ed-lung protective ventilation-slide deck white no … mechanical ventilation leads to pulmonary...

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• Inhalation

• Active process

• Diaphragm and intercostal muscles contract to increase thoracic

volume vertically creating a NEGATIVE change in thoracic pressure.

• At end inhalation alveolar pressure equalizes with atmospheric

pressure (approximately 0 cmH2O)

• Exhalation:

• Passive process

• Lungs recoil, thoracic volume decreases.

• At end exhalation alveolar & interstitial pressures return to

atmospheric (approximately 0 cmH2O)

• 2013 – Gilstrap – AJRCCM

• Spontaneous ventilatory pattern (Vt, Rate & I:E) is controlled by the

brainstem Ventilatory Control Center (VCC)

• Respiratory Rhythm Generator in VCC interacts with:

• Chemoreceptors (PO2, PCO2 & pH receptors)

• Located in great vessels and 4th ventricle of brain

• Mechanoreceptors (stretch and irritant receptors)

• Located in thorax and ventilatory muscles

• Ultimate ventilatory pattern generated by VCC:

• Adequate gas exchange

• Least amount of ventilatory muscle loading

• Least amount of air trapping

• Just what is it that is delivered by the ventilator to the patients’ lungs?

• Volume

• Flow

• Pressure

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• Physics of positive-pressure ventilation differs radically from those of

spontaneous ventilation.

• During inhalation:

• Positive intra-thoracic pressures

• Flow distributed heterogeneously throughout the lung

• Effectively distributed through compliant lung

• Attenuated in low-compliant areas

• Inspiratory flow heterogenicity can result in:

• Over-distension of compliant “healthy” lung

• Under-distension of non-compliant “injured” lung


• Muscle loading inherent in mechanical ventilation can effect the VCC:

• Delayed or missed triggers ↘

• Uncomfortable isometric load ↘

• Increased inspiratory effort intensity

• Increased muscle loading during inhalation ↘

• Spontaneous breathing pattern changes to reduce this

increased load ↘

• Rapid, shallow breathing

• Dyspnea

• Overdistension (mechanoreceptors) ↘

• Shortening of neural Ti

• Activation of expiratory muscles

• 2013 – Biehl – Respiratory Care

• Results from injury to the blood-gas barrier in the lung

• Caused by mechanical ventilation

• Initial stretch of blood-gas barrier ↘

• Disruption of pores in the endothelium ↘

• Leakage of protein into the interstitial space

• Subsequent stretch of blood-gas barrier ↘

• Membrane stress insult/failure ↘

• Disruption of endothelium & alveolar epithelium ↘

• Leakage of protein into alveolar space

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• 1998 – Dreyfuss – AJRCCM


• Duration of exposure

• <24 h in large mammals

• Intensity of exposure

• Vt

• Too high → membrane strain/volutrauma

• FRC and the size of the available lung

• “Baby lung”

• PEEP

• Amount needed is influenced by prior recruitment and

chest-wall compliance



• Heterogeneity of Flow Distribution:

• Atelectasis

• Consolidation

• Edema

• End-inspiratory lung volume (FRC)

• Too low promotes derecruitment

• Too high promotes overdistension

• Inspiratory flow and flow profile (strain rate)

• Too high = ↓ risk of VILI



• Breathing frequency

• Low RR = ↓ risk of VILI

• RR must be adequate to meet patient demand

• Most patients in ARF require 20-30 bpm to meet metabolic

needs

• Vascular pressures

• Higher transpulmonary pressures promotes higher hydrostatic

pressures

• ↑ risk of pulmonary edema

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• The First “Hit”

• ↑ suscepDbility to “second” hit of VILI

• Endotoxin/sepsis

• Tissue injury

• Fluid/transfusion

• 1744 – Fothergill:

• May be the earliest description of ventilator-induced lung injury

• Described the mouth-to-mouth resuscitation of a coal miner

• “The lungs of one may bear, without injury, as great a force as those

of another man can exert; which by the bellows cannot always be

determined”

• 1952 - Lassen - Lancet:

• Copenhagen polio outbreak

• Several problems with positive-pressure ventilation identified:

• “When bag ventilation is administered for weeks there is a risk of

emphysema”

• “The weaning period from positive-pressure ventilation is not

infrequently difficult”

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• 1967 – Nash – NEJM

• Postmortem of patients who had undergone mechanical ventilation

revealed alveolar infiltrates and hyaline membranes

• The term “Respirator Lung” coined

• 1970 – Mead – J Appl Physiol

• “In mechanical ventilation, by applying high transpulmonary

pressures to heterogeneously expanded lungs could contribute to the

development of lung hemorhage and hyaline membranes”

• 1972 - Pontoppidian – NEJM

• ARDS patients experienced discomfort when using small Vt’s.

• Beginning of the practice of using Vt’s in the 10-15 ml/kg range

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• For decades Barotrauma was considered as the major cause of VILI

• It was accepted that as long as Peak Inspiratory Pressures were

maintained in the “safe” range the lungs were protected from injury

� In the 1980’s and 1990’s further research identified the more subtle

effects of VILI:

� Volutrauma

� Atelectrauma

� Oxygen Toxicity

� 1974 - Webb & Tierney – ARRD

� Two important concepts that were contrary to the barotrauma

focus:

• Distending pressures & volumes above normal maximums

but below that which was required for alveolar rupture still

produced lung edema, surfactant abnormalities, tissue

inflammation and hemorrhage.

• Preventing cyclical alveolar collapse & reopening could also

significantly reduce the incidence of lung injury.

• Unfortunately, these concepts were not widely applied at the

time.

• 1988 – Dreyfus – ARRD

• Applied normal & excessive alveolar pressures to both volume-

limited lungs (chests bound to prevent alveolar expansion) and

volume-unlimited lungs (chests unbound with unchecked alveolar

expansion)

• Alveolar pressures caused considerably less lung damage in the

alveoli with limited expansion than in the alveoli in the unbound

chest.

• Alveoli that do not overdistend were unlikely to experience

damage

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• Measured “Lung Flooding” factors in rodents ventilated with three different ventilatory styles:

• HiP/HiV

• High Pressure (45 cmH2O)

• High Volume

• LoP/HiV

• Low Pressure (neg.pres.ventilator)

• High Volume

• HiP/LoV

• High Pressure (45 cmH2O)

• Low Volume (chest strapped) Dreyfuss,D ARRD 1988;137:1159

• 1985 – Dreyfus – ARRD

• High-volume mechanical ventilation leads to pulmonary edema

of the permeability type

• 2000 – Tschumperlin – AJRCCM

• Limiting Vt reduces injury of alveolar epithelium

• Large cyclic increases in alveolar surface area are much more

damaging than static increases in alveolar surface area

• Alveolar epithelial viability is not adversely affected by

application of large static deformations (PEEP)

• Occasional deep inspirations to recruit collapsed alveoli

should not have a serious negative impact on alveolar

epithelial viability.

daviddarling.com

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• EXCESSIVE END-INSPIRATORY ALVEOLAR VOLUME IS THE MAJOR

DETERMINANT OF VOLUTRAUMA.

• Diffuse alveolar damage at the pulmonary/capillary membrane.

• ↑ epithelial & microvascular permeability → pulmonary edema

• May be indicated by excessive PPLAT

• May result from a combination of PEEP + Vt

• GOAL: Prevent excessive end-inspiratory volume

• Target 4-6cc/kg (may try 8cc/kg first)

Slutsky, Chest, 1999

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• CYCLICAL END-EXPIRATORY ALVEOLAR COLLAPSE/RE-EXPANSION IS THE

PRIMARY DETERMINANT OF ATELECTRAUMA

• 2003 – Bilek – J Appl Physiol

• Repeated cyclical recruitment/de-recruitment of small airways/lung

units↘

• Abrasion of the epithelial airspace lining

• GOAL: Prevent end-expiratory alveolar de-recruitment


• 2016 – Marini – Critical Care Medicine

• Consensus that for the same plateau pressure minimizing the number

of collapsed units at jeopardy is a key objective

• Lungs with extensive collapse need higher pressure to ventilate:

• Overstretch already open lung units

• Amplify tensions at the borders of open and closed lung units

• Promote tidal opening-closure cycles

• Amplified border tension & tidal opening/closure cycles:

• Deplete or inactivate surfactant

• Accentuate tissue tensions

• Tear delicate membranes

• Evoke inflammatory signaling in the endothelium &

microvasculature

• EXCESSIVE FIO2 IS THE PRIMARY DETERMINANT OF OXYGEN TOXICITY

• Excessive FiO2 ↘

• Progressive alveolar damage/death secondary to generation of

Reactive Oxygen Species (ROS) ↘

• Formation of disruptive chemical bonds with surrounding lipids,

proteins and carbohydrates ↘

• Damage to cell membranes, collagen, connective tissue & DNA

• Alter enzymatic reactions within these tissues.

