Chapter 8 Mechanical ventilation (MV) is an important tool for resuscitation of critically ill patients in the emergency department (ED). It is vital that ED practitioners have a thorough understanding of the basics of MV and to know when to apply these principles and how to support patients in respiratory or cardiac failure. Hospital overcrowding has led to a delay in transfer of mechanically ventilated patients out of the ED, and ventilator management often falls on the emergency medicine physician. Also, during nights and weekends in some facilities, the ED physician may be called on to troubleshoot or stabilize mechanically ventilated patients in the intensive care unit (ICU). The traditional view of MV as a prescription that fits virtually all patients equally should be discarded as a gross misunderstanding of pulmonary pathophysiology. Increasing evidence has shown that the mechanism of lung ventilation by MV may be as deleterious as it is helpful.1 Because patients remain in the ED while mechanically ventilated, ED clinicians should embrace the established paradigm of pulmonary-protective MV strategies as a cornerstone of care. Normal is 7 to 10 L/min. Vt can be further broken down into alveolar volume (Va) and dead space volume (Vds): In healthy young persons, the anatomic dead space is accounted for by the trachea and the larger airways and is approximately 2.2 mL/kg lean body weight. In disease states, in addition to the anatomic dead space, there is a variable amount of “pathologic” dead space, which corresponds to ventilated alveoli and respiratory bronchioles that are not adequately perfused. The sum of anatomic and pathologic dead space is often referred to as physiologic dead space. Alveolar minute ventilation () is the product of rate times Vt minus dead space: and the rate of CO2 production by the body determine the partial pressure of CO2 in the alveoli (Paco2), which is approximately equal to systemic arterial CO2 tension. Conversely, this relationship also holds for volume. For example, a pressure of 20 cm H2O will create a certain volume based on the compliance of the system. Increasing pressure will result in higher volume. Decreasing pressure will result in lower volume. Decreasing compliance will result in lower volume. Increasing compliance will result in higher volume. Plateau pressure is measured at the end of inspiration with a short breath-hold (Fig. 8-1). At this point no airflow should be occurring. This is considered a static pressure. By understanding the aforementioned volume-pressure relationship, one can easily deduce how plateau pressure is inversely related to respiratory system compliance and directly related to volume. Anything that decreases compliance will increase plateau pressure. Increasing compliance will decrease plateau pressure. Decreasing volume will decrease plateau pressure (a major tenet in lung-protective ventilation). A physiologically appropriate means of detecting and monitoring bronchospasm is the peak-plateau gradient. A normal gradient is less than 4 cm H2O pressure, and elevated values indicate increased airway resistance. The efficacy of treatment with β2-agonists, steroids, intravenous magnesium, or diuresis may be assessed by monitoring the changes in this gradient (Fig. 8-2). Extrinsic PEEP: When discussing MV and PEEP, most often authors are referring to extrinsic PEEP (PEEPe). This is also referred to as applied PEEP. It is the PEEP that is extrinsically applied by the ventilator. When PEEP is used without a subscript in this chapter, it refers to PEEPe. The useful PEEP range is from 3 to 20 cm H2O.2 PEEP is used to increase FRC and move the zero pressure point of each alveolar unit more proximally in the airway and thereby prevent early alveolar collapse.3 By so doing, PEEP increases the available number of alveolar units that can participate in gas exchange. The primary effect of PEEP on gas exchange is improvement in oxygenation, not removal of CO2. CO2 clearance is rather efficient and will be well preserved, even in hypoxic situations. By opening one alveolar unit, the tendency of adjacent units is to open as well (i.e., alveolar codependency) (Fig. 8-3).4 Excessive PEEP will compromise hemodynamics. There are two primary questions to ask when using PEEP to augment oxygenation: (1) What is the “optimal PEEP” and (2) Is the current amount of PEEP compromising the patient’s hemodynamics? PEEP is not without untoward side effects, and increased levels of PEEP can lead to lung injury and hemodynamic compromise.5 Increased intrathoracic pressure can result in cardiac compression and collapse, principally of the right atrium. It is imperative that the patient be adequately volume-resuscitated because preload depletion compounds this problem. Desired levels of PEEP simply may not be possible because of deleterious effects on cardiac output. Another excellent method of determining the optimal PEEP is guided by assessing changes in plateau