Author: Allon Amitai, MD, Clinical Assistant Instructor, Department of Emergency Medicine, Kings County Hospital, State University of New York-Downstate School of Medicine
Coauthor(s): Richard Sinert, DO, Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center; Daniel M Joyce, MD, Consulting Staff, Department of Emergency Medicine, Saint Vincent's and Saint Mary's Medical Centers
Allon Amitai, MD, is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure
Many different strategies of positive-pressure ventilation are available; these are based on various permutations of triggered volume-cycled and pressure-cycled ventilations and are delivered at a range of rates, volumes, and pressures. Given both the risks of poor ventilatory management (inflicting serious pulmonary damage) and the increasing length of stay of ventilated patients in emergency departments, it is necessary for emergency physicians to have a good understanding of tactics to optimize mechanical ventilation and to minimize complications.
Because many of the effects of ventilator-induced lung injury are delayed and not seen while patients are in the ED, much of our understanding of the adverse consequences of volutrauma, air-trapping, barotrauma, and oxygen toxicity has come from the critical care literature. While the fundamental principles underlying mechanical ventilatory support have changed little over the decades, much progress has been made in our understanding of the secondary pathophysiologic changes associated with positive-pressure ventilation. Ventilatory strategies have been devised for different disease processes to protect pulmonary parenchyma while maintaining adequate gas exchange, and they may be responsible for the increased rates of survival for pathologies such as acute respiratory distress syndrome (ARDS). Additionally, an upsurge in utilization of noninvasive ventilation has permitted many patients to avoid the risks and complications of tracheal intubation.
Volume-cycled mode
Inhalation proceeds until a set tidal volume (TV) is delivered and is followed by passive exhalation. A feature of this mode is that gas is delivered with a constant inspiratory flow pattern, resulting in peak pressures applied to the airways higher than that required for lung distension (plateau pressure). Since the volume delivered is constant, applied airway pressures vary with changing pulmonary compliance (plateau pressure) and airway resistance (peak pressure).
Because the volume-cycled mode ensures a constant minute ventilation, it is a common choice as an initial ventilatory mode in the ED. A major disadvantage is that high airway pressures may be generated, potentially resulting in barotrauma. Close monitoring and use of pressure limits are helpful in avoiding this problem. Note that ventilators set to volume-cycled mode function well as monitors of patients' pulmonary compliance, which will be decreased in physiological states such as worsening ARDS, pneumothorax, right mainstem intubation, chest-wall rigidity, increased intra-abdominal pressure, and psychomotor agitation (“fighting the vent”). These pathophysiological states increase peak pressure and should be considered whenever pressure alarms are sounded. In pressure-cycled settings, by contrast, such states result only in reduced delivered volumes and may not trigger alarms. Given that the airway resistance and pulmonary compliance of the critical ED patient is unknown and potentially unstable, the authors recommend the volume-cycled mode for initial ventilation of most patients.
Pressure-cycled mode
A set peak inspiratory pressure (PIP) is applied and the pressure difference between the ventilator and the lungs results in inflation until the peak pressure is attained, and passive exhalation follows. The delivered volume with each respiration is dependent on the pulmonary and thoracic compliance.
A theoretical advantage of pressure-cycled modes is a decelerating inspiratory flow pattern, in which inspiratory flow tapers off as the lung inflates. This usually results in a more homogeneous gas distribution throughout the lungs. No definite evidence exists, however, that this results in a reduction of the rate of ventilator-induced lung injury or overall mortality. Nevertheless, pressure-cycled ventilation has achieved considerable popularity in the intensive care setting for management of patients with ARDS, whose lungs are most likely to be characterized by a broad range of alveolar dysfunction and are also most vulnerable to the effects of barotrauma and volutrauma.
A major disadvantage is that dynamic changes in pulmonary mechanics may result in varying tidal volumes. This necessitates close monitoring of minute ventilation and limits the usefulness of this mode in many emergency department patients. However, newer ventilators can provide volume-assured pressure-cycled ventilation, which increase peak pressures as needed to deliver a preset minimum tidal volume.
High-frequency oscillatory support
In this ventilatory strategy, ultra-high respiratory rates (180-900 breaths per minute) are coupled with tiny tidal volumes and high airway pressures. This is a commonly accepted ventilatory setting for premature infants and has now also been used in small critical care unit studies on patients with ARDS, with reports of improving oxygenation and lung recruitment.
While this setting cannot currently be recommended for routine ED use, it may in the future be found appropriate for the management of patients with ARDS.