• Absorption atelectasis

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• 1967 – Nash – NEJM

• Prolonged exposure to excessive FiO2 in mechanically ventilated pts:

• Worsens gas exchange

• Decreases ciliary efficacy

• Produces hyperoxic bronchitis and atelectasis

• 2012 – Rachmale – Respir Care

• Prolonged exposure to excessive FiO2 :

• Worse OI at 48 hrs.

• ↑ VLOS & ICU days

• May be associated with worsening lung function


• EXCESSIVE TRANSPULMONARY PRESSURE ASSOCIATED WITH LUNG

OVER-DISTENSION IS THE PRIMARY DETERMINANT OF BAROTRAUMA

• Gross tissue injury permits transfer of air into the interstitial tissues.

• Clinically presents as:

• Pneumothorax

• Pneumomediastinum

• Pneumopericardium

• Subcutaneous emphysema.

BLOWING UP LUNGS…

BETTER

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42Ann Intern Med 1938, 12:754-795

• The goal of Lung-Protective Ventilation is to limit VILI through the early

application of strategies that:

• Limit alveolar over-expansion

• Prevent cyclical alveolar collapse/re-recruitment

• Prevent oxygen toxicity

LUNG PROTECTIVE VENTILATION RCT’S

1988Amato et al

Brazil

29 pts: Vt < 6ml/kg, Pplat < 20cmH2O 38% Mortality

24 pts: Vt = 12ml/kg, PaCO2 35-38 mmHg 71% Mortality

1998Stewart et al

Canada

60 pts: Vt < 8ml/kg, Ppeak < 30cmH2O 50% Mortality at disch

60 pts: Vt 10-15ml/kg, Ppeak < 50cmH2O 47% Mortality at disch

1998Brochard et al

Multinational

58 pts: Vt 6-10ml/kg, Pplat < 25-30 cmH2O 47% Mortality at 60 d

58 pts: Vt 10-15ml/kg, PaCO2 38-42 mmHg 38% Mortality at 60 d

1999Brower et al

USA

26 pts: Vt 5-8ml/kg, Pplat <30 cmH2O 50% Mortality at disch

26 pts: Vt 10-12ml/kg, Pplat < 45-55 cmH2O 46% Mortality at disch

2000ARDSnetwork

USA

432 pts: Vt 6ml/kg, Pplat < 30 cmH2O 31% Mortality at disch/180 d

429 pts: Vt 12ml/kg, Pplat < 50 cmH2O 40% Mortality at disch/180 d

2006Villar et al

Spain

50 pts: Vt 5-8ml/kg, PEEP @ LIP + 2cmH2O 32% Mortality in ICU

53 pts: Vt 9-11ml/kg, PEEP >5 cmH2O 53% Mortality in ICU

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• What caused the different survival outcomes of the six previous RCT’s?

• 2002 – Eichacher et al – AJRCCM (Meta-Analysis):

• Could the survival benefit of the two Low Vt RCT’s be related to the

larger-than-routine Vt’s in the control arms?

• The control arms of the “non-beneficial” Low Vt RCT’s actually had

lower Pplat’s than in the two beneficial arms

• Could the differences be related to Pplat rather than Vt?

• 2016 – Guo – Critical Care (Network Meta-Analysis)

• 17 RCT’s with a total of 575 patients without ALI/ARDS

• Objective was to identify the optimal mechanical ventilation strategy :

• Strategy C (lower VT + higher PEEP)

• Highest PaO2/FiO2 ratio.

• Strategy B (higher VT + lower PEEP)

• Highest pulmonary compliance.

• Strategy A (lower VT + lower PEEP)

• Shortest length of ICU stay

• Strategy D (lower VT + ZEEP)

• Lowest P/F ratio

• Lowest pulmonary compliance.

• 2005 – Gattinoni – Intensive Care Medicine

• Suggested PPLAT and Vt limits may not be safe for all ARDS patients

• 2008 – Chiumello – AJRCCM

• PPLAT and Vt may be inadequate in assessing lung stress and strain

• 2016 – Borsellino – Expert Review of Respiratory Medicine

• Potential benefit of LPV in neuro-critical patients is unclear

• LPV can increase intracranial pressure:

• Permissive hypercapnia

• High airway pressures during recruitment maneuvers

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• Stable Vt in the presence of varying compliance

• Clinician control of Minute Ventilation and CO2 clearance

• Inspiratory flow is “Back-End” loaded

• More gradual filling of alveoli

• Pre-set inspiratory flow

• May be less comfortable for actively breathing patients

• Variable airway and transpulmonary pressures.

• Stable PIP in the presence of variable compliances

• Inspiratory Flow is “Front-End” loaded

• More rapid filling of alveoli

• Variable inspiratory flow, based on distending pressure

• The high initial flow of Pressure-Limited ventilation may be injurious

• May overinflate with improving compliance

• Higher Mean Paw may improve ventilation/perfusion matching

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• Variable inspiratory flow of pressure-limited ventilation with a pre-set

target Vt

• Variable PIP

• Less variation in Vt with varying compliance

• Advantages:

• Positive attributes of pressure-limited ventilation

• More consistent Vt & Ve than conventional pressure-limited

• Automated weaning of PIP as compliance improves and/or patient

effort increases

• Disadvantages:

• Require volume-limited test breath(s) at initiation and following

alarms and changes

• Intermittent patient effort leads to variable Vt

VOLUME/PRESSURE HYBRID MODES

PRVC/AUTOFLOW/VC+/APV

• 2003 – MacIntyre - New Approaches to Mechanical Ventilatory Support

• Currently no evidence of benefit for any one mode.

• The choice of volume- or pressure-limited mode depends on which

feature is required for the clinical goal.

• Volume-limited is preferable if CO2 clearance is of primary concern

and patient comfort and lung stretch are less of an issue,

• Pressure-limited is preferable if volutrauma risk is high and/or

patient synchrony is more of an issue than CO2 clearance.

• Many clinicians have a bias in favor of Pressure-Limited ventilation in

patients with ALI/ARDS but supporting evidence for this choice is

weak.

• 2015 - Rittayamai - Chest

• Systematic review & meta-analysis to determine whether

pressure-control ventilation has demonstrated advantages over

volume-control ventilation

• Outcomes included:

• Compliance

• Gas exchange

• Hemodynamics

• Work of breathing

• The two modes have different working principles but clinical

available data do not suggest any difference in outcomes

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• It is against this background that intermittent

• mandatory ventilation (IMV) was introduced in 1973.

• This allowed partial ventilatory support, in which

• some of the minute ventilation is provided by the ventilator

• and the remainder is provided by the patient’s

• respiratory muscles. In their original report, Downs

• et al 4 promoted several advantages for IMV: re

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• Marini et al 8

• reported that inspiratory work increased progressively

• for both spontaneous and mandatory breaths as ventilator

• support was withdrawn, suggesting little adaptation

• to the mandatory volume-control breaths during

• IMV. Imsand et al 9 reported that electrical activations

• of the sternocleidomastoid and diaphragm were similar

• in successive spontaneous and mandatory breaths

• during SIMV. They concluded that inspiratory motor

• output is not regulated breath by breath but rather is

• constant for a given level of ventilator support. Leung

• et al 10 reported that the addition of PS of 10 cm H 2 O

• with IMV resulted in respiratory muscle unloading

• for both the mandatory and spontaneous breaths.

• The results of these studies suggest that, unlike what

• has been commonly taught, SIMV does not allow

• partitioning the work of breathing between that done

• by the ventilator and that done by the patient.

• The most common use of IMVSIMV has been


• IMV modes do not allow the patients Ventilatory Control Center to accurately anticipate the loading pattern of the next breath

• Adapting to the applied pattern of support may be more difficult to achieve

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• 2015 – Luo – J Thor Diseases

• Conclusions: In patients with moderate ARDS, SIMV + PS can safely and

effectively improve

• oxygenation, but does not decrease mortality, incidence of delirium and

patient-ventilator asynchrony,

• dosages of analgesics and sedatives, and duration of mechanical

ventilation and hospital stay.

