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Veterinary Focus

Issue number 32.3 Other Scientific

How I approach… The dog in respiratory distress

Published 25/01/2023

Written by Jasper E. Burke and Deborah C. Silverstein

Also available in Français , Deutsch , Italiano , Português and Español

How do you deal with a dog in respiratory distress? This article reviews the optimal approach required to assess and stabilize the critically ill patient.

© Dr Céline Pouzot-Nevoret

© Dr Céline Pouzot-Nevoret

Key points

Dogs presenting in respiratory distress can decompensate quickly.

Initial stabilization involves oxygen supplementation, minimal handling, and – when appropriate – sedatives.

A rapid but thorough examination allows the clinician to characterize the respiratory pattern and then localize the abnormality.

There are 8 categories of possible localization of the respiratory distress that need to be investigated.


There are many conditions that can cause respiratory distress or apparent dyspnea in veterinary patients. Strictly speaking, the word “dyspnea” refers to a feeling of being unable to catch one’s breath; therefore, although animals are frequently described as being “dyspneic”, the clinician is observing “apparent dyspnea” or increased respiratory effort. Regardless of the terminology used, rapid identification of the problem is critical for treatment, but as these patients tend to be fragile and can decompensate quickly, a thorough diagnostic work-up may be challenging. History and physical examination, and particularly characterization of the respiratory pattern, can help localize the area of concern, which can then inform the differentials and diagnostic and therapeutic strategy for the patient. This article will review the different sections of the respiratory tract that can be involved in cases of canine dyspnea, and discuss differentials, emergent diagnostics, and treatments for each.

The initial approach

Given that dyspneic patients are often critically ill, appropriate initial stabilization is important while a more tailored plan is formulated. In general, two key principles should be kept in mind for all animals presenting in respiratory distress, namely oxygen supplementation and minimal stress.

Oxygen supplementation, in the short term, is not harmful; this can be administered with a face mask or flow-by during examination and then transitioned to a nasal cannula if the animal tolerates it, or an oxygen cage if preferred. Oxygen cages allow for a quiet, low stress environment with a relatively high fraction of inspired oxygen (40-80%); however, if the patient is at risk of upper airway obstruction (as discussed below), they should be in a cage that allows people nearby to hear any change in their respiratory noises (i.e., worsening obstruction). If an animal has severe airway obstruction, is fatiguing, or is unable to breathe on its own, intubation should be pursued. The general rule is that if the clinician is worried that intubation is necessary, intubation should be performed; this allows for delivery of 100% oxygen and also bypasses any upper airway obstruction and takes over the work of breathing. Occasionally, oral intubation is very challenging or not possible, and other methods are described below.

Minimizing stress frequently means minimal handling, and can be eased by use of sedatives. After a brief physical examination, venous access should be secured (if possible), and sedatives administered if needed. Butorphanol is typically preferred as a sedative over full-mu opioids as it causes less respiratory depression; however, in painful conditions, such as following trauma, full-mu opioids (e.g., fentanyl for its short-acting nature) are preferred given the lack of analgesia from butorphanol (an opioid with mu-antagonist and kappa-agonist activity). Ideally, this is given intravenously to decrease time to efficacy, but if placement of an intravenous catheter risks causing the patient to decompensate, intramuscular injections are an alternative option. After sedatives are administered, the patient should be placed in a temperature and humidity-controlled cage to deliver supplemental oxygen and to provide a quiet environment to minimize hospital stress.

The full physical examination may need to be staged depending on the severity of the respiratory distress; part of the examination is hands-on and requires a stethoscope, but a visual examination, even from outside the oxygen cage, is also valuable. Examination should focus on:

  1. a quick overview looking for external abnormalities (e.g., evidence of trauma or abdominal distension),
  2. the respiratory pattern (e.g., looking for tachypnea, abnormal inspiratory or expiratory effort, stertor or stridor, a restrictive pattern, orthopnea, paradoxical breathing, or nasal flaring),
  3. pulmonary auscultation (e.g., checking for crackles, wheezes, increased or decreased respiratory sounds), and
  4. cardiac auscultation (e.g., to detect a murmur, gallop, or abnormal rhythm).

