2. Outlines
Introduction
Type and working principle of MV
Modes of ventilation and initial ventilator setting
Common alarm settings and MV Troubleshooting
Respiratory failure
References
9/8/2022 2
4. Introduction
Mechanical ventilation
Used to replace fully or partially the functions of
spontaneous breathing by performing the WB and
gase exchange
Apart from its supportive role in OR, MV support
is indicated when spontaneous ventilation is
inadequate for the sustenance of life
9/8/2022 4
5. Cont,
History of MV
Galen’s observations on the respiratory and
circulatory systems in the 2nd century
The Drinker Respirator,
“iron lung” was offered by John Emerson in 1932.
In the 1940s and 1950s, polio epidemics
Copenhagen in 1952, when Bjorn Ibsen…positive
pressure ventilation
9/8/2022 5
7. Cont,
As a result two basic methods have been
developed to replace the normal mechanisms
of breathing:
Negative pressure ventilation
Positive pressure ventilation
9/8/2022 7
9. Cont,
Positive Pressure Ventilation
PPV occurs when a MV is used to deliver air into
the patient’s lungs by way of an endotracheal tube
or positive pressure mask.
During inspiration the pressure in the alveoli
progressively builds and becomes more positive.
At the end of inspiration, the ventilator stops
delivering PPV mouth pressure returns to ambient
pressure.
And the direction of airflow changes then
9/8/2022 9
11. Cont,
Power Source Or Input
Power
an electrical or
pneumatic (compressed
gas) source.
Pneumatic Circuit:
is a series of tubes that
allow gas to flow inside the
ventilator and between the
ventilator and the patient.
Divided as internal and
external pneumatic circuits
Control Systems And
Circuits:
Can be open closed loop
system
Closed-loop systems
The control panel, or user
interface,
is located on the surface of
the ventilator
It is monitored and set by
the ventilator operator.
Adjuncts?
9/8/2022 11
12. Cont,
Pressures In PPV:
Baseline Pressure:
Airway pressures are measured relative to a baseline
value.
The baseline pressure is zero (or atmospheric).(ZEEP)
The baseline pressure is higher than zero when non
zero value is set(PEEP)
9/8/2022 12
13. Cont,
Positive end expiratory pressure
PEEP increases the volume of gas remaining in the
lungs
At the end of a normal exhalation PEEP increases the
FRC.
PEEP applied by the operator is referred to as extrinsic
PEEP.
Auto-PEEP (or intrinsic PEEP), is air that is accidentally
trapped in the lung.
9/8/2022 13
15. Cont,
Peak Pressure:
This is the highest pressure recorded at the end of
inspiration.
PinP is also called peak inspiratory pressure (PIP) or
peak airway pressure.
These pressures measured during inspiration are the
sum of:
a) the pressure required to force the gas through the
resistance of the airways (PTA)
b) and the pressure of the gas volume as it fills the alveoli
(Palv).
9/8/2022 15
16. To assist a breath, the ventilator drops the pressure below baseline by 1cm H2O. The
assist effort is set at +9cm H2O.
9/8/2022 16
17. Cont’d
Plateau Pressure :
The plateau pressure is measured after a breath
has been delivered to the patient and before
exhalation begins.
Exhalation is prevented by the ventilator for a
brief moment (0.5 to 1.5 s).
9/8/2022 17
21. Modes of mechanical ventilations
Each ventilator-controlled respiratory cycle
can be divided into four phases
9/8/2022 21
22. Cont,
Variables
Variables are elements of a breath that a ventilator
can control during breath delivery.
There are two kinds of variables, control variables and
phase variables.
Control(targeted) Variables
Only one of the three control variables – volume, pressure,
or flow – can be used to control the shape of a breath.
Accordingly the MV mode become volume, pressure, or
flow controlled
9/8/2022 22
23. Cont,
Phase Variables
How the ventilator controls the phases of the
respiratory cycle .
Can be trigger variable, cycle variable, and
baseline variable.
The Triggerring Variable
Triggering is the mechanism that the ventilator uses to
cycle from expiration to inspiration.
A ventilator-driven breath
patient initiated (patient-triggered).
9/8/2022 23
24. Cont,
Cycle Variable
The changeover from inspiration to expiration and
from expiration to inspiration is called cycling.
different ways to cycle between inspiration and
expiration
• time, volume or flow cycled
9/8/2022 24
25. Cont,
Baseline Variable
This is the variable that is controlled at end
exhalation.
Most often, the baseline variable controlled is
pressure.
