Keywords
Key points
Intermittent positive pressure ventilation (PPV) through the use of mechanical ventilators has been a mainstay of therapy in people with respiratory failure since the poliomyelitis epidemic in the 1940s. Veterinary patients with respiratory failure can also benefit from the use of mechanical ventilation. Two major indications for initiation of PPV include hypoxemia refractory to conventional therapy and ventilatory failure. In addition, patients with severe sepsis and septic shock and those with respiratory muscle fatigue can benefit from mechanical ventilation. An intensive care unit (ICU) ventilator differs from an anesthesia ventilator through its ability to vary the inspired oxygen concentration and to humidify the inspired air. Thus, patients can be maintained on an ICU ventilator for as many days as is necessary. With the advent of positive pressure ventilators, intensivists emerged as the primary physicians caring for these patients in the ICU. In veterinary medicine, the role of long-term mechanical ventilation has been primarily assumed by specialists in emergency and critical care. However, patients that present with imminent respiratory failure must be managed quickly and assuredly by the primary attending veterinarian. First and foremost, an adequate and patent airway must be established. Following rapid sedation, hand ventilation with an Ambu bag connected to an oxygen source can be administered. An anesthesia ventilator can be temporarily used (eg, for up to 8 hours); however, because of the potential for oxygen toxicity from delivery of 100% fraction of inspired oxygen (Fio2) by the anesthesia ventilator, the use of an ICU ventilator is more suitable if longer ventilation is necessary. With support, veterinary patients with severe respiratory failure have the potential to survive.
Indications for ventilation
Mechanical ventilation is indicated when adequate gas exchange can no longer be maintained and there is a significant risk of patient death as a consequence. There are 4 main indications for mechanical ventilation. These are
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- 1.Severe hypoxemia despite oxygen therapy (Pao2 <60 mm Hg)
- 2.Severe hypoventilation (defined as Pco2 >60 mm Hg)
- 3.Excessive work of breathing
- 4.Severe circulatory shock
Severe Hypoxemia Despite Oxygen Therapy
The oxygenation status of a patient is ideally assessed by measurement of the partial pressure of oxygen in an arterial blood sample (Pao2). Hypoxemia is commonly defined as a Pao2 of less than 80 mm Hg at sea level, while a Pao2 of less than 60 mm Hg is considered severe hypoxemia. Severe hypoxemia is also known as hypoxemic respiratory failure.
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The need for mechanical ventilation in the hypoxemic patient will depend on the underlying mechanism of hypoxemia and the patient’s response to oxygen therapy. Also, if the arterial sample is taken at significant altitude, the cut-off for hypoxemia will be lower. In the emergency room setting, collection of an arterial blood gas (ABG) may not be feasible and unfortunately venous blood gas (VBG) samples cannot be used to evaluate oxygenation. In the absence of ABG samples, pulse oximetry can provide a measure of oxygenation. Pulse oximetry is appealing, as it is noninvasive; however, it is prone to inaccuracies. A pulse oximeter reading of 95% is equivalent to a Pao2 of ∼80 mm Hg, while 90% is approximately 60 mm Hg (indicating severe hypoxemia).1
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Mechanical ventilation is a consideration for patients with severe hypoxemia despite oxygen therapy, in other words, patients with a Pao2 of less than 60 mm Hg or an SpO2 of less than 90% despite oxygen therapy.General mechanisms of hypoxemia include
- 1.Inadequate inspired oxygen
- 2.Hypoventilation
- 3.Venous admixture
Inadequate inspired oxygen is not likely to be relevant to the emergency room patient. It can occur in patients on a breathing circuit when the oxygen supply is disconnected or the oxygen tank is empty. It is also the cause of hypoxemia when at high altitude. This problem is readily resolved with oxygen administration.
Hypoventilation is defined by an elevation in the partial pressure of carbon dioxide (Pco2). Elevations in Pco2 will reduce the partial pressure of alveolar oxygen as defined by the alveolar air equation.
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When patients are breathing room air, moderate-to-severe hypercapnia will be associated with hypoxemia. This cause of hypoxemia is readily resolved with oxygen administration and is not an indication for PPV.4
It is important to note that hypercapnia itself may be an indication for PPV.Venous admixture describes any mechanism by which blood can pass from the right side of the heart to the left side of the heart without being fully oxygenated. This includes ventilation–perfusion (V/Q) mismatch, right-to-left anatomic shunts, and diffusion defects. Right-to-left anatomic shunts are associated with congenital cardiovascular defects (eg, right-to-left patent ductus arteriosus) and generally become clinically relevant in young animals. These cases are not usually considered candidates for PPV. Lung diseases associated with a true diffusion defect are associated with changes to the gas exchange surface of the alveoli. In small animal patients, such diseases include smoke inhalation, oxygen toxicity, and acute respiratory distress syndrome (ARDS). The alveolar changes typified by these diseases are the loss of the type 1 pneumocytes and their replacement with the large, cuboidal type 2 pneumocytes. This process is slow, taking several days after the initial pulmonary insult to occur. Hypoxemia subsequent to a diffusion defect improves with oxygen therapy and should not require PPV. As the diseases that can cause a diffusion defect can also cause severe V/Q mismatch, PPV maybe indicated in those patients failing to respond to therapy. V/Q mismatch refers to pulmonary parenchymal disease that leads to alveoli receiving decreased ventilation for the degree of perfusion (low V/Q) or no ventilation but ongoing perfusion (no V/Q or shunt). In small animal medicine, V/Q mismatch is associated with all forms of pulmonary parenchymal disease including pulmonary edema, hemorrhage, and pneumonia. When pulmonary parenchymal disease is associated with severe hypoxemia despite high levels of oxygen therapy, PPV is indicated. As a general guideline, a Pao2 of less than 60 mm Hg despite greater than 60% Fio2 is an indication for PPV unless the underlying cause for the hypoxemia can be readily resolved.