The abnormality is localized once the clinician has this information, and diagnostic and therapeutic plans can then be tailored to the most likely disease process; the owner can be given more information, and ultimately morbidity and mortality are minimized. Pulse-oximetry is often the first objective measurement of oxygenation status, given its non-invasive nature. Ultimately, it is a useful tool to assess severity of disease and track improvement/decompensation over time; however, some animals are stressed by this procedure, and the result must be correlated with the clinical picture as an animal that is struggling to breath but maintaining a normal pulse-ox should still be considered critical and in respiratory distress until proven otherwise. An arterial blood gas measurement is more reliable – and allows for calculation of an A-a (alveolar-arterial) gradient – but more technically challenging to obtain and can also cause the animal excessive stress. A venous blood gas assessment, when possible, can also give valuable information about acid/base and perfusion status (e.g., lactate), but importantly can also demonstrate hypercarbia, which would raise concern for lack of appropriate ventilatory ability.

There are several ways to break down how to localize the cause of respiratory distress; we use eight categories of potential disease localization: upper airway, lower airway, pulmonary parenchymal, vascular, pleural space, chest wall, abdominal distension, and “look-alikes” (Table 1a and b).

Table 1a. Causes, treatments, and diagnostics for types of respiratory distress by localization.

Localization Examination findings Differentials
Upper airway
  • Inspiratory dyspnea
  • +/- stertor/stridor
  • +/- honking cough, choking, gagging
  • Brachycephalic airway disease
  • Tracheal collapse
  • Laryngeal collapse
  • Nasopharyngeal collapse/stenosis
  • Trauma 
  • Coagulopathy 
  • Swelling/edema secondary to envenomation or heat stroke
  • Obstruction secondary to mass, foreign body, or abscess
Lower airway
  • Expiratory dyspnea
  • Expiratory wheeze
  • Bronchitis
  • Lungworm
  • Smoke inhalation
  • Trauma
  • Obstruction secondary to mass, foreign body, or abscess
Pulmonary parenchyma
  • Increased effort (inspiratory and/or expiratory) 
  • Crackles/harsh lung sounds 
  • +/- decreased lung sounds if severe
  • +/- restrictive pattern
  • Pneumonia
  • Pulmonary edema (cardiogenic vs. non-cardiogenic)
  • Interstitial lung disease
  • Neoplasia
  • Trauma/contusions
  • Acute onset tachypnea with increased effort
  • +/- cough
  • +/- syncope
  • +/- harsh lung sounds 
  • +/- crackles/wheezes
  • +/- dull lung sounds 
  • Pulmonary thromboembolism
Pleural space
  • Inspiratory effort
  • Restrictive breathing pattern
  • +/- paradoxical breathing pattern
  • Decreased lung sounds 
  • Pleural effusion (pyothorax, chylothorax, hemothorax, neoplasia, other)
  • Pneumothorax
  • Mass effect (neoplasia vs. diaphragmatic hernia)
Chest wall
  • Decreased chest wall excursion
  • +/- abdominal movement on inspiration
  • +/- external wounds
  • Traumatic
  • Neurologic 
Abdominal distension
  • Distended abdomen, possible tympanic or with a fluid wave
  • Mass
  • Ascites
  • Organomegaly
  • Gastric dilatation (+/- volvulus) 
  • Pregnancy
  • Variable 
  • Hyperthermia
  • Excitement
  • Anxiety
  • Pain
  • Metabolic acidosis
  • Anemia
  • Shock 
  • Hypoglycemia
  • Medications (steroids, opioids, stimulants)
  • Abdominal distension


Upper airway

Physiologically, the upper respiratory tract is from the nose and mouth to the trachea at the level of the thoracic inlet. If this section is affected, examination will typically reveal inspiratory dyspnea (although some animals have expiratory effort as well). Animals may also exhibit inspiratory stertor or stridor, have a honking cough, or they may be observed choking or gagging. History and signalment will be helpful; for example, an excited Bulldog, an older Labrador running around on the first warm day in spring, or a young Pitbull Terrier seen playing with a stick may make us concerned about brachycephalic airway disease, laryngeal paralysis, or an oral foreign body, respectively. Other differentials include obstruction anywhere along the airways (secondary to mass, foreign body, or abscess), tracheal collapse, laryngeal collapse, nasopharyngeal collapse/stenosis, trauma, coagulopathy, or swelling/edema secondary to envenomation or heat stroke.