The end expiratory pressure may be set to zero
(ZEEP), or may be non zero PEEP
9/8/2022 25
26. Cont,
Waveforms
are graphical representation of data collected by the
ventilator.
Waveform analysis can help in determining & early pick
ventilation problems
Two types of waveforms
a) Scalars - variables plotted against time.
Pressure Vs time
Flow Vs time
Volume vs time.
b) Loops - two variables plotted against each other.
Pressure-volume loop,
Flow-volume loop
9/8/2022 26
32. Cont,
Controlled mechanical
ventilation(CMV)
Does not need any patient
effort
Paralysed, heavily sedated
and comatose pts are
candidates
Can be either pressure or
volume targeted
Most Modern Mechanical
ventilators have no this
mode, Why?
Asisst control (AC) mode:
Has risk of hyperventilation
and VILI when the patient
has breathing effort
Can be volume or pressure
controlled
Better option for critically
ill patients who requires
constant VT or full support
9/8/2022 32
34. Cont,
Synchronized intermittent
mandatory ventilation
(SIMV)
Variation of IMV in which the
ventilators breath is
synchronized with the
patients inspiratory effort
The support ranges from zero
to full supports and is
important for weaning from
MV
was introduced to avoid the
problems associated with
IMV.
Advantages over AC modes?
Intermittent mandatory
ventilation (IMV)
the spontaneous breath is not
machine supported and
mandatory breathes are not
synchronized with patient
effort
Has risk of of asynchrony,
breath stacking and increased
work of breathing
9/8/2022 34
35. Pressure-Regulated
Volume Control(PRVC)
is designed to deliver a
volume-targeted, pressure-
control breath.
the ventilator automatically
adjusts pressure between
breaths to reach the targeted
volume in response to varying
patient conditions.
The pressure-control value is
then gradually increased or
decreased until the target tidal
volume .
Advantages?
dual Modes and
Adaptive Control
best characteristics of
both pressure-and volume-
control ventilation.
When using a single
variable as the control, with
pressure control, volume
varied and with volume
control, pressure varied.
9/8/2022 35
36. Cont,
High-Frequency Ventilation
have been in use since the 1960s.
High-frequency ventilation employs very low VT,
less than physiologic VD (about 3rd of VT) and very
rapid RR (> 60 breaths/min).
Used for:
patients in the face of large air leaks with major airway
disruption
rescue technique in adult ARDS
in infants with RF unresponsive to conventional MV
9/8/2022 36
37. Cont,
There are four major types of HFV that differ
based on breath delivery design.
High-frequency positive pressure ventilation
(HFPPV)
High-frequency jet ventilation (HFJV)
High-frequency oscillatory ventilation (HFOV)
High-frequency percussive ventilation (HFPV)
Neurally adjusted ventilatory assist (NAVA)
9/8/2022 37
39. Cont,
Spontaneous Modes
There are three basic means of providing support
for continuous spontaneous breathing (CSV)
during MV:
Spontaneous breathing
Continuous positive airway pressure (CPAP)
Pressure support ventilation (PSV)
APRV
9/8/2022 39
40. cont,
PSV
is a special form of assisted ventilation.
provides a constant pressure during inspiration
once it senses that the patient has made an
inspiratory effort
the patient must have a consistent, reliable
spontaneous respiratory pattern
The operator sets the inspiratory pressure, PEEP,
flow cycle criteria, and the sensitivity level.
9/8/2022 40
41. Cont,
CPAP
Ventilators can also provide CPAP for spontaneously
breathing patients.
In the acute care setting, CPAP may be helpful for
improving oxygenation in Pts with refractory hypoxemia .
The ventilator can provide a means of monitoring the
patient.
BPAP
also called bilevel pressure assist, often used in NIV. .
The operator sets two pressure levels:
Inspiratory positive airway pressure
Expiratory positive airway pressure
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42. Cont,
The Indications for Mechanical Ventilation
Hypoxic RF
Hypoventilation(hypercarbic RF)
Increased Work of Breathing
Airway protections
Other Indications
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43. Initial ventilator settings
Regardless of the method used for selecting the
VT ,be aware of risks below:
a) Overdistention of lung tissue
b) Repeated opening and closing
c) Inadequate VT setting
modes of ventilation are frequently chosen based
on:
the lung pathology & hemodynamics,
oxygenation,
lung mechanics,
clinician familiarity
9/8/2022 43
44. Initial ventilator settings
The MV monitor screen
contains mainly 3 data
types:
The set data value, alarm
settings and patient data
What we set on MV:
VT/Pinsp, RR
PEEP, FIO2
I:E ratio, Flow rate
Trigger sensitivity
Flow triggers
Alarm setting
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45. Cont,
PCV
Lower PAP?
