ARDS and Ventilator Management

ARDS and Ventilator Management
Behrouz Jafari, M.D. Pulmonary & Critical Care Section University of California-Irvine/VA Long Beach

27-year-old woman with dyspnea
4 days s/p C-section Gradual increase in dyspnea over 24 hours with fever of 101 Evaluation Crackles R > L No peripheral edema Hypoxia (7.25/67/41 on 40% VM) Normal Echo Let me start my talk with a case….

27 yo female, 4 days post c-section, progressive shortness of breath, normal echo, mild hypertension, no peripheral edema, fever to 101, PCWP 15 on high PEEP subsequently, right sided crackles.

Clinical Course FiO2 100%; PEEP 20 cm H2O Peak and plateau airway pressures: 40s

Clinical Course FiO2 100%; PEEP 20 cm H2O Peak and plateau airway pressures: 40s Key questions What is the cause of acute respiratory failure? How to oxygenate the patient? How to save her life?

Common Causes of Hypoxemic Respiratory Failure
Acute lung injury (ALI) / ARDS Pulmonary Edema Diffuse alveolar Hemorrhage Pulmonary Embolism Interstitial lung disease Pneumonia Neoplasm Pulmonary contusion Atelectasis COPD Asthma Bronchiolitis There are many reasons to have respiratory failure as you know But REALLY the majority of my focous would be ARDS A LITTLE ABOUT DEFINITION, epidemiology, pathophysiology . But most on management which has impact on your practice.

ARDS: Berlin Deﬁnition
Category Criterion Timing Within 1 week of clinical insult or new/worsening respiratory sx Chest Imaging Bilateral opacities – not fully explained by effusions, lobar/lung collapse, or nodules Origin of edema Not fully explained by cardiac failure or fluid overload. Objective measure to rule out hydrostatic edema Oxygenation: Mild 200 mm Hg < PaO2/FIO2 < 300 mm Hg* Oxygenation: Moderate 100 mm Hg < PaO2/FIO2 < 200 mm Hg** Oxygenation: Severe PaO2/FIO2 < 100 mm Hg** * PEEP or CPAP > 5 cm H2O; ** PEEP > 5 cm H2O So they came up with new definition called Berlin definition , which is very similar to old one except three new changes: 1-the pulmonary capillary wedge pressure criterion has been removed, 2-the term “acute lung injury” has been eliminated, 3- and minimal ventilator settings have been added. JAMA 2012;307:

Diffuse bilateral infiltrates
Patchy, confluent Alveolar, ground- ‐glass In contrast to CHF, no prominence of.. Cardiomegaly Pleural effusion Widened vascular pedicle A few quick comments about chest radiographs. This is a typical appearance It is diffuse bil can be patchy, ggo, importantly, we do not see cardiomegaly….. Having said that you can have both together , having chf and ARDS together. So you need to be aware. But classically pure ARDS doesnot have that component.

ARDS: Chest Radiograph Criteria
Radiographic findings not attributable to: Chronic changes Atelectasis Mass Pleural effusion

As we look at the ct though, you can get a better picture of where densities are. When u look at cxr it looks more homogenous but in ct you see the density follow gravity.

If you make pt in prone position the density will follow the gravity..
Imagine lung is like a wet sponge sitting on table, most of lower part will be collapsed and more wet.

So how does ARDS work? Something trigger, this trigger can either directly injure the alveolo-capillary interface the classic example is asp. PNA, or indirectly through systemic inflammatory process hit the lung like any other systems, the heart brain, kidneys,…also hit the lung and cause a-c injury. The confusing issue is this injured lung can produce more inflammatory markers going out of the lung and cause systemic inflammation elsewhere in the body. So direct and indirect injury and feed back from lung potentiating the systemic inflammation causing permeability edema, surfactant is not low but is not working, cap. Thrombi, which all result is stiff lung, hypoxia….

