Mechanical Ventilation: Indications, Goals, and Prognosis

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.

echanical ventilation is currently an time so that it can be viewed as a useful and uncommon supportive measure in vet- lifesaving adjunct to critical care. Merinary medicine, and its use is largely restricted to academic institutions and specialty INDICATIONS practices. As the discipline of veterinary critical Mechanical ventilation is indicated in care continues to grow, application of mechani- patients with severe hypoxemia despite oxygen cal ventilation will likely become more wide- therapy, severe hypercapnia, or excessive work spread. Human intensive care physicians view of breathing.2 Guidelines for initiating ventila- mechanical ventilation as an essential aspect of tory support are based on measurements of critical patient care, with 1.5 million patients blood gasses, pulse oximetry, and capnography ventilated yearly in the United States.1 It is or on the more subjective criteria of excessive inevitable that mechanical ventilation will have ventilatory effort. a significant role in veterinary medicine. Patients with respiratory compromise can be Successful application of positive-pressure broadly divided into two groups: those with pri- ventilation (PPV), the most prevalent form of mary pulmonary disease and those with nonpul- mechanical ventilation, requires appropriate monary causes of inadequate ventilation. The patient selection, an understanding of ventilator clinical presentation of patients in these two function, and most important, intensive nursing groups may be very different. Pulmonary and care. Many veterinary patients upper airway disease are characterized by hypox- Send comments/questions via email can benefit from PPV. It is emia and increased work of breathing, whereas [email protected], hoped that the perception of animals with extrapulmonary pathology often fax 800-556-3288, or web the ventilator as a harbinger have few clinical signs of respiratory distress.2–4 CompendiumVet.com of death will change with Because patients requiring mechanical venti-

March 2005 195 COMPENDIUM 196 CE Mechanical Ventilation: Indications, Goals, and Prognosis

The A-a Gradient SpO2 of 91% should correspond

to a PaO2 of approximately 60 Patient hypoventilating without 5,9,10 pulmonary pathology Patient with pulmonary pathology mm Hg. Pulse oximetry is not only prone to inaccuracy but FIO2 = 21% FIO2 = 21% also insensitive to changes in PaO = 74 mm Hg PaO = 74 mm Hg 2 2 oxygenation at levels of PaO PaCO = 58 mm Hg PaCO = 31 mm Hg 2 2 2 greater than 100 mm Hg. For PAO2 = FIO2 (PB – PH2O) – (PaCO2 ÷RQ) PAO2 = FIO2 (PB – PH2O) – (PaCO2 ÷RQ) example, a patient receiving = 0.21 (760 – 50) – (58 ÷ 0.8) = 0.21 (760 – 50) – (31 ÷ 0.8) 100% inspired oxygen is ex- = 76.6 mm Hg = 110.4 mm Hg pected to have a PaO2 of approx- PAO2 – PaO2 = 2.6 mm Hg PAO2 – PaO2 = 36.4 mm Hg imately 500 mm Hg and a Assessment: A-a gradient <15 (normal) Assessment: A-a gradient >25 (abnormal) corresponding pulse oximeter reading of 99% to 100%. This RQ = respiratory quotient; P = barometric pressure; PH O = partial pressure of water. B 2 patient’s ability to oxygenate could drop significantly so that

the PaO2 falls as low as 100 to lation are in need of urgent intervention, it is important 120 mm Hg without a corresponding change in the pulse that clinicians understand the indications for mechanical oximeter reading. Therefore, pulse oximeter readings of ventilation and are willing to begin ventilation manually 99% to 100% in animals receiving oxygen therapy can be or by machine to stabilize patients in the acute period. interpreted only as adequate. There is no way to ascertain whether the degree of oxygenation is appropriate for the HYPOXEMIA animal’s level of inspired oxygen. Accurate pulse oximeter Recognition readings of less than 99% in animals receiving supplemen- Hypoxemia is defined as a partial pressure of oxygen in tal oxygen can be considered abnormal.5 the arterial blood (PaO2) of less than 80 mm Hg. A PaO2 Although the partial pressure of oxygen in venous of less than 60 mm Hg is considered severe hypoxemia blood (PvO2) is not reflective of pulmonary function, 5 and warrants rapid intervention. Measuring PaO2 re- when all other measurements are unavailable, it can be quires an arterial blood sample and a blood gas analyzer. used as an indication that an animal is receiving ade-

Approximately 50% of dogs and cats ventilated for neuromuscular pathology are successfully weaned from the ventilator compared with 25% of those with pulmonary pathology.