Homogenous gas
distributions
Improved pt-vent
synchrony
Earlier liberation from
MV
VCV
Can guarantee constant
VT
Good forlung protective
ventilation protocol
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46. Specific considerations
COPD and asthma an initial VT of 6 to 8 mL/kg
with a rate of 8 to 12 breaths/min
chronic or acute restrictive disease, such as
pulmonary fibrosis or ARDS, an initial VT of 4
to 6 mL/kg +rate 15 to 25bpm
The VT should be adjusted to maintain Ppl <30
cm H2O and RR adjusted to minimize auto-
PEEP
9/8/2022
46
47. Cont,
ARDS pts…VC/PC?
COPD/asthma…VC/PC?
intracranial pathology?
Significant air leak?
For those with bariatric surgery?
o No statistically significant difference in mortality,
oxygenation & WB b/n VCV &PCV in general
9/8/2022 47
50. Cont,
Hypoxia:
occurs when oxygen supplies are
insufficient to meet oxygen demands in a
particular compartment (PaO2<80%)
Tissue hypoxia may be subdivided into four
main Types: hypoxaemic, anaemic, stagnant
or histotoxic.
Oxygen therapy may only correct hypoxia
due to hypoxaemia,
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51. Hypoxemic respiratory failure
is a consequence of gas exchange failure and is
recognized by hypoxemia (PaO2<60mmHg)
Hypoxaemic hypoxia( hypoxic hypoxia):
is present when the oxygen content in the blood
is low due to low PaO2.
This occurs naturally at high altitude or occurs
secondary to right-to-left shunts, V/Q mismatch,
alveolar hypoventilation or diffusion impairment.
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54. Cont,
Anaemic hypoxia:
Anaemic hypoxia results from a reduced level of Hbn
available for oxygen transport.
Circulatory (Stagnant hypoxia):
s a low level of oxygen in the tissues due to
inadequate blood flow (either globally or regionally).
Histotoxic hypoxia:
Due to inability of the tissues to use oxygen due to
interruption of normal cellular metabolism..
9/8/2022 54
58. Cont,
Treatment of Acute Respiratory Failure
find and treat the underlying cause, if possible.
Support can be given to the patient during the workup
and treatment and should not be delayed.
Noninvasive support measures including supplemental
oxygen, inhaled bronchodilators and NIV with CPAP&BPAP
More severe manifestations of respiratory failure like
ARDS, multilobar pneumonia, neuromuscular diseases,
and cardiogenic shock usually require intubation and
mechanical ventilation.
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59. 9/8/2022 59
is not a therapeutic intervention.
The goal of ventilation is to simply maintain
adequate gas exchange and metabolic function
while the underlying disease process gets treated
or resolves on its own.
Focus be on treating reversible causes of RF and
minimizing further injury to the patient.
60. Acute Respiratory Distress Syndrome
is a diffuse inflammatory injury of the lungs responsibl
for 10% of ICU admission and 25% of cases of
prolonged MV worldwide
Chxzed by acute onset, severe hypoxemia, and bilateral
pulmonary infiltrates without evidence of left HF
Pathogenesis:
activation of circulat neutrophils W/C attach to the
endothelium… migrate into the lung parench …
degranulati and release inflamm cytokine
damages the capillary endothelium,
exudation of protein-rich fluid that fills the distal airspaces
and impairs pulmonary gas exchange
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64. Cont,
CLINICAL FEATURES:
The earliest signs of ARDS
are the sudden appearance
of hypoxemia and signs of
RD
The chest x-ray can be
unrevealing in the first few
hours after symptom onset,.
Progressive hypoxemia
requiring mechanical
ventilation often occurs in
the first 48 hours of the
illness.
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66. Diagnostic criteria
Many clinical features of ARDS are nonspecific, and
are shared by other conditions that cause hypoxemic
respiratory failure.
This creates a tendency for misdiagnosis
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68. ARDS management
MECHANICAL VENTILATION
about 80% of patients with ARDS require
mechanical ventilation.
There are two general goals of mechanical
ventilation in ARDS:
(a) limit the stretch imposed on the distal airspaces
during lung inflation,
(b) prevent the distal airspaces from collapsing during
lung deflation.
Lung protective ventilation
9/8/2022 68
69. Cont,
Conventional Mechanical Ventilation uses large
VT(10-15ml/Kg).
