VENTILASI MEKANIK

 Objective

 Discuss the indications and techniques for noninvasive positive pressure ventilation

 Describe the characteristics of different types of breaths and modes of mechanical

ventilation. .

 Outline ventilator settings and monitoring needs for the initiation of mechanical ventilation.

 Describe interactions between ventilatory parameters and modilications needed to avoid

harmful effects of mechanical ventilation

 Review the guidelines for initial ventilator management that apply to specific clinical
situations. .

Case Study

A 65-year-old woman with an exacerbation of chronic obstructive pulmonary disease is

admitted to the hospital. She is receiving oxygen at 3 lein by nasal cannula. She continues to
have significant respiratory distress after receiving two bronchodilator nebulizer treatments.
Her vital signs are blood pressure 160/1 10 mm Hg, heart rate 110! min, respirations 301mm,
and temperature 99 .0°F (37 2°C). Physical examination is remarkable for use of accessory
muscles of respiration and diffuse wheezing bilaterally. An arterial blood gas analysis
demonstrates a pH 7.24, P002 60 mm Hg (8 kPa), and P02 65 mm Hg (8.7 kPa).

- What type of respiratory support should be initiated?

- What settings should be selected for respiratory support?

- What are the goals of respiratory support?

I. INTRODUCTION

When hypoxic or hypercapnic respiratory failure cannot be treated by other means as

discussed in Chapter 4: 3, anvanced support With positive pressure ventilation maybe
needed. a ventylator is a device used to assist or replace the work of the respiratory
system. positive pressure ventilation can be delivered noninvasively via mask or helmet
or invasively via an endotracheal tube. Generally accepted indications for initiating
positive pressure ventilatory support are summarized in Table 5-1.

Tabel 5.1

Table 5.1 Indications For Positive Pressure Ventilatory Support

Ventilation abnormalities Respiratory muscle dysfunction

 Respiratory muscle fatigue

 Chest wall abnormalities

 Neuromuscular disease

Decreased ventilatory drive

Increased airway resistance and/or obstruction

Oxygenation abnormalities
Refractory hypoxemia

Need for positive end expiratory pressure

Excessive work of breathing

Need for sedation and/or neuromuscular

blockade

Need to decrease systemic or myocardial

oxygen consumption

Use of hyperventilation to reduce intracranial

pressure

Facilitation of alveolar recruitment and

prevention of atelectasis
 The choice between noninvasive or invasive positive pressure ventilation is dependent on
patient characteristics, the type and severity of the respiratory and/or systemic condition,
anticipated clinical course, availability of resources, as well as the experience and training of the
clinician and healthcare team.

II. NON INVASIVE POSITIF PRESSURE VENTILATION

A. What is noninvasive positif pressure ventilation

Noninvasive positive pressure ventilation (NPPV) refers to a form of mechanical
ventilation that . provides respiratory assistance without an invasive artificiai
airway; The potential beneficial effects of NPPV ate simiia! to those of invasive
mechanical ventilation and include decreased work of breathing, improved
oxygenation, and improved gas exchange. In addition, this type of ventilation
avoids many of complications associated with intubation and invassive
mechanical ventialtion. Potential advantages and disadvantages of NPPV are
listed in Table 5-2
Table 5-2 Advantages Dan Disadvantages Of NPPV

Advantages
 Reduced need for sedation
 Preservation of airway-
protective reflexes
 Avoidances of upper airway
trauma
 Decreased in incidance of
nosocomial sinusitis and
pneumonia
 Improved patient comfort
 Shorter lenght of stays in
ICU and hospital
 improved survival
Disadvantages
 Claustropobia
 Increased workload for respiratory
practitioner
 Facial/ nasal presure lesions
 Unprotected airway
 Inabillity to suction deep airway
 Gastric distension with use of mask or
helmet
 Possible upper-extremity edema, axillary
vein thrombosis, tympanic membran
disfungction, and intrahelmet noise with
use of helmet
 Delay in intubation

B. How does NPPV work

NPPV utilizes two levels of positive airway pressure, combining the modalities of
pressure support ventilation (PSV) and continuous positive airway pressure (CPAP)
 (see Section 111). By convention, the PSV modality is referred to as IPAP
(inspiratory positive airway pressure), and the CPAP modality is referred to as EPAP
(expiratory positive airway pressure). CPAP alone can also be delivered
noninvasively but does not provide support of ventilation. CPAP allows ' spontaneous
breathing from a gas source at an elevated baseline system pressure (higher than
atmospheric pressure) and is functionally equivalent to positive end-expiratory
pressure (PEEP). The difference between these two pressure levels (AP) determines
tidal volume generated. NPPV can be delivered using a standard ICU ventilator or a
portable device. The benefits of using an ICU ventilator include delivery of a more
precise and higher concentration of oxygen, the separation of inspiratory and
expiratory tubing to prevent rebreathing C02, better monitoring and alarm features,
and improved detection of air leaks. Alarm setups may need to be altered on standard
ventilators because the alarms are typically triggered by exhalation, and noninvasive
ventilation inherently has more gas leakage compared to ventilation via an
endotracheal tube. Ventilators specifically designed to provide patient-triggered
noninvasive pressure support or patient~ triggered volume-cycled breaths are
optimal.