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Tidal Volume

Accurately measured

Respiratory Rate

Accurately measured

FiO2

Accurately measured

PEEP

Measured but not accurately

Plateau Pressure


Tidal Volume

Accurately measured

Respiratory Rate

Accurately measured

FiO2

Accurately measured

PEEP


Plateau Pressure


• GOAL: Vt = 4-6 ml/kg IBW

• IBW Males: 50 + 2.3 [height (inches) - 60]

• IBW Females: 45.5 + 2.3 [height (inches) -60]

• An initial Vt of 8ml/kg may be beneficial followed by subsequent

reductions in Vt by 1 ml/kg at intervals ≤ 2 hours until Vt = 6ml/kg IBW.

• Cell death can be reduced by limiting the amplitude of alveolar

deformation, even at constant peak deformations.

• Strategies that limit changes in Vt may limit epithelial injury

Tschumerlin, Am J Respir Crti Care Med, 2000

Rocco, Curr Op Anesth, 2012

Spieth P, AJRCCM - 2009

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• 2000 – The ARDSNetwork - NEJM

• “In patients with acute lung injury and the acute respiratory distress

syndrome, mechanical ventilation with a lower tidal volume than is

traditionally used results in decreased mortality and increases the

number of days without ventilator use

• Volume Controlled Continuous Mandatory Ventilation

• Control Group – Vt set at 12ml/kg IBW

• Vt reduced to maintain Pplat < 50cmH2O

• Test Group – Vt set at 6ml/kg IBW

• Vt reduced to maintain Pplat < 30 cmH2O

• Vt increased to 8ml/kg IBW in patients with severe dyspnea

• Trial was stopped after enrollment of 861 patients

• Mortality was lower in Test Group (31% vs 39.8% P=.007)60

• 1990 – Lee – Chest

• Surgical ICU patients randomized to receive Vt of 6cc/kg or 12cc/kg

• Lower Vt = ↓VLOS

• Lower vt = ↓ ICU days

• 2004 – Gajic – Critical Care Medicine

• First observational study of VILI in patients without ARDS

• Patients ventilated with Vt’s of >12cc/kg IBW

• Excessive Vt identified as a risk factor for development of ARDS

• Odds Ratio of 1.3 for each cc above 6cc/kg IBW

• 2015 – Ghamioush – Respiratory Care

• Determine the optimal VT setting for each patient rather than

applying the same set VT to lungs that are mildly, moderately, or

severely diseased.

• Set VT may be a fluid value that varies with the degree of aerated

lung, not a single value from intubation to extubation.

• Verify that the chosen VT is achieving the desired physiologic effect

and adjust it when necessary”.

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63

Conditions where LOWER Vt

may be beneficialRationale

ARDS Functional lung size is smaller

Lung Resection Functional lung size is smaller

Single-lung Ventilation Functional lung size is smaller

Chest Wall Deformaties Functional lung size is smaller

ECMO Lung Rest

2016 –Davies – Respiratory Care

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Conditions where HIGHER Vt

may be beneficialRationale

COPD and AsthmaIncreased Vd, increased metabolic demands,

increased WOB, acidosis, prolonged time constant

Metabolic AcidosisIncreased metabolic requirements, increased neural

drive, increased WOB

Neurological InjuryIncreased neural drive unable to control with any

mode

Neuromuscular PatientsNeed to avoid atelectasis, preserve chest wall mobility,

aid cough

Drug OD or WithdrawlIncreased neural drive, agitation, increased WOB,

increased metabolic requirements

Exercise (Rehabilitation) Increased metabolic demand

2016 –Davies– Respiratory Care

• 2016 – Davies – Respiratory Care

• Two reasons to strongly consider the use of an initial Vt of 6 mL/kg

PBW in all patients:

• Pulmonary damage can happen only a few hours after the

initiation of mechanical ventilation with inappropriate settings.

• ARDS is frequently recognized after a delay in onset of the

inflammatory process.

• Early use of 6 mL/kg PBW may be preventive as opposed to

therapeutic.

• Especially protective in at-risk conditions, such as sepsis,

trauma, transfusions, or high-risk surgeries.

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• Low Vt’s may cause ventilator/patient dys-synchrony and/or double-

triggering.

• Insufficient Inspiratory Time (Ti)

• Low Vt’s require shorter Ti’s to be delivered

• Ventilator Ti may be shorter than the patients neural Ti

• Insufficient Inspiratory Flow (PIFR):

• Whether PIFR is set directly or as a function of Ti, it is integral

to promoting synchrony.

• Low Vt’s require lower PIFR’s to deliver set volume during Ti

• 2 large RCT’s currently underway:

• PRe-VENT-NL (Netherlands)

• Critically ill patients without ARDS

• 4–6 mL/kg PBW vs 8–10 mL/kg PBW

• EPALI (Spain)

• Critically ill patients at risk of developing ARDS

• 6 mL/kg PBW vs 8 mL/kg PBW

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• 2000 – Rich – J.Trauma, Injury, Infection and Crit Care

• ↓ PIFR = ↓ risk of VILI

• 2004 – Maeda - Anesthesiology

• The ↑ PIFR in pressure-limited ventilation induced significantly more

severe lung damage than the ↓ PIFR’s in volume-control ventilation

• 2013 – Gajic – Respiratory Care

• Square wave flow profile of volume-control ventilation may be

preferable than the more aggressive decelerating flow profile of

pressure-control ventilation

• Square wave flow may be less well tolerated unless the patient is

paralyzed

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• 2012 – Aboab – J Critical Care

• Abrupt cessation of inspiratory flow enhances CO2 elimination.

• In ARDS patients an end-inspiratory pause:

• Reduces deadspace

• Reduces CO2’s

• No clinically significant increase in the intrinsic PEEP or negative

hemodynamic effects

• GOAL: RR = rate adequate to approximate the patients baseline

spontaneous Ve (along with Vt)

• Adjust Vt and RR to achieve pH and plateau pressure goals

• Current consensus is that RR should not to exceed 30-35 bpm

• Often needs to match the patients demand

• 2000 – Blanch AJRCCM

• At the same pulmonary artery pressure, lower breathing frequencies

lessened VILI

• 2012 – Hartmann – Critical Care

• For the same VT/strain, higher breathing frequencies intensify VILI

• Multiple strategies can be employed to improve patient/ventilator

synchrony during lung-protective ventilation:

• Sedation, Analgesia, Paralysis

• Adjust RR

• Adjust Vt

• Adjust trigger sensitivity

• Minimize Auto-PEEP

• Adjust PIFR

• Adjust Ti

• Adjust inspiratory flow cycling

• Adjust rise time

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• 2011 - de Graaff - Intensive Care Med

• Although most clinicians are aware of the adverse effects of

hyperoxia, prevention of hypoxia often takes priority and liberal

oxygenation targets tend to be preferred

• 2104 - Gilbert-Kawai - Cochrane Database Systematic Review

• Goal of oxygen titration is to achieve:

• PaO2 60–65 mm Hg

• SpO2 approximately 90%

• Critically ill patients may tolerate lower PaO2 levels

• Permissive hypoxemia

• Don’t automatically increase FiO2 in response to low PaO2’s

Tidal Volume

Accurately measured

Respiratory Rate

Accurately measured

FiO2

Accurately measured

PEEP


Plateau Pressure


• PPLAT – Static pressure exerted by the volume of gas in the lungs at the

end of an inhalation.

• Indicator of “lung fullness”

• 1993 – Slutsky – Chest - ACCP Consensus Conference Recommendation

• Maintain PPLAT < 35cm H2O

• 2007 – Jardin – Intensive Care Medicine

352 ARDS patients

PPLAT MORTALITY

> 35 cmH2O 80%

27 – 35 cmH2O 42%

<27 cmH2O 30%

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• 2003 – Gattinoni – Critical Care Medicine

• Avoidance of stretch by maintaining a low plateau pressure is one

of the physiologic cornerstones of mechanical ventilation

• 2007 – Malhotra – NEJM

• The goal of low-Vt ventilation is to maintain a PPLAT <30 cm H2O

• If PPLAT > 30 cmH2O then reduce Vt to 4cc/kg

• It is reasonable to allow PPLAT >30cmH2O in patients with stiff

chest wall/increased abdominal pressures

• Pleural pressures are elevated but transpulmonary pressures

are not

• Check PPLAT (with a minimum 0.5 second inspiratory pause) at least

q 4h and after each change in PEEP or VT.

