History

The history begins with the signalment (age, sex, breed), with breed predilections for respiratory disease considered (such as brachycephalic syndrome, hypoplastic trachea, and tracheal collapse). Hereditary causes of heart disease could be a cause of pulmonary edema or other respiratory distress. The past medical history could identify problems such as heart murmur, vomiting, asthma or other findings that could contribute to the onset of breathing abnormalities. The recent history can reveal vaccination status, exposure to other animals or a travel history that may pose a risk for infectious disease. The current problems should be described to include the onset and progression of clinical signs. Exercise intolerance, potential exposure to inhaled toxins (such as smoke, strong perfumes, incense, gases, sprayed chemicals) and a description of any breathing changes, such as coughing, open‐mouth breathing or loud breathing, warrant further investigation.

It is important to have a description of the respiratory rate (such as fast, slow, normal) and effort (such as open‐mouth, lips drawn back, elbow abducted with neck extended) observed in the patient. A description of any coughing heard can be important. There are three main types of cough that can be described for the dog and cat. Purposeful coughing is the beneficial expelling of foreign material or mucopurulent exudate such as might occur due to foreign body inhalation, infectious tracheobronchitis or pneumonia. This cough is loud and harsh, often occurring in a series until the animal swallows or there is expulsion of sputum or foreign material. Cautionary coughing is a manifestation of a systemic disruption, which can be life‐threatening, such as pulmonary edema (congestive heart failure, acute respiratory distress syndrome) and pulmonary hemorrhage (rodenticide, leptospirosis). This type of cough has a soft sound, often occurring in a series. An irritating cough is a nuisance to the patient, as might occur in animals with mild tracheal collapse or chronic bronchitis. This is often a progressive chain of “goose‐honking” sounds.

Physical examination

The physical examination is the most important tool to help narrow down the cause of respiratory failure when other diagnostic tools are not possible due to the fragile condition of the patient. Characterizing the respiratory pattern by simple observation can be an incredibly informative initial approach. Common respiratory rates and patterns are described with possible localization within the respiratory tract in Table 8.2. An abnormal breathing pattern develops as an adaptive process to minimize the effect of abnormal forces applied to the respiratory system. Distinct breathing patterns, if observed, may be helpful in determining the underlying pathology and next diagnostic or therapeutic steps.

Patients with mild upper airway disease can have a change in voice, gagging, retching, and coughing. Severe upper airway abnormalities cause noises that are audible without a stethoscope, as well as gasping, retching or vomiting, and orthopnea. Two types of upper airway sounds are recognized. Stertor is a low‐pitched or snoring inspiratory sound, due to a lesion located in the nasal passages, soft palate or nasopharynx. Stridor is a coarser, more raspy and higher pitch sound, that is due to a laryngeal or tracheal abnormality. Upper airway sounds may be underappreciated if the patient is enclosed in an O₂ chamber [4]. Upper airway obstruction is associated with an “obstructive” breathing pattern with the loudest sounds on inspiration (such as laryngeal paralysis). Lower airway obstruction primarily affects exhalation [5].

Rapid, shallow breathing suggests a “restrictive” breathing pattern, most compatible with lung parenchymal pathology (such as pulmonary edema, pneumonia, pulmonary fibrosis). Paradoxical respiration is characterized by asynchrony between the movement of the chest and the abdomen, more typical of pleural space disease or of respiratory muscle fatigue [6,7].

Body posture can be important in assessing the severity of respiratory distress (Figure 8.2). In cats, open‐mouth breathing is commonly a sign of respiratory failure or severe anxiety. In dogs, open‐mouth breathing allows direct air flow through the oropharynx rather than the nasopharynx to avoid the increased airway resistance within the nasal turbinates. The neck is extended to straighten the trachea and further decrease airway resistance. Dogs tend to stand or prefer sternal recumbency, and abduct their elbows, all of which optimize thoracic compliance by avoiding compression of the expanding chest. Open‐mouth breathing in dogs must be differentiated from panting secondary to hyperthermia, fear or anxiety. In panting dogs, the tidal volume is small and each breath primarily moves dead space rather than excessively ventilating the alveoli. The minute ventilation and arterial CO₂ remain normal.

During clinical evaluation, a cough should be induced by palpation and compression of the cervical trachea. The resultant cough is categorized as moist or productive, dry or hacking or honking. However, the cough in itself is not pathognomonic for any particular disease process. Differentials for an inducible cough include collapsing trachea, laryngeal and pharyngeal dysfunction, tracheitis, tracheal masses, and bronchitis. A cough may also be elicited in patients with esophageal dilation (megaesophagus), esophagitis, allergic airway disease, asthma, pulmonary hemorrhage, pneumonia, heartworm infection, and pulmonary edema (dogs). Mediastinal masses, pulmonary thromboemboli, tracheobronchial lymphadenopathy, and left atrial enlargement should also be on the differential list. Patients assessed as having a potentially contagious cause of coughing should be in isolation if hospitalized. In dogs, canine infectious respiratory disease complex includes viral and bacterial agents as well as parasites, while in cats contagious diseases targeting the respiratory tract include viruses, Mycoplasma species, and lungworms.

A more thorough examination can be performed once life‐threatening problems have been stabilized. Common physical examination findings associated with respiratory distress are listed in Table 8.3.