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Severe Hypoventilation
Hypoventilation is marked by hypercapnia (Pco2 >50 mm Hg). As arterial and venous carbon dioxide levels correlate well in hemodynamically stable patients, with Pvco2 running approximately 4 mm Hg higher than Paco2, venous blood gases can be used to evaluate ventilation (but not oxygenation) status in most patients.
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In hemodynamically unstable animals, measurement of Paco2 is ideal, as carbon dioxide can accumulate in venous blood in association with low flow states and is no longer representative of ventilation. Hypoventilation is defined as a Pco2 greater than 50 mm Hg, while severe hypoventilation is a Pco2 greater than 60 mm Hg (eg, hypercapnic respiratory failure).1
Severe hypoventilation that cannot be readily resolved by treatment for the primary disease (eg, reversal agent for a sedative) may be an indication for PPV. The extreme of hypoventilation is apnea, a clear indication for manual or PPV. As elevations of Pco2 may be associated with increases in intracranial pressure, animals considered at risk of intracranial hypertension (eg, head trauma) may require PPV to maintain a Paco2 less than 45 mm Hg and greater than 35 mm Hg.The Pco2 is controlled primarily by alveolar minute ventilation, which is equal to the product of the respiratory rate and effective (alveolar) tidal volume (TV). Consequently, causes of severe hypoventilation are diseases that impair the ability of patients to maintain an adequate respiratory rate and/or TV. Such diseases include brain disease, cervical spinal cord disease, peripheral neuropathies, diseases of the neuromuscular junction, and myopathies. Hypoventilation will cause hypoxemia when the patient is breathing room air, as it reduces (dilutes out) the partial pressure of oxygen in the alveolus.
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The higher the Pco2, the lower the alveolar oxygen partial pressure and hence the greater the severity of hypoxemia. Oxygen therapy will increase the partial pressure of oxygen in the alveolus, and hypoxemia should rapidly resolve (although the Pco2 will be unchanged). For this reason, oxygen therapy should be provided as soon as hypoventilation is identified. Hypoventilation is life-threatening, because it is associated with inadequate respiratory rate and/or TV, which can easily result in apnea and death. When hypoventilation is severe or the underlying disease thought to be progressive in nature, PPV is indicated.1
Excessive Work of Breathing
Animals that are breathing so hard that they are becoming exhausted or appear to be at risk of developing exhaustion (eg, orthopnea or eyes closed during breathing) may require PPV to prevent imminent death. While some of these patients may be maintaining adequate blood gases, they are at risk for respiratory fatigue and arrest. Also, in these fragile patients, there may be no time for blood gas evaluation to be performed. This decision is based on clinical judgment and is particularly important in the emergency room setting where patients can present in a near-death state, and rapid intervention is the only chance to stabilize them.
Animals in severe respiratory distress due to lung disease are expected to have increased respiratory rate and effort with hypoxemia and hypocapnia (Pco2 <35 mm Hg). The presence of normal or elevated Pco2 in the respiratory distress patient can be a sinister sign suggestive of respiratory muscle fatigue and may support the decision to initiate PPV even if hypoxemia can be adequately resolved with oxygen therapy. Again, this should be determined based on clinical evaluation of work of breathing and signs consistent with respiratory fatigue.
Severe Circulatory Shock
Clinical signs of circulatory shock include obtundation, mucous membrane pallor, tachycardia or bradycardia, tachypnea, weak pulse quality, and cold extremities. Circulatory shock can be due to hypovolemia, cardiac disease, and loss of vasomotor tone. In patients with severe circulatory shock that is persistent despite initial resuscitation efforts, PPV may be indicated. The main goal of PPV in these patients is to reduce oxygen consumption by relieving the work of the respiratory muscles.
