Acute respiratory distress syndrome mechanical ventilation therapy: Difference between revisions

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{{Acute respiratory distress syndrome}}
{{Acute respiratory distress syndrome}}
{{CMG}}
{{CMG}}; {{AE}} {{BShaller}}


==Overview==
==Overview==
Acute respiratory distress syndrome is usually treated with mechanical ventilation in the Intensive Care Unit. Ventilation is usually delivered through oro-tracheal intubation, or tracheostomy whenever prolonged ventilation (≥2 weeks) is deemed inevitable. The origin of [[infection]], when surgically treatable, must be operated on. When [[sepsis]] is diagnosed, appropriate local medical protocols should be enacted.
Most patients with ARDS will require [[endotracheal intubation]] and [[mechanical ventilation]] at some point during the course of their illness and recovery. A mechanical ventilation strategy using lower [[Lung volumes|tidal volumes]] of 6 mL/kg predicted body weight and higher levels of [[PEEP|positive end-expiratory pressure (PEEP)]] has been shown to be most effective at improving oxygenation and minimizing [[barotrauma|volutrauma]] (injury to stiff lungs resulting from overdistention).


Commonly used supportive therapy includes particular techniques of mechanical ventilation and pharmacological agents whose effectiveness with respect to the outcome has not yet been proven. It is now debated whether mechanical ventilation is to be considered mere supportive therapy or actual treatment, since it may substantially affect survival.
As an overview, a quasi-experimental, before-after trial<ref name="pmid28157140">{{cite journal| author=Fuller BM, Ferguson IT, Mohr NM, Drewry AM, Palmer C, Wessman BT et al.| title=A Quasi-Experimental, Before-After Trial Examining the Impact of an Emergency Department Mechanical Ventilator Protocol on Clinical Outcomes and Lung-Protective Ventilation in Acute Respiratory Distress Syndrome. | journal=Crit Care Med | year= 2017 | volume=  | issue=  | pages=  | pmid=28157140 | doi=10.1097/CCM.0000000000002268 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28157140  }} </ref> found reduced mortality associated with the following strategy quoted from Journal Watch<ref>{{Cite web| title = Lung Protective Strategy for Acute Respiratory Distress Syndrome Saves Lives| journal=NEJM Journal Watch | year=2017|accessdate = 2017-03-07| url = http://www.jwatch.org/na43522/2017/03/03/lung-protective-strategy-acute-respiratory-distress?query=etoc_jwhospmed&jwd=000000590141&jspc=IM}}</ref>:
* use tidal volumes <6.5 mL/kg,
* use a PEEP of 5–24 cm H20 within a plateau pressure <30 cm H20,
* decrease FiO2 as permitted to achieve saturation of 88%–95%,
* and elevate the head of the bed. Hypercapnia with a pH >7.25 is permissible.
* Use a higher flow rate (up to 100 L/min) for obstructive airway disease when necessary to achieve a satisfactory I:E ratio


==Mechanical ventilation==
==Mechanical ventilation==
{{ Further|[[Pressure Regulated Volume Control]] }}
*'''Lower [[Lung volume|tidal volume]] [[Mechanical ventilation|ventilation]]''' (6 mL/kg predicted body weight) is associated with reduced mortality and a greater number of ventilator-free days<ref name="pmid10793162">{{cite journal| author=| title=Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. | journal=N Engl J Med | year= 2000 | volume= 342 | issue= 18 | pages= 1301-8 | pmid=10793162 | doi=10.1056/NEJM200005043421801 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10793162  }} </ref>
The overall goal is to maintain acceptable gas exchange and to minimize adverse effects in its application. Three parameters are used: PEEP (positive end-expiratory pressure, to maintain maximal recruitment of alveolar units), mean airway pressure (to promote recruitment and predictor of hemodynamic effects) and plateau pressure (best predictor of alveolar overdistention). <ref>{{cite journal | author =Malhotra A | title = Low-tidal-volume ventilation in the acute respiratory distress syndrome | journal = N Engl J Med | volume = 357 | issue = 11 | pages = 1113-20| year = 2007 | id = PMID 17855672 }}</ref>
:*Lower tidal volume ventilation should be continued even if the [[PaCO2|arterial partial pressure of carbon dioxide (PaCO<sub>2</sub>)]] rises (this is called ''permissive [[hypercapnia]]'')
:*Permissive hypercapnia usually results in a drop in blood [[pH]], however, treatment of [[acidemia]] (e.g., intravenous administration of [[sodium bicarbonate]] or [[tromethamine]]) is not indicated if the pH remains at or above 7.15 to 7.20
:*Predicted body weight (PBW) in kilograms (kg) may be calculated from height in inches (in) as follows:
::*PBW (men) = '''50 + 2.3 (height in inches – 60)'''
::*PBW (women) = '''45.5 + 2.3 (height in inches – 60)'''
*'''Higher [[positive end-expiratory pressure|positive end-expiratory pressure (PEEP)]]''' combined with lower tidal volume ventilation is associated with decreased mortality in patients with '''moderate or severe ARDS (PaO<sub>2</sub>/FIO<sub>2</sub> ≤ 200)'''<ref name="pmid20197533">{{cite journal| author=Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD et al.| title=Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis. | journal=JAMA | year= 2010 | volume= 303 | issue= 9 | pages= 865-73 | pmid=20197533 | doi=10.1001/jama.2010.218 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20197533  }} </ref>
*'''[[Mechanical ventilation initial ventilator settings#Proning|Prone positioning''']] for at least 16 consecutive hours each day is associated with improved 28-day and 90-day survival in patients with '''ARDS and a PaO<sub>2</sub>/FIO<sub>2</sub> ratio < 150 on an FIO<sub>2</sub> ≥ 60% and PEEP ≥ 5 mmHg'''
:*Prone positioning is thought to improve [[oxygenation]] by improving [[Ventilation/perfusion ratio|ventilation/perfusion (V/Q) mismatching]] via reduced [[Shunt|shunting of blood]] through under-ventilated lung tissue
*'''[[Cisatracurium]]''', when started within the first 48 hours of ARDS diagnosis and continued for 48 hours, has been associated with improved 90-day survival, a greater number of ventilator-free days, and a decreased incidence of [[barotrauma|volutrauma]]<ref name="pmid20843245">{{cite journal| author=Papazian L, Forel JM, Gacouin A, Penot-Ragon C, Perrin G, Loundou A et al.| title=Neuromuscular blockers in early acute respiratory distress syndrome. | journal=N Engl J Med | year= 2010 | volume= 363 | issue= 12 | pages= 1107-16 | pmid=20843245 | doi=10.1056/NEJMoa1005372 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20843245  }} [http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21242357 Review in: Ann Intern Med. 2011 Jan 18;154(2):JC1-3] </ref>