The temperature, pulse rate and intensity, mucous membrane color, and capillary refill time are assessed. The perfusion and hydration status are assessed. The circulatory status and severity of hypoxemia can change the mucous membrane color from pink to pale or white, or even to gray, purple or blue. Pale mucous membranes can occur due to peripheral vasoconstriction or anemia. Anemia decreases the O₂ content of the blood, and can also result in tachypnea. Red mucous membranes occur in animals with peripheral vasodilation or certain toxicities such as cyanide and carbon monoxide exposure. Dark mucous membranes, including those that are gray, purple or blue, indicate severe hypoxemia, termed cyanosis. Cyanosis is the presence of deoxyhemoglobin, and can only be appreciated if sufficient Hgb (>5 mg/dL) is circulating through the capillaries in the mucosa. Cyanosis is not visible in animals with severe anemia, even if they are hypoxic. Cyanosis is a late indication of respiratory dysfunction.

The entire facial structure should be evaluated, including the parts of the palate and dental arcade that can be visualized on an awake oral examination. Nasal discharge can be characterized as serous, mucoid, purulent, sanguineous, or hemorrhagic. Unilateral versus bilateral nasal patency can be assessed by holding a microscope slide in front of each external nares and observing steam upon exhalation. Discharge from the external nares can be due to intranasal or extranasal diseases. As a general rule, younger patients tend to have more infectious or congenital nasal abnormalities whereas older patients are more likely to have neoplastic, fungal or dental‐related causes. Immunocompromised patients are prone to secondary bacterial or fungal infections. Hunting dogs are susceptible to inhaled foreign material such as grass or ground debris [8,9].

Auscultation of the cardiorespiratory system (including the larynx, cervical trachea, lungs, and heart while palpating peripheral pulses) can better distinguish the type and location of respiratory disease. Pathology of the conducting airways can manifest as auscultatable stridor, stertor, or wheezes. Depending on the severity of airway obstruction, these sounds can be noticeable without a stethoscope or only evident during auscultation over the trachea. Wheezes are defined as whistling or squeaky sounds, due to obstruction of lower airways, which could be caused by edema, mucus, inflammation, bronchoconstriction or a mass. True wheezes are most prominent during expiration, and are highly suggestive of lower airway disease (such as feline asthma).

Pleural space disease can be suspected if there is a decrease in audible resonance of the lung and heart sounds due to the presence of pleural fluid, air, or tissue. Dull lung sounds can be identified dorsally or ventrally; they can be focal or diffuse, unilateral or bilateral. Ventral dull sounds are more consistent with pleural fluid, whereas air tends to accumulate dorsally. Common pleural diseases include pneumothorax, pleural effusion, masses, and diaphragmatic hernia. These changes on auscultation are often difficult to distinguish in the cat, since lung sounds may be heard throughout their thorax even with pleural space disease. In large dogs, percussion of the chest wall may demonstrate dull sounds with pleural fluid and hyperresonant sounds with pleural air.

Increased bronchovesicular sounds and crackles may be heard in animals with lung parenchymal disease. However, increased or harsh lung sounds may be present in normal animals. Increased bronchovesicular sounds warrant further diagnostics for evidence of lung disease. Crackles are popping, discontinuous sounds that result from the presence of fluid in distal airways and alveoli, or alveolar/bronchial collapse and reexpansion. Crackles can be further characterized as fine end‐inspiratory crackles, which confirm parenchymal disease and suggest the presence of fluid such as pulmonary edema, hemorrhage, or inflammatory exudate. This is distinct from loud crackles that can occur during any phase of the respiratory cycle, which indicate stiffening of the lower airways, occurring with bronchitis or pulmonary fibrosis. Often in the cat, the only change on auscultation is that the lung sounds are louder than normal.

An effort is made to auscultate the lungs when the patient is closed‐mouth breathing to minimize large airway sounds that can mask the lower airway and lung sounds. All lung fields should be auscultated since focal disease is not uncommon. Cranioventral abnormalities tend to occur due to aspiration pneumonia, whereas perihilar, diffuse or dorsocaudal distribution can be due to cardiogenic pulmonary edema, acute respiratory distress syndrome, hemorrhage, pulmonary thromboembolism, and many other alveolar diseases [5].

Respiratory distress can also be a result of cardiovascular or hematological disorders that can impair oxygen delivery (DO₂). The heart should be auscultated for at least 60 seconds while simultaneously palpating the peripheral pulses. The presence of a murmur, gallop rhythm or arrhythmia warrants further diagnostics for heart failure as a cause of or contributor to labored breathing. Cats are more difficult to diagnose with congestive heart failure on physical examination since they may only have an intermittent murmur or arrhythmia. In cats, an audible gallop rhythm may be the only cardiac abnormality heard. In both dogs and cats, pulse quality may be decreased in the presence of cardiovascular disease, but is often normal in animals with respiratory system disease [10].

The neurological examination is done to evaluate for evidence of cervical or thoracic spinal lesions or brain abnormalities that could affect the control of ventilation. The respiratory centers are located in the brainstem and disease in this area can cause an abnormal depth or rate of breathing (see Table 8.2).

