Positive pressure ventilation (PPV) is invasive, time-consuming, often frustrating, and consumes tremendous resources, both financial and emotional. Despite all of these drawbacks, it provides a wonderful means of life support that can truly make the difference between life and death. As criticalists, our job is to recognize the patients who will most benefit, and then to apply positive pressure ventilation in such a way as to minimize its adverse effects and therefore optimize patient outcome.
The decision to initiate PPV is made based on the clinical condition of the animal and the degree of dyspnea, the arterial blood gas results and response to oxygen supplementation while spontaneously breathing, the prognosis, and the wishes of the owner. Animals with elevated PaCO2 (> 50 mmHg), those with PaO2 values less than 55 mmHg on oxygen supplementation, or those with obvious ongoing respiratory distress or paradoxical respiration despite oxygen supplementation, are candidates for PPV. In general, we believe that better outcomes may be achieved if PPV is initiated early, rather than waiting until the animal is moribund before providing aggressive respiratory support. Furthermore, PPV is not necessarily a benign procedure, since inappropriately delivered PPV can result in worsening of lung disease and hasten the death of the patient.
Ventilator Settings in Animals with Lung Disease
General recommendations suggest that during positive pressure ventilation we should aim to achieve a peak airway pressure of 10-20 cm H2O. In animals with normal lungs, this is not a problem, as the low end of this airway pressure range will usually be achieved if the patient is ventilated with tidal volumes of 10-12 ml/kg. When the lungs are abnormal or diseased they become less compliant, and if 'normal' tidal volumes (10-15 ml/kg) are delivered to the airway, since the lungs are stiffer than normal, the airway pressures may reach values as high as 50 or 60 cm H2O.
This creates a problem, however, as numerous experimental studies in multiple species have been published confirming adverse effects in the lungs if airway pressures exceed 30 cm H2O. These adverse effects include inflammatory changes within the alveoli, rupture of alveolar septae, emphysema and pneumothorax. In contrast to normal lungs, the diseased lung can be very heterogeneous. Lung units with normal alveoli may be side-by-side with lung units with severely abnormal alveoli. If the lung contains many abnormal alveoli, positive pressure ventilation with normal tidal volumes can result in very high peak airway pressures and over-distension of normal alveoli, which are relatively compliant, rather than the less compliant diseased alveoli, which may not open at all. Over-distension of the normal alveoli in turn results in progression of alveolar injury and lung inflammation. In addition, some alveoli and terminal bronchioles may be 'recruitable': collapsed at end expiration but expanded during inspiration. In these recruitable alveoli and the alveoli immediately adjacent to them, further lung injury and inflammation may occur due to shear stress as they are opened and closed with each breath. Pro-inflammatory cytokines produced in the lung as a result of ventilator-induced inflammation may be released into the systemic circulation, especially in animals with severe disruption of the alveolar epithelial and endothelial barrier. Systemic release of these cytokines can then initiate or contribute to systemic inflammatory response syndrome (SIRS), eventually resulting in multiple organ failure. Pneumothorax is the most dramatic and easily recognized complication of barotrauma in the ventilated patient.
Pneumothorax due to barotrauma can rapidly progress to tension pneumothorax in the patient receiving PPV, resulting in life-threatening desaturation and hypotension. The most common clinical signs that a pneumothorax has developed are sudden desaturation, patient/ventilator dyssynchrony, and sometimes drops in blood pressure. Interestingly, in this author's experience, although pneumothorax seems to be caused by high peak airway pressures, the airway pressure does not become any higher after the pneumothorax develops. If pneumothorax is suspected, confirmatory radiographs may be obtained, although the patient is often too unstable to move and may not tolerate manipulation for radiography. Diagnostic and therapeutic thoracocentesis should be attempted to confirm the diagnosis.
Previous standards for ventilator settings in human and veterinary acute respiratory distress syndrome (ARDS) patients have recommended tidal volumes of 10-15 ml/kg, with positive end expiratory pressure (PEEP) as required to maintain adequate oxygenation. Emphasis has been placed on maintenance of adequate PaO2 and PaCO2. Multiple recent studies suggest that lung protective ventilation strategies may result in decreased lung inflammation and improved survival in human ARDS patients. The general approach is to provide quite high levels of PEEP (10-20 cm H2O) to recruit alveoli and increase functional residual capacity, thereby preventing the cycle of alveolar re-opening and stretching with each breath.
Current recommendations suggest that tidal volumes and peak airway pressures should be kept as low as possible (ideally 6-8 ml/kg and < 30 cm H2O) in order to prevent over-distention of relatively normal alveoli and shear stress.Tidal volumes should be calculated based on predicted ideal body weight for that patient, rather than actual body weight in overweight individuals.