This graph depicts the concept of permeability edema, this is looking at the lung water and this is left atrial pressure. You and I do not develop lung water until our LA pressure gets quite high but in this syn. With acute capillary injury you get much earlier lung edema. Which is called non-cardiogenic pul. Edema. This is ards vs you and I .In CHF, the edema safety factor prevents pulmonary edema fluid accumulation until pulmonary capillary pressure is elevated to approximately 22 mm Hg. In ARDS, an increase in capillary permeability produces edema at normal capillary pressures and greatly increases the rate of edema formation at elevated capillary pressures.

Lung Compliance in ARDS
Normal Volume ARDS This stiff lungs the best described by pressure-volume curves. You and I have a very steep curve , can generate fair amount of volume with pretty low pressure, but as u develop ards it becomes more flat . This is classical mechanical changes u see in pt with acute lung injury. Pressure

Primary - Direct lung injury (eg aspiration,
ARDS Triggers - primary vs secondary Primary - Direct lung injury (eg aspiration, pneumonia, contusion, inhalation) Patchy If it doesn’t evolve into SIRS/MODS, Outcome better than secondary Let’s talk about triggers, as I said it ca be primary or secondary, primary like….., they are usually patchy and perhaps less peep responsive of course it is a more controversial issue.. Also if it does not evlove……

ARDS Triggers - primary vs secondary
Secondary - Lung is one of many organs involved in SIRS/MODS (sepsis, pancreatitis, hypotension) Diffuse Outcome worse than primary Let’s talk about triggers, as I said it ca be primary or secondary, primary like….., they are usually patchy and perhaps less peep responsive of course it is a more controversial issue.. Also if it does not evlove……

ARDS - clinical progression
STAGE DAYS XRAY PATHOLOGY I Initiation Nl PMNs ARDS moves through various stages, at the beginning cxr look normal but if u do pathology u will see lots of neutrophills, in the next couple of days cxr develops patchy infiltrates , again neutrophils are dominant cells, u see edema and type I cells , type I are the lining cells in alveoli participate in gas exchange of lung . Over the next week or so , x ray become more diffuse , now the fluid in the lung become more exudative and u see more type II cells, the surfactant and repair cells will proliferate. Over the next several weeks if it last that long lym enter the lung and fibrosis start to develop. I want you focous on lym here , because this is the rational to start steroid in late stage to prevent fibrosis. I will discuss later in the management section.

STAGE DAYS XRAY PATHOLOGY I Initiation Nl PMNs II 1-2 days Patchy PMNs, edema, Type I ARDS moves through various stages, at the beginning cxr look normal but if u do pathology u will see lots of neutrophills, in the next couple of days cxr develops patchy infiltrates , again neutrophils are dominant cells, u see edema and type I cells , type I are the lining cells in alveoli participate in gas exchange of lung . Over the next week or so , x ray become more diffuse , now the fluid in the lung become more exudative and u see more type II cells, the surfactant and repair cells will proliferate. Over the next several weeks if it last that long lym enter the lung and fibrosis start to develop. I want you focous on lym here , because this is the rational to start steroid in late stage to prevent fibrosis. I will discuss later in the management section.

STAGE DAYS XRAY PATHOLOGY I Initiation Nl PMNs II 1-2 days Patchy PMNs, edema, Type I III 2-10 days Diffuse cell damage Exudate, Type II ARDS moves through various stages, at the beginning cxr look normal but if u do pathology u will see lots of neutrophills, in the next couple of days cxr develops patchy infiltrates , again neutrophils are dominant cells, u see edema and type I cells , type I are the lining cells in alveoli participate in gas exchange of lung . Over the next week or so , x ray become more diffuse , now the fluid in the lung become more exudative and u see more type II cells, the surfactant and repair cells will proliferate. Over the next several weeks if it last that long lym enter the lung and fibrosis start to develop. I want you focous on lym here , because this is the rational to start steroid in late stage to prevent fibrosis. I will discuss later in the management section.

STAGE DAYS XRAY PATHOLOGY I Initiation Nl PMNs II 1-2 days Patchy PMNs, edema, Type I III 2-10 days Diffuse cell damage Exudate, Type II IV >10 days proliferation Lymph, fibrosis ARDS moves through various stages, at the beginning cxr look normal but if u do pathology u will see lots of neutrophills, in the next couple of days cxr develops patchy infiltrates , again neutrophils are dominant cells, u see edema and type I cells , type I are the lining cells in alveoli participate in gas exchange of lung . Over the next week or so , x ray become more diffuse , now the fluid in the lung become more exudative and u see more type II cells, the surfactant and repair cells will proliferate. Over the next several weeks if it last that long lym enter the lung and fibrosis start to develop. I want you focous on lym here , because this is the rational to start steroid in late stage to prevent fibrosis. I will discuss later in the management section.