• If PPLAT >30 cmH2O:

• �VT by 1ml/kg to minimum of 4 ml/kg.

• If PPLAT < 25 cmH2O and VT< 6 ml/kg:

• � VT by 1 ml/kg until PPLAT > 25 cmH2O or VT = 6 ml/kg.

• If PPLAT < 30 but patient/ventilator dysynchrony is evident:

• � VT by 1ml/kg to a VT of 7-8 ml/kg if PPLAT remains < 30 cm

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• 2002 – Eichacker – AJRCCM

• Excessive reduction in plateau pressure might increase mortality in

ARDS patients

• 2005 – Hager – AJRCCM

• Increased mortality in ARDS with day-1 PPLAT > 26–28 cm H2O

• 2013 – Terragni – Anesthesiology

• A PPLAT <30 cmH2O does not identify all patients a risk of lung injury

due to mechanical venton

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• PEEP - The pressure exerted by the volume of gas remaining in the lungs at

end exhalation (FRC) necessary to prevent intra-tidal collapse.

• 1937 – Barach – Annals of Internal Medicine

• First description of PEEP, used to treat pulmonary edema

• 1967 – Ashbaugh – Lancet

• Widespread use of PEEP in the treatment of ARDS begins.

• 2006 – Gattinoni – NEJM

• PEEP reduces injurious alveolar shear stresses

• PEEP improves ventilation–perfusion matching

• PEEP improves arterial oxygenation.

• 2010 – ARDSNet – NEJM

• ↑ survival benefit with PEEP combined with Low Vt ventilation

• 2013 – Ed-Khatib-CCMJournal

• Optimal PEEP is that which either results in:

• Best lung compliance

• Lowest intrapulmonary shunt

• Best conteract of compressive atelctasis

• Maximized alveolar recruitment

• 2001 – Brower – NEJM (the ALVEOLI Study)

• Low PEEP Arm (273 pts) High PEEP arm (276 pts)

Mean PEEP = 8.9 cmH2O Mean PEEP = 14.7 cmH2O

Mortality = 27.5% Mortality = 25%

• Mortality and VLOS not significantly different between both arms

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• 2008 – Meade – JAMA (the LOVS Study)



Mortality = 40% Mortality = 36%

• No significant difference in mortality or barotrauma with “Open

Lung” protocol vs “Low Vt” protocol

• Open-Lung protocol did appear to improve hypoxemia

• 2008 – Mercat – JAMA (the EXPRESS Study)



Mortality = 39% Mortality = 35%

• No significant difference in mortality.

• High PEEP arm:

• Improved lung function

• ↓VLOS

• Duration of organ failure.

• 2010 – Briele – JAMA

• Difference in hospital mortality between high and low PEEP arms

was not statically significant (32.9% vs 35.2%)

• Statistically significant reduction of death in the ICU for patients

in the High PEEP arm

• Clinicians needed to institute “rescue therapies” for profound

hypoxemia less frequently in patients in the High PEEP group

• Rate of death following “rescue therapy” was also lower

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• 2013 – Santa Cruz – Cochrane Databse of Systematic Reviews

• High levels of PEEP did not reduce hospital mortality compared to

low levels of PEEP

• No significant difference in the risk of barotrauma with high

levels of PEEP

• High levels of PEEP improved oxygenation to the first, third, and

seventh days.

• 2016 – Chikhani – British Journal of Anesthesia

• Not certain whether Low-PEEP vs High-PEEP strategies result in

improvements in mortality and ventilator-free days.

• Select PEEP to improve Oxygenation

• 1975 – Suter – NEJM

• Select PEEP based upon best oxygenation and cardiac output

• Optimum PEEP is that which provides best respiratory compliance

• Select PEEP to Protect the Lung

• 1993 – Bone – JAMA

• Target of PEEP should not be oxygenation but prevention of

intratidal collapse and decollapse.

• Open the lung and keep it open

Gas Exchange/

Oxygenation

Lowest shunt (highest PaO2), lowest deadspace (lowest PaCO2) , best

oxygen delivery (CaO2 x C.O.)

Maximal PEEP while

avoiding over-

distension

Use highest PEEP while maintaining Pplat < 30cmH20

ComplianceUse the highest PEEP that results in the highest respiratory-system

compliance

Imaging Computed tomography, electrical impedance tomography, ultrasound

ARDSNet

PEEP Table

Table of FiO2 and PEEP combinations to achieve PaO2 or SpO2 in target

range

Pressure/Volume

CurveSet PEEP slightly higher than the Lower Inflection Point

Stress

Index

Observe the pressure-time curve during constant-flow inhalation for

signs of tidal recruitment and overdistension

Esophageal

Pressures

Estimate the intra-pleural pressure with an esophageal balloon

measurement of esophageal pressure, then determine optimal PEEP

4/1/2017

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• 2004 – ARDSNet – NEJM

• ARDSNet suggested that the clinician consider the use of Incremental

FiO2/PEEP tables to achieve goal of improved oxygenation.

Low PEEP/High FiO2 ProtocolFiO2 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0

PEEP 5 5 8 8 10 10 10 12 14 14 14 16 16 18-24

High PEEP/Low FiO2 ProtocolFiO2 0.3 0.3 0.3 0.3 0.3 0.4 0.4 0.5 0.5 0.5-0.8 0.8 0.9 1.0 1.0

PEEP 5 8 10 12 14 14 16 16 18 20 22 22 22 24

• Couple of caveats:

• Assumes a Pleural Pressure of ZERO!

• Does not address “PEEP Hunger”

• Need for higher PEEP’s with lower FiO2’s that some patients

exhibit

• The Pressure/Volume loop can be used for PEEP selection with the

hypothesis that:

• A Lower Inflection Point (A) indicates the end of recruitment

• Set PEEP at the Lower Inflection Point pressure

• A Upper Inflection Point (B) indicates the beginning of hyperinflation

• 2001 – Croti – AJRCCM

• Collapsed units open-up at different pressures

• Recruitment is not limited to the LIP but occurs along the entire curve

• At pressures of 30 cmH2O up to 15-30% of the lung remains closed

• May require pressures up to 60 cmH2O to open

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2007 – Terragni – AJRCCM

SI = 0.75 SI = 1.06 SI = 1.38

• 2004 – Grasso – Critical Care Medicine

• At a CONSTANT PIFR:

• Concave Paw waveform = Stress Index <1.0 = Inadequate PEEP

• Linear Paw waveform = Stress Index = 1.0 = Adequate PEEP

• Convex Paw waveform = Stress Index >1.0 = Excessive PEEP

• 2013 – Terragni – Anesthesiology

• Stress IndexRS >1.05 may be indicative of developing VILI

AIRWAY PRESSURE (PAW)

• Measured at the circuit wye or ventilator outlet

• Reflects both lung and pleural pressures

PLEURAL PRESSURE (PPL)

• Pressure imposed upon the lungs by the Chest

Wall and Abdomen

• Can be approximated by measuring pressures

within the esophagus

TRANSPULMONARY PRESSURE (PTP)

• The true pressure within the lung

• PTP = PAW – PES

Paw

PesPtp

Ppl

4/1/2017

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• Airway pressures do not reflect pressures within the lung but pressures of

the entire Respiratory System

• To know true Lung Pressure (Transpulmonary Pressure) you must

account for the pressures outside of the lung (Pleural Pressures)

• Numerous studies have demonstrated reasonable correlation between

Esophageal Pressures and Pleural Pressures

• Pleural pressures adjacent to the esophagus transmitted to esophagus.

• GOAL: Avoid alveolar collapse after recruitment by providing a PEEP that

is greater than the compressive forces operating on the lung

• 2008 – Talmor – NEJM

• Could PEEP be managed better with PTP PEEP rather than the ARDSNet

PEEP Tables?

• PTP PEEP Arm:

• ↑ P/F raDo

• ↑ respiratory-system compliance

• ↓ mortality

• 2010 – Talmor – Respiratory Care

• Estimate pleural pressures from PES

• Set PEEP to achieve a target PTP

• May allow higher PEEP in many patients without overdistending

lung regions that are already recruited.