11 PaO2 is the most sensitive measure of a patient’s ability to quate oxygen to the tissue. A PvO2 of less than 30 mm oxygenate and is the ideal parameter for monitoring the Hg suggests that the total content of delivered oxygen is response to therapy. inadequate to meet the patient’s oxygen consumption.5

If an arterial blood gas sample cannot be obtained, pulse A low PvO2 can be a consequence of reduced oxygen oximetry can be used to approximate the adequacy of oxy- delivery and/or increased oxygen consumption and can- genation.6–8 Pulse oximeters measure the percent saturation not be simply interpreted as an indicator of pulmonary of hemoglobin with oxygen (SpO2) in pulsatile vessels. dysfunction. When interpreting PvO2 in patients with Although simple to use, pulse oximeters can be inaccurate, cardiovascular compromise, it is recommended that only especially in moving, darkly pigmented, or poorly perfused central venous or mixed venous samples be evaluated. animals; thus they should be interpreted with caution.6,7 Peripheral venous samples can reflect abnormalities of

Based on the oxyhemoglobin dissociation curve, an SpO2 of the local tissue bed that are not globally representative 11 96% should approximate a PaO2 of 80 mm Hg, whereas an of the patient.

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5 The PaO2:FIO2 Ratio Causes of Hypoxemia Low inspired oxygena FIO = 40% = 0.40 FIO = 80% = 0.80 2 2 • High altitude PaO = 200 mm Hg PaO = 200 mm Hg 2 2 • Equipment malfunction PaO ÷FIO = 500 PaO ÷FIO = 250 2 2 2 2 Hypoventilationa Assessment: Normal Assessment: Venous admixture Moderate Pathology • Anatomic shunt • Diffusion defects • V/Q mismatch Cyanosis is blue discoloration of the mucous mem- — Low V/Qa branes indicating the presence of deoxygenated hemo- — No V/Q a globin. Once cyanosis has been appreciated, the PaO2 is Likely to be very oxygen responsive. 50 mm Hg or less and hypoxemia is severe; this is a late indicator of respiratory failure.12,13

PaO2 by the decimal value of FIO2 yields the ratio. A Evaluation normal PaO2:FIO2 ratio is 500. A PaO2:FIO2 ratio of 300 The PaO2 must be interpreted with regard to the frac- to 500 is consistent with mild disease, 200 to 300 with tion of inspired oxygen (FIO2) at the time of the meas- moderate disease, and less than 200 with severe pathol- 5,16 urement. This evaluation allows a clinician to determine ogy. The PaO2:FIO2 ratio is a quick method of evaluat- whether the animal’s ability to oxygenate is normal. ing oxygenation and is widely used in human medicine Abnormal or lower than expected PaO2 measurements but is less accurate than the A-a gradient because it does can be quantified to reflect the degree of disease severity not account for the influence of varying partial pressure O and allow comparisons between Pa 2 measurements in of carbon dioxide (PCO2) levels. the same patient at different times and on varying levels The five times rule is an approximate guideline for pre- IO of F 2. dicting the expected normal PaO2 in a patient at sea level O In patients with healthy lungs, the Pa 2 should be sim- for a given FIO2. The FIO2 measured as a percentage and ilar to the partial pressure of oxygen in the alveolus multiplied by five is the approximate PaO2 expected in an 16,17 (PAO2). Calculation of the alveolar–arterial (A-a) gradi- animal with normal lungs. Therefore, a patient on ent gives a measure of pulmonary dysfunction by evalu- room air would be expected to have a PaO2 of approxi- ating the difference between these two partial pressures. mately 100 mm Hg, which should increase to approxi- The PAO2 primarily depends on the inspired partial pres- mately 500 mm Hg on 100% oxygen. sure of oxygen (PO2) and the quantity of carbon dioxide