ARDS Mortality Trend Outcome has improved over the last 2 decades , but since mid 90s kinda flat which is probably good because we are treating much sicker pt , older, immunosuppressed pts. So my take is vent. Strategies paid off.

ARDS Management

Again Pathogenesis slide blocking initiation sequence , blocking mediators, but unfortunately this does not consume whole lot of our time, most we are doing down here to block the manifestations to buy time so pt own defense systme overcome the current problem meantime minimize the complications.

ARDS: Blocking the trigger
Appropriate infection management Antibiotics Surgical drainage Foreign body removal So looking at the triggering process. What can we do there. Probably the most we can do is controlling infections .

ARDS - mediator modulation
Failed trials Coagulation cascade Immuno-nutrition How about blocking mediator activity. This is consumed lot of money and time but yielded a little. There are areas failed trials, coag cascade, and immuno nutrition.

ARDS - blocking manifestations
Goals are to “buy time” and avoid complications Support gas exchange/lung protective ventilator strategies Assure other components of DO2 are optimal Altering lung fluid fluxes

ARDS Management Mechanical Ventilation : Low TV (ARDSNET protocol)
Unconventional approach: APRV HFV To achive this goal we use two different measures: 1- MV which includes lung protective stategies which I am going to discuss ARDSNET data and role PEEP as well as unconventioal approach like APRV and HFV

ARDS Management Mechanical Ventilation : General Measures:
Low TV (ARDSNET protocol) Unconventional approach: APRV HFV General Measures: Prone positioning Nitric oxide NMBA Fluid Management ECMO 2- and general measures to improve oxygentation and or outcome including ….

Ventilator Management

861 Patients 432 Patients 429 Patients
Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and Acute Respiratory Distress Syndrome 861 Patients 6 cc/kg 12 cc/kg 432 Patients 429 Patients ARDSNET N Engl J Med 2000;342:1301-8

ARDSNET: Setting the Ventilator
FiO2 .3 .4 .5 .6 .7 .8 .9 1 PEEP 5 8 10 12 14 16 18 20-24

Hypothesis of ARDSnet 6 vs 12 Trial
The classic ARDS net trial showing benefits of reducing TV which is associated with improve mortality.

While the target is <30 but As you see higher plt translates to higher mortality, so here lower is better so if your patient is comfortable at plt pressure of 20 then keep it that low. 20 is better than 25 or 30 as while as pt is comfortable an have synchrony , etc. Brower et al, AJRCCM 2002;166: Brower et al, AJRCCM 2005;172:1241-5

General Measures

In patients with severe ARDS, early administration of a neuromuscular blocking
agent improved the adjusted 90-day survival and increased the time off the ventilator without increasing muscle weakness

Eﬀect of Prone Positioning on Oxygenation
Gattinoni, et al. N Engl J Med 2001; 345: prone supine The same thing for prone postioning , improve oxygenation Change in PaO2:FiO2 from baseline to 1h to end of period to next morning

Multicenter RCT comparing prone (n = 237) and supine (n = 229) positioning in severe (P/F <150) ARDS So this is we should consdier if u have enough staff to make sure it is done in a safe way.