� 2013 – Yang – Chinese Medical Journal

� In patients with ARDS and IAH

� PEEP titrated by transpulmonary pressure was higher than PEEP

titrated by ARDSnet protocol

� Oxygenation improved

� 2016 – Kassis – Intensive Care Medicine

� Compared to conventional PEEP titration using Pes for PEEP titration:

� Improved elastance

� Decreased driving pressures

PTP PEEP RESEARCH

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• 2006 – Borges – AJRCCM

• Best recruitability with stepwise PEEP increases

• PEEPs up to 45 cmH2O

• Driving Pressure fixed at 15 cmH2O

• DP = PPLAT - PEEP

• 2011 – Silva – Critical Care Medicine

• Compared to sustained inflation, stepwise increase in pressures:

• ↓hemodynamic compromise

• ↓ microscopic and biochemical signs of lung injury

• 2010 – Briele – JAMA

• PEEP is beneficial in ARDS lungs with a high potential for recruitment

• PEEP can result in over-distension in ARDS lungs with a low potential

for recruitment.

• 2007 – Malhotra – NEJM

• Potential for lung recruitment can be inferred at the bedside:

• Recruitable Lung:

• If PEEP is � and PPLAT then �’s in a lesser increment as the

change in PEEP

• Non-Recruitable Lung:

• If PEEP is � and PPLAT then �’s in an equal or greater

increment as the change in PEEP

• 2015 – Gattinoni – Critical Care

• “The “best PEEP” does not exist. To pretend and claim that we may

find a PEEP level that avoids intratidal recruitment-derecruitment,

providing in the meantime the best compliance, best oxygenation

and lowest deadspace, without causing hyperinflation and

affecting hemodynamics, reflects a wishful dream that has nothing

to do with the reality”

• A reasonable approach may simply be tailoring PEEP according to

the Berlin ARDS severity scale:

• Mild ARDS 5-10 cmH2O

• Moderate ARDS 10- 15 cmH2O

• Severe ARDS 15-20 cmH2O

4/1/2017

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• 2012 – Gattinoni – Current Opinion in Anesthesiology

• Stress – distribution of distending forces per unit area

• In the lung this distending force = transpulmonary pressure

• Strain – deformation of the area in response to the stress

• 2016 – Protti – Critical Care Medicine

• Lung Strain – Ratio between Vt and FRC

• Lung Strain Rate – Ratio between Lung Strain and Ti

• Low Strain Rate – I:E of 1:2 – 1:3

• High Strain Rate – I:E of 1:9

• 2015 – Amato – NEJM

• Driving Pressure of the Respiratory System (DPRS) may be a superior

marker of VILI

• DPRS = PPLAT - PEEP

• ↑ DPRS correlated with ↑ mortality even in patients receiving low-

volume lung-protective ventilation

• However, did not account for effect of chest-wall

• 2016 – Kassis – Int Care Med

• Chest wall pressures may account for up to 33% of DPRS

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• 2015 – Loring – NEJM

• Driving Pressure of the Lung (DPL) takes into consideration the

effect of the Pleural Pressure impinging upon the Lung by using

transpulmonary pressures in the equation:

• DPL = PTP PLAT - PTP PEEP

• DPL, instead of DPRS, may be the more appropriate measure of lung

injury due to the varying chest wall compliance and pleural

pressures between patients.

• 2016 – Cressoni – J.AmSociety of Anesth

• Vt and PPLAT represent static work of a single breath.

• Does the dynamic work applied to the lung also contribute to VILI?

• Mechanical Power considers both static and dynamic energy applied

over the lung over time.

• Mechanical Power (W) = PTP x Vt

• “Lethally” ventilated piglets (Vt=38cc/kg, PTP PLAT=27cmH2O) with

varying RR’s

• While RR only varied 5 fold (3-15bpm), power increased 11 fold as

PIFR is augmented at higher RR.

• Determined that a power of 12 Joules/minute was threshold for

VILI

• Does PIP still play a role in VILI?

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• 1987 – Downs – Critical Care

• First description of Airway Pressure Release Ventilation

• 2001 – Frawley – AACN Clinical Issues

• Relatively high CPAP with regular, brief, intermittent releases in airway

pressure

• Unlike CPAP, APRV facilitates both oxygenation and CO2 clearance

• Release phase permits alveolar ventilation & removal of CO2

• Time-triggered, pressure-limited, time-cycled mode of mechanical

ventilation

• Allows unrestricted spontaneous breathing

2011 – MODRYKAMIEN – Cleveland Clinic Journal of Medicine

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• 2016 – Jain – Intensive Care Medicine Experimental

• Care must be exercised when reviewing APRV research as there are

two “eras” in the application of APRV:

• Early Methodology (Downs/Stock) - Fixed APRV (F-APRV):

• Relatively short Thigh (<90% total cycle time)

• Fixed Tlow not adjusted based on changing lung mechanics

• Recent Methodology (Habashi) – Personalized (P-APRV)

• Phigh set at previous PPLAT

• Thigh > 90% of total cycle time

• Tlow adjusted based on changes in lung mechanics

• Analysis of expiratory flow curve

• Plow set at 0 cmH2O

Personalized

Fixed

113

• 2011 – Mondrykamien – Cleveland Clinic Journal of Medicine

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PROMireles-Cabodevila

CONKacmarek

Serves the goals of safety and

comfort.

No human studies have demonstrated

a reduction in WOB

Promotes alveolar stability and

recruitment (animal studies)


a reduction in the need for sedation

and narcotics

Minimizes airway pressure (animal

studies)


a minimized likelihood of VILI

Seems to decrease or prevent lung

injury


a reduction in VLOS or ICU stay

Allows unrestricted spontaneous

breathing


a effect on mortality.

• 2016 – Mireles-Cabodevila & Kacmarek – Respiratory Care

• Mireles-Cabodevila

• Spontaneous breathing seems like a positive but research on

spontaneous breathing during APRV is scant.

• Modes of ventilation are just like medications; you need the correct

one, at the correct dose, and for the right time for a given condition.

• APRV, like many other modes, is still looking for definition of the dose,

the timing, and optimization of its delivery.

• Kacmarek:

• APRV has a greater potential for adversely affecting patient outcome

than improving it

• Unless definitive data are forthcoming demonstrating outcome

benefits from the use of APRV in ARDS or any other patient group,

there is no reason to consider this approach to ventilatory support.

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• High Frequency ventilators are described by their delivery method

and classified by their exhalation mechanism (active or passive).

• High-Frequency Oscillatory Ventilation (HFOV)

• Active Exhalation

• High-Frequency Percussive Ventilation (HFPV)

• Passive Exhalation

• 2011 – Ali – Crit Care Clin

• Constant mean airway pressure

• Pressure waves in the ventilatory circuit (generated by a

diaphragm) at frequencies between 3 and 15 Hz (180–900 bpm)

• Active exhalation as diaphragm creates both inspiratory and

expiratory pressure waves

• May be beneficial in preventing hyperinflation and controlling

CO2 elimination

• 1972 – Lunkenheimer – Br J Anaesth

• First published findings of adequate CO2 clearance with HFOV

• Numerous RCT’s of HFOV in neonatal respiratory distress have been

conducted but there is a smaller body of work in adult HFOV

119

• 2000 – FDA approval of Adult HFOV

• Initially a rescue therapy for patients failing conventional ventilation

• Expanding into treatment of patients with severe ARDS

• 2002 – Derdak – AJRCCM (MOAT Trial)

• First RCP comparing HFOV with conventional ventilation

• HFOV group:

• Significant ↑ in P/F raDo

• Did not persist past 24 hrs

• No significant difference in hemodynamic variables

• Trend towards ↓ mortality

120

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• 2002 – Derdak - AJRCCM

• Early but non-sustained ↑ in the P/F raDo

• Similar complication rates

• Non-significant trend towards reduced 30-day mortality

• 2003 – Sedeek – Anesthesiology

• ↓ histological damage & lung inflammaDon with HFOV vs CMV

• 2013 – Mashael – Semin Respir Crit Care Med

• Mean airway pressures during HFOV often exceed the 30-35 cm H2O

lung-protective threshold employed during CMV.

• Could tolerance of higher mean’s during HFOV be 2° to better

maintained alveolar structure with a slowly applied constant pressure

as opposed to cyclical brief tidal pressures?