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Both experimental animal studies and human clinical studies have found that PPV can improve outcome from shock, and PPV is part of the early goal-directed therapy algorithm for the treatment of septic shock.6
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A secondary goal is to allow airway protection by supporting the animal appropriately during anesthesia.Prognosis
Mechanical ventilation in emergency room patients plays several important roles. In many situations, PPV may need to be initiated before any specific diagnosis can be obtained as part of life-saving stabilization efforts. In this setting, stabilization of the ABCDs (ie, airway, breathing, circulation, dysfunction) is imperative, and further prognostication of the patient can be made once the patient is successfully stabilized, allowing further diagnostic tests to be performed. Some animals may not need PPV for more than a few hours, and the owners of patients that need longer term PPV will have the benefit of a more informed prognosis once further diagnostic tests have been performed in a more controlled manner. That said, it is important to keep in mind that some patients may be difficult to wean off PPV once initiated, and the costs associated with short-term (or long-term) PPV is high. Another important role for PPV in the emergency room patient is to relieve suffering and prevent further clinical deterioration while owners spend some time to consider all their options or say good bye to their pet.
The prognosis of weaning from PPV is largely dependent on the underlying disease for which the animal requires ventilation. In general, patients that require PPV for hypoventilation (eg, cervical disc disease) have a greater likelihood of weaning than those with pulmonary parenchymal disease (eg, ARDS, pulmonary contusions, fungal pneumonia).
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For example, in a study evaluating 128 dogs and cats that received PPV for more than 24 hours, 50% of animals with hypoventilation were weaned, while only 36% of animals with pulmonary parenchymal disease were weaned.10
It is more helpful to consider prognosis of weaning from PPV in terms of the primary disease process present. For example, in the pulmonary parenchymal group in this study, 50% of animals with aspiration pneumonia were successfully weaned, while only 8% of animals with ARDS were weaned. This study largely reflects ICU patients, not emergency room patients, and only enrolled patients ventilated for 24 hours or longer. Other factors that have been reported to be associated with a poorer outcome from PPV include age, weight, and species. The weaning rates reported for feline patients are consistently lower than that of canine patients, reported to be 10% to 25%, overall.10
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Disease processes that may have a fair prognosis for weaning from PPV include
- •Congestive heart failure
- •Pulmonary contusions
- •Aspiration pneumonia
- •Cervical spinal cord compression
- •Polyradiculoneuritis
- •Intoxications
Disease processes that may have a poor prognosis to be weaned from PPV include
- •Cardiopulmonary arrest
- •Intracranial disease
- •ARDS
Overview of ventilation modes
To understand how to appropriately manage a patient undergoing PPV, an understanding of the ventilation modes and ventilator settings is imperative.
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Pressure Versus Volume Control
Modern ICU ventilators have the capability to generate several different breath types to the patient. The more basic machines tend to be either volume control ventilators or pressure control ventilators. These ventilators can generate a breath in 1 of 2 basic ways. It can deliver a preset TV over a given inspiratory time (volume control, or VC), or the machine can maintain a preset airway pressure for a given inspiratory time (pressure control, or PC). In a volume-controlled breath, the peak inspired airway pressure (PIP) generated will be dependent on the preset TV chosen by the operator and the compliance of the respiratory system. In a pressure-controlled breath, the TV will depend on the preset airway pressure chosen by the operator and the compliance of the respiratory system.
Assist-Control Ventilation
In this mode of ventilation, a minimum respiratory rate is set by the operator. If the trigger sensitivity is set appropriately, the patient can increase the respiratory rate, but all breaths delivered will be full ventilator breaths, either pressure- or volume-controlled. Breaths triggered by the ventilator are controlled breaths, while breaths triggered by the patient are considered assisted breaths (eg, patient initiates the breath, but the ventilator generates the full breath). This mode of ventilation provides maximum support of the respiratory system and is used in patients with severe disease or patients with no respiratory drive.
Synchronized Intermittent Mandatory Ventilation
In this mode of ventilation, a set number of mandatory breaths is delivered. Between these breaths, the patient can breathe spontaneously. In modern ventilators, the machine tries to synchronize the mandatory breaths with the patient’s inspiratory efforts, thus the term synchronized intermittent mandatory ventilation (SIMV). Between these mandatory breaths, the patient can breathe spontaneously, as often or as few times as desired. The operator can only control the minimum respiratory rate and minute ventilation; there is no control over the maximum rate or maximum minute ventilation. As this mode combines full ventilator breaths with spontaneous patient breaths, it is generally used for animals that do not require 100% assistance from the ventilator, such as neurologically inappropriate animals with an unreliable respiratory drive (eg, brain injury), or patients with lung disease that are improving and do not need as much support as assist–control provides.
Continuous Positive Airway Pressure
Continuous positive airway pressure (CPAP) is a completely spontaneous mode of ventilation; in other words, the patient determines both the respiratory rate and TV. The ventilator delivers no breaths; the operator can only control the baseline airway pressure, a form of positive end-expiratory pressure (PEEP). This mode of ventilation provides support for the patient’s spontaneous breaths and is only suited for patients with a strong respiratory drive and minimal pulmonary dysfunction. The ventilator will alarm if the animal does not generate adequate breaths or develops apnea, so it is a useful monitoring mode for weaning patients or for monitoring intubated patients.
