Respiratory Distress

"Suspect a thoracic injury with any sort of trauma!"

1.  Description of important terms used in conjunction with respiratory distress.

2.  Describe the causes of respiratory distress in trauma.

Pneumothorax -- Open or Closed
Pulmonary Contusions
Airway Obstruction
Flail Chest
Tension Pneumothorax
Diaphragmatic Hernia

3. What is acute hypercapnic respiratory failure?

Hypercapnic respiratory failure is defined as acute respiratory distress resulting in an arterial partial pressure of carbon dioxide (PaCO2) greater than 45 mmHg. Typically, this involves abnormalities with central nervous system control of respiration, the peripheral nervous system as it interacts with the respiratory apparatus, the chest wall/bellows apparatus, and/or the airways involved with gas transport. Hypercapnic respiratory failure is thus often called "respiratory pump failure" or "ventilatory failure."

4. What is acute hypoxemic respiratory failure?

Hypoxemic respiratory failure is defined as acute respiratory distress resulting in a PaO2 of less than 60 mmHg, despite addition of supplemental oxygen of at least 60%. Typically, this involves the pulmonary alveoli component of the pulmonary system. Hypoxemic respiratory failure is also called "lung failure" or "oxygenation failure." Causes include 1) decreased inspired oxygen content [FIO2] (e.g., high altitude ascent or reduction in the FIO2 setting on a mechanical ventilator), 2) hypoventilation (e.g., respiratory paralysis, airway obstruction, or atelectasis), 3) diffusion impairment (e.g., severe pneumonia, interstitial fibrosis, or interstitial pulmonary edema), 4) ventilation-perfusion (V/Q) mismatch (e.g., emphysema, alveolar pulmonary edema, pneumothorax, atelectasis), and 5) intra- and extrapulmonary shunting (technically the most severe form of V/Q mismatch; e.g., lung consolidation, atelectasis).

5. What are the fundamental initial treatment priorities in any patient with respiratory distress?

It is crucial to always remember that re-establishment of adequate arterial oxygen tension and removal of excessive CO2 are the overriding aims of the immediate treatment of patients with severe respiratory distress. The major ways in which to achieve this aim, regardless of the underlying cause of distress, are establishing a patent airway, instituting or assisting ventilation, and maintaining an adequate oxygen tension, by administration of supplemental oxygen, to maximize oxygen delivery.

6. What are the most useful diagnostic "tools" for use in evaluation patients with respiratory distress?

The simplest and often most useful tools are a good history, detailed physical exam, and careful chest auscultation. Other tools useful in diagnosing causes of respiratory distress include arterial blood gas analysis, pulse oximetry, capnography, thoracic radiography, and lung perfusion scans (not usually in the emergent patient, however).

7. Describe measures that allow differentiation of the various causes of hypoxemia in emergency patients with respiratory distress.

Hypoxemia is diagnosed by the presence of an SpO2 of less than 90% or an arterial blood gas (ABG) analysis that reveals a PaO2 of less than 60 mmHg. ABG analysis is essential for proper interpretation of causes of hypoxemia. Alternatively, use of pulse oximetry and capnography can be useful in diagnosis. Hypoxemia with hypercapnia defines hypoventilation as the underlying cause. Hypoxemia with normocapnia implies diffusion impairment, ventilation/perfusion imbalance ("V/Q mismatch"), or shunt as underlying causes. In veterinary patients, diffusion impairment is rarely severe enough to cause hypoxemia in and of itself. Response to oxygen supplementation usually allows differentiation between V/Q mismatch and shunting. Typically, the patient with a V/Q mismatch will demonstrate marked response (i.e., improved PaO2) with supplemental oxygen; whereas, the patient with shunt only minimally shows improvement in PaO2, if at all (i.e., by definition, refractory hypoxemia with < 10 mmHg increase with at least 40% oxygen administration).

8. How will I recognize a patient with severe respiratory distress?

Usually, they aren’t hard to recognize. Abnormal sounds (stridor, wheezes), abnormal posture (orthopnea, head and neck extended, elbows abducted, sternal recumbency), abnormal mucous membrane color (cyanosis or pale), tachypnea, weakness and exhaustion, altered respiratory effort (shallow and rapid, or labored and forceful, or absent), and vigorous resistance to restraint are the typical signs present in animals with respiratory distress. However, pets can have significant respiratory compromise and yet outwardly show minimal clinical signs of distress. Cats are more likely to have this type of presentation. Careful and quiet examination is essential to avoid sending the patient into stress-induced overt distress or respiratory arrest.