In patients with ARDS, such VT are delivered into
compromised lungs leading to increased risk of
VILI
So the the ARDS Clinical Network developed MV
protocol consisting of low VT and application of
optimal PEEP w/c showed decreased mortality
9/8/2022 69
71. Cont,
REFRACTORY HYPOXEMIA
10 to 15% of patients with ARDS develop severe
hypoxemia that is refractory to oxygen therapy
with conventional MV.
immediate threat to life, and need quick “rescue
therapies”
But the rescue measures available often provide
little or no survival benefit.
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72. Cont,
High Frequency Oscillatory Ventilation
delivers small VT (1–2 mL/kg) using rapid pressure
oscillations (300 cycles/min)
improve arterial oxygenation, but there is no documented
survival benefit
Inhaled Nitric Oxide (5–10 ppm)
improve arterial oxygenation in ARDS temporarily(1-4days)
and has no associated survival benefit
Prone Positioning
Improve oxygenation but has little impact on mortality in
ARDS,
ECHMO: last resort and has variable success
9/8/2022 72
73. Nonventilatory management
9/8/2022
Underlying cause treatment
Fluid management
Avoid positive fluid balalance and correct deficit
Steroid therapy
Early severe ARDS and Unresolving ARDS
Provide Multi-organ Supportive care
73
The development of respiratory care progressed through history from Galen’s observations on the respiratory and circulatory systems in the 2nd century to the early 20th century, when great strides in pulmonary physiology were made.
The Drinker Respirator, which provided negative pressure ventilation, was introduced in 1928, and a commercial version of this “iron lung” was offered by John Emerson in 1932.
In the 1940s and 1950s, polio epidemics were sweeping across Europe and the United States.
The birth of modern-day critical care occurred in Copenhagen in 1952, when Bjorn Ibsen realized that positive pressure ventilation could save lives during a polio epidemic when the iron lungs (a negative pressure ventilator) were failing.
The combination of endotracheal intubation and positive pressure ventilation has likely saved hundreds of thousands, if not millions, of lives.
Artificial ventilation has prolonged the lives of thousands of people afflicted with spinal cord injuries and devastating NM diseases.
The combination of endotracheal intubation and positive pressure ventilation has likely saved hundreds of thousands, if not millions, of lives.
Artificial ventilation has prolonged the lives of thousands of people afflicted with spinal cord injuries and devastating NM diseases
Negative pressure ventilation (NPV) attempts to mimic the function of the respiratory muscles to allow breathing through normal physiological mechanisms.
The patient’s head and neck are exposed to atmospheric or zero pressure while
The thorax and the rest of the body are enclosed in an airtight container that is subjected to negative pressure .
Negative pressure generated around the thoracic area is transmitted across the chest wall, into the intrapleural space, and finally into the intraalveolar space.
The intrapleural space becomes negative, the space inside the alveoli becomes increasingly negative in relation to the pressure at the airway opening
This pressure gradient results in the movement of air into the lungs.
Expiration occurs when the negative pressure around the chest wall is removed.
The normal elastic recoil of the lungs and chest wall causes air to flow out of the lungs passively.
The use of negative pressure ventilators declined considerably in the early 1980s.
The resultant positive alveolar pressure is transmitted across the visceral pleura and the intrapleural space.
During inspiration, the inflating pressure at the upper (proximal) airway equals the sum of:
resistance of the airways and
elastance of the lung and chest wall.
Alveolar pressure is still positive, which creates a gradient between the alveolus and the mouth, and air flows out of the lungs
pneumatically Powered Ventilators
PCurrent generation ICU ventilators are typically pneumatically powered devices.
These machines use one or two 50-psi gas sources and have built-in internal reducing valves so that the operating pressure is lower than the source pressure.
Pneumatically powered ventilators are classified according to the mechanism used to control gas flow.
Two types of devices are available: pneumatic ventilators and fluidic ventilators.
Most pneumatically powered ICU ventilators also have an electrical power source incorporated into their design to energize a computer that controls the ventilator functions.
The gas sources, mixtures of air and oxygen, supply the power for ventilator function and allow for a variable FIO2.
The electrical power is required for operation of the computer microprocessor, which controls capacitors, solenoids, and electrical switches that regulate the phasing of inspiration and expiration, and the monitoring of gas flow.
Electrically powered ventilators rely entirely on electricity from a standard electrical outlet
The electricity provides the energy to operate and control the timing mechanisms for inspiration and expiration, gas flow, and alarm systems.
