Article #2 CE Mechanical Ventilation: Indications, Goals, and Prognosis Monica Clare, VMD Advanced Critical Care & Internal Medicine Tustin, California Kate Hopper, BVSc, DACVECC University of California, Davis ABSTRACT: 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. Send comments/questions via email compendium@medimedia.com, fax 800-556-3288, or web CompendiumVet.com 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. INDICATIONS 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 venti- March 2005 195 COMPENDIUM
196 CE The A-a Gradient Patient hypoventilating without pulmonary pathology FIO 2 = 21% PaO 2 = 74 mm Hg PaCO 2 = 58 mm Hg PAO 2 = FIO 2 (P B PH 2 O) (PaCO 2 RQ) = 0.21 (760 50) (58 0.8) = 76.6 mm Hg PAO 2 PaO 2 = 2.6 mm Hg Assessment: A-a gradient <15 (normal) lation 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 Recognition Hypoxemia is defined as a partial pressure of oxygen in the arterial blood (PaO 2 ) of less than 80 mm Hg. A PaO 2 of less than 60 mm Hg is considered severe hypoxemia and warrants rapid intervention. 5 Measuring PaO 2 requires an arterial blood sample and a blood gas analyzer. Patient with pulmonary pathology FIO 2 = 21% PaO 2 = 74 mm Hg PaCO 2 = 31 mm Hg PAO 2 = FIO 2 (P B PH 2 O) (PaCO 2 RQ) = 0.21 (760 50) (31 0.8) = 110.4 mm Hg PAO 2 PaO 2 = 36.4 mm Hg Assessment: A-a gradient >25 (abnormal) RQ = respiratory quotient; P B = barometric pressure; PH 2 O = partial pressure of water. Approximately 50% of dogs and cats ventilated for neuromuscular pathology are successfully weaned from the ventilator compared with 25% of those with pulmonary pathology. PaO 2 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 (SpO 2 ) 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 SpO 2 of 96% should approximate a PaO 2 of 80 mm Hg, whereas an SpO 2 of 91% should correspond to a PaO 2 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 PaO 2 greater than 100 mm Hg. For example, a patient receiving 100% inspired oxygen is expected to have a PaO 2 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 PaO 2 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 (PvO 2 ) 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 PvO 2 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 PvO 2 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 PvO 2 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
CE 197 The PaO 2 :FIO 2 Ratio FIO 2 = 40% = 0.40 PaO 2 = 200 mm Hg PaO 2 FIO 2 = 500 Assessment: Normal FIO 2 = 80% = 0.80 PaO 2 = 200 mm Hg PaO 2 FIO 2 = 250 Assessment: Moderate Pathology Cyanosis is blue discoloration of the mucous membranes indicating the presence of deoxygenated hemoglobin. Once cyanosis has been appreciated, the PaO 2 is 50 mm Hg or less and hypoxemia is severe; this is a late indicator of respiratory failure. 12,13 Evaluation The PaO 2 must be interpreted with regard to the fraction of inspired oxygen (FIO 2 ) 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 PaO 2 measurements can be quantified to reflect the degree of disease severity and allow comparisons between PaO 2 measurements in the same patient at different times and on varying levels of FIO 2. In patients with healthy lungs, the PaO 2 should be similar to the partial pressure of oxygen in the alveolus (PAO 2 ). Calculation of the alveolar arterial (A-a) gradient gives a measure of pulmonary dysfunction by evaluating the difference between these two partial pressures. The PAO 2 primarily depends on the inspired partial pressure of oxygen (PO 2 ) and the quantity of carbon dioxide (CO 2 ) in the alveolus. PAO 2 is calculated by the alveolar air equation. The A-a gradient can then be determined by subtracting the PaO 2 from the PAO 2. 14 The A-a gradient (see the box on page 196) is one of the few calculations of oxygenation that accounts for the impact of changes in partial pressure of arterial carbon dioxide (PaCO 2 ). 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 FIO 2 increases (approximately 5 to 7 mm Hg per 10% increase in FIO 2 ). 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 PaO 2 :FIO 2 ratio (see the box on this page) is a less complicated method for quantifying the ability to oxygenate at different levels of FIO 2. Dividing the value for Causes of Hypoxemia 5 Low inspired oxygen a High altitude Equipment malfunction Hypoventilation a Venous admixture Anatomic shunt Diffusion defects V/Q mismatch Low V/Q a No V/Q a Likely to be very oxygen responsive. PaO 2 by the decimal value of FIO 2 yields the ratio. A normal PaO 2 :FIO 2 ratio is 500. A PaO 2 :FIO 2 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 PaO 2 :FIO 2 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 (PCO 2 ) levels. The five times rule is an approximate guideline for predicting the expected normal PaO 2 in a patient at sea level for a given FIO 2. The FIO 2 measured as a percentage and multiplied by five is the approximate PaO 2 expected in an animal with normal lungs. 16,17 Therefore, a patient on room air would be expected to have a PaO 2 of approximately 100 mm Hg, which should increase to approximately 500 mm Hg on 100% oxygen. Causes The three main causes of hypoxemia are a low FIO 2, hypoventilation, and venous admixture 5 (see the box on this page). 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 CO 2 level can cause significant dilution of the PAO 2 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 PCO 2 is addressed. If hypercapnia is severe and the primary cause cannot be rapidly March 2005 COMPENDIUM
198 CE Figure 1. Ventilation perfusion abnormalities. 19 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 PaO 2. 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 FIO 2 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 FIO 2 is increased. Oxygen therapy is therefore not effective in regions of no V/Q. 17 Patients with a large proportion of The goals of mechanical ventilation include optimizing oxygenation and ventilation, reducing the work of breathing, and allowing patient stabilization while diagnostic and therapeutic plans are implemented with the ultimate goal of weaning the patient from the ventilator. resolved, the animal may require PPV to restore a more acceptable PCO 2. 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 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 gasexchange 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.