Careful palpation of the abdomen is done to identify any abdominal masses, effusions or gastric distension that could impair ventilation by increasing the intraabdominal pressure and restricting the movement of the diaphragm. In addition, many intraabdominal diseases can be complicated by secondary respiratory distress (such as peritonitis with acute respiratory distress syndrome (ARDS) or acute lung injury (ALI), gastrointestinal (GI) foreign body with aspiration pneumonia or gastric dilation‐volvulus with impaired ventilation).

Point of Care testing

The initial POC testing begins with the collection of samples for the packed cell volume (PCV), total protein (TP), blood urea nitrogen (BUN), glucose, electrolytes, venous blood gas, coagulation profile, urinalysis (UA), and cytology of any collected pleural fluid or respiratory tract secretions. When the patient can tolerate the procedure, arterial blood is sampled for an arterial blood gas (ABG). The technique for collecting an arterial sample is outlined in Box 8.1.

Hemoconcentration may indicate dehydration, common with open‐mouth breathing, profuse nasal discharge, severe pulmonary edema or pleural effusion. Anemia (low PCV) can be a cause of hypoxemia or a consequence of pleural or pulmonary hemorrhage. Hypoproteinemia (low TP) can be present due to albumin loss and is of concern due to loss of pulmonary capillary colloidal osmotic pressure during fluid therapy (see Chapter 4).

The BUN is evaluated in conjunction with the specific gravity of the urine for the initial assessment of renal function. Uremic pneumonitis and oliguric or anuric renal failure can each affect the fluid balance in the lungs and result in pulmonary edema (see Chapter 13). Prolongation of coagulation times can be associated with lung parenchymal or pleural hemorrhage. A hypercoagulable state can result in pulmonary thromboembolic disease (see Chapter 9).

Arterial blood gas analysis

Arterial blood gas analysis provides invaluable and specific data regarding the patient’s respiratory status. The PaO₂ and PaCO₂ are directly measured. ABG analysis is the gold standard for the diagnosis for respiratory failure, allows quantitation of the severity of disease, and sometimes even allows categorization of the type of respiratory dysfunction. In addition, the ABG provides information regarding the patient’s acid–base status [15]. As a general rule, ABG analysis should be performed in dogs exhibiting clinical signs of respiratory failure to assess the severity and cause of signs. However, clinical judgment is required since restraint is needed for sample collection. This test is difficult to perform in cats and is not usually ordered in awake cats.

Arterial blood can be sampled by direct puncture of an artery or using an indwelling arterial catheter. The most common artery used is the dorsal pedal artery (Figure 8.3), but other options include the femoral, auricular, and coccygeal arteries [11]. The sublingual artery can be sampled in anesthetized patients. The method of collection is outlined in Box 8.1. The sample should be run as soon as possible or placed on ice to stop ongoing cell metabolism for transport to a laboratory [16]. Samples should be analyzed within two hours of being obtained. If the PaO₂ is low, it may be difficult to determine whether a sample is arterial or inadvertently obtained venous blood. A known venous sample can be obtained for comparison.

Arterial catheter placement requires a similar technique to puncture the artery. Standard “over‐the‐needle” peripheral venous catheters can be used, or specialized arterial lines can be placed using the Seldinger technique. Once the catheter is taped in place, it can be capped or attached to a pressure transducer for continuous monitoring of arterial blood pressure (see Chapter 3). Blood samples can be obtained from the catheter using the three‐syringe technique, by first withdrawing a “pre‐sample” of at least 2 ml of blood mixed with saline, that will be injected back into a venous catheter. Then the actual sample for analysis is withdrawn and the catheter flushed (see Box 10.2). Most modern ABG analyzers require <0.5 ml of blood.

In respiratory patients, ABGs should not be sampled until a steady state has been achieved after ventilator settings have been changed or oxygen supplementation has been started. Typically this requires about 5–10 minutes, but some patients with chronic airway disease may require longer equilibration times.

Guidelines for the interpretation of the respiratory components of the ABG are provided in Table 8.4, with two separate but interconnected values evaluated: PaO₂ and PaCO₂. The CO₂ is readily diffusible (about 20 times more diffusible than O₂), therefore the arterial CO₂ (PaCO₂) is directly proportional to the minute ventilation. Changes in CO₂ cause predictable alterations in plasma pH; severe changes result in enzymatic and cellular disturbances, potentially leading to life‐threatening conditions and even death (see Chapter 7).

ABG Value	Interpretation	Effect	Intervention
PaCO2
32–43 mmHg (dog)* 26‐36 mmHg (cat)*	Normal Normal	N/A	None
<32 mmHg (dog) <26 mmHg (cat)	Hyperventilation	Loss of respiratory drive, respiratory alkalosis, vasoconstriction	Treat underlying disease; alleviate pain, anxiety
>43 mmHg (dog) >36 mmHg (cat)	Inadequate ventilation	Respiratory acidosis, vasodilation, coma, death	Identify and treat underlying cause. Intubation and manual or mechanical ventilation if underlying cause cannot be treated
PaO2
80–105 mmHg (dog)* 95–115 mmHg (cat)*	Must be interpreted based on oxygen supplementation levels	N/A	None
<80 mmHg <60 mmHg	Hypoxemia Severe hypoxemia	Poor oxygen delivery to tissues	Oxygen supplementation, or mechanical ventilation
>100 mmHg	Usually due to oxygen supplementation	Increased likelihood of oxygen toxicity	Discontinue or taper oxygen therapy

^*Normal values may vary between laboratory equipment. ABG, arterial blood gas.