Table 1b. Causes, treatments, and diagnostics for types of respiratory distress by localization.

Localization Emergency treatments Diagnostics
Upper airway
  • Oxygen 
  • Sedation (butorphanol, acepromazine)
  • +/- intubation
  • +/- corticosteroids 
  • Sedated airway examination
  • Cervical/thoracic radiographs
  • +/- fluoroscopy
  • +/- tracheoscopy
  • +/- thoracic CT
Lower airway
  • Oxygen
  • +/- bronchodilators 
  • Thoracic radiographs
  • +/- endotracheal or transtracheal wash
  • +/- fluoroscopy
  • +/- bronchoscopy
  • +/- thoracic CT
  • +/- fenbendazole
Pulmonary parenchyma
  • Oxygen
  • +/- furosemide vs. antibiotics vs. corticosteroids vs. other 
  • Thoracic radiographs
  • +/-echocardiogram
  • +/- thoracic CT 
  • +/- endotracheal wash
  • Oxygen
  • Heparin
  • Treatment of underlying cause
  • +/- thrombolysis
  • Thoracic radiographs
  • Complete blood cell count
  • Chemistry panel
  • D-dimers
  • Echocardiogram
  • +/- abdominal ultrasound
  • +/- CT with angiography
Pleural space
  • Oxygen
  • +/- thoracocentesis
  • Thoracic radiographs
  • +/- fluid analysis
Chest wall
  • Oxygen
  • +/- intubation
  • +/- pain medication
  • +/- antibiotics
  • Blood gases 
  • Thoracic radiographs
  • +/- POCUS
  • +/- complete blood cell count
  • +/- chemistry panel
  • +/- MRI/CSF tap
  • +/- anti-acetylcholine receptor antibody testing
  • +/- botulinum toxin testing
  • +/- EMG 
Abdominal distension
  • +/- oxygen
  • +/- abdominocentesis, decompression, surgery if indicated
  • +/- POCUS
  • Abdominal radiographs or ultrasound
  • Variable
  • +/- pain medication
  • +/- anxiolytic
  • Treat underlying disease process
  • Pulse-oximetry
  • Blood pressure
  • Bloodwork (PCV, blood gases, acid/base status)
  • Thoracic radiographs


These patients are typically very stressed because they are struggling to breathe, so sedation with butorphanol and/or acepromazine is recommended. Close monitoring after sedation is required in case the animal becomes excessively relaxed and is unable to ventilate, or if the upper airway further narrows as muscle tone decreases. When upper airway obstruction is suspected, preparation for imminent intubation is recommended. When a dog’s airway becomes obstructed, the quality of noise produced may change, or the animal may suddenly make no sound despite significantly increased respiratory effort; at this point intubation will be required, but may be challenging depending on the cause of obstruction (e.g., mass, inflammation, etc.). Oral intubation with a smaller endotracheal tube is recommended, but if the airway is compromised, a red rubber catheter or airway exchange device can be used to provide oxygen (Figure 1). Certain functional diseases such as laryngeal paralysis are easily diagnosed with an airway examination at intubation, so if required emergently, the upper airway (laryngeal tissues, soft palate, oropharynx) should be evaluated, but this should not delay expedient intubation and delivery of oxygen. If intubation with anything larger than a catheter or airway exchanger is not possible, an emergent temporary tracheostomy may be required (ideally once the smaller tube is in place, to allow for even some degree of oxygenation during this procedure). Tracheostomy can be performed with an endotracheal tube if transtracheal (ideally cannulated) tubes are unavailable, and the technique is described elsewhere 1.

