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Compendium March 2005 (Vol 27, No 3)

Mechanical Ventilation: Indications, Goals, and Prognosis

by Monica Clare, VMD, Kate Hopper, BVSc, DACVECC


    Mechanical ventilation is the use of a machine to perform some or all of the work of breathing. The principle indications for mechanical ventilation include hypoxemia, hypercapnia, and excessive work of breathing that do not resolve with less invasive therapy. The prognosis varies with the underlying disease and the degree of pulmonary pathology. This article reviews the indications, goals, and prognosis of mechanical ventilation in small animals.

    Mechanical ventilation is currently an uncommon supportive measure in veterinary medicine, and its use is largely restricted to academic institutions and specialty practices. As the discipline of veterinary critical care continues to grow, application of mechanical ventilation will likely become more widespread. Human intensive care physicians view mechanical ventilation as an essential aspect of critical patient care, with 1.5 million patients ventilated yearly in the United States.1 It is inevitable that mechanical ventilation will have a significant role in veterinary medicine.

    Successful application of positive-pressure ventilation (PPV), the most prevalent form of mechanical ventilation, requires appropriate patient selection, an understanding of ventilator function, and most important, intensive nursing care. Many veterinary patients can benefit from PPV. It is hoped that the perception of the ventilator as a harbinger of death will change with time so that it can be viewed as a useful and lifesaving adjunct to critical care.


    Mechanical ventilation is indicated in patients with severe hypoxemia despite oxygen therapy, severe hypercapnia, or excessive work of breathing.2 Guidelines for initiating ventilatory support are based on measurements of blood gasses, pulse oximetry, and capnography or on the more subjective criteria of excessive ventilatory effort.

    Patients with respiratory compromise can be broadly divided into two groups: those with primary pulmonary disease and those with nonpulmonary causes of inadequate ventilation. The clinical presentation of patients in these two groups may be very different. Pulmonary and upper airway disease are characterized by hypoxemia and increased work of breathing, whereas animals with extrapulmonary pathology often have few clinical signs of respiratory distress.2-4

    Because patients requiring mechanical ventilation are in need of urgent intervention, it is important that clinicians understand the indi­cations for mechanical ventilation and are willing to begin ventilation manually or by machine to stabilize patients in the acute period.



    Hypoxemia is defined as a partial pressure of oxygen in the arterial blood (Pao2) of less than 80 mm Hg. A Pao2 of less than 60 mm Hg is considered severe hypoxemia and warrants rapid intervention.5 Measuring Pao2 re­quires an arterial blood sample and a blood gas analyzer. Pao2 is the most sensitive measure of a patient's ability to oxygenate and is the ideal parameter for monitoring the response to therapy.

    If an arterial blood gas sample cannot be obtained, pulse oximetry can be used to approximate the adequacy of oxygenation.6-8 Pulse oximeters measure the percent saturation of hemoglobin with oxygen (Spo2) in pulsatile vessels. Although simple to use, pulse oximeters can be inaccurate, especially in moving, darkly pigmented, or poorly perfused animals; thus they should be interpreted with caution.6,7 Based on the oxyhemoglobin dissociation curve, an Spo2 of 96% should approximate a Pao2 of 80 mm Hg, whereas an Spo2 of 91% should correspond to a Pao2 of approximately 60 mm Hg.5,9,10 Pulse oximetry is not only prone to inaccuracy but also insensitive to changes in oxygenation at levels of Pao2 greater than 100 mm Hg. For example, a patient receiving 100% inspired oxygen is ex­pected to have a Pao2 of approximately 500 mm Hg and a corresponding pulse oximeter reading of 99% to 100%. This patient's ability to oxygenate could drop significantly so that the Pao2 falls as low as 100 to 120 mm Hg without a corresponding change in the pulse oximeter reading. Therefore, pulse oximeter readings of 99% to 100% in animals receiving oxygen therapy can be interpreted only as adequate. There is no way to ascertain whether the degree of oxygenation is appropriate for the animal's level of inspired oxygen. Accurate pulse oximeter readings of less than 99% in animals receiving supplemental oxygen can be considered abnormal.5