pressure with changes in PEEP. As PEEP is increased from a minimal level, the patient’s peak airway pressure and plateau pressure will increase by the amount of PEEPe. When the optimal PEEP for the lung units is achieved, plateau pressure will no longer increase. As the lung is optimally recruited, peak and plateau pressure may decrease because more volume of lung is available to receive a set Vt. Once this level is exceeded, there will be further increases in plateau pressure beyond the incremental increase in PEEP as the units overdistend. Therefore, the clinician must readily identify the plateau in this plateau pressure trend. The same relationship may be displayed graphically in the dynamic pressure-volume loop (Fig. 8-4). The lower limb of the loop represents the pressure required to open the alveolar units.6,7 In the absence of PEEP (or inadequate PEEP), this limb is prolonged and flattened and has an inflection point far to the right of the origin of the loop (Fig. 8-5). As PEEP is progressively increased, the inflection point travels to the left. When the optimal PEEP is achieved, there will be a rapid upstroke of the loop because the vast majority of the functional lung units are already open and ready to be ventilated (see Fig. 8-4). This strategy is known as the open lung model of MV.6 Figure 8-5 Inadequate positive end-expiratory pressure (PEEP) and the pressure-volume loop. Compare this curve with that in Figure 8-4. Note that the loop is initially flat (lower segment) along the x-axis. Once airway pressure is high enough to open the alveolar units, each increase in airway pressure is matched by a corresponding increase in tidal volume. Irrespective of what technique is used, it is currently widely agreed that plateau pressure should not exceed 30 cm H2O. If respiratory system compliance is so low that plateau pressure exceeds 30 cm H2O, either PEEP or Vt has to be decreased. If this is not possible because of either recalcitrant hypoxia or acidosis, rescue therapies may need to be used (see the section “Acute Lung Injury and Acute Respiratory Distress Syndrome”). Intrinsic PEEP: Intrinsic PEEP (PEEPi) is additional pressure that is generated within the airways from trapped gas that should have been exhaled but for various reasons (commonly obstruction to exhalation such as in chronic obstructive pulmonary disease [COPD]) was not. PEEPi is also referred to as auto-PEEP, dynamic hyperinflation, and breath stacking. For the remainder of this chapter it will be referred to as PEEPi. PEEPi can cause hemodynamic instability secondary to decreased venous return, just like high levels of PEEP.7 PEEPi may be detected in two ways: (1) evaluation of the flow-time trace or (2) disconnection of the patient from the ventilator and listening for additional exhaled gas after an exhalation should have occurred.6 The flow-time trace will demonstrate that the exhalation is not yet completed before the next breath has been initiated (Fig. 8-6).8 Perhaps one of the most confusing aspects of MV is the plethora of terms and acronyms that are used. Understanding the basic terminology helps clarify this subject. The following discussion explores machine features and settings. Regardless of which ventilator is used, a limited number of standard features are common to each (Fig. 8-7). All ventilators can deliver an adjustable fraction of inspired oxygen (Fio2). Recommendations are to set it initially at 1.0 because the act of transitioning from negative pressure ventilation (normal physiologic breathing) to positive pressure ventilation (PPV) may unpredictably alter ventilation-perfusion () matching. Although initially an Fio2 of 100% is optimal, it is beneficial to quickly titrate Fio2 down because of the theoretical risk for oxygen toxicity. Make adjustments based on ABG analysis or pulse oximetry, with a goal of keeping arterial Po2 higher than 60 mm Hg or arterial oxygen saturation at 88% to 92% to avoid potential oxygen toxicity (see Table 3-3 in Chapter 3). Such adjustments may best be accomplished in the ICU rather than the ED, after the entire clinical scenario can be analyzed and all interventions are appropriately adjusted. PEEPe is typically set at 5 to 8 cm H2O. Most patients should be started at a PEEP of 5 cm H2O, which is considered a physiologic level. It is used to offset the gradual loss of functional residual volume (FRC) in supine, mechanically ventilated patients. PEEP can be increased by 2 cm H2O every 10 to 15 minutes as needed or tolerated by patients who remain hypoxic. The initial goal is to reduce Fio2 to nontoxic levels. This goal is coming under increasing scrutiny as new information challenges the time frame and concept of O2-induced lung injury at Fio2 levels greater than 0.6.9 Exercise care when using PEEP levels higher than 8 cm H2O in the setting of elevated intracranial pressure (ICP),10 unilateral lung processes, hypotension, hypovolemia, or pulmonary embolism. High PEEP