Types of support
Most ventilators can be set to apply the delivered tidal volume in a control mode or a support mode.
Control mode
In control mode, the ventilator delivers the preset tidal volume once it is triggered regardless of patient effort. If the patient is apneic or possesses limited respiratory drive, control mode can ensure delivery of appropriate minute ventilation.
Support mode
In support mode, the ventilator provides inspiratory assistance through the use of an assist pressure. The ventilator detects inspiration by the patient and supplies an assist pressure during inspiration. It terminates the assist pressure upon detecting onset of the expiratory phase. Support mode requires an adequate respiratory drive. The amount of assist pressure can be dialed in.
Continuous mandatory ventilation
Breaths are delivered at preset intervals, regardless of patient effort. This mode is used most often in the paralyzed or apneic patient because it can increase the work of breathing if respiratory effort is present. Continuous mandatory ventilation (CMV) has given way to assist-control (A/C) mode because A/C with the apneic patient is tantamount to CMV. Many ventilators do not have a true CMV mode and offer A/C instead.
Assist-control ventilation
The ventilator delivers preset breaths in coordination with the respiratory effort of the patient. With each inspiratory effort, the ventilator delivers a full assisted tidal volume. Spontaneous breathing independent of the ventilator between A/C breaths is not allowed. As might be expected, this mode is better tolerated than CMV in patients with intact respiratory effort.
Intermittent mandatory ventilation
With intermittent mandatory ventilation (IMV), breaths are delivered at a preset interval, and spontaneous breathing is allowed between ventilator-administered breaths. Spontaneous breathing occurs against the resistance of the airway tubing and ventilator valves, which may be formidable. This mode has given way to synchronous intermittent mandatory ventilation (SIMV).
Synchronous intermittent mandatory ventilation
The ventilator delivers preset breaths in coordination with the respiratory effort of the patient. Spontaneous breathing is allowed between breaths. Synchronization attempts to limit barotrauma that may occur with IMV when a preset breath is delivered to a patient who is already maximally inhaled (breath stacking) or is forcefully exhaling.
The initial choice of ventilation mode (eg, SIMV, A/C) is institution and physician dependent. A/C ventilation, as in CMV, is a full support mode in that the ventilator performs most, if not all, of the work of breathing. These modes are beneficial for patients who require a high minute ventilation. Full support reduces oxygen consumption and CO2 production of the respiratory muscles. A potential drawback of A/C ventilation in the patient with obstructive airway disease is worsening of air trapping and breath stacking.
When full respiratory support is necessary for the paralyzed patient following neuromuscular blockade, no difference exists in minute ventilation or airway pressures with any of the above modes of ventilation. In the apneic patient, A/C with a respiratory rate (RR) of 10 and a TV of 500 mL delivers the same minute ventilation as SIMV with the same parameters.
Pressure support ventilation
For the spontaneously breathing patient, pressure support ventilation (PSV) has been advocated to limit barotrauma and to decrease the work of breathing. Pressure support differs from A/C and IMV in that a level of support pressure is set (not TV) to assist every spontaneous effort. Airway pressure support is maintained until the patient's inspiratory flow falls below a certain cutoff (eg, 25% of peak flow). With some ventilators, there is the ability to set a back-up IMV rate should spontaneous respirations cease.
PSV is frequently the mode of choice in patients whose respiratory failure is not severe and who have an adequate respiratory drive. It can result in improved patient comfort, reduced cardiovascular effects, reduced risk of barotrauma, and improved distribution of gas.
Noninvasive ventilation
The application of mechanical ventilatory support through a mask in place of endotracheal intubation is becoming increasingly accepted and used in the emergency department. Considering this modality for patients with mild-to-moderate respiratory failure is appropriate. The patient must be mentally alert enough to follow commands. Clinical situations in which it has proven useful include acute exacerbation of chronic obstructive pulmonary disease (COPD) or asthma, decompensated congestive heart failure (CHF) with mild-to-moderate pulmonary edema, and pulmonary edema from hypervolemia. It is most commonly applied as continuous positive airway pressure (CPAP) and biphasic positive airway pressure (BiPAP). BiPAP is commonly misunderstood to be a form of pressure support ventilation triggered by patient breaths; in actuality, BiPAP is a form of CPAP that alternates between high and low positive airway pressures, permitting inspiration (and expiration) throughout.