Pressure Support Ventilation
Pressure support ventilation (PSV) allows the operator to augment the TV of spontaneous breaths. For example, a patient has a PSV of 6 cm H2O. This patient will begin and end inspiration, and the ventilator will maintain a pressure of 6 cm H2O in the airway during this inspiration; this effectively provides the patient with a greater tidal volume for less patient effort. Pressure support ventilation is generally used in conjunction with CPAP or to support the spontaneous breaths in SIMV.
Overview of ventilator settings
The parameters the operator is able to adjust on a ventilator will vary between machines. On advanced ICU ventilators, there tend to be more options for adjusting breath parameters compared with simpler, anesthesia-type machines. It is important to note that there is no consistency in the terminology for ventilator settings between companies; therefore, it may be necessary to read the manufacturer’s instructions to fully understand how the settings on an individual machine operate.
Trigger Variable
This is the parameter that initiates a ventilator breath. In patients that are not making any respiratory effort, the trigger variable will be time (which is determined from the set respiratory rate). The patient trigger setting is usually a change in airway pressure or a change in flow of the circuit. Appropriate trigger sensitivity is an essential safety measure to ensure ventilator breaths are synchronized with genuine respiratory efforts made by the patient.
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This increases patient comfort and allows the patient to increase its RR as required. The trigger variable can be too sensitive, such that nonrespiratory efforts such as patient handling may initiate breaths; this should also be avoided.Respiratory Rate and Inspiration: Expiration Ratio
The respiratory rate can be set on all ventilators either directly or by manipulation of variables such as minute ventilation, inspiratory time, or exhalation time. The ideal respiratory rate for an individual patient generally needs to be titrated according to patient comfort and Pco2. Respiratory rates are commonly set in the range of 10 to 20 breaths per minute initially. The ratio of the duration of inspiration to expiration (called the I:E ratio) may be preset by the operator or may be a default setting within the machine. Commonly, an I:E ratio of 1:2 is used to ensure the patient has fully exhaled before the onset of the next breath.
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This is similar to a physiologic normal breath, where expiration lasts approximately twice as long as inspiration. As respiratory rates are increased, the expiratory time will have to be reduced accordingly. It is advised to prevent the I:E ratio from increasing more than 1:1 to avoid a situation known as breath stacking or intrinsic PEEP.15
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Inspiratory Time and Flow Rate
Inspiratory time is commonly set at 1 second, but shorter inspiratory times are suitable for patients with high respiratory rates.
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Many smaller patients seem to tolerate shorter inspiratory times well. Many volume control ventilators have the option to set the flow rate instead of the inspiratory time. The faster the inspiratory flow rate, the more quickly the breath is delivered. Flow rates of 60 L/min are suggested as a good starting point.2
The flow rate may be adjusted between 40 and 80 L/min as needed to provide an inspiratory time that suits the patient’s needs.16
Tidal Volume
The normal TV reported for dogs and cats is in the range of 10 to 15 mL/kg. Lower TV (6–8 mL/kg) may be targeted in animals with severe lung disease.
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When using volume control ventilation, the operator presets the desired TV. Overdistension of the lung is extremely dangerous, as it is a major mechanism of ventilator-induced lung injury and can have severe, even fatal consequences. It is recommended to start with no more than 10 mL/kg as a preset TV. The TV can always be increased if it is determined to be insufficient once the patient is connected to the machine. If pressure control ventilation is used, then the operator presets the pressure used to generate inspiration; once the animal is connected to the machine, the TV achieved with the preset pressure is assessed. A TV of around 10 mL/kg would be a very acceptable result. A simple evaluation of TV is to observe the patient's chest movements to see if normal chest excursions are occurring, although direct measurement of TV should be performed when ever possible.Positive End-Expiratory Pressure
Pulmonary parenchymal disease can lead to areas of poorly ventilated alveoli (eg, alveoli smaller than normal) and alveolar collapse; this is the primary cause of inefficient oxygenating ability of the diseased lung. PEEP will maintain pressure in the airway during exhalation. This prevents full exhalation occurring, holding the lung in a semiinflated state, which can help open up previously collapsed alveoli to improve lung-oxygenating ability and potentially protect against some forms of ventilator-associated lung injury.
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As lung disease tends to be heterogeneous, there is a risk that while increases in PEEP may recruit areas of diseased lung, it may also cause overdistension or volutrauma of healthier lung regions. In general, PEEP is likely to be beneficial in patients with cardiogenic and noncardiogenic pulmonary edema and acute lung injury (ALI) or ARDS.13
There are some potential dangers from the use of PEEP that must be considered. The use of PEEP in diseases such as pneumonia, where the diseased lung may not be recruited, should be done with caution. Also, as PEEP increases peak airway pressure, it can contribute to barotrauma (eg, pressure trauma to the lung). Also, as PEEP maintains elevated intrathoracic pressure during exhalation, it may compromise venous return (eg, hypotension). Cardiovascular monitoring is recommended for all ventilator patients and is essential when high levels of PEEP and/or more aggressive ventilator settings are used. Ultimately, optimizing PEEP requires balancing the potential gain with the concern for adverse effects.