An airway exchange catheter

Figure 1. An airway exchange catheter. This can be used for difficult intubations where the airway is narrow or partially obstructed. Note that the tip has holes to allow oxygen flow, and the top has a connector that can attach to an Ambu bag or a ventilator circuit. Once successfully placed, the connector can be detached and a larger endotracheal tube guided over the exchange catheter, which is then removed, leaving the more appropriately sized tube in place. Alternatively, if a larger tube cannot be placed, the airway exchange catheter can be used as a temporary measure to provide oxygen while an emergent tracheostomy is performed. 
© D. Silverstein/J. Burke/University of Pennsylvania

Some of these patients may present with an elevated body temperature (e.g., heatstroke) or they may start to overheat in hospital if they continue to struggle and cannot lose heat through their respiratory tract. If this is the case, cooling may be required (wetting the fur with tepid water, fans, cool environment, etc.) to reduce the body temperature to 39.4 oC/103 °F; however, aggressive cooling below this point is not recommended, as this can lead to rebound hypothermia. Many of these dogs develop airway inflammation because of trauma to the tissues while breathing against an obstruction; an anti-inflammatory dose of steroids can be considered (e.g., dexamethasone sodium phosphate, 0.1 mg/kg IV once). Some animals will also develop post-obstructive pulmonary edema; close monitoring of oxygenation levels, and auscultation and/or chest radiographs may be helpful in detecting this complication.

Once stabilized, diagnostics should be directed at determining the cause of the upper airway obstruction. A sedated airway examination is indicated to look for abnormalities of the oropharynx and larynx, such as brachycephalic airway disease, laryngeal paralysis or collapse, or any masses or foreign bodies. Cervical and thoracic radiographs, followed by fluoroscopy, may be considered if looking for tracheal collapse or mass effect. Advanced diagnostics, such as CT and scoping (e.g., tracheoscopy, nasopharyngoscopy) may be required if the cause of obstruction cannot be easily identified with less invasive methods.

Jasper E. Burke

The full physical examination may need to be staged depending on the severity of the respiratory distress; part of the examination is hands-on and requires a stethoscope, but a visual examination, even from outside the oxygen cage, is also valuable.

Jasper E. Burke

Lower airway

Lower respiratory tract disease encompasses the remainder of the conducting airways from the thoracic inlet to the alveoli. Patients with lower airway disease often have narrow bronchial lumens that are open at inhalation but have a tendency to close during expiration, thus causing an expiratory dyspnea, sometimes with an expiratory push. Expiratory wheezes may be heard on auscultation. In dogs this localization most frequently represents bronchomalacia seen in end-stage bronchitis, but trauma, lungworm, smoke or toxic substance inhalation, and obstructions (e.g., secondary to stricture or foreign body) remain possible.

In addition to oxygen, these patients may benefit from bronchodilators such as terbutaline; however, caution should be used in dogs suspected of having significant heart disease, as terbutaline may increase the heart rate. Once stable, thoracic radiography to look for a bronchial or bronchointerstitial pattern is recommended (Figure 2), although the diagnostic sensitivity of radiography for bronchial diseases in dogs is relatively poor 2. Thus, further diagnostics – such as an endotracheal or transtracheal wash and cytologic evaluation – should be considered. Fluoroscopy, bronchoscopy or CT could be considered to look for dynamic tracheal and/or mainstem bronchial collapse (if not observed on radiographs), tracheal masses or nodules, bronchiectasis, or excessive mucus production. The agreement between these tests can be relatively poor for lower airway disease, so ideally a combination of modalities is performed 3,4. Finally, a Baermann fecal test can be considered to diagnose lungworm infection, although empirical treatment with fenbendazole is often elected. If bronchitis is suspected, a corticosteroid taper may be recommended; some clinicians prefer inhaled fluticasone if required long term to decrease systemic absorption and side-effects.