    Although the partial pressure of oxygen in venous blood (Pvo2) is not reflective of pulmonary function, when all other measurements are unavailable, it can be used as an indication that an animal is receiving adequate oxygen to the tissue.11 A Pvo2 of less than 30 mm Hg suggests that the total content of delivered oxygen is inadequate to meet the patient's oxygen consumption.5 A low Pvo2 can be a consequence of reduced oxygen delivery and/or increased oxygen consumption and cannot be simply interpreted as an indicator of pulmonary dysfunction. When interpreting Pvo2 in patients with cardiovascular compromise, it is recommended that only central venous or mixed venous samples be evaluated. Peripheral venous samples can reflect abnormalities of the local tissue bed that are not globally representative of the patient.11

    Cyanosis is blue discoloration of the mucous membranes indicating the presence of deoxygenated hemoglobin. Once cyanosis has been appreciated, the Pao2 is 50 mm Hg or less and hypoxemia is severe; this is a late indicator of respiratory failure.12,13


    The Pao2 must be interpreted with regard to the fraction of inspired oxygen (Fio2) at the time of the measurement. This evaluation allows a clinician to determine whether the animal's ability to oxygenate is normal. Abnormal or lower than expected Pao2 measurements can be quantified to reflect the degree of disease severity and al­low comparisons between Pao2 measurements in the same patient at different times and on varying levels of Fio2.

    In patients with healthy lungs, the Pao2 should be similar to the partial pressure of oxygen in the alveolus (Pao2). Calculation of the alveolar-arterial (A-a) gradient gives a measure of pulmonary dysfunction by evaluating the difference between these two partial pressures. The Pao2 primarily depends on the inspired partial pressure of oxygen (Po2) and the quantity of carbon dioxide (CO2) in the alveolus. Pao2 is calculated by the alveolar air equation. The A-a gradient can then be determined by subtracting the Pao2 from the Pao2.14 The A-a gradient (see box) is one of the few calculations of oxygenation that accounts for the impact of changes in partial pressure of arterial carbon dioxide (Paco2).14 A normal A-a gradient is less than 15 mm Hg when breathing room air (i.e., 21% oxygen).5 The normal A-a gradient increases as the Fio2 increases (approximately 5 to 7 mm Hg per 10% increase in Fio2).15 If the A-a gradient is normal in a hypoxemic patient, the cause of hypoxemia is either hypercapnia or decreased inspired oxygen. An increased A-a gradient usually indicates the presence of pulmonary or cardiovascular pathology.14

    The Pao2:Fio2 ratio (see box) is a less complicated method for quantifying the ability to oxygenate at different levels of Fio2. Dividing the value for Pao2 by the decimal value of Fio2 yields the ratio. A normal Pao2:Fio2 ratio is 500. A Pao2:Fio2 ratio of 300 to 500 is consistent with mild disease, 200 to 300 with moderate disease, and less than 200 with severe pathology.5,16 The Pao2:Fio2 ratio is a quick method of evaluating oxygenation and is widely used in human medicine but is less accurate than the A-a gradient because it does not account for the influence of varying partial pressure of carbon dioxide (Pco2) levels.

    The five times rule is an approximate guideline for predicting the expected normal Pao2 in a patient at sea level for a given Fio2. The Fio2 measured as a percentage and multiplied by five is the approximate Pao2 expected in an animal with normal lungs.16,17 Therefore, a patient on room air would be expected to have a Pao2 of approximately 100 mm Hg, which should increase to approximately 500 mm Hg on 100% oxygen.


    The three main causes of hypoxemia are a low Fio2, hypoventilation, and venous admixture5 (see box). A low inspired level of oxygen can occur with equipment malfunction or human error when establishing a patient on a breathing circuit. When hypoxemia is identified in an animal on a breathing circuit, it is essential to ensure that the oxygen supply is adequate before considering other causes of hypoxemia.

    Hypoventilation by definition causes hypercapnia. In patients breathing room air, this elevated CO2 level can cause significant dilution of the Pao2 so that a patient can become hypoxemic. Patients with this hypoxemia readily respond to oxygen therapy.18 Therefore, hypercapnic animals should receive oxygen supplementation while the cause of elevated Pco2 is addressed. If hypercapnia is severe and the primary cause cannot be rapidly resolved, the animal may require PPV to restore a more acceptable Pco2.