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Peak Inspired Airway Pressure
Patients with normal lungs (such as anesthetic patients or patients with ventilatory failure) typically only require low PIPs in the range of 8 to 15 cm H2O, ideally not exceeding 20 cm H2O. Patients with lung disease often have stiff, noncompliant lungs and consequently will require higher airway pressures to achieve the same TV. Peak airway pressures as high as 30 cm H2O may be required in animals with very severe lung disease.
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High airway pressure can cause lung injury (barotrauma) and should be avoided where possible. When using pressure control ventilation, the desired airway pressure is preset by the operator. Once the animal is connected to the ventilator, the TV achieved with that airway pressure can be assessed. Alternatively in volume control, the TV is preset, and the associated airway pressure must be assessed once PPV commences. Initially, airway pressures of 10 to 15 cm H2O should be targeted; higher airway pressures can be used if indicated by inadequate pulmonary function.Selection of initial settings
There is no way to accurately predict the ideal ventilator settings for a specific patient. The choice of initial settings is based on an understanding of the underlying disease process present.
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Once the patient is attached to the ventilator, the settings are then titrated to target adequate blood gases with an acceptable Fio2.Animals that do not have pulmonary disease are expected to have compliant, easy-to-ventilate lungs. As a result, low airway pressures, higher TV, and less PEEP are likely to be well tolerated (Table 1). When initially placing a patient on the ventilator, the use of 100% oxygen should be utilized as a safety measure (and weaned down once ventilator settings are determined and the patient stabilized).
Table 1Suggested initial ventilator settings for patients with normal pulmonary function
| Ventilator Parameter | Initial Setting |
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| Fraction of inspired oxygen | 100% |
| Tidal volume | 8–15 mL/kg |
| Respiratory rate | 10–20 breaths per minute |
| Inspiratory pressure (above PEEP) | 8–12 cm H2O |
| PEEP | 0–4 cm H2O |
| Inspiratory time | ∼1 s |
| Inspiratory: Expiratory (I:E) ratio | 1:2 |
| Inspiratory trigger | −1 to −2 cm H2O or 0.5 to 2.0 L/min |
Animals that require PPV for pulmonary disease are expected to have poor lung compliance and will require higher airway pressures than animals with healthy lungs (Table 2). PEEP may improve the oxygenating efficiency of the diseased lung and can be a very important aspect of management of some ventilator patients. Studies have shown that limiting TV to approximately 6 mL/kg in human patients with ALI and ARDS improves survival.
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The role of small TV ventilation in other lung diseases is unknown, but limiting TV when possible may be beneficial.Table 2Suggested initial ventilator settings for patients with pulmonary disease
| Ventilator Parameter | Initial Setting |
|---|---|
| Fraction of inspired oxygen | 100% |
| Tidal volume | 6–8 mL/kg |
| Respiratory rate | 20–30 breaths per minute |
| Inspiratory pressure (above PEEP) | 10–15 cm H2O |
| PEEP | 4–8 cm H2O |
| Inspiratory time | ∼1 s |
| I:E ratio | 1:2 |
| Inspiratory trigger | −1 to −2 cm H2O or 0.5 to 2.0 L/min |
Once the patient is attached to the ventilator, the patient’s chest should be observed for appropriate movement (eg, if there is insufficient or overaggressive chest inflation, the ventilator settings should be adjusted appropriately). The thorax should then be auscultated bilaterally to ensure there is ventilation of bilateral lung fields. All monitoring parameters need to be rapidly and continuously evaluated including blood pressure, electrocardiography (ECG), pulse oximeter and end-tidal carbon dioxide (etco2) monitoring. Any concerning changes should be addressed immediately.
Once the patient is adequately stabilized on the ventilator, assessment of ABGs is ideally performed. The target of PPV is to maintain adequate gas exchange while minimizing the likelihood of ventilator-associated lung injury. Target values are commonly a Pao2 between 80 and 120 mm Hg and a Paco2 of 35 to 50 mm Hg.
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Pao2
The first aim in titration of ventilator settings is to lower the Fio2 to no more than 60% while maintaining an acceptable Pao2. In the absence of ABGs, reductions in the Fio2 will have to be based on the saturation of oxygen (SpO2) based off the pulse oximeter. The implantation of PEEP may help increase the oxygenating efficiency of the sick lung. If the Pao2 is not high enough to allow adequate reductions in Fio2, increases in PEEP may be of benefit.
Paco2
The Paco2 will be inversely proportional to alveolar minute ventilation (eg, TV × respiratory rate). When titrating the initial ventilator settings, if Paco2 is higher than desired, increases in TV and/or respiratory rate are made and vice versa if the Paco2 is too low. If ABGs are not available, venous Pco2 can be used to guide ventilator settings. Initially, Pco2 should be measured on a blood gas machine to evaluate the correlation with etco2. Once this relationship has been established, etco2 can be used as a noninvasive measure to titrate ventilator settings further. If a significant change in the patient status occurs, the Pco2 should be measured directly, as the relationship and accuracy with etco2 can rapidly change.