Hypercapnia is an elevated PaCO₂ and is almost always caused by inadequate ventilation, although on rare occasions it can be caused by severe pulmonary parenchymal disease. Considerations for the cause of ventilatory failure include depressed brainstem function (such as during anesthesia), neuromuscular dysfunction (including electrolyte abnormalities), upper airway obstruction, and respiratory muscle fatigue. The accumulation of CO₂ results in respiratory acidosis. Elevated CO₂ levels are not well tolerated, with PaCO₂ values >50 mmHg significant and prompting intervention. PaCO₂ values >70 mmHg can quickly lead to life‐threatening consequences, such as vasodilation and central nervous system abnormalities (including coma and death) [17]. Immediate intervention requires establishing an airway and providing positive pressure ventilation if the underlying cause cannot be identified and immediately treated [18].

Low PaCO₂ values (hypocapnia) occur due to hyperventilation, a rather common physical manifestation of respiratory compromise, anxiety or pain. However, when severe, the hypoxemia caused by pulmonary dysfunction can take over the previously CO₂ driven respiratory control of the brainstem and result in hypocapnia [19].

The PaO₂, representing the O₂ dissolved in plasma, defines the amount of O₂ that can bind to Hgb, therefore the PaO₂ controls the amount of Hgb that is saturated with O₂ (SaO₂). The relationship between the PaO₂ and Hgb‐O₂ saturation is represented by a sigmoid curve (see Figure 8.1). As PaO₂ values increase, the SaO₂ rises rapidly and plateaus when the PaO₂ is around 60 mmHg. PaO₂ is the most important determinant of SaO₂, but other variables can cause a shift in the curve. A rise in body temperature, PaCO₂, and level of 2,3‐DPG in the blood all cause the curve to shift to the right. This reflects a decrease in Hgb O₂ affinity and results in improved release of O₂ to the tissues. A decrease in these variables produces the opposite effect. A PaO₂ < 80 mmHg is considered hypoxemic and corresponds with SaO₂ around 93%. Severe hypoxemia is defined as a PaO₂ < 60 mmHg. Hypoxic patients require further investigation of the cause as well as immediate oxygen support and possibly ventilation [2].

Clinicopathological testing

A complete blood count (CBC) and serum biochemical profile should be performed in animals with problems affecting ventilation and oxygenation. An inflammatory leukogram could be compatible with pneumonia, ALI or ARDS as a cause of respiratory failure. The serum creatinine is assessed with the BUN and urinalysis results for evidence of renal disease, with consequences potentially affecting the respiratory tract (see Chapter 13). When pulmonary thromboemboli are suspected, adrenocorticotropic hormone (ACTH) stimulation testing for hyperadrenocorticism, a urine protein:creatinine ratio for glomerular disease, and thromboelastography (TEG) to define the coagulation status can be requested. The Baermann fecal examination is a method used to determine if there are Strongyloides or Aelurostrongylus species of lungworms present.

Several techniques are available to collect samples from the respiratory system to diagnose the underlying etiology. Endotracheal wash, transtracheal wash, bronchoscopic brush, and bronchoalveolar lavage samples can all be collected with fluid or cytology samples sent for laboratory analysis. The cytology of collected fluid is examined for evidence of infectious organisms (fungal infections, bacteria, and parasites) and to classify the disease process (inflammatory, neoplastic). Samples can also be sent for aerobic culture and susceptibility as well as the polymerase chain reaction (PCR) diagnosis of many infectious diseases.

Radiographic, fluoroscopic or ultrasound‐guided aspiration of abnormal lung tissue is another way of collecting samples. There is risk of iatrogenic hemorrhage and pneumothorax with this procedure, but the procedure can be well tolerated in many patients. Collected samples may be useful for cytological analysis and culture and susceptibility testing.

A variety of fungal species can infect the pulmonary system in dogs and cats. Fungal antigen and antibody tests are available, requiring relatively noninvasive procedures to collect samples. Reported sensitivity of the urine antigen test for detection of blastomycosis in dogs is as high as 93.5%, and considered more sensitive than serum antibody tests. This urine test can also be used as a tool to monitor clinical remission [20,21]. Other fungal organisms, such as Coccidioides, require serum antibody testing or identification of the organism in collected samples [22].

Diagnostic imaging

Diagnostic imaging is used in the stabilized patient to define the underlying cause of any respiratory failure and, under some circumstances, to demonstrate progression or resolution of the disease over time. Imaging begins with survey thoracic radiographs and can incorporate ultrasound, bronchoscopy, fluoroscopy, and computed tomography (CT) scans.