    Venous admixture, the most common cause of hypoxemia, refers to blood passing from the right to left side of the circulation without being fully oxygenated, thus diluting arterial blood with deoxygenated blood.5 Causes of venous admixture can be divided into right- to left-sided anatomic shunts, diffusion defects, and ventilation-perfusion (V/Q) mismatch. Clinically, V/Q mismatch is by far the most important cause of hypoxemia.5

    Pathologic anatomic shunts are associated with abnormal communication between the right and left sides of the circulation (e.g., right- to left-sided shunting ventricular septal defects, right- to left-sided shunting patent ductus arteriosus) and tend not to be oxygen responsive.16

    Diffusion defects are caused by thickening or pathology of the gas exchange surface of the alveoli. Although frequently discussed, diffusion defects are rare because the diffusion surface of the alveolus is highly protected by virtue of its anatomic structure.12,16 Although pulmonary parenchymal diseases such as pulmonary edema can increase the thickness of the pulmonary interstitium, there is minimal change to the barrier to gas exchange between the surface of the alveolar epithelial cell and the pulmonary capillary. The abnormality in gas exchange occurring in patients with pulmonary edema is largely due to alveolar flooding and collapse leading to V/Q mismatch.5

    Venous admixture occurring in patients with pulmonary parenchymal disease is due to discrepancies in the ventilation and perfusion of alveoli. These changes are best characterized by the V/Q ratio (Figure 1).19 The ideal alveolus is optimally ventilated and perfused, resulting in a V/Q of 1. Inadequately ventilated alveoli with low V/Q and collapsed alveoli, which have no V/Q, contribute to venous admixture and can result in hypoxemia or a lower than expected Pao2.19

    Diseases that create partial filling of alveoli with fluid or partial obstruction of the terminal airways result in areas of low V/Q. These alveoli are still capable of gas exchange, and increasing the Fio2 improves the arterial oxygen content of the capillaries perfusing these regions. In no-V/Q areas, the alveoli or airways are completely occluded (i.e., ventilation = 0) and are therefore not able to contribute to gas exchange even if the Fio2 is in­creased. Oxygen therapy is therefore not effective in regions of no V/Q.17 Patients with a large proportion of no-V/Q regions usually have pulmonary parenchymal disease, fail to respond to oxygen therapy, and require ventilation. PPV may reopen some of these collapsed, no-V/Q alveoli and convert them into functional gas- exchange units—a process referred to as recruitment. This is one of the major benefits of PPV in patients with pulmonary parenchymal disease. In reality, most pulmonary diseases create a heterogenous mixture of low- and no-V/Q areas. As the relative proportion of no-V/Q regions increases, the effectiveness of oxygen therapy declines and the requirement for PPV increases. All pulmonary parenchymal diseases can create collapse or filling of alveoli, leading to V/Q mismatch. Examples include pneumonia, cardiogenic and noncardiogenic pulmonary edema, pulmonary contusions, infiltrative neoplasia, pulmonary hemorrhage, and compressive masses.12,16,20

    Diagnostic Approach

    Initial management of hypoxemic patients should always include oxygen therapy. Evaluation of hypoxemic patients can follow a simple diagnostic algorithm (Figure 2).

    For intubated patients on a breathing circuit, the first concerns are the adequacy of oxygen supply and correct placement of the endotracheal tube. Once the patient is receiving the appropriate Fio2, the remaining causes of hypoxemia are hypoventilation or venous admixture.