DV (a) and lateral (b) thoracic radiographs

Figure 2. DV (a) and lateral (b) thoracic radiographs from a dog with end-stage bronchitis. Note the severe diffuse bronchial pattern.
© D. Silverstein/J. Burke/University of Pennsylvania

Pulmonary parenchymal

Pulmonary parenchymal diseases incorporate abnormalities of the interstitium. Typical examination findings include crackles or loud breath sounds, although lung sounds can be decreased in dogs with severe disease that causes fluid accumulation and collapse of a portion of the lungs and thus lack of airflow. These dogs may have inspiratory effort, expiratory effort, or both, and may exhibit restrictive respiratory patterns, with short shallow breaths with or without abdominal effort.

Differentials are quite broad, and include pneumonia, pulmonary edema, interstitial lung disease, neoplasia (primary or metastatic), or traumatic injury (contusions), or ARDS (acute respiratory distress syndrome). Pneumonia may be secondary to infectious causes (bacterial, viral or parasitic) or aspiration events. Pulmonary edema can be cardiogenic or non-cardiogenic in origin. Interstitial lung disease includes idiopathic pulmonary fibrosis, heartworm disease, and (uncommonly) eosinophilic bronchopneumopathy. If detected, more specific clinical signs may help increase suspicion of the underlying cause; for example, murmurs or arrhythmias may be seen in dogs with cardiogenic pulmonary edema, while coughing, mucopurulent nasal discharge, and occasionally a fever may be seen in dogs with pneumonia, and hemoptysis can occur in cases with hemorrhage/contusions. Dogs that are suspected to have ARDS typically develop respiratory distress within 3-7 days of an underlying trigger or risk factor (e.g., sepsis, pneumonia, surgery) and have evidence of edema on imaging that is not secondary fluid overload or cardiac dysfunction. These patients should be referred to a specialty hospital for work-up and aggressive supportive care. Signalment can also be used to narrow differential diagnoses (e.g., West Highland White Terriers and idiopathic pulmonary fibrosis, or Huskies with eosinophilic bronchopneumopathy).

Given the many differentials, diagnostics are generally necessary to determine definitive treatment recommendations; however, until the animal is stable enough to safely perform tests, empirical treatment can be initiated, since oxygen therapy alone may not improve their respiratory status. For example, the index of suspicion for congestive heart failure may be higher in a small dog with localizable pulmonary disease, a loud murmur, and tachycardia, therefore empiric furosemide may be administered. Ideally, if ultrasound is available, it is worthwhile measuring the diameters of the left atrium and the aortic root in order to calculate the ratio and thus assess the size of the cardiac chamber; if the value is greater than 1.6, left atrial enlargement due to possible heart disease would be considered more likely (Figure 3) 5. A dog with dyspnea, an elevated temperature and mucopurulent nasal discharge would be concerning for pneumonia, and empirical antibiotics should be started.

Point-of-care ultrasound

Figure 3. Point-of-care ultrasound (POCUS) evaluating the left atrium to aortic root ratio. The red dashed line represents the diameter of the aortic root, while the blue dashed line is the left atrium. This patient had a ratio of 3:1, consistent with left atrial enlargement. 
© D. Silverstein/J. Burke/University of Pennsylvania

Thoracic radiographs are the primary diagnostic for dogs with pulmonary parenchymal disease (Figure 4), along with point-of-care ultrasound (POCUS) if possible, and an echocardiogram if cardiac disease is high on the differential list (Figure 5). Pending initial diagnostic work-up, a thoracic CT and endotracheal wash may be recommended. Findings will help determine if treatment should consist of antibiotics, diuretics, steroids, bronchodilators, or oxygen alone.

DV (a) and lateral (b) thoracic radiographs from a dog

Figure 4. DV (a) and lateral (b) thoracic radiographs from a dog with infectious pneumonia. Note the alveolar pattern in the right cranial, right middle, and left cranial lung lobes.
© D. Silverstein/J. Burke/University of Pennsylvania 

dog with congestive heart failure

Figure 5. DV (a) and lateral (b) thoracic radiographs from a dog with congestive heart failure. Note the left-sided cardiomegaly, perihilar to diffuse interstitial to alveolar pattern, and moderate pulmonary venous distension. 
© D. Silverstein/J. Burke/University of Pennsylvania