Prone positioning associated with:
Multicenter RCT comparing prone (n = 237) and supine (n = 229) positioning in severe (P/F <150) ARDS – > 16 hr / d prone positioning Prone positioning associated with: Lower 28 and 90 day mortality More patients extubated at 90 days More ventilator-free days (at 28, 90 d) No difference in complications So this is we should consdier if u have enough staff to make sure it is done in a safe way. Guerin et al. N Engl J Med 2013

Inhaled Nitric Oxide Endogenous vasodilator
Inhalation of ppm produces selective dilation of pulmonary vessels Rapidly inactivated by combining with hemoglobin and by oxidation Inhaled NO as you know is a vasoilator and rapidly inactivated by attaching to hgb

What is the Role for Nitric Oxide in ARDS?
Oxygenation beneﬁt for up to 4 days (5-‐20ppm) No outcome beneﬁt (survival, duration of mechanical ventilation, ICU LOS) Routine use of inhaled NO is not supported Potential role for inhaled NO as rescue therapy for severe refractory hypoxemia It improves oxygenation but hasn’t shown improve mortality. It is expensive, it is safe, it is very unlikely to cause methgb with the does we use. You would not use it routinely, however if u have that pt can not oxygenate it maybe a bridge.

ECMO for ARDS Venovenous (VV-‐ ECMO) for respiratory failure
Blood removed and pumped through oxygenator and returned to circulation; no cardiac support Large vascular cannula, and coagulation, infection risk The last thing I wana point is ECMO, which is available in a limited centers. There are 2 types: VV which is for respiratory failure and VA which is for cardiac failure.

The Bottom Line Identify ARDS using conventional parameters (predisposition / timing, CXR, ABG) Use “lung protective approach” – 6 ml/kg PBW Vt Avoid trans-alveolar pressure > 30 cmH2O; Avoid cyclic alveolar collapse by applying PEEP, particularly for severe ARDS

The Bottom Line Conservative ﬂuid management: aim for balanced I = O
Consider NMBA, prone positioning, NO, or ECMO for severe hypoxemia – moving from least invasive to most invasive. Prove that it helps to continue rx

Randomized, blinded controlled trial of methylprednisilone vs
Randomized, blinded controlled trial of methylprednisilone vs. placebo for ALI persisting > 7 days 2 mg/kg/day x 14 days; then 1 mg/kg/day x 7 days then tapered over 4 days. How about steroid ? In ARDS net trial adding steroid after a week

Methylprednisilone vs. placebo results
You can see no difference in survival or in MV

Pressure vs Volume-‐Targeted Ventilation in ARDS?
No large, recent (low Vt) RCTs comparing only pressure vs volume-‐targeting Potential advantages of pressure-‐targeting Easily adjust inspiratory time Better patient-‐ventilator synchrony Avoid regionally excessive transalveolar pressure Potential advantages of volume-‐targeting Avoid high tidal volume, simplify implementation Pressure vs volume target? Does it matter? We stuck with lack of outcome studies. Some of the potential advantages of using pressure modes are easily adjusting inspiratory time (u can do it with volume mode but easier with pressure mode). Better synchrony But the risk is u don’t have a control on volume it can change with MacIntyre & Sessler. Respir Care 2010; 55:43-55 Marini & MacIntyre Chest 2011; 140:

There is a this notion of recruitable vs non-recruitable lung in ards
There is a this notion of recruitable vs non-recruitable lung in ards. In the top there is a pt with bil lung injury but it is pretty patchy, there is not a whole lung to recruit, down here however the injury is more diffuse and this respond to peep better.

Mortality according to % of recruitable lung
It appear more recruitable lung have higher mortality, I think it is a little misleading. because more recruitable lung means you have more lung injured , so I am not sure if this curve reflects the extent of inflammation. But the data is out there. And people talk about recruitable as predictor of mortality.

RM Techniques Wide variety of proposed approaches :
40 cm H2O pressure for 40 seconds (40-40 rule) But why do we do recruitment manuver? Remember peep does not recruit, peep only prevents derecruitment. Peep only keeps open what you opened during inspiration. So the idea of recruitment is bring the lung all the way to TLC and bring it back to the peep level , but if you do not have PEEP in the system, the effect will be lost fairly quickly., so it is got to be tied to the PEEP strategy. It does not make sense to do rec manuver and bring pt to where he was. You will lose that effect. So this manuver should be used if you lose the peep like disconnect or suctioning Demonstrated to improve oxygenation Transient benefit alone Recommended prior to increasing PEEP Clearly beneficial for interventions that promote loss of airway pressure / PEEP But overall has No effect on mortality, barotrauma, blood pressure CCM 2004:32:2371