Conventional therapy aimed at tidal volumes (''V''<sub>t</sub>) of 12-15 ml/kg. Recent studies have shown that high tidal volumes can overstretch alveoli resulting in volutrauma (secondary lung injury). The ARDS Clinical Network, or [http://www.ardsnet.org/index.php ARDSNet], completed a landmark trial that showed improved [[Mortality rate|mortality]] when ventilated with a tidal volume of 6 ml/kg compared to the traditional 12 ml/kg. Low tidal volumes (''V''<sub>t</sub>) may cause [[hypercapnia]] and [[atelectasis]].<ref name=Rippe-ARDS>{{cite book | author = Irwin RS, Rippe JM | title = Irwin and Rippe's Intensive Care Medicine | edition = 5th ed. | publisher = Lippincott Williams & Wilkins | year = 2003 | id = ISBN 0-7817-3548-3 }}</ref>
=== ARDS Network Mechanical Ventilation Protocol ===
In 1994 the [[NIH|National Institutes of Health (NIH)]] and [[NHLBI|National Heart, Lung, and Blood Institute (NHLBI)]] founded the '''ARDS Clinical Trial Network''' (often abbreviated as ''ARDSnet'') – a consortium of over 40 hospitals that conduct [[Clinical trial|clinical research trials]] aimed at improving care for patients with ARDS. In order to simplify the mechanical ventilation of patients with ARDS, the NIH-NHLBI ARDS Network has compiled a [http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf '''Mechanical Ventilation Protocol Summary''']<ref>NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary. (2008). http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf Accessed on June 28, 2016</ref> that outlines the [[mechanical ventilation]] strategies associated with better outcomes in an easy-to-use format for [[ICU]] health care providers.