    Hypoventilation is identified by an elevated Pco2 and results from an inadequate respiratory rate and/or tidal volume and causes an elevated Pco2.21 Patients may have both hypoventilation and venous admixture; therefore, it is important to confirm the impact of an elevated Pco2. Calculating the alveolar air equation in patients with hypoventilation alone reveals a normal A-a gradient, confirming that hypoventilation is the sole cause of hypoxemia. Animals with hypoventilation as their primary problem frequently have no evidence of pulmonary disease on radiographs, and their hypoxemia responds to oxygen therapy.22

    Patients with a lower than expected ability to oxygenate and an abnormal A-a gradient have venous admixture. Most of these animals have pulmonary parenchymal disease and would be expected to have radiographic changes. A small number of patients with an abnormal A-a gradient have an anatomic shunt. These animals are identified usually by history and signalment and possibly by the presence of a cardiac murmur. They may have cardiac and/or pulmonary changes evident on thoracic radiographs.5,19

    The severity of pulmonary parenchymal disease can be estimated by calculating the A-a gradient, Pao2:Fio2 ratio, and response to oxygen therapy. Patients that do not achieve adequate oxygenation despite oxygen therapy are candidates for ventilation and should be recognized and treated aggressively before they are in danger of cardiopulmonary arrest. These animals should be promptly anesthetized and intubated to gain control over their ventilation. They can be manually ventilated on 100% oxygen with a nonrebreathing circuit or anesthetic machine until they can be safely established on a ventilator.

    Patients that require a high Fio2 to maintain adequate oxygenation may also be candidates for mechanical ventilation because of the risk of oxygen toxicity. Exposure to 60% or more oxygen for longer than 24 hours is believed to lead to pulmonary damage.17,23 The full impact of these toxic effects may not be appreciated until the damage is irreversible. Mechanical ventilation can recruit collapsed alveoli and improve gas exchange so that patients may achieve acceptable blood gas values on a lower Fio2 with PPV compared with spontaneous breathing. Ventilatory assistance should therefore also be considered in patients that require an Fio2 of greater than 60% for longer than 24 hours.17



    The arterial CO2 level is an indicator of the adequacy of alveolar ventilation. A Paco2 greater than 43 mm Hg in dogs and greater than 36 mm Hg in cats is considered elevated, whereas a Paco2 greater than 60 mm Hg suggests severe hypoventilation and warrants therapy.6,11 An elevated Pco2 causes acidosis and can have serious metabolic and neurologic consequences. Elevated Pco2 leads to cerebral vasodilation and increased intracranial pressure. Patients with preexisting brain disease may not tolerate such fluctuations in intracranial pressure and often require their Pco2 to be maintained in a narrow range of 35 to 45 mm Hg to prevent deterioration of their neurologic status.24 Although a Paco2 greater than 60 mm Hg despite therapy is an indication for PPV in most patients, a Paco2 of greater than 45 mm Hg may be an indication for PPV in animals with brain disease.24

    Although venous oxygen measurements do not reflect arterial oxygen values, venous Pco2 (Pvco2) values are usually 3 to 6 mm Hg higher than arterial values and therefore provide a good indication of ventilatory status.11 In animals with poor perfusion, a central venous sample is more accurate than a peripheral Pco2.11

    A capnograph, which allows measurement of end-tidal CO2 (ETCO2), can also be used to assess the adequacy of ventilation. These monitors measure the CO2 levels of expired gas, and the last portion of exhalation is assumed to have a composition similar to alveolar gas. ETCO2 is approximately 2 to 6 mm Hg lower than Paco2 in dogs.25-27 ETCO2 is not an accurate reflection of Paco2 in patients with poor perfusion or substantial alveolar dead space as seen in patients with pulmonary thromboembolism; therefore, it is important to compare the ETCO2 with at least one blood gas analysis when possible.25,26


    Hypoventilation leading to ineffective alveolar ventilation elevates Pco2. Effective alveolar ventilation is the portion of the tidal volume that reaches the alveoli and participates in gas exchange. A decrease in minute ventilation, which is the product of the tidal volume and the respiratory rate, reduces the effective alveolar ventilation. Dead space refers to the portion of the tidal volume that does not participate in gas exchange.22 Diseases (e.g., pulmonary thromboembolism) that increase dead space can also lead to hypercapnia. Dead space can also be created by an increase in the length of the breathing circuit between the Y piece and the patient. This is especially important in very small patients in which an excessively long endotracheal tube or extensions such as an ETCO2 adapter can create significant dead space.22