(CO2) in the alveolus. PAO2 is calculated by the alveolar Causes air equation. The A-a gradient can then be determined The three main causes of hypoxemia are a low FIO2, 14 5 by subtracting the PaO2 from the PAO2. The A-a gradi- hypoventilation, and venous admixture (see the box on ent (see the box on page 196) is one of the few calcula- this page). A low inspired level of oxygen can occur with tions of oxygenation that accounts for the impact of equipment malfunction or human error when establish- changes in partial pressure of arterial carbon dioxide ing a patient on a breathing circuit. When hypoxemia is 14 (PaCO2). A normal A-a gradient is less than 15 mm Hg identified in an animal on a breathing circuit, it is essen- when breathing room air (i.e., 21% oxygen).5 The normal tial to ensure that the oxygen supply is adequate before

A-a gradient increases as the FIO2 increases (approxi- considering other causes of hypoxemia. 15 mately 5 to 7 mm Hg per 10% increase in FIO2). If the Hypoventilation by definition causes hypercapnia. In

A-a gradient is normal in a hypoxemic patient, the cause patients breathing room air, this elevated CO2 level can of hypoxemia is either hypercapnia or decreased inspired cause significant dilution of the PAO2 so that a patient oxygen. An increased A-a gradient usually indicates the can become hypoxemic. Patients with this hypoxemia presence of pulmonary or cardiovascular pathology.14 readily respond to oxygen therapy.18 Therefore, hyper-

The PaO2:FIO2 ratio (see the box on this page) is a less capnic animals should receive oxygen supplementation complicated method for quantifying the ability to oxy- while the cause of elevated PCO2 is addressed. If hyper- genate at different levels of FIO2. Dividing the value for capnia is severe and the primary cause cannot be rapidly

March 2005 COMPENDIUM 198 CE Mechanical Ventilation: Indications, Goals, and Prognosis

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 Figure 1. Ventilation–perfusion abnormalities.19 The ideal alveolus is optimally ventilated and perfused, resulting in a V/Q of 1. Inad- equately ventilated alveoli with low V/Q resolved, the animal may require PPV to restore a more and collapsed alveoli, which have no V/Q, contribute to acceptable PCO2. venous admixture and can result in hypoxemia or a 19 Venous admixture, the most common cause of hypox- lower than expected PaO2. emia, refers to blood passing from the right to left side of Diseases that create partial filling of alveoli with fluid the circulation without being fully oxygenated, thus dilut- or partial obstruction of the terminal airways result in ing arterial blood with deoxygenated blood.5 Causes of areas of low V/Q. These alveoli are still capable of gas venous admixture can be divided into right- to left-sided exchange, and increasing the FIO2 improves the arterial anatomic shunts, diffusion defects, and ventilation–perfu- oxygen content of the capillaries perfusing these regions. sion (V/Q) mismatch. Clinically, V/Q mismatch is by far In no-V/Q areas, the alveoli or airways are completely the most important cause of hypoxemia.5 occluded (i.e., ventilation = 0) and are therefore not able

Pathologic anatomic shunts are associated with abnor- to contribute to gas exchange even if the FIO2 is in- mal communication between the right and left sides of creased. Oxygen therapy is therefore not effective in the circulation (e.g., right- to left-sided shunting ventric- 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. ular septal defects, right- to left-sided shunting patent no-V/Q regions usually have pulmonary parenchymal ductus arteriosus) and tend not to be oxygen responsive.16 disease, fail to respond to oxygen therapy, and require Diffusion defects are caused by thickening or pathol- ventilation. PPV may reopen some of these collapsed, ogy of the gas exchange surface of the alveoli. Although no-V/Q alveoli and convert them into functional gas- frequently discussed, diffusion defects are rare because exchange units—a process referred to as recruitment. the diffusion surface of the alveolus is highly protected This is one of the major benefits of PPV in patients by virtue of its anatomic structure.12,16 Although pul- with pulmonary parenchymal disease. In reality, most monary parenchymal diseases such as pulmonary edema pulmonary diseases create a heterogenous mixture of can increase the thickness of the pulmonary intersti- low- and no-V/Q areas. As the relative proportion of tium, there is minimal change to the barrier to gas no-V/Q regions increases, the effectiveness of oxygen exchange between the surface of the alveolar epithelial therapy declines and the requirement for PPV increases.

