5/1/2017
Ron Pasewald BS, RRT-ACCS, RCP
Respiratory Therapy
Froedtert Hospital
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I have no conflicts of interest to disclose.
The views and opinions in this lecture are my
own.
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Define ARDS and causes of ARDS
Provide the definitions for APRV
Provide indications/contraindications
for APRV
Explain the benefits of spontaneous
breathing with APRV.
APRV Initial setup
APRV Adjustments
APRV Weaning
Acute respiratory distress syndrome (ARDS)
is a medical condition occurring in critically
ill patients characterized by widespread
inflammation in the lungs.
ARDS is not a particular disease, rather it is
a clinical phenotype which may be triggered
by various pathologies such as trauma,
pneumonia and sepsis.
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Direct or indirect pulmonary injury
Proliferation of inflammatory mediators
Neutrophil accumulation in pulmonary microcirculation.
Neutrophil migration in alveoli epithelial
Protease and Cytokine release
Vascular permeability, gap formation and necrosis of
Type I & II Alveolar cells
Pulmonary edema, Hyaline membrane formation, & loss
of surfactant.
Infiltration of fibroblasts leads to collagen formation
and fibrosis.
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ARDSnet criteria:
◦ Bilateral Infiltrates on CXR
◦ PaO2/FIO2 ratio
 Mild 200-300, moderate 100-200,
severe <100
◦ Plateau pressures greater than 30 cm H2O
◦ No evidence of left heart failure
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Sepsis
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Inhalation injury
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Pneumonia
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Trauma
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Pulmonary Embolism
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Oxygenation – The severity of hypoxemia determines whether
the patient has mild ARDS (P/F >200-300 mmHg), moderate
ARDS (P/F >100-200 mmHg), or severe ARDS (P/F≤100
mmHg).
Mortality appears to increase as ARDS becomes more severe,
according to an observational study of 3670 patients with
ARDS that found that patients with mild, moderate, and
severe ARDS had mortality rates of 27, 32, and 45 percent,
respectively (1)
Pulmonary vascular dysfunction is indicated by an elevated
trans-pulmonary gradient ≥12 mmHg or pulmonary vascular
resistance index >285 dyne s/cm.
Pulmonary vascular dysfunction appears to be an independent
risk factor for 60-day mortality. (2)
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Higher extra vascular lung water and pulmonary vascular
permeability indices correlate independently with 28 day
mortality (3)
Dead space ventilation early in the course of ARDS appears to
correlate with mortality.
This was illustrated by a series of 179 patients with early
ARDS who had their ratio of dead space to tidal volume
(Vd/Vt) determined by measuring exhaled carbon dioxide
(EtC02) levels.
The dead space fraction was markedly elevated and there was
a linear correlation between the degree of dead space
ventilation and mortality. For every 0.05 increase in dead
space fraction, the odds of death increased by 45 percent. (4)
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Infection and/or multi-organ dysfunction are better
predictors of mortality than respiratory parameters
This is probably because they predict death from a nonrespiratory cause, which is more common than death due to
respiratory failure. (5)
Severity of illness scores appear to correlate with mortality.
◦ As an example, patients with a higher APACHE III score have
an increased likelihood of death. (16)
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Severe but not mild or moderate alcohol misuse, in patients
with acute lung injury, is associated with an increased risk of
death or persistent hospitalization at 90 days. (8)
The presence of diffuse alveolar damage (DAD) on lung
biopsy is also associated with a worse prognosis compared
with those who had non DAD-associated ARDS. (9.)
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Fluid balance – A positive fluid balance may be associated
with higher mortality.
◦ This was demonstrated by the ARDSnet low tidal volume
trial, which found that a negative fluid balance at day 4
was associated with decreased mortality compared to a
positive fluid balance. (10, 11)
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Treatment with glucocorticoids (IV steroids)
Patients who received glucocorticoids prior to the onset of
ARDS may have an increased likelihood of death. (12)
Packed red blood cell transfusion
◦ Patients who receive packed red blood cell transfusions
may have an increased likelihood of death. (13)
Organization of the ICU
◦ Patients cared for in an ICU that mandates transfer to an
intensivist or co-management by an intensivist may have a
decreased likelihood of death. (14)
Late intubation
◦ Patients who are intubated late in the course of the disease
may have a higher risk of death from ARDS when
compared with patients who are intubated early and those
who are never intubated. Initial strategies (eg, NIPPV & HF
02) may impact the timing of intubation & ultimately affect
mortality. (15)
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Currently, routine laboratory parameters are not helpful for
predicting the outcome of ARDS.