    Hypoventilation is frequently due to neuromuscular disease and is a common indication for PPV. Impairment to the neuromuscular pathway controlling respir­ation can lead to hypoventilation, and patients may re­quire PPV to maintain adequate minute ventilation and ensure an acceptable Pco2. This includes lesions affecting the respiratory muscles themselves and/or the function of the central respiratory center, brain stem, cervical spinal cord, peripheral nerves, and/or neuromuscular junction.22,28-31

    Minute ventilation can also be reduced by large airway obstruction such as laryngeal paralysis or foreign body obstruction leading to hypercapnia. PPV is not indicated in patients with these conditions because specific therapy to relieve obstructions (e.g., tracheostomy) can resolve their hypercapnia.

    Malfunction of one-way valves or scavenging systems and inadequate flow rates in a nonrebreathing circuit can be iatrogenic causes of hypercapnia. It is important to rule out these causes because they are reversible and affected patients do not require PPV.32

    Animals with pulmonary parenchymal disease frequently become hypoxemic while maintaining a normal or even reduced Pco2. This is because CO2 is approximately 20 times more diffusible in water than in oxygen; therefore, less alveolar surface area is required to remove CO2 from blood than to add oxygen to it.18

    Diagnostic Approach

    Evaluation of hypercapnic patients should follow a systematic approach. Hypoventilating animals breathing room air are likely to be hypoxemic as well as hypercapnic and should be given supplemental oxygen. As discussed previously, these patients should have a normal A-a gradient, and rapid resolution of their hypoxemia would be expected with oxygen supplementation.

    If a hypercapnic animal is on a breathing circuit or anesthetic machine, the system should first be checked for a valve or scavenging system malfunction and inadequate flow rates. Excessive dead space between the Y piece and patient should be removed.

    A primary cause of hypoventilation should be investigated and addressed when possible. Reversal of anesthetic or narcotic agents, decompression of cervical lesions, normalization of intracranial pressure, and intubation or medical management for airway obstructions may all increase effective ventilation in appropriate situations. A Paco2 above 60 mm Hg (or >45 mm Hg in patients with intracranial disease) despite specific treatment is sufficient indication for PPV.22

    Excessive Work of Breathing

    A patient that responds to oxygen therapy and has acceptable blood gas values may still require ventilation if its respiratory effort is not sustainable; work of breathing and muscle fatigue must be considered when evaluating a patient in respiratory distress.33 Human studies have demonstrated a four- to sixfold increase in inspiratory effort in acute respiratory failure.34 In fact, reducing the work of the respiratory muscles is the most common reason for mechanical ventilation in humans.34

    Likewise, animals with pulmonary pathology must expend more energy to maintain adequate gas exchange.35 This increase in work of breathing increases oxygen consumption and exacerbates hypoxemia.36 Dyspneic patients may also become hyperthermic, which further increases respiratory effort and oxygen consumption. Animals with excessive work of breathing can become exhausted and develop acute respiratory failure leading to cardiopulmonary arrest.35

    Making the decision to implement PPV in a patient based on clinical signs alone can be challenging. In some cases, the degree of respiratory distress may be so severe that it precludes any measure of oxygenation. Tests to measure or estimate work of breathing are not readily available, and clinicians are left with subjective evaluation as their only guide. A rule of thumb used by one human critical care specialist is that if a patient is distressed enough that mechanical ventilation is being considered, it is likely that mechanical ventilation is indicated.15 Patients demonstrating excessive work of breathing can acutely arrest. Early recognition of these patients and prompt intubation and mechanical ventilation can be lifesaving.

    Goals of Ventilation

    The ultimate goal of mechanical ventilation is to wean the patient from the ventilator. The goals during ventilation are to optimize oxygenation and ventilation in a patient while reducing work of breathing and minimizing complications. Because PPV is not benign, clinicians should ideally use the least-aggressive ventilator settings possible to maintain acceptable Pao2 and Paco2 levels (i.e., Pao2 of 80 to 120 mm Hg and Paco2 of approximately 40 mm Hg).2 From the time an animal is placed on a ventilator, efforts to reduce the level of support should be made. Many patients need long-term (>12 to 24 hours) ventilation; in these animals, the aim is to provide adequate medical and nursing care to minimize complications and maximize patient comfort.