Low tidal volume ventilation was the primary independent variable associated with reduced mortality in the NIH-sponsored ARDSnet trial of tidal volume in ARDS.  Plateau pressure less than 30 cm H2O was a secondary goal, and subsequent analyses of the data from the ARDSnet trial (as well as other experimental data) demonsrtate that there appears to be NO safe upper limit to plateau pressure; that is, regardless of plateau pressure, patients fare better with low tidal volumes (see Hager et al, American Journal of Respiratory and Critical Care Medicine, 2005).
===Non-Invasive Positive Pressure Ventilation===
Many patients who develop ARDS will receive a trial of [[Positive airway pressure|non-invasive positive pressure ventilation (NIPPV)]] before [[intubation]] and [[mechanical ventilation]] become necessary to maintain adequate [[oxygenation]], or before the degree of clinical deterioration precludes the use of NIPPV and necessitates [[endotracheal intubation]] for airway protection. Several studies have examined the utility of NIPPV in the management of ARDS:
*'''NIPPV observational data from [[Cohort study|cohort studies]]: Early application of NIPPV appears to reduce the rate of [[intubation]] and [[mechanical ventilation]] in patients with [[Acute respiratory distress syndrome diagnostic criteria|mild-to-moderate ARDS]] (PaO<sub>2</sub>/FIO<sub>2</sub> ratio 150 to 200)<ref name="pmid17133177">{{cite journal| author=Antonelli M, Conti G, Esquinas A, Montini L, Maggiore SM, Bello G et al.| title=A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome. | journal=Crit Care Med | year= 2007 | volume= 35 | issue= 1 | pages= 18-25 | pmid=17133177 | doi=10.1097/01.CCM.0000251821.44259.F3 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17133177  }} </ref><ref name="pmid24215648">{{cite journal| author=Thille AW, Contou D, Fragnoli C, Córdoba-Izquierdo A, Boissier F, Brun-Buisson C| title=Non-invasive ventilation for acute hypoxemic respiratory failure: intubation rate and risk factors. | journal=Crit Care | year= 2013 | volume= 17 | issue= 6 | pages= R269 | pmid=24215648 | doi=10.1186/cc13103 | pmc=4057073 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24215648  }} </ref>
*'''NIPPV versus high-flow [[nasal cannula]] (HFNC) or supplemental oxygen via face mask''': 310 patients with ARDS and a PaO<sub>2</sub>/FIO<sub>2</sub> ratio ≤ 300 were randomized to either NIPPV, high-flow nasal cannula, or supplemental oxygen via face mask<ref name="pmid25981908">{{cite journal| author=Frat JP, Thille AW, Mercat A, Girault C, Ragot S, Perbet S et al.| title=High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 23 | pages= 2185-96 | pmid=25981908 | doi=10.1056/NEJMoa1503326 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25981908  }} </ref>
:*At 28 days, no differences in were seen in rates of [[intubation]] and [[mechanical ventilation]] between the three groups
:*At 90 days, there were significantly more [[ICU]]-free days and significantly fewer mortalities in the high-flow nasal cannula group as compared to the other two groups
*'''NIPPV via face mask versus NIPPV via helmet''': 83 patients with ARDS were randomized to either NIPPV via face mark or NIPPV via helmet<ref name="pmid27179847">{{cite journal| author=Patel BK, Wolfe KS, Pohlman AS, Hall JB, Kress JP| title=Effect of Noninvasive Ventilation Delivered by Helmet vs Face Mask on the Rate of Endotracheal Intubation in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial. | journal=JAMA | year= 2016 | volume= 315 | issue= 22 | pages= 2435-41 | pmid=27179847 | doi=10.1001/jama.2016.6338 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27179847  }} </ref>
:*At 28 days, there was a significantly lower rate of intubation and significantly  more ventilator-free days in the helmet group
:*At 90 days, there were significantly fewer mortalities in the helmet group
:*Study was terminated early due to the significantly higher [[mortality rate]] seen in the face mask group


===APRV (Airway Pressure Release Ventilation) and ARDS / ALI===
=== Alternative Mechanical Ventilation Strategies ===
Although a particular ventilation mode has yet to be "proven in clinical trials"* more effective than others in treating patients with ARDS, ever increasing empirical evidence and clinical experience is showing that [http://www.aacn.org/pdfLibra.NSF/Files/ci120205/$file/ci120205.pdf APRV]is the primary mode of choice when ventilating a patient with ARDS or ALI (Acute Lung Injury).
Several specialized modes of [[mechanical ventilation]] have been tested in ARDS, however, none has been proven to carry a [[morbidity]] or [[mortality]] benefit and should only be considered if [[oxygenation]] does not improve with a judicious trial of the first-line mechanical [[ventilation strategies]] as outlined by the ARDS Network.<ref>NIH-NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary. "http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf"</ref>
*[[Mechanical ventilation modes of ventilation#High Frequency Ventilation (HFV)|'''High-frequency oscillatory ventilation (HFOV)''']] may improve [[oxygenation]] in patients with '''[[Acute respiratory distress syndrome diagnostic criteria|moderate to severe ARDS]] and severe refractory [[hypoxemia]]''', however, initiation of HFOV early in the course of ARDS (i.e., prior to low [[tidal volume]]/high [[PEEP]] [[mechanical ventilation]]) has been associated with ''increased mortality'' compared to lower [[tidal volume]]/high [[PEEP]] ventilation<ref name="pmid12231488">{{cite journal| author=Derdak S, Mehta S, Stewart TE, Smith T, Rogers M, Buchman TG et al.| title=High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. | journal=Am J Respir Crit Care Med | year= 2002 | volume= 166 | issue= 6 | pages= 801-8 | pmid=12231488 | doi=10.1164/rccm.2108052 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12231488  }} </ref><ref name="pmid23339639">{{cite journal| author=Ferguson ND, Cook DJ, Guyatt GH, Mehta S, Hand L, Austin P et al.| title=High-frequency oscillation in early acute respiratory distress syndrome. | journal=N Engl J Med | year= 2013 | volume= 368 | issue= 9 | pages= 795-805 | pmid=23339639 | doi=10.1056/NEJMoa1215554 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23339639  }} </ref>
*'''[[Acute respiratory distress syndrome mechanical ventilation therapy#APRV (Airway Pressure Release Ventilation) and ARDS / ALI |Airway pressure release ventilation (APRV)]]''' appears to be safe in ARDS, and may be associated with reduced [[paralytic]] and [[sedative]] use as well as an increase in the number of ventilator-free days<ref name="pmid19727373">{{cite journal| author=Daoud EG| title=Airway pressure release ventilation. | journal=Ann Thorac Med | year= 2007 | volume= 2 | issue= 4 | pages= 176-9 | pmid=19727373 | doi=10.4103/1817-1737.36556 | pmc=2732103 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19727373  }} </ref><ref name="pmid21762559">{{cite journal| author=Daoud EG, Farag HL, Chatburn RL| title=Airway pressure release ventilation: what do we know? | journal=Respir Care | year= 2012 | volume= 57 | issue= 2 | pages= 282-92 | pmid=21762559 | doi=10.4187/respcare.01238 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21762559  }} </ref>


