This chapter will discuss the principles of mechanical ventilation, indications, modes of mechanical ventilation, weaning and spontaneous breathing trials, tracheostomy, complications of mechanical ventilation, special situations, and noninvasive mechanical ventilation.

Proximal Airway Pressure, Alveolar Pressure, and Plateau Pressure

Proximal airway pressure applied by the ventilator (P_vent) is approximated during the expiratory phase in the inspiratory limb when flow is 0 and during the inspiratory phase in the expiratory limb when the flow is 0.¹ It uses the following equation²:

In this equation, C_RS is respiratory system compliance, PEEP is peak end-expiratory pressure, iPEEP is intrinsic PEEP, P_mus is pressure from patient’s inspiratory muscles, P_vent is proximal airway pressure from the ventilator, R_aw is airway resistance, VI is the inspiratory volume, inertance (cm H₂O L⁻¹ s²) is pressure difference to cause change in rate of change in volume flow rate in time, and VT is tidal volume. Alveolar pressure (PA) during inspiration in volume control ventilation is V/C_RS + PEEP, and during inspiration in pressure control ventilation is ΔP × (1 − e^−t/T) + PEEP.¹ In this equation, t is the elapsed time after initiation of inspiration, and T is the time constant.

Due to R_aw, the presence of flow causes proximal airway pressure to be greater than PA. Plateau pressure (P_plat) is determined by applying an end-inspiratory breath hold for 0.5 to 2 seconds, where the pressure equilibrates when the flow is 0. It is calculated via P_plat = VT/C_RS during passive inflation and via P_plat = (VT × PIP) − (VT × PEEP)/(VT + [T_E × VI]) in spontaneous breathing modes.¹ In this equation, PIP is peak inspiratory pressure and T_E is the expiratory time constant. During end-inspiratory breath hold, the P_plat approximates PA. Ideally, P_plat is less than 30 cm H₂O (Fig. 12-1).¹

Understanding the relationship between peak and plateau pressures can help troubleshoot mechanically ventilated patients. PIP without increase in plateau pressure suggests an increase in airway resistance from a kinked or blocked endotracheal (ET) tube, bronchospasm, or increased secretions.³ Increased PIP with increased plateau pressure suggests decreased compliance such as extrathoracic compression, bronchial intubation, atelectasis, pulmonary edema, pneumothorax, and hyperinflation.³ Decreasing PIP, low tidal volumes, gurgling sounds, and stridor can indicate cuff leak.

When the difference between peak and plateau pressures is greater 5 cm H₂O, increased airway pressure can likely be attributed to increased airway resistance. Acute causes of elevated airway resistance are bronchospasm, ET tube obstruction, or ventilator circuit obstruction (eg, the ventilator tubing is kinked). If the difference between peak and plateau pressures is low, increased airway pressure is likely secondary to acute decrease of lung compliance and resultant increased elastic work. Acute causes of elevated elastic work are pneumothorax, tension pneumothorax, evolving pneumonia, pulmonary edema, acute respiratory distress syndrome (ARDS), and auto-PEEP caused by breath stacking.

Plateau pressure, low tidal volumes, and high PEEP are suggested to improve survival in ARDS but their relative relationship is uncertain. Driving pressure explores this relationship and is the amount of cyclic parenchymal deformation imposed on ventilated lung units. Driving pressure (change in P = VT/C_RS) is calculated via P_plat − PEEP if there is no inspiratory effort.⁴ Decreasing driving pressure is associated with better outcomes in ARDS.⁴ The driving pressure limit varies, from 14 cm H₂O to 18 cm H₂O, but patients without ARDS have a driving pressure of 10.^5,6 One group of authors suggests limiting the driving pressure to 15 cm H₂O.⁵ This relationship of driving pressure and mortality is not seen in nonARDS patients.⁷

Mean Airway Pressure

This is a major determinant of oxygenation. Airway pressure or P_aw that is too low can result in hypoventilation and atelectasis. A P_aw that is too high can result in barotrauma and hemodynamic compromise. This can be calculated several ways. Flow-volume ventilation uses the following equation:

where T_I is the inspiratory phase and T_tot is the total respiratory cycle. Pressure ventilation uses the following equation¹:

