In pressure-controlled ventilation (PCV), the targeted pressure level is set by the clinician and achieved rapidly, as is the case with PSV. However, in PSV, the patient’s spontaneously initiated flow triggers the breath, and a decrease in flow terminates the breath. In contrast, with PCV the initiation of the breath, duration of inspiration, and duration of expiration are determined by the clinician and set on the ventilator. However, changes in lung compliance and airway resistance do alter the volume of gas delivered as the specified target pressure is reached. Because the ventilator rather than the patient primarily controls the breathing pattern, PCV can be uncomfortable for the patient, who must be heavily sedated to tolerate the imposed ventilatory pattern. PCV is used primarily in patients with ARDS in whom problems with oxygenation and decreased lung compliance are particularly severe. In these cases, the clinician’s control of peak pressure and the relative timing of inspiration and expiration can facilitate improved oxygenation and reduce the risk of complications from high pressure delivered by the ventilator.
Volume-cycled ventilation
When the ventilator is used in a volume-cycled fashion, each inspiration is terminated (and passive expiration allowed to occur) after a specified volume has been delivered by the machine. Volume cycling is much more reliable than pressure-limited ventilation in delivering constant, specified tidal volumes. However, the pressure required to deliver a particular volume will vary depending on lung compliance and airway resistance and may change over time as these parameters get better or worse.
A hybrid mode termed volume-targeted pressure-control is sometimes employed. In this mode, initial pressure control settings are entered, but these are then automatically and continuously adjusted by the ventilator in order to achieve a selected tidal volume.
With volume-cycled ventilation, inspiration terminates after a specified tidal volume has been delivered by the ventilator. With pressure-limited ventilation, inspiration terminates after the targeted airway pressure has been achieved.
Several ventilatory patterns or modes are available with most mechanical ventilators when used in a volume-cycled fashion (Fig. 30.1). In controlled ventilation, ventilation is supplied entirely by the ventilator at a respiratory rate, tidal volume, PEEP, and inspired O2 concentration chosen by the physician. If the patient attempts to take a spontaneous breath between the machine-delivered breaths, he or she does not receive any inspired gas. Rarely used anymore, this type of ventilation is extremely uncomfortable for the conscious patient capable of initiating inspiration and therefore can only be used for patients who are comatose, anesthetized, or unable to make any inspiratory effort.
FIGURE 30.1 Airway pressure during spontaneous ventilation and during mechanical ventilation with several different ventilatory patterns. E, expiration; I, inspiration; IMV, intermittent mandatory ventilation; PCV, pressure-controlled ventilation; PEEP, positive end-expiratory pressure; PSV, pressure support ventilation. *Inspiratory positive-pressure support ceases when patient’s flow rate falls below a threshold level. †Relative timing of inspiration and expiration is
controlled by physician-determined ventilator settings.
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In the assist-control mode of ventilation, the ventilator is set to “sense” when the patient initiates inspiration, at which point the machine assists by delivering a specified tidal volume. Although the tidal volume is set by the machine, the respiratory rate is determined by the number of spontaneous inspiratory efforts made by the patient. However, should the patient’s spontaneous respiratory rate fall below a specified level, the machine provides backup by delivering at least this minimal number of breaths. For example, if the backup rate set on the machine is 10 breaths/min, the ventilator will automatically deliver a breath if and when 6 seconds have elapsed from the previous breath. In this example, if the patient is spontaneously initiating breaths at 16 breaths/min, all breaths are triggered by the patient. Because the respiratory rate with assist-control mode is determined by the patient (after the rate exceeds the specified minimal level), fluctuations in minute ventilation can occur if the patient’s respiratory rate changes significantly.
Available modes of volume-cycled mechanical ventilation are controlled ventilation, assist-control ventilation, and synchronized intermittent mandatory ventilation (SIMV).
A third ventilatory mode is intermittent mandatory ventilation (IMV). With IMV, the machine delivers a preset number of breaths per minute at a specified tidal volume and inspired O2 concentration. Between the machine-delivered breaths, the patient can breathe spontaneously from a gas source providing the same inspired O2 concentration given during the machine-delivered breaths. However, the machine does not assist the spontaneous breaths; therefore, the tidal volume for these breaths is determined by the patient. In a much more commonly used variant of IMV called synchronized IMV (SIMV), each of the machine-delivered breaths is timed to coincide with and assist a patient-initiated breath. If the patient being ventilated by IMV or SIMV modes changes his or her spontaneous respiratory rate significantly, the variation in minute ventilation theoretically is less than in the assist-control mode of ventilation, because each breath has not been supplemented by a comparatively large tidal volume delivered by the ventilator. In practice, both assist-control and SIMV are clinically useful and effective modes of ventilation. The assist-control mode is used more commonly because the problem of patient-ventilator dyssynchrony is more likely to occur in the SIMV mode.