• 2010 – Sud – BMJ

• 8 RCT’s with a total of 419 patients were included

• Almost all patients had ARDS

• HFOV may ↓ mortality in ARDS paDents

• HFOV ↑ P/F raDo

• No significant difference in

• VLOS

• Ventilator-free days

• No significant differences in the risk of:

• Barotrauma

• Hypotension

• Endotracheal tube obstruction

• 2013 – Ferguson – NEJM (The OSCILLATE Study)

• ↑ mortality with HFOV compared to CMV with high PEEP’s

• ↑ need for pressor medications

• High mean-airway pressures led to hemodynamic compromise

• 2013 – Young – NEJM (The OSCAR Study)

• No major difference in outcome between HFOV and CMV

• 2013 – Malhotra – NEJM (Editorial Response)

• OSCILLATE & OSCAR underscore the notion that HFOV should be:

• Reserved for patients failing conventional lung protective strategies

• Provided by clinicians with expertise in the technology.

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• 2010 – Allan – J Burn Care Res

• Small high-frequency pulses

of gas

• Pulses accumulate/stack to

form a “low”-frequency Vt

• Emulates a typical pressure-

limited, time-cycled

waveform

124

• 2005 – Salim – Critical Care Medicine

• HFPV provides favorable gas exchange in several well-defined patient

populations

• ↑ oxygenaDon and ↓ PIP’s vs convenDonal venDlaDon

• 2006 – Eastman – American Journal of Surgery

• HFPV may ↑ oxygenation in patients with ARDS without a concomitant

increase in mPaw

• 2010 – Allan – J Burn Care Res

• Lack of literature regarding the practical application of HFPV theory

toward improving gas exchange.

• No discussion has been held regarding the possible risk of HFPV-

associated VILI.

125

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38

• 1957 – Saxon – J Appl Physiol

• First published report of closed-loop ventilation

• Described a servo mechanism to automatically adjust the negative

pressure of an iron lung ventilator in response to EtCO2.

• 2007 – Wysocki – Critical Care Clinics

• Early closed-loop systems designed to maintain ABG’s at normal levels

• Current closed-loop systems designed to:

• Improve lung-protection

• Disease is a dynamic process so closed-loop system may be

able to automatically adjust in response

• Reduce clinician errors

• Cover resource limitations

• 2002 – Branson – Respiratory Care

• Simple - control of one output based on the measurement of one

input.

• The constant modification of inspiratory flow (output) to maintain

the pre-set PSV pressure (input).

• Complex - measurement of multiple inputs (eg, compliance, oxygen

saturation, respiratory rate) to control multiple outputs (eg, ventilator

frequency, airway pressure, tidal volume).

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• 1977 – Hewlett – Anesthesia

• First description of Mandatory Minute Ventilation (MMV)

• ASV is based upon MMV with adaptive pressure control

• 1994 – Laubscher - IEEE Trans Biomed Eng

• First description of clinical application of ASV

• Measured respiratory mechanics applied to algorithms of

pressure control to maintain a target Ve

• 2007 – ASV commercially available in the US

• 2014 – Chopra – Journal of Association of Chest Physicians

• Assist-control, pressure-targeted, time-cycled mode

• RR/Vt pattern automatically set according to minimize ventilator

work.

• Selects the appropriate RR and Vt for mandatory breaths

• Selects the appropriate Vt or spontaneous breaths

• This minimal ventilator work may translate into minimal stretching

forces on the lungs

132

• 2008 – Chen - J lntern Med Taiwan

• Small studies have demonstrated that ASV can be used as a safe

weaning mode for specific postoperative and chronically ventilated

patient groups

• May save manpower and management,

• May reduce VILI

• There is concern regarding patient/ventilator asynchrony if there is

no awareness of the underlying mechanism for respiratory distress

in the patients

• Could worsen the patient's condition or prolong weaning

process

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• 2015 – Kirakli – Chest

• RCT comparing ASV vs pressure A/C in Medical ICU patients

• Previous RCT’s focused on post-op cardiac patients

• ASV arm outcomes:

• ↓VLOS

• ↓ number of manual ventilator setting changes

• ↑ paDents extubated successfully on the first aaempt

• Weaning success and mortality at day 28 were comparable between

the two arms

• 2016 –Greico – Chest

• Aspects of the Kirakli RCT require further discussion

• Reasons of weaning failure were not presented.

• PSV was contemplated in the PC-CMV arm only after failure of the

third SBT

• Delay in applying PSV hampers the understanding of to what

extent the benefit described in patients receiving ASV

• No mention of sedation in either arms

• Patients in the PC-CMV arm may have required more sedation

to achieve adequate patient/ventilator interaction.

• No data on fluid balance and cardiac function even though cardiac

decompensation and fluid overload are recognized as the most

common causes of SBT failure

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• 1992 – Younes – ARRD

• First description of Proportional Assist Ventilation (PAV_

• 2007 – Wysocki – Critical Care Clinics

• Pressure-regulated mode of ventilation

• Inspiratory airway pressure is titrated within each breath in

proportion to the patients inspiratory airflow

• Surrogate of the patient’s respiratory muscle effort

• The proportionality between flow and airway pressure is determined

by the clinician determining the proportions of the total WOB to be

performed by both ventilator and patient.

• PAV+ measures resistance (Rrs) and compliance (Crs) of the respiratory

system and the percentage of assistance adjusted accordingly.139


• All PAV breaths are spontaneous.

• Patient controls the timing and size of the breath.

• No present pressures, flow, or volume goals

• Safety limits on the volume and pressure delivered can be set.

• Patient effort is boosted according to a pre-set proportion of the

measured WOB.

• ↑ paDent effort = ↑delivered flow

• PAV is contraindicated in:

• Respiratory depression (bradypnea)

• Large air leaks (e.g. bronchopleural fistulas)

• 2008 – Gruber – Anesthesiology

• ↓ WOB vs PSV

• 2006 – Kondili – Anesthesiology

• Hemodynamic profile similar to that of PSV

• Vt’s are variable but are usually within the lung-protective range

• 2008 – Xirouchaki – Intensive Care Medicine

• ↓ patient/ventilator dys-synchrony vs PSV

• ↑ probability of spontaneous breathing without assistance vs PSV

• No trial has reported effect of PAV on mortality

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• 2015 – Teixiera – Respiratory Care

• RCT compared weaning with PAV+, PSV, or T-tube

• When subjects were ready to perform the SBT:

• PAV+ group - ventilated in PAV mode up to 40% support

• PSV group - ventilated with 7 cmH2O

• T-tube group - connected to T-piece with supplemental oxygen.

• No significant differences in the groups was observed regarding:

• Rate of extubation failure

• VLOS

• Duration of ICU and hospital stay

• 2016 – Gautam – IJRCCM

• Crossover study comparing PAV+ to PSV

• Ventilator Ti was significantly longer than patient Ti in PSV vs PAV+

• ↑ paDent/venDlator dys-synchronies were in PAV+ vs PSV while

patients were awake

• Variable end inspiratory hold observed in PAV+ .

• Non-significant ↑ in compliance and P/F ratio in PAV+

• PSV and PAV+ modes perform similarly for patient-ventilator

interactions in awake and sedated states.

• Changeover between modes resulted in swings in hemodynamics

and respiratory mechanics

• Patient “tunes” to ventilator deliveries over time.

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• 1999 – Sinderby – Nature Medicine

• First published report of NAVA technology


• Diaphragmatic EMG signal (EAdi) triggers and cycles ventilator breath.

• EMG sensor positioned in esophagus at crural level of the

diaphragm.

• Triggering - virtually simultaneous with phrenic nerve excitation of

inspiratory muscles.

• Termination - linked to the cessation of inspiratory muscle contraction.

• 2015 – Patthum - JBI Database of Systematic Rev & Implemen Reports

• Ventilatory assist proportional to EAdi

145


• Small clinical studies have demonstrated improved trigger and cycle

synchrony with NAVA

• Data lacking showing improved outcomes (e.g. VLOS, sedation needs).

• Concern with NAVA is the expense associated with the EMG sensor.

• 2015 – Diniz-Silva – ATS 2016

• ↑ variability of Vt and Paw with NAVA vs PSV

• 2016 – Carteaux – Critical Care Medicine

• Can be excessively sensitive to EAdi in terms of triggering

• 2016 – Demoule – Critical Care Medicine

• Associated with less frequent application of post-extubation

noninvasive mechanical ventilation. 146

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• Volutrauma & atelectrauma are more detrimental to patient outcomes

than respiratory acidosis.