However, a large body of emerging evidence suggests that
many biomarkers and gene polymorphisms are associated
with both susceptibility to ARDS and outcome from ARDS. (6)
The practical utility of these observations is uncertain, but the
research may lead to new preventative and therapeutic
strategies in the future.
Patients with trauma-related ARDS appear to have a lower
likelihood of death at 90 days than patients with ARDS that is
unrelated to trauma. (7)
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Early application of airway pressure release ventilation may reduce mortality
in high-risk trauma patients: A systematic review of observational trauma
ARDS literature Penny L. Andrews, RN, BSN, Joseph R. Shiber, MD, Ewa Jaruga-Killeen, PhD, Shreyas Roy, MD, CM,
Benjamin Sadowitz, MD, Robert V. O’Toole, Louis A. Gatto, PhD, Gary F. Nieman, BA, Thomas Scalea, MD, and Nader M.
Habashi, MD, Baltimore, Maryland
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Alveolar instability (atelectrauma) is not identified by arterial oxygenation
predisposing the development of an occult ventilator-induced lung injury
Penny L Andrews2, Benjamin Sadowitz1, Michaela Kollisch-Singule1, Joshua Satalin1*, Shreyas Roy1, Kathy Snyder1, Louis A
Gatto3, Gary F Nieman1 and Nader M Habashi3
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Early stabilizing alveolar ventilation prevents acute respiratory distress
syndrome: A novel timing-based ventilatory intervention to avert lung injury
Shreyas Roy, MD, CM, Benjamin Sadowitz, MD, Penny Andrews, RN, Louis A. Gatto, PhD, William Marx, DO, Lin Ge, PhD,
Guirong Wang, PhD, Xin Lin, PhD, David A. Dean, PhD, Michael Kuhn, BA, Auyon Ghosh, BSc, Joshua Satalin, BA, Kathy
Snyder, BA, Yoram Vodovotz, PhD, Gary Nieman, BA, and Nader Habashi, MD, Syracuse, New York
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Mechanical Ventilation as a Therapeutic Tool to Reduce ARDS Incidence
Gary F. Nieman , BS ; Louis A. Gatto , PhD ; Jason H. T. Bates , PhD ; and
Nader M. Habashi , MD
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APRV is spontaneous breathing CPAP with
short releases.
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The short releases of pressure allows C02
release from the conducting airways.
◦ ~90% CPAP phase
◦ Spontaneous breathing augments CO2 elimination
and helps prevent alveolar collapse and promotes
alveolar recruitment. (especially posterior
dependent regions)
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Diffusion is the main principle.
◦ Keeping the alveoli open allows diffusion to occur.
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To provide lung protective ventilation
To provide an “Open lung” approach
Minimize alveolar over distension.
Avoid repeated alveolar collapse and
re-expansion.
Restore FRC through recruitment
maintain FRC by creating intrinsic PEEP.
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Unmanaged increased intracranial pressure.
Large proximal bronchopleural fistulas.
Pre-existing obstructive and restrictive lung
diseases?
◦ Set the TLow correctly.
 Obstructive will need a longer T low
 Restrictive will need a shorter T low
 PHigh – the upper CPAP level.
 PLow – the lower CPAP level.
*P High – P Low = Δ P
 THigh – the time phase for the PHigh.
 TLow – the time phase for PLow.
* T High + T low is the set cycle time.
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P High – Set at plateau pressure in AC/VC or
AC/PC. Ideally, target upper inflection
point.
◦ Ideally, start at 20-25 cm H2O early.
◦ Maximum Phigh 35 cmH20, is controversial.
 High intra-abdominal pressure, obesity, and/or severely
low thoracic compliance
 Optimal patient positioning is recommended.
 Reverse Trendelenburg
 Prone
 Avoid Semi-Fowlers
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The inspiratory time phase (Thigh) is set at a
minimum of 4.0-6.0 sec
Increase your (Thigh) in .5 second
increments.
Your target is lung recruitment, increased
alveolar surface area, and efficient
diffusion.
Set Plow at 0 cm H2O.