Mechanical Ventilation in ARDS: Prolonged Inspiratory Time
Methods Inspiratory Pause Decreased PIFR Prolonged TI Potential benefits Higher mean pressure Autopeep

Mechanical Ventilation in ARDS: Prolonged Inspiratory Time
Impaired DO2 Barotrauma Need for heavy sedation Doesn’t work

Female IBW = 45.5 + 2.3(ht(in) - 60)
Ventilation with Lower Tidal Volumes as Compared with Traditional Tidal Volumes for Acute Lung Injury and Acute Respiratory Distress Syndrome Male IBW = (ht(in) - 60) Female IBW = (ht(in) - 60) ARDSNET N Engl J Med 2000;342:1301-8

ARDSNET: Setting the Ventilator: Subtleties
RR can be increased to correct pH VT can be increased for Dyspnea and breath stacking (if PPl < 30) PPl < 25 and VT < 6 ml/kg VT may go as far as 4 ml/kg if needed to keep PPl <30 cmH20 Paralysis rarely needed (~6%) Vast majority complied with protocol

Eisner MD et al., Am J Resp Crit Care Med 2001; 164:225
Eisner et al, AJRCCM july 2001 Eisner MD et al., Am J Resp Crit Care Med 2001; 164:225

Causes of Death in ARDS (%)
* Ferring M, Vincent JL. Eur Respir J 1997; 10:

ARDS: Organ Failure(s) and Mortality
Ferring M, Vincent JL. Eur Respir J 1997; 10:

Inflammatory Cytokines in ARDS (D1)
Headley et al., Chest 1997; 111:1306 44

n=16 Elliot, C.G. et al., ARRD 1987; 135:634

McHugh, L.G. et al., AJRCCM 1994; 150:90-94

ARDS: AECC Consensus Definition
American-european consensus definition, by definition is bilateral

Criticism Problems with the definition: PEEP not specified
CXR criteria vague ALI vs ARDS: Does it matter? One man’s infiltrate is another man’s lung collapse, interobserver difference, and this causes lots of issues defining this syndrome and another problem is pretty non-specific. Again this is a problem we are dealing with. It can apply to whole bunch of lung dis.

ALI vs ARDS: Does it Matter?
Characteristic ALI (n=66) ARDS (n=221) P/F 239.8 ± 27.1 130.7 ± 37.5 Age 55.0 ± 19.8 61.3 ± 16.5 APACHE II 17.2 ± 7.9 19.2 ± 7.9 Quadrants on CXR 2.8 ± 0.8 3.0 ± 0.9 Mortality (90 d) 42.2% 41.2% Lure, O.R. et al., Am J Respir Crit Care Med 1999; 159:1849

Lung protection tradeoffs: PO2
This may involve trade off u may have worse hypoxemia, but because u are protecting healthier part of the lung those have a better outcome What novel strategies is the best to keep gas exchange? In ARDS trial if u look at the P/F ratio u see those with high TV actually did much better oxygenation at least at the beginning . But are not they the group had more mortality? It is a heterogenous dis. High TV opens up more alveoli and better oxygentation at the beginning but cause damage to thos normal areas and VILI and higher mortality. Crs also better in the HIGH Vt group

Lung protection tradeoffs: pH
Similarly you might get low PH and high co2 as a result of low TV and that is ok too. ARDSnet rules allowed pH values as low as 7.15

Unconventional vent. approach

ARDS Unconventional approaches: Long I time strategies (APRV) HFOV
So these are conventioanl approach, low tv , low plt and peep how about non conventional approaches. sLet’s talk about gas exchange and lung protective startegies. Vent mgm: start with 6 ml/kg ibw u can go up to 8 while keeping plat <30. the caveat is if u have a morbidly obese or significant intraabdominal path can accept higher plt. These are unconventioanl approaches, I will touch on later.

APRV Long I time, short E time strategy. And spontanous breath allowed throughout the cycle. Long I time let more time to more units open up , increase mean airway pressure without set vol .