Transpulmonary Pressure and Esophageal Pressure

Transpulmonary pressure (TPP) is the pressure gradient between alveolar pressure and pleural pressure which drives the flow of air.^1,8,9 Atmospheric air is always constant so the dynamic changes in the lungs propels the flow of air. Due to hysteresis, the pressure required to generate inspiration is higher than expiration. To inflate the lung, pressure must overcome airway resistance, inertance (pressure gradient required to accelerate gas), and pressure required to overcome elastance.⁹ When flow is zero, the transpulmonary pressure (alveolar pressure – pleural pressure) is the principle pressure maintaining the lung inflation.⁹

Esophageal pressure (P_es) is an indirect measure of pleural pressure. It is accomplished by inserting a thin catheter orally and nasally down to the esophagus (approximately 35–40 cm) and behind the heart. Identification of cardiac oscillations is used to determine accurate placement. Esophageal pressure is used to TPP.¹ It uses the following equation:

Transpulmonary pressure is used to assess lung recruitability and usually kept below 25 cm H₂O.^10,11 The ideal TPP is obtained from observations from the volume and transpulmonary pressure curve (Fig. 12-2). The lower inflection point (LIP) is the junction between the first and second portions of the curve or 20% decrease in steepest slope there is end of alveolar recruitment.^12-14 Amato’s study suggested decreased mortality with pressure more than 2 cm above LIP and plateau less than 20 cm H₂O.¹³ The upper inflection point (UIP) is 20% increase from the steepest slop and pressures above UIP are noted to cause overdistention and decreased alveolar recruitment. Based on these observations, it has been suggested that the pressures between LIP and UIP is where the lung has the highest compliance; alveoli is recruited throughout the inspiratory limb; and improved mortality is not solely dependent on PEEP which is an expiratory process.^14-19

Esophageal pressure is used to titrate PEEP in ARDS as long as TPP between 0 to 25 cmH₂O.^1,11,20 In ARDS, there is a propensity for alveolar collapse. One single center randomized control study suggested that TPP are negative in ARDS due to flooding or atelectasis.¹¹ An esophageal directed ventilation with TPP goal of 0 to less than 25 cm H₂O improved mortality.¹¹

Other roles of esophageal pressure is measurement of intrinsic PEEP and improve patient-ventilatory synchrony. Measurements of P_aw and flow mask true patient and ventilator asynchrony. Patients who are heavily sedated, respiratory muscles are actively contracting and going against ventilator support.^8,21-24 This is called reverse triggering or respiratory entrainment. Consequences are higher tidal volumes, erroneous plateau pressures, double inspiration, ineffective efforts, and prolonged mechanical ventilation (PMV).^8,21-24

Intra-abdominal Pressure

Intra-abdominal hypertension (abdominal pressure > 12 mmHg) can cause cephalic displacement of the diaphragm leading to compression of pulmonary parenchyma and decreased lymphatic drainage.^25,26 This leads to atelectasis, decreased oxygenation, reduced carbon dioxide removal, reduced capillary blood flow, increased airway pressures, and reduced tidal volume and pulmonary compliance.^25,26 Intra-abdominal pressure is measured indirectly via bladder pressures. In mechanically ventilated patients, inhalation with diaphragmatic contraction increases the pressure. Subsequently, an increase in abdominal pressure decreases C_RS with flattening and rightward shift of the pressure-volume (PV) curve.^27-29

Stress Index

Stress index (SI) is a parameter used to identify injurious mechanical ventilation. It is determined by the following equation:

P is Pressure for P_aw or TPP, T is time interval from time 0—time 1, a is the slope of P_aw-time or TPP-time, b is the stress index and c is P_aw or TPP at time 0. It assesses the pressure-time curve during constant-flow volume control.¹ The SI is 1 if there is adequate requirement without overcompensation. An SI greater than 1 suggests overdistention and recommends a decrease of PEEP, VT, or both.¹ An SI less than 1 suggests the addition of PEEP¹ (Fig. 12-3).