Advantages to APRV ventilation include: decreased airway pressures, decreased minute ventilation, decreased dead-space ventilation, promotion of spontaneous breathing, almost 24 hour a day alveolar recruitment, decreased use of sedation, near elimination of neuromuscular blockade and an often positive effect on cardiac output (due to the negative inflection from the elevated baseline with each spontaneous breath).
===Recruitment Maneuvers===
A '''recruitment maneuver''' is the application of very high (up to 40 cm H<sub>2</sub>O) positive airway pressure to open collapsed [[alveolus|alveoli]], thereby reducing [[Shunt|shunting]], decreasing [[Ventilation-perfusion mismatch|V/Q mismatching]], and improving [[gas exchange]]. The decision to apply recruitment maneuvers must take into account various factors including the extent of lung injury (due to the risk of causing [[barotrauma|volutrauma]] through overdistention of stiff and inflamed lungs) and patient [[hemodynamics]] (due to the risk of further worsening [[hypotension]] by impeding [[venous return]] to the [[right heart]]). Recruitment maneuvers have not been standardized and there are insufficient data to support or discourage their use in ARDS.


A patient with ARDS on average spends 8 to 11 days on a mechanical ventilator; APRV may reduce this time significantly.
=== Extracorporeal Membrane Oxygenation (ECMO) ===
There is growing evidence to support the use of [[extracorporeal membrane oxygenation|extracorporeal membrane oxygenation (ECMO)]] for severe ARDS that fails to improve despite judicious application of the ARDS Network low tidal volume/high PEEP ventilation strategy.<ref name="pmid3090285">{{cite journal| author=Gattinoni L, Pesenti A, Mascheroni D, Marcolin R, Fumagalli R, Rossi F et al.| title=Low-frequency positive-pressure ventilation with extracorporeal CO2 removal in severe acute respiratory failure. | journal=JAMA | year= 1986 | volume= 256 | issue= 7 | pages= 881-6 | pmid=3090285 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3090285  }} </ref><ref name="pmid19762075">{{cite journal| author=Peek GJ, Mugford M, Tiruvoipati R, Wilson A, Allen E, Thalanany MM et al.| title=Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial. | journal=Lancet | year= 2009 | volume= 374 | issue= 9698 | pages= 1351-63 | pmid=19762075 | doi=10.1016/S0140-6736(09)61069-2 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19762075  }} </ref> ECMO facilitates gas exchange in circumstances where adequate oxygenation and ventilation cannot be achieved through the lungs themselves. There are two main forms of ECMO, both of which have been used successfully in the treatment of [[Acute respiratory distress syndrome diagnostic criteria|severe ARDS]]:
*'''Veno-venous (VV)-ECMO''': [[Venous blood]] is removed through an outflow [[cannula]] placed in a large [[vein]] (usually the right [[femoral vein]] or [[inferior vena cava]]) and passed through an [[oxygenator]] where [[gas exchange]] occurs (CO<sub>2</sub> is removed and O<sub>2</sub> is introduced) before being returned to the body through an inflow cannula placed in another large vein (usually the right [[internal jugular vein]] or [[superior vena cava]])
:*Supports [[gas exchange]] but does not provide any [[hemodynamic]] support
*'''Veno-arterial (VA)-ECMO''': Venous blood is removed through an outflow [[cannula]] placed in a large [[vein]] (usually the right femoral vein or inferior vena cava) and passed through an oxygenator where [[gas exchange]] occurs (CO<sub>2</sub> is removed and O<sub>2</sub> is introduced) before being returned to the body through an inflow cannula placed in a large [[artery]] (usually the right [[femoral artery]] or right [[carotid artery]])
:*Supports [[gas exchange]] and provides [[hemodynamic]] support by bypassing the heart completely