    The prognosis in animals treated with mechanical ventilation has not been well established in the literature. The weaning and survival rates in veterinary patients are substantially lower than those in humans.2-4,23,28-31,34,37-39 This may be partly due to poor case selection, lack of experience, and the greater financial and time limits imposed on veterinarians.

    One retrospective study of mechanical PPV in dogs and cats cited a 39% overall survival rate.4 Data from another veterinary study on long-term ventilation had an overall survival rate to discharge of 28%.3 The prognosis in patients requiring mechanical ventilation varies with the underlying disease process. Approximately 50% of veterinary patients that required ventilation because of neuromuscular pathology were successfully weaned compared with 25% of those requiring ventilation because of pulmonary pathology.3,4 Patients with a combination of pulmonary and extrapulmonary diseases had weaning rates between these two numbers.29,37,39

    In comparison, mortality rates in humans with nonpulmonary diseases or mild pulmonary changes are reportedly less than 5%. Severe pulmonary conditions such as acute respiratory distress syndrome are associated with a 40% to 50% mortality.34


    Mechanical ventilation is becoming a critical component of caring for animals with respiratory compromise. One of the most challenging aspects of mechanical ventilation is making the decision to initiate it. All clinicians will be faced with patients that require mechanical ventilation and need to be prepared to intubate and manually ventilate a patient to stabilize it. Mechanical ventilation can have a role in supporting patients with oxygenation and ventilation issues. The goal is to stabilize critically ill patients, maintain them until there is clinical improvement, and ultimately wean them from machine support. The prognosis for successful weaning depends on the underlying disease and the severity of concurrent issues.

    Downloadable PDF

    1. MacIntyre NR: Mechanical Ventilation. Philadelphia, WB Saunders, 2001.

    2. Haskins SC, King LG: Positive pressure ventilation, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 217-229.

    3. Mellema MS, Haskins SC: Weaning from mechanical ventilation. Clin Tech Small Anim Pract 15(3):157-164, 2000.

    4. King LG, Hendricks JC: Use of positive-pressure ventilation in dogs and cats: 41 cases (1990-1992). JAVMA 204(7):1045-1052, 1994.

    5. Haskins SC: Interpretation of blood gas measurements, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 181-193.

    6. Grosenbaugh DA, Muir WW III: Accuracy of noninvasive oxyhemoglobin saturation, end-tidal carbon dioxide concentration, and blood pressure monitoring during experimentally induced hypoxemia, hypotension, or hypertension in anesthetized dogs. Am J Vet Res 59(2):205-212, 1998.

    7. Matthews NS, Hartke S, Allen JC Jr: An evaluation of pulse oximeters in dogs, cats and horses. Vet Anaesth Analg 30(1)2-4, 2003.

    8. Jubran A, Tobin MJ: Reliability of pulse oximetry in titrating supplemental oxygen therapy in ventilator-dependent patients. Chest 97(6):1420-1425, 1990.

    9. Hackett TB: Pulse oximetry and end tidal carbon dioxide monitoring. Vet Clin North Am Small Anim Pract 32(5):1021-1029, 2002.

    10. Hendricks JC: Pulse oximetry, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 193-197.

    11. Ilkiw JE, Rose RJ, Martin IC: A comparison of simultaneously collected arterial, mixed venous, jugular venous and cephalic venous blood samples in the assessment of blood-gas and acid-base status in the dog. J Vet Intern Med 5(5):294-298, 1991.

    12. Lee JA, Drobatz KJ: Respiratory distress and cyanosis in dogs, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 1-12.

    13. Drager LF, Abe JM, Martins MA, et al: Impact of clinical experience on quantification of clinical signs at physical examination. J Intern Med 254:257-263, 2003.

    14. King LG, Anderson JG, Rhodes WH, Hendricks JC: Arterial blood gas tensions in healthy aged dogs. Am J Vet Res 53(10):1744-1748, 1992.