Reviews of the literature have shown noninvasive positive-pressure ventilation to be beneficial for COPD, reducing the rate of tracheal intubations as well as length of stay. Their benefit increases with increasing severity of disease. In patients with mild cases of COPD and CHF who would not otherwise require ventilatory support do not benefit from noninvasive positive-pressure ventilatory support. The use of noninvasive positive-pressure ventilation has been less well studied in asthma, but, in one small randomized trial, it reduced hospital admission rates.
Pulmonary effects
Barotrauma may result in pulmonary interstitial emphysema, pneumomediastinum, pneumoperitoneum, pneumothorax, and/or tension pneumothorax. High peak inflation pressures (>40 cm H2O) are associated with an increased incidence of barotrauma. However, note that separating barotrauma from volutrauma is difficult, since increasing barometric pressure is usually accompanied by increasing alveolar volume. Experimental models of high peak inflation pressures in animals with high extrathoracic pressures have not demonstrated direct alveolar damage from increased pressure without increased volume as well. Thus, saying that high airway pressures result in alveolar overdistention (volutrauma) and accompanying increased microvascular permeability and parenchymal injury might be more accurate. Alveolar cellular dysfunction occurs with high airway pressures. The resultant surfactant depletion leads to atelectasis, which requires further increases in airway pressure to maintain lung volumes.
High-inspired concentrations of oxygen (fraction of inspired oxygen [FiO2] >0.5) result in free-radical formation and secondary cellular damage. These same high concentrations of oxygen can lead to alveolar nitrogen washout and secondary absorption atelectasis.
Cardiovascular effects
The heart, great vessels, and pulmonary vasculature lie within the chest cavity and are subject to the increased intrathoracic pressures associated with mechanical ventilation. The result is a decrease in cardiac output due to decreased venous return to the right heart (dominant), right ventricular dysfunction, and altered left ventricular distensibility.
The decreased cardiac output from reduction in right ventricular preload is more pronounced in the hypovolemic patient and those with a low ejection fraction.
Exaggerated respiratory variation on the arterial pressure waveform is a clue that positive-pressure ventilation is significantly affecting venous return and cardiac output. In the absence of an arterial line, a good pulse oximetry waveform can be equally instructive. A reduction in the variation after volume loading confirms this effect. These effects will most frequently be seen in patients with preload-dependent cardiac function (that is, operating on the right side of the Starling curve) and in hypovolemic patients or those with otherwise compromised venous return.
For patients with Swan-Ganz catheterization in place for whom cardiac output may be measured (usually in the ICU setting), PEEP studies may be performed. This is performed by adjusting PEEP, monitoring oxygenation by peripheral oxygen saturation or arterial oxygen measurement via blood gas sampling, and measuring the associated cardiac output. The process is repeated at various PEEP settings, and the results are recorded. The physician can then review the results and determine the optimal PEEP for that patient at that time. This procedure is not generally performed in the ED but underlies the association of ventilation strategy and cardiac output.
Renal, hepatic, and gastrointestinal effects
Positive-pressure ventilation is responsible for an overall decline in renal function with decreased urine volume and sodium excretion.
Hepatic function is adversely affected by decreased cardiac output, increased hepatic vascular resistance, and elevated bile duct pressure.
The gastric mucosa does not have autoregulatory capability. Thus, mucosal ischemia and secondary bleeding may result from decreased cardiac output and increased gastric venous pressure.
Author Information Ventilator Management Modes Of Mechanical Ventilation Methods Of Ventilatory Support Adverse Consequences Of Mechanical Ventilation Indications Guidelines For Ventilator Settings Monitoring During Ventilatory Support Initial Ventilator Settings In Various Disease States Pictures Bibliography
The principal indications for mechanical ventilation are airway protection and respiratory failure. A compromised airway, or an airway at risk of compromise, may be identified by physical examination and ancillary testing.
Respiratory failure in the ED is almost always–and most appropriately–a clinical diagnosis. The decision to intubate and mechanically ventilate or to institute noninvasive ventilation support is generally made purely on clinical grounds without delay for laboratory evaluation.
Respiratory failure may also be easily identified with laboratory or pulmonary function data.
Mechanical ventilation is indicated for both hypercapnic respiratory failure and hypoxemic respiratory failure. It is also indicated for treatment of certain critical conditions such as correction of life-threatening acidemia in the setting of salicylate intoxication, for intentional hyperventilation in the setting of major head injury with elevated intracranial pressure, for suspicion of clinical brain herniation from any cause, or for a patient in critical condition with cyclic antidepressant toxicity.
Laboratory criteria
Laboratory Criteria for Mechanical Ventilation
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