The internal control system reads and uses the operator’s settings to control the machine
has various knobs or touch pads for setting components
heat-moisture exchanger, heated humidifier)
A thermometer or sensing device
An apnea or low-pressure alarm
A nebulizer line, Bacterial filters
A pressure gauge to measure pressures in the upper airway
In-line suction catheter
Air can be trapped in the lungs during mechanical ventilation if no enough time is allowed for exhalation.
The most effective way to prevent this complication is to monitor the pressure in the ventilator circuit at the end of exhalation.
If no extrinsic PEEP is added and the baseline pressure is greater than zero ,air trapping, or auto-PEEP, is present
The plateau pressure reflects the effect of the elastic recoil on the gas volume inside the alveoli and
Any pressure exerted by the volume in the ventilator circuit that is acted upon by the recoil of the plastic circuit.
At the point of breath holding, the pressures inside the alveoli and mouth are equal (no gas flow)…PPl
The expiratory phase encompasses the period from the end of inspiration to the beginning of the next breath.
During mechanical ventilation, expiration begins when inspiration ends, the expiratory valve opens, and expiratory flow begins.
Opening of the expiratory valve may be delayed if an inflation hold is used to prolong inspiration.
This controlling variable is called independent variable; the other two variables automatically become dependent variables.
Determined by the mode of MV.
The mode describes how a breath is delivered.
A breath has two components (inspiratory phase & expiratory phase).
There are 3 variables to the inspiratory phase.
1. Trigger variable – how a breath is initiated.
Time, flow or pressure triggered
2. Control variable
Pressure controlled vs volume (flow) controlled
3. Cycling variable – what terminates a breath.
When triggered, the ventilator detects the onset of a patient-initiated inspiration (by detecting changes in pressure & flow/volume that occur within the ventilator circuitTime cycled, volume (flow) cycled
The type of breath delivered & the mode of MV
Triggering variable
Control variable
Cycling variable
Patient ventilator asynchrony
Imposed ventilatory work
Respiratory system resistance and compliance
Presence of circuit leak
Accumulation of secretion
Presence of auto-PEEP
Response to bronchodialatory therapy.
These ventilator graphics tells the clinician about patient-ventilator interaction & gives a “window” into what is happening to the patient in real time
The goal of adjusting PSV is threefold.
To help increase VT (4 to 8 mL/kg)
To decrease respiratory rate (to <30 breaths/min)
To decrease the WOB associated with breathing through an artificial airway
For patients with lung disease, levels of 8 to 14 cm H2O are typically used to compensate for additional work associated with breathing through a tube and ventilator system.
The clinician will set the minimum mandatory control variable value and the pt can trigger a breath and the machine will give the full breath
This was achieved by allowing a window of time to open during which the patient could trigger a mandatory breath
Advantages over AC modes: has better Patient vent synchrony, preserve respiratory muscle fun, lower mean Airway pressure and greater control over the level of support
Simply put, PRVC is a pressure-controlled mode of ventilation with a backup rate and set VT
Advantages of PRVC include maintaining a stable tidal volume delivery with pressure control in the face of changing lung mechanics or changing patient inspiratory effort.
Potential problems include inappropriate automatic pressure adjustments that may occur under certain conditions
he pressure is “regulated” to deliver the clinician set VT from breath to breath. If the volume falls short or exceeds the set VT , the pressure can increase or decrease incrementally +/– 3 cm H2O for the next breaths. The range of the auto-adjusting pressures are confined to within 5 cm H2O of the peak pressure alarm setting and minimum set PEEP; an alarm will sound at both extremes
Various forms of high-frequency ventilation (HFV) have been in use since the 1960s.
High-frequency ventilation employs very low tidal volumes, typically less than physiologic dead space volume(about 3rd of VT) and very rapid respiratory rates (> 60 breaths/min).
An advantage of HFV is the ability to ventilate patients in the face of large air leaks in pts with major airway disruption (e.g., tracheal esophageal fistula, bronchopleural fistula) that is unmanageable by conventional ventilation.
HFV has also been advocated for use as a rescue technique in adult ARDS patients who are failing conventional support
in infants with respiratory failure unresponsive to conventional mechanical ventilation
uses the natural electrical discharge from the diaphragm (i.e., electrical activity of the diaphragm or EAdia ) during inspiration to trigger a breath from the ventilator.
The inspiratory signal trigger is the primary difference between NAVA and other modes of mechanical ventilation.
The inspiratory signal is detected using diaphragmatic electromyography (EMGdia ).