Increased physiologic and anatomic dead space and low tidal volumes can result in problems with CO2 elimination during PPV, particularly at low tidal volumes. The term 'permissive hypercapnia' refers to acceptance of a higher than normal PaCO2 (as long as respiratory acidosis is not severe), in order to minimize tidal volumes and airway pressures. Concurrent administration of bias flow oxygen (tracheal insufflation of oxygen) is another option, flushing out carbon dioxide from the dead space, thereby improving oxygenation and assisting with carbon dioxide removal. In addition, studies in human patients and experimental dogs suggest that recruitment maneuvers and sighs can be used to attempt to open up increased numbers of atelectatic alveoli, thereby improving oxygenation.The usual approach to recruitment is to impose a short-term sustained inflation of the lung at very high airway pressures and long inspiratory times, followed by resumption of the previous baseline or a higher level of PEEP. The experimental studies suggest that responses to recruitment maneuvers may be variable depending on the type of lung injury, and there is currently no information available about their use in dogs and cats with naturally occurring ARDS. Despite our best efforts, pneumothorax occurs commonly during ventilation of animals with severe lung disease. Immediate placement of a thoracostomy tube and continuous negative pressure pleural evacuation are needed if it occurs.
Oxygen Toxicity
Animals with severe lung disease may require ventilation with high concentrations of oxygen. High FiO2 values may cause alveolar inflammation due to oxidative injury caused by high concentrations of oxygen free radicals; this type of lung injury is known as oxygen toxicity. Experimental studies in many animals with normal lungs document that the earliest changes due to oxygen toxicity begin after FiO2 values greater than 0.6 have been administered for more than 12-18 hours. In the clinical setting, lung inflammation due to oxygen toxicity may be difficult or impossible to differentiate from that caused by infection, SIRS or barotrauma. In reality, multiple causes of alveolar inflammation probably exist concurrently in most ventilated patients with lung disease. However, some degree of oxygen toxicity should be assumed if the FiO2 exceeds 0.6 for more than 12 hours.
If possible therefore, FiO2 should be kept less than 0.6 to prevent oxygen toxicity from contributing to the acute lung injury. In animals with lung disease, PEEP should be added to increase functional residual capacity and open alveoli, thereby reducing the FiO2 required. Despite the addition of PEEP, higher FiO2 values may be required to achieve oxygenation in some of the most severely affected animals. In these cases, target goals for PaO2 may be set lower than usual (i.e., a PaO2 value of 70 mmHg might be acceptable) in order to minimize the FiO2 used. In the worst case scenario, if hypoxia is severe, use of high FiO2 levels may be unavoidable and the benefit of achieving tissue oxygen delivery must be weighed against possible oxygen-induced injury to the lungs.
Hemodynamic Alterations Due to Positive Intrathoracic Pressure
Normal spontaneous respiration is achieved by generation of negative intrathoracic pressures during inspiration, followed by slightly positive pressures during exhalation. Overall, the airway pressures tend to be quite low, and oscillate around a baseline of 0 cm H2O. Positive pressure ventilation is quite unphysiologic, in that there is never a negative pressure in the chest at any time during the respiratory cycle. Instead, the ventilator creates positive pressure during inspiration, and the application of PEEP further increases the baseline and peak airway pressures. This increase in pleural pressure can have adverse effects on the cardiovascular system by decreasing venous return to the heart, which then decreases stroke volume and cardiac output. These effects are most severe during the inspiratory phase of the respiratory cycle, and tend to be most profound when the patient also has other problems that might compromise hemodynamic stability, most commonly concurrent hypovolemia. If positive intrathoracic pressures are contributing to cardiovascular compromise, the resulting tachycardia and systemic hypotension may significantly decrease tissue oxygen delivery, contributing to ongoing SIRS and multiple organ failure.
Cardiovascular instability may be recognized by the presence of tachycardia and/or hypotension. The role of increased intrathoracic pressure may be assessed by observing whether the arterial waveform or blood pressure changes with the phase of respiration. The mean airway pressure should be minimized in order to reduce the adverse hemodynamic effects of positive pressure ventilation, and also of course to minimize the adverse effects on the lung at the same time. Airway pressures may be decreased by reducing the PEEP, the peak airway pressure or the duration of inspiration, and by ensuring that the expiratory phase of the respiratory cycle is as long as possible. Assuming that the airway pressures are as low as possible, adverse cardiovascular consequences can also be avoided by ensuring that the animal is adequately volume expanded. Fluids must be administered with care, however, to avoid exacerbating pulmonary dysfunction. Other factors that might contribute to hypotension, including anesthetic and sedative drugs such as barbiturates, propofol, or alpha 2 agonists, should be avoided.
References
Available are available upon request.