This provides a rapid drop in pressure and
unimpeded expiratory gas flow.
◦ Setting a P Low above zero will slow down
expiratory flow.
◦ There are certain rare conditions where a
Plow > 0 may be appropriate. (5-10 cmH20)
Severe ARDS with high E and low C, to
prevent alveolar collapse. (extremely low
Tce)
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Set Tlow @ 50-75% of PEFR
Use the flow/time curve to set this.
◦ Freeze expiratory waveform
◦ Scroll to PEF
◦ Multiply PEF x .75
 For example, PEF 60 lpm x 75% = 45 lpm
 Set Tlow to terminate expiratory flow @ 45lpm
Ideally, 0.4 to 0.8 seconds
Regional auto-PEEP is a desired outcome with APRV
◦ Perform an expiratory hold, freeze waveform, scroll to
measure amount of auto-peep.
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APRV uses lower peak airway pressures
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Spontaneous diaphragmatic breathing is
maintained
 Less dynamic alveolar stress/strain
 Increased cardiac index
 Decreased central venous pressure
 Improves renal perfusion and urine output.
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APRV enhances oxygen delivery through
improved diffusion and reduces the need for
chemical sedation/paralysis. (
VD/VT)
 Less delirium
 Less neurologic functional decline
 Less diaphragmatic muscle atrophy
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Increased Raw (i.e. Asthma)
◦ the ability to eliminate CO2 may be more
difficult due to limited emptying of the lung
and short release periods.
Irresponsible settings may lead to asynchrony
during pressure changes.
 Typically due to Thigh settings too low.
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Limited staff experience with this mode may
make implementation of its use difficult.
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Due to APRV being a pressure-targeted mode of
ventilation, volume delivery depends on lung
compliance, airway resistance and the patient’s
spontaneous effort.
APRV may not completely support CO2 elimination,
but relies on augmentation from spontaneous
breathing.
◦ Using this mode on a paralyzed, non spontaneous
breathing patient is acceptable, but some of the benefits of
this mode are diminished.
◦ Although, hospitals that have implemented APRV for use
with organ donation, have seen an increase in viable tissue
for donation.
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Decrease THigh
◦ Increases the amount of releases/minute
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Increase THigh
◦ Increasing Thigh may lead to increased alveolar recruitment,
which improves normal gas diffusion
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Increase PHigh to increase DP
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Increase TLow.
◦ Delta P (PHigh – PLow) determines flow out of the lungs and
volume exchange.
◦ Extending TLow will give more time to empty conducting
airspaces. If you go too far, alveolar collapse may develop
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Increase THigh. (fewer releases/min)
◦ Slow increments of 0.5-1.0 seconds.
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Decrease PHigh to lower DP.
◦ Do not wean PHigh until patients spontaneous
VE is >= 40-50% of total VE
*This may be a sign that your patient is ready to
wean.
To Increase Pa02
1.
Increase Fi02
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Increase mAP by increasing PHigh in 2 cm H2O
increments.
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Increase THigh slowly (0.5 seconds at a time)
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Shorten TLow to increase PEEPi in 0.1 second
increments.
5.
Recruitment Maneuvers
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Fi02 should be weaned first.
Stretch Thigh slowly, to increase patients
spontaneous efforts (EtC02)
Once Spontaneous Ve >= 40-50% of total
Ve, start drop/stretch wean
Wean Phigh by 2-3 and Stretch Thigh 1.0
sec every 2-4 hours
Goal of 8-10 cmh20 and T high >15 sec
Weaning- Habashi method: Drop-and-Stretch
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1. The ARDS Definition Task Force. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA 2012; May 21:Epub
ahead of print.
2. Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent prognostic factor in patients with acute
respiratory distress syndrome. Crit Care Med 2013; 41:472.
3. Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent prognostic factor in patients with acute
respiratory distress syndrome. Crit Care Med 2013; 41:472.
4. Nuckton TJ, Alonso JA, Kallet RH, et al. Pulmonary dead-space fraction as a risk factor for death in the acute respiratory
distress syndrome. N Engl J Med 2002; 346:1281.
5. Stapleton RD, Wang BM, Hudson LD, et al. Causes and timing of death in patients with ARDS. Chest 2005; 128:525.
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Putensen, AJRCCM, 1999
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Any questions?
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