COMPENDIUM March 2005 200 CE Mechanical Ventilation: Indications, Goals, and Prognosis

Figure 2. Diagnostic approach to hypoxemic patients.

All pulmonary parenchymal diseases can create collapse placement of the endotracheal tube. Once the patient is or filling of alveoli, leading to V/Q mismatch. Examples receiving the appropriate FIO2, the remaining causes of include pneumonia, cardiogenic and noncardiogenic hypoxemia are hypoventilation or venous admixture. pulmonary edema, pulmonary contusions, infiltrative Hypoventilation is identified by an elevated PCO2 and neoplasia, pulmonary hemorrhage, and compressive results from an inadequate respiratory rate and/or tidal 12,16,20 21 masses. volume and causes an elevated PCO2. Patients may have both hypoventilation and venous admixture; there- Diagnostic Approach fore, it is important to confirm the impact of an elevated

Initial management of hypoxemic patients should always PCO2. Calculating the alveolar air equation in patients include oxygen therapy. Evaluation of hypoxemic patients with hypoventilation alone reveals a normal A-a gradi- can follow a simple diagnostic algorithm (Figure 2). ent, confirming that hypoventilation is the sole cause of For intubated patients on a breathing circuit, the first hypoxemia. Animals with hypoventilation as their pri- concerns are the adequacy of oxygen supply and correct mary problem frequently have no evidence of pul-

COMPENDIUM March 2005 Mechanical Ventilation: Indications, Goals, and Prognosis CE 203

monary disease on radiographs, and their hypoxemia of alveolar ventilation. A PaCO2 greater than 43 mm Hg responds to oxygen therapy.22 in dogs and greater than 36 mm Hg in cats is consid-

Patients with a lower than expected ability to oxy- ered elevated, whereas a PaCO2 greater than 60 mm Hg genate and an abnormal A-a gradient have venous suggests severe hypoventilation and warrants therapy.6,11 admixture. Most of these animals have pulmonary An elevated PCO2 causes acidosis and can have serious parenchymal disease and would be expected to have metabolic and neurologic consequences. Elevated PCO2 radiographic changes. A small number of patients with leads to cerebral vasodilation and increased intracranial an abnormal A-a gradient have an anatomic shunt. pressure. Patients with preexisting brain disease may not These animals are identified usually by history and sig- tolerate such fluctuations in intracranial pressure and nalment and possibly by the presence of a cardiac mur- often require their PCO2 to be maintained in a narrow mur. They may have cardiac and/or pulmonary changes range of 35 to 45 mm Hg to prevent deterioration of 5,19 24 evident on thoracic radiographs. their neurologic status. Although a PaCO2 greater than The severity of pulmonary parenchymal disease can be 60 mm Hg despite therapy is an indication for PPV in estimated by calculating the A-a gradient, PaO2:FIO2 most patients, a PaCO2 of greater than 45 mm Hg may ratio, and response to oxygen therapy. Patients that do not be an indication for PPV in animals with brain disease.24 achieve adequate oxygenation despite oxygen therapy are Although venous oxygen measurements do not reflect candidates for ventilation and should be recognized and arterial oxygen values, venous PCO2 (PvCO2) values are treated aggressively before they are in danger of car- 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. diopulmonary arrest. These animals should be promptly therefore provide a good indication of ventilatory anesthetized and intubated to gain control over their ven- status.11 In animals with poor perfusion, a central venous 11 tilation. They can be manually ventilated on 100% oxygen sample is more accurate than a peripheral PCO2. with a nonrebreathing circuit or anesthetic machine until A capnograph, which allows measurement of end- they can be safely established on a ventilator. tidal CO2 (ETCO2), can also be used to assess the ade-