can potentially lead to hypotension as it increases intrathoracic pressure and decreases venous return and subsequently cardiac output. The normal I/E ratio in a spontaneously breathing, nonintubated patient is 1 : 4.11 Intubated patients commonly achieve I/E ratios of 1 : 2. Shorter ratios may lead to decreased exhalation by compromising Te. In its extreme form, inverse ratio ventilation (IRV), the normal pattern of breathing is reversed. A longer time is spent in inhalation to allow more time for oxygenation and recruitment. The decrease in Te can lead to air trapping, elevated mean airway pressure, and rising Pco2. These problems lead to hypercapnia, respiratory acidosis, and PEEPi12 (Fig. 8-8). This refers to the sensitivity of the trigger. If the trigger is set too high (not sensitive enough), the work of breathing incurred by the patient can be substantial. Some providers have been known to set the sensitivity at a high level if the patient is markedly overbreathing the set rate. This is not recommended because it causes an undue increase in the work of breathing. Many ventilators are set to a pressure trigger with a sensitivity of 1 to 3 cm H2O.13 If the sensitivity is set too low (too sensitive), the ventilator can “auto-trigger” (inappropriate initiation of machine-generated breaths) because of oscillating water in the ventilator tubing, hyperdynamic heartbeats, or patient movement. Once some of the standard features are understood, the next step is determining the ventilator’s target. Most ventilators can be set to achieve spontaneous breathing, volume-targeted ventilation, pressure-targeted ventilation, or some combination. In volume-targeted ventilation, the ventilator is set to reach a determined volume regardless of the pressure required to do so. Pressure-targeted modes are set to reach a determined pressure regardless of the volume generated. Dual modes combine the benefits of both strategies (Fig. 8-9). An advantage of PCV is that airway pressure is tightly managed to limit or eliminate alveolar overdistention and to reduce ventilator-induced lung injury.14 It should be noted that the clinician does not control waveform or peak inspiratory flow. Patients can generate their desired flow rate and thus reduce air hunger. Pressure-targeted modes, which are growing in popularity, might have better pressure distribution, improved dissemination of airway pressure, and greater distribution of ventilation.14 Caution should be exercised to avoid auto-PEEP (also known as breath stacking) when using volume-targeted AC modes. Because each mechanically delivered breath is given at full Vt, patients with a high actual respiratory rate on AC may not have sufficient time to completely exhale between breaths. This results in progressive air trapping, which leads to an increase in auto-PEEP (PEEPi) (see Fig. 8-6). This is of clinical concern in patients with asthma, in whom auto-PEEP can significantly reduce cardiac output and even promote cardiovascular collapse. SIMV provides breaths at a preset rate (machine breath), similar to the AC mode. The patient can initiate an additional spontaneous breath between the mandated or preset number of ventilator-supported breaths. Such spontaneous breaths above the preset ventilatory rate are not supported by the ventilator, and the patient receives only a spontaneous Vt that reflects the depth and time spent in the patient-controlled inspiration. For each of these nonmandatory (i.e., spontaneous) breaths, the patient has a high work of breathing. SIMV is typically partnered with PSV to aid in spontaneous breathing support and to overcome the intrinsic resistance associated with MV. This mode was initially recommended by those who thought that as a patient’s need for mechanical ventilatory support decreased, the set respiratory rate could be decreased and the patient “weaned” to PSV alone and ensuing extubation. Subsequent data have shown that this method of liberation actually increases the number of ventilator days.15 The synchronized version of intermittent MV allows the ventilator to attempt to coordinate spontaneous and machine breaths to prevent it from delivering a scheduled breath on top of a spontaneous breath or during exhalation after a spontaneous breath. This could lead to elevated mean airway pressure, alveolar overdistention, and biotrauma.16 Advanced modes of mechanical ventilation use a closed-loop ventilator logic that combines the features of volume- and pressure-targeted ventilation (Box 8-1). These modes automatically alter control variables, either breath to breath or within a breath, to ensure a minimum Vt or minute ventilation.17 Detailed explanation of these modes is beyond the scope of this chapter. If these modes are encountered, one should discuss options with a respiratory therapist and critical care medicine specialist. High-frequency ventilation (HFV) attempts to achieve adequate gas exchange by using asymmetric velocity profiles