9 

General Principles of
Mechanical Ventilation
ISMAIL CINEL AND R. PHILLIP DELLINGER

CHAPTER OUTLINE
History Pulse Oximetry
Mechanical Ventilation End-Tidal Capnography
Basic Concepts Transcutaneous Carbon Dioxide Monitoring
The Ventilator Circuit Ventilator Waveforms
Alarms and Safety Maintaining Support of the Ventilated Patient
Automatic Tube Compensation Sedation and Analgesia
Indications for Mechanical Ventilation Positioning
Secretion Clearance
Mechanical Breath Generation Early Physical Therapy in Acute Respiratory Failure
Ventilator Modes Weaning From Mechanical Ventilation
Continuous Mandatory Ventilation
Assist Control Ventilation Complications of Mechanical Ventilation
Synchronized Intermittent Mandatory Ventilation Hemodynamics
Stand-Alone Pressure Support Ventilation Ventilator-Induced Lung Injury
Dual Control Modes Ventilator-Associated Events
Gastrointestinal Bleeding
Other Modes of Mechanical Ventilation Venous Thromboembolism
Airway Pressure Release Ventilation
High-Frequency Oscillatory Ventilation Noninvasive Positive-Pressure Ventilation
Effort-Adapted Modes of Mechanical Ventilation High-Flow Nasal Cannula: A Potential Alternative to Mechanical
Ventilation
Positive End-Expiratory Pressure
Monitoring the Ventilated Patient
Hemodynamics

T
he institution of mechanical ventilation can be a lifesaving This chapter, which briefly discusses those modes, focuses on the
measure. However, the mechanical ventilator also has traditional and still most frequently used modes of mechanical
potential for great harm and, in and of itself, does not ventilation.
reverse underlying disease. Limiting iatrogenic injury from
ventilator-induced lung injury (VILI) should take high priority, History
along with acceptable levels of oxygenation and ventilation. The
clinician should be aware of basic and advanced principles involving In 1530, Paracelsus (1493–1541) used a fire bellows connected
mechanical ventilation, allowing flexibility when applying evidence- to a tube inserted into a patient’s mouth as a ventilator device.3
based practices to the individual patient. Knowledge of guidelines The first known mechanical device designed specifically to provide
and large clinical trials is vitally important, and the consideration ventilation for the patient was the foot pump developed by Fell
of patient trajectory, individual physiology, timing of therapy, and and O’Dwyer in the 1880s.4
severity of illness will make tailoring the ventilator prescription The first generation of mechanical ventilators focused primarily
most effective.1 The evolution of mechanical ventilation is fascinating on the intermittent delivery of a bulk volume of gas to the patient
(Fig. 9.1) with current newer modes often with complex computer with limited monitoring.5 Negative-pressure ventilators were
interaction and automatic adjustments of ventilation parameters.2 invented and applied a negative pressure around the body or chest

129
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 130 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

mechanism of the device and in the monitoring systems, enabling

automatic adjustment of most aspects of the mechanical breath
being delivered.

Mechanical Ventilation
Basic Concepts
A For a breath to be generated, flow must exist. During normal
spontaneous breathing, the diaphragm and other respiratory muscles
create gas flow by lowering pleural, alveolar, and airway pressures
relative to atmospheric pressure. Alveolar pressure is normally
atmospheric at end-inspiration and end-expiration. Diaphragmatic
and intercostal muscle activation during normal inspiration expands
the chest and decreases intrapleural pressure from −5 cm H2O to
−8 cm H2O. Alveolar pressure fluctuates from +1 cm H2O during
exhalation to −1 cm H2O during inspiration.
B A ventilation-perfusion (V̇ /Q̇ ) mismatch occurs when areas of
the lung are perfused but either poorly ventilated (low V̇ /Q̇ ) or
not ventilated at all (shunt). The latter is an intrapulmonary (IP)
(capillary) shunt. Shunt may also be intracardiac (anatomic). Venous
admixture, as a measure of less than fully oxygenated blood after
passing through the lung, includes both low V̇ /Q̇ areas of lung
and IP shunt. Normal venous admixture is about 2% to 5%.
Mechanical ventilation may increase the venous admixture to
approximately 10% in the normal individual. Mechanical ventilation
C usually decreases venous admixture in alveolar lung disease, such
as acute respiratory distress syndrome (ARDS), improving the
• Fig. 9.1  Evolution of the concept of mechanical ventilation. A, The first distribution of ventilation, especially in previously underventilated
mechanical ventilators were not equipped with sensors. B, Mechanical
ventilators monitor all the ventilation parameters, allowing both closed-
lung areas. Pressures greater than alveolar opening and closing
loop control of the generated waveform and providing information to the pressures expand the collapsed alveolus and prevent its collapse,
clinicians. C, Mechanical ventilators monitor the condition of the patients respectively. However, if positive-pressure ventilation produces
and automatically adjust the ventilatory parameters on the basis of overdistention, redistribution of pulmonary blood flow to unven-
patients’ needs. (From Dellaca’ RL, Veneroni C, Farre R. Trends in tilated regions may occur, resulting in hypoxemia. Dead space refers
mechanical ventilation: are we ventilating our patients in the best possible to areas of the lung with a higher V̇ /Q̇ ratio. Anatomic dead space
way? Breathe (Sheff). 2017;13:85–98.) is the volume of the conducting airways of the lungs, about 150 mL.
Alveolar dead space refers to alveoli that are overventilated relative
to perfusion; it is increased by any condition that reduces pulmonary
blood flow, such as pulmonary embolism (PE) or with overdistention
cavity. Two classic devices that provided negative-pressure ventilation of the lung. Mechanical dead space refers to the rebreathed volume
were the iron lung and the chest cuirass or chest shell.6 Iron lungs of the ventilator circuit; this volume behaves like an extension of
were widely used during the poliomyelitis epidemics of the 1930s the anatomic dead space. Mechanical ventilation can also increase
and 1940s. These devices encased the patient from the neck down dead space if it leads to overdistention.
and applied negative pressure around the patient to expand the An increased dead space fraction requires a greater minute
lungs. The chest cuirass was intended to alleviate the problems of ventilation to maintain alveolar ventilation and PaCO2 (partial
patient access and “tank shock” that occurred secondary to venous pressure of carbon dioxide in arterial blood). Hyperventilation
pooling during the application of negative pressure associated with lowers PaCO2. Hypoventilation raises PaCO2; a modest elevation
iron lungs.7 Although the chest cuirass improved patient access (50–70 mm Hg) reduces pH and is usually not by itself injurious
and decreased the potential for tank shock, ventilation with this in the mechanically ventilated patient. It has become increasingly
device was limited by the difficulties in maintaining an airtight recognized that hypercapnia during mechanical ventilation is well
seal between the shell and the patient’s chest wall. tolerated and may not be harmful. An exception occurs in the
After the polio epidemic of the 1960s, the era of respiratory presence of increased intracranial pressure.
intensive care emerged, as positive-pressure ventilation via an Although modern ventilators have evolved into complex machines,
artificial airway became commonplace.6 Controlled mechanical the basic premise remains: a ventilator is designed to replace or
ventilation eventually led to assisted modes of support, and positive augment a patient’s muscles in performing the work of breathing.8
end-expiratory pressure (PEEP) was introduced in the late 1960s. Ventilators use input power (electricity or compressed gas) to ventilate
The improvements in mechanical ventilators came about as the lungs. To generate a breath (whether it be spontaneous or
understanding was gained in manipulating variables of flow and positive pressure), a pressure gradient must be generated from the
pressure for patient benefit. Further technical evolution of ventilators airway opening to the alveoli. The volumes delivered and pressures
included advances such as intermittent mandatory ventilation and generated largely depend on the mechanical properties of the
synchronous intermittent mandatory ventilation. Modern ventilators respiratory system: the lungs and chest wall as well as the abdomen.8
now boast microprocessors that serve both in the operating Each of these components has mechanical properties that determine

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 CHAPTER 9  General Principles of Mechanical Ventilation 131

the overall behavior of the respiratory system. Although the respira- Gases delivered from mechanical ventilators are typically dry,
tory system can be quite complex, the main variables of interest and the upper airways of patients being ventilated are functionally
are pressure, flow, and volume. The ventilator must generate a bypassed by artificial airways, necessitating the use of an external
pressure to cause flow through an open circuit and therefore increase humidifying apparatus in the breathing circuit. Because the upper
lung volume.9 The pressure required to do this reflects a combination airway is bypassed during mechanical ventilation, the inspired gas
of the pressures to inflate the lung and chest wall. This can be temperature should be kept close to the body temperature. Inspired
illustrated by the equation of motion9,10: gases that bypass the upper respiratory tract through ETs or tra-
cheostomy tubes should be heated to at least 32°C to 34°C at
Musclepressure + Ventilatorpressure 95% to 100% relative humidity. The temperature probe for the
= (Elastance Volume ) + (Resistance Flow) heated humidifier should be placed inside the inspiratory limb of
the ventilator circuit as close to the patient as possible. Moisture
Compliance describes the ease or difficulty of the respiratory loss and subsequent dehydration of the respiratory tract result in
system to expand in response to a delivered pressure and volume. epithelial damage.
Simplistically, compliance is defined by the change in volume (ΔV) An HME, which is placed between the artificial airway and
divided by the change in pressure (ΔP), and the compliance of the ventilator circuit, may be used to replace the traditional heated
the respiratory system (CRS) is ΔV/ΔPalveolar. Elastance is the inverse humidifier. During exhalation, moisture and heat from the patient
of compliance, or the ratio of pressure change to volume change, are absorbed into the honeycomb structure of the exchanger and
and describes the tendency to recoil. Resistance describes the are transferred back to the patient during the next inhalation.
impedance to airflow through the respiratory system, or the ratio Ventilator circuits with bacterial-viral filtering HMEs cost less to
of pressure change to flow change. The elastic load is the pressure maintain and are less likely to colonize bacteria than those with
required to overcome the elastance of the respiratory system, and heated humidifiers.12,13 Contraindications for use of an HME are
the resistive load is the pressure required to overcome flow resistance thick or large amounts of secretions, minute volume exceeding
of the ventilator circuit, endotracheal tube (ET), and airways.8 10 L/min, body temperature less than 32°C, and need for aerosolized
The equation of motion illustrates several basic principles. To medications.14
drive gas into the patient, a ventilator can directly control either
the pressure or the flow and volume applied at the airway. Despite Alarms and Safety
its complexity a ventilator is simply a machine controlling one of
these two variables (control variables). For example, in pressure Current ventilators are equipped with monitors that constantly or
control and PSV, pressure is the control variable and is held constant, periodically assess the ventilator’s operation and the patient’s status
although flow and lung inflation vary based on the patient’s (Fig. 9.2). These monitors are usually associated with alarms that
respiratory mechanics and inspiratory time (I time) (the latter set visually or audibly notify the operator of any variation from the
directly in pressure control and patient influence with pressure preset norm. Ventilator alarms can warn of potentially life-
support). In volume ventilation, flow is the control variable and threatening events, must have an appropriate level of sensitivity
pressure and lung inflation vary with the patient’s respiratory and specificity, and must be evaluated clinically and in a clinical
mechanics. Flow and volume are intimately linked: volume (L) = context.15 There are some alarms related to power input (e.g., low
flow (L/sec) × I time (sec). battery, loss of power, loss of air supply) and control circuit (e.g.,
nonfunctioning ventilator, incompatible settings), but most alarms
are related to measured output, such as pressure, volume, and flow.8
The Ventilator Circuit High-pressure alarms are triggered by patient factors (such as
The ventilator circuit consists of plastic tubing connecting the decreased compliance and increased resistance of the respiratory system)
artificial airway or mask with the mechanical ventilator. Within or by ventilator circuit malfunction (obstruction or kinking of the
the circuit may reside humidifiers, devices for the delivery of ET). Low-pressure alarms are generally secondary to a leak in the
aerosolized medications, filters, suction catheters for secretion system (ventilator circuit, ET or cuff) or patient (large pressure loss
clearance, and heated wires.11 The length and compliance (2–3 cm3/ from a bronchopleural fistula). A high expired volume alarm could
cm H2O) of the ventilator circuit are responsible for a volume of be seen with improved pulmonary mechanics during pressure-control
gas contained within the circuit, termed the compressible volume. ventilation. Low expired volume could be secondary to patient-
This is partly responsible for the discrepancy between the set tidal ventilator disconnect or a leak in the system or patient. A high-
volume (VT) delivered and the expiratory volume measured and frequency alarm is secondary to either autotriggering or hyperventilation,
displayed by the ventilator. The ventilator circuit also adds resistance and a low-frequency alarm indicates bradypnea or apnea.8,15
to the system, but it is minimal compared to either the patient’s
inherent mechanics or the ET. Although frequently colonized with Automatic Tube Compensation
bacterial pathogens, the routine change of the ventilator circuit
for infection prevention (e.g., ventilator-associated pneumonia Traditionally, most clinicians apply some amount of pressure support
[VAP]) is not recommended. during inspiration to compensate for the increased work of breathing
In the body, inspired gases are conditioned in the airway just related to artificial airway resistance. The amount of pressure support
before the carina so that they are fully saturated with water at needed to counterbalance this resistance is highly variable, depending
body temperature by the time they reach the alveoli (37°C, 100% not only on the internal diameter of the ET but also on flow, bend
relative humidity, 44 mg/L absolute humidity, 47 mm Hg water of the tube, and changing demands of the patient. This variability
vapor pressure). This portion of the airway acts as a heat and makes one level of pressure insufficient to meet these changing
moisture exchanger (HME). Under normal conditions, about demands.16
250 mL of water is lost from the lungs each day to humidify the Automatic tube compensation (ATC) compensates for ET
inspired gases. resistance via closed-loop control of calculated tracheal pressure.

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 132 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

• Fig. 9.2  The alarm panel of a Draeger Evita 4 ventilator showing the alarms typically used on current
ventilators. (From Draeger Medical, Inc., Lübeck, Germany.)