* *This would require a side by side study of APRV and the current ARDSNet protocol.  There seems to be little political will, within the medical community, to address the need for this study, in spite of the successes seen with APRV.
The use of ECMO in the treatment of ARDS is an ongoing area of research, and referral to a medical center with ample experience in the use of ECMO for ARDS should be considered for patients with ARDS who are failing traditional management strategies and may be candidates for ECMO. The use of ECMO requires systemic [[anticoagulation]] (usually with [[heparin]]) and is associated with the risk of major [[hemorrhage]] as well as [[thrombosis]]. Additionally, the use of VA-ECMO may result in [[Ischemia|ischemic injury]] to the limb [[distal]] to the site of the inflow [[cannula]] (although rates of limb ischemia have been mitigated by the addition of a [[reperfusion]] cannula that takes blood from the inflow cannula and delivers it distally to the otherwise-affected limb).
 
===Positive end-expiratory pressure===
[[Positive end-expiratory pressure]] (PEEP) must be used in mechanically-ventilated patients in order to contrast the tendency to collapse of affected alveoli.
 
Ideally, a 'perfect' PEEP would match the increased alveolar [[surface tension]], caused by surfactant deficiency and external pressure (edema), thus restoring a normal time constant in all affected units.
 
However, because of the cited inherent inhomogeneity, surface tension varies, and so do PEEP requirements for the diseased units. Furthermore, high levels of PEEP may impair [[venous blood]] return to the right [[heart]], although the actual impact of PEEP on [[hemodynamics]] is still debated.
 
The 'best PEEP' used to be defined as 'some' cmH<sub>2</sub>O above the lower inflection point (LIP) in the sigmoidal pressure-volume relationship curve of the lung. Recent research has shown that the LIP-point pressure is no better than any pressure above it, as recruitment of collapsed alveoli, and more importantly the overdistention of aerated units, occur throughout the whole inflation. Despite the awkwardness of most procedures used to trace the pressure-volume curve, it is still used by some to define the ''minimum'' PEEP to be applied to their patients. Some of the newest ventilators have the ability to automatically plot a pressure-volume curve. The possibility of having an 'instantaneous' tracing trigger might produce renewed interest in this analysis.
 
PEEP may also be set empirically. Some authors suggest performing a 'recruiting maneuver' (i.e., a short time at a very high continuous positive airway pressure, such as 50 cmH<sub>2</sub>O (4.9 kPa), to recruit, or open, collapsed unit with a high distending pressure) and then to increase PEEP to a rather high level before restoring previous ventilation. The final PEEP level should be the one just before the drop in PaO<sub>2</sub> (or [[hemoglobin|peripheral blood oxygen saturation]]) during a step-down trial.
 
PEEP 'stacks up' to P<sub>l</sub> during volume-controlled ventilation. At high levels, it may cause significant overdistension of (and injury to) compliant, aerated units, and higher plateau pressures at the same ''V''<sub>t</sub>.
 
Intrinsic positive end-expiratory pressure (Intrinsic PEEP, iPEEP) or auto-PEEP, is not detected during normal ventilation. However, when ventilating at high frequencies, its contribution may be substantial, both in its positive and negative effects. There are 'underground', unproven claims that the Amato and NIH/ARDS Network studies got a positive result because of the high iPEEP levels reached by spontaneously breathing patients in low-volume assist-control ventilation. Whether or not that is true, it is a fact that iPEEP has been measured in very few formal studies on ventilation in ARDS patients, and its entity is largely unknown. Its measurement is recommended in the treatment of ARDS patients, especially when using high-frequency (oscillatory/jet) ventilation.
 
A compromise between the beneficial and adverse effects of PEEP is, as usual, inevitable.
 