Patients that require a high FIO2 to maintain adequate quacy of ventilation. These monitors measure the CO2 oxygenation may also be candidates for mechanical ven- levels of expired gas, and the last portion of exhalation is tilation because of the risk of oxygen toxicity. Exposure assumed to have a composition similar to alveolar gas. to 60% or more oxygen for longer than 24 hours is ETCO2 is approximately 2 to 6 mm Hg lower than 17,23 25–27 believed to lead to pulmonary damage. The full PaCO2 in dogs. ETCO2 is not an accurate reflection impact of these toxic effects may not be appreciated of PaCO2 in patients with poor perfusion or substantial until the damage is irreversible. Mechanical ventilation alveolar dead space as seen in patients with pulmonary can recruit collapsed alveoli and improve gas exchange thromboembolism; therefore, it is important to compare so that patients may achieve acceptable blood gas values the ETCO2 with at least one blood gas analysis when 25,26 on a lower FIO2 with PPV compared with spontaneous possible. breathing. Ventilatory assistance should therefore also be considered in patients that require an FIO2 of greater Causes than 60% for longer than 24 hours.17 Hypoventilation leading to ineffective alveolar ventila-

tion elevates PCO2. Effective alveolar ventilation is the HYPERCAPNIA portion of the tidal volume that reaches the alveoli and Recognition participates in gas exchange. A decrease in minute venti-

The arterial CO2 level is an indicator of the adequacy lation, which is the product of the tidal volume and the

March 2005 COMPENDIUM 204 CE Mechanical Ventilation: Indications, Goals, and Prognosis

respiratory rate, reduces the effective alveolar ventilation. quate flow rates. Excessive dead space between the Y Dead space refers to the portion of the tidal volume that piece and patient should be removed. does not participate in gas exchange.22 Diseases (e.g., A primary cause of hypoventilation should be investi- pulmonary thromboembolism) that increase dead space gated and addressed when possible. Reversal of anes- can also lead to hypercapnia. Dead space can also be cre- thetic or narcotic agents, decompression of cervical ated by an increase in the length of the breathing circuit lesions, normalization of intracranial pressure, and intu- between the Y piece and the patient. This is especially bation or medical management for airway obstructions important in very small patients in which an excessively may all increase effective ventilation in appropriate situ- long endotracheal tube or extensions such as an ETCO2 ations. A PaCO2 above 60 mm Hg (or >45 mm Hg in adapter can create significant dead space.22 patients with intracranial disease) despite specific treat- Hypoventilation is frequently due to neuromuscular ment is sufficient indication for PPV.22 disease and is a common indication for PPV. Impair- ment to the neuromuscular pathway controlling respir- EXCESSIVE WORK OF BREATHING ation can lead to hypoventilation, and patients may A patient that responds to oxygen therapy and has require PPV to maintain adequate minute ventilation acceptable blood gas values may still require ventilation and ensure an acceptable PCO2. This includes lesions if its respiratory effort is not sustainable; work of affecting the respiratory muscles themselves and/or the breathing and muscle fatigue must be considered when function of the central respiratory center, brain stem, evaluating a patient in respiratory distress.33 Human cervical spinal cord, peripheral nerves, and/or neuro- studies have demonstrated a four- to sixfold increase in muscular junction.22,28–31 inspiratory effort in acute respiratory failure.34 In fact, Minute ventilation can also be reduced by large air- reducing the work of the respiratory muscles is the most way obstruction such as laryngeal paralysis or foreign common reason for mechanical ventilation in humans.34 body obstruction leading to hypercapnia. PPV is not Likewise, animals with pulmonary pathology must indicated in patients with these conditions because spe- expend more energy to maintain adequate gas cific therapy to relieve obstructions (e.g., tracheostomy) exchange.35 This increase in work of breathing increases can resolve their hypercapnia. oxygen consumption and exacerbates hypoxemia.36 Dys- Malfunction of one-way valves or scavenging systems pneic patients may also become hyperthermic, which and inadequate flow rates in a nonrebreathing circuit further increases respiratory effort and oxygen con- can be iatrogenic causes of hypercapnia. It is important sumption. Animals with excessive work of breathing can to rule out these causes because they are reversible and become exhausted and develop acute respiratory failure affected patients do not require PPV.32 leading to cardiopulmonary arrest.35 Animals with pulmonary parenchymal disease fre- Making the decision to implement PPV in a patient quently become hypoxemic while maintaining a normal based on clinical signs alone can be challenging. In some or even reduced PCO2. This is because CO2 is approxi- cases, the degree of respiratory distress may be so severe mately 20 times more diffusible in water than in oxygen; that it precludes any measure of oxygenation. Tests to therefore, less alveolar surface area is required to remove measure or estimate work of breathing are not readily 18 CO2 from blood than to add oxygen to it. available, and clinicians are left with subjective evaluation as their only guide. A rule of thumb used by one human Diagnostic Approach critical care specialist is that if a patient is distressed Evaluation of hypercapnic patients should follow a enough that mechanical ventilation is being considered, it systematic approach. Hypoventilating animals breathing is likely that mechanical ventilation is indicated.15 Patients room air are likely to be hypoxemic as well as hypercap- demonstrating excessive work of breathing can acutely nic and should be given supplemental oxygen. As dis- arrest. Early recognition of these patients and prompt cussed previously, these patients should have a normal intubation and mechanical ventilation can be lifesaving. A-a gradient, and rapid resolution of their hypoxemia would be expected with oxygen supplementation. GOALS OF VENTILATION If a hypercapnic animal is on a breathing circuit or The ultimate goal of mechanical ventilation is to wean anesthetic machine, the system should first be checked the patient from the ventilator. The goals during venti- for a valve or scavenging system malfunction and inade- lation are to optimize oxygenation and ventilation in a