C. What types of lnterface Are Available?

The ventilator connects to a tightly fitted face mask, nasal mask, nasal plugs, or
ahelmet [Figure 5.. 1). Many patients with acute respiratory failure are mouth
breathers, thus the face mask is preferred as it is associated with smaller leaks than
the nasal plugs and nasal mask. The nasal passages may offer significant resistance to
airflow, limiting the benefits of NPPV‘ Some gas leakage is anticipated with both
masks and can be compensated for by increasing pressure settings or increasing the
set tidal volume (VT) level. When a nasal mask is used, the patient’s mouth should
be kept closed or chin straps should be employed to reduce leakage.
D. Which Patients Benefit From NPPV?
Before NPPV is initiated, patient charateristic and potential for successfully treating
the underlying respiratory condition should be eavluated. Table 5-3 lists conditions
leading to respiratory failure that are likely to improve with use of NPPV. Of these,
acute exacerbations of chronic obstructive pulmonary disease and cardiogenic
pulmonary edema are teh two best studied and accepted indications for the
applications OF NPPV.

Table 5-3 Respiratory conditions ilkely to respond to NPPV

Hipoxemic respiratory failure

 Cardiogenic pulmonary edema without hemodynamic instability
 Respiratory failure in patients with pneumocystis pneumonia
 Respiratory failure in immunocompromised patients
Hipercapnic respiratory failure
 Acute exacerbations of chronic obstructive pulmonary disease
 Acute exaserbations of asthma
 Respiratory failure in patients with cystic fibrosis

E. Which Patient Should Not Receive Non Invasive Mechanical Ventilation ?

In general, NPPV should not be initiate din the following circumtances;
uncooperative patients; patient with difficulty clearing secretions, recurrent emesis,
or post cardiac or respiratory arrest; and patients with hemodynamic instability. A
more detailed list of contraindications for the use of NPPV is presented in table 5-5

Table 5-5 contraindications to use of NPPV

  Cardiac or respiratory arest
 Hemodinamic instability
 Myocardial ischemia or arrhythmia
 Patient who unable cooperative
 Instability to protect the airway
 High risk for aspiration
 Active upper gastrointestinal hemorrhage
 Severe hypoxemia
 Severe enchepalopathy
 Facial trauma
 Significant agitation

F. How Are Patient Monitored On Nppv

Patients receiving N PPV must be monitored closely in a proper setting, and
continuous pulse oximetry and cardiac monitoring are suggested. Close clinical
follow-up assessments are required, ' including evaluations of the pH, Pao2, and
Paco2. Consider transition to invasive ventilation when a clear trend toward
improvement has not been observed over the first 1 or 2 hours or when the therapeutic
goals have not been achieved within the first 4 to 6 hours. Sedation should be used
cautiously and with adequate monitoring as NPPV is initiated. Additional measures .
that may be considered include application of a protective nose patch when using a
nasal mask and gastric decompression if a face mask or helmet is used. Oral intake
should be restricted until the patient has stabilized and intubation is no longer a
consideration. An algorithm for assessing NPPV is presented in Figure 5-2.
III. INVASIVE MECHANICAL VENTILATION

Mechanical ventilation via an endotracheal tube is commonly used to support critically

ill patients. it is a definitive intervention to ensure acceptable oxygenation and
ventilation with a secure airway.

Each mechanical ventilation respiratorycycle can be divided into two phases: inspiration
and expiration (Figure 5-3). Inspiration is the point at which the exhalation valve doses
and fresh gas under pressure from the ventilator enters the chest. The amount of gas
delivered during inspiration is determined by three targets that can be set on the
ventilator: volume, pressure, and! or flow. cycling the changeover from the end of
inspiration to the expiratory phase, and occurs in response to one of three parameters:
elapsed time, delivered volume, or a decrease in flow rate. During expiration, the
ventilator gas flow is stopped and the exhalation circuit is opened to allow gas to
escape passively from the lungs Expiration continues until the next inspiration begins.
trigering is the changeover from expiration to inspiration. All mechanical ventilators
require some signal from the patient (except when the patient does not interact with the
ventilator) to determine when inspiration should begin. When the patient initiates a
breath, it is called an assisted breath, and a triggering signal results when the patient's
inspiratory effort produces a drop in airway pressure or a diversion of constant gas flow
in the ventilator circuitry. In the absence of patient interaction with the ventilator,
breaths are delivered based on elapsed time (eg, at a set rate of lo breaths/minute and no
detection of patient effort. the ventilator will be triggered every 6 seconds). This is
called an unassisted or mandatory breath. Using these definitions, two ventilator breath
types are possible: full ventilator control (mandatory or unassisted) and partial ventilator
control (assisted). Spontaneous breaths (no ventilator assist) are also possible in modes
such as synchronized intermittent mandatory ventilation (SIMV) and bi-level
ventilation. The most common ventilator breaths are further described later. CPAP
allows spontaneous breathing but is a not mode of ventilation.

