Mechanical Ventilation

Introduction

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.

Basic Physiology

Understanding basic pulmonary physiology is essential to understanding how to initiate MV. This ensures that the method of gas delivery meshes with the patient’s underlying physiology to avoid ventilator-induced lung injury.

Minute Volume and Alveolar Ventilation

The volume of air that moves in and out of a patient’s lungs per minute is termed minute volume (). is the product of tidal volume (Vt) and respiratory frequency or rate (f):

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.

Volume-Pressure Relationship

Volume and pressure are related for a given respiratory system. A given volume (V) will create a certain pressure (P) relative to the compliance (C) of the respiratory system. The respiratory system consists of the ventilator tubing, endotracheal (ET) tube, trachea, airways, lung parenchyma, chest wall, and diaphragm tension. For example, a 500-mL volume will create a certain pressure based on the compliance of the respiratory system. Increasing the volume will increase the pressure in the system. Decreasing the volume will result in lower pressure. Decreasing the compliance (i.e., making the system “stiffer”) will increase the pressure in the system. Increasing the compliance will decrease the pressure in the system.

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.

Airway Pressures

Plateau Pressure

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).

Figure 8-1 Schematic of a pressure-time curve showing an inspiratory breath-hold and subsequent plateau pressure (P_plat) measurement. P_aw, airway pressure; PEEP, positive end-expiratory pressure.

Peak Airway Pressure

Peak airway pressure is derived during inspiration and thus incorporates airflow. Because there is air movement during this measurement, it is considered a dynamic pressure. It reflects the dynamic compliance of the entire respiratory system and incorporates static compliance and airflow. Peak airway pressure can never be lower than plateau pressure. In addition, because its main distinction is that it incorporates airflow, it is reflective of resistance to airflow. Anything that decreases compliance or increases resistance to airflow will increase peak airway pressure. Increasing compliance or decreasing resistance to airflow will decrease peak airway pressure.

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).

Figure 8-2 Schematic of two superimposed pressure-time curves showing an isolated decrease in peak inspiratory pressure (P_peak) with no change in plateau pressure (P_plat) as airflow resistance improves. P_aw, airway pressure.

Positive End-Expiratory Pressure

Positive end-expiratory pressure (PEEP) is the pressure in the airway at the end of exhalation. PEEP helps keep the large noncartilaginously supported airways and the smaller alveoli open to prevent collapse, atelectasis, and ensuing hypoxia. The ventilation required to compensate for this triad commonly worsens lung compliance and is associated with ventilator-induced lung injury. Progressive increases in PEEP result in elevations in both total lung pressure and total lung volume. For example, serial elevations in PEEP often result in increased plateau pressure and elevated functional residual capacity (FRC; i.e., lung volume).

Extrinsic PEEP: When discussing MV and PEEP, most often authors are referring to extrinsic PEEP (PEEP_e). 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 PEEP_e. 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?

Figure 8-3 Alveolar interdependence. Note that alveoli are not round in shape; instead, they are polygons. Polygons have corners and may have two opposing surfaces that may adhere to one another via surface tension. Surfactant works to reduce this surface tension and allow alveoli to open with reduced shear stress at the junction of closed and open alveoli. Alveoli are connected via the pores of Kohn. These pores allow opening alveoli to pull a relatively closed alveolus open while equalizing pressure between adjacent alveoli. The central alveolus on the right is fairly closed in the upper part of the diagram, but it is pulled open by its neighbors as they expand and accept gas.

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.

Optimal PEEP can be determined in several ways. One is to increase PEEP until there are no longer increases in Po₂. However, this method may result in several untoward events. First, oxygen tension may increase steadily, but carbon dioxide pressure (Pco₂) may increase as a result of alveolar overdistention. With overdistention, alveolar pressure may exceed pulmonary arteriolar pressure and actually decrease pulmonary blood flow and clearance of CO₂. Second, alveolar overdistention may increase total intrathoracic pressure and result in diminished venous return and cardiac output. Third, decreased venous return may cause cerebral venous hypertension. The optimal PEEP for one organ system may be deleterious for another. For example, the optimal PEEP for ideal oxygenation may be the worst PEEP for cerebral venous drainage.

An alternative is to increase PEEP until a complication of PEEP occurs (e.g., elevation in Pco₂, hypotension) and then reduce PEEP if needed (inability to tolerate hypercapnia) or expand the patient’s intravascular volume to combat the decreased venous return.