A ventilator with ATC compensates for the pressure drop across demands of a physiologically stressed patient. Clinical indicators,
the ET during inspiration by increasing the airway pressure and such as tachycardia, arrhythmias, hypertension, and tachypnea;
during expiration by decreasing airway pressure according to actual use of accessory respiratory muscles; diaphoresis; and cyanosis, are
gas flow.17–19 This technique uses a continuous calculation of the used to diagnose respiratory distress. Type I respiratory failure is
flow-dependent drop in pressure across the ET. ATC is similar to hypoxemic respiratory failure, defined as a partial pressure of oxygen
PSV, but the pressure applied by the ventilator varies as a function in arterial blood (PaO2) less than 60 mm Hg. Type II respiratory
of ET resistance and flow demand. Most of the interest in ATC failure is hypercarbic respiratory failure, defined as PaCO2 greater
revolves around eliminating the imposed work of breathing during than 50 mm Hg, if elevated from patient baseline and associated
inspiration. During expiration, however, ATC may also compensate with acidosis.22 Blood pH is generally a better indicator than PaCO2
for that flow resistance by lowering the pressure in the expiratory for adjusting minute ventilation. Hypercapnia should not prompt
limb transiently from its PEEP setting, helping reduce effective aggressive intervention if pH remains acceptable and the patient
expiratory resistance and auto-PEEP.17,20 In addition to overcoming remains alert. Hypercapnia is generally well tolerated, but this
the work of breathing imposed by the artificial airway, ATC may clearly depends on the underlying pathophysiology and comorbid
improve patient-ventilator synchrony by varying the flow com- conditions of the patient (e.g., right ventricular dysfunction).
mensurate with demand and may reduce air trapping by compensat- However, a sustained pH of 7.65 or greater or 7.10 or less is often
ing for imposed expiratory resistance. During weaning trials, this considered sufficiently dangerous in itself to require control of
technique may allow a more reliable prediction of patient perfor- minute ventilation by mechanical ventilation. Mechanical ventilation
mance when the tube is removed. may also be instituted to maintain normal blood pH, decrease
work of breathing, assist left ventricular function in the setting of
Indications for Mechanical Ventilation acute decompensated heart failure, or for airway protection in the
setting of toxic overdose, traumatic brain injury, or any other
Mechanical ventilation is instituted for a number of reasons significant acute central nervous system illnesses. Box 9.1 suggests
(Table 9.1).21 Most commonly, these indications are a combination guidelines for setting basic operating parameters in a mechanical
of a failure to adequately oxygenate, ventilate, or meet the metabolic ventilator.

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 CHAPTER 9  General Principles of Mechanical Ventilation 133

TABLE
9.1  Potential Indications for Mechanical Ventilation

Value(s)/Finding(s) Supporting Need for

Physiologic Mechanism Clinical Assessment Normal Range Mechanical Ventilation
Hypoxemia P(A-a)O2 gradient (mm Hg) 25–65 >350
PaO2/FIO2 ratio 425–475 <300
SaO2 98% <90% despite supplemental oxygen
Hypercarbia/inadequate alveolar PaCO2 35–45 mm Hg Acute increase from patient’s baseline
ventilation pH <7.20
Mental status decline
Oxygen delivery/oxygen consumption Elevated lactate ≤2.2 mg/dL ≥4 mg/dL despite adequate resuscitation
imbalance Decreased mixed venous oxygen saturation 70% <70% despite adequate acute resuscitation
Increased work of breathing Minute ventilation 5–10 L/min >15–20 L/min
Dead space 0.15–0.30 ≥0.5 (acute)
Inspiratory muscle weakness NIP 80–100 cm H2O <20–30
VC 60–75 mL/kg <15–20
Acute decompensated heart failure Jugular venous distention Clinical judgment combined with the listed
Pulmonary edema factors
Decreased EF
Inadequate lung expansion VT (mL/kg) 5–8 <4–5
VC (mL/kg) 60–75 <10–15
Respiratory rate (breaths/min) 12–20 ≥35

EF, Ejection fraction; FIO2, fraction of inspired oxygen; NIP, negative inspiratory pressure; P(A-a)O2, alveolar-arterial oxygen pressure difference; PaO2, partial pressure of oxygen; PaCO2, partial pressure
of carbon dioxide; SaO2, arterial oxygen saturation; VC, vital capacity; VT, tidal volume.

• BOX 9.1  Guidelines for the Initiation of Mechanical Breath Generation

Mechanical Ventilation
The breath generated by a mechanical ventilator can be separated
1. Choose the ventilator mode with which you are most familiar. The primary into four phases: triggering, inspiration, cycling, and expiration.
goals of ventilatory support are adequate oxygenation/ventilation, reduced Triggering represents the change from expiration to inspiration
work of breathing, synchrony between the patient and ventilator, and
avoidance of high end-inspiratory alveolar pressures.
and occurs either because of a drop in circuit pressure or diversion
2. The initial FIO2 (fraction of inspired oxygen) value should be 1.0. of flow (when patient triggered) or because of elapsed time. Sensitiv-
The FIO2 thereafter can be titrated downward to maintain the SpO2 ity refers to a preset threshold of pressure or flow. When this
(oxyhemoglobin saturation) at 92% to 94%. In severe ARDS, >88% threshold is reached, a mechanical breath is delivered. This threshold
SpO2 may be acceptable to minimize complications of mechanical can be adjusted, and is usually set at −1 to −2 cm H2O. If sensitivity
ventilation. is set too low, the ventilator will be triggered by any process that
3. Initial VT should be 8–10 mL/kg. Patients with acute respiratory failure causes the airway pressure to drop below the set threshold. Such
from neuromuscular disease often require VT of 10–12 mL/kg to satisfy air processes include patient motion, external compression, gastric
hunger. In patients with ARDS, it is recommended to use a VT of 6 mL/kg suctioning, and air leaks in the circuit. Conversely, if the threshold
and to keep inspiratory plateau pressure 30 cm H2O or less. is set too high, the work of breathing increases, as the patient must
4. Choose a respiratory rate and minute ventilation appropriate for
the particular clinical requirements. Target pH, not PaCO2 (partial
make a significant effort to overcome the threshold limit for
pressure of carbon dioxide). Initial respiratory rate is typically 10–12 inspiratory flow to occur. In the setting of pressure triggering,
breaths/min. airway pressure is reduced (by patient effort) in the proximal circuit,
5. Use PEEP in diffuse lung injury to support oxygenation and reduce the FIO2. the expiratory valve closes, pressurization of the inspiratory limb
6. In patients with chronic obstructive pulmonary disease, avoid choosing of the circuit occurs, and the patient receives a breath. Flow sensing
settings that limit expiratory time and cause or worsen auto-PEEP. was developed as an alternative to pressure triggering to reduce
7. When poor oxygenation, inadequate ventilation, or excessively high peak the delay in response time between neural input from the patient
inspiration pressures are thought to be related to patient intolerance of and delivery of gas volume by the ventilator.23,24 In the setting of
ventilator settings and are not corrected by ventilator adjustment, consider flow triggering, the patient’s inspiratory effort induces a disruption
initiating or increasing sedation or analgesia. of the constant flow in the ventilator inspiratory circuit. This
ARDS, Acute respiratory distress syndrome; PEEP, positive end-expiratory pressure; VT, tidal volume. change in flow signals the expiratory valve to close and for the
Adapted from Fundamental Critical Care Support. Des Plaines, IL: Society of Critical Care Medicine; ventilator to deliver the next breath. Flow triggering was initially
2007.
demonstrated to decrease the work of breathing compared with
pressure triggering. However, with improvement in response time,

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 134 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

monitoring, and feedback, pressure and flow triggering are similar minute ventilation is not guaranteed. It is a function of the compli-
in this regard.25,26 Fig. 9.3 is a representation of patient effort and ance and resistance of the respiratory system. The clinician therefore
ventilator response time. should monitor these physiologic changes closely to avoid untoward
During inspiration, flow is channeled through the open inspira- changes in either airway pressure or PaCO2 levels.
tory valve of the ventilator to the patient with the exhalation valve With pressure control and pressure support (PS) breaths, the
closed. This phase can be controlled by how one sets flow or pattern of inspiratory flow is a natural decelerating pattern as the
pressure in the ventilator proximal to the open inspiratory valve. pressure gradient for flow decreases as pressure rises in the patient’s
For example, volume-assist control is flow controlled and pressure- lungs. The pattern of inspiratory flow with a flow-controlled breath
assist control is pressure controlled. The choice of control variable (volume cycled) is typically square with an almost instantaneous
is largely the discretion of the clinician, as either can be manipulated rise to a preset level (40 L/min, 60 L/min, and so on) followed
to achieve set goals. It should be noted, however, that in volume- by constant flow until cycling occurs. The flow pattern can be
targeted ventilation, excessive airway pressures can arise secondary computer altered to be decelerating or sinusoidal (Fig. 9.5). Decelerat-
to worsening pulmonary mechanics. In this situation, the pressure ing flow results in a rapid rise to a maximum level followed by a
alarm will cause a pressure limit to cycle to expiration. At the end gradual decrease until cycling. Sinusoidal flow pattern most closely
of inspiration in volume-targeted ventilation, an inspiratory hold represents normal physiologic breathing. It results in flow that
maneuver can be performed (Fig. 9.4), which can distinguish the gradually increases and then decreases during inspiration. The
peak airway pressure from the plateau pressure (because flow is choice of inspiratory flow pattern should be based on patient
stopped, resistance is negligible). In pressure-targeted ventilation, characteristics, and a few common clinical scenarios should be
familiar to the clinician. Square flow over time results in a shorter
inspiratory time (I time) for a given VT, and therefore longer
expiratory time (E time). For this reason it may be preferred in
Response time
60 patients with obstructive physiology (chronic obstructive pulmonary
disease [COPD] or asthma).27,28 It is also usually tolerated better
in patients with demand for high minute ventilation, such as severe
40 metabolic acidosis or elevated intracranial pressure. In this situation,
there is a potential for dyssynchrony to occur during the progression
20
of the inspiratory phase if decelerating flow is chosen. The trade-off
is higher peak airway pressures with a square waveform, which
cm H2O

may be ameliorated if it leads to a reduction in hyperinflation and

-S iPEEP. Decelerating flow results in a longer I time and likely a
better distribution of flow. With pulmonary pathophysiology
RT = 6 msec involving heterogeneous distribution of injury (ARDS as the
prototype example), decelerating flow is likely the best choice, as
the longer I time can lead to more homogeneous distribution of
ventilation. The distribution of ventilation can be quite different
when the flow pattern changes. A decelerating flow pattern yields
the most even distribution under most abnormal airway conditions.29
40 80 120
Studies have also demonstrated that a decelerating flow pattern
• Fig. 9.3  Pressure wave showing time relationship between patient inspi- improves the geographic distribution of lung vibration as a presumed
ratory effort and ventilator response time (RT). surrogate of airflow.30 The length of inspiration depends on several
factors. In the pressure control mode of ventilation, the clinician
directly controls the I time and I:E ratio. With pressure support
Peak inspiratory the patient primarily controls I time. In flow-controlled (volume-
pressure Plateau targeted) ventilation, the I time is a function of set VT and flow
pressure rate (VT/inspiratory flow rate) as well as flow wave characteristics
(shape). The end-inspiratory alveolar pressure, as measured by an
end-inspiratory hold, is the same for a given VT regardless of the
Pressure type of ventilator breath.
Inspiratory
hold

Flow •
V

LPM

Inspiration Expiration

• Fig. 9.5  Depicted left to right are square, decelerating, and sine inspira-
Volume tory flow waveforms as options for delivery of volume ventilation. Note that
• Fig. 9.4
  A plateau pressure measurement can be obtained in assist the square waveform produces the shortest inspiratory time and that the
volume control mode by the performance of an inspiratory hold to better decelerating waveform does not return to zero flow at end inspiration.
estimate the pressure in the lungs. LPM, Liters per minute; V̇ , flow.

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 CHAPTER 9  General Principles of Mechanical Ventilation 135

Cycling is the transition from inspiration to expiration (closing Ventilator Modes

inspiratory valve and opening expiratory valve). It can occur due
to a threshold of decrease in flow, elapsed time, or delivered volume. A ventilator mode describes ventilation over time and a set of
Flow-cycled breaths are PS breaths. With PS breaths flow rate specific combinations of breath characteristics delivered to a patient,
decreases dramatically as (a) patient inspiratory effort decreases including types of breaths, phase variables, and mandatory versus
and then ceases and (b) the pressure rises in the patient’s lungs as spontaneous breaths.16 Clinician familiarity, unit, and institutional
the breath is delivered. With a fixed pressure application the gradient practice patterns determine to a large extent the mode that is
for flow decreases. The patient often senses control not only of used. Also, data showing definitive improvement in clinically relevant
initiation of breath but also of its termination. When a predeter- outcomes comparing one mode to another are lacking. Patient
mined decrement in flow occurs, inspiration is terminated and need and response to therapy should guide mode selection.
the patient cycles to expiration. This is typically set at 25% of Table 9.2 summarizes the features of some of the modes of mechani-
initial flow, but can be manipulated based on different clinical cal ventilation, and Table 9.3 lists some of their advantages and
conditions. For example, if a large leak occurs (bronchopleural disadvantages. Fig. 9.6 also shows some characteristic waveforms
fistula or ventilator circuit leak) it may be wise to set the cycle at of various modes of mechanical ventilation.
a higher percentage of initial flow to terminate inspiration at the
appropriate time. Strength and duration of patient inspiratory Continuous Mandatory Ventilation
effort influence VT. For safety reasons, PS breaths can be cycled
due to excessive pressures (e.g., coughing during inspiration) or With continuous mandatory ventilation (CMV), the patient has
elapsed time (e.g., secondary to a leak in the system which would no influence on mechanical ventilation, and all breaths are time
prolong inspiration). In time-cycled breaths (pressure control), (ventilation) triggered. Patient-ventilator interaction is solely from
inspiration is terminated after a preset interval, regardless of whether the ventilator to the patient; it is time triggered and cycled by the
preset pressure has been achieved or a desired VT has been delivered. ventilator. Current ventilators do not have a CMV setting; this
Pressure is maintained at a preset level throughout inspiration, mode is essentially what is achieved when a patient using assist
yielding a square pressure waveform. Pressure-targeted ventilation control (AC) ventilation has no interaction with the ventilator
is time cycled, and the time can be adjusted to yield a precise secondary to conditions such as heavy sedation, neuromuscular
inspiration/expiration (I:E) ratio. In volume-cycled breaths (flow blockade, or central nervous system injury.
controlled), the clinician has selected the targeted VT. Volume is
delivered until that volume is reached. Airway pressure is directly Assist Control Ventilation
dependent on the VT and the mechanical characteristics of the
patient’s respiratory system. For safety reasons, volume-cycled breaths In AC ventilation, a mandatory number of breaths are set and
will be pressure cycled if airway pressures exceed the pressure alarm delivered with a set pressure or flow (assisted or unassisted), and if
limit. In this situation, the delivered V T will not reach the set the patient’s respiratory rate is higher than this backup setting (rate),
volume target unless the pressure alarm limit is increased. additional assisted breaths to the preset pressure or flow are delivered.
At the end of inspiration, flow from the ventilator ceases, the The target variable can be pressure (PC/AC) or volume (VC/AC).
exhalation valve opens, and gas is allowed out from the lungs. This
release occurs passively. Expiratory flow should cease prior to Synchronized Intermittent
expiration. If this does not occur, the patient has auto-PEEP or
intrinsic PEEP (iPEEP). This is most commonly seen in patients Mandatory Ventilation
with expiratory flow limitation (COPD or asthma) or high With synchronized intermittent mandatory ventilation (SIMV),
inspiration/expiration (I:E) ratios (see later text). the ventilator delivers a mandatory number of breaths with a set

