fluid collection and brush cytology, using specialized equipment.60 As such, BAL is not a modality routinely used on an emergency basis despite its increased sensitivity compared with TTW and BAL.59 The main complication seen with airway sampling is oxygen desaturation or cyanosis, with other potential complications to include pneumothorax, and tracheal laceration with subsequent SQ emphysema.67 Oropharyngeal swabs are often utilized for respiratory polymerase chain reaction (PCR) panels, showing high sensitivity and specificity for the detection of canine adenovirus type 2, canine distemper virus, and Bordetella bronchiseptica in dogs.68–70 The diagnostic use of deep oropharyngeal swabs was shown not to be useful for culture samples in a population of puppies with community-acquired pneumonia.68 Ultrasound-guided fine needle aspirates can be considered in consolidated lung lobes or masses that are on the periphery of the lung field. Although rare, complications include pneumothorax, pulmonary hemorrhage, and death.71 Clinicopathologic Evaluation Comprehensive bloodwork, such as a complete blood cell count and biochemistry, often is performed to systemically evaluate the metabolic status of a patient but tends to not be diagnostic for any specific underlying respiratory disease. Certain findings with corresponding clinical signs, however, may lead a clinician to consider specific disorders, such as peripheral eosinophilia in a dog with eosinophilic bronchopneumopathy. The SNAP prohormone brain natriuretic peptide (proBNP) test measures N-terminal fragment of the proBNP (NT-proBNP), which is released during increased myocardial wall stretch. Its use in differentiating cardiac and noncardiac causes of respiratory distress has been demonstrated in both dogs and cats.56,72 The NT-proBNP levels in pleural fluid may differentiate cardiac versus noncardiac cause of pleural effusion in cats.73 The NT-proBNP levels can be increased in other conditions, such as pulmonary hypertension, dysrhythmias, renal disease, and systemic hypertension, where secondary myocardial stretch may occur.74 Serologic testing for fungal, viral, and protozoal pathogens, in addition to PCR and virus isolation assays, should be considered when deemed appropriate. Viscoelastic testing may serve the most use when evaluating for hypercoagulability as support for a suspected PTE. Thromboelastography is a well-established modality for in-hospital viscoelastic testing.75 Its use is limited, however, by need for specialized equipment and delicate sample collection in order to minimize erroneous results. 1253 1254 Tong & Gonzalez Box 3 Endotracheal wash procedure Equipment required 1. IV catheter 2. Short-acting anesthetic agents (eg, propofol and alfaxalone) 3. Laryngoscope 4. Sterile gloves 5. 3 to 5 syringes with sterile 0.9% saline A. 3-mL to 5 mL-aliquots for cats and small dogs B. 10-mL to 20-mL aliquots for larger dogs 6. Sterile endotracheal tubes 7. Sterile red rubber catheter (5–8F) 8. Sterile specimen container 9. A suction catheter and wall-mount mechanical suction unit 10. Aerobic culture transport medium 11. Ethylenediamine tetraacetic acid (EDTA) and nonserum separator tubes Procedure 1. The patient is positioned into sternal recumbency. 2. An injection of short-acting anesthetic agents is given IV and titrated to effect to allow endotracheal intubation. 3. A laryngoscope is used to assist intubation with a sterile endotracheal tube, taking care to avoid contamination of the tube with oropharyngeal secretions. 4. Once the patient is intubated, a sterile red rubber catheter is introduced through the endotracheal tube. 5. An aliquot of sterile saline is instilled through the catheter and flushed into the airways. 6. Retrieval of fluid A. The syringe used to flush the saline into the airway can be used to manually aspirate the fluid instilled. B. Alternatively, a suction catheter is inserted into the endotracheal tube. The suction catheter can be connected to a suction unit through a sterile specimen container, where fluid can be aspirated into the container. Gentle, intermittent suction is applied to retrieve fluid sample. 