Positive end-expiratory pressure
PEEP is an important option available for the intubated patient with hypoxemic respiratory failure (especially when it is due to ARDS). PEEP consists of the maintenance of positive pressure during expiration, which functions to keep small airways open and avoid microatelectasis. When a patient is assisted by a mechanical ventilator without PEEP, airway (and alveolar) pressure falls during expiration from the positive level achieved at the height of inspiration down to zero. However, if the expiratory portion of the tubing is connected to a valve requiring a pressure of at least 10 cm H2O, for example, to open it, the valve closes and expiration ceases when the airway pressure falls to 10 cm H2O. Consequently, airway pressure at the end of expiration does not fall to zero but remains at the level determined by the settings of the expiratory valve. The level of PEEP can be set as desired by adjusting the pressure required to open the expiratory valve.
A variation of PEEP that works on the same principle is continuous positive airway pressure (CPAP, see Chapter 18). The term CPAP is used when the patient is breathing spontaneously (without machineassisted breaths) and expiratory tubing is connected to a PEEP valve. To use CPAP, the patient can be either intubated or given a tightly fitting face mask. Although no positive pressure is provided by a mechanical ventilator during inspiration, inspired gas is delivered from a reservoir bag under tension or
Discontinuation of ventilatory support
When the underlying problem that precipitated the need for mechanical ventilation has improved, ventilatory support is discontinued, typically after observing the patient during a short (30-120 minutes) trial of spontaneous breathing with minimal or no positive pressure delivered by the mechanical ventilator. A useful guideline for assessing the patient’s initial response to the spontaneous breathing trial and predicting successful discontinuation of mechanical ventilation is provided by the rapid shallow breathing index. This index is the ratio of the patient’s respiratory rate divided by the tidal volume (expressed in liters) measured when the patient is not receiving assistance from the ventilator (i.e., during the spontaneous breathing trial). An index less than 105 is predictive of successful extubation (i.e., removal of the endotracheal tube), whereas an index greater than 105 is associated with a much higher likelihood of recrudescent respiratory failure after extubation.
Although the term weaning is still applied to discontinuation of mechanical ventilation, the older technique of slowly decreasing the amount of support provided by the ventilator is generally no longer used. As rational as it seems to wean the patient gradually from ventilatory support, an alternative strategy that tends to discontinue mechanical ventilation more rapidly is to perform an empiric daily trial of spontaneous breathing. If the patient tolerates the trial, then the patient is extubated. In many cases, the patient continues to receive some ventilatory assistance following extubation through NIPPV applied with a tight-fitting face mask, as described earlier, with the goal of avoiding the need for reintubation.
Mechanical ventilation can be discontinued after a successful trial of spontaneous breathing.
Noninvasive ventilatory support for acute respiratory failure
When patients with acute respiratory failure require mechanical ventilation, support traditionally has been provided by positive pressure administered through a tube placed into the trachea (i.e., endotracheal tube). However, use of an endotracheal tube is associated with risks and complications, such as patient discomfort from the tube itself, injury to the larynx or trachea, and development of lower respiratory tract infection (Table 30.1). An alternative to endotracheal intubation is to provide positive pressure noninvasively through a tightly fitting mask placed over the mouth and nose. This approach has been used for support of patients with a variety of types of acute respiratory failure, including patients with cardiogenic pulmonary edema, those with hypercapnic acute exacerbation of COPD, and patients who are not considered suitable candidates for intubation. High-flow (up to 60 L/min) warmed, humidified oxygen delivered via large nasal prongs may be another option to avoid endotracheal intubation in patients with less severe forms of acute hypoxemic respiratory failure in whom hypercapnia is not a prominent concern. However, noninvasive ventilatory support is not appropriate if a patient is unable to protect the airway; it is most useful when respiratory failure most likely is readily reversible and therefore of relatively short duration.