Pulse oximetry

Pulse oximetry is a noninvasive tool that provides rapid, continuous assessment of oxygenation, allowing detection of minor changes in respiratory status [26]. The pulse oximeter uses both oximetry and plethysmography. Oximetry (measurement of the saturation of Hgb with O₂ (SaO₂)) is determined through spectrophotometry. The Beer–Lambert law states that all atoms absorb specific wavelengths of light, which coincides with the concentration of the substance being measured. This principle is used to measure the concentration of oxygenated Hgb in blood, which absorbs red light at a wavelength of about 660 nm, and deoxygenated Hgb, which absorbs infrared light at a wavelength of 940 nm [27]. The pulse oximeter measures light absorption using two light‐emitting diodes (660 nm and 940 nm) on one side of the tissue bed and two photodectors on the other. The two photodetectors quantify the transmitted light and calculate the concentration of oxyhemoglobin and deoxyhemoglobin. Oxygenated Hgb is then expressed as a percentage (SpO₂). Phlethysmography identifies only arterial pulsatile flow characteristics, distinguishing flow from nonarterial blood. Many pulse oximeters display the pulse rate but also an image of the pulsatile waveform. This can be used for continuous monitoring of heart rate and to confirm the accuracy of the SpO₂ reading as well as the strength of the signal (Figure 8.4) [28].

The results from the pulse oximeter have been validated in both canine and feline patients. Normal SpO₂ should be greater than 95%, bearing in mind that this may correlate with PaO₂ values as low as 70 mmHg (see Figure 8.1). Valid SpO₂ values of 91–94% indicate significant hypoxemia that may require intervention. Valid SpO₂ values <90% indicate potentially life‐threatening hypoxemia that should be managed by O₂ supplementation or positive pressure ventilation [29,30].

Two main sensors are used in veterinary medicine: transmittance probes, detecting light that passes through the tissue, and reflectance probes, wherein the sensor is placed flat against a tissue. The lingual sensor can be placed on the tongue in sedated or anesthetized patients, or on the outer pinna, lips, prepuce, vulva, toe webbing, or Achilles tendon of awake patients. Wetting and parting or clipping the fur will increase skin contact. When using the lingual sensor, frequent repositioning may be necessary to avoid decreased blood flow due to compression, and tissue dessication can be avoided by placing a wet gauze square between the tongue and the probe. The reflectance probe is a linear probe that is used on the ventral base of the tail (not into the rectum). This type of probe has also been used with success directly over arteries, such as the femoral artery, pedal arteries, on the palmar aspect of the feet, proximal to the carpal or tarsal pad and in the rectum, facing the caudal abdominal aorta. Lubricant does not alter SpO₂ readings [31].

Following application of the probe, there is a 10–15 second delay before a reading is obtained because the signal is averaged. Mild to moderately hypoxemic patients may still be on the plateau of the O₂ Hgb dissociation curve where the PaO₂ can decrease significantly with little change in the SpO₂ reading. In addition, the quality of the signal can significantly alter the accuracy of SpO₂ readings, with factors such as motion, skin pigmentation, and anemia affecting the SpO₂ result. A list of common causes of inaccurate pulse oximetry readings is given in Table 8.6.

Of note, the concentration of oxygen in arterial blood (CaO₂) in anemic animals may be low even if the SpO₂ is normal. SpO₂ values may be 98–100% in patients receiving O₂ supplementation, regardless of whether the PaO₂ is 100 mmHg or 500 mmHg [2]. Therefore, it is necessary to measure PaO₂ to assess lung function in these patients. The pulse oximeter does not provide quantitative data regarding ventilation as it provides no measurement of PaCO₂ [32].

Continuous pulse oximetry is recommended in sedated or anesthetized patients, including those on ventilators. In awake patients, intermittent measurements are indicated on a scheduled timetable or when pertinent clinical signs change. Frequent evaluation of SpO₂ aids in quantification of response to therapy and can provide early detection of deterioration, facilitating intervention.

Other oximeters

While traditional pulse oximeters only measure deoxyhemoglobin and oxyhemoglobin, the co‐oximeter also measures methemoglobin and carboxyhemoglobin by using additional wavelengths of light. Smoke inhalation is the most common cause of carboxyhemoglobinemia, which is a stable complex of carbon monoxide (CO) and Hgb. CO has a much higher affinity for Hgb than O₂ (about 200 times), and accumulation of carboxyhemoglobin prevents adequate tissue DO₂.

Exposure to certain intoxicants can cause methemoglobinemia, including acetaminophen, local anesthetics, nitrates, nitrites, nitroglycerin, nitroprusside, certain antibiotics (sulfonamides), benzocaine, oxidative drugs, naphthalene (mothballs), garlic, and onions. Methemoglobin contains oxidized ferric iron instead of ferrous, which has a higher affinity for O₂, thus preventing release of O₂ in tissues. There is normally less than 2% methemoglobin in healthy patients, and it is converted back to Hgb by nicotinamide adenine dinucleotide (NADH)‐dependent methemoglobin reductase [33]. Higher concentration of CO or methemoglobin warrants an investigation of cause and specific therapeutic intervention.

A large amount of research has been performed evaluating the benefit of monitoring tissue oxygenation levels (StO₂) with near infrared spectroscopy (NIRS). Oxygen must diffuse down its concentration gradient into the tissues, typically making StO₂ much lower than arterial oxygen levels. Monitoring the StO₂ shows promise for the clinical monitoring of tissue oxygenation in the future [34,35].