COMPENDIUM March 2005 206 CE Mechanical Ventilation: Indications, Goals, and Prognosis

patient while reducing work of breathing and minimiz- ment, and ultimately wean them from machine support. ing complications. Because PPV is not benign, clini- The prognosis for successful weaning depends on the cians should ideally use the least-aggressive ventilator underlying disease and the severity of concurrent issues. settings possible to maintain acceptable PaO2 and PaCO2 levels (i.e., PaO2 of 80 to 120 mm Hg and PaCO2 of Watch for an upcoming article on ventilator 2 approximately 40 mm Hg). From the time an animal is settings, patient management, and nursing care. 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 REFERENCES is to provide adequate medical and nursing care to mini- 1. MacIntyre NR: Mechanical Ventilation. Philadelphia, WB Saunders, 2001. 2. Haskins SC, King LG: Positive pressure ventilation, in King LG (ed): Text- mize complications and maximize patient comfort. book of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 217–229. PROGNOSIS 3. Mellema MS, Haskins SC: Weaning from mechanical ventilation. Clin Tech Small Anim Pract 15(3):157–164, 2000. The prognosis in animals treated with mechanical 4. King LG, Hendricks JC: Use of positive-pressure ventilation in dogs and ventilation has not been well established in the litera- cats: 41 cases (1990–1992). JAVMA 204(7):1045–1052, 1994. ture. The weaning and survival rates in veterinary 5. Haskins SC: Interpretation of blood gas measurements, in King LG (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB Saunders, patients are substantially lower than those in 2004, pp 181–193. 2–4,23,28–31,34,37–39 humans. This may be partly due to poor 6. Grosenbaugh DA, Muir WW III: Accuracy of noninvasive oxyhemoglobin case selection, lack of experience, and the greater finan- saturation, end-tidal carbon dioxide concentration, and blood pressure monitoring during experimentally induced hypoxemia, hypotension, or hyperten- cial and time limits imposed on veterinarians. sion in anesthetized dogs. Am J Vet Res 59(2):205–212, 1998. One retrospective study of mechanical PPV in dogs 7. Matthews NS, Hartke S, Allen JC Jr: An evaluation of pulse oximeters in and cats cited a 39% overall survival rate.4 Data from dogs, cats and horses. Vet Anaesth Analg 30(1):3–14, 2003. another veterinary study on long-term ventilation had 8. Jubran A, Tobin MJ: Reliability of pulse oximetry in titrating supplemental 3 oxygen therapy in ventilator-dependent patients. Chest 97(6):1420–1425, 1990. an overall survival rate to discharge of 28%. The prog- 9. Hackett TB: Pulse oximetry and end tidal carbon dioxide monitoring. Vet nosis in patients requiring mechanical ventilation varies Clin North Am Small Anim Pract 32(5):1021–1029, 2002. with the underlying disease process. Approximately 50% 10. Hendricks JC: Pulse oximetry, in King LG (ed): Textbook of Respiratory Dis- of veterinary patients that required ventilation because ease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 193–197. 11. Ilkiw JE, Rose RJ, Martin IC: A comparison of simultaneously collected of neuromuscular pathology were successfully weaned arterial, mixed venous, jugular venous and cephalic venous blood samples in compared with 25% of those requiring ventilation the assessment of blood-gas and acid-base status in the dog. J Vet Intern Med because of pulmonary pathology.3,4 Patients with a com- 5(5):294–298, 1991. 