AutoPEEP & Tidal Volume Creep
APRV Concerns: AutoPEEP & Tidal Volume Creep Tidal volume pressure 700 650 600 550 500 450 400 350 300 but short E time prouduce good amount of auto peep. And variable TV . Also plt pressure might be higher than what u set because of pt ‘s breathing on top of it. Does it work? Yes, it might improve oxygenation but does not change the outcome. 6 ml/kg IBW flow 10pm 2am 6am 10am Incomplete emptying (i.e. autoPEEP)

HFOV – CPAP with a “wiggle”
HFO is a CPAP with a wiggle, with a very high RR like /min with a very low TV <1 ml/kg, gas diffusion is funky uses augmented diffusion , it is like CPAP try to minimize overdistension and prevent under-recruitment injury

HFOV for Severe ARDS Multicenter RCT of 548
patients of HFOV vs LTVV (Vt 6 ml/kg, high PEEP) for ARDS (PaO2:FiO2 < 200 mmHg) Stopped early for harm HFOV associated with: Higher mortality (ICU, hosp) More sedation, NMBA More vasopressors Less refractory hypoxemia Ferguson et al. N Engl J Med 2013

HFOV for Severe ARDS Multicenter RCT of 548 •
patients of HFOV vs LTVV (Vt 6 ml/kg, high PEEP) for ARDS (PaO2:FiO2 < 200 mmHg) Stopped early for harm HFOV associated with: Higher mortality (ICU, hosp) More sedation, NMBA More vasopressors Less refractory hypoxemia Multicenter RCT of 795 UK patients of HFOV vs usual care for ARDS (PaO2:FiO2 < 200 mmHg) – Vt = 8.3 ml/kg, PEEP 11 cm H2O No diﬀerence in: 30 day all cause mortality ICU, Hosp LOS Vent-‐free days Ferguson et al. N Engl J Med 2013 Young et al. N Engl J Med 2013

ECMO for ARDS Extracorporeal Life Support (ECLS) Large RCT in UK :
lower mortality and/or disability in group (but many other Rx diﬀerences) Peek et al. Lancet 2009 There was a large study should lower mortality with ECMO, there are some questions about the study including the difference in treatments they got, but this is another option in those who fail or refractory to the conventional treatment.

This is how often you see the ards
This is how often you see the ards. sepsis alone will produse % of the time, if it is with other risk factors maybe 2/3 of these pts. Asp pna alone produce 10% of ards cases. Others include overdose, transfusion,etc (open bars the factor alone , closed bar in conjunction with other risk factors increase the risk of developing ards.

What PEEP should we choose?
High or Low? So now what about after set your ventilator on 6 ml/kg, what sort of peep should achive .

I want u look at the orange bar in front which is peep and pink is fio2 . So if u are in range peep in 5 range , move to 9 range u r still in single digit until u get to >80%. Which u move to double digit. That is the general framework u mostly see, now if u add 5-6 to peep what happens?

There are three trials I am going to talk, first was published in nejm by the ards net back in 2004
Three study: alveoli (ards study) used peep table I just showed u , in all plt<30 LOVS was canadian which was in 3 continents 30 hosp, and in 2 arms plt was <30 and 40, and EXPREE trial which is french trial in 37 icus in control group used peep 5-9 and in treatment arm increased peep to keep plt in all slightly different approaches but all got the same results.

At the end mortality was the same in all studies and no significant difference.

But there a few caveat, mortality was the same but in a subgroup analysis of very severe /bad ARDS survival was higher in EXPREE trial in high peep group the sicker u were u intended to benefit a little more. So if u are a person who like high peep u have a little evidence toward use of high peep in vary severe /bad ards. This is because it is heterogenous and if it is severe ards maybe benefits of high peep outweight the risks , but at the same time if the dis is not that severe then low peep is more beneficial. But also found a couple of other interesting , first in all the major cause of ards was sepsis, also all used 2 h sbt and if pt passed prompted the MD for possible extubation, if this is not happening in our icu, then we should consider a better communication, in LOVS 95% were on sedatives>1 weeks. This is not acceptble. I know we want pain free but many data shows this keeps pt on the vent more than anything else u r doing.