TABLE
9.2  Overview of Features of Selected Modes of Mechanical Ventilation

Ventilator Mode Trigger Control Cycling Inspiratory Flow

Continuous mandatory ventilation Time Flow or pressure Volume or time Selected or decelerating
Volume control/assist control (VC/AC) Patient or Flow Volume Square, decelerating, or sinusoidal
time
Pressure control/assist control (PC/AC) Patient or Pressure Time Decelerating
time
Synchronized intermittent mandatory Patient or Pressure for patient Flow for spontaneous Decelerating for spontaneous breath
ventilation time breaths breaths
Flow (VC) or pressure (PC) Volume or time for Square (VC), decelerating (VC or PC),
for ventilator breaths ventilator breaths sinusoidal for spontaneous breaths
Stand-alone pressure-support Patient None Flow Decelerating
ventilation

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 136 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

TABLE
9.3  Potential Advantages and Disadvantages of Selected Modes of Mechanical Ventilation

Mode Advantage(s) Disadvantage(s)

Controlled mechanical ventilation Rests muscles of respiration Requires use of heavy sedation/neuromuscular blockade
Assist volume control Reduced work of breathing Potential adverse hemodynamic effects
Guarantees delivery of set tidal volume (unless May lead to inappropriate hyperventilation and excessive
peak pressure limit alarm is exceeded) inspiration pressures
Assist pressure control Allows limitation of peak inspiratory pressures Same as for assist volume control
Potential hyperventilation or hypoventilation with lung
resistance/compliance changes
Synchronized intermittent mandatory Less interference with normal cardiovascular Increased work of breathing compared with assist control
ventilation function Patient may find it difficult to adjust to two different types
of ventilator breaths
Stand-alone pressure-support Patient comfort Apnea alarm is only backup
ventilation Improved patient-ventilator interaction Variable patient tolerance
Decreased work of breathing

Spontaneous Assist volume Assist pressure Pressure support

breath control control and pressure- ventilation
regulated volume control

Pressure

Flow

Volume
A B C D
• Fig. 9.6   Characteristic pressure-flow waveforms with breathing spontaneously and various types of

ventilation. A, Spontaneous breath. Such breaths are spontaneous, and inspiratory flow is achieved by
the negative pressure generated by the respiratory muscles. Expiration occurs as these muscles relax.
The combination of mandatory ventilator breaths (B or C) with spontaneous breaths (with or without
pressure support) is called synchronized intermittent mandatory ventilation. B, Assist volume control
ventilation. The flow is constant and pressure increases throughout inspiration. C, Assist pressure control
ventilation or pressure-regulated volume control (PRVC). The pressure is constant and flow decreases
throughout inspiration. In PRVC, the level of applied pressure may vary from one breath to the next. D,
Pressure support ventilation. The pressure is constant and flow decreases throughout inspiration. When
the flow reaches one-fourth of its initial value, inspiration ends (flow-cycled). The flow and respiratory time
are determined by patient effort and level of pressure support applied. The tidal volume varies from one
breath to the next.

pressure or flow (assisted or unassisted), similar to AC. However, ventilator will deliver a regularly scheduled mandatory breath (time
spontaneous breaths are delivered upon patient triggering during triggered).
a timing window created around the delivery of mandatory breaths.
These spontaneous breaths can be totally driven by patient effort Stand-Alone Pressure Support Ventilation
or pressure-enhanced as pressure-controlled/flow-cycled (PS) breaths.
The ventilator will attempt to synchronize the delivery of this This mode of ventilation is patient triggered, pressure controlled,
mandatory breath with the spontaneous effort of the patient (if and flow cycled with a decelerating flow inspiratory waveform.
effort is present). If the patient does not trigger a breath, then the Cycling to expiration typically occurs when the flow rate decreases

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 CHAPTER 9  General Principles of Mechanical Ventilation 137

to a set percentage of inspiratory flow (typically 25% of initial

inspiratory flow). However, if there is a leak in the system, inspira- Other Modes of Mechanical Ventilation
tory flow may never decrease to the cycle threshold. In this situation, Airway Pressure Release Ventilation
for safety purposes, flow can be time cycled as well. During
inspiration, the ventilator will adjust flow to maintain the preset Airway pressure release ventilation (APRV) has been described in
pressure, and VT is dependent on patient effort and the mechanics the literature since 1987.37 It is a time-triggered, pressure-controlled,
of the respiratory system. The pressurization rate to the goal pressure time-cycled mode of mechanical ventilation that exactly resembles
is determined by the rise time, which can be adjusted on many AC/PC with very extended I:E ratios if the patient is not spontane-
ventilators. If the rise time is set too low, increased work of breathing ously breathing.38,39 It has been described as continuous positive
can occur; if it is set too high, the preset pressure may be exceeded airway pressure (CPAP) with an intermittent time-cycled release
(overshoot), causing early cycling to expiration. PSV is effective phase to a set lower pressure. Whereas conventional modes of
at decreasing patient effort and work of breathing.31–33 Data suggest mechanical ventilation elevate airway pressure up from a set baseline
that most clinicians view PSV as a weaning mode of mechanical to accomplish tidal ventilation, APRV uses very high I:E ratios to
ventilation, despite its being fully capable of appropriate full support maintain mean airway pressure and brief deflations to accomplish
in patients with respiratory failure and intact respiratory drive.34 ventilation. When APRV is used in ARDS (primary use) short
time low (Tlow) is used, whereas this mode can be used in patients
without ARDS with longer Tlow and is often called “bilevel positive
Dual Control Modes airway pressure” in that circumstance (Fig. 9.7). The expiratory
The preceding modes of mechanical ventilation are classically referred valve in APRV also facilitates spontaneous breathing throughout
to as “conventional” ventilator modes, which is purely arbitrary. the ventilatory cycle, facilitating ventilation. Because this mode is
Dual control modes of ventilation manipulate pressure or volume primarily used with ARDS with long time high (Thigh) and very
on either a breath-to-breath basis or within the same breath. short time low (Tlow), breathing occurs primarily during Thigh.
Breath-to-breath modes include volume support (VS) and pressure- Pressure high (Phigh) is the baseline airway pressure that occupies
regulated volume control (PRVC), also called “pressure control most of the ventilatory cycle. Pressure low (Plow) is the release
volume guarantee.” VS is PSV (pressure limited, flow cycled) that pressure and is set at 0 cm H2O. Thigh is the length of time for
uses VT as a feedback to adjust the pressure support level.16 PRVC which Phigh is maintained, and Tlow is the length of time for which
is pressure control ventilation (pressure limited, time cycled), but Plow is maintained. This is primarily semantics, but the term APRV
uses VT as a conditional variable to adjust pressure to achieve implies longer I:E ratios than bilevel positive airway pressure, and
desired VT. Proportional assist ventilation (PAV) measures patient a Plow setting of 0 at all times.
inspiratory demand while calculating compliance and resistance Although outcome data are lacking compared with conventional
to offload inspiratory muscles in proportion and in synchrony ventilation using protective lung strategies, the reported advantages
with patient effort.35 When compared to PSV it has been shown of APRV include sustained alveolar recruitment with improved
in one study to be associated with less dyschromy.36 oxygenation, higher mean airway pressures accomplished with

Phigh
Pressure

Plow
Thigh
Tlow
A APRV with pressure-supported breaths

Phigh
Pressure

Plow
Thigh
Tlow

B BiPAP with pressure-supported breaths

• Fig. 9.7  Pressure-time waveforms showing the use of airway pressure release ventilation (APRV). A,
APRV as used in ARDS with pressure-supported breaths taken on Thigh only and short Tlow (dump time)
to allow CO2 removal and PEEP setting. B, A variant of APRV often called bilevel positive airway pressure
with longer Tlow and pressure-supported breaths allowed on both Thigh and Tlow. Phigh, Pressure high; Plow,
pressure low; Thigh, time high; Tlow, time low.

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 138 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

lower Ppeak and Ppl, spontaneous breathing throughout the ventilatory frequencies, higher VTs and bulk flow can be achieved, which
cycle, and decreased use of sedation and neuromuscular blockade assists in ventilation (and may contribute to VILI). The percentage
in severe ARDS.39 The maintenance of spontaneous breathing may of I time is set at 33% or 50%, depending on ventilation goals.
improve V̇ /Q̇ matching by preferential ventilation of dependent This effect would be predicted to be most beneficial when applied
lung regions, and the higher mean airway pressure, relative to Ppeak early in the course of severe ARDS.44,46 Clinical trials of the
and Ppl, may limit VILI. comparison of HFOV with ARDS net setting standard ventilation
Alveolar recruitment is a pan-inspiratory phenomenon and in patients at the onset of moderate or severe ARDS showed no
alveoli that are recruited are more compliant than recruiting or benefit of HFOV, and one of the two trials showed an increased
nonrecruited alveoli. With prolonged elevated pressures, APRV mortality rate in the HFOV arm.46,47 This would imply consideration
likely recruits alveoli, which require a longer inflation with higher of HFOV use only as salvage therapy in ARDS. The clinician
threshold opening pressures.38,39 Sustained inflation maintains should note that patients ventilated with HFOV require heavy
recruitment, decreases shunt and dead space, and uses the more sedation or neuromuscular blockade.
compliant expiratory limb of the pressure-volume (PV) curve.
Ventilation is determined by the stored kinetic energy at the high Effort-Adapted Modes of Mechanical Ventilation
pressure, the intermittent release phase, and is augmented by
spontaneous breathing. Although minute ventilation is decreased Early mechanical ventilators, such as the CMV mode setting,
with this mode of ventilation, ventilation is also improved by a performed work on the patient and adapted the patient to the
decrease in dead space. ventilator, with complete ventilator and physician control over
Clinical data are limited but have shown improved oxygenation, breath characteristics and delivery. Although this can achieve
less shunt and dead space, as well as decreased need for sedation adequate oxygenation and ventilation, it can come at a great expense
and neuromuscular blockade.39–43 Data on clinically relevant to the patient, with side effects including dyssynchrony, increased
outcomes, such as mortality rates, mechanical ventilation days, work of breathing, respiratory muscle weakness, and increased
and intensive care unit (ICU) days, are limited. This mode remains use of sedative infusions. Advances in ventilator technology
physiologically attractive for its effects on oxygenation and potential and increased recognition of the side effects of mechanical ventilation
to limit VILI, but no specific recommendations can be made given have led to an increased awareness to adapt the ventilator to the
the lack of good outcome data. patient, using the patient’s physiology and demand to assist
the respiratory muscles in proportion to effort and need.
These effort-adapted modes of mechanical ventilation include PAV,
High-Frequency Oscillatory Ventilation neurally adjusted ventilatory assist (NAVA), and adaptive support
High-frequency oscillatory ventilation (HFOV) is very different ventilation (ASV).
from conventional bulk flow ventilation and uses respiratory frequen- PAV is a mode of partial support in which ventilator assist is
cies much higher and VTs much lower than conventional modes. delivered in proportion to patient effort. A defined level of assist,
It is similar to APRV in that it aims to elevate mean airway pressure or unloading, relieves the resistive and elastic burden of the respira-
to maximize recruitment and oxygenation while limiting Ppeak.44 tory system.48,49 The ventilator responds to the mechanical output
Oxygenated, humidified gas (bias flow) passes in front of an oscil- of the patient and will amplify patient effort with a preset pro-
lating membrane and generates very small V Ts at very high portional amount of pressure support. The theory behind PAV is
respiratory rates. This is actively driven by a piston pump that based on the equation of motion; based on changes in flow and
oscillates the diaphragm. This produces sinusoidal or somewhat volume, flow-proportional and volume-proportional pressure support
erratic pressure waves that are actively driven in both inspiration is given. A percentage of effort is set by the clinician, and applied
and expiration (unique in that expiration is not passively driven airway pressure develops as a function of volume to overcome
by elastic recoil). This component is created by the backward elastance or a function of flow to overcome resistance.48 Reported
movement of the diaphragm or piston of the oscillator. Resistance benefits of PAV include improved synchrony, better physiologic
valves are used to apply a constant distending airway pressure, breathing pattern, and improved sleep quality.50–56 A limitation of
over which small VTs are superimposed at a high respiratory PAV is that it relies on the mechanical output from the patient;
frequency; in this fashion, it uncouples, for the most part, oxy- therefore continuous knowledge of the elastic and restrictive
genation and ventilation. properties of the patient is a necessity. If PAV incorrectly estimates
Given the fact the VT is often less than anatomic dead space, the mechanical properties, the ventilator may overassist, causing
HFOV relies on gas transport mechanisms much different from delayed inspiratory ending (“runaway phenomenon”). This problem
those used by bulk flow ventilation. These mechanisms include has been improved by the development of PAV+ (PAV with load
some convective gas transport, but also molecular diffusion, adjustable gain).
pendelluft, coaxial flow, and Taylor dispersion.45 NAVA is similar to PAV in that it is also an effort-adapted
When initiating HFOV, the patient’s ET should be verified to mode of partial assist. Unlike PAV, which responds to the mechanical
be patent, as heavy secretions or kinks in the ET will significantly output from the patient, NAVA responds to the neural input from
harm ventilation. The mean airway pressure should be set at about the electrical activity of the diaphragm (Edi). Pressure is applied
5 cm H2O higher than that achieved with conventional settings. in a linear proportion to Edi, and this requires the placement of
The bias flow delivers fresh gas into the ventilator circuit at 40 to an esophageal electrode (similar to nasogastric tube placement).
60 L/min and helps maintain mean airway pressure.45 The power The ventilator is triggered based on Edi or conventional signals
control allows adjustment of amplitude (Δpressure), which is set (whichever comes first), therefore improving synchrony, as the
high enough to elicit vibrations of the patient to the lower abdomen time delay from patient effort to breathe is very brief. In addition,
or midthigh. Frequency helps determine ventilation and is set the amount of ventilator assistance varies based on Edi. As such,
typically at 3 to 5 Hz. It should be noted, however, that at low to achieve greater assistance, the patient must increase Edi. Reported