12. Lee JA, Drobatz KJ: Respiratory distress and cyanosis in dogs, in King LG bination of pulmonary and extrapulmonary diseases had (ed): Textbook of Respiratory Disease in Dogs and Cats. Philadelphia, WB weaning rates between these two numbers.29,37,39 Saunders, 2004, pp 1–12. In comparison, mortality rates in humans with non- 13. Drager LF, Abe JM, Martins MA, et al: Impact of clinical experience on quantification of clinical signs at physical examination. J Intern Med pulmonary diseases or mild pulmonary changes are 254:257–263, 2003. reportedly less than 5%. Severe pulmonary conditions 14. King LG, Anderson JG, Rhodes WH, Hendricks JC: Arterial blood gas ten- such as acute respiratory distress syndrome are associ- sions in healthy aged dogs. Am J Vet Res 53(10):1744–1748, 1992. ated with a 40% to 50% mortality.34 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. CONCLUSION 17. Manning AM: Oxygen therapy and toxicity. Vet Clin North Am Small Anim Mechanical ventilation is becoming a critical compo- Pract 32(5):1005–1020, v, 2002. 18. Lumb AB: Diffusion of respiratory gasses, in Lumb AB (ed): Nunn’s Applied nent of caring for animals with respiratory compromise. Respiratory Physiology, ed 5. Woburn, Reed Educational and Professional One of the most challenging aspects of mechanical venti- Publishing Ltd, 2000, pp 200–221. lation is making the decision to initiate it. All clinicians 19. Lumb AB: Distribution of pulmonary ventilation and perfusion, in Lumb AB (ed): Nunn’s Applied Respiratory Physiology, ed 5. Woburn, Reed Educa- will be faced with patients that require mechanical venti- tional and Professional Publishing Ltd, 2000, pp 163–189. lation and need to be prepared to intubate and manually 20. Hackner SG: Emergency management of traumatic pulmonary contusions. ventilate a patient to stabilize it. Mechanical ventilation Compend Contin Educ Pract Vet 17(5):677–686, 1995. can have a role in supporting patients with oxygenation 21. Drellich S: Principles of mechanical ventilation. Vet Clin North Am Small Anim Pract 32(5):1087–1100, 2002. and ventilation issues. The goal is to stabilize critically ill 22. Campbell VL, Perkowski SZ: Hypoventilation, in King LG (ed): Textbook of Res- patients, maintain them until there is clinical improve- piratory Disease in Dogs and Cats. Philadelphia, WB Saunders, 2004, pp 53–61.

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23. Parent C, King LG, Walker LM, Van Winkle TJ: Clinical and clinicopatho- logic 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 side- stream 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 attrib- utable 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 hydrox- yzine 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 Mechanical Ventilation: Indications, Goals, and Prognosis

2. Which of the following is the most common 10. The ETCO2 is most likely to vary substantially

cause of hypoxemia? from the PaCO2 when the a. diffusion defects a. respiratory rate is high. b. hypoventilation b. patient is in cardiovascular shock. c. venous admixture c. mucous membranes are darkly pigmented. d. equipment failure d. patient is on supplemental oxygen.

3. An SpO2 of 91% should correspond to a PaO2 of ____ mm Hg. a. 40 b. 50 c. 60 d. 80

4. At sea level, the PaO2 should be approximately

____ times the FIO2. a. two b. three c. four d. five

5. The ______is helpful in evaluating oxygena-

tion because it accounts for the effect of CO2. a. A-a gradient

b. PaO2:FIO2 ratio c. V/Q ratio

d. PvO2

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. PaCO2. b. A-a gradient. c. effective alveolar ventilation.

d. PaO2:FIO2 ratio.

8. Cyanosis is not usually appreciated until the PaO2 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

COMPENDIUM March 2005