an aortic thromboembolism."/>
Figure 1.1 Cat with open mouth breathing secondary to the pain associated with an aortic thromboembolism.
If decreased lung sounds relative to respiratory effort are heard dorsally, pneumothorax should be suspected. However, if decreased lung sounds are heard ventrally, pleural effusion should be considered. Lung sounds may not be completely absent in the presence of pleural effusion or pneumothorax, they may be reduced relative to the other lung fields but still present. See Chapter 34 for stabilization of the patient with pleural space disease. Diseases of the chest wall such as masses, rib fractures, and flail segments may also result in abnormal auscultation of the pulmonary parenchyma. For more information on chest wall disease, see Chapter 41.
For patients in respiratory distress with a heart murmur, arrhythmia, pleural effusion, or pulmonary crackles present on auscultation, cardiogenic and hypoxemic shock should be considered as possible differentials. This is particularly important since fluid therapy is often contraindicated in most patients with cardiac dysfunction or failure and must be ruled out, to the best of the clinician's ability on triage, prior to administering intravenous (IV) fluid therapy.
Hypoxemic Shock
Hypoxemic shock occurs secondary to decreased arterial blood oxygen content. Common causes of hypoxemic shock include pulmonary parenchymal disease, such as pneumonia, severe anemia, and hypoventilation (Figure 1.2). Many veterinary patients in hypoxemic shock are at the limits of their physiologic reserves, and are intolerant of excessive handling, restraint, and manipulation; they should be handled carefully. Clinical signs include weakness, mental depression, pale mucous membranes, dyspnea, crackles or increased bronchovesicular lung sounds, or decreased lung sounds ventrally (pleural effusion) or dorsally (pneumothorax), and cyanosis. Patients with diaphragmatic hernia may have decreased lung sounds dorsally or ventrally. Cyanosis is only seen with severe hypoxemia (at least 5 g/dl of deoxygenated hemoglobin), and thus the absence of cyanosis absolutely does not rule out hypoxemia. In anemic animals, cyanosis is unlikely to be detected due to decreased hemoglobin concentration, and therefore should not be relied upon to diagnose hypoxemia [8].
Figure 1.2 Lateral thoracic radiograph showing cranioventral pulmonary infiltrates creating an alveolar pattern consistent with aspiration pneumonia.
In any patient with suspected hypoxemic shock, supplemental oxygen should be provided until the ability to adequately oxygenate is confirmed. Diagnostics that can be helpful for the patient in hypoxemic shock include pulse oximetry (peripheral capillary oxygen saturation, SpO2), arterial blood gas analysis, thoracic radiographs, thoracic/trauma computed tomography (CT), and thoracic ultrasound. SpO2 may be less effective with bright lighting, poor perfusion, high motion, and pigmentation of the skin. It is convenient since it can noninvasively determine percentage of oxygenated hemoglobin, and, for sedentary patients, can be left in place for continuous monitoring (Figure 1.3). Many patients in respiratory distress will not tolerate the restraint necessary for arterial blood gas collection and thoracic radiographs, especially on presentation. If obtaining an arterial blood gas is feasible, findings may include decreased SpO2, decreased partial pressure of carbon dioxide (PaCO2) consistent with hyperventilation, increased PaCO2 consistent with hypoventilation, decreased partial pressure of oxygen (PaO2) consistent with hypoxemia, and an increased partial pressure of alveolar–arterial oxygen gradient P(A–a)O2). Calculation of the P(A–a)O2 gradient provides objective information on pulmonary function by removing the influence of ventilation on PaO2. When a patient is breathing 21% oxygen, the P(A–a)O2 should be less than 10–15 mmHg. When a patient is breathing 100% oxygen, the P(A–a)O2 should be less than 150 mmHg. If the P(A–a)O2 gradient is greater than 15 mmHg while breathing 21% oxygen, it is consistent with pulmonary dysfunction. For A–a gradient calculation, see the formula in Box 1.1.
Figure 1.3 Continuous pulse oximetry assessment in a laterally recumbent dog receiving oxygen supplementation via nasal prongs.
Preliminary evaluation of the ratio of SpO2 to fraction of inspired oxygen (FiO2) to the partial pressure of oxygen in arterial blood to FiO2 (PaO2/FiO2) showed good correlation between the two values in dogs. It is possible that with further investigation, the SpO2/FiO2 may become a reliable, less invasive alternative to determining PaO2/FiO2 [9].
Thoracic radiographs may show pulmonary parenchymal infiltrates ventrally consistent with pneumonia, caudodorsally consistent with non‐cardiogenic pulmonary edema, and in the perihilar region consistent with congestive heart failure. In the trauma patient, pulmonary contusions, which can be present in any lung field(s), may not become radiographically apparent for up to 48 hours, although peak opacification has been shown to occur at 6 hours in human trauma patients [10]. Additionally, up to 30% of human trauma patients do not have radiographic evidence of contusions on initial thoracic radiographs, which is why CT is often proposed as the preferred method of thoracic imaging [10–12]. In a study of dogs that had succumb to vehicular trauma, thoracic radiographs underestimated the presence of contusions, while also overestimating their severity. The same study also noted that thoracic radiographs were less sensitive than CT for detecting rib fractures [13]. Initial investigation in the use of thoracic ultrasound for detection of pulmonary contusions in dogs with vehicular trauma showed a high sensitivity for diagnosing contusions compared with CT, and even noted improved sensitivity compared with thoracic radiographs [14]. Therefore, cautious respiratory monitoring and repeat thoracic imaging may be indicated in any patient with a history of known or suspected trauma.
Box 1.1 Formula Used for A–a Gradient Calculation
The partial pressure of alveolar–arterial oxygen (P(A–a)O2) gradient provides objective information on pulmonary function by removing the influence of ventilation on PaO2.
PAO2 = alveolar gas equation
FiO2 = percentage of inspired O2
Patm = atmospheric pressure (760 mmHg used at sea level)
PH2O = water vapor pressure (53 mmHg 39°C for dogs/cats; 47 mmHg at 37°C in humans)
R = respiratory quotient (approximately 0.8–0.9)
Example