The respiratory cycle is the time from the initiation of one breath until the initiation of the next
breath. Triggering (A) signals the transition from expiration to inspiration; cycling (C) indicates
the transition from inspiration to eXpiration. Inspiratory pause (BC). total respiratory cycle
(ABCD). inspiration (ABC). and expiration (CD). Spontaneous breaths do not include an
inspiratory pause. The spontaneous respiratory cycle is ACD.
A. Volume Cycle A Breath

A volume-cycled breath, often called volume assist-control breath, ensures the

delivery of a prese tidal volume (unless the peak pressure limit is exceeded). On
most ventilators. the setting of peak inspiratory flow rate and the choice of
inspiratory flow waveform (square, sine, or decelerating) determine the length of
inspiration. Some ventilators change the peak inspiratory flow rate to maintain
constant inspiratory time on switching between a constant flow (square) and
decelerating flow (ramp) waveforms. With volume-cycled breaths, worsening
airway resistance or lung/chest-wall compliance results in increases in peak
inspiratory pressure with continued delivery of the set tidal volume (unless the peak
pressure limit is exceeded).

B. Time Cycled Breath

A time-cycled breath, often called pressure assist-comm! breath, applies a constant

pressure for a preset time. The application of constant pressure throughout
inspiration results in a square pressure-overtime waveform during inspiration and a
decelerating inspiratory flow waveform as the pressure gradient falls between the
ventilator (pressure remains constant) and the patient ( pressure rises as the lung
fills). Flow in this breath format is variable and this leads to variable tidal volumes.
Flow depends on the resistance of the lung. the compliance of the lung, and patient
effort. With this type of breath, changes in airway resistance or lung] chest-wall
compliance will alter tidal volume (ie, worsening of airway resistance or lung
compliance results in a decrease in tidal volume). This disadvantage of time-cycled
(pressure assist-control) breaths may be overcome by delivering pressure-regulated
volume-control breaths, in which the ventilator adjusts the pressure up or down in
response to a fall or rise of the tidal volume. Each delivered breath is a pressure-
targeted and time-cycled breath, with the ventilator adjusting the amount of
pressure applied to the airway to maintain a constant tidal volume. However, in this
dual control mode of mechanical ventilation, abnormally increased patient efforts
may lead to a pressure decrease due to the ventilator algorithm, resulting in under-
support of the acutely ill patient
 C. Flow Cycled- Breath

A flow-cycled breath, usually called a pressure support breath, is very similar to a

time-cycled breath in that a set pressure is applied constantly throughout the patient
triggered inspiration and the inspiratory flow waveform is decelerating. Pressure
support breaths are terminated when the flow rate decreases to a predetermined
percentage of the initial peak flow rate (typically 25%). As the patient’s inspiratory
effort decreases, the flow decreases, marking the proximity of the end of
inspiration.

IV. Modes Of Mechanical Ventilation

The mode of ventilation describes how one or more types of ventilator breaths
interface with the patient to provide ventilatory support. When mechanical ventilation is
initiated, the optimum ventilatory support for a given clinical circumstance and the
specific needs of the patient must be determined. CPAP is seldom used as initial support
for acute respiratory failure in an intubated patient. It is not considered a mode of
mechanical ventilation because positive pressure is not applied during inspiration. The
respiratory rate and vt are dependent on the patient’s inspiratory effort as the patient
inspires against the resistance of the endotracheal tube. it is mainly used in the final
stages of invasive ventilation, when patients are being assessed for their potential
readiness for extubation.

Commonly used modes of ventilation include assist-control (AC) ventilation, SIMV, and
PSV.The various modes are achieved by using some combination of the three types of
ventilator breaths (described earlier) and may be combined with the application of PEEP.
Airway pressure and flow tracings of spontaneous respiration, CPAP, and the different
modes of mechanical ventilation are illustrated in Figure 5-4.

These tracings have been obtained from a clinical ventilator and represent pressure and
flow tracings. Note, for example, in the tracing for pressure assist-control, the irregular
respiratory pattern created by the combination of patient-initiated breaths and the
programmed respiratory rate in the ventilator.
Airway pressure and flow tracings for spontaneous breathing, for CPAP, and for commonly used
modes of mechanical ventilation. Time Is represented on the horizontal axis and pressure or flow
on the vertical axis. The tracings for this figure have been provided courtesy of Paul Ouellet, PhD
(c) RRT, FCCM.

Each has advantages and disadvantages, as summarized in Table 5-6. In choosing a mode
of ventilation, it is important to consider specific goals, the most important of which are
adequacy of ventilation and oxygenation, reduction in the work of breathing, and the
assurance of patient comfort and synchrony with the ventilator.

Potensial advantages and disadvantages of selected mode of

mechanical ventilation

Mode Advantages disadvantages

Assist-control(AC) Patient can increease ventilatory Adverse hemodinamic effect;

ventilation support; reduced work of inappropriate hiperventilasi;
breathing compared with increased work of breathing if Vt
pernapasan spntan and flow do not meet patients
 demands

AC volume ventilation Guarantees delivery of set Vt Excessive tekanan inspirasi

(pressure assist-control (unless peak pressure limit is
) exceede)

Ac tekanan ventilasi Limitation of peak inspiratory Vt decreases or increases with

tekana; variabel flow lung resistence
rateaccomodate patients
demands

Ventilasi tekanan Patient comfort; improved Apnea alarm may not tringger
pattient-ventilator interaction; backup ventilation mode;
decreased work of berathing variabble patient tolerance

Sychronized Less interference with normal Increased work of breathing

intermittent mandatory cardiovascular unction compared with Ac
ventilation

Controlled mechanical Rests muscles of respiration Requires use of sedation/

ventilation (CMV) completely neuromuscular blockade, adverse
efek hemodinamic

A. Assist-Control Ventilation

AC ventilation is typically delivered with either volume-cycled (volume assist-

control) or time cycled (pressure assist-control) breaths. In volume AC, a preset VT
with a preset flow rate is delivered at a preset minimum rate. Similarly in pressure
AC, a preset airway pressure is delivered for a preset length of inspiratory time. The
patient receives the minimum number of ventilator breaths (set rate); however, the
total number of breaths may be higher if the patient triggers the ventilator with
additional inspiratory efforts. This mode of ventilation is commonly used when
mechanical ventilation is initiated in patients with acute respiratory failure.