when combining very high respiratory rates with Vt levels that are smaller than the volume of anatomic dead space. It is used more commonly in neonates and infants with neonatal respiratory failure. There has been renewed interest in using HFV in adult patients with ALI or ARDS under the rationale that the small Vt may cause less ventilator-associated lung injury. More trials are necessary to determine whether HFV can improve mortality outcomes in these patients.18 Both these modes are proprietary names yet function in essentially the same manner. The clinician sets a pressure high, a pressure low, and a time at each level (time high and time low). Although at first glance this appears to be similar to PCV, it differs markedly in that the majority of time is spent at pressure high with brief periods at pressure low. The patient typically spends 4 to 6 seconds in time high. Pressure high may be as high as 40 cm H2O or greater. Ventilation occurs during the release from pressure high to pressure low. Time low is typically 0.2 to 0.8 second in restrictive lung disease and 0.8 to 1.5 seconds in obstructive lung disease. It is probably prudent to start at 0.8 and titrate to meet individual patient requirements. Time low is also referred to as the release phase.19 The long time that high-level pressure is maintained achieves oxygenation, and the short release period achieves clearance of CO2 (Fig. 8-10). The long time at high-level pressure results in substantial recruitment of alveoli from markedly different regional time constants at rather low gas flow rates. The establishment of PEEPi by the short release time enhances oxygenation. CO2 clearance is aided by recruitment of the patient’s lung at close to total lung capacity. Elastic recoil creates large-volume gas flow during the release period. In a paralyzed patient, airway pressure release ventilation and bilevel ventilation (APRV/Bi-Level) are identical to pressure-targeted IRV. For these reasons, some have described this mode as inverse ratio ventilation. A major difference between APRV/Bi-Level and IRV is that IRV typically requires chemical paralysis or heavy sedation. APRV/Bi-Level is a fundamentally different mode from cyclic ventilation. This mode allows the patient to spontaneously breathe during all phases of the cycle, thus making it relatively more comfortable and reducing the level of sedation or paralysis needed. This mode is enabled to succeed by having a floating valve that is responsive to the patient’s needs, regardless of the location within the respiratory cycle. The patient is allowed to breathe in or out during the pressure high phase and during the release phase. Accordingly, the sequence is called a phase cycle. There is no set Ti or Te and no readily identifiable respiratory rate in the traditional sense. During the pressure high phase, patients may exhale 50 to 200 mL or more of gas as the lung volume becomes full of gas. This is not a full exhalation, and the release of excess gas should not be counted as a breath. APRV has been used successfully for neonatal, pediatric, and adult forms of respiratory failure. It is considered an alternative open–lung model approach to MV.19 Given the spontaneous nature of the mode, there should be virtually no need for continuous infusion of neuromuscular blocking drugs in patients placed on this mode of ventilation. This may result in a shorter length of ICU stay and a reduced incidence of prolonged neuromuscular blockade syndrome. The need for sedatives is reduced because patients are more comfortable on this spontaneous mode than on cyclic ventilation.20 APRV/Bi-Level has gained popularity in patients with hypoxemic respiratory failure because it improves oxygenation by optimizing alveolar recruitment and matching.21 A common mistake with this mode is setting time low too long. This essentially mimics a pressure-targeted SIMV strategy. Transport of patients on APRV with pressure high greater than 20 cm H2O should occur with the patient attached to the ventilator instead of being hand-ventilated.22 Hand ventilation is unable to match the manner of gas delivery and pressure dynamics that the patient requires. Attempts at hand ventilation, even with an appropriately set PEEP valve, are frequently complicated by unexpected hypoxemia and hemodynamic instability.
Mechanical Ventilation
Introduction
Basic Physiology
Minute Volume and Alveolar Ventilation
Volume-Pressure Relationship
Airway Pressures
Peak Airway Pressure
Positive End-Expiratory Pressure
Equipment—standard Options
Fraction of Inspired Oxygen
Positive End-Expiratory Pressure
I/E Time Ratio
Sensitivity
Modes of Ventilation
Pressure-Cycled Ventilation
Modes of Ventilation Commonly Used in the ED
Assist/Control Ventilation
Synchronized Intermittent Mechanical Ventilation
Advanced Modes of Mechanical Ventilation
Other Modes
Airway Pressure Release Ventilation and Bi-Level Ventilation
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