7. If insufficient sample is obtained, instillation of saline aliquots can be repeated. 8. The fluid retrieved is placed into aerobic culture transport medium, EDTA, and nonserum separator tubes to be submitted for laboratory analysis. 9. Once the procedure is performed, patients should be monitored until they are awake and can be extubated. 10. Patients may need additional suction if excessive fluid is suspected in the airway via auscultation. Adapted from Syring RS. Tracheal Washes. In: King LG, ed. Textbook of Respiratory Disease in Dogs and Cats. 1st ed. St. Louis, MO: Saunders; 2004: 128-134; with permission. Respiratory Emergencies The recent availability of point-of-care viscoelastic devices have allowed rapid cageside in vitro assessment of global coagulation. Readers are referred to evidencebased guidelines on viscoelastic testing in veterinary medicine created by the Partnership on Rotational ViscoElastic Test Standardization initiative.76 Heartworm testing can be performed utilizing bedside rapid SNAP tests, which are widely available and have a high sensitivity and specificity.77 Canine SNAP tests detect the adult worm antigen, whereas the feline tests detect the antibody.77,78 Clinicians also are encouraged to evaluate a blood smear for evidence of circulating microfilaria. A Baermann fecal test is traditionally used for evaluation of lung worms (Angiostrongylus vasorum); however, its accuracy is variable due to intermittent shedding of the parasite.79 Alternatively, an ELISA SNAP test is available for cage-side use with a high sensitivity and specificity in detecting lungworm antigens.80 SUMMARY Respiratory distress is a common emergency in dogs and cats and can have a wide spectrum of clinical signs that range from mild to severe at the time of initial presentation, often in patients that are critical. As such, it is crucial for clinicians to feel confident in the recognition of respiratory distress and subsequent localization of the disease. Care must be exercised when evaluating patients in respiratory distress and a strategic diagnostic plan should be created that minimizes the risk of further respiratory compromise to the patient. Clear communication and planning with support staff will help alleviate any unnecessary stress and uncertainties, allowing the most effective handling of these patients while in hospital and ultimately optimizing outcome. DISCLOSURE The authors have nothing to disclose. REFERENCES 1. West JB. Chapter 1 Structure and function. In: Respiratory physiology: the essentials. 9th edition. Baltimore (MD): Lippincott Williams & Wilkins; 2012. p. 1–11. 2. Haskins SC. Hypoxemia. In: Silverstein DC, Hopper K, editors. Small Animal Critical Care Medicine. 2nd edition. St. Louis: Saunders; 2015. p. 81–6. 3. Sigrist NE, Adamik KN, Doherr MG, et al. Evaluation of respiratory parameters at presentation as clinical indicators of the respiratory localization in dogs and cats with respiratory distress. J Vet Emerg Crit Care 2001;21(1):13–23. 4. Holt DE. Upper Airway Obstruction, Stertor, and Stridor. In: King L, editor. Textbook of Respiratory Disease in Dogs and Cats. 1st edition. St Louis: Saunders; 2004. p. 34–42. 5. Fonfara S, de la Heras Alegret L, German AJ, et al. Underlying diseases in dogs referred to a veterinary teaching hospital because of dyspnea: 229 cases (20032007). J Am Vet Med Assoc 2011;239(9):1219–24. 6. Johnson LR, Vernau W. Bronchoscopic findings in 48 cats with spontaneous lower respiratory tract disease (2002-2009). J Vet Intern Med 2011;25(2):236–43. 7. Bertolani C, Hernandez J, Gomes E, et al. Bromide-associated lower airway disease: A retrospective study of seven cats. J Feline Med Surg 2012;14(8):591–7. 8. Mandell DC. Respiratory Distress in Cats. In: King L, editor. Textbook of Respiratory Disease in Dogs and Cats. 1st edition. St Louis: Saunders; 2004. p. 12–7. 1255 1256 Tong & Gonzalez 9. Adamantos S, Hughes D. Pulmonary Edema. In: Silverstein DC, Hopper K, editors. Small Animal Critical Care Medicine. 2nd edition.