With proper use of AC, the work of breathing may be significantly decreased. If the
ventilator and the patient are not in synchrony, orif the ventilator inspiratory flow
rates are not matched to the patient’s demand, however, this mode may result in an
increase in the patient’s work of breathing.
 This mode has aiso been called continuous mandatory ventilation (CNN), which
more accurately represents a situation in which the patient doesn’t trigger additional
breaths (ie, absent respiratory drive) (Section D) .

B. Pressure Support Ventilation

PSV provides a preset level of inspiratory pressure assist with each ventilator
detected patient effort. This inspiratory assist is selected to overcome the increased
work of breathing imposed by the disease process, endotracheal tube, inspiratory
valves, and other mechanical aspects of ventilatory support. The set amount of
pressure that is applied augments each patient-triggered breath. All breaths are flow
cycled. With PSV, the patient controls the respiratory rate and exerts a strong
influence on the duration of inspiration, inspiratory flow rate, and Vr. In addition. the
delivered Vr is influenced by pulmonary compliance and resistance. Rapid changes
in these parameters potentially alter the tidal volume and work of breathing. PSV
may be coupled with SIMV. primarily as a means to diminish excess work of
breathing for spontaneous breaths occurring between mandatory breaths (Section C).

The amount of pressure support is titrated according to the patient’s Vr measured by

the ventilator during expiration. Suggested parameters include a setting that achieves
one or more of the following goals:

- AVr of 6 to 10 mLIltg, depending on patient needs

- A slowing of spontaneous breathing rate to an acceptable range

- The desired minute ventilation

Appropriate apnea alarms and a backup ventilation setting are essential. Potential
benefits of PSV include the comfort and tolerance this ventilatpry mode offers some
patients. In addition, PSV may reduce the work of breathing by diminishing patient-
ventilator asynchrony. Typically, as pressure support is increased in patients with
lung disease, the patient's work of breathing and respiratory rate decrease and Vt
increases. With PSV, an endotracheal tube cuff leak may interfere with appropriate
 cycling because flow may never drop to the preset threshold for cycling (typically
25% of the peak flow rate).

C. Syncronized Intermitent Mandatory Ventilation

SIMV delivers either volume-cycled or timecycled breaths at a preset mandatory

rate. Volume cycling is most commonly used for the mandatory breaths. Between
mandatory breaths. the Patient can breathe spontaneously through either a demand
valve or a continuous flow of gas. The addition of pressure support to these patient-
initiated breaths is recommended, using a value, that offsets the resistance of the
endotracheal tube. Typically, SIMV is initiany set to deliver full ventilatory support.
and support is then decreased as the patient tolerates spontaneous breathing.
Synchronization allmws for enhanced patient-ventilator interaction by delivering the
presset vt

V. CHOSING A MODE AND INITIAL VENTILATOR SETTINGS

The most important goals of mechanical ventilation are adequacy of ventilation and
oxygenation, a reduction in the work of breathing, and the assurance of patient comfort
and synchrony with the ventilator. Choosing a mode of mechanical ventilation depends
on the reason it is required and the underlying disease process. In general, AC is used as
the initial mode for a patient needing invasive mechanical ventilation. Each mode has
both advantages and disadvantages, as summarized in Table 5-6. When initiating
ventilatory support in adults, an Fio2 of 1.0 is used to ensure maximal amount of
available oxygen during the patient’s adjustment to the ventilator and during the initial
attempts to stabilize the patient’s condition. In addition, the high level of oxygen offers
support for complications that may have occurred before and during intubation. The
usual recommended VT level is 8 to 10 mLI kg and should be calculated by using
predicted body weight (to estimate predicted body weight, see the formulas on the next
page). Higher VT levels should be avoided to reduce the possibility of pulmonary
injury. An appropriate respiratory rate should be set to achieve the desired minute
ventilation. Normal minute ventilation (vt x respiratory rate) is approximately 7 to 8
lein, but certain conditions may require levels that more than double this baseline.
Minute ventilation should be adjusted to produce the paco2 level that allows an
acceptable acid-base (pH) status for the patient's clinical condition. As a general rule,
F102, mean airway pressure, and PEEP affect the Pao2 whereas the respiratory rate, VI),
and VT affect alveolar minute ventilation and Paco2. One should be cognizant of the
fact that in many circumstances (acute respiratory distress syndrome and severe
obstructive lung disease), the goals of mechanical ventilation are not to normalize blood
gases. Hypercapnia and respiratory acidosis are tolerated in such situations to achieve
goals such as minimizing dynamic hyperinflation and avoiding ventilator-associated
lung injury. guidelines for the iniyiation of mechanical ventilation are listed in Table 5-
7.