Capnography

Capnography uses infrared spectrophotometry to measure the CO₂ level in expired air. By emitting a constant infrared beam from a phototransmitter and detecting absorption on the other side of the sampling compartment, the device continuously quantitates CO₂ during the respiratory cycle. There are two main types of capnographs: sidestream and mainstream. Sidestream devices aspirate air into a side chamber on the instrument for CO₂ measurement, which can cause a slight delay in the reading and increase dead space, especially in smaller patients. If the aspirated air contains inhalants, it must be returned to the anesthetic machine circuit for safety reasons. Mainstream instruments attach directly onto the endotracheal tube and directly measure CO₂ as exhaled air flows through the device [36].

Because CO₂ is approximately 20 times more rapidly diffusible than O₂, alveolar CO₂ is almost identical to the PCO₂ in the pulmonary capillaries. Alveolar CO₂ is exhaled at the end of each breath (ETCO₂), and when measured it can be used as an indirect estimation of PCO₂; there is a small amount of blood shunted (e.g. through bronchiole arterioles and coronary artery) that bypasses the lungs without being oxygenated, accounting for a ETCO₂‐PaCO₂ difference of up to 5 mmHg. The capnograph produces a waveform and numerical display of CO₂ throughout the respiratory cycle (Figure 8.5). The plateau CO₂ level is reported by the instrument as the ETCO₂ [37].

End‐tidal CO₂ is commonly used as a surrogate for the PvCO₂, but variability of the gradient between ETCO₂ and PCO₂ makes the use of trends most informative. The capnograph is typically used in patients intubated for an anesthetic event, cardiopulmonary cerebral resuscitation (CPCR), or positive pressure ventilation. The normal ETCO₂ range for dogs and cats is 35–45 mmHg. Values greater than 50 mmHg indicate hypercapnia and hypoventilation; those less than 30 mmHg may indicate hyperventilation. A sudden decline in the ETCO₂ towards zero may indicate a leak in the ventilator circuit, airway occlusion, severe pulmonary thromboembolism, or cardiopulmonary arrest (CPA). It can help to troubleshoot endotracheal tube placement, as the ETCO₂ will be zero if the tube is in the esophagus.

End‐tidal CO₂ is influenced by several factors, especially problems that affect the ventilation‐perfusion relationship within the lung. Decreased perfusion of alveolar units results in lower concentration of CO₂ in those alveoli. If these alveoli are ventilated, dead space air from the underperfused alveoli mixes with air from perfused alveoli, and the ETCO₂ decreases, creating a gradient between PCO₂ and ETCO₂. In addition, tachypnea and panting cause decreases in ETCO₂ due to mixing of gases within the sampling chamber. Hyperventilation (during anesthesia or CPR) will cause a falsely decreased ETCO₂ reading, requiring ventilation to remain fairly constant to obtain a significant reading. Sidestream capnographs aspirate 50–100 mL/min from the circuit, which may require adjustment of minute ventilation, especially in smaller patients.

Capnography is used extensively in ventilated patients because it provides continuous, real‐time readings that can be used for ventilator setting adjustment. It can be used to measure dead space using the dead space to tidal volume ratio (VD/VT), which is determined partly from ETCO₂ where: VD/VT = (PaCO₂ – P end‐tidal CO₂)/PaCO₂. This ratio can provide information regarding the presence of V/Q mismatch.

Capnography can also be used to monitor patients with tracheostomy tubes, as well as those that are spontaneously breathing. A sidestream capnograph can be used in combination with a nasal cannula to monitor ETCO₂ in the awake, nontachypneic, nonintubated patient [38].

Capnography is an invaluable tool for early detection of apnea and CPA, and is now standard of care for intubated critically ill patients [39]. During a CPA event, the capnograph tracing rapidly becomes zero before the decline of other monitored parameters such as O₂ saturation and electrocardiography. Upon initial intubation during initiation of CPR, the ETCO₂ may be elevated due to respiratory failure or zero due to decreased cardiac output. ETCO₂ measurement during CPR is directly correlated with efficacy of ventilation and with coronary blood flow [40]. ETCO₂ values near zero may indicate esophageal intubation; values greater than 15 during CPR in dogs appear to be predictive of a better outcome [41]. ETCO₂ values will rise with an increase in cardiac output and during the return of spontaneous circulation [42].

Treatment of hypoxemia

Stabilization of the critical small animal patient with hypoxemia commonly begins with providing anxiolytic/analgesic agents (examples include butorphanol 0.2–0.4 mg/kg IV or IM or acepromazine 0.0025–0.02 mg/kg IV or IM), assuring a patent airway, and providing supplemental oxygen. The SpO₂ and PaO₂ values can be used to confirm the need for O₂ supplementation and should be provided for critically ill patients with SpO₂ < 95% or PaO₂ < 80 mmHg. The clinical signs of respiratory distress (such as abnormal breathing pattern, respiratory rate or work of breathing) or poor perfusion will also prompt oxygen support when the patient is not stable enough for testing. Each method of oxygen supplementation has advantages and limitations depending on the patient size, O₂ requirement and tolerance, hypoxemia etiology, clinical skill level, and available monitoring.

There are noninvasive methods of oxygen supplementation that are fast and easy to initiate: flow‐by, mask, hood and cage oxygen, while more invasive nasal cannulas or catheters are used for prolonged oxygen support. Endotracheal intubation and tracheostomy provide a means for controlling the airway and providing therapeutic PPV.