With this mode patients can breathe spontaneously through a ventilator circuit without receiving any mandatory breaths.
This is sometimes called a T-piece method because it mimics having the patient’s endotracheal tube connected to a Briggs adapter (T-piece) and a humidified oxygen source using large-bore tubing.
The advantage of this approach is that the ventilator can be used to monitor the patient’s breathing and activate an alarm if an undesirable circumstance arises
The disadvantage is that some ventilator systems require considerable patient effort to open inspiratory valves to receive gas flow, thus increasing WOB.
Ventilator manufacturers have attempted to minimize this problem by incorporating rapidly responsive valves into their designs.
A spontaneous breathing trial (SBT) can be used to evaluate a patient’s readiness to have ventilation discontinued
The patient establishes the rate, inspiratory flow, and TI.
PSV is always an assist mode (patient triggered).
A pressure support breath is patient triggered, pressure limited, and flow cycled.
With flow cycling, the ventilator senses a decrease in flow and determines that inspiration is ending.
The decrease in flow corresponds to a decrease in the pressure gradient between the mouth and lungs as the lungs fill.
All ventilators that provide pressure support also have a maximum preset inspiratory time.
Most ventilators use a fixed value, such as 1.5 to 2 seconds for adult patients and 0.5 seconds for infants, for the maximum inspiratory time.
Other ventilators use different maximum time-cycle criteria
PSV is used for three basic functions:
To reduce work of breathing (WOB) for spontaneously breathing patients breathing through a ventilator circuit.
To reduce WOB in patients receiving continuous positive airway pressure or spontaneous intermittent mechanical ventilation.
This is accomplished by setting the pressure level higher than that required to overcome system resistance
To provide full ventilatory support in the assist mode, in which each patient breath is a pressure support (PS) breath.
The patient must have a dependable, intact respiratory center and a fairly stable lung condition, because tidal volume can vary when used in this mode.
Commonly used in pts Cardiogenic pulmonary edema
BPAP is use of higher positive airway pressure during inspiration and lower pressure during expiration
Best used for hypercapnic respiratory failure, COPD, obesity hypoventilation disorder, drug overdose
Other Indications In addition to these major indications, mechanical ventilation may be of value in certain specific conditions. The vasoconstriction produced by deliberate hyperventilation can reduce the volume of the cerebral vascular compartment, helping to reduce raised intracranial pressures. In flail chest, mechanical ventilation can be used to provide internal stabilization of the thorax when multiple rib fractures compromise the integrity of the chest wall; in such cases, mechanical ventilation using positive end-expiratory pressure (PEEP) normalizes thoracic and lung mechanics, so that adequate gas exchange becomes possible. Where postoperative pain or neuromuscular disease limits lung expansion, mechanical ventilation can be employed to preserve a reasonable functional residual capacity within the lungs and prevent atelectasis
VT=6-8ml/kg, PIP:12-25cm H2O
RR=12-16
PEEP=5-24
I:E=1:2,1:3
FIO2 targeting SPO2 of 90-95%
Flow rate: 40-60L/min(for COPD60-75L/min)
Trigger sensitivity: flow triggering: 2L/min
Pressure triggering: -1 to -3 cm H2O which means a breath can be triggered only when the alveolar pressure drops 1-3cm of H20 below ATM pressure, used I A/C and SIMV modes, avoid in those who are at risk of AutoPEEP
PS for SIMV: 5-10cm H2O
Risk of excessive PEEP=decreased CO+barotrauma+increased ICP+increased Work of breathing if pressure triggering is used
Low PEEP= risk of atelectasis+hypoxemia
PEEP may be avoided for patients with barotrauma or those with prolonged air leak from pneumothorax
Be cautiously used in perioperative period for pts with:intracranial diseases, focal lung disease,hypotension, hypovolemia, P. Embolism, autopeep without airflow limitations, bronchopleural fistula, prone position
Autopeep can develop in three common situations: in the presence of high MV, expiratory flow limitations and expiratory resistance
Treatment of autopeep:correcting underlying cause, appling PEEP, giving bronchodilator, steroids…
Delivery of an inspiratory volume is perhaps the single most important function a ventilator accomplishes.
Two factors determine the way the inspiratory volume is delivered:
The structural design of the ventilator and
The ventilator mode set by the clinician
Keep alveolar pressure
Keep alveolar pressure <30 cm H2O (assumes thoracic compliance is normal)
Respiratory Frequency (f)
f = f = VE/VT
Respiratory rate typically ranges from 12 to 18 breaths per minute.