Tabel 5.7

Guidlenes For The Initiations Of Mechanical Ventilation

1. Choose the ventilator mode with which you are most familiar. The primary goals of
ventilatory support are adequate oxygenation! ventilation. reduced work of
breathing synchrony between patient and ventilator, and avoidance of high end-
inspiration alveolar pressures.

2. The initial fio2, should be 1.0. The Fro2 thereafter can be titrated downward to
maintain the Spo2 at 92% to 94%. In severe acute respiratory distress syndrome an
Spoz 288% may be acceptable to minimize complications of mechanical
ventilation.

3. Initial Vt: -8 to 10 ml/kg In patients with relatively normal lung compliance. in

patients with poor lung compliance leg, ARDS a target Vrof 6 mng by PBW Is
recommended to avoid overdistension and to maintain an inspiratory plateau
pressure <30 cm H20. (See Section Vlll for more information.)

4. Choose a respiratory rate and minute ventilation appropriate for the particular
clinical requirements. Target pl-l. not Paco2

5. Use PEEP to diffuse lung Injury to maintain open alveoli at and expiration. If
volume Is held constant. PEEP may increase peak inspiratory plateau pressure a
 potentially undesirable effect In ARDS. PEEP levels >15 cm H20 are rarely
necessary.

6. Set the trigger sensitivity to allow minimal patient effort to initiate inspiration.
Beware of auto-cycling if the trigger setting is too sensitive.

7. In patients at risk of obstructive airway disease, avoid choosing ventilator settings

that limit expiratory time and cause or worsen autoE PEEP (see Section Vl)

8. Call the critical care consultant or other appropriate consultant for assistance.

VI. CONTINUNG CARE DURING MECHANICAL VENTILATION

After mechanical ventilation has been initiated. the following parameters should be
assessed and titrated to achieve the desired goals. Many important inter-relationships
exist amongventilator settings, and the consequences of making any change must be
appreciated. This interdependency alparameters may lead to beneficial or harmful
effects in the respiratory andlor cardiovascular systems. Critical care consultation
should be obtained for complex patients.

A. Inspiratory Pressure
During positive pressure volume assist-control ventilation, airway pressure rises
progressively to a peak inspiratory pressure (Ppeak; Figure 5-5), which is reached
at end inspiration. The Ppeak is the sum of the pressure required to overcome
airway resistance and the pressure required to overcome the elastic properties of the
lung and chest wall. Ppeak, sometimes referred to as peak airway pressure, is
affected by many other variables, such as the flow rate, diameter of the
endotracheal tube, secretions, and diminished bronchial diameter. When an
inspiratory hold is applied at the end of inspiration, gas flow ceases, all dynamic
factors are eliminated, and the pressure drops to a measurement called the
inspiratory plateau pressure (Pplat). The Pplat reflects the pressure required to
 overcome the elastic recoil within the lung and chest wall and is, contrary to the
Ppeak. a static pressure. The Pplat is the best estimate of peak alveolar pressure,
which is an important indicator of alveolar distension. Accurate measurement of
Pplat requires the absence of any patient effort, and an inspiratory hold for a
minimum of 0.5 seconds.
Potential adverse effects from high inspiratory pressures include barotrauma,
volutrauma, and reduced cardiac output. Barotrauma (pneumothorax,
pneumomediastinum) and volutrauma (lung parenchymal injury due to
overinflation), although linked to high Ppeak, correlate best with Pplat. As
mentioned earlier, an example of the relationship of Ppeak and Pplat to alveolar
distension is demonstrated by the effect of endotracheal tube size on Ppeak and
Pplat. As the intemal diameter of an endotracheal tube is decreased in a patient
receiving volume ventilation, the same V'r will result in higher Ppeak, yet Pplat and
alveolar distension remain unchanged as the pressure is dissipated across the
resistance of the endotracheal tube. The same VT, regardless of the type of breath,
produces the same alveolar distension at end inspiration. To avoid injury in patients
receiving mechanical ventilation, inspiratory plateau pressure should be maintained
<30 cm H20. The relation of Ppeak and Pplat is illustrated in Figure 5-5.
This figure demonstrates airway pressure tracings for typical volume assist-control
ventilation under conditions of normal compliance and resistance, increased airway
resistance, and decreased respiratory system compliance. When resistance is
increased, the waveform of pressure versus time will demonstrate an increase in
peak inspiratory pressure to reflect the pressure required to deliver a lixed tidal
volume against increased airway resistance. Plateau pressure, obtained during an
inspiratory hold, is unchanged. When compliance is decreased, as in the third
tracing, both peak inspiratory pressure and plateau pressure rise for a fixed tidal
volume. As resistance is unchanged, the difference between peak pressure and
plateau pressure is not affected.
Elevated Pplat may be reduced by the following interventions :
 Decreased PEEP, which may also decrease oxygenation and worsen alveolar
collapse ( if PEEP is used to improve oxygenattion and alveolar stability).
  Decrease VT, which may lead to hypercapnia due to a reduction in minute
ventilation.
 Decrease auto-PEEP (see next section) with interventions that prolong the
expiratory time, understanding that this may lead to hypercapnia.
B. Relation Of Inspiratory Time To Expiratory Time And Auto PEEP