Initial Patient Stabilization on the Ventilator
Placing a veterinary patient on an ICU ventilator requires knowledge about how the specific ventilator is connected with inflow and outflow tubing, a humidifier, and airway suction. Because of the time it takes to assemble the ventilatory equipment, the unstable patient should be anesthetized, intubated, and manually ventilated in the emergency room until the ventilator is ready to use. An anesthesia circuit breathing bag or purpose-made practice lung can be placed on the Y-piece of the ventilator circuit, allowing for input of initial ventilator settings before placing the patient directly on the breathing circuit. The initial settings used are based on general guidelines such as those described previously. When the ventilator settings are verified and the patient is anesthetized, transfer to the ventilator breathing circuit can occur. Intensive monitoring should be initiated before or soon after anesthetic induction. As the patient is being placed on the ventilator, an inspired oxygen concentration of 100% should be provided. Once the patient has stabilized on the ventilator, the aim is to decrease the Fio2 in an effort to decrease the likelihood of oxygen toxicity. A sustained Fio2 of less than 60% oxygen within the first 12 hours is desired, especially in patients with severe hypoxemic respiratory failure.
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Sustaining a minimally adequate oxygenation (Pao2 of 60 mm Hg, SpO2 of ∼90% or above) is essential, and this may limit the degree to which Fio2 can be reduced.Mechanically ventilated patients require intense monitoring and supportive care. Intravenous catheters (ideally, a multilumen catheter), an arterial catheter, a body temperature probe, and urinary catheterization should be used. Monitoring should include continuous ECG, continuous pulse oximetry, continuous direct arterial blood pressure, intermittent blood gas analysis (via an arterial catheter), and etco2 measurements. Nursing care should include catheter asepsis, oral antibacterial rinse, tracheal tube suction, passive range of motion of all limbs, ocular care, and intermittent change of body position.
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The ventilator itself requires management, including emptying water traps that collect condensation from the tubing and filling of the humidifier with sterile water as needed. Most ventilator patients need a dedicated veterinary nurse constantly, and an attentive veterinarian who can troubleshoot ventilator problems and make adjustments to ventilator settings as needed. As such, placing and maintaining a patient on a mechanical ventilator is a significant financial and time obligation.Induction and Maintenance of Anesthesia
To successfully ventilate neurologically intact dogs and cats, appropriate anesthesia must be maintained. This is to allow maintenance of the endotracheal tube (ETT), to prevent patient movement, to provide patient comfort, and to stop animals from bucking or fighting the ventilator, as the sensation of receiving a positive pressure breath is unpleasant. In neurologically inappropriate animals, anesthesia may not be necessary. Paralyzed animals may only need anesthesia to allow ETT intubation or placement of a tracheostomy tube (which allows PPV with minimal to no anesthetic or sedative drugs). Comatose patients may also tolerate ETT intubation without drug administration and are another group of patients that often can be ventilated without anesthesia.
There are several options for induction and maintenance of anesthesia in the ventilated patient. Induction of anesthesia should be performed using at least 1 fast-acting intravenous drug allowing rapid ETT placement (eg, fentanyl or midazolam). All animals should be preoxygenated before induction. Consideration of the patient’s cardiovascular status when selecting induction drugs is important. Propofol, administered slowly and to effect, is an ideal induction drug for hemodynamically stable patients. In the emergency room, where animals are often hemodynamically unstable or there is insufficient time to assess the cardiovascular system adequately, the use of induction drugs such as ketamine or etomidate may be preferable.
Maintenance anesthesia of the PPV patient is generally achieved by combinations of injectable drugs, as inhalant anesthesia is not an option when ventilating patients on an ICU ventilator. However, if an anesthesia ventilator is temporarily used, low concentrations of inhalant anesthesia can also be employed. Care must be taken, however, as inhalants can exacerbate hypotension and worsen pulmonary gas exchange. The choice of anesthesia protocol for individual PPV patients will be influenced by their cardiovascular stability, the duration of PPV anticipated, and in some situations, cost. A further consideration is recovery time. It is ideal to be able to recover animals as soon as they are ready to be weaned from PPV. This may require reducing drug doses ahead of time or changing the anesthetic protocol when weaning is thought to be imminent. Injectable anesthetics such as propofol and pentobarbital will provide an adequate plane of anesthesia when used as constant rate infusions (CRI) and generally are the basis for most ventilator patient anesthetic protocols. It is ideal to provide balanced anesthesia by the addition of drugs such as benzodiazepines and/or opioids. This allows minimal dosing of any 1 drug to reduce the likelihood of adverse effects. Sample protocols include fentanyl-lidocaine-ketamine and fentanyl-dexmedetomidine in addition to propofol or pentobarbital. See Table 3 for suggested dosing regimens. Long-term administration of propofol in dogs can lead to lipemia, which can have adverse effects and should be avoided. By minimizing the dose of propofol with the addition of other drugs, lipemia can often be avoided. Cats cannot tolerate long-term (>48 hours) propofol administration, as it leads to Heinz body formation; therefore, other anesthetic regimes need to be considered for long-term PPV in this species.