Oxygen supplementation for more than a few hours can cause epithelial desiccation, which leads to inflammation and increased mucus production. Humidification of inspired gas with water vapor is mandatory whenever supplemental O₂ bypasses the nasal turbinates [43]. Humidification is achieved by inserting a canister (Hudson Rci, Temecula, CA) filled with distilled water into the oxygen delivery system. As the O₂ travels out of the diffuser, bubbles are created that rise through the water. Evaporation of water occurs at the contact surface of each bubble, loading the gas passing through with water vapor. Greater quantities of water vapor can be added if the water is heated, the bubbles are smaller or the water is made deeper for longer diffusion times. The humidified O₂ above the water then travels along the tubing to the patient.

Oxygen therapy is not without risk, and hyperoxia and oxygen toxicity must be avoided. As a general rule, a patient should not receive more than 60% FiO₂ for more than 12 hours [44]. During mitochondrial aerobic metabolism, highly reactive O₂ species (including hydrogen peroxide, hydroxyl radicals, superoxide radicals) are formed that will disrupt and damage essential cellular lipid membranes, cytoplasmic proteins, and nuclear DNA [45]. Administration of excessive FiO₂ for long periods of time results in production of much higher concentrations of these reactive oxygen species [46], causing oxidative injury. Ideally, the lowest possible FiO₂ should be used to maintain the patient’s O₂ saturation above 93%. However, it may be impossible to avoid use of high FiO₂ values in animals with severe respiratory disease.

Chronic hypercapnia in patients with longstanding respiratory disease (such as chronic obstructive lung disease) results in central nervous system adaptations. In these patients, hypoxemia has taken over from hypercarbia as the main trigger for brainstem respiratory centers. Therefore, providing O₂ supplementation to these animals can result in hypoventilation and worsening of their respiratory function [2].

Noninvasive oxygen delivery

Flow‐by O₂ is one of the least invasive methods of supplementation, commonly used in the emergency setting while the patient is being evaluated and stabilized. O₂ tubing is placed close to the mouth or nose, with O₂ flow rates of 1–5 L per minute. FiO₂ achieved is variable depending on the flow rate, size of the patient, and whether the animal is breathing through the nose or mouth. This technique is not recommended after the initial stabilization of the patient [43].

An O₂ mask acts as a reservoir system. Masks of various sizes have been designed specifically for the dog and cat (Surgivet, Waukesh, WI). The mask size should ideally be slightly larger than the muzzle or head of the patient to prevent rapid equilibration of O₂ with the surrounding air and minimize the accumulation of CO₂, heat, and humidity inside the mask. A flow rate of 2–10 L/minute is recommended to clear the exhaled gas from the reservoir. FiO₂ values of 30–90% can be achieved depending on the size of the mask and patient [47]. Frequent monitoring is required to ensure proper mask placement and patient tolerance. This method is best applied in patients with minimal voluntary movement or during initial stabilization to transition to a self‐supporting mechanism.

Commercially available oxygen hoods (Oxyhood, Jorgen Kruuse, Denmark) are available or an oxygen hood can be made by taping O₂ tubing to the inside bottom of an Elizabethan collar. The wide opening of the collar is covered with plastic wrap to create a reservoir system, with a small opening (approximately 5 cm) made at the top of the plastic to allow escape of CO₂ and water vapor. Use of clear material to make the hood allows easy patient monitoring. This system can achieve FiO₂ values of 30–50% or more [48]. Larger patients, and those that are panting, are at risk of hyperthermia when using this technique.

Oxygen cages provide excellent O₂ delivery, controlled humidity, and regulation of chamber temperature. They can be used long term in hypoxic patients, or during the emergency management of stressed patients that cannot handle restraint. FiO₂ levels achieved vary depending on the manufacturer, but values as high as 80–90% should be available for short‐term use in a crisis. The main disadvantage is the inability to handle the patient when necessary. Opening the cage immediately results in equilibration to room air. Additionally, temperature regulation may be difficult with larger, panting or brachycephalic dogs, due to the small size of the enclosure. The placement of ice bags inside the cage can help with temperature regulation with regular monitoring of the body temperature recommended. The use of O₂ cages in patients with upper airway obstructions should be avoided because of the inability to hear upper airway sounds when monitoring the patient.

Given the varying ability of cages to control O₂ concentration, oxygen monitors (MSA, Pittsburg, PA) that measure the FiO₂ in the cage are recommended (Figure 8.6). The accumulation of CO₂ is of concern and some cages come with a CO₂ scavenging system built in. When that is not available, CO₂ and temperature monitors (CO2Meter.com, Ormond Beach, FL) should be placed within O₂ cages to allow intervention if necessary (Figure 8.7).

Endotracheal intubation

Endotracheal (ET) intubation is indicated for patients requiring general anesthesia, developing hypoxia from hypoventilation, respiratory fatigue or apnea and for aggressive or overtly anxious patients that are not tolerating less invasive forms of O₂ supplementation. In addition, animals with upper airway obstruction or those given O₂ but remaining severely hypoxemic (PaO₂ < 60 mmHg) or hypercapnic (PaCO₂ > 50 mmHg) can benefit from an ET intubation and oxygenation.