9. Are there physical exam findings that might help me differentiate the cause or location of the primary respiratory problem?

YES! Patients with a rapid, shallow respiratory pattern frequently have pleural space disease (pleural effusion, hemothorax, pneumothorax). Patients with end-expiratory effort and wheezes on chest auscultation frequently have small airway obstructive disease (asthma). Patients with deep, labored chest movements frequently have pulmonary parenchymal disease (pulmonary edema, pulmonary contusions, space-occupying masses). Patients with obvious stridor, minimal air movement at the nares or mouth, and marked inspiratory effort typically have upper airway obstruction (laryngeal edema or paralysis, foreign body aspiration). These patterns are hardly exclusive: Often patients have multiple problems, and some patients may have serious underlying respiratory problems and yet clinically appear normal.

10. Define cyanosis, its causes and significance, and the treatment of an emergent patient with cyanosis.

Cyanosis develops 1) when blood is insufficiently oxygenated in the lungs, 2) when hemoglobin is unable to carry oxygen, and 3) when blood stagnates in peripheral capillary beds. To be detected clinically, unoxygenated hemoglobin concentration must be > 5 gm/dL of blood. At this level, significant hypoxemia can already be present (< 50 mmHg), thus reinforcing the significance of cyanosis in a critical patient with respiratory distress. Additionally, anemic patients may not demonstrate cyanosis. Cyanosis is centrally-mediated (right-to-left cardiovascular shunts, hypoventilation, airway obstruction, V/Q mismatching, methemoglbinemia) or peripherally-mediated (arterial thromboembolism, venous obstruction, arteriolar constriction, low cardiac output heart failure, shock). Emergency treatment is provision of supplemental oxygen and rapid identification and correction of the underlying cause.

11. What nonrespiratory conditions can mimic acute respiratory distress?

Numerous disorders cause tachypnea, orthopnea, and other signs referable to the respiratory system in the absence of true respiratory disease. These disorders can confuse the clinician. Disorders such as hyperthermia, shock, metabolic acidosis and alkalosis, hyperthyroidism, fear or anxiety, pericardial tamponade, anemia, abdominal organ enlargement or ascites, and abnormalities with central control of respiration from drugs and metabolic or organic central nervous system disease are all causes of signs that may mimic true respiratory distress.

12. What are the 2 broad categories of traumatic respiratory emergencies in dogs and cats?

The categories are blunt thoracic trauma (e.g., vehicular trauma, falls from height) and penetrating trauma (e.g., bullets, arrows, bite wounds, penetrating foreign bodies).

13. Categorize the location and most common types of traumatic respiratory emergencies in small animal veterinary patients.

Larynx and major extrathoracic airways: Commonly caused by collars, bite wounds, and gun shot injury; airway obstruction may occur from blood clots, edema, foreign debris, tissue debris, and secretions; typical signs include labored inspiration, stridor, cyanosis; aspiration pneumonia may be present.

Chest wall: Rib fractures (including flail chest segments) and open (sucking) chest wounds are not infrequent in patients suffering thoracic trauma.

Pleural space: Pneumothorax and hemothorax are the most common complications seen after chest trauma. Diaphragmatic hernias are infrequent, and can be difficult to diagnose.

Pulmonary parenchyma and major intrathoracic airways: Pulmonary contusions are seen in about 45% of blunt trauma cases. Lung lacerations and pulmonary hematomas are infrequently seen. Intrabronchial hemorrhage carries a grave prognosis, and is seen in major chest trauma cases fairly commonly. Rupture or disruption of intrathoracic airways probably occurs frequently, as many cases of pneumothorax have no outward source of air leakage. Blatant disruption of major airways from the parenchyma likely leads to rapid death.

14. What are the 3 goals of supplemental oxygen therapy when treating hypoxemic patients? When should supplemental oxygen administration be used?

The goals are to 1) treat the hypoxemia, 2) decrease the work of breathing, and 3) decrease myocardial work. Supplemental oxygen therapy is indicated for virtually any patient with any degree of respiratory embarrassment: Using conventional delivery methods (see next question), it is never possible to harm a patient with additional oxygen, and may mean the difference between life and death.

15. Describe the ways in which supplemental oxygen therapy can be administered, listing the advantages and disadvantages of each.

Four methods are commonly used to provide supplemental oxygen: 1) face mask, 2) nasal oxygen insuflation, 3) oxygen cage, and 4) intratracheal oxygen administration.