Some clinicians classify vascular disease (i.e., pulmonary thromboembolic disease) as a subcategory of pulmonary disease; however, as it does not involve the parenchyma, we distinguish it from other causes. Pulmonary thromboembolism (PTE) is a challenging diagnosis to make and requires a full work-up to identify the underlying cause of hypercoagulability, as animals will be at risk of continued embolic disease without identification and correction of the primary source. Many disorders can cause hypercoagulability that may then lead to PTE, including protein-losing nephropathies or enteropathies, hyperadrenocorticism, immune-mediated hemolytic anemia, neoplasia, sepsis, and trauma. Examination findings vary, but typically include acute onset tachypnea and increased respiratory effort, and possibly coughing, syncope, or abnormal mentation. Auscultation may be normal or reveal loud lung sounds, crackles or wheezes. If concurrent pleural effusion is present, lung sounds may be decreased.

As with other conditions discussed, initial supportive care includes oxygen supplementation and intravenous catheter placement while diagnostics are pursued. Thoracic radiographs may reveal a variety of changes, including main pulmonary artery enlargement, interstitial or alveolar infiltrates, hyperlucent areas of peripheral parenchyma secondary to oligemia (“Westermark sign”), cardiomegaly, pleural effusion, or no abnormalities at all. In fact, PTE should be a differential in a patient with tachypnea and apparent dyspnea but with normal radiographs, especially if concurrent risk factors exist. A complete blood count and biochemistry panel should be performed to look for underlying causes; thrombocytopenia and/or schistocytes may be present. A coagulation panel (looking specifically at D-dimers) may be helpful to increase the index of suspicion, but normal D-dimers do not exclude PTE, and elevated D-dimers are not specific for the condition 6,7. Abdominal ultrasound should be performed to rule out neoplasia or a source of sepsis if clinically indicated. Echocardiography occasionally reveals evidence of thrombi, or can show changes in cardiac structure and function associated with thromboembolic disease (e.g., pulmonary hypertension) 8. A CT with angiography can be offered to identify emboli, but this may require general anesthesia; additionally, a negative scan does not exclude thromboembolic disease. Ultimately, the underlying cause should be treated, and if there is a high index of suspicion, anti-coagulants such as heparin are recommended. Thrombolytic therapy could also be considered, but must be weighed against the potential risk of hemorrhage.

Deborah C. Silverstein

In general, two key principles should be kept in mind for all animals presenting in respiratory distress, namely oxygen supplementation and minimal stress.

Deborah C. Silverstein

Pleural space

Diseases of the pleural space result in a build-up of substance between the lungs and the chest wall, which compresses the lungs and prevents expansion. The substance can be fluid (as in pleural effusion), air (pneumothorax), or a mass effect (neoplasia or diaphragmatic hernia). Typically, these animals have a restrictive breathing pattern, with short shallow breaths, an inspiratory effort with abdominal effort, and decreased lung sounds (ventrally for fluid, dorsally for air). Animals may also have a paradoxical breathing pattern as the diaphragm moves caudally during inspiration, with the abdomen rising while the chest falls. In these cases, POCUS is useful to confirm effusion or pneumothorax (i.e., absence of a glide sign), but thoracic radiographs can also be confirmatory. If examination is consistent with pleural space disease, ultrasound is not available, and the patient is too unstable for radiography, a therapeutic thoracocentesis is recommended to relieve the patient’s distress. If effusion is obtained, it should be analyzed, and culture/susceptibility testing considered, as differentials are variable and include neoplasia, pyothorax, chylothorax, heart failure, hemothorax, lung lobe torsion, and diaphragmatic hernia. Packed cell volume, total solids, glucose, lactate, and in-house cytology of the effusion are recommended to look for hemothorax, transudate vs. exudate, or a septic effusion. Following thoracocentesis, radiographs are recommended to identify a possible underlying cause, such as a pulmonary bulla, pulmonary mass, or cardiomegaly (Figures 6 and 7). A CT scan may also be indicated pending initial work-up. If the patient requires multiple thoracocenteses, placement of a chest tube should certainly be considered while further diagnostics are followed and/or until definitive treatment can be performed (e.g., surgery for spontaneous pneumothorax secondary to a bulla).