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Another concern for PPV in cats is the delayed recovery time they have after prolonged injectable anesthesia. After 24 hours of anesthesia, recovery time has been reported to be 18 to 35 hours in one study.23
In the authors’ experience, it can take many days for cats to recover from long-term anesthesia. As they often require ventilator support during the prolonged recovery period, it adds significantly to the cost and challenge of management of cats needing PPV.Table 3Anesthetic/analgesic agents commonly used in ventilated patients
| Anesthetic/Analgesic Agent | Suggested Dose |
|---|---|
| Fentanyl | 1–7 μg/kg/h CRI Loading dose: 2–5 μg/kg |
| Midazolam | 0.1–0.5 mg/kg/h CRI Loading dose: 0.2–0.4 mg/kg |
| Diazepam | 0.1–1.0 mg/kg/h CRI Loading dose: 0.5 mg/kg |
| Morphine-lidocaine-ketamine CRI | Morphine: 0.2 mg/kg/h; loading dose: 0.1–0.2 mg/kg slow intravenously Lidocaine: 3 mg/kg/h; loading dose 1–2 mg/kg Ketamine: 0.6 mg/kg/h; loading dose 0.5 mg/kg |
| Propofol | 0.05–0.4 mg/kg/min CRI |
| Dexmedetomidine | 0.5 to 1.0 μg/kg/h |
All doses indicate intravenous route.
Monitoring
Continuous monitoring of cardiovascular parameters, respiratory parameters, body temperature, and fluids both administered and lost (eg, evaporative, urinary, gastrointestinal losses, etc.) is of utmost importance when managing a patient on a mechanical ventilator. Continuous pulse oximetry, ECG, etco2, blood pressure, and body temperature should be measured. In addition, charting of results on an hourly basis will help to identify trends, diagnosing both clinical improvement and areas of concern that must be addressed. Ideally, an arterial catheter should be placed to measure both blood pressure and intermittent blood gas analysis. In smaller dogs and cats, placement of an arterial catheter may not be possible; in these cases, one must rely on results of pulse oximetry readings and VBG analysis to assess presence of significant hypoxemia and effective ventilation.
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Po2 and Pco2 Targets
Traditionally, patients should be ventilated to endpoints of normal blood levels of Po2 and Pco2: Pao2 of 80 to 120 mm Hg (SpO2 of 95%–99%) and a Paco2 of 35 to 45 mm Hg. In most patients, these goals can be reached with an Fio2 of no more than 60% and mild-to-moderate ventilator settings. In patients with severe lung disease, far more aggressive ventilator settings (eg, higher PEEP, Fio2, and PIP) may be necessary to achieve the normal blood gas goals. Ventilating with high TV and pressures can cause lung trauma, including pulmonary biotrauma and barotrauma and worsening patient outcome. A study by the ARDSnet group in 2000 showed a decrease in mortality when using a low TV strategy when ventilating patients with ARDS.
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Current recommendations for ARDS patients include ventilating to an oxygen saturation of 85% to 90% (eg, Pao2 55–80 mm Hg) and allowing Paco2 to rise above normal, as long as blood pH is maintained above 7.2 (eg, permissive hypercapnia).18
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Although this strategy may not be as relevant to patients with other forms of lung disease, lowering the target Pao2 to 60 mm Hg (SpO2 of 90%) and increasing the tolerance for hypercapnia (eg, Pco2 >50 mm Hg) may reduce the magnitude of the ventilator settings needed in animals with severe hypoxemic respiratory failure. This may reduce the likelihood of ventilator-induced lung injury.Troubleshooting
Problems involving PPV include hypoxemia/oxygen desaturation, hypercapnia, hypotension, patient–ventilator dyssynchrony, air leak, resistance to air flow, and barotrauma.
Hypoxemia is a common problem faced by patients undergoing PPV. The approach to management of hypoxemia differs when it is an acute development versus a more gradual onset. If acute desaturation is detected on the pulse oximeter, repositioning of the pulse oximeter or confirmation with an ABG is ideal. Acute desaturation of a ventilator patient that was previously oxygenating adequately indicates a dramatic decrease in pulmonary function. Potential causes include pneumothorax, machine malfunction, circuit disconnection, and loss of oxygen supply. The Fio2 should be immediately increased to 100%, the thorax auscultated, and the ventilator function reviewed. If a pneumothorax is suspected, thoracocentesis should be performed immediately. A gradual decline in oxygenating efficiency of the lung is not uncommon in the ventilator patient and is more suggestive of progressive pulmonary disease such as pneumonia, ARDS, or ventilator-induced lung injury rather than a pneumothorax or machine issue. This can be addressed in several ways. The Fio2 can be increased; however, high levels of inspired oxygen over a long period of time can induce ALI and secondary oxygen toxicity. Other methods include increasing the PEEP level, increasing the TV, and increasing the peak pressure at which the tidal breath is delivered.