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 CHAPTER 9  General Principles of Mechanical Ventilation 139

benefits include improved synchrony57–61 and preserved variability PEEP is not without side effects. Given the heterogeneous
in breathing pattern.48,62,63 High NAVA levels and high Edi may distribution of lung injury in ARDS, PEEP can overdistend more
result in high inspiratory pressures and VT delivery, especially in compliant lung units, contributing to VILI.68 If PEEP leads to
patients with unstable respiratory patterns or high respiratory overdistention, it can augment dead space, increase pulmonary
drive.64,65 vascular resistance, and cause right-sided heart dysfunction. It can
ASV ensures a set target minute ventilation based on measure- also decrease venous return and, in the setting of volume depletion,
ments of the patient’s E time constant and dynamic compliance, decrease cardiac output.
along with preset information of predicted body weight, minimum The optimal way to set PEEP is debated and controversial, as
minute volume limit, and a pressure limit.48 The ventilator attempts is the optimal level of PEEP to use.69–84 See Chapter 11 for a
to minimize the work of breathing by combining the most effective detailed discussion of PEEP application in ARDS.
combination of rate and VT, while limiting pressure support. ASV
potential benefits include decreased work of breathing and improved
patient-ventilator interaction. Monitoring the Ventilated Patient
Effort-adapted modes of ventilator assist are physiologically Hemodynamics
attractive, especially considering that most conventional modes of
mechanical ventilation are decades old. The decision to use these Positive-pressure ventilation causes predictable physiologic changes
modes should be tailored to the individual patient. Patients with and cardiopulmonary function is intimately linked—respiratory
a high amount of dyssynchronous breaths and iPEEP secondary function alters cardiovascular function and vice versa.85,86 The venous
to obstructive physiology may benefit from a switch to these modes. system is a low-pressure reservoir that contains about three-fourths
They do not, however, ameliorate iPEEP, and extrinsic PEEP should of our total blood volume.85,87 This can be divided into the stressed
be delivered appropriately. In patients who are severely hypoxemic and unstressed volume. The stressed volume contributes to the return
or hemodynamically unstable, these modes should likely be avoided. of blood to the heart. The right ventricle’s main function is to accept
All require an intact ventilator drive, and ongoing assessments of venous return and eject the optimal amount of blood into a (usually)
pulmonary mechanics are a necessity. Finally, the clinician must highly compliant pulmonary vascular system.86–89 This maintains a
give up a significant amount of control with these modes of ventila- low right atrial pressure, thereby maximizing venous return and
tion (which may be unappealing to some practitioners), and outcome overall myocardial performance. A positive-pressure breath increases
data are currently lacking. lung volume and increases intrathoracic pressure, which increases
juxtacardiac pressure and therefore right atrial pressure. This can
Positive End-Expiratory Pressure decrease venous return and therefore left ventricular preload several
cardiac cycles later. At the same time, positive-pressure ventilation
CPAP maintains airway pressure above atmospheric pressure decreases left ventricular afterload by increasing the juxtacardiac
throughout the respiratory cycle by pressurization of the ventilator pressure, therefore assisting ventricular contraction.
circuit. In mechanically ventilated patients, the purpose of CPAP With respect to the mechanical ventilator, arterial blood pressure
is to achieve therapeutic PEEP in the presence of ARDS or pulmonary monitoring is commonplace in all ICUs. Although noninvasive
edema (Fig. 9.8). In these patients PEEP restores functional residual cuff measurements can be adequate, invasive, continuous monitoring
capacity, reduces IP shunt, shifts ventilation to a more compliant is much more informative when ventilator settings are dynamically
portion of the PV curve, and prevents end-expiratory volume loss changing. A fall in blood pressure temporally related to a ventilator
(derecruitment).66 PEEP recruits previously nonaerated lung tissue change is a fairly specific indicator of a drop in cardiac output.87
and homogenizes regional distribution of tidal ventilation. The net A narrow pulse pressure may indicate relative hypovolemia, although
effect on gas exchange reflects the balance between recruitment and a widened pulse pressure may point to vasodilation or regurgitant
overdistention. In the setting of obstructive physiology or expiratory cardiac valve disease. Pulse pressure variation (secondary to previ-
flow limitation, PEEP serves less to improve oxygenation but more ously described heart-lung interactions) in mechanically ventilated
to improve patient-ventilator synchrony and triggering.27,28,67 patients is also the most accurate predictor of determining preload
responsiveness.90 Central venous pressure (CVP) is a reflection of
CPAP Mode right atrial pressure and normally is low to maximize venous return.
Despite the commonality of its use in determining volume status
Airway pressure (cm H2O) and preload responsiveness, data and physiology have shown that
to be inaccurate.91 This does not indicate that the measurement
of CVP is not of value. The absolute value and morphologic
appearance (e.g., large v wave) of the CVP tracing can serve as
valuable surrogates for right ventricular function, and an inspiratory
fall in CVP can indicate preload responsiveness.92 There are multiple
0 other hemodynamic variables that could be measured in the
Time mechanically ventilated patient, such as pulmonary artery occlusion
0 = Ambient pressure pressure and mixed venous oxygenation, and these should be based
• Fig. 9.8A pressure-time waveform in a patient with continuous positive
 
on individual patient characteristics.
airway pressure (CPAP) without application of pressure support ventilation
is demonstrated. The patient is breathing spontaneously at an elevated Pulse Oximetry
baseline system pressure. With initiation of inspiration (arrows), pressure
becomes more negative (but remains positive), and with expiration, pres- Pulse oximeters determine oxygen saturation by determining arterial
sure becomes more positive. blood light absorption at 660-nm and 940-nm wavelengths. The

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 140 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

ratio of absorption of these two wavelengths is then calibrated

against computer-stored algorithms to determine the oxygen satura- Maintaining Support of
tion. Pulse oximeters are quite accurate at their upper range but
lose accuracy at lower oxygen saturations, require a good pulsatile the Ventilated Patient
signal, and have other limitations. These limitations include Sedation and Analgesia
hypoperfusion, motion artifact, dyshemoglobinemias, ambient
light, certain intravenous dyes, and deeply pigmented skin. Pulse Critically ill patients who are mechanically ventilated often require
oximetry is virtually ubiquitous in the ICU. Its use includes detec- sedative and analgesic drugs, and pain is common among ICU
tion of hypoxemia, monitoring response to ventilator changes (such patients.103 The ideal sedative and analgesic regimen would provide
as PEEP setting), weaning fraction of inspired oxygen (FIO2), and adequate sedation and pain control, rapid onset of action, rapid
as a surrogate for pulmonary gas exchange.93 recovery after discontinuation, minimal systemic accumulation,
and minimal adverse effects—without raising health care costs.104
The primary aim of these medications is to reduce the physiologic
End-Tidal Capnography stress of respiratory failure and to improve the tolerance of mechani-
End-tidal capnography (ETCO2) is a useful way to monitor the cal ventilation. As more patients survive acute illness, the importance
concentration of exhaled carbon dioxide (CO2), plotting it against of goal-oriented sedation and analgesia has emerged, and the deleteri-
time. A normal capnogram consists of a low value at baseline ous side effects of these medications are evident.105
during inspiration and while emptying CO2-free dead space. This Historically, mechanically ventilated patients have been treated
is followed by a steep increase as alveolar units empty CO2, with continuous infusions of benzodiazepines, opiates, and
and this increases progressively until a plateau is reached. A normal propofol.106–108 Unfortunately, emerging data point to increased
value (e.g., when ventilation and perfusion are matched) is side effects associated with these medications, such as delirium,
about 5 mm Hg less than the PaCO2, and a normal shape consists increased mechanical ventilation days, increased lengths of hospital
of a low baseline, steep ascending portion, plateau, and steep stay, and higher mortality rate.105,109,110 This has prompted interest
decline. The ETCO2/PaCO2 gap can widen in patients with altered in novel regimens with agents such as dexmedetomidine, an α2-
V̇ /Q̇ relationships or changes in cardiac output; the morphologic agonist with sedative and analgesic properties. Data have shown
pattern of the waveform can be altered in patients with endobron- that dexmedetomidine use is associated with a reduction in delirium,
chial intubation, expiratory flow limitation, and ventilator improved cognitive function, and a decrease in mechanical ventila-
dyssynchrony. tion days.111–115
Regardless of the sedation regimen chosen, the mechanically
ventilated patient should have sedation and analgesia titrated to
Transcutaneous Carbon Dioxide Monitoring a validated scale, such as the Richmond Agitation-Sedation Scale,
Transcutaneous carbon dioxide (PtCO2) monitoring allows non- and delirium should be monitored at least daily, also with a validated
invasive and continuous approximation of PaCO2. This technique scale (Confusion Assessment Method-Intensive Care Unit). All
was described by Severinghaus in 1960. Pt CO2 monitoring patients should be assessed daily for readiness to be liberated from
uses disposable skin electrodes.94,95 Measurement of PtCO2 has the ventilator (spontaneous awakening trial [SAT]), and this should
been examined in patients with acute and chronic respiratory be paired with a spontaneous breathing trial (SBT).
failure and as a monitoring tool. In these studies, PtCO2 monitoring
shows a good correlation with PaCO2.96–99 Some studies support Positioning
PtCO2 as superior to ETCO2 monitoring in terms of reflecting
PaCO2.100,101 There is no optimal position for an individual patient and certainly
Limitations of the measurement for approximating PaCO2 include no evidence-based gold standard. Predictable physiologic changes
frequency of the need for recalibrations, time needed to achieve occur in patients when placed in the supine position, including
skin warming, accuracy of measurements with thick skin, and the reduced functional residual capacity, alteration in pleural pressure,
need for adequate tissue perfusion.102 reduced lung compliance, and change in V̇ /Q̇ matching. The supine
position should be avoided, as it is a risk factor for VAP.116,117 In
patients with unilateral lung injury, the “good side” should be
Ventilator Waveforms placed in the dependent position to optimize V̇ /Q̇ match. Patients
Modern ventilators allow continuous monitoring of pressure, volume, with severe hypoxemia (PaO2:FIO2 ratio <100) should be considered
and flow waveforms, all of which are plotted against time. They for prone positioning early in the course of ARDS, as this will
are useful in readily identifying the mode of mechanical ventilation likely improve oxygenation and may offer survival benefit in this
being used, as well as identifying physiologic abnormalities. Examina- patient cohort.118
tion of the flow waveform can allow detection of iPEEP. A ripple-like
waveform can indicate water or secretion buildup in the ventilator Secretion Clearance
circuit. A prolonged expiratory flow pattern can indicate expiratory
flow limitation. The pressure waveform allows calculation of compli- Secretion clearance is impaired in the mechanically ventilated patient
ance of the respiratory system, and an estimation of transalveolar owing to decreased mucociliary activity and inability to cough
pressure with an end-inspiratory hold maneuver to calculate plateau effectively. Removal of oral and tracheobronchial secretions is
pressure. An initial overshoot in the pressure waveform may signal commonplace and standard care of the mechanically ventilated
high patient effort or an overshoot on ramp speed. An upward patient. Because of insufficient data and complications, scheduled
inflection at the end of the pressure waveform could signal overdisten- and routine suctioning should be avoided, but the decision is based
tion, and a dip in an otherwise square pressure waveform can signal on patient assessment. The use of closed-circuit catheters is now
patient effort and dyssynchrony. commonplace, but data are conflicting with regard to patient benefit

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 CHAPTER 9  General Principles of Mechanical Ventilation 141

when compared to open-circuit catheters. Before the suctioning secretions). The ability to predict successful extubation is challenging,
procedure, the caregiver should be aware of the potential for and if the clinician never experiences a reintubation, he or she is
complications, such as hypoxia, airway trauma, and cardiac likely not extubating patients based on the best available
arrhythmias. evidence.

Early Physical Therapy in Acute Complications of Mechanical Ventilation

Respiratory Failure
Hemodynamics
Although overall evidence is limited and controversial, a recent clinical
practice guideline “suggests” protocolized rehabilitation directed Blood pressure (BP) is simply the product of cardiac output (CO)
toward early mobilization for patients with acute respiratory failure and systemic vascular resistance (SVR; BP = CO × SVR). Although
and mechanical ventilation for greater than 24 hours.35,119 It notes the transition of positive-pressure ventilation is associated with a
early physical therapy beneficial effects on duration of mechanical predictable set of physiologic responses, the overall hemodynamic
ventilation and ability to walk at discharge. These are mixed findings response is largely a consequence of underlying patient comorbid
with regard to improvement in functional performance in various conditions (such as left ventricular dysfunction) and preload status.
studies, and studies have not been able to demonstrate shortened Immediately after endotracheal intubation, worsening hemodynam-
mechanical ventilation, ICU stay, or hospital stay.36,120 Early physical ics are usually secondary to a decrease in preload, as right atrial
therapy is likely beneficial for select patients. Studies that inform pressure will increase, or a drop in arteriolar tone from sedation
on patient selection and dose of therapy are needed. and analgesia. Any change in hemodynamics in the mechanically
ventilated patient should prompt a thorough and almost algorithmic
Weaning From Mechanical Ventilation evaluation for potential causes.