Face Mask

  • Simple
  • Inexpensive
  • Readily available
  • Provides an FIO2 of 40-60%
  • requires high O2 flow rates
  • patient may not tolerate mask
  • patient must be attended at all times

Nasal Oxygen

  • More freedom of movement for the patient
  • FIO2 is not known (24-44%?)
  • excessive flow may cause gastric dilatation

Oxygen Cage

  • Noninvasive
  • Provides known FIO2 in a humidity and temperature-controlled environment
  • Less stressful to patient
  • Patient is physically separated from caregivers
  • Opening doors drops FIO2
  • Maximum FIO2 is 40-50% at economic rates


  • Can place transtracheal catheter during emergencies
  • FIO2 from 40-80%, depending on whether catheter or endotracheal tube is used
  • Endotracheal tube placement may require sedation or anesthesia
  • Tracheostomy tube may be required
  • Requires continuous monitoring

16. List the common causes of airway obstruction in dogs and cats.

Common causes include trauma; infections involving the nasal passages, pharynx, and larynx; obstruction with foreign material; localized or systemic anaphylaxis with edema formation and bronchoconstriction; compressive tumors of the airways and surrounding soft tissues; brachycephalic syndrome components (stenotic nares, elongated soft palate, laryngeal malformation, everted laryngeal saccules, hypoplastic [collapsing] trachea); laryngeal paralysis; and tracheal stenosis.

17. List the common pulmonary parenchymal disorders that cause respiratory distress, and briefly describe findings that might aid in diagnosis in the acute setting.

Pneumonia (acute fulminant bronchopneumonia, aspiration pneumonia, and smoke inhalation pneumonia), pulmonary contusions, pulmonary edema, asthma (in cats), and pulmonary thromboembolism are the common parenchymal disorders causing respiratory distress. Patients with pneumonia are usually depressed, anorectic, and febrile and may or may not have a deep, moist, productive cough. Abnormal lung sounds (crackles) may suggest bronchopneumonia. Patients with contusions invariably have a history of trauma, and areas of the chest on auscultation, especially adjacent to rib fractures or skin bruising, may be "quiet," reflecting alveolar and small airway filling with blood and edema. Patients with pulmonary edema usually have fine or coarse crackles on auscultation and may have cardiac findings or other exam findings to suggest either cardiac or noncardiac causes of the edema, in addition to historical information to suggest an underlying cause (e.g., CHF, electric cord shock). Cats with asthma typically have a supporting history, and usually have wheezes on chest auscultation and a characteristic end-expiratory effort caused by forcing air in the small airways against partial or complete small airway closure. Patients with pulmonary thromboembolism (PTE) frequently have another significant medical problem that predisposes them to embolize (hyperadrenocorticism, diabetes mellitus, trauma, DIC). The hallmark findings in patients with PTE are acute, severe respiratory distress with minimal radiographic changes and minimal response to oxygen supplementation in the absence of signs suggesting another cause.

18. How will I recognize and manage a patient with a pleural space disorder presenting with respiratory distress?

Patients with pleural cavity disease or with disruption of the integrity of the chest wall tend to present with a characteristic restrictive respiratory pattern (rapid, shallow breathing with other attendant signs of distress). Chest auscultation usually demonstrates generalized loss of lung sounds ("muffled"). Common causes of pleural space disease include open chest wounds, flail chest, pneumothorax, pleural effusions, hemothorax, and diaphragmatic hernia. Management depends on the cause, but generally, rapid careful thoracentesis is required for pneumothorax, hemothorax, and severe pleural effusions. Cautious handling until definitive surgery is possible is required for patients with diphragmatic hernias. Chest wall trauma is managed by appropriate wound care with local anesthetic blocks at sites of rib fractures.

19. How do I manage the patient with fulminant pulmonary edema?

Management depends on the pathophysiologic mechanism responsible for the edema formation. Acute cardiogenic edema is managed by 1) minimizing cardiac work (cage rest, sedation, inotropic support), 2) improve oxygenation (supplemental oxygen, bronchodilators, airway suctioning, mechanical ventilation), 3) resolve pulmonary edema (diuretics, vasodilators, phlebotomy), and 4) improve cardiac performance (inotropic support). Management of noncardiogenic edema (due to increased capillary permeability) is more challenging, as the underlying cause is not frequently found. Oxygen supplementation is the key tool, and mechanical ventilation with positive end-expiratory pressure may be required. Cautious fluid therapy is essential, and diuretics and vasodilators are recommended only if the patient is normovolemic. Cardiovascular support is important, to include inotropic support and blood transfusions to maintain oxygen delivery.