If the expiratory time is too short to allow full exhalation, the previously delivered
bréath is not completely expired and the next lung inflation is superimposed upon the
residual gas in the lung. This results in lung hyperinflation and PEEP over and above
the preset level on the ventilator. This increase in end-expiratory pressure is called
auto-PEEP, or intrinsic, inadvertent, or occult ' PEEP. Auto-PEEP can be quantified by
using manual methods or through electronic programs within some ventilators during
an expiratory hold maneuver. However, it is most easily diagnosed qualitatively by
viewing the flow-versus-time graphic waveform tracing available on most mechanical
ventilators, as the expiratory flow fails to reach the zero flow level before the initiation
of the next breath (Figure 5-6). The potentially harmful physiologic effects of auto-
PEEP on peak. plateau. and mean airway pressures are the same as those of preset
PEEP. In addition, high levels of PEEP may decrease venous return to the heart,
resulting in hypotension and higher Pooz due to increased dead space, and adversely
affect oxygenation (especially with asymmetric lung disease)
Figure 5-6. Flow-versus-time Waveform Demonstrating Auto-PEEP

Auto-PEEP is demonstrated by the failure of the expiratory flow to return to zero

before inspiratory flow is initiated. Auto-PEEP may be reduced by the following
interventions:

 I Decrease respiratory rate by changing the set rate or sedating the patient. These
interventions result in fewer inspirations per minute and thus increase the total
expiratory time available; this is the most effective way of decreasing auto-PEEP.

 I Decrease vt, which requires less time to deliver a smaller breath and allows more
time for exhalation.

 I Increase gas flow rate. delivering the VT faster and allowing more time in the
cycle for exhalation. This intervention has little impact unless the initial how rate
was set at an extremely low level.

 Changing the inspiratory waveform from decelerating (ramp) to constant (square).

The first two interventions, as discussed earlier, may lead to hypercapnia due to a
reduction in minute ventilation; however; the benefits of a decrease in auto-PEEP
despite the lower minute ventilation may lead to little change in Paco2. When severe
 air trapping occurs, allowing sufficient expiratory time may improve ventilation and
C02 removal. Hypercapnia and a controlled reduction in pH (permissive hypercapnia)
may be acceptable in some clinical conditions but requires expert consultation. This
approach may not be suitable for patients with intracranial hypertension because
hypercapnia causes cerebral vasodilation and further increases in the intracranial
pressure.

C. Fio2

High levels of inspired oxygen may be harmful to lung parenchyma after prolonged
exposure. Although the prease threshold for concern is not known, it is desirable to
reduce the Fi02 <0.5 (50% oxygen) within the first 24 hours. However, hypoxemia is
always considered a greater risk to the patient than high Fro2 levels.

The primary determinants of oxygenation during mechanical ventilation are Flo2 and
mean airway pressure (Paw), VT, [:13 ratio, inspiratory flow rate, PEEP, auto-PEEP,
use of inspiratory pause, and the inspiratory: flow warreformn pattern (volume
breaths). In the patient with acute lung injury (All) and acute respiratory distress
syndrome (ARDS). PEEP becomes a major determinant of mean airway pressure. The
Inter-relationships of these various parameters, as already demonstrated. often lead to
complex adjustments Within the plan for mechanical ventilation. ‘

D. Minute ventilation and alveolar minute ventilation

Minute venyilation. defined as the amount of gas exchanged by an individual in 1

minute, is calculated as the respiratory rate multiplied by mean Vt. The primary
determinant og co2 excange during mevhanical ventilation is the alveolar minute
ventilation. calcuhted as va=(vt-vd)f

where Vn is dead space and f is the respiratory rate (Chapter 4). The Vr, the respiratory
rate, and their inter-relationships with other ventilatory parameters have already been
discussed. Physiologic VD represents, in general, lung units that are relatively well
ventilated but underperfused. The physiologic effect of high amounts of V0 is
hypercapnia. Dead space may result from the pathologic process in the lung or from
 mechanical ventilation complicated byliigh airway pressures. low intravascular
volume, or low cardiac output. It may be necessary to use a low Vt to avoid high
airway pressure and] or a low respiratory rate to avoid auto~PEEB thus permitting
hypoventilation and hypercapnia.

As previously discussed, adequate ventilation is assessed by consideration of both the

Paco2, and the pH. Hyperventilation resulting in a low Paco2, level may be an
appropriate short-term compensatory goal during metabolic acidosis while the primary
etiology is corrected. Similarly, a patient with chronic hypercapnia has an increased
baseline Paco2, and maintains a near-nomial pH by renal compensation (increased
bicarbonate retention). Patients with chronic compensated hypercapnia should receive
sufficient minute ventilation during mechanical ventilation to maintain the Paco2 at
their usual level, and utmost attention should be paid to the pH to avoid severe
alkalemia and loss of retained bicarbonate.