The five essential steps that facilitate achieving ventilation inde- Ventilator-Induced Lung Injury
pendence are (1) preparation (such as cardiovascular status, fluid
balance), (2) evaluation (such as spontaneous breathing trial), (3) Mechanical ventilation can be a lifesaving intervention. However,
withdrawal of ventilation support, (4) extraction of ET, and (5) it has great potential for harm, and the clinician’s focus should
peri-extubation care.121 (A more extensive discussion of weaning extend beyond normalization of gas exchange to providing safe
is found in Chapter 14). and physiologically sound mechanical ventilation. Perhaps nowhere
Shortly after a patient is endotracheally intubated to initiate is this demonstrated more significantly than with the concept of
mechanical ventilation, thoughts should turn toward liberation VILI. Most patients with ARDS do not die of hypoxia, but rather
from the ventilator. The withdrawal of mechanical support is a multiple organ dysfunction syndrome.132–135 Applied airway pressures
continuum from intubation until hospital discharge.122,123 Depending in patients with ARDS distribute in a heterogeneous fashion, leaving
on severity of illness, patient comorbid conditions, and critical more compliant lung units overdistended and others collapsed and
care treatments needed, the timing of this may range from hours nonrecruited. Respiratory system compliance is related to the
to weeks or months. There are several evidence-based guiding amount of normally aerated lung tissue that remains, the so-called
principles that shorten mechanical ventilation days across a broad baby lung.136 This heterogeneity leads to a maldistribution of
cohort of critically ill patients. ventilation, with some alveoli overdistended, others collapsed
A key component in liberation from the ventilator is the targeted throughout the respiratory cycle, and others cyclically opening
use of sedation, limitation of sedative and opioid infusions, and and closing. VILI is a spectrum, classically defined as barotrauma,
the monitoring for and aggressive treatment of delirium.105 Patients atelectrauma, and volutrauma (stretch injury).137 All of these can
should also undergo daily interruption of sedative medications lead to biotrauma, or the decompartmentalization of the inflam-
(SAT), which has been shown to decrease ventilator days and ICU matory response secondary to increased alveolar epithelial-capillary
length of stay.124 After awakening, the patient should be assessed endothelial permeability. This results in the release of biologic
for readiness to wean. The literature abounds with weaning predic- inflammatory mediators and the spread of injury to distant organs,
tors, all of which have modest sensitivity and specificity, including causing multiple organ dysfunction syndrome and death. VILI is
the frequency/VT ratio.123 Given this, as opposed to weaning much more complex than the preceding definitions and involves
predictors, the patient should undergo an SBT based on common tissue stress and strain modifiers, complex molecular mechanisms,
sense, overall clinical trajectory, lack of hypoxia, and hemodynamic as well as gene activation and upregulation.138,139
stability. The SAT should be paired with an SBT, as the SAT-SBT Human studies support the concept of VILI and the importance
pairing decreases ventilator days, shortens ICU and hospital length of a protective ventilation strategy with low VTs and the use of
of stay, and improves mortality rate.125 An SBT can be conducted PEEP. Low VT ventilation is the only intervention shown to
unassisted through a T-piece, on low-level PSV or on CPAP, once consistently improve outcome in ARDS, and support for protective
or multiple times a day and from 30 to 120 minutes; SIMV lung ventilation to decrease VILI from several well-conducted
weaning is not recommended.126–131 If a patient has an unsuccessful clinical trials exists.73,74,140 This includes data showing a decrease
SBT, a reason for that failure should be sought and corrected. This in inflammatory mediators in patients ventilated with a protective
could include sedation, weakness, delirium, respiratory muscle lung strategy. In the absence of a patient-specific factor to suggest
fatigue, or left ventricular dysfunction. Also, afterward the ET otherwise, a protective ventilation strategy, consisting of low VT
should be placed immediately on comfortable full mechanical ventilation, PEEP setting, and limitation of plateau pressure, should
support, as delaying this and prolonging the SBT to the point of be attempted at all times. Emerging data suggest that these strategies
respiratory muscle exhaustion can delay extubation. After a successful should be used not only in patients with ARDS, but in all patients
SBT, the patient should be extubated unless a reason exists to leave receiving mechanical ventilation, especially those with known risk
the ET in place (e.g., no cough reflex and heavy pulmonary factors for the development of ARDS.141

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 142 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

Spontaneous breathing during mechanical ventilation may lead develops have worse clinical outcomes, including prolonged
to improved oxygenation through better aeration and ventilation- mechanical ventilation.167 Furthermore, VTE is common and
perfusion matching, reduced need for sedation, and a smaller risk frequently asymptomatic in mechanically ventilated patients. Given
of diaphragm deconditioning.35 However, it also potentially increases the adverse clinical outcomes associated with VTE, thrombopro-
transpulmonary pressure and risk for ventilation-associated lung phylaxis with low–molecular-weight heparin or unfractionated
overinflation injury.35 It may displace gas from nondependent heparin, both administered subcutaneously, should be given unless
more-recruited areas to dependent less-recruited areas, the so-called contraindicated.168–170
pendelluft effect. With strong diaphragm contractions during early
inspiration spontaneous breathing may lead to regional overinflation Noninvasive Positive-Pressure Ventilation
and ventilation induced lung injury. Properly applied higher PEEP
may decrease this pendelluft effect.142 Noninvasive positive-pressure ventilation (NIPPV) offers the
potential to provide ventilatory assistance without an invasive
artificial airway. NIPPV may be accomplished using a face mask
Ventilator-Associated Events or nasal mask fitted to the face and connected through standard
Diagnosis of VAP has been a controversial issue in the critical care ventilator tubing to either a standard mechanical ventilator or
setting. Problematic is that clinical findings for VAP are subjective smaller ventilators made specifically to deliver noninvasive mechani-
and nonspecific. In 2013, the Centers for Disease Control and cal ventilation.
Prevention published a new algorithm for surveillance of what are In patients with COPD and type II respiratory failure, NIPPV
called ventilator-associated events (VAEs).143–145 reduces dyspnea, decreases intubation rates, and improves mortality
The new three-tier algorithm defines associated events as a rates.171–173 Similarly, in patients with cardiogenic pulmonary edema,
significant and sustained worsening in oxygenation variables after NIPPV decreases intubation rates and improves survival. 173,174
an initial period of stabilization or improvement. This deterioration NIPPV may also serve a critical role in decreasing mechanical
in oxygenation can occur from infectious and noninfectious ventilation days and improving weaning success, especially in
conditions. patients with COPD recovering from type II respiratory failure.175,176
This three-tier definition is as follows: Finally, immunocompromised patients, especially those with
1. Tier 1: Ventilator-associated condition (VAC) defined as new hematologic malignancies, should be considered for NIPPV.177
respiratory deterioration. Before initiation of NIPPV, the patient should be assessed for an
2. Tier 2: Infection-related ventilator-associated complication adequate mental status for airway protection, hemodynamic stability,
(IVAC) defined as VAC − clinical signs of infection. and lack of excessive secretions. (See a more detailed discussion
3. Tier 3: Possible or probable VAP defined as IVAC + evidence of NIPPV in Chapters 36 and 38.)
of pulmonary infection.
Patients with VAEs have a high morbidity and mortality rate High-Flow Nasal Cannula: A Potential
compared with patients without VAEs.146,147 Avoiding intubation,
minimizing the duration of mechanical ventilation, and targeting Alternative to Mechanical Ventilation
the specific causes of VAEs are three important approaches to High-flow nasal cannula (HFNC) oxygen therapy is a noninvasive
improve outcome in critically ill patients.148 respiratory support system that delivers heated and humidified
One of the most frequent complications of mechanical ventilation high-flow oxygen via special nasal prongs at a rate of up to 60 L/
is the development of VAP.149–160 VAP is discussed in Chapter 40. min as the FIO2 is set from 0.21 to 1.0.178
HFNC oxygen therapy is considered to have multiple physiologic
effects other than providing a high FIO2, including (1) washout
Gastrointestinal Bleeding of nasopharyngeal space CO2 to reduce the anatomic dead space,
Mechanical ventilation is a risk factor for gastrointestinal bleeding (2) a therapeutic PEEP effect, (3) constant FIO2 without intubation
secondary to stress ulceration, trauma (especially traumatic brain or noninvasive ventilation by mask, and (4) humidification of
injury), and major burns. Mechanical ventilation for longer than inspired gas. Results of these physiologic effects of HFNC reduce
48 hours is regarded as the most frequent risk factor.161 The most the work of breathing.179–183
effective treatment of stress ulceration is prevention. H2-receptor In patients with acute hypoxemic respiratory failure, HFNC
antagonists and proton pump inhibitors have been shown to reduce offers patient tolerance and comfort and has been associated with
the incidence of clinically important bleeding compared with sucralfate improved oxygenation, reduced need for intubation, decreased
and are considered the first-line therapy among many clinicians.162–166 respiratory rate, decreased work of breathing, and decreased
mortality.184–191 Also, in immunocompromised patients with acute
respiratory failure one study showed that patients treated with
Venous Thromboembolism HFNC had lower intubation and mortality rates than noninvasive
Venous thromboembolism (VTE) refers to the development mechanical ventilation.192
of deep venous thrombosis or pulmonary embolism in the HFNC oxygen therapy has potential value in postextubation
critically ill patient. Patients in whom deep venous thrombosis respiratory failure but remains controversial.193,194

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 CHAPTER 9  General Principles of Mechanical Ventilation 143

Key Points
• Consideration of patient trajectory, individual physiology, timing • With SIMV, the ventilator delivers a mandatory number of
of therapy, and severity of illness will make tailoring the ventilator breaths with a set pressure or flow (assisted or unassisted), similar
prescription most effective. to AC ventilation. However, spontaneous breaths are delivered
• High-pressure alarms are triggered by patient factors (such as upon patient triggering during a timing window created around
decreased compliance and increased resistance of the respiratory the delivery of mandatory breaths. These spontaneous breaths
system) or by ventilator circuit malfunction (obstruction or can be totally driven by patient effort or pressure enhanced as
kinking of the ET). pressure-controlled/flow-cycled (PS) breaths.
• Low-pressure alarms are generally secondary to a leak in the • Although outcome data are lacking compared with conventional
system (ventilator circuit, ET or cuff) or patient (large pressure ventilation using protective lung strategies, the reported advan-
loss from a bronchopleural fistula). tages of APRV include sustained alveolar recruitment with
• Closed-loop control of calculated tracheal pressure, as seen with improved oxygenation, higher mean airway pressures accom-
ATC, allows compensation for ET resistance. plished with lower Ppeak and Ppl, spontaneous breathing
• The breath generated by a mechanical ventilator can be separated throughout the ventilatory cycle, and decreased use of sedation
into four phases: triggering, inspiration, cycling, and expiration. and neuromuscular blockade in severe ARDS.
• With pressure control and pressure support breaths the pattern • PAV is a mode of partial support in which ventilator assist is
of inspiratory flow is a natural decelerating pattern as the pressure delivered in proportion to patient effort.
gradient for flow decreases as pressure rises in the patient’s lungs. • NAVA is similar to PAV in that it is also an effort-adapted
• In AC ventilation, a mandatory number of breaths are set and mode of partial assist. Unlike PAV, which responds to the
delivered with a set pressure or flow (assisted or unassisted), mechanical output from the patient, NAVA responds to the
and if the patient’s respiratory rate is higher than this backup neural input from the Edi. Pressure is applied in a linear propor-
setting (rate), additional assisted breaths to the preset pressure tion to Edi, and this requires the placement of an esophageal
or flow are delivered. The target variable can be pressure (PC/ electrode (similar to nasogastric tube placement).
AC) or volume (VC/AC).

Selected References Marini JJ. Unproven clinical evidence in mechanical ventilation. Curr
Opin Crit Care. 2012;18:1–7.
Bellani F, Laffey JG, Pham T, et al. Noninvasive ventilation of patients Morris PE, Berry MJ, Files DC, et al. Standardized rehabilitation and
with acute respiratory distress syndrome: insights from the LUNG hospital length of stay among patients with acute respiratory failure;
SAFE Study. Am J Respir Crit Care Med. 2017;195:67–77. a randomized clinical trial. JAMA. 2016;315:2694–2702.
Bosama KJ, Read BA, Bahrgard Nikoo MJ, et al. A pilot randomized Papazian L, Corley A, Hess D, et al. Use of high-flow nasal cannula
trial comparing weaning from mechanical ventilation on pressure oxygenation in ICU adults: a narrative review. Intensive Care Med.
support versus proportional assist ventilation. Crit Care Med. 2016;42:1336–1349.
2016;44:1098–1108. Pettenuzzo T, Fan E. 2016 year in review: mechanical ventilation. Respir
Dellaca’ RL, Veneroni C, Farre R. Trends in mechanical ventilation: are Care. 2017;62:629–635.
we ventilating our patients in the best possible way? Breathe (Sheff). Raoof S, Baumann MH, Critical Care Societies, et al. Ventilator-associated
2017;13:85–98. events: the new definition. Am J Crit Care. 2014;23:7–9.
Holets SR, Marini JJ. Is Automated weaning superior to manual spontane- The complete list of references can be found at www.expertconsult.com.
ous breathing trials? Respir Care. 2016;61:749–760.
Magill SS, Klompas M, Balk R, et al. Developing a new, national approach
to surveillance for ventilator-associated events. Crit Care Med.
2013;41:2467–2475.