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 PEEP_e. 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 8-4 Dynamic pressure-volume (PV) loop. Note that as soon as pressure is delivered to the airway, there is an increase in measured tidal volume. The lower arrow denotes inspiration and the upper arrow indicates exhalation. This indicates that the airways are open and do not need to be forced open by increasing the pressure in the airway. If this latter case were true, the PV loop would initially be flat along the x-axis.

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 (PEEP_i) 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. PEEP_i is also referred to as auto-PEEP, dynamic hyperinflation, and breath stacking. For the remainder of this chapter it will be referred to as PEEP_i.

PEEP_i can cause hemodynamic instability secondary to decreased venous return, just like high levels of PEEP.⁷ PEEP_i 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

Figure 8-6 Schematic of a flow-time curve showing potential air trapping. Note that full exhalation has not occurred before initiation of the next breath. This is seen by the fact that flow has not reached zero when the next breath is given. A square waveform is being used in this example. Continuation of this state can lead to intrinsic positive end-expiratory pressure.

Indications for Mechanical Ventilation

There are wide-ranging reasons for patients to require MV in the ED, and there are no absolute contraindications. Many time-honored indications for invasive ventilation are now identified as appropriate indications for noninvasive ventilation and are addressed later. Indications for MV range from loss of airway anatomy (edema, direct or indirect trauma, burns, infection), loss of protective airway mechanisms (intoxicants, brain injury, stroke), inability to ventilate, inability to oxygenate, or the expected clinical course. Indications for ET intubation may be separated into several categories—emergency, urgent, delayed, and elective—based on the urgency of establishing a definitive airway.

Equipment—standard Options

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).

Figure 8-7 The Nellcor Puritan Bennett 840 Ventilator system (Mansfield, MA). Selected features common to all ventilators include the respiratory rate (A), Fio₂ (B), positive end-expiratory pressure (PEEP) (C), waveform (D), inspiratory-to-expiratory ratio (I/E) (E), and trigger (F).

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 T_e. 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 T_e can lead to air trapping, elevated mean airway pressure, and rising Pco₂. These problems lead to hypercapnia, respiratory acidosis, and PEEP_i¹² (Fig. 8-8).

Figure 8-8 Effect of flow rate on inspiratory (T_i) and expiratory (T_e) time. Note that as the flow rate changes, there are corresponding alterations in the effective times for inspiration and exhalation. Deflections above the x-axis (time) indicate inspiration, and those below indicate exhalation. The tidal volume (Vt) delivered for each cycle is the same, but T_i and T_e are different.

Trigger

The trigger is the aspect that initiates a machine-generated breath. The trigger can be set to detect either a pressure or a flow gradient. It should be set so that the patient can trigger the ventilator without great effort.

Sensitivity

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.

Modes of Ventilation

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).

Figure 8-9 Initial ventilator settings for standard patients. AC, assist/control mode; Fio₂, fraction of inspired oxygen; IBW, ideal body weight; PEEP, positive end-expiratory pressure; PCV, pressure-cycled ventilation; PSV, pressure support ventilation; RR, respiratory rate; SIMV, synchronized intermittent mandatory ventilation; VCV, volume-cycled ventilation; Vt, tidal volume.

Spontaneous Breathing

Spontaneously breathing patients can be supported on the ventilator by pressure support ventilation (PSV). In this mode the ventilator provides a supplemental inspiratory pressure to each of the patient-generated breaths. The clinician sets Fio₂ and PEEP. The patient dictates the respiratory rate and generates the desired flow rate. The applied pressure is turned off once the flow decreases to a predetermined percentage. Vt is dictated by the pressure support given, patient effort, and compliance of the respiratory system. There is no set respiratory rate, although most modern ventilators have a backup apnea rate.

Volume-Cycled Ventilation

Volume-cycled ventilation (VCV) may also be termed volume-limited, volume-control, volume-assist, or volume-targeted ventilation. Volume-targeted modes are the most commonly used and the most familiar mode of MV in adults. As its name implies, “volume”—in this case Vt—is the ventilator’s targeted parameter. With this target, the ventilator seeks to deliver a preset amount of gas. The ventilator will generate the necessary driving pressure to reach this “target.” In addition to Vt, the clinician sets the desired respiratory rate, Fio₂, and PEEP. It should be noted that other important aspects of the mechanical ventilator can be controlled in this setting, such as waveform (decelerating or square), I : E ratio, flow rate, trigger, and sensitivity.

The time of gas flow is determined by the set volume, flow rate, and waveform of gas delivery. When the set volume is reached, gas flow is terminated and expiration passively begins. An advantage is that VCV delivers a reliable volume, but it does not take into account dynamic changes in lung compliance, which may alter the ability of the lung to accept delivered gas in gas-exchanging alveoli.