Time Constant

The time constant (T) is a product of resistance and compliance and determines the rate of volume change that is passively inflated or deflated.¹ It is based on this equation: V_t = V_i × e^-t/τ, where V_t is the volume of a lung unit at time t, V_i is the initial volume of the lung unit, e is the base of the natural logarithm, and τ is the time constant.¹ For 1τ, there is a 63% volume change, 2τ there is 87% volume change, 3τ there is 95% volume change, 4τ there is 98% volume change, and 5τ there is more than 99% volume change.¹

A higher resistance and compliance will have a longer time to fill and empty, and a lower resistance and compliance will have a shorter time to fill and empty.¹ For example, the value for a normal lung is 0.2 seconds, for asthmatic lungs is 0.4 seconds, and for fibrotic lungs is 0.1 seconds.³⁰

Flow and Resistance

Flow (V̇) can be turbulent or laminar. Transition from laminar to turbulent can be determined via Reynold’s Number is greater than 2000. The equation for Reynold’s number is 2rvd/η (r = radius of tube, v = velocity of flow, d = gas density, η = gas viscosity). Just like in fluid, radius is the major determinant in laminar flow as suggested by Poiseuille’s law. Reduction of the radius by one-half with all the parameters constant will reduce flow by 1/16. The reduction of flow means higher resistance in smaller bronchi compared to larger bronchi. However, due to the large number of small bronchi, the area of greatest resistance is the intermediate bronchi between the 4th and 8th bifurcation.

Airway resistance (R_aw) is the change in pressure divided by the change in flow (PIP-P_plat/change in V̇). The normal R_aw is 0.6 − 2.4 cm H₂O/L/sec. Factors that increase R_aw include increased airway diameter such as bronchodilation, decrease airway length, decrease viscosity, laminar flow, and increased volume. Factors that decrease R_aw include decrease airway diameter such as bronchoconstriction, increased airway length, increase viscosity, turbulent flow, and decreased volume.

Flow is monitored in the ventilator at the inspiratory valve and expiratory valve during volume-control ventilation.¹ During pressure control, inspiratory flow is determined via the following equation:

τ is the time constant. t is time elapsed after inspiration. e is the base of natural algorithm. This value typically is positive.¹ Expiratory flow is typically negative and is determined via the following equation:

It has been suggested that there is a maximum threshold for flow before respiratory rate increases. Inspiratory time is often increased to prolong expiration time in episodes of hypercapnia but there is a reflex increase in respiratory rate when the flow is increased from 60 L/min to 90 L/min.³¹

Lung Volumes and Capacities

Tidal volume (VT) is the volume during normal volume and typically is 500 mL. Inspiratory reserve volume (IRV) is the maximum volume that can be inhaled after normal inhalation. It can range from 1900 to 3300 ml. Expiratory reserve volume (ERV) is the maximum volume exhaled after normal exhalation. It can range from 700 to 1200 mL/breath. Residual volume (RV) is air left after exhalation. Maximum amount is 1200 mL/breath. Inspiratory capacity (IC) is the total amount of air inhaled and is the sum of VT and IRV. Functional residual capacity (FRC) is amount of air remaining in the lungs after exhalation and is the sum of RV and ERV. FRC has a direct correlation to PEEP. Vital capacity (VC) is the total exchangeable air and typically around 4800 mL. Total lung capacity (TLC) is the total of all volumes and is around 6000 mL.

Respiratory System Compliance

Lung and chest wall compliance is determined via the following equation:

Acceptable values are 50 to 100 mL/cm H₂O. Respiratory system compliance also determines the slope of the PV curve. Chest wall compliance is determined via the following equation¹:

The normal value is 200 mL/cm H₂O, and is decreased in patients with obesity, abdominal compartment syndrome, chest wall abnormalities, and burns.¹ Lung compliance is determined via the following equation:

The normal value is 200 mL/cm H₂O, and is decreased in patients with ARDS, pulmonary edema, pneumothorax, fibrosis, bronchial intubation, and atelectasis, and it is increased in patients with emphysema.¹

Work of Breathing

The work of breathing (WOB) is normally 4 to 8 J/min and is calculated via Volume × Pressure.

Minute Ventilation

Minute ventilation is the product of respiratory rate (RR) and tidal volume (V̇E = RR × VT). At rest, minute ventilation is 5 to 8 L/min. At mild exertion, minute ventilation can increase more than 12 L/min. There must be reciprocal changes between respiratory rate and tidal volume to meet the minute ventilation requirements for adequate carbon dioxide exchange.