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 CHAPTER 9  General Principles of Mechanical Ventilation
143.e1

References 24. Fabry B, Guttmann J, Eberhard L, et al. An analysis of desyn-

chronization between the spontaneously breathing patient and
1. Marini JJ. Unproven clinical evidence in mechanical ventilation. ventilator during inspiratory pressure support. Chest. 1995;107(5):
Curr Opin Crit Care. 2012;18(1):1. 1387–1394.
2. Dellaca RL, Veneroni C, Farre R. Trends in mechanical ventilation: 25. Tutuncu AS, Cakar N, Camci E, et al. Comparison of pressure and
are we ventilating our patients in the best possible way? Breathe. flow-triggered pressure-support ventilation on weaning parameters
2017;13(2):85–98. in patients recovering from acute respiratory failure. Crit Care Med.
3. Morch E. History of mechanical ventilation. In: Kirby RR, Smith 1997;25(5):756.
RA, Desautels DA, eds. Mechanical Ventilation. New York: Churchill 26. Branson RD, Campbell RS, Davis K Jr, et al. Comparison of
Livingstone; 1985. pressure and flow triggering systems during continuous positive
4. Fell G. Forced respiration in opium poisoning—its possibilities, airway pressure. Chest. 1994;106(2):540–544.
and the apparatus best adapted to produce it. Buffalo Med Surg J. 27. Marini JJ. Ventilatory management of obstructive airway disease.
1887;145–157. In: Parrillo JE, Dellinger RP, eds. Critical Care Medicine Principles
5. Dräger H. Das Werden des Pulmotors. Drägerhefte. 1917;57/58: of Diagnosis and Management in the Adult. 3rd ed. Philadelphia:
495–496. Mosby Elsevier; 2008:177–190.
6. Linton D. Cuirass ventilation: a review and update. Crit Care 28. MacIntyre NR. Management of obstructive airway disease. In:
Resuscitation. 2005;7:22–28. MacIntyre NR, Branson RD, eds. Mechanical Ventilation. 2nd ed.
7. Kotur P. Mechanical ventilation—past, present, and future. Indian St. Louis: Elsevier; 2009:297–305.
J Anaesth. 2004;48(6):430–432. 29. Davis K, Branson RD, Campbell RS, et al. Comparison of volume
8. Chatburn R, Branson RD. Classification of mechanical ventilators. control and pressure control ventilation: is flow waveform the
In: MacIntyre NR, Branson RD, eds. Mechanical Ventilation. 2nd difference? J Trauma. 1996;41(5):808.
ed. St. Louis: Elsevier; 2009:1–48. 30. Dellinger RP, Jean S, Cinel I, et al. Regional distribution of
9. MacIntyre NR. Respiratory system mechanics. In: MacIntyre NR, acoustic-based lung vibration as a function of mechanical ventilation
Branson RD, eds. Mechanical Ventilation. 2nd ed. St. Louis: Elsevier; mode. Crit Care. 2007;11(1):R26.
2009:159–170. 31. Brochard L, Harf A, Lorino H, et al. Inspiratory pressure support
10. Lucangelo U, Bernabe F, Blanch L. Lung mechanics at the bedside: prevents diaphragmatic fatigue during weaning from mechanical
make it simple. Curr Opin Crit Care. 2007;13(1):64. ventilation. Am J Respir Crit Care Med. 1989;139(2):513–521.
11. Branson RD. The patient-ventilator interface: ventilator circuit, 32. Tokioka H, Saito S, Kosaka F. Effect of pressure support ventilation
airway care, and suctioning. In: MacIntyre NR, Branson RD, on breathing patterns and respiratory work. Intensive Care Med.
eds. Mechanical Ventilation. 2nd ed. St. Louis: Elsevier; 2009: 1989;15(8):491–494.
89–110. 33. Van de Graaff W, Gordey K, Dornseif S, et al. Pressure support.
12. Boots RJ, Howe S, George N, et al. Clinical utility of hygroscopic Changes in ventilatory pattern and components of the work of
heat and moisture exchangers in intensive care patients. Crit Care breathing. Chest. 1991;100(4):1082–1089.
Med. 1997;25(10):1707. 34. Esteban A, Anzueto A, Frutos F, et al. Characteristics and out-
13. Kirton OC, DeHaven B, Morgan J, et al. A prospective, randomized comes in adult patients receiving mechanical ventilation. JAMA.
comparison of an in-line heat moisture exchange filter and heated 2002;287(3):345–355.
wire humidifiers. Chest. 1997;112(4):1055–1059. 35. Pettenuzzo T, Fan E. 2016 year in review: mechanical ventilation.
14. Kacmarek RM, Dimas S, Mack CW. Aerosol and humidity therapy. Respir Care. 2017;62(5):629–635.
In: Kacmarek RM, Dimas S, eds. Essentials of Respiratory Care. 4th 36. Bosama KJ, Read BA, Bahrgard Nikoo MJ, et al. A pilot randomized
ed. St. Louis: Mosby; 2005. trial comparing weaning from mechanical ventilation on pressure
15. MacIntyre N, Day S. Essentials for ventilator-alarm systems. Respir support versus proportional assist ventilation. Crit Care Med.
Care. 1992;37(9):1108. 2016;44(6):1098–1108.
16. Branson RD. Modes of ventilator operation. In: MacIntyre NR, 37. Stock MC, Downs JB, Frolicher DA. Airway pressure release
Branson RD, eds. Mechanical Ventilation. 2nd ed. St. Louis: Elsevier; ventilation. Crit Care Med. 1987;15(5):462.
2009:49–88. 38. Habashi N, Andrews P. Ventilator strategies for posttraumatic acute
17. Guttmann J, Haberthür C, Mols G. Automatic tube compensation. respiratory distress syndrome: airway pressure release ventilation
Respir Care Clin North Am. 2001;7(3):475. and the role of spontaneous breathing in critically ill patients. Curr
18. Haberthür C, Elsasser S, Eberhard L, et al. Total versus tube-related Opin Crit Care. 2004;10(6):549.
additional work of breathing in ventilator-dependent patients. Acta 39. Habashi NM. Other approaches to open-lung ventilation: airway pres-
Anaesthesiol Scand. 2000;44(6):749–757. sure release ventilation. Crit Care Med. 2005;33(suppl):S228–S240.
19. Mols G, Rohr E, Benzing A, et al. Breathing pattern associated 40. Putensen C, Zech S, Wrigge H, et al. Long-term effects of spontane-
with respiratory comfort during automatic tube compensation and ous breathing during ventilatory support in patients with acute lung
pressure support ventilation in normal subjects. Acta Anaesthesiol injury. Am J Respir Crit Care Med. 2001;164(1):43–49.
Scand. 2000;44(3):223–230. 41. Putensen C, Mutz NJ, Putensen-Himmer G, et al. Spontaneous
20. Marini JJ, Wheeler AP. Indications and options for mechanical breathing during ventilatory support improves ventilation-perfusion
ventilation. In: Critical Care Medicine: The Essentials. 3rd ed. distributions in patients with acute respiratory distress syndrome.
Philadelphia: Lippincott Williams & Wilkins; 2006. Am J Respir Crit Care Med. 1999;159(4):1241.
21. Cinel I, Jean S, Dellinger RP. General principles of mechanical 42. Sydow M, Burchardi H, Ephraim E, et al. Long-term effects of
ventilation. In: Parrillo JE, Dellinger RP, eds. Critical Care Medicine: two different ventilatory modes on oxygenation in acute lung
Principles of Diagnosis and Management in the Adult. 3rd ed. injury. Comparison of airway pressure release ventilation and
Philadelphia: Mosby Elsevier; 2008:153–176. volume-controlled inverse ratio ventilation. Am J Respir Crit Care
22. Gurka DP, Balk RA. Acute respiratory failure. In: Parrillo JE, Med. 1994;149(6):1550.
Dellinger RP, eds. Critical Care Medicine: Principles of Diagnosis 43. Rathgeber J, Schorn B, Falk V, et al. The influence of controlled
and Management in the Adult. 3rd ed. Philadelphia: Mosby Elsevier; mandatory ventilation (CMV), intermittent mandatory ventilation
2008:771–794. (IMV) and biphasic intermittent positive airway pressure (BIPAP)
23. Aslanian P, Isabey D, Valente E, et al. Effects of flow triggering on on duration of intubation and consumption of analgesics and
breathing effort during partial ventilatory support. Am J Respir Crit sedatives. A prospective analysis in 596 patients following adult
Care Med. 1998;157(1):135–143. cardiac surgery. Eur J Anaesthesiol. 1997;14(6):576–582.

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143.e2 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

44. Chan KPW, Stewart TE. Clinical use of high-frequency oscillatory 65. Patroniti N, Bellani G, Saccavino E, et al. Respiratory pattern during
ventilation in adult patients with acute respiratory distress syndrome. neurally adjusted ventilatory assist compared with pressure support
Crit Care Med. 2005;33(suppl):S170–S174. ventilation in acute respiratory failure patients. Intensive Care Med.
45. Gentile MA, MacIntyre NR, Neil R. High-frequency ventilation. 2012;38(2):230–239.
In: MacIntyre NR, Branson RD, eds. Mechanical Ventilation. 2nd 66. Cressoni M, Caironi P, Polli F, et al. Anatomical and functional
ed. St. Louis: Elsevier; 2009. intrapulmonary shunt in acute respiratory distress syndrome. Crit
46. Young D, Lamb SE, Shah S, et al. High-frequency oscillation for acute Care Med. 2008;36(3):669–675.
respiratory distress syndrome. N Engl J Med. 2013;368(9):806–813. 67. Dominguez-Cherit G, Posadas-Calleja JG, Borunda D. Chronic
47. Ferguson ND, Cook DJ, Guyatt GH, et al; for the OSCILLATE Trial obstructive pulmonary disease. In: Parrillo JE, Dellinger RP, eds.
Investigators and the Canadian Critical Care Trials Group. High- Critical Care Medicine: Principles of Diagnosis and Management in
frequency oscillation in early acute respiratory distress syndrome. the Adult. 3rd ed. Philadelphia: Mosby Elsevier; 2008:811–826.
N Engl J Med. 2013;368(9):795–805. 68. Rouby JJ, Puybasset L, Nieszkowska A, et al. Acute respiratory
48. Moerer O. Effort-adapted modes of assisted breathing. Curr Opin distress syndrome: lessons from computed tomography of the whole
Crit Care. 2012;18(1):61. lung. Crit Care Med. 2003;31(4 suppl):S285–S295.
49. Grasso S, Puntillo F, Mascia L, et al. Compensation for increase 69. Brower R, Lanken P, MacIntyre NR, et al. Higher versus lower
in respiratory workload during mechanical ventilation. Am J Respir positive end-expiratory pressures in patients with the acute respiratory
Crit Care Med. 2000;161(3):819–826. distress syndrome. N Engl J Med. 2004;351(4):327.
50. Bosma K, Ferreyra G, Ambrogio C, et al. Patient-ventilator interaction 70. Gainnier M, Michelet P, Thirion X, et al. Prone position and positive
and sleep in mechanically ventilated patients: pressure support versus end-expiratory pressure in acute respiratory distress syndrome. Crit
proportional assist ventilation. Crit Care Med. 2007;35(4):1048. Care Med. 2003;31(12):2719–2726.
51. Ranieri VM, Giuliani R, Mascia L, et al. Patient-ventilator interaction 71. Girard TD, Bernard GR. Mechanical ventilation in ARDS: a
during acute hypercapnia: pressure-support vs. proportional-assist state-of-the-art review. Chest. 2007;131(3):921–929.
ventilation. J Appl Physiol. 1996;81(1):426–436. 72. Villar J, Kacmarek RM, Perez-Mendez L, et al. A high positive
52. Giannouli E, Webster K, Roberts D, et al. Response of ventilator- end-expiratory pressure, low tidal volume ventilatory strategy
dependent patients to different levels of pressure support and pro- improves outcome in persistent acute respiratory distress syndrome: a
portional assist. Am J Respir Crit Care Med. 1999;159(6):1716–1725. randomized, controlled trial. Crit Care Med. 2006;34(5):1311–1318.
53. Wrigge H, Golisch W, Zinserling J, et al. Proportional assist versus 73. Amato MBP, Barbas CSV, Medeiros DM, et al. Effect of a protective-
pressure support ventilation: effects on breathing pattern and ventilation strategy on mortality in the acute respiratory distress
respiratory work of patients with chronic obstructive pulmonary syndrome. N Engl J Med. 1998;338(6):347.
disease. Intensive Care Med. 1999;25(8):790–798. 74. Ranieri VM. Effect of mechanical ventilation on inflammatory
54. Wysocki M, Meshaka P, Richard JC, et al. Proportional-assist mediators in patients with acute respiratory distress syndrome: a
ventilation compared with pressure-support ventilation during randomized controlled trial. JAMA. 1999;282(1):54–61.
exercise in volunteers with external thoracic restriction. Crit Care 75. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy
Med. 2004;32(2):409. using low tidal volumes, recruitment maneuvers, and high positive
55. Mols G, von Ungern-Sternberg B, Rohr E, et al. Respiratory comfort end-expiratory pressure for acute lung injury and acute respiratory
and breathing pattern during volume proportional assist ventilation distress syndrome: a randomized controlled trial. JAMA. 2008;
and pressure support ventilation: a study on volunteers with artificially 299(6):637.
reduced compliance. Crit Care Med. 2000;28(6):1940. 76. Mercat A, Vielle B, Jaber S, et al. Positive end-expiratory pressure
56. Alexopoulou C, Kondili E, Vakouti E, et al. Sleep during proportional- setting in adults with acute lung injury and acute respiratory distress
assist ventilation with load-adjustable gain factors in critically ill syndrome: a randomized controlled trial. JAMA. 2008;299(6):646.
patients. Intensive Care Med. 2007;33(7):1139–1147. 77. Halter JM, Steinberg JM, Schiller HJ, et al. Positive end-expiratory
57. Piquilloud L, Vignaux L, Bialais E, et al. Neurally adjusted ventilatory pressure after a recruitment maneuver prevents both alveolar
assist improves patient-ventilator interaction. Intensive Care Med. collapse and recruitment/derecruitment. Am J Respir Crit Care Med.
2011;37(2):263–271. 2003;167(12):1620–1626.
58. Colombo D, Cammarota G, Bergamaschi V, et al. Physiologic 78. Mols G, Priebe HJ, Guttmann J. Alveolar recruitment in acute lung
response to varying levels of pressure support and neurally adjusted injury. Br J Anaesth. 2006;96(2):156–166.
ventilatory assist in patients with acute respiratory failure. Intensive 79. Gattinoni L, Pelosi P, Suter PM, et al. Acute respiratory distress
Care Med. 2008;34(11):2010–2018. syndrome caused by pulmonary and extrapulmonary disease. Different
59. Breatnach C, Conlon NP, Stack M, et al. A prospective crossover syndromes? Am J Respir Crit Care Med. 1998;158(1):3.
comparison of neurally adjusted ventilatory assist and pressure-support 80. Talmor D, Sarge T, Malhotra A, et al. Mechanical ventilation
ventilation in a pediatric and neonatal intensive care unit population. guided by esophageal pressure in acute lung injury. N Engl J Med.
Pediatr Crit Care Med. 2010;11(1):7. 2008;359(20):2095.
60. Terzi N, Pelieu I, Guittet L, et al. Neurally adjusted ventilatory 81. Foti G, Cereda M, Sparacino M, et al. Effects of periodic lung
assist in patients recovering spontaneous breathing after acute recruitment maneuvers on gas exchange and respiratory mechanics in
respiratory distress syndrome: physiological evaluation. Crit Care mechanically ventilated acute respiratory distress syndrome (ARDS)
Med. 2010;38(9):1830. patients. Intensive Care Med. 2000;26(5):501–507.
61. Clement KC, Thurman TL, Holt SJ, et al. Neurally triggered breaths 82. Richard JC, Maggiore SM, Jonson B, et al. Influence of tidal volume
reduce trigger delay and improve ventilator response times in ventilated on alveolar recruitment. Respective role of PEEP and a recruitment
infants with bronchiolitis. Intensive Care Med. 2011;37(11):1–7. maneuver. Am J Respir Crit Care Med. 2001;163(7):1609.
62. Rozé H, Lafrikh A, Perrier V, et al. Daily titration of neurally 83. Nemer SN, Caldeira JB, Azeredo LM, et al. Alveolar recruitment
adjusted ventilatory assist using the diaphragm electrical activity. maneuver in patients with subarachnoid hemorrhage and acute
Intensive Care Med. 2011;37(7):1087–1094. respiratory distress syndrome: a comparison of 2 approaches. J Crit
63. Schmidt M, Demoule A, Cracco C, et al. Neurally adjusted Care. 2011;26(1):22–27.
ventilatory assist increases respiratory variability and complexity 84. Pelosi P, Cadringher P, Bottino N, et al. Sigh in acute respiratory
in acute respiratory failure. Anesthesiology. 2010;112(3):670. distress syndrome. Am J Respir Crit Care Med. 1999;159(3):872.
64. Barwing J, Linden N, Armbold M, et al. Neurally adjusted ventilatory 85. Pinsky MR. Effect of mechanical ventilation on heart-lung interac-
assist vs. pressure support ventilation in critically ill patients: an tions. In: Tobin MJ, ed. Principles and Practice of Mechanical
observational study. Acta Anaesthesiol Scand. 2011;55:1261–1271. Ventilation. 2nd ed. New York: McGraw-Hill; 2006:729–757.