focal alveolar

Figure 6. DV (a) and lateral (b) thoracic radiographs from a dog with pleural effusion. This patient also had focal alveolar changes in the right middle lung lobe, potentially secondary to pleural effusion or concurrent pneumonia.
© D. Silverstein/J. Burke/University of Pennsylvania

dog with a pneumothorax

Figure 7. DV (a) and lateral (b) thoracic radiographs from a dog with a pneumothorax. This patient had been hit by a car and had concurrent subcutaneous emphysema and peritoneal effusion (hemoabdomen).
© D. Silverstein/J. Burke/University of Pennsylvania

Chest wall

Diseases of the chest wall refer to abnormalities of the skeleton, musculature, and nerves related to the wall of the thorax. These animals typically hypoventilate, with decreased chest wall excursions and sometimes increased abdominal movement during inspiration. Differentials are most commonly trauma and neuromuscular etiologies. With traumatic injuries, the history or external examination will frequently give clues as to what is going on. In addition to any external wounds, a flail segment may be present: a flail chest is a two or more adjacent ribs that are each fractured in at least two places, dorsally and ventrally, causing a section of the chest wall to become unstable and therefore move inwards during spontaneous inspiration. In these cases, pain medication (ideally full-mu opioids, e.g., fentanyl or methadone) should be given, wounds should be covered, and the dog placed in lateral recumbency with the flail segment side to the table to stabilize the chest wall and allow for better ventilation with the less damaged side of the chest. These cases may also have pulmonary and/or pleural space disease (e.g., pulmonary contusions or pneumothorax), so auscultation changes are variable; POCUS may be useful to identify some of these changes (e.g., pleural effusion, pulmonary edema, or absence of a glide sign). If not immediately obvious, thoracic radiographs may be helpful to look for evidence of intrathoracic penetration, as that will warrant surgical intervention (Figure 8). Ultimately, all external wounds should be explored and the surgeon prepared for a thoracic exploration, regardless of the imaging findings. This is because external wounds often do not reveal the entire extent of the damage.

Neurologic etiologies include central causes such as intracranial (e.g., neoplasia, infectious, inflammatory, vascular), cervical spinal (e.g., intervertebral disc herniation, neoplasia, infectious, inflammatory, vascular), or phrenic nerve abnormalities, as well as peripheral causes such as myasthenia gravis, botulism, tick paralysis, polyradiculoneuritis, or tetanus. Neurologic and musculoskeletal examination will help differentiate these causes; animals with intracranial disease may have abnormal mentation, while those with cervical spinal disease may have normal mentation but be tetraplegic, and peripheral causes may have either flaccid or stiff paralysis depending on the cause. In these cases, the chest wall muscles and diaphragm may not work effectively, so very shallow breaths, along with open-mouth (“fish-mouth”) breathing, may be seen. These patients are likely to require intubation and manual or mechanical ventilation. In less obviously severe cases, venous blood gases may be helpful to determine if the patient is hypercarbic, which would also be an indication for intubation and assisted ventilation. More specific treatments will depend on the diagnostic work-up and cause of hypoventilation. Dogs suspected of having intracranial or cervical spinal disease may ultimately require an MRI, but initial work-up should include bloodwork (complete blood cell count, chemistry panel), and thoracic radiographs (and cervical, in the case of cervical myelopathy). Those with peripheral causes may benefit from a thorough examination to look for ticks (as well as one dose of topical tick preventative), anti-acetylcholine receptor antibody testing for diagnosis of myasthenia gravis, and/or neostigmine response assessment, testing of serum or feces for botulinum toxin, and electromyography once stabilized.