20. What are the indications for placement of an indwelling thoracotomy tube (chest tube)?

Indications include intractable persistence of air in the chest due to continued leakage, large volumes of air accumulating in a very short time (e.g., tension pneumothorax), or accumulation of fluid (blood, chyle, pus) in significant quantities in the pleural space. Good clinical judgment is required when deciding on placement of an indwelling tube - they are not without potentially serious complications, increase client costs and patient discomfort, and mandate continuous observation. Exact guidelines are impossible to recommend, but the author will usually place a tube immediately if tension pneumothorax is developing, and a soon as practicable when large volumes of air or fluid are repeatedly removed from the chest over a period of 6-8 hours, or sooner if the patient is clinically affected.

21. What are the indications for performing a tracheotomy in the emergent patient with respiratory distress?

The most common indications are emergency management of extrathoracic airway obstruction and hypoventilation due to CNS and neuromuscular diseases and severe hypoxemia requiring ventilatory support due to underlying pulmonary disease.

22. What are the indications for mechanical ventilation in a patient with respiratory distress?

Mechanical ventilation is indicated for patients with ventilatory failure and for patients with severe hypoxemia unresponsive to supplemental oxygen administration by face mask, nasal cannula, or oxygen cage. Specific indications in ventilatory failure are 1) apnea, 2) administration of paralyzing agents, and 3) ineffective respiratory efforts with progressive hypercarbia and acidosis (usually defined as a PaCO2 > 60 mmHg and an arterial pH < 7.30), regardless of cause. Specific indications for treating hypoxemic patients include 1) presence of an arterial PO2 < 50-60 mmHg on a test of 100% oxygen, and 2) inability to maintain a PaO2 above 50-60 mmHg with a nontoxic level of oxygen supplementation (< 60% O2).

23. What is the emergency treatment for acute small airway disease (asthma) in the cat?

The mainstays of emergency treatment include oxygen administration, corticosteroids (prednisolone sodium succinate, 10-20 mg/kg IV), bronchodilators (aminophylline, 2-4 mg/kg IM or slowly IV). If these agents failed to resolve the crisis in 5-15 minutes, additional agents may be necessary, including epinephrine (0.5 to 1.0 mL of 1:10,000 dilution IM or SQ), beta-adrenergic agonists (terbutaline, 1.25-2.5 mg PO), and parasymphatholytics (atropine, 0.04 mg/kg SC or IM).

24. What is the alveolar-arterial oxygen difference, and how is it useful in managing a patient with respiratory distress?

The alveolar-arterial oxygen tension difference ("A-a gradient") is a calculation that allows the clinician to estimate adequacy of oxygen transfer from the alveolus to pulmonary capillary blood. In the ideal alveolus, every bit of oxygen inspired would rapidly cross over into the capillary blood, with an A-a gradient of 0. In physiologic systems, with "normal" shunting of some blood, the A-a gradient can be up to 10 mmHg. In certain pathologic conditions (diffusion impairment, V/Q mismatching, and shunt), the A-a gradient increases, reflecting inadequacy of oxygen transfer. The alveolar component of the equation is calculated using the alveolar gas equation:

PAO2 = (Barometric pressure - 47)FIO2 - (PaCO2/0.8)

where PAO2 is the expected alveolar partial pressure of oxygen, 47 is the vapor pressure of water, FIO2 is the inspired oxygen concentration (21% or 0.21 for room air), and 0.8 is the Respiratory Quotient. Once solved for PAO2, subtract the measured arterial partial pressure of oxygen (PaO2) from the PAO2 to yield the A-a gradient.

Example: Patient has a PaO2 of 50 mmHg breathing room air, a PaCO2 of 50 mmHg, and the barometric pressure is 760 mmHg. The estimated alveolar O2 tension, from the formula above, is 87 mmHg. Subtract the actual PaO2 from this (87-50) to give the A-a gradient, in this case 37 mmHg.

A gradient of 0-10 mmHg is considered normal; 10-20 is considered mild impairment of oxygen exchange; 20-30 is considered moderate impairment; and > 30 is considered severe gas exchange abnormality. Clinically, the A-a gradient can be used to assess gas exchange function over time, and is thus useful in monitoring patients with certain types of respiratory distress.