• 1990 – Hickling – Intensive Care Medicine

• First description of Permissive Hypercapnia

• 50 ARDS patients with 16% mortality (predicted to be 40%)

• PaCO2 averaged 60 mmHg

• Effects of Respiratory Acidosis:

• Cellular: In the absence of hypoxemia, intracellular acidemia appears

to be well tolerated.

• Cardiovascular: Increased HR, BP & stroke volume.

• CNS: Variable, some agitation may occur.

• I:E of 1:1 or inverse (I>E)

• Possible alternative to PEEP

• Usually reserved for patients with plateau pressures >35 cm H20

• ↑ Ti may improve shunt in severe ventilatory failure

• Understanding of ventilator graphics very important

• 1998 – Tharrat – Chest

• Inverse ratio ventilation improves arterial oxygenation

• ↑ mean alveolar pressure with ↓ PIP

• 2013 – Lee – Anesthesia

• I:E ratio of 1:1 vs I:E ratio of 1:2 in one-lung ventilation:

• Modest ↑ in oxygenation

4/1/2017

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• 2015 – Naik – Respiratory Care

• Biological systems are characterized by a continuously variable

response to changing intrinsic or extrinsic input (noise)

• Bad Noise = irregular, random input

• Good Noise = frequency and amplitude of input controlled

• Signal output can be improved with good noise

• This paradoxical effect of noise is termed stochastic

resonance.

• 1996 – Lefevre – AJRCCM

• First description of Variable Ventilation

• Variable ventilation arm:

• RR range of 15–27 breaths/min with over 360 RR changes

• Vt varied 75% - 135% of mean Vt

• Variable ventilation arm:

• Significant↑ in arterial oxygenation

• Significant ↑ respiratory compliance

• ↓ postmortem wet/dry lung weight

• Currently no commercially available ventilators capable of performing

variable ventilation.

• 2003 – Pelosi – AJRCCM

• The application of intermittent sigh breaths offers the opportunity

to introduce some limited variability.

• 2009 – Steimback – Intensive Care Medicine

• Sigh breath frequency should be limited to 2–3 breaths/min

• Facilitates maximum recruitment without inducing volume-

related lung injury.

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• 2007 - Terragni – AJRCCM

• Low-Vt ventilation does not definitively protect the lung from

overdistention during a tidal breath.

• End-inspiratory over-distention occurs in 30% of ARDS patients

receiving lung-protective ventilation

• May be 2° extensive consolidated dorsal lung regions not

recruited during the tidal breath.

• Maneuvers to recruit alveoli might counteract those adverse effects

of low VT and improve oxygenation

• 2007 – Kacmarek – Respiratory Care

• Intentional, transient increase in transpulmonary pressure

• Reopen non-aerated/poorly aerated alveoli.

• Immediate expected benefits are improvements in oxygenation and

respiratory system compliance

• 2015 – Suzumura – Intensive Care Medicine

• RMs have a clear role as rescue therapy for patients with severe

hypoxemia, refractory to protective ventilation strategies and prone

position.

4/1/2017

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2015 – Suzumura – Intensive Care Medicine

• 2008 – Badet – Respiratory Care

• Sighs superimposed on lung-protective ventilation significantly

improve oxygenation and Cstat in patients with ALI/ARDS

• Sigh/decremental PEEP Procedure:

1. Sustained inflation of 40 cmH2O for 30 seconds

2. Adjust PEEP to 24 cmH2O for 10 minutes

• Adjusted Vt to maintain PPLAT < 32 cmH2O

3. Stepwise decrement of PEEP of 4 cmH2O every 10 min

• Measure ABG & CSTAT after each decrement

4. Re-set PEEP to “optimal” PEEP

• The PEEP below which PaO2/FIO2 fell by at least 20%.

2015 – Suzumura – Intensive Care Medicine

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• 2016 – Pirrone - Critical Care Medicine

• Determining optimal PEEP in morbidly obese patients:

• Method #1 - Decremental PEEP Protocol

1. PEEP ↑ in a stepwise manner unDl PTP PEEP = 0 - +2 cmH2O

2. PEEP then set 4 cmH2O higher than the PTP PEEP PEEP level.

3. After 2 minutes PPLAT & PEEP were measured and Driving Pressure

(Pplat – PEEP) was calculated

4. PEEP ↓ by 2 cmH2O, step 3 repeated for at least 5 increments

5. Best decremental PEEP = PEEP with lowest Driving Pressure

6. PEEP set at best decremental PEEP plus 2 cmH2O

• Method #2 - Stepwise Recruitment Maneuver

1. Initial PEEP = 15 cmH2O

2. PEEP ↑ by 5 cmH2O every 30 seconds

3. Total duration of the RM was 2 minutes

• PEEP selected by the ICU team prior to the trial averaged 9 cmH2O lower

than PEEP determined by titration methods

• RM followed by PEEP titration significantly improves EELV

• RM performed with lowest PEEP with a positive PTP PEEP :

• ↑ EELV by 3 mL/kg

• PTP INSP ↓ by 1.5 cm H2O

• Suggests a more favorable distribution of volume among

alveolar units.

• RM followed by PEEP titration significantly improves lung elastance and

oxygenation

• PEEP ↑ without a RM did not significantly improve lung elastance

• 2004 – Chu – Critical Care Medicine

• Atelectatic lung is relatively inert with scant cytokine production

• Cytokine production may be markedly increased by inadequate

recruitment or repeated derecruitment.

• 2009 – Rzezinski – Respir Physiol Neurobiol

• Progressive RM significantly reduced lung inflammation, alveolar

epithelial cell apoptosis, and alveolar-capillary membrane injury

• Epithelial damage more pronounced if high distending pressures are

applied abruptly as compared to progressive approaches

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• 2015 - Koutsoukou – Health Science Journal

• High distending pressure may impair hemodynamics

• Correcting patients volume status prior to RM may attenuate potent

circulatory depression

• 2010 – Silva – Critical Care

• Fluid management, used to minimize hemodynamic instability

associated with RM’s, may have an impact on lung and distal organ

injury

• In hypervolemic animals RM’s:

• Improved oxygenation

• Increased lung injury

• Increased inflammatory and fibrogenic responses.

• May promote recruitment of dependent, atelectatic lung regions by

relieving external compressive forces

• Abdominal contents push upward on the diaphragm and collapse

lower lobes of the lung.

• Over 40% of left lung and 15% of right lung are located under the

heart and may be compressed

• 2006 – Mancebo – AJRCCM

• Trend towards ↑ survival when prone positioning:

• Administered early

• For a much as 20h /day

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• 2009 – Taccone – JAMA

• No significant survival benefit in ARDS patients or in patients with

moderate and severe hypoxemia.

• 2010 – Sud – BMJ (meta-analysis)

• ↑mortality (by about 10%) in the most hypoxic patients (P/F < 100)

• 2013 – Guerin – NEJM – The PROSEVA Trial

• RCT involving 566 patients

• Test arm patients were proned at least 16 h/day

• Early application of prolonged prone-positioning sessions

significantly ↓ 28-& 90-day mortality.

• 2009 – Taccone – JAMA

• ↑ need for increased sedaDon/muscle relaxants

• Airway obstruction

• Transient desaturation

• Vomiting

• Hypotension, arrhythmias, increased vasopressors

• Loss of venous access

• Displacement of endotracheal tube

• Displacement of thoracotomy tube

4/1/2017

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• Endotracheal tubes provide a significant resistance to flow during both

inspiration and expiration.

• May result in significant initial flow dys-synchrony in patients with

vigorous inspiratory efforts.

• 2014 – Frutos-Vivar – Intensive Care Medicine

• Designed to overcome the imposed WOB due to artificial airways by

providing dynamic ventilatory support of each spontaneous breath

• Delivers the exact amount of pressure necessary to overcome the

resistive load of the endotracheal tube for the flow measured at

that time

169

• 2014 – Frutos-Vivar – Intensive Care Medicine

• Mode evaluated as a method for the first trial of withdrawal from

mechanical ventilation in a few studies

• Favorable results in the rate of successful first weanings

• Rate of extubation failure was similar to that reported using other

weaning modes

• 1998 – Strauss – AJRCCM

• A 2-hour trial of spontaneous breathing through an ETT mimicked the

WOB performed after extubation.

• The WOB dissipated against the ETT represented around 10% of

the overall work performed by the patient.