===Mechanical stress===
*[[Mechanical ventilation]] is an essential part of the treatment of ARDS. As loss of aeration (and the underlying disease) progress, the work of breathing (WOB) eventually grows to a level incompatible with life.
* Mechanical ventilation is initiated to relieve respiratory muscles of their work, and to protect the usually obtunded patient's [[airway]]s.
* Mechanical ventilation may constitute a risk factor for the development, or the worsening, of ARDS.
* Aside from the infectious complications arising from invasive ventilation with tracheal [[intubation]], positive-pressure ventilation directly alters lung mechanics during ARDS. The result is higher mortality, when injudicious techniques are used.
* In 1998, Amato ''et al'' published a paper showing substantial improvement in the outcome of patients ventilated with lower tidal volumes (''V''<sub>t</sub>) (6 mL·kg<sup>-1</sup>).<ref name=Amato_1998>{{cite journal | author = Amato M, Barbas C, Medeiros D, Magaldi R, Schettino G, Lorenzi-Filho G, Kairalla R, Deheinzelin D, Munoz C, Oliveira R, Takagaki T, Carvalho C | title = Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. | journal = N Engl J Med | volume = 338 | issue = 6 | pages = 347-54 | year = 1998 | id = PMID 9449727}}</ref> This result was confirmed in a 2000 study sponsored by the [[National Institutes of Health|NIH]].<ref name=MacIntyre_2000>{{cite journal | author = MacIntyre N | title = Mechanical ventilation strategies for lung protection. | journal = Semin Respir Crit Care Med | volume = 21 | issue = 3 | pages = 215-22 | year = 2000 | id = PMID 16088734}}</ref> Although both these studies were widely criticized for several reasons, and although the authors were not the first to experiment lower-volume ventilation, they shed new light on the relationship between mechanical ventilation and ARDS.
* One opinion is that the forces applied to the lung by the [[ventilator]] may work as a lever to induce further damage to lung parenchyma. It appears that shear stress at the [[Interface (chemistry)|interface]] between collapsed and aerated units may result in the breakdown of aerated units, which inflate asymmetrically due to the 'stickiness' of surrounding flooded alveoli. The fewer such interfaces around an alveolus, the lesser the stress.
* Indeed, even relatively low stress forces may induce [[signal transduction]] systems at the cellular level, thus inducing the release of inflammatory mediators.
* This form of stress is thought to be applied by the [[transpulmonary pressure]] (gradient) (''P''<sub>l</sub>) generated by the ventilator or, better, its cyclical variations. The better outcome obtained in patients ventilated with lower ''V''<sub>t</sub> may be interpreted as a beneficial effect of the lower ''P''<sub>l</sub>. [[Transpulmonary pressure|transpulmonary pressure]], is an indirect function of the ''V''<sub>t</sub> setting on the ventilator, and only trial patients with plateau pressures (a surrogate for the actual ''P''<sub>l</sub>) were less than 32 cmH<sub>2</sub>O]] (3.1 kPa had improved survival.
* The way ''P''<sub>l</sub> is applied on alveolar surface determines the shear stress to which lung units are exposed. ARDS is characterized by an usually inhomogeneous reduction of the airspace, and thus by a tendency towards higher ''P''<sub>l</sub> at the same ''V''<sub>t</sub>, and towards ''higher'' stress on ''less'' diseased units.
* The inhomogeneity of alveoli at different stages of disease is further increased by the gravitational gradient to which they are exposed, and the different perfusion pressures at which blood flows through them. Finally, abdominal pressure exerts an additional pressure on inferoposterior lung segments, favoring compression and collapse of those units.
* The different mechanical properties of alveoli in ARDS may be interpreted as having varying ''time constants'' (the product of alveolar [[compliance]] &times; [[pulmonary alveolus#details|resistance]]). A long time constant indicates an alveolus which opens slowly during tidal inflation, as a consequence of contrasting pressure around it, or altered water-air interface inside it (loss of surfactant, flooding).
* Slow alveoli are said to be 'kept open' using [[mechanical ventilation|positive end-expiratory pressure]], a feature of modern ventilators which maintains a positive airway pressure throughout the whole respiratory cycle. A higher mean pressure cycle-wide slows the collapse of diseased units, but it has to be weighed against the corresponding elevation in ''P''<sub>l</sub>/plateau pressure.
* The prone position also reduces the inhomogeneity in alveolar time constants induced gravity and edema.


==References==
==References==
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[[Category:Pulmonology]]
[[Category:Pulmonology]]
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Latest revision as of 15:12, 7 March 2017

Acute respiratory distress syndrome Microchapters

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Brian Shaller, M.D. [2]

Overview

Most patients with ARDS will require endotracheal intubation and mechanical ventilation at some point during the course of their illness and recovery. A mechanical ventilation strategy using lower tidal volumes of 6 mL/kg predicted body weight and higher levels of positive end-expiratory pressure (PEEP) has been shown to be most effective at improving oxygenation and minimizing volutrauma (injury to stiff lungs resulting from overdistention).

As an overview, a quasi-experimental, before-after trial[1] found reduced mortality associated with the following strategy quoted from Journal Watch[2]:

  • use tidal volumes <6.5 mL/kg,
  • use a PEEP of 5–24 cm H20 within a plateau pressure <30 cm H20,
  • decrease FiO2 as permitted to achieve saturation of 88%–95%,
  • and elevate the head of the bed. Hypercapnia with a pH >7.25 is permissible.
  • Use a higher flow rate (up to 100 L/min) for obstructive airway disease when necessary to achieve a satisfactory I:E ratio

Mechanical ventilation

  • Lower tidal volume ventilation (6 mL/kg predicted body weight) is associated with reduced mortality and a greater number of ventilator-free days[3]
  • PBW (men) = 50 + 2.3 (height in inches – 60)
  • PBW (women) = 45.5 + 2.3 (height in inches – 60)
  • Higher positive end-expiratory pressure (PEEP) combined with lower tidal volume ventilation is associated with decreased mortality in patients with moderate or severe ARDS (PaO2/FIO2 ≤ 200)[4]
  • Prone positioning for at least 16 consecutive hours each day is associated with improved 28-day and 90-day survival in patients with ARDS and a PaO2/FIO2 ratio < 150 on an FIO2 ≥ 60% and PEEP ≥ 5 mmHg
  • Cisatracurium, when started within the first 48 hours of ARDS diagnosis and continued for 48 hours, has been associated with improved 90-day survival, a greater number of ventilator-free days, and a decreased incidence of volutrauma[5]