Hypercapnia in the ventilator patient may be due to one or more of the following causes:
- •Pneumothorax
- •ETT or tracheostomy tube kink or obstruction
- •Increased apparatus dead space—excess tubing/connectors between the patient and the ventilator circuit Y-piece
- •Incorrect assembly of the ventilator circuit, including large airway leaks, obstruction of the exhalation circuit, or any problem that would prevent effective generation or delivery of a TV
- •Increased pulmonary dead space, which may occur with overdistension of alveoli or large pulmonary embolism
- •Inadequate ventilator settings, in particular inadequate TV, inadequate respiratory rate, or both; settings that can impair exhalation such as insufficient expiratory time can also cause hypercapnia
A sudden increase in Paco2 (eg, hypoventilation or hypercapnia) in a previously stable patient is suggestive of an acute abnormality such as an ETT or tracheostomy tube obstruction or dislodgement, ventilator circuit leak, or pneumothorax. If evaluation of the machine and patient rules out major complications, then it is to be assumed that there is insufficient alveolar minute ventilation, and appropriate changes in the ventilator settings should be made.
Hemodynamic compromise can be an adverse effect of PPV. Subatmospheric pressure generated within the thoracic cavity during normal, spontaneous inspiration promotes venous return to the right side of the heart (eg, preload). When a patient is placed on PPV, it causes positive intrathoracic pressure during inspiration, which opposes venous return. As a result, venous return occurs primarily during exhalation during PPV and may be reduced. With the addition of PEEP, which generates positive intrathoracic pressure during exhalation, venous return may be further compromised. Perfusion parameters and blood pressure should be closely monitored in the PPV patient, especially when high PEEP levels and high peak pressures are used. If hemodynamic compromise occurs, volume support to improve preload may be beneficial. In patients that are hypotensive despite fluid therapy, vasopressor therapy may be indicated.
Patient–ventilator dyssynchrony occurs when the patient’s breath and the mechanical breath conflict with one another. When a patient fights or bucks the ventilator, it can prevent effective ventilation of the animal and may lead to desaturation and hypercapnia. In addition, it increases the work of breathing and can increase both patient discomfort and patient morbidity. Bucking the ventilator is 1 of the most common challenges for PPV patient management. It is ideal to have a thorough, systematic approach to this problem to avoid missing potential causes. Potential causes of patient–ventilator dyssynchrony include
- •Hypoxemia— loss of oxygen supply, worsening of underlying disease, or development of new pulmonary disease such as pneumothorax, pneumonia, or ARDS
- •Hypercapnia— circuit disconnect/leak, tube obstruction or kink, pneumothorax
- •Pneumothorax— Typified by a rapidly climbing Pco2 and a plummeting Pao2; auscultation and diagnostic thoracocentesis is warranted
- •Hyperthermia
- ○Anesthetized animals like to have relatively low temperatures, and even a rectal temperature of 102°F/38.9°C may cause dogs to pant on the ventilator; active cooling is required to control panting in hyperthermic ventilator patients
- ○A common cause of hyperthermia is increased breathing efforts when patients fight the ventilator; airway humidification makes it difficult for patients to lose heat, and humidification may have to be discontinued for short periods to allow hyperthermia to be resolved.
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- •Inappropriate ventilator settings— observe when the patient is trying to inhale and exhale and evaluate if the patient’s breathing pattern is appropriate or consistent with the ventilator settings
- •Inadequate depth of anesthesia— monitor routine clinical signs of anesthetic depth; this may be the most common cause of bucking, but care should be taken not to blindly increase the anesthetic drug dose when patients begin bucking the machine without fully assessing the patient or the ventilator settings
It is very important to appropriately set the high- and low-pressure alarms on the ventilator. Low pressure in the ventilator circuit indicates air leak, which is usually due to inadvertent disconnection of the ventilator tubing. The high-pressure alarm is activated due to increased resistance to airflow. This may be caused by ETT obstruction from a mucous plug or a large amount of secretions or due to the development of a pneumothorax. Resistance to airflow can also be due to worsening of pulmonary disease, requiring higher pressures to adequately ventilate the patient. Plateau airway pressures of greater than 30 cm H2O should be avoided.
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Summary
Mechanical ventilation can be a life saving tool for dogs and cats experiencing hypoxemic respiratory failure and those that develop ventilatory failure. Ventilation of patients with ventilatory failure has been shown to have a better prognosis than ventilation of those ventilated for hypoxemic respiratory failure.
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An anesthesia machine can be used to provide PPV to patients for a short period of time; this may be suitable for initial stabilization of animals in the emergency room. If longer-term ventilation is required, referral to a veterinary hospital with an ICU ventilator should be considered. Recognizing and treating dogs and cats with imminent respiratory failure with anesthesia, intubation, and PPV can be practical and life saving.References
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Published online: May 01, 2013
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© 2013 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