Tension-Time Index and Pressure-Time Product

Both the tension-time index and the pressure-time product assess diaphragmatic fatigue. Tension-time index (TTI) = (Pdi/Pdimax)x Ti/Ttot) where Pdimax id maximum inhalation, Pdi/Pdimax is contractile force of diaphragm, and Ti/Ttot is contraction duration.1 A TTI > 0.15 predicts respiratory muscle fatigue. Work of breathing does not account for isometric phase and pressure-time product (PTP) account for energy expenditures during dynamic and isometric phases of respiration.

Auto-PEEP

Auto-PEEP occurs when air remains in the alveoli at the end of expiration, which increases the functional residual capacity (FRC). Auto-PEEP can be due to either flow restriction (as in chronic obstructive pulmonary disease), or insufficient time for lungs to return to FRC. Consequences of auto-PEEP include: (1) increased work of breathing because more work is required for inspiration; (2) worsening gas exchange; and (3) hemodynamic compromise due to increased intrathoracic pressure, decreased preload of right and left ventricle, and increased right ventricle afterload from increased pulmonary vascular resistance.^32-34

Auto-PEEP can be recognized by: (1) delay between inspiratory effort and drop in airway pressure; (2) failure of peak airway pressure to change when external PEEP is applied; (3) reduction of plateau after prolonged exhalation; (4) static auto-PEEP via expiratory hold; (5) dynamic auto-PEEP via esophageal pressures; and (6) depiction on mechanical waveforms.^32-34 On a flow-volume loop, volume does not return to baseline (depicting volume still trapped in alveoli). On a flow-time scalar, expiratory flow does not return to baseline (depicting flow still trapped in alveoli). The less the return is, the greater the air-trapping is. The dashed line in Figure 12-5 depicts normal flow return to baseline.

Treatment strategies include the following: (1) decreasing respiratory rate/tidal volume or minute ventilation; (2) decreasing the inspiration-to-expiration (I:E) ratio or increase expiration time; (3) if with hemodynamic compromise remove from the ventilator; (4) if with dynamic hyperinflation and intrinsic expiratory flow limitation such as COPD apply PEEP by 75% to 85% of autoPEEP; and (5) heliox.^32-34 Heliox is a blend of helium and oxygen (usually at a 70:30 ratio), which is less dense than air, theoretically permitting higher flow rates through a given airway segment for the same driving pressure, thereby alleviating dynamic hyperinflation. Several small studies have shown heliox reduce peak inspiratory pressure and arterial carbon dioxide tension, and improve oxygenation in mechanically ventilated patients by decreasing work of breathing, Paco₂, gas trapping, auto-PEEP, peak inspiratory pressures and plateau pressures, barotrauma, I:E ratio, and shunting.³⁵

The waveform of a ventilator cycle has 3 initiation phases variables (trigger, limit, and cycle)^36,37 (Fig. 12-6).

The trigger variable (point A), which causes inspiration to begin, can be a preset pressure variation (pressure triggering), a preset volume (volume triggering), a designated flow change (flow triggering), or an elapsed time (time triggering). The limit variable (point B) is the pressure, volume, or flow target that cannot be exceeded during inspiration. An inspiration thus may be limited when a preset peak airway pressure is reached (pressure limiting), when a preset volume is delivered (volume limiting), or when a preset peak flow is attained (flow limiting). Cycling (point C), refers to the factors that terminate inspiration. A breath may be pressure, volume, or time cycled when a preset pressure, volume, or flow as the time interval has been reached, respectively.

Three types of breath can be provided during mechanical ventilation, depending on whether the ventilator or the patient does the work and whether the ventilator or the patient initiates (triggers) the breath. These types are mandatory, assisted, and spontaneous breaths (Table 12-1). Controlled breaths are machine cycled, trigger limited, and cycled by the ventilator. The patient is entirely passive, and the ventilator performs the work of breathing. Assisted breaths are like controlled breaths in that they are limited and cycled by the ventilator, but are triggered by the patient. Breathing work thus is provided partly by the ventilator and partly by the patient. Spontaneous breaths are triggered, limited, and cycled by the patient, who performs all the work of breathing.

The relationship between the various possible types of breath and the inspiratory phase variables just discussed is called a mode of ventilation. The different modes of ventilation differ in the trigger, limit, and cycle phase variables (Table 12-2).