Prior to ET intubation, all equipment and drugs needed for induction and tube placement, suction, and crisis management should be prepared. There are two main types of ET tubes: the Murphy tube (most common) and the Cole tube. The Murphy tube has a distal side fenestration to allow for continued air flow despite the end being occluded by secretions or anatomical abnormalities. The larger tubes are cuffed, but those less than 3 mm internal diameter are usually uncuffed. Cole tubes are all uncuffed but have a distal shoulder that is placed just rostral to the larynx in order to obtain a tight seal. Both types of tubes are available in a large variety of sizes and different materials, including polyvinyl chloride, rubber, and silicone. Clear tubes are ideal, allowing visualization of secretions within the tube.

Multiple ET tubes in different sizes (the anticipated size, one larger and two sizes smaller) should be readily available prior to induction of anesthesia. The ET tube size selected is based on the normal body weight of the patient and adjusted for anticipated individual variations (such as brachycephalic dogs with hypoplastic tracheas). The recommended ET tube size according to body weight is shown in Table 8.8 for the dog and Table 8.9 for the cat. Cats have a more uniform tracheal diameter.

Body weight (kg)	ET tube size (mm)	Body weight (kg)	ET tube size (mm)
2	5.0	14	8.5
3.5	5.5	16	9
4.5	6	18	9.5
6	6.5	20	10
8	7	25	11
10	7.5	30	12
12	8	>40	14–16

Body weight (kg)	ET tube size (mm)
1	3.0
2	3.5
3.5	4.0
>4	4.5

Intubation of cats tends to be more difficult because their highly sensitive larynx will spasm closed when touched. Avoiding tactile stimulation with the tube and laryngoscope is helpful, along with applying a topical anesthetic such as lidocaine spray.

A source of oxygen and ventilation equipment (either manual or mechanical) is prepared and supplemental oxygen is provided before, during, and after intubation. Rapid‐acting injectable anesthetics are necessary to facilitate rapid sequence intubation. It is recommended that an anesthetic agent or combination of agents be chosen that supports the cardiovascular status of the patient. Possible induction agents can include:

• propofol (2–6 mg/kg IV)
  
• ketamine/benzodiazepine combination (ketamine 1–2 mg/kg and diazepam/midazolam 0.25–0.5 mg/kg)
  
• alfaxalone (1–3 mg/kg)
  
• etomidate/benzodiazepine combination (1–3 mg/kg etomidate and 0.25–0.5 mg/kg diazepam or midazolam).

Induction with gas anesthetics is not recommended due to slow speed, stress to the patient, excitatory phase of induction, and exposure to inhalant by personnel.

Preoxygenating the patient with flow‐by O₂ for approximately five minutes will help prevent prolonged hypoxemic events. After induction, the patient is positioned in sternal recumbency and an assistant holds the maxilla by placing the finger and thumb behind the canine teeth while pulling the lips dorsally. The mandible can be held open with the other hand by grasping the tongue and pulling it forward and downward (avoid tongue contact with the mandibular canines). Rapid visual assessment of the upper airway increases the chances of successful intubation and can identify upper airway obstruction, abnormal anatomical structures, upper airway secretions, and dynamic functional changes in the pharynx and larynx. It is vital to be prepared for difficult intubations in every critically ill patient, with special emphasis on brachycephalic dogs, small patients, cats, and those with oropharyngeal or orofacial obstructions, trauma or other disease.

A laryngoscope can provide light and open the epiglottis, allowing better visualization and access to the trachea. The chosen lubricated ET tube is advanced orally through the larynx and into the trachea, providing a patent airway. Inflation of a cuff protects the patient from aspiration. O₂ or gaseous anesthetics and PPV can be provided.

With practice, intubating dogs and cats in dorsal recumbency may actually become easier than sternal since it allows the head and neck to be held straight. The laryngoscope can be used as designed for humans (Figure 8.8).

Once the ET tube is advanced through the larynx, the distal end is estimated to lie at or near the thoracic inlet. Tracheal tube placement is confirmed by auscultating both sides of the thoracic cavity for air movement and visualization of thoracic wall excursions during PPV and humidification of the tube during exhalation. ETCO₂ is the most accurate indirect method of confirming placement, and values should be >20 mmHg to confirm correct placement in the trachea. The ET tube is then secured with a tie anchored around the maxilla in dogs with a long muzzle or behind the ears of cats and brachycephalic dogs.

Endotracheal tube cuffs are inflated to protect the airway and during general anesthesia when PPV or inhalants are being administered. Cuff pressure should be maintained between 25 and 35 cmH₂O (18.3–25.7 mmHg). Overinflation of the cuff applies excessive pressure on the tracheal mucosa, causing mucosal ischemia and occasionally tracheal rupture [50,51]. High‐volume, low‐pressure endotracheal cuffs are recommended for all patients.

Patients predisposed to complications during ET tube placement include cats and brachycephalic dogs, animals with orofacial and dynamic airway abnormalities, and those with suboptimal positioning. Preoxygenating these patients is especially important. Besides multiple ET tube sizes, several red rubber catheters and stiff peripheral intravenous catheters should be available in case tracheal catheterization is required. For patients that are difficult to intubate, it may help to stiffen the softer ET tubes with a guidewire or stylet [52]. However, a stylet should never extend beyond the tip of the ET tube.