    15. Marino PL: The ICU Book, ed 2. Baltimore, Williams and Wilkins, 1998.

    16. Powell LL: Causes of respiratory failure. Vet Clin North Am Small Anim Pract 32(5):1049-1058, 2002.

    17. Manning AM: Oxygen therapy and toxicity. Vet Clin North Am Small Anim Pract 32(5):1005-1020, v, 2002.

    18. Lumb AB: Diffusion of respiratory gasses, in Lumb AB (ed): Nunn's Applied Respiratory Physiology, ed 5. Woburn, Reed Educational and Professional Publishing Ltd, 2000, pp 200-221.

    19. Lumb AB: Distribution of pulmonary ventilation and perfusion, in Lumb AB (ed): Nunn's Applied Respiratory Physiology, ed 5. Woburn, Reed Educational and Professional Publishing Ltd, 2000, pp 163-189.

    20. Hackner SG: Emergency management of traumatic pulmonary contusions. Compend Contin Educ Pract Vet 17(5):677-686, 1995.

    21. Drellich S: Principles of mechanical ventilation. Vet Clin North Am Small Anim Pract 32(5):1087-1100, 2002.

    22. Campbell VL, Perkowski SZ: Hypoventilation, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 53-61.

    23. Parent C, King LG, Walker LM, Van Winkle TJ: Clinical and clinicopathologic findings in dogs with acute respiratory distress syndrome: 19 cases (1985-1993). JAVMA 208(9):1419-1427, 1996.

    24. Dewey CW: Emergency management of the head trauma patient. Vet Clin North Am Small Anim Pract 30(1):207-225, 2000.

    25. Teixeira Neto FJ, Carregaro AB, Mannarino R, et al: Comparison of a sidestream capnograph and a mainstream capnograph in mechanically ventilated dogs. JAVMA 221(11):1582-1585, 2002.

    26. Wagner AE, Gaynor JS, Dunlop CI, et al: Monitoring adequacy of ventilation by capnometry during thoracotomy in dogs. JAVMA 212(3):377-379, 1998.

    27. Raffe MR: Oximetry and capnography, in Wingfield WE, Raffe MR (eds): The Veterinary ICU Book. Jackson, Teton NewMedia, 2002, pp 86-95.

    28. Beal MW, Poppenga RH, Birdsall WJ, Hughes D: Respiratory failure attributable to moxidectin intoxication in a dog. JAVMA 215(12):1806, 1813-1817, 1999.

    29. Beal MW, Paglia DT, Griffin GM, et al: Ventilatory failure, ventilator management, and outcome in dogs with cervical spinal disorders: 14 cases (1991-1999). JAVMA 218(10):1598-1602, 2001.

    30. Hopper K, Aldrich J, Haskins SC: Ivermectin toxicity in 17 collies. J Vet Intern Med 16(1):89-94, 2002.

    31. Tegzes JH, Smarick SD, Puschner B: Coma and apnea in a dog with hydroxyzine toxicosis. Vet Hum Toxicol 44(1):24-26, 2002.

    32. Cantwell SL, Modell JH: Inadvertent severe hypercarbia associated with anesthesia machine malfunction in one cat and two dogs. JAVMA 219(11): 1551, 1573-1576, 2001.

    33. Laghi F, D'Alfonso N, Tobin MJ: Pattern of recovery from diaphragmatic fatigue over 24 hours. J Appl Physiol 79(2):539-546, 1995.

    34. Tobin MJ: Advances in mechanical ventilation. N Engl J Med 344(26): 1986-1996, 2001.

    35. Barton L: Respiratory muscle fatigue. Vet Clin North Am Small Anim Pract 32(5):1059-1071, 2002.

    36. Tobin MJ: Mechanical ventilation. N Engl J Med 330(15):1056-1061, 1994.

    37. Campbell VL, King LG: Pulmonary function, ventilator management, and outcome of dogs with thoracic trauma and pulmonary contusions: 10 cases (1994-1998). JAVMA 217(10):1505-1509, 2000.

    38. 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(9):1428-1433, 1996.

    39. Powell LL, Rozanski EA, Tidwell AS, Rush JE: A retrospective analysis of pulmonary contusion secondary to motor vehicular accidents in 143 dogs: 1994-1997. JVECCS 9(3):127-136, 1999.

    References »

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