Descargado para carlos urquijo ([email protected]) en New Granada Military University de ClinicalKey.es por Elsevier en abril 11, 2020.
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 CHAPTER 9  General Principles of Mechanical Ventilation
143.e3

86. Pinsky MR. Heart-lung interactions. Curr Opin Crit Care. 109. Pandharipande P, Shintani A, Peterson J, et al. Lorazepam is an
2007;13(5):528. independent risk factor for transitioning to delirium in intensive
87. Magder S. Hemodynamic monitoring in the mechanically ventilated care unit patients. Anesthesiology. 2006;104(1):21.
patient. Curr Opin Crit Care. 2011;17(1):36. 110. Pisani MA, Murphy TE, Araujo KLB, et al. Benzodiazepine and
88. Calzia E, Ivanyi Z, Radermacher P. Determinants of blood flow opioid use and the duration of ICU delirium in an older population.
and organ perfusion. Funct Hemodynamic Monit. 2005;19–32. Crit Care Med. 2009;37(1):177.
89. Mebazaa A, Karpati P, Renaud E, et al. Acute right ventricular 111. Pandharipande PP, Pun BT, Herr DL, et al. Effect of sedation with
failure—from pathophysiology to new treatments. Intensive Care dexmedetomidine vs. lorazepam on acute brain dysfunction in
Med. 2004;30(2):185–196. mechanically ventilated patients. JAMA. 2007;298(22):2644–2653.
90. Michard F, Boussat S, Chemla D, et al. Relation between respiratory 112. Riker RR, Shehabi Y, Bokesch PM, et al. Dexmedetomidine
changes in arterial pulse pressure and fluid responsiveness in septic vs midazolam for sedation of critically ill patients. JAMA.
patients with acute circulatory failure. Am J Respir Crit Care Med. 2009;301(5):489–499.
2000;162(1):134–138. 113. Reade MC, O’Sullivan K, Bates S, et al. Dexmedetomidine vs.
91. Marik PE, Baram M, Vahid B. Does central venous pressure predict haloperidol in delirious, agitated, intubated patients: a randomised
fluid responsiveness? Chest. 2008;134(1):172–178. open-label trial. Crit Care. 2009;13(3):R75.
92. Magder S, Lagonidis D, Erice F. The use of respiratory variations 114. Mirski MA, Lewin JJ, LeDroux S, et al. Cognitive improvement
in right atrial pressure to predict the cardiac output response to during continuous sedation in critically ill, awake and responsive
PEEP. J Crit Care. 2001;16(3):108–114. patients: The Acute Neurological ICU Sedation Trial (ANIST).
93. Jubran A. Pulse oximetry. Crit Care. 1999;3(2):R11–R17. Intensive Care Med. 2010;36(9):1505–1513.
94. Severınghaus JW. Methods of measurement of blood and gas carbon 115. Pandharipande PP, Sanders RD, Girard TD, et al. Research effect
dioxide during anesthesia. Anesthesiology. 1960;21:717–726. of dexmedetomidine versus lorazepam on outcome in patients with
95. Huttmann SE, Windisch W, Storre JH. Techniques for the measure- sepsis: an a priori-designed analysis of the MENDS randomized
ment and monitoring of carbon dioxide in the blood. Ann Am controlled trial. Crit Care. 2010;14(2):R38.
Thorac Soc. 2014;11(4):645–652. 116. Torres A, Serra-Batlles J, Ros E, et al. Pulmonary aspiration of
96. Bobbia X, Claret PG, Palmier L, et al. Erratum: concordance and gastric contents in patients receiving mechanical ventilation: the
limits between transcutaneous and arterial carbon dioxide pressure effect of body position. Ann Intern Med. 1992;116(7):540.
in emergency department patients with acute respiratory failure: a 117. Kollef MH. The prevention of ventilator-associated pneumonia. N
single-center, prospective, and observational study. Scand J Trauma Engl J Med. 1999;340(8):627–634.
Resusc Emerg Med. 2015;23:77. 118. Sud S, Friedrich JO, Taccone P, et al. Prone ventilation reduces
97. Nicolini A, Ferrari MB. Evaluation of a transcutaneous carbon mortality in patients with acute respiratory failure and severe
dioxide monitor in patients with acute respiratory failure. Ann hypoxemia: systematic review and meta-analysis. Intensive Care
Thorac Med. 2011;6(4):217–220. Med. 2010;36(4):585–599.
98. Hazenberg A, Zijlstra JG, Kerstjens HA, et al. Validation of a 119. Colice GL. Historical perspective on the development of
transcutaneous CO(2) monitor in adult patients with chronic mechanical ventilation. In: Tobin MJ, ed. Principles and Practice of
respiratory failure. Respiration. 2011;81(3):242–246. Mechanical Ventilation. 3rd ed. New York: McGraw Hill Medical;
99. Rafiq MK, Bradburn M, Proctor AR, et al. Using transcutaneous 2012:3–41.
carbon dioxide monitor (TOSCA 500) to detect respiratory failure 120. Morris PE, Berry MJ, Files DC, et al. Standardized rehabilitation
in patients with amyotrophic lateral sclerosis: a validation study. and hospital length of stay among patients with acute respiratory
Amyotroph Lateral Scler. 2012;13(6):528–532. failure; a randomized clinical trial. JAMA. 2016;315(24):2694–2702.
100. Spelten O, Fiedler F, Schier R, et al. Transcutaneous PTCCO2 121. Holets SR, Marini JJ. Is automated weaning superior to manual
measurement in combination with arterial blood gas analysis spontaneous breathing trials? Respir Care. 2016;61(6):749–760.
provides superior accuracy and reliability in ICU patients. J Clin 122. Boles JM, Bion J, Connors A, et al. Weaning from mechanical
Monit Comput. 2017;31(1):153–158. ventilation. Eur Respir J. 2007;29(5):1033–1056.
101. Lermuzeaux M, Meric H, Sauneuf B, et al. Superiority of trans- 123. Epstein SK. Weaning from ventilatory support. Curr Opin Crit
cutaneous CO2 over end-tidal CO2 measurement for monitoring Care. 2009;15(1):36.
respiratory failure in nonintubated patients: a pilot study. J Crit 124. Kress JP, Pohlman AS, O’Connor MF, et al. Daily interruption of
Care. 2016;31(1):150–156. sedative infusions in critically ill patients undergoing mechanical
102. Cuvelier A, Grigoriu B, Molano LC, et al. Limitations of transcutane- ventilation. N Engl J Med. 2000;342(20):1471–1477.
ous carbon dioxide measurements for assessing long-term mechanical 125. Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a paired
ventilation. Chest. 2005;127(5):1744–1748. sedation and ventilator weaning protocol for mechanically ventilated
103. Kress JP, Pohlman AS, Hall JB. Sedation and analgesia in the patients in intensive care (Awakening and Breathing Controlled trial):
intensive care unit. Am J Respir Crit Care Med. 2002;166(8): a randomised controlled trial. Lancet. 2008;371(9607):126–134.
1024–1028. 126. Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods
104. Ostermann ME, Keenan SP, Seiferling RA, et al. Sedation in the of weaning patients from mechanical ventilation. N Engl J Med.
intensive care unit. JAMA. 2000;283(11):1451–1459. 1995;332(6):345–350.
105. Morandi A, Brummel NE, Ely E. Sedation, delirium and mechani- 127. Esteban A, Alia I, Tobin MJ, et al. Effect of spontaneous breathing
cal ventilation: the “ABCDE” approach. Curr Opin Crit Care. trial duration on outcome of attempts to discontinue mechanical
2011;17(1):43. ventilation. Am J Respir Crit Care Med. 1999;159(2):512–518.
106. Arroliga AC, Thompson BT, Ancukiewicz M, et al. Use of sedatives, 128. Esteban A, Alia I, Gordo F, et al. Extubation outcome after spontane-
opioids, and neuromuscular blocking agents in patients with acute ous breathing trials with T-tube or pressure support ventilation. Am
lung injury and acute respiratory distress syndrome. Crit Care Med. J Respir Crit Care Med. 1997;156(2):459–465.
2008;36(4):1083. 129. Farias J, Retta A, Alia I, et al. A comparison of two methods to
107. Jacobi J, Fraser GL, Coursin DB, et al. Clinical practice guidelines perform a breathing trial before extubation in pediatric intensive
for the sustained use of sedatives and analgesics in the critically ill care patients. Intensive Care Med. 2001;27(10):1649–1654.
adult. Crit Care Med. 2002;30(1):119. 130. Meade MO, Cook DJ, Guyatt GH, et al. Ventilation strategy
108. Weinert CR, Calvin AD. Epidemiology of sedation and sedation using low tidal volumes, recruitment maneuvers, and high positive
adequacy for mechanically ventilated patients in a medical and end-expiratory pressure for acute lung injury and acute respiratory
surgical intensive care unit. Crit Care Med. 2007;35(2):393. distress syndrome. JAMA. 2008;299(6):637–645.

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143.e4 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