• This increased work load was not different from what was related

to upper airways obstruction immediately following extubation

• The use of such a compensatory mode may falsify spontaneous

breathing trial relevance. 170

• 2009 – Aggarwal – Respiratory Care

• 41 patients requiring mechanical ventilation due to acute respiratory

failure secondary to poisoning from snakebites.

• Compared weaning time of PS with ETRC vs PSV alone

• PSV with ETRC – median weaning time was 8h

• PSV alone – median weaning time was 12h

• 2012 – Oto – Respiratory Care

• ETRC does not necessarily compensate for an ETT-imposed respiratory

work load.

• ETT configuration changes and tracheal secretions can increase

ETT resistance and decrease the ability of ETRC to compensate for

the increased respiratory work load

171

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• 1998 – 2014 – Frutos-Vivar – Intensive Care Medicine

• Designed to overcome the imposed work of breathing due to

artificial airways.

• Provides dynamic ventilatory support of each spontaneous breath

• Delivers the exact amount of pressure necessary to overcome

the resistive load of the endotracheal tube for the flow

measured at that time

• This mode has been evaluated as a method for the first trial of

withdrawal from mechanical ventilation in a few studies

• Favorable results in the rate of successful first weanings

• Rate of extubation failure was similar to that reported using

other weaning modes

172

• 2013 – El-Gendy – Ther Deliv

• Almost all of the currently used exogenous surfactants have a high

efficacy in treating neonatal respiratory distress syndrome, yet

almost none of them are as successful in treating surfactant

dysfunction in adults.

• 2015 – Willson – Chest

• Administration of calfactant was not associated with improved

oxygenation or longer-term benefits relative to placebo in this

randomized, controlled, and masked trial.

• At present, exogenous surfactant cannot be recommended for

routine clinical use in ARDS.

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53

• 2012 – Meng – J Cardiothoracic and Vasc Anesthesia (Meta-Analysis)

• Nine trials involving 2,575 patients

• Surfactant replacement therapy:

• Does not significantly decrease mortality.

• Increases P/F ratio in the first 24 hours

• Lost by 120 hours.

• Causes a non-significant trend towards lower VLOS

• Slightly higher risk of adverse effects.

• 2005 – Griffiths – JAMA

• iNO induces vasodilatation in ventilated lung areas

• 2015 – Bhatraju – Nitric Oxide

• iNO diffuses across the alveolar membrane and binds with Hb

• Allows for iNO to positively modulate the pulmonary circulation.

• iNO selectively works on area of lung that maintains ventilation

• Lung units that maintain ventilation

• Vasculature will dilate and preferentially receive more of the

systemic blood flow.

• Improves V/Q

• Lung units with impaired ventilation

• Lower ratio of perfusion

• Provide a lower amount of the body's total arterial oxygenation

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• 2000 – Payen – Clin Ches Med

• When dissolved in alveolar fluid iNO may react with Reactive

Oxygen Species to form reactive Nitrogen species which may be

cytotoxic to epithelial calls

• 2007 - Adhikari - BMJ

• Trend towards increased mortality rates in groups using iNO

• Significantly increased risk for renal dysfunction

• 2014 – Adhikari – Critical Care Medicine

• Nitric oxide does not reduce mortality in adults or children with

ARDS, regardless of the degree of hypoxemia.

• 2016 – Gebistorf – Cochrane Reviews

• Evidence is insufficient to support INO in any category of critically ill

patients with acute hypoxemic respiratory failure

• Inhaled NO results in a transient improvement in oxygenation

• Inhaled NO does not reduce mortality

• Inhaled NO seems to increase renal impairment.

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“It is remarkable how little is known about alveolar deformation during breathing.”

Rolf Hubmayr

Am J Respir Crit Care Med, 2002

The most meaningful cost reduction strategies will involve standardization of clinical care and elimination of variation in patient procedures.

May 9, 2012

• Positive-pressure ventilation is a proven, effective modality but is the

cause of immense physiological derangements:

• Redistribution of alveolar ventilation

• Altered capillary perfusion

• Functional changes in surfactant

• Transcapillary fluid shifts

• Impaired lymphatic drainage

• Impeded venous return

• These derangements all contribute to wet, harder-to-ventilate lungs

which necessitate even more aggressive positive-pressure ventilation.

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• To minimize these derangements clinical evidence supports:

• Small Vt (4-6 ml/kg IBW)

• Optimal PEEP therapy

• Plateau Pressure maintained below 30cmH2O

• Acute Lung Injury: Prevention May Be the Best Medicine, Litell J, Resp Care

2011

• Dynamic Alveolar Mechanics and Ventilator-Induced Lung Injury, Carney, Crit

Care Med 2005

• Acute Respiratory Distress Syndrome and Acute Lung Injury, Dushianthan,

Postgrad Med Journal, 2011

• Ventilator-Induced Lung Injury in Healthy and Diseased Lungs, Pelosi,

Anesthesiology 2011

• Acute Lung Injury and Acute Respiratory Distress Syndrome, Mackay, Cont Ed

in Anaesthesia, Crit Care and Pain, 2009

• New Insights Into the Pathogenesis of the Acute Respiratory Distress

Syndrome, Slutsky, Medscape Crit Care

191

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57

• Therapeutic Stragegies for Severe Acute Lung Injury, Diaz, Crit Care Med 2010

• ARDSNet Ventilatory Protocol and Alveolar Hyperinflation, Grasso, Am J

Respir Crit Care Med, 2007

• Higher vs Lower End-Exipiratory Pressure in Patients with Acute Lung Injury

and Acute Respiratory Distress Syndrome, Briel, JAMA 2010

• Approaches to Conventional Mechanical Ventilation of the Patient with Acute

Respiratory Distress Syndrome, Hess, Resp Caer 2011

• Approaches to Refractory Hypoxemia in Acute Respiratory Distress Syndrome,

Collins, Resp Care 2011

• What Is Acute Respiratory Distress Syndrome?, Villar, Resp Care 2011

• Measures to Assess Potential Lung Injury During Ventilation Inadequate,

Gattinoni, Am J Resp Crit Care Med 2011

192

• Ventilation with Lower Tidal Volumes as Compared to Conventional Tidal

Volumes for Patients Without ARDS, Determann, Crit Care 2010

• Pathogenesis of Ventilator-Induced Lung Injury: Trials and Tribulations,

Tremblay, American Journal of Physiology-Lung Cellular and Molecular

Physiology, 2005

• Pathophysiology of Ventilator-Associated Lung Injury, Rocco, Current Opinion-

Anesthesiology, 2012

• The Pulmonary Physician in Critical Care 7: Ventilator-Induced Lung Injury,

Whitehead, Thorax, 2002

• Deformation-induced injury of alveolar epithelial cells, Tschumperlin, Am J

Respir Crit Care Med, 2000

• Acute Respiratory Distress Syndrome: Evaluation and Management, Cortes,

Minerva Anesthesiologica, 2012

193

• Low Mortality associated with low volume pressure linked ventilatino with

permissive hypercapnea in severe ARDS, Hickling, Intensive Care Medicine

1990

• High Frequency Oscillatino in Patients with Acute Lung Injury and ARDS:

Systematic Review and Meta-Analysis, Sud, British Medical Journal 2010 ,

• Effect of Rate and Inspiratory Flow on Ventilatior-induced Lung Injury, Rich,

Journal of Trauma, Injury, Infection and Critical Care 2000

• Mechanical Power and the Development of Ventilator-Induced Lung Injury;

Cressoni, The Journal of the American Society of Anesthesiologists, 2016

• Driving Pressure and Survival in the Acute Respiratory Distress Syndrome;

Amato, NEJM 2015

• Ventilator-Induced Lung Injury: Historical Perspectives and Clinical

Implications, deProst, Annals of Intensive Care 2011

194

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• Ventilator-Induced Lung Injury, Slutsky, NEJM 2013

• Influence of respiratory rate and end-expiratory pressure variation on

cyclic alveolar recruitment in an experimental lung injury model.

Hartmann EK, Crit Care 2012

• Effects of decreased respiratory frequency on ventilator-induced lung

injury, Blanch L, Am J Respir Crit Care Med 2000

• Tidal volume reduction in patients with acute lung injury when plateau

pressure are not high, Hager D, Am J Respir Crit Care Med 2005

• Low-tidal-volume ventilation in the acute respiratory distress syndrome,

Malhotra, NEJM 2007

195

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