These lower VT rates are described as protective strategies that minimize the damaging effects associated with over-distention of the alveoli.
An adult’s lungs do not get larger as he or she gains weight.
A person’s tidal volume increases linearly with body weight up to that person’s ideal body weight.
TThe upper airway pressure limit is typically set at 10–15 cm H2 O above the observed peak inspiratory pressure
the apnea alarm should be set such that it is activated if the patient makes no attempt to breathe for at least 15–20 s,
When a particular FIO2 is chosen for the patient, the upper and lower FIO2 limits are set approximately 5–10% above and below the chosen FIO2 , respectively. This allows monitoring the delivered FIO2 within narrow limits.
HYPOXEMIA AND HYPOXIA: COMMON SYMPTOMS
Both hypoxemia and hypoxia can share a list of common symptoms which include:
Changes in skin color, ranging from blue to cherry red
Confusion
Cough
Fast heart rate
Rapid breathing
Shortness of breath
Slow heart rate
Sweating
Wheezing
Cytopathic: the heart pumps enough oxygen to the tissues, but something inhibits effective oxidative phosphorylation (septic shock, cyanide poisoning, salicylate poisoning).
The best known example of this occurs during cyanide poisoning which impairs cytochrome function
With the exception of reducing the shunt fraction with positive end expiratory pressure, mechanical ventilation is not a therapeutic intervention. The goal of ventilation is to simply maintain adequate gas exchange and metabolic function while the underlying disease process either gets treated or (more commonly) resolves on its own. Thus, the physician should focus on treating reversible causes of respiratory failure and minimizing further injury to the patient. When the patient is ready to come off the ventilator, he’ll let you know.
Predisposing Conditions ARDS is not a primary disorder, but is a consequence of a variety of infectious and noninfectious conditions. The common conditions that predispose to ARDS are listed in Table 23.1. The most frequent offenders are pneumonia and the “sepsis syndromes” (i.e., septicemia, severe sepsis, and septic shock) (1,5). One feature shared by many of these conditions is the ability to trigger a systemic inflammatory response, which involves neutrophil activation, the principal inciting event in ARDS.
Only half of the patients with the premortem diagnosis of ARDS had evidence of ARDS on postmortem examination, and the conditions most commonly mistaken for ARDS were pneumonia and hydrostatic pulmonary edema. The likelihood of identifying ARDS was 50% in this study, which is no better than the likelihood of heads or tails with a coin flip!
The chest x-ray can be unrevealing in the first few hours after symptom onset, but bilateral pulmonary infiltrates begin to appear within 24 hours.
Most (>90%) cases of ARDS appear within one week of a known predisposing condition, and 80% of cases require mechanical ventilation (
Radiographic Appearance The characteristic appearance of ARDS on a portable chest x-ray is shown in Figure 17.1. The infiltrate has a finely granular or ground-glass appearance, and is evenly distributed throughout both lungs. Also note the lack of a prominent pleural effusion, which helps to distinguish ARDS from cardiogenic pulmonary edema
. 2. Oxygenation The impairment in oxygenation in ARDS is assessed using the PaO2 /FIO2 ratio, measured at a positive end-expiratory pressure (PEEP) of ≥5 cm HThe diagnosis of ARDS requires a PaO2 /FIO2 ratio 2O. (For patients who are not on a ventilator, continuous positive airway pressure, or CPAP, is used instead of PEEP.)
shows a severity of illness classification (mild, moderate, or severe) based on the PaO2 /FIO2 ratio, which is intended for predicting the likelihood of a fatal outcome. The reported mortality rates for mild, moderate, and severe ARDS are 27%, 32%, and 45% (mean values), respectively
(3In a study of interobserver variability in the radiographic diagnosis of ARDS, a group of 21 experts in ARDS agreed on the diagnosis (ARDS or no ARDS) in only 43% of cases (4). 2. In a large retrospective study designed to identify patients with ARDS based on the clinical criteria in Table 17.2, 40% of the cases of ARDS were not clinically recognized (1). 3. An autopsy study of patients who died with a clinical diagnosis of ARDS showed that only 50% of the patients had postmortem evidence of ARDS (5). This implies that the likelihood of identifying ARDS based on clinical criteria is no greater than the likelihood of predicting heads or tails in a coin toss. 4. The Wedge Pressure The pulmonary artery occlusion pressure (wedge pressure) has been used to distinguish between ARDS and cardiogenic pulmonary edema; i.e., a wedge pressure ≤18 mm Hg is considered evidence of ARDS (6). This is problematic because the wedge pressure is not a measure of capillary hydrostatic pressure, as explained in Chapter 5, Section II-B. Although the wedge pressure is no longer a required measurement in the diagnosis of ARDS, the limitations of this
Ventilator-Induced Lung Injury One of the most important discoveries in critical care medicine in the last quartercentury is the role of mechanical ventilation as a source of lung injury, particularly in patients with ARDS. This injury is related to excessive stretch of distal airspaces, as described next.