E. Humidification

Gases delivered by mechanical ventilators are typically dry, and the upper respiratory
tract is bypassed by artificial airways, resulting in loss of heat and moisture. Heating
and humidification of gases are routinely provided during mechanical ventilation to
prevent mucosal damage and minimize inspissation of secretions. Available systems
include passive humidifiers (artificial nose) or active, microprocessor-controlled heat
and humidifying systems (heated humidifiers).'l‘he passive humidiiiers are
contraindicated in the presence of copious secretions, minute ventilation >12 Ll min,
air leaks >15% of delivered tidal volume, or blood-in the airway.

F. Use of Positive end-expiratory Pressure (PEEP)

PEEP is the cornerstone strategy employed for disease states that cause alveolar
collapse or airway closure (eg. ARDS). It causes alveolar recruitment and prevents
repeated opening and closing of the alveoli (atelectrauma). Titration of PEEP for
hypoxernic respiratory failure secondary to ARDS can be performed according to the
PEEP! Fro2 combinations given in Table 5-8. In cases of severe obstructive lung
disease, applying external PEEP and setting it close to the auto-PEEP value can help
 offset the work of breathing to trigger the ventilator. Seeking expert consultation is
prudent if higher levels of PEEP are required to maintain oxygenation.

G. Prophylactic Therapies

Mechanical intubation is a risk factor for venous thromboembolism, gastric stress

ulceration, and nosocomial pneumonia. Measures to prevent venous thromboembolism
include the prophylactic use of antiooagulation (unless contraindicated) and/or
pneumatic compression devices. Using a proton pump inhibitor or histaminez-receptor
blocker is warranted for stress ulcer prevention. The risk of ventilator-associated
pneumonia (ventilator bundle) is reduced by elevating the head of the bed to 230°. oral
hygiene, and daily evaluations for liberation from mechanical ventilation. Please see
Appendix 12 for prophylactic therapies and Appendix 10, Table A1 0-3 for the
ventilator bundle

VII. SEDASI, ANALGESIA DAN BLOKADE NEUROMUSCULAR

Endotracheal intubation and mechanical ventilation can be uncomfortable and anxiety

provoking. To improve the patient’s comfort and synchrony with the ventilator, anxiolytics,
sedatives, and analgesics may be administered. Neuromuscular blocking agents should be
used with caution, and expert consultation should be sought beforehand. Guidelines for the
use of these agents are outlined in the Society of Critical Care Medicine's Clinical Practice
guidlines for sustained neuromuscular blokade in the Adult Critically 111 Patient. Caution
 also should be taken with use of sedation in nonintubated patients with acute respiratory
insutiiciency or impending respiratory failure

VIII. VENTILAGORY GUIDLINES FOR SPESIFIC CLINICAL SITUATIONS

A. Acute lung injury/ acute respiratory distress sindrom

case study

An 18-year~old female patient is brought to the emergency department after being

found unresponsive at a party where alcohol was consumed. The paramedics reported
vomitus in the oral cavity and a difiicult intubation due to copious foreign matter. In
spite of baq-mask ventilation with 100% oxygen her oxyhemoglobin saturation
remained 87% to 88% during transport. The initial assessment reveals diffuse crackles.
more prominent on the right hemithorax. and a chest radiograph shows diffuse
bilateral infiltrates. The ventilator alarm is constantly warning of high pressure.

- What ventilator settings are recommended for this patient?

- What steps should be taken to avoid triggering the pressure alarm?

- What parameters should be measured and monitored?

ALI and ARDS cause a decrease in lung compliance, making the lungs stiff and
difficult to inflate, and produce hypoxemic respiratory failure (Chapter 4). Guidelines
for mechanical ventilation in ALI and ARDS are outlined in Tables 5-8 and 5-9. High
Ppeak and Pplat complicate mechanical ventilation because of the low lung
compliance or high airway resistance. Lower Vr is required and the Pplat should be
maintained at the desired level of 530 cm H20; permissive hypercapnia may be
required to accomplish that goal. The F102 is increased as necessary to prevent
hypoxemia but reduced as soon as other ventilatory interventions are effective.
Because of increased shunt in ARDS, hypoxemia may be severe. PEEP is the most
effective way to improve oxygenation and is typically applied in the range of 8 to 15
cm H20, based on the severity of hypoxemia. Higher PEEP levels may be indicated in
severe lung injury. Although patients with ARDS are somewhat less likely to develop
 auto-PEEP because expiratory time requirements are reduced due to decreased lung
compliance (stiffness), its presence should be monitored, especially at higher 11E
ratios. Table 5-9 outlines the recommended strategy for ventilating patients with
ARDS. Table 5-8 outlines the recommended Fro2 and PEEP combinations.

B. Obstrukif Airway Disease

Mechanical ventilation for patients with asthma and chronic obstructive pulmonary
disease is designed to support oxygenation and assist ventilation until airway
obstruction has improved. Mechanical ventilation in these patients may produce
hyperinflation, auto-PEEP, and resultant hypotension. Therefore, careful attention is
needed to balance cycle, inspiratory, and expiratory times.

The initial VT should be «6 to 8 mL/kg, and the minute ventilation should be adjusted
to a low normal pH. With volume ventilation, the inspiratory flow rate should be set to
optimize the 1:13 ratio and allow complete exhalation. Such management reduces
breath stacking and the potential for auto-PEEP. As flow rate increases, Ppeak may rise
but not be mirrored in the Pplat; this is a function of airways resistance and not an
indication of worsening lung compliance.