200 CE Figure 2. Diagnostic approach to hypoxemic patients. 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 FIO 2, the remaining causes of hypoxemia are hypoventilation or venous admixture. Hypoventilation is identified by an elevated PCO 2 and results from an inadequate respiratory rate and/or tidal volume and causes an elevated PCO 2. 21 Patients may have both hypoventilation and venous admixture; therefore, it is important to confirm the impact of an elevated PCO 2. 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 pul-
CE 203 of alveolar ventilation. A PaCO 2 greater than 43 mm Hg in dogs and greater than 36 mm Hg in cats is considered elevated, whereas a PaCO 2 greater than 60 mm Hg suggests severe hypoventilation and warrants therapy. 6,11 An elevated PCO 2 causes acidosis and can have serious metabolic and neurologic consequences. Elevated PCO 2 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 PCO 2 to be maintained in a narrow range of 35 to 45 mm Hg to prevent deterioration of their neurologic status. 24 Although a PaCO 2 greater than 60 mm Hg despite therapy is an indication for PPV in most patients, a PaCO 2 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 PCO 2 (PvCO 2 ) values are usually 3 to 6 mm Hg higher than arterial values and The indications for ventilation include hypoxemia, hypercapnia, or excessive work of breathing that is not adequately responsive to other therapies. monary 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, PaO 2 :FIO 2 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 FIO 2 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 FIO 2 with PPV compared with spontaneous breathing. Ventilatory assistance should therefore also be considered in patients that require an FIO 2 of greater than 60% for longer than 24 hours. 17 HYPERCAPNIA Recognition The arterial CO 2 level is an indicator of the adequacy therefore provide a good indication of ventilatory status. 11 In animals with poor perfusion, a central venous sample is more accurate than a peripheral PCO 2. 11 A capnograph, which allows measurement of endtidal CO 2 (ETCO 2 ), can also be used to assess the adequacy of ventilation. These monitors measure the CO 2 levels of expired gas, and the last portion of exhalation is assumed to have a composition similar to alveolar gas. ETCO 2 is approximately 2 to 6 mm Hg lower than PaCO 2 in dogs. 25 27 ETCO 2 is not an accurate reflection of PaCO 2 in patients with poor perfusion or substantial alveolar dead space as seen in patients with pulmonary thromboembolism; therefore, it is important to compare the ETCO 2 with at least one blood gas analysis when possible. 25,26 Causes Hypoventilation leading to ineffective alveolar ventilation elevates PCO 2. 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 March 2005 COMPENDIUM
204 CE 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 ETCO 2 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 PCO 2. 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 PCO 2. This is because CO 2 is approximately 20 times more diffusible in water than in oxygen; therefore, less alveolar surface area is required to remove CO 2 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 PaCO 2 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
206 CE 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 PaO 2 and PaCO 2 levels (i.e., PaO 2 of 80 to 120 mm Hg and PaCO 2 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. PROGNOSIS 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 CONCLUSION 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. Watch for an upcoming article on ventilator settings, patient management, and nursing care. REFERENCES 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):3 14, 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.
207 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. ARTICLE #2 CE TEST This article qualifies for 2 contact hours of continuing CE education credit from the Auburn University College of Veterinary Medicine. Subscribers may purchase individual CE tests or sign up for our annual CE program. Those who wish to apply this credit to fulfill state relicensure requirements should consult their respective state authorities regarding the applicability of this program. To participate, fill out the test form inserted at the end of this issue or take CE tests online and get real-time scores at CompendiumVet.com. 1. Inhaled oxygen above % is associated with toxicity after 24 hours. a. 40 c. 70 b. 60 d. 80 March 2005 COMPENDIUM
208 CE 2. Which of the following is the most common cause of hypoxemia? a. diffusion defects b. hypoventilation c. venous admixture d. equipment failure 3. An SpO 2 of 91% should correspond to a PaO 2 of mm Hg. a. 40 b. 50 c. 60 d. 80 10. The ETCO 2 is most likely to vary substantially from the PaCO 2 when the a. respiratory rate is high. b. patient is in cardiovascular shock. c. mucous membranes are darkly pigmented. d. patient is on supplemental oxygen. 4. At sea level, the PaO 2 should be approximately times the FIO 2. a. two b. three c. four d. five 5. The is helpful in evaluating oxygenation because it accounts for the effect of CO 2. a. A-a gradient b. PaO 2 :FIO 2 ratio c. V/Q ratio d. PvO 2 6. is defined as the portion of the tidal volume not participating in gas exchange. a. Venous admixture b. Diffusion impairment c. V/Q mismatch d. Dead space 7. An animal that is hypoxemic from hypoventilation should have a normal a. PaCO 2. b. A-a gradient. c. effective alveolar ventilation. d. PaO 2 :FIO 2 ratio. 8. Cyanosis is not usually appreciated until the PaO 2 is mm Hg or less. a. 50 b. 60 c. 70 d. 80 9. The overall prognosis for survival of ventilated veterinary patients is approximately %. a. 5 b. 15 c. 35 d. 50