Reduce the FiO2 by 10-20% at a time every 5-10 minutes until the SpO2 levels off at 88-94%
Once the FiO2 has been reduced, begin dropping the PEEP in 2 cm increments every 5-10 minutes until the SpO2 falls below 88%, or until there’s a notable drop in compliance. Either of these would indicate alveolar derecruitment. Repeat the recruitment maneuver (40 for 40) and set the PEEP at 2 cm higher than the level where derecruitment occurred.
Permissive Hypercapnia One of the consequences of low tidal volume ventilation is a decrease in CO2 elimination in the lungs, which can result in hypercapnia and respiratory acidosis. Because of the benefits of low volume ventilation, hypercapnia is allowed to persist as long as there is no evidence of harm. This practice is known as permissive hypercapnia (22). The limits of tolerance to hypercapnia and respiratory acidosis are unclear, but data from clinical trials of permissive hypercapnia show that arterial PCO2 levels of 60–70 mm Hg and arterial pH levels of 7.2–7.25 are safe for most patients ( 23). The target pH is 7.30–7.45 in the protocol for lung protective ventilation in
Impact on Survival Lung protective ventilation is one of the few measures that has been shown to improve survival in ARDS. The largest and most successful trial of lung protective ventilation was conducted by the ARDS Network (20), and enrolled over 800 ventilator-dependent patients with ARDS who were randomly assigned to receive tidal volumes of 6 mL/kg or 12 mL/kg (using predicted body weight). Ventilation with the lower tidal volume (6 mL/kg), and an end-inspiratory plateau pressure (Ppl) ″30 cm H2O, was associated with a shorter duration of mechanical ventilation and a 9% absolute reduction in mortality rate (40% to 31%, P=0.007). A total of 5 clinical trials have compared tidal volumes of 6 mL/kg and 12 mL/kg during mechanical ventilation in patients with ARDS. In two of the trials, low tidal volumes were associated with fewer deaths, while in three of the trials, there was no survival benefit associated with low tidal volumes (24). Despite the lack of a consistent survival benefit, lung protective ventilation using tidal volumes of 6 mL/kg has become a standard practice in patients with ARDS. A recent multicenter survey of lung protective ventilation in ARDS showed an in-hospital mortality rate of 48% (5), which is no better than mortality rates reported before the introduction of lung protective ventilation. An observation that is relevant in this context is that mortality rates for ARDS tend to be lower in controlled clinical trials than in clinical practice surveys (25). (Note: A possible explanation for the lack of a consistent survival benefit with low tidal volumes is presented in
Inhaled Nitric Oxide Inhaled nitric oxide (5–10 ppm) is a selective pulmonary vasodilator that can improve arterial oxygenation in ARDS by increasing flow to areas of high dead space ventilation (34). However, the increase in arterial oxygenation is temporary (1–4 days), and there is no associated survival benefit
Prone Position Switching from the supine to prone position can improve pulmonary gas exchange by diverting blood away from poorly aerated lung regions in the posterior thorax and increasing blood flow in aerated lung regions in the anterior thorax (see Figure 23.4). Prone positioning has had little impact on mortality in ARDS, but a recent study combining lung protective ventilation with prone positioning showed a lower than expected mortality rate in patients with severe ARDS (PaO2/FIO2
ECMO Extracorporeal membrane oxygenation (ECMO) has had variable success in patients with refractory hypoxemia, and is a consideration only in medical centers with established ECMO programs, and only when other rescue therapies have failed
The treatment of ARDS begins by treating the inciting condition (e.g., septicemia), if possible. Therapies directed at the ARDS have been marked by failure more than success. The failed therapies in ARDS in-clude surfactant (in adults), inhaled nitric oxide, pentoxyphylline, ibuprofen, prostaglandin E1, and antifungal agents (to inhibit thromboxane) (26). Clinical benefits have been reported with fluid management that avoids fluid accumulation in the lungs, and with high-dose corticosteroids in severe or unresolving ARDS. The management described in this section is limited to the measures that have documented benefits.
Early Severe ARDS In early severe ARDS, defined as a PaO2/FIO2