'while the patient is support with mechanical ventilation, airway obstruction should be
aggressively treated with bronchodilators (Chapter 4). As airflow improves, the
patient Will tolerate higher Vr levels and longer inspiratory times

XI. MONITORING MECHANICAL VENTILAGORY SUPPORT

Patients who receive mechanical ventilatory support require continuous monitoring to assess
the beneficial and potential adverse effects of treatment (Table 510). Arterial blood gas
measurements provide valuable information about the adequacy of oxygenation, ventilation,
and acid-base balance. This information is essential during the initial phases of ventilatory
support and during periods of patient instability. If available, a pulse oximeter (Chapter 6)
and end-tidal capnometer (for measuring end-tidal c02) can be used to further monitor the
patient progress
 Rekomendations For Monitoring Mechanical Ventilation

1. Obtain a chest radiograph after intubation and additional chest radiographs as indicated to
evaluate any deterioration in status.

2. Obtain arterial blood gas measurements after initiation of mechanical ventilation and
intermittenly. based on patient status.

3. Measure vital signs frequently and observe the patient directly (including patient-
ventilator interaction).

4. Measure inspiratory plateau pressure as clinically appropriate.

5. Use pulse oximetry to monitor oxygenation.

6. Use ventilator alarms to monitor key physiologic and ventilator parameters.

X. HIPOTENSION ASSOCIATED WITH INITIATION OF MECHANICAL

VENTILATION

A. Tension Pneumothorax

When hypotension occurs immediately after initiation of mechanical ventilation, tension

pneumothorax should be one of the first considerations. This diagnosis is based on a
physical examination that finds decreased or absent breath sounds and tympany to
percussion on the side of the pneumothorax. Ttacheal deviation away from the side of the
pneumothorax may be observed. although it is uncommon after placement of an
endotracheal tube. Treatment includes emergent decompression by inserting a large-bore
catheter or needle into the second or third intercostal space in the midclavicular line
(Appendix 8). Treatment should not be delayed awaiting a chest radiograph. The insertion
of a catheter or needle is both diagnostic and therapeutic: it improves blood pressure and
reverses the findings of physical examination. The insertion of the catheter or needle must
be followed by chest tube placement.
B. Conversion From Negativ To Positive Intrathoracic Pressure

Normal intrathoracic pressure is slightly negative relative to the atmosphere. When

positive pressure ventilation is initiated, intrathoracic pressure becomes positive. As
intrathoracic pressure rises, right atrial pressure rises and the intravascular pressure
gradient for return of blood from the large extrathoracic veins into the right heart
decreases. As a result, blood return to the heart may be reduced. Left ventricular preload,
stroke volume, cardiac output, and blood pressure then may decrease in sequence.
Underlying intravascular volume depletion exacerbates the deleterious effects of the
increased intrathoracic pressure on cardiac output and blood pressure. 'lreatment of this
common complication includes volume resuscitation by means of rapidly infused fluid
boluses to raise extrathoracic venous pressure and increase venous return to the right
heart until the blood pressure increases. Oxygen saturation should be monitored to avoid
overly aggressive fluid resuscitation. Use of ventilation techniques associated with high
mean airway pressure may

C. Auto – PEEP

Auto-PEEP occurs when the combination of ventilator settings and patient physiology
results in an inadequate expiratory time. Excessive end expiratory pressure may increase
intratlroraeie pressure and cause hypotension due to decreased venous return to the heart.
Although aim-PEEP may occur in any patient. those with obstructive airway disease are
particularly predisposedto this condition. Assessment and treatment of auto-PEEP are
performed as previously described.

D. Acute Myocardial Ischemia

Stress from the cause of acute respiratory failure, as well as the stress of intubation itself,
may lead to increased myocardial oxygen demand and to acute myocardial ischemia,
infarction, and subsequent hypotension. Patients at high risk should be evaluated with
serial electrocardiograms and myocardial markers of injury.
 Key points

 The primary goals of noninvasive and invasive positive pressure ventilation are to
support ventilation and oxygenation and to reduce writ of breathing while orienting
patient comfort.

 NPPV is best utilized in the alert. Cooperative patient whose inspiratory condition is
expect to improve in 48 to 72 hours.

 The advantages and disadvantages of the different modes of invasive mechaniml

ventilation must be considered when determining the optimal ventilatory support £0! the
patient’s clinical condition.

 Guidelines for initiating mechanical ventilation should be carefully followed, with

adjustments made based on patient assessment and monitoring.

 The complex intetactions of inspiratorypressures, I:E ratio Fi02 and PEEP must be
appreciated to evaluate the potential benefits and harmfull effects in each patient.

 The primary determinants of oxygenation are Fio2, and mean airway pressure whereas
alveolar ventilation primarily affects co2 exchange

 During mechanical ventilation a patient must be closely monitored using the ventilator
alarm systems, continuous pulse axitnetry, attentive physicald assessment. measurement
of inspiratory plateau pressure (as clinically appropriate), and intermittent arterial blood
gases and chest radiographs as needed.

 The inspiratory plateau pressure should be maintained below 30 cm H20

 Hypotension occurring immediately after initiation of invasive mechanical ventilation

should prompt evaluation for tension pneumothorax. decreased venous blood return due
to intrathoratic pressure, auto-PEEp or myocardial ishcemia. , ‘