131. Perren A, Domenighetti G, Mauri S, et al. Protocol-directed label, clustered group-randomised, crossover study. Lancet Infect
weaning from mechanical ventilation: clinical outcome in patients Dis. 2011;11:372–380.
randomized for a 30-min or 120-min trial with pressure support 155. Oostdijk EA, de Smet AM, Blok HE, et al. Ecological effects of
ventilation. Intensive Care Med. 2002;28(8):1058–1063. selective decontamination on resistant gram-negative bacterial
132. Del Sorbo L, Slutsky AS. Acute respiratory distress syndrome and colonization. Am J Respir Crit Care. 2010;181:452–457.
multiple organ failure. Curr Opin Crit Care. 2011;17(1):1–6. 156. Poelaert J, Depuydt P, De Wolf A, et al. Polyurethane cuffed
133. Shock C, Montgomery AB, Stager MA, et al. Causes of mortality endotracheal tubes to prevent early postoperative pneumonia after
in patients with the adult respiratory distress syndrome. Am Rev cardiac surgery: a pilot study. J Thorac Cardiovasc Surg. 2008;135:
Respir Dis. 1985;132:485–489. 771–776.
134. Stapleton RD, Wang BM, Hudson LD, et al. Causes and timing 157. Lorente L, Lecuona M, Jimenez A, et al. Influence of an endotracheal
of death in patients with ARDS. Chest. 2005;128(2):525. tube with polyurethane cuff and subglottic secretion drainage on
135. Suchyta MR, Orme JF, Morris AH. The changing face of organ pneumonia. Am J Respir Crit Care. 2007;176:1079–1083.
failure in ARDS. Chest. 2003;124(5):1871. 158. Muscedere J, Rewa O, McKechnie K, et al. Subglottic secretion drain-
136. Gattinoni L, Pesenti A. The concept of “baby lung.” Intensive Care age for the prevention of ventilator-associated pneumonia: a systematic
Med. 2005;31(6):776–784. review and meta-analysis. Crit Care Med. 2011;39:1985–1991.
137. Stapleton RD, Steinberg KP. Ventilator-induced lung injury. In: 159. Lacherade JC, De Jonghe B, Guezennec P, et al. Intermittent
MacIntyre NR, Branson RD, eds. Mechanical Ventilation. 2nd ed. subglottic secretion drainage and ventilator-associated pneumonia:
St. Louis: Elsevier; 2009. a multicenter trial. Am J Respir Crit Care. 2010;182:910–917.
138. Gattinoni L, Carlesso E, Caironi P. Stress and strain within the 160. Kollef MH, Afessa B, Anzueto A, et al. Silver-coated endotracheal
lung. Curr Opin Crit Care. 2012;18(1):42–47. tubes and incidence of ventilator-associated pneumonia: the
139. Ngiam N, Kavanagh BP. Ventilator-induced lung injury: the role NASCENT randomized trial. JAMA. 2008;300:805–813.
of gene activation. Curr Opin Crit Care. 2012;18(1):16–22. 161. Quenot JP, Thiery N, Barbar S. When should stress ulcer prophylaxis
140. De Campos T. Ventilation with lower tidal volumes as compared be used in the ICU? Curr Opin Crit Care. 2009;15(2):139–143.
with traditional tidal volumes for acute lung injury and the acute 162. Cook D, Guyatt G, Marshall J, et al. A comparison of sucralfate
respiratory distress syndrome. The Acute Respiratory Distress and ranitidine for the prevention of upper gastrointestinal bleed-
Syndrome Network. N Engl J Med. 2000;342:1301–1308. ing in patients requiring mechanical ventilation. N Engl J Med.
141. Determann RM, Royakkers A, Wolthuis EK, et al. Ventilation with 1998;338(12):791–797.
lower tidal volumes as compared with conventional tidal volumes 163. Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis
for patients without acute lung injury: a preventive randomized in critically ill patients: resolving discordant meta-analyses. JAMA.
controlled trial. Crit Care. 2010;14(1):R1. 1996;275:308–314.
142. Bellani F, Laffey JG, Pham T, et al. Noninvasive ventilation of patients 164. Geus WP. Are there indications for intravenous acid-inhibition in
with acute respiratory distress syndrome: insights from the LUNG the prevention of upper GI bleeding? Scand J Gastroenterol Suppl.
SAGE Study. Am J Respir Crit Care Med. 2017;195(1):67–77. 2000;30:254–256.
143. Magill SS, Klompas M, Balk R, et al. Developing a new, national 165. Conrad SA, Gabrielli A, Margolis B, et al. Randomized, double-blind
approach to surveillance for ventilator-associated events*. Crit Care comparison of immediate-release omeprazole suspension versus
Med. 2013;41(11):2467–2475. intravenous cimetidine for the prevention of upper gastrointestinal
144. Raoof S, Baumann MH, et al. Ventilator-associated events: the new bleeding in critically ill patients. Crit Care Med. 2005;33:760–765.
definition. Am J Crit Care. 2014;23(1):7–9. 166. Dial S, Alrasadi K, Manoukian C, et al. Risk of Clostridium
145. Spalding MC, Cripps MW, Minshall CT, et al. Ventilator- difficile diarrhea among hospital inpatients prescribed proton pump
associated pneumonia: new definitions. Crit Care Clin. 2017;33(2): inhibitors: cohort and case-control studies. Can Med Assoc J.
277–292. 2004;171(1):33–38.
146. Boyer AF, Schoenberg N, Babcock H, et al. A prospective evaluation 167. Cook DJ, Crowther M, Meade M, et al. Deep vein thrombosis
of ventilator-associated conditions and infection-related ventilator- in medical surgical ICU patients: prevalence, incidence and risk
associated conditions. Chest. 2015;147(1):68–81. factors. Crit Care Med. 2005;33:1565–1571.
147. Hayashi Y, Morisawa K, Klompas M, et al. Toward improved 168. Cook DJ, Rocker G, Meade M, et al. Prophylaxis of Thrombo-
surveillance: the impact of ventilator-associated complications on embolism in Critical Care (PROTECT) Trial: a pilot study. J Crit
length of stay and antibiotic use in patients in intensive care units. Care. 2005;20:364–372.
Clin Infect Dis. 2013;56(4):471–477. 169. Cade JF. High risk of the critically ill for venous thromboembolism.
148. Klompas M. Potential strategies to prevent ventilator-associated Crit Care Med. 1982;10:448–450.
events. Am J Respir Crit Care Med. 2015;192(12):1420–1430. 170. Crowther M, Cook DJ. Thromboprophylaxis in medical-surgical
149. Safdar N, Dezfulian C, Collard HR, et al. Clinical and economic critically ill patients. Curr Opin Crit Care. 2008;14:520–523.
consensus of ventilator-associated pneumonia: a systematic review. 171. Nava S, Hill N. Non-invasive ventilation in acute respiratory failure.
Crit Care Med. 2005;33:2184–2193. Lancet. 2009;374(9685):250–259.
150. American Thoracic Society. Guidelines for the management of adults 172. Bott J, Carroll M, Conway J, et al. Randomised controlled trial
with hospital acquired, ventilator-associated, and healthcare-associated of nasal ventilation in acute ventilatory failure due to chronic
pneumonia. Am J Respir Crit Care. 2005;171:388–416. obstructive airways disease. Lancet. 1993;341(8860):1555–1557.
151. Liberati A, D’Amico R, Pifferi S, et al. Antibiotics for preventing 173. Boldrini R, Fasano L, Nava S. Noninvasive mechanical ventilation.
respiratory tract infections in adults receiving intensive care. Cochrane Curr Opin Crit Care. 2012;18(1):48.
Database Syst Rev. 2000;(2):CD000022. 174. Peter JV, Moran JL, Phillips-Hughes J, et al. Effect of non-invasive
152. Liberati A, D’Amico R, Pifferi S, et al. Antibiotics for preventing positive pressure ventilation (NIPPV) on mortality in patients with
respiratory tract infections in adults receiving intensive care. Cochrane acute cardiogenic pulmonary oedema: a meta-analysis. Lancet.
Database Syst Rev. 2000;(4):CD000022 (update). 2006;367(9517):1155–1163.
153. De Smet A, Kluytmans JA, Cooper BS, et al. Decontamination of 175. Burns K, Adhikari N, Keenan SP, et al. Use of non-invasive ventilation
the digestive tract and oropharynx in ICU patients. N Engl J Med. to wean critically ill adults off invasive ventilation: meta-analysis
2009;360:20–31. and systematic review. BMJ. 2009;338:1574.
154. De Smet A, Kluytmans JA, Blok HE, et al. Selective digestive tract 176. Girault C, Bubenheim M, Abroug F, et al. Noninvasive ventilation and
decontamination and selective oropharyngeal decontamination and weaning in chronic hypercapnic respiratory failure patients: a random-
antibiotic resistance in patients in intensive-care units: an open ized multicenter trial. Am J Respir Crit Care. 2011;184:672–679.

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 CHAPTER 9  General Principles of Mechanical Ventilation
143.e5

177. Gristina GR, Antonelli M, Conti G, et al. Noninvasive versus invasive 187. Sztrymf B, Messika J, Mayot T, et al. Impact of high flow nasal
ventilation for acute respiratory failure in patients with hematologic cannula oxygen therapy on intensive care unit patients with acute-
malignancies: a 5-year multicenter observational survey. Crit Care respiratory failure:a prospective observational study. J Crit Care.
Med. 2011;39(10):2232–2239. 2012;27(3):324.e9–324.e13.
178. Papazian L, Corley A, Hess D, et al. Use of high-flow nasal cannula 188. Rello J, Perez M, Roca O, et al. High-flow nasal therapy in adults
oxygenation in ICU adults: a narrative review. Intensive Care Med. with severe acute respiratory infection:cohort study in patients with
2016;42(9):1336–1349. 2009 influenza A/H1N1v. J Crit Care. 2012;27(5):434–439.
179. Dysart K, Miller TL, Wolfson MR, et al. Research in high flow 189. Nagata K, Morimoto T, Fujimoto D, et al. Efficacy of high-flow nasal
therapy: mechanisms of action. Respir Med. 2009;103(10):1400–1405. cannula therapy in acute hypoxemic respiratory failure: decreased
180. Parke RL, Eccleston ML, McGuinness SP. The effects of flow on use of mechanical ventilation. Respir Care. 2015;60(10):1390–1396.
airway pressure during nasal high-flow oxygen therapy. Respir Care. 190. Kang BJ, Koh Y, Lim CM, et al. Failure of high-flow nasal cannula
2011;56(8):1151–1155. therapy may delay intubation and increase mortality. Intensive Care
181. Riera J, Pérez P, Cortés J, et al. Effect of high-flow nasal cannula Med. 2015;41(4):623–632.
and body position on end-expiratory lung volume: a cohort study 191. Frat JP, Thille AW, Mercat A, et al. High-flow oxygen through
using electrical impedance tomography. Respir Care. 2013;58(4): nasal cannula in acute hypoxemic respiratory failure. N Engl J Med.
589–596. 2015;372(23):2185–2196.
182. Nishimura M. High-flow nasal cannula oxygen therapy in adults. 192. Coudroy R, Jamet A, Petua P, et al. High-flow nasal cannula oxygen
J Intensive Care. 2015;3(1):15. therapy versus noninvasive ventilation in immunocompromised
183. Mauri T, Turrini C, Eronia N, et al. Physiologic effects of high-flow patients with acute respiratory failure: an observational cohort study.
nasal cannula in acute hypoxemic respiratory failure. Am J Respir Ann Intensive Care. 2016;6(1):45.
Crit Care Med. 2016. 193. Hernández G, Vaquero C, Colinas L, et al. Effect of postextubation
184. Sztrymf B, Messika J, Bertrand F, et al. Beneficial effects of humidified high-flow nasal cannula vs noninvasive ventilation on reintubation
high flow nasal oxygen in criticalcare patients: a prospective pilot and postextubation respiratory failure in high-risk patients: a
study. Intensive Care Med. 2011;37(11):1780–1786. randomized clinical trial. JAMA. 2016;316(15):1565–1574.
185. Roca O, Riera J, Torres F, et al. High-flow oxygen therapy in acute 194. Futier E, Paugam-Burtz C, Godet T, et al. Effect of early postextuba-
respiratory failure. Respir Care. 2010;55(4):408–413. tion high-flow nasal cannula vs conventional oxygen therapy on
186. Parke RL, McGuinness SP. Pressures delivered by nasal high flow hypoxaemia in patients after major abdominal surgery: a French
oxygen during all phases of the respiratory cycle. Respir Care. multicentre randomised controlled trial (OPERA). Intensive Care
2013;58(10):1621–1624. Med. 2016;42(12):1888–1898.

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143.e6 Pa rt 1 Critical Care Procedures, Monitoring, and Pharmacology

Review Questions
1. A patient is triggering the ventilator and is being ventilated the back pressure for venous return, right ventricular venous
with a pressure-controlled, time-cycled breath, using a decel- return decreases. At the same time, compression of the pulmonary
erating inspiratory waveform pattern. Flash pulmonary edema veins causes an increase in left ventricular return and stroke
develops. Which of the following statements are true? volume on the left side of the heart increases. Several cardiac
a. Owing to a decrease in compliance, airway pressure will cycles later, the decreased venous return from the right side
increase until the alarm limit is reached. now presents itself to the left side (usually during expiration),
b. Owing to a decrease in compliance, flow and tidal volume and left-sided stroke volume decreases. This is one example of
will decrease, and airway pressure will stay the same. ventricular interdependence and is what generates pulse pressure
c. Owing to a change in mechanics, intrinsic positive end- variation. The overall hemodynamic effects, such as arterial
expiratory pressure (PEEP) will develop, as exhalation will hypotension, are typically dependent on volume status and
be prolonged. baseline left ventricular function. Decreasing flow during volume-
d. Tidal volume will stay the same, but flow will increase controlled ventilation will increase inspiratory time and worsen
owing to increased work of breathing. intrinsic PEEP. Positive-pressure ventilation always decreases
Answer: b. The patient is being ventilated with pressure-assist left ventricular afterload.
control ventilation (i.e., “pressure control”). This mode of ventila- 3. All of the following statements about mechanical ventilation
tion is patient triggered, because the patient is actively triggering are correct except:
and can use pressure or flow triggering (like many modes). During a. A decrease in the end-tidal carbon dioxide (ETCO2)–partial
inspiration, a clinician-set pressure is controlled, or targeted, and pressure of carbon dioxide (PaCO2) gap indicates an increase
pressure control is always time-cycled with a decelerating inspira- in dead space.
tory waveform pattern. In pressure-targeted breaths, if mechanics b. Pairing a spontaneous awakening trial (SAT) with a spon-
change, flow and volume will change. In the case of pulmonary taneous breathing trial (SBT) effectively reduces ventilator
edema, the problem lies in reduced compliance. As such, flow time and days in the intensive care unit.
and tidal volume will decrease. Answer a would be correct if the c. An SBT can be conducted through a T-piece or on low-level
patient was on volume-assist control, as tidal volume would stay pressure support.
the same, but pressure would increase. A decrease in compliance d. Mechanical ventilation in acute respiratory distress syn-
will not cause a reduction in expiratory flow; therefore answer c drome (ARDS) is approached with the knowledge that
is incorrect. In reference to answer d, because this is a pressure- overdistention can result in alveolar injury.
targeted breath, flow may indeed increase if the patient’s work Answer: a. A normal ETCO2-PaCO2 gap is about 5 mm Hg,
of breathing and inspiratory effort increases. However, tidal volume with ETCO2 being less than PaCO2. An increase in that gap is
will decrease as a result of the decreased compliance. typically indicative of an increase in dead space, whether due
2. Which one of the following is most correct concerning hemo- to altered ventilation-perfusion relationships or an acute drop
dynamic effects of positive-pressure ventilation? in cardiac output. Daily assessment of readiness to liberate from
a. A positive-pressure breath is always associated with a drop the ventilator, along with protocolized SATs and SBTs and
in arterial blood pressure. targeted sedation practices, are the most effective means of
b. During volume-assist controlled ventilation, intrinsic posi- safely discontinuing mechanical ventilation. The literature
tive end-expiratory pressure (PEEP)-induced elevated intra- supports the fact that SBTs can be conducted via a T-piece,
thoracic pressure can be minimized by decreasing inspiratory low levels of pressure support or continuous positive airway
flow. pressure (CPAP), once or twice daily, and for 30 minutes up
c. The immediate effect of a positive-pressure breath is a to 120 minutes.
decrease in venous return secondary to an elevation in right The literature support exists for a greater beneficial effect of
atrial pressure and an increase in left ventricular stroke PEEP when applied immediately after the onset of ARDS.
volume secondary to increased venous return from the pul- Overinflation at end inspiration produces an upper deflection
monary veins. zone on the pressure-volume curve. Mechanical ventilation in
d. By increasing pleural pressure, mechanical ventilation ARDS is approached with the knowledge that overdistention
increases left ventricular afterload. can result in barotrauma, whereas allowing alveoli to collapse
Answer: c. The physiology of a positive-pressure breath is predict- at the end of each expiration (below lower inflation point) may
able: an increase in intrathoracic pressure causes an increase in result in shearing-type airway and alveolar injury. Overdistention
juxtacardiac and right atrial pressure. As right atrial pressure is is a prime driver of ventilator-associated lung injury.

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