ARDS Network Mechanical Ventilation Protocol

In 1994 the National Institutes of Health (NIH) and National Heart, Lung, and Blood Institute (NHLBI) founded the ARDS Clinical Trial Network (often abbreviated as ARDSnet) – a consortium of over 40 hospitals that conduct clinical research trials aimed at improving care for patients with ARDS. In order to simplify the mechanical ventilation of patients with ARDS, the NIH-NHLBI ARDS Network has compiled a Mechanical Ventilation Protocol Summary[6] that outlines the mechanical ventilation strategies associated with better outcomes in an easy-to-use format for ICU health care providers.

Non-Invasive Positive Pressure Ventilation

Many patients who develop ARDS will receive a trial of non-invasive positive pressure ventilation (NIPPV) before intubation and mechanical ventilation become necessary to maintain adequate oxygenation, or before the degree of clinical deterioration precludes the use of NIPPV and necessitates endotracheal intubation for airway protection. Several studies have examined the utility of NIPPV in the management of ARDS:

  • NIPPV observational data from cohort studies: Early application of NIPPV appears to reduce the rate of intubation and mechanical ventilation in patients with mild-to-moderate ARDS (PaO2/FIO2 ratio 150 to 200)[7][8]
  • NIPPV versus high-flow nasal cannula (HFNC) or supplemental oxygen via face mask: 310 patients with ARDS and a PaO2/FIO2 ratio ≤ 300 were randomized to either NIPPV, high-flow nasal cannula, or supplemental oxygen via face mask[9]
  • At 28 days, no differences in were seen in rates of intubation and mechanical ventilation between the three groups
  • At 90 days, there were significantly more ICU-free days and significantly fewer mortalities in the high-flow nasal cannula group as compared to the other two groups
  • NIPPV via face mask versus NIPPV via helmet: 83 patients with ARDS were randomized to either NIPPV via face mark or NIPPV via helmet[10]
  • At 28 days, there was a significantly lower rate of intubation and significantly more ventilator-free days in the helmet group
  • At 90 days, there were significantly fewer mortalities in the helmet group
  • Study was terminated early due to the significantly higher mortality rate seen in the face mask group

Alternative Mechanical Ventilation Strategies

Several specialized modes of mechanical ventilation have been tested in ARDS, however, none has been proven to carry a morbidity or mortality benefit and should only be considered if oxygenation does not improve with a judicious trial of the first-line mechanical ventilation strategies as outlined by the ARDS Network.[11]

Recruitment Maneuvers

A recruitment maneuver is the application of very high (up to 40 cm H2O) positive airway pressure to open collapsed alveoli, thereby reducing shunting, decreasing V/Q mismatching, and improving gas exchange. The decision to apply recruitment maneuvers must take into account various factors including the extent of lung injury (due to the risk of causing volutrauma through overdistention of stiff and inflamed lungs) and patient hemodynamics (due to the risk of further worsening hypotension by impeding venous return to the right heart). Recruitment maneuvers have not been standardized and there are insufficient data to support or discourage their use in ARDS.

Extracorporeal Membrane Oxygenation (ECMO)

There is growing evidence to support the use of extracorporeal membrane oxygenation (ECMO) for severe ARDS that fails to improve despite judicious application of the ARDS Network low tidal volume/high PEEP ventilation strategy.[16][17] ECMO facilitates gas exchange in circumstances where adequate oxygenation and ventilation cannot be achieved through the lungs themselves. There are two main forms of ECMO, both of which have been used successfully in the treatment of severe ARDS:

  • Veno-arterial (VA)-ECMO: Venous blood is removed through an outflow cannula placed in a large vein (usually the right femoral vein or inferior vena cava) and passed through an oxygenator where gas exchange occurs (CO2 is removed and O2 is introduced) before being returned to the body through an inflow cannula placed in a large artery (usually the right femoral artery or right carotid artery)

The use of ECMO in the treatment of ARDS is an ongoing area of research, and referral to a medical center with ample experience in the use of ECMO for ARDS should be considered for patients with ARDS who are failing traditional management strategies and may be candidates for ECMO. The use of ECMO requires systemic anticoagulation (usually with heparin) and is associated with the risk of major hemorrhage as well as thrombosis. Additionally, the use of VA-ECMO may result in ischemic injury to the limb distal to the site of the inflow cannula (although rates of limb ischemia have been mitigated by the addition of a reperfusion cannula that takes blood from the inflow cannula and delivers it distally to the otherwise-affected limb).