Pressure vs Volume-‐Targeted Ventilation in ARDS?
No large, recent (low Vt) RCTs comparing only pressure vs volume-‐targeting Potential advantages of pressure-‐targeting Easily adjust inspiratory time Better patient-‐ventilator synchrony Avoid regionally excessive transalveolar pressure Potential advantages of volume-‐targeting Avoid high tidal volume, simplify implementation Pressure vs volume target? Does it matter? We stuck with lack of outcome studies. Some of the potential advantages of using pressure modes are easily adjusting inspiratory time (u can do it with volume mode but easier with pressure mode). Better synchrony But the risk is u don’t have a control on volume it can change with MacIntyre & Sessler. Respir Care 2010; 55:43-55 Marini & MacIntyre Chest 2011; 140:

But keep in mind if u look at subgroup analysis u will see it Impacted by underlying diseases
ARDS with MOF 81% ARDS without MOF 40%

ARDS outcome Long term mortality depends on underlying health status (11% mortality in 1st year) Long term mortality, if pt survive u are not home free, still there is 11% mortality. It is not because of resp problems, it is due to comorbidities caused ards in the first place. At one year still there are some functional changes : vc comes back up well but 6 MW is still low. There are important psycho-social issues measured by SF-36 , PTSD like syndrome, we r not sure why , is it due drugs….? Do not know. NEJM 2003; 348: 8

ARDS outcome Long term mortality depends on underlying health status (11% mortality in 1st year) At one year: – 6 MW 49%, VC 85%, DLCO 72% PTSD like syndrome Are these long term effects of hypoxemia? hypotension? drugs ? Long term mortality, if pt survive u are not home free, still there is 11% mortality. It is not because of resp problems, it is due to comorbidities caused ards in the first place. At one year still there are some functional changes : vc comes back up well but 6 MW is still low. There are important psycho-social issues measured by SF-36 , PTSD like syndrome, we r not sure why , is it due drugs….? Do not know. NEJM 2003; 348: 8

Controversies in VILI - Overdistention
Is it “maximal” stretch or “tidal” stretch (or both) that causes VILI? If “maximal” , goal is to keep Pplat <30 with any VT Pplat < 30 is “safe” If “tidal”, goal is to reduce VT and Pplat to minimums No Pplat is “safe” So there was immediate controversy . Was it low TV or low pla pressure kept them safe or both….. It is important clinicaly because if u belive in pl pressure<30 then u can give any TV as while as pressure <30, but if u believe tidal strtch is important then there is no safe plateau pressure and u need to minimize both

Stretch injury - Is it max stretch or tidal stretch?
What is the data on this? This is ARDS net data organized based on quartiles , 25% sickest, healthiest and middle pts. And as u see even with low TV but plat >30 had higher mortalitiy.

Controversies in VILI - Overdistention
Is it “maximal” stretch or “tidal” stretch (or both) that causes VILI? If “maximal” , goal is to keep Pplat <30 with any VT Pplat < 30 is “safe” If “tidal”, goal is to reduce VT and Pplat to minimums No Pplat is “safe” So as per Dr Macintyre says minimize both plt and TV

Steroids in ARDS: Use of low dose, longer duration steroids is associated with more rapid recovery and may be associated with reduced mortality risk But, small studies, methodological quality issues However in some small studies showed low does steroi is associated with rapid recovery but they are small studies an have some methodological issues. The bottom line is it is still controversial issue and many clinical trials is on going at this point to answer this , but if you choose to use it should avoid to use it after 14 days and avoi using with NMBA

Steroids in ARDS: Use of low dose, longer duration steroids is associated with more rapid recovery and may be associated with reduced mortality risk But, small studies, methodological quality issues If use steroids in ARDS Avoid starting after day 14 Avoid NMBA Infection surveillance Methylprednisolone 2m g/kg/d, taper over 4 weeks However in some small studies showed low does steroi is associated with rapid recovery but they are small studies an have some methodological issues. The bottom line is it is still controversial issue and many clinical trials is on going at this point to answer this , but if you choose to use it should avoid to use it after 14 days and avoi using with NMBA

Lower Tidal Volumes and Survival in ARDS
ARDSNET N Engl J Med 2000;342:1301-8

ARDS and Ventilator Management

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