Pressure-Cycled Ventilation

Pressure-cycled ventilation (PCV) may also be termed pressure-limited, pressure-control, pressure-assist, or pressure-targeted ventilation. As its name implies, “pressure” is the ventilator’s targeted parameter. The ventilator will generate an inspiratory pressure that has been set by the clinician. With this target, the ventilator alters gas flow to achieve and maintain a preset airway pressure for the duration of a preset inspiratory time (T_i). Gas flow is terminated when the preset pressure is achieved. The volume delivered is determined by the compliance of the patient’s respiratory system, airway resistance, T_i, and the pressure target. In addition, the clinician sets the desired PEEP, respiratory rate, Fio₂, T_i, I : E ratio, and trigger mode. Pressure is maintained with a variable or intermittent flow rate for the set T_i. In the setting of hypoxemia, T_i may be increased quite precisely to increase mean airway pressure and oxygenation. This strategy is much more difficult, if not impossible, to manipulate with VCV.

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

One problem with PCV is that the volume received by the patient is potentially variable. Any change in system compliance or resistance (or both) will affect the Vt generated. For example, if the patient bites on the ET tube or a mucus plug develops, the set pressure that was generating an adequate volume will no longer do so. In contrast, a sudden increase in system compliance might result in the generation of Vt that may be considerably larger than desired. Instead of the traditional pressure alarm limits, one must adjust and be cognizant of Vt and minute ventilation alarm settings. Uncertainties such as these have led many clinicians to favor volume-targeted strategies or dual controlled strategies in the acute care setting.

Modes of Ventilation Commonly Used in the ED

Assist/control (AC) and synchronized intermittent mandatory ventilation (SIMV) are the ventilation modes most commonly used in the ED. Both are acceptable, and no data have demonstrated a better outcome with either mode. Other modes are also acceptable based on clinician preference.

Assist/Control Ventilation

Here, ventilator-initiated breaths, known as machine breaths (i.e., control breaths), are provided at a preset rate. Every breath is fully supported by the ventilator, regardless of whether the breath is initiated by the patient or the ventilator. The clinician sets the base ventilation rate, but if the patient tries to breathe faster than the set rate, additional breaths can be initiated by the patient, known as spontaneous breaths (i.e., assist breaths). A potential downside is inappropriate hyperventilation.

AC modes may be either volume or pressure cycled. Both assist breaths and control breaths will reach the set target, be it a set volume (in a volume-targeted mode) or a set pressure (in a pressure-targeted mode). In VCV, the spontaneous breath receives the same Vt that is set for the machine breath. In PCV, the spontaneous breath receives the same pressure that is set for the machine breath. To be more specific, in the volume-targeted mode, the clinician sets Vt, as well as the inspiratory flow rate, flow waveform, sensitivity to the patient’s respiratory effort (i.e., trigger), and the basal ventilatory rate. In the pressure-targeted mode, the clinician determines the basal ventilatory rate and how sensitive the ventilator will be to the patient’s respiratory effort and also selects pressure levels and T_i. Hence in this mode Vt is not set by the ventilator but is dependent on the compliance of the lung and chest wall and airway pressure. This helps avoid pressure-induced lung injury, but a specific Vt is not guaranteed.

For the patient to trigger the ventilator and initiate flow for a spontaneous breath, mean airway pressure must decrease by a preset amount below PEEP if set on a pressure trigger or flow to be generated if set on a flow trigger. The amount necessary to open the inflow valve is the sensitivity setting.

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 (PEEP_i) (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.

Synchronized Intermittent Mechanical Ventilation

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

Both volume-targeted ventilation and pressure-targeted ventilation modes can be set to either an AC or SIMV mode to achieve the desired minute ventilation. In a chemically paralyzed patient with no intrinsic respiratory drive, AC and SIMV look virtually identical. Both will reach their target (volume or pressure) at the set rate. If a patient triggers the ventilator at a rate greater than the set rate, these two strategies diverge. In AC, each breath above the set respiratory rate will result in a full mechanically supported breath to reach either the set volume or pressure target. In SIMV, the ventilator will give only the set number of breaths that the clinician has selected. Each additional breath will require the patient to generate a spontaneous Vt without mechanical assistance. This patient-generated breath must overcome any resistance caused by the artificial airway and ventilator circuitry. Pressure support should be added to SIMV for patient-generated breaths to reduce any increase in the work of breathing related to the resistance imposed by the ventilator circuit and ET tube.

Advanced Modes of Mechanical Ventilation

Dual Control Modes

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.

Box 8-1 Advanced Modes of Mechanical Ventilation

Breath to Breath