References

  1. ↑ Fuller BM, Ferguson IT, Mohr NM, Drewry AM, Palmer C, Wessman BT; et al. (2017). "A Quasi-Experimental, Before-After Trial Examining the Impact of an Emergency Department Mechanical Ventilator Protocol on Clinical Outcomes and Lung-Protective Ventilation in Acute Respiratory Distress Syndrome". Crit Care Med. doi:10.1097/CCM.0000000000002268. PMID 28157140.
  2. ↑ "Lung Protective Strategy for Acute Respiratory Distress Syndrome Saves Lives". NEJM Journal Watch. 2017. Retrieved 2017-03-07.
  3. ↑ "Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network". N Engl J Med. 342 (18): 1301–8. 2000. doi:10.1056/NEJM200005043421801. PMID 10793162.
  4. ↑ Briel M, Meade M, Mercat A, Brower RG, Talmor D, Walter SD; et al. (2010). "Higher vs lower positive end-expiratory pressure in patients with acute lung injury and acute respiratory distress syndrome: systematic review and meta-analysis". JAMA. 303 (9): 865–73. doi:10.1001/jama.2010.218. PMID 20197533.
  5. ↑ Papazian L, Forel JM, Gacouin A, Penot-Ragon C, Perrin G, Loundou A; et al. (2010). "Neuromuscular blockers in early acute respiratory distress syndrome". N Engl J Med. 363 (12): 1107–16. doi:10.1056/NEJMoa1005372. PMID 20843245. Review in: Ann Intern Med. 2011 Jan 18;154(2):JC1-3
  6. ↑ NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary. (2008). http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf Accessed on June 28, 2016
  7. ↑ Antonelli M, Conti G, Esquinas A, Montini L, Maggiore SM, Bello G; et al. (2007). "A multiple-center survey on the use in clinical practice of noninvasive ventilation as a first-line intervention for acute respiratory distress syndrome". Crit Care Med. 35 (1): 18–25. doi:10.1097/01.CCM.0000251821.44259.F3. PMID 17133177.
  8. ↑ Thille AW, Contou D, Fragnoli C, Córdoba-Izquierdo A, Boissier F, Brun-Buisson C (2013). "Non-invasive ventilation for acute hypoxemic respiratory failure: intubation rate and risk factors". Crit Care. 17 (6): R269. doi:10.1186/cc13103. PMC 4057073. PMID 24215648.
  9. ↑ Frat JP, Thille AW, Mercat A, Girault C, Ragot S, Perbet S; et al. (2015). "High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure". N Engl J Med. 372 (23): 2185–96. doi:10.1056/NEJMoa1503326. PMID 25981908.
  10. ↑ Patel BK, Wolfe KS, Pohlman AS, Hall JB, Kress JP (2016). "Effect of Noninvasive Ventilation Delivered by Helmet vs Face Mask on the Rate of Endotracheal Intubation in Patients With Acute Respiratory Distress Syndrome: A Randomized Clinical Trial". JAMA. 315 (22): 2435–41. doi:10.1001/jama.2016.6338. PMID 27179847.
  11. ↑ NIH-NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary. "http://www.ardsnet.org/files/ventilator_protocol_2008-07.pdf"
  12. ↑ Derdak S, Mehta S, Stewart TE, Smith T, Rogers M, Buchman TG; et al. (2002). "High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial". Am J Respir Crit Care Med. 166 (6): 801–8. doi:10.1164/rccm.2108052. PMID 12231488.
  13. ↑ Ferguson ND, Cook DJ, Guyatt GH, Mehta S, Hand L, Austin P; et al. (2013). "High-frequency oscillation in early acute respiratory distress syndrome". N Engl J Med. 368 (9): 795–805. doi:10.1056/NEJMoa1215554. PMID 23339639.
  14. ↑ Daoud EG (2007). "Airway pressure release ventilation". Ann Thorac Med. 2 (4): 176–9. doi:10.4103/1817-1737.36556. PMC 2732103. PMID 19727373.
  15. ↑ Daoud EG, Farag HL, Chatburn RL (2012). "Airway pressure release ventilation: what do we know?". Respir Care. 57 (2): 282–92. doi:10.4187/respcare.01238. PMID 21762559.
  16. ↑ Gattinoni L, Pesenti A, Mascheroni D, Marcolin R, Fumagalli R, Rossi F; et al. (1986). "Low-frequency positive-pressure ventilation with extracorporeal CO2 removal in severe acute respiratory failure". JAMA. 256 (7): 881–6. PMID 3090285.
  17. ↑ Peek GJ, Mugford M, Tiruvoipati R, Wilson A, Allen E, Thalanany MM; et al. (2009). "Efficacy and economic assessment of conventional ventilatory support versus extracorporeal membrane oxygenation for severe adult respiratory failure (CESAR): a multicentre randomised controlled trial". Lancet. 374 (9698): 1351–63. doi:10.1016/S0140-6736(09)61069-2. PMID 19762075.
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