When supplemental oxygen is administered, the A-a gradient as calculated above is not accurate. Dividing the measured PaO2 by the fraction of inspired oxygen yields the PaO2/FIO2 ratio, which is accurate. Normal values for this ratio are > 200 mmHg; patients with severe respiratory failure have values < 200.

Example: A patient with a PaO2 of 50 mmHg breathing 50% oxygen would have a PaO2/FIO2 ratio of 100 (50/0.50), indicating severe respiratory failure.

25. What is the Acute Respiratory Distress Syndrome (ARDS), and does it occur in dogs and cats?

ARDS is a life-threatening form of respiratory failure due to acute lung injury. Numerous causes are described in people, and despite recent advances, the mortality rate remains high in people who develop ARDS. Recently, a syndrome similar to human ARDS has been reported in dogs (Parent et al, 1996). Diagnostic criteria in people that were applicable in this study include severe respiratory distress, severe hypoxemia refractory to supplemental oxygen, bilateral alveolar infiltrates on thoracic radiography, decreased lung compliance, and near normal cardiac function. These findings reflect the severe pulmonary edema and profound pulmonary inflammatory response characteristic of ARDS. Treatment is nonspecific, aimed at correcting the underlying condition, correcting the hypoxemia (which frequently requires mechanical ventilation using positive end-expiratory pressure), fluid and nutritional therapy, and prevention of secondary infection.

26. What are the most common immediately reversible acute respiratory causes of cardiopulmonary arrest (CPA)?

Clinicians should always be alert for tension pneumothorax and obstructive asphyxia. These rapidly developing conditions are immediately reversible and carry a grave prognosis if not corrected immediately. Tension pneumothorax is typically seen in trauma patients or patients being mechanically ventilated, as is characterized by rapid-onset hypotension, hypoxia, high airflow resistance (in ventilated patients), subcutaneous emphysema, and reduced lung sounds. Obstructive asphyxia is typically seen after foreign body aspiration, laryngeal paralysis, retropharyngeal abscessation, or cervicofacial trauma.


Crowe DT, Jr. Managing respiration in the critical patient. Vet Med 1:55-76, 1989.

Drobatz KJ, Concannon K. Noncardiogenic pulmonary edema. Comp Cont Ed Pract Vet 16:333-345, 1994.

Frevert CW, Warner AE. Respiratory distress resulting from acute lung injury in the veterinary patient. J Vet Intern Med 6:154-165, 1992.

Hackner SG. Emergency management of traumatic pulmonary contusions. Comp Cont Ed Pract Vet 17:677-686, 1995.

Harpster N. Pulmonary Edema. Current Veterinary Therapy X. Ed by Kirk RW and Bonagura JD. Philadelphia, WB Saunders Company, 1989, pp 385-392.

Keyes ML, Rush JE, Knowles KE. Pulmonary thromboembolism in dogs. J Vet Emerg Crit Care 3:23-32, 1993.

Kovacic JP. Management of life-threatening trauma. Vet Clin North Am: Small Anim Pract 24:1057-1094, 1994.

Lanken PN. Respiratory Failure: An Overview. Principles and Practice of Medical Intensive Care. Ed by Carlson RW and Geheb MA. Philadelphia, WB Saunders Company, 1993, pp 754-762.

Murtaugh RJ, Spaulding GL. Initial Management of Respiratory Emergencies. Current Veterinary Therapy X. Ed by Kirk RW and Bonagura JD. Philadelphia, WB Saunders Company, 1989, pp 195-201.

Parent C, King LG, Van Winkle TJ, Walker LM. Respiratory function and treatment in dogs with acute respiratory distress syndrome: 19 cases (1985-1993). JAVMA 208:1428-1433, 1996.

Taboada J, Hoskins JD, Morgan RV. Respiratory emergencies. The Compendium Collection: Emergency Medicine and Critical Care in Practice. Trenton, VLS Books, 1996, pp 227-247.

Tams TR, Sherding RG. Smoke Inhalation Injury. The Compendium Collection: Emergency Medicine and Critical Care in Practice. Trenton, VLS Books, 1992, pp 42-49.

Van Pelt DR, Wingfield WE, Hackett TB, Martin LG. Application of airway pressure therapy in veterinary critical care, Part 1: Respiratory mechanics and hypoxemia. J Vet Emerg Crit Care 3:63-70, 1993.

Return to Primary Survey

dyspnea.jpg (292467 bytes)

Respiratory distress in a dog.  Note the posture of the dog.
Return to respiratory terms