TABLE 30.1
Complications of Intubation and Mechanical Ventilation
Associated With Intubation
Malposition of tube
Tube in esophagus
Tube in mainstem bronchus (usually right mainstem bronchus)
Dysrhythmias
Hypoxemia
Laryngospasm
Associated With Endotracheal or Tracheostomy Tubes
Vocal cord ulcers
Laryngeal stenosis/granulomas
Tracheal stenosis
Nasal necrosis
Sinusitis/otitis media (with nasotracheal tubes)
Occlusion or kinking of tube
Infection (ventilator-associated pneumonia)
Associated With Mechanical Ventilation
Barotrauma (volutrauma)
Pneumothorax
Pneumomediastinum
Subcutaneous emphysema
Biotrauma (alveolar injury related to overdistention and cytokine release)
Atelectrauma (associated with cyclic alveolar opening and closing)
Decreased cardiac output (hypotension)
Alveolar hypoventilation or hyperventilation
Complications of intubation and mechanical ventilation
Intubation and mechanical ventilation of patients in respiratory failure are associated with potential risks and complications (see Table 30.1). The procedure of intubation can be complicated acutely by problems such as arrhythmias, laryngospasm, and malposition of the endotracheal tube (either in the esophagus or in a mainstem bronchus). When a tube remains in the trachea for days to weeks, complications affecting the larynx and trachea can occur. Vocal cord ulcerations and laryngeal stenosis and granulomas may develop. The trachea is subject to ulcerations, stenosis, and tracheomalacia (degeneration of supporting tissues in the tracheal wall) resulting from pressure applied by the inflated balloon at the end of the tube. As a
precaution to decrease tracheal complications, tubes are made with cuffs that minimize the pressure
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exerted on the tracheal wall and the resulting pressure necrosis. For prolonged ventilatory support (weeks to months), a tracheostomy tube placed directly into the trachea through an incision in the neck has some advantages over prolonged orotracheal or nasotracheal intubation, including patient comfort, reduced need for sedation, and prevention of further vocal cord and laryngeal injury.
The presence of an endotracheal tube puts the patient at significant risk for nosocomial pneumonia, usually called ventilator-associated pneumonia. Several factors appear to contribute to the patient’s increased risk for developing pneumonia when intubated and receiving mechanical ventilation. They include bypassing of the normal anatomic barriers and upper airway clearance mechanisms that prevent organisms from reaching the lower respiratory tract, aspiration of oropharyngeal secretions around the endotracheal tube and into the lower respiratory tract, and bacterial contamination of the endotracheal tube or the ventilator circuitry connected to the endotracheal tube. Organisms causing ventilatorassociated pneumonia are often relatively antibiotic-resistant bacteria that are resident in the hospital environment, including Gram-negative bacilli and Staphylococcus aureus, leading to significant increases in both duration of hospitalization and mortality.
Administration of positive pressure by a mechanical ventilator has its own attendant problems. Patients receiving positive-pressure ventilation are subject to barotrauma—development of pneumothorax or pneumomediastinum as a result of high alveolar pressures. Because alveolar overdistention with rupture is currently thought to be the cause of these complications, the term volutrauma is now often used instead of barotrauma. Development of a pneumothorax in patients receiving mechanical ventilation can have catastrophic consequences if not detected and treated quickly. The ventilator continues to deliver gas under positive pressure, and the gas enters the pleural space through the rupture. The pressure in the pleural space and thorax increases, and a tension pneumothorax can result (see Chapter 15), which severely diminishes venous return and cardiac output and causes rapid cardiovascular collapse. In such situations, a tube, catheter, or needle must be immediately inserted through the chest wall in order to decompress the pleural space, allow resumption of venous return, and enable reexpansion of the lung.
Barotrauma/volutrauma, atelectrauma, biotrauma, and impairment of systemic venous return to the heart are important adverse effects of positive-pressure ventilation.
Prolonged exposure to excessive volumes and high levels of pressure delivered to the alveoli is injurious to alveolar structures. Because lung injury in ARDS is often heterogeneously distributed (see Chapter 29), inspired gas is preferentially distributed to the more normal, more compliant alveoli than to the abnormal, less compliant alveoli. This puts the more normal alveoli at particular risk for overdistention. At the same time, more diseased alveoli are subject to collapse (atelectasis) during the expiratory phase of the respiratory cycle because of intraalveolar fluid and/or a disrupted or insufficient surfactant layer. Alveoli that are open during inspiration but collapse during expiration are subject to abnormal shear stresses during the repetitive process of opening and closing, a complication termed atelectrauma.
Repeated alveolar overdistention and atelectrauma are accompanied by microscopic injury to cells of the alveolar wall and to intercellular attachments, leading to disruption of the normal permeability barrier provided by alveolar epithelial and capillary endothelial cells. In addition, proinflammatory cytokines may be released, a phenomenon that has been called biotrauma, resulting in ongoing alveolar injury and also systemic effects, such as increasing the likelihood of developing multiorgan dysfunction syndrome. As a result, positive-pressure ventilation for respiratory failure, especially ARDS, can potentially compound or worsen the process for which it was initiated. Therefore, the pattern of ventilation should avoid both alveolar closure (atelectasis) during expiration and overdistention during inspiration, the former by use of PEEP and the latter by limiting tidal volume to 6 to 8 mL/kg of predicted body weight