DV (a) and lateral (b) thoracic radiographs from a dog with a penetrating chest wound secondary to a bite wound

Figure 8. DV (a) and lateral (b) thoracic radiographs from a dog with a penetrating chest wound secondary to a bite wound. Note the disruption of the right cranial thoracic wall around the level of the third intercostal space. This patient also sustained a displaced fracture of the right third rib.
© Christiana Fischer, VMD

Abdominal distension

Diseases causing abdominal distension can lead to respiratory distress by preventing caudal movement of the diaphragm and therefore inhibiting lung expansion. This can be due to a variety of etiologies, including masses, ascites, organomegaly, gastric dilatation (+/- volvulus), and pregnancy. Physical examination will usually reveal an obvious distension, which may include a palpable fluid wave or tympanic abdomen that will prompt abdominal imaging (radiographs, ultrasound, or even POCUS where available). Oxygen supplementation will not harm these patients, but ultimately treatment of the abdominal disease is required to relieve the pressure on the diaphragm.


A number of other disease processes can mimic apparent dyspnea – hyperthermia, anxiety, excitement, pain, metabolic acidosis (e.g., Kussmaul respiration associated with severe acidemia), anemia, shock, hypoglycemia, and various medications (including stimulants, opioids, or corticosteroids) can all mimic dyspnea. History, physical examination, and other diagnostics such as pulse-oximetry (normal), bloodwork (e.g., arterial blood gases to ensure normal oxygenation, or a venous blood gas test for assessment of acid base-status, PCV, anion gap, etc.), and thoracic radiographs can help differentiate these from true distress. A trial of pain medication or an anxiolytic may also be useful, but ultimately treatment of the underlying cause is necessary to resolve respiratory changes on examination.


Treating dogs that present in respiratory distress can be stressful; they are fragile and require the clinician to work efficiently with minimal handling to prevent decompensation. Initial assessment includes stabilization with oxygen supplementation and possibly sedation, along with intravenous access if possible, and blood gas results may help. A brief examination focusing on auscultation and characterization of respiratory pattern will assist in localizing the disease process. Once this is achieved, systematic and appropriate diagnostics can help find and treat the cause, although empiric therapy is occasionally indicated based on the history and physical examination in animals that are too unstable for additional diagnostics.


  1. MacPhail C, Fossum TW. Surgery of the Upper Respiratory System. In: Fossum TW, (ed.) Small Animal Surgery, 5th ed. Philadelphia: Elsevier Saunders; 2018;842-844. 

  2. Mantis P, Lamb CR, Boswood A. Assessment of the accuracy of thoracic radiography in the diagnosis of canine chronic bronchitis. J. Small Anim. Pract. 1998;39(11):518-520.

  3. Johnson LR, Singh MK, Pollard RE. Agreement among radiographs, fluoroscopy and bronchoscopy in documentation of airway collapse in dogs. J. Vet. Intern. Med. 2015;29(6):1619-1626.

  4. Johnson LR, Johnson EG, Vernau W, et al. Bronchoscopy, imaging, and concurrent diseases in dogs with bronchiectasis: 2003-2014. J. Vet. Intern. Med. 2016;30(1):247-254.

  5. Keene BW, Atkins CE, Bonagura JD, et al. ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs. J. Vet. Intern. Med. 2019;33(3):1127-1140. 

  6. Nelson OL, Andreason C. The utility of plasma D-dimer to identify thromboembolic disease in the dog. J. Vet. Intern. Med. 2003;17(6):830-834. 

  7. Epstein SE, Hopper K, Mellema MS, et al. Diagnostic utility of D-Dimers in dogs with pulmonary embolism. J. Vet. Intern. Med. 2013;27(6):1646-1649.

  8. Nazeyrollas P, Metz D, Chapoutot L, et al. Diagnostic accuracy of echocardiography-Doppler in acute pulmonary embolism. Int. J. Cardiol. 1995;47(3):273-280.

Jasper E. Burke

Jasper E. Burke

Dr. Burke graduated from the University of Pennsylvania and subsequently completed a small animal rotating internship at the Animal Medical Center in New York City Read more

Deborah C. Silverstein

Deborah C. Silverstein

Dr. Silverstein graduated from the University of Georgia Read more

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By Rafael Obrador de Aguilar

Issue number 32.3 Published 29/03/2023

Acute heart failure in dogs

Acute heart failure in dogs carries a serious risk of death, and optimizing diagnosis and treatment is paramount, as discussed by Luca Ferasin.

By Luca Ferasin