Waveforms usually plot 1 of 3 parameters (pressure, flow, or volume) against time (Fig. 12-7). Time is plotted on the horizontal (x) axis and the other parameter is plotted on the vertical (y) axis. Flow-delivery waveforms are the next parameters to consider. Flow delivery can be set as square (rectangular), ascending ramp, descending ramp, sine (sinusoidal), or decay (exponential). See Figure 12-8.¹

Loops are representations of pressure versus volume or flow versus volume. Expiration is typically depicted on the superior limb, and inspiration is on the inferior limb. A widened loop typically depicts increased airway resistance, whereas a narrowed loop typically depicts increased compliance (Fig. 12-9).²

Mechanical ventilators are set to deliver a constant volume (volume cycled), a constant pressure (pressure cycled), or a combination of both with each breath. Modes of ventilation that maintain a minimum respiratory rate regardless of whether the patient initiates a spontaneous breath are referred to as assist-control (A/C) ventilation. Because pressures and volumes are directly linked by the pressure-volume curve, any given volume will correspond to a specific pressure, and vice versa, regardless of whether the ventilator is pressure or volume cycled.³

Each type of mechanical ventilation is a variation of ventilation and pressure; settings include respiratory rate, tidal volume, trigger sensitivity, flow rate, waveform, and inspiratory/expiratory (I/E) ratio. Each ventilation mode offers its own set of advantages and disadvantages.

Volume-Cycled Ventilation

Each breath delivers a preset tidal volume (volume control).The desired carbon dioxide removal is achieved via a fixed minute volume (VT × RR). This includes modes such as volume-controlled, volume-controlled spontaneous intermittent mechanical ventilation (SIMV), and volume-controlled continuous mandatory ventilation (Fig. 12-10A).

Spontaneous Intermittent Mechanical Ventilation

This mode is similar to A/C with 1 notable difference: Only the set breaths are fully supported. If the set rate is 6 and the patient is breathing 12, then 6 of the breaths get the full set tidal volume and the other 6 get no support, pressure support, or volume support (Fig. 12-10B).

Pressure-Regulated Volume-Cycled Ventilation

Also known as VC+ on certain ventilators, pressure-regulated volume-cycled ventilation (PRVC) combines a pressure limit (pressure control) with volume assurance, thus guaranteeing a minimum minute ventilation. The ventilator adjusts the pressure from breath to breath, as the patient’s airway resistance and respiratory system compliance changes to deliver the set tidal volume. The ventilator monitors each breath and compares the delivered tidal volume with the set tidal volume and adjusts the inspiratory pressure on the next breath appropriately (Fig. 12-11A).

Pressure-Cycled Ventilation

Parameters such as pressure and inspiratory time are set by the operator. Volume and flow are variable according to patient needs. The patient can breathe spontaneously during the inspiratory and expiratory phases of the PC mandatory breath cycle. This includes PCV, PC-SIMV, and APRV (Fig. 12-11B).

Airway Pressure Release Ventilation

This modified bilevel mode allows spontaneous breathing to occur at the upper pressure level (IRV), which is usually maintained throughout a long inspiratory phase. It is essentially the sum of continuous positive airway pressure (CPAP) and time-cycled pressure release.³⁸ Advantages include improved oxygenation and compliance secondary to spontaneous breathing, which improves V̇/Q̇ matching, increased cardiac output from improved venous return due to decreased intrathoracic pressure and right atrial pressure, improved perfusion to gastrointestinal tract and glomerular filtration rate, and decreased sedation and neuromuscular blockade use. The increased time at high pressures may improve recruitment. The pressure release feature allows for improved tidal volume (VT) for given ΔP by utilizing increased elastic recoil. There is less chance of overdistension given not “filling” lung but “emptying.” The short release time does not allow significant derecruitment. Initial settings would include P_high at the P_plat, desired P_mean + 3 cm H₂O, or previous mean airway pressure, with a maximum of less than 35 cm H₂O; T_high at 4.5 to 6 seconds with respiratory rate of 8 to 12 beats/min; P_low at 0 cm H₂O; and T_low at 0.5 to 0.8 seconds with a target tidal volume of 4 to 6 mL/kg. The T_low is increased if VT is inadequate or shortened if VT is too high. (Fig. 12-12A).