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ARDS Objectives Updated definition of ARDSBriefly review Pathophysiology and Pathogenesis Etiology/Risk factors Clinical PresentationDiagnosis, Differential DiagnosisManagement

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Слайд 1 JSC “Astana Medical University”


ACUTE RESPIRATORY

DISTRESS SYNDROME

Done by: Nessipbay A.
Group:433 GM
Checked by: Akhmetzhanova


JSC “Astana Medical University” ACUTE RESPIRATORY DISTRESS SYNDROME Done by: Nessipbay A.Group:433 GMChecked

Слайд 2ARDS Objectives
Updated definition of ARDS
Briefly review Pathophysiology and Pathogenesis


Etiology/Risk factors
Clinical Presentation
Diagnosis, Differential Diagnosis
Management

ARDS  	Objectives Updated definition of ARDSBriefly review Pathophysiology and Pathogenesis Etiology/Risk factors Clinical PresentationDiagnosis, Differential DiagnosisManagement

Слайд 3 ARDS



New Definition

ARDS

Слайд 4ARDS, New Definition
ESICM convened an international panel of experts, with

representation of ATS and SCCM
The objectives were to update the

ARDS definition using a systematic analysis of:
current epidemiologic evidence
physiological concepts
results of clinical trials
ARDS, New DefinitionESICM convened an international panel of experts, with representation of ATS and SCCMThe objectives were

Слайд 5ARDS, New Definition
All modifications were based on the principle that

syndrome definitions must fulfill three criteria:
Feasibility
Reliability
Validity

ARDS, New DefinitionAll modifications were based on the principle that syndrome definitions must fulfill three criteria:Feasibility ReliabilityValidity

Слайд 6Acute Respiratory Distress Syndrome The Berlin definition
JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669

Acute Respiratory Distress Syndrome  	The Berlin definitionJAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669

Слайд 7ARDS The Berlin Definition
JAMA. 2012;307(23):2526-2533.

doi:10.1001/jama.2012.5669

ARDS       The Berlin DefinitionJAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669

Слайд 8ARDS The Berlin Definition
No change

in the underlying conceptual understanding of ARDS

“acute diffuse, inflammatory

lung injury, leading to increased pulmonary vascular permeability, increased lung weight, and loss of aerated lung tissue…[with] hypoxemia and bilateral radiographic opacities, associated with increased venous admixture, increased physiological dead space, and decreased lung compliance.”

Although the authors emphasize the increased power of the new Berlin definition to predict mortality compared to the AECC definition, in truth it’s still poor, with an area under the curve of only 0.577, (95% CI, 0.561-0.593) compared to 0.536, (95% CI, 0.520-0.553;P < 001 ) for the old definition.
ARDS       The Berlin DefinitionNo change in the underlying conceptual understanding of

Слайд 9ARDS Pathophysiology

ARDS  	Pathophysiology

Слайд 10ARDS Pathological Stages
Initial "exudative" stage-diffuse alveolar damage within the first week


“Proliferative" stage-resolution of pulmonary edema, proliferation of type II alveolar

cells, squamous metaplasia, interstitial infiltration by myofibroblasts, and early deposition of collagen.
Some patients progress to a third "fibrotic" stage, characterized by obliteration of normal lung architecture, diffuse fibrosis, and cyst formation
ARDS 	Pathological StagesInitial

Слайд 11ARDS Pathophysiology

ARDS       Pathophysiology

Слайд 12Risk Factors
Sepsis
Severe trauma
Surface burns
Multiple blood transfusions


Drug overdose
Following bone marrow transplantation
Multiple fractures

Aspiration
Pneumonia
Pulmonary contusion
Pulmonary embolism


Inhalational injury
Near drowning
Risk Factors  Sepsis Severe trauma Surface burns Multiple blood transfusions Drug overdoseFollowing bone marrow transplantationMultiple fractures

Слайд 13Negative Pressure Pulmonary Edema
Type of Non-Cardiogenic Pulmonary Edema
Mechanism
Rapid

resolution of large levels of negative intra-thoracic pressures by removal

of airways obstruction ------leads to alveolar and capillary damage ------ leads to increased vascular permeability
Negative Pressure Pulmonary Edema Type of Non-Cardiogenic Pulmonary EdemaMechanism Rapid resolution of large levels of negative intra-thoracic

Слайд 14ARDS Clinical Presentation
Dyspnea, Tachypnea
Persistent hypoxemia, despite the administration

of high concentrations of inspired oxygen
Increase in the shunt

fraction
Decrease in pulmonary compliance
Increase in the dead space ventilation
ARDS  Clinical Presentation Dyspnea, Tachypnea Persistent hypoxemia, despite the administration of high concentrations of inspired oxygen

Слайд 15Management of ARDS

Management of ARDS

Слайд 16Basic Management Strategies for Patients with ALI/ARDS
Identify and treat underlying

causes
Ventilatory support
Lung protective ventilatory support strategy
Application of

PEEP
Restore and maintain hemodynamic function
Conservative fluid replacement strategy
Vasopressors and inotropics support
Prevent complications of critical illness
Ensure adequate nutrition
Avoid oversedation
Using weaning protocol with spontaneous breathing trials
Continous use of steroids for fibroproliferative phase ?questionable
Basic Management Strategies for Patients with ALI/ARDSIdentify and treat underlying causes Ventilatory support Lung protective ventilatory support

Слайд 17Fluid management and vasoactive support
SAFE trial
Resuscitation with saline is

as beneficial as resuscitation with albumin in critically ill patients

with shock
FACTT trial
Prospective, Randomized, Multi-Center Trial
Utility and safety of using a pulmonary artery catheter versus central venous catheter to guide the volume replacement
Liberal versus conservative fluid replacement
Fluid management and vasoactive support SAFE trialResuscitation with saline is as beneficial as resuscitation with albumin in

Слайд 18ARDS FACTT
Patients were treated with the specific fluid management strategy

(to which they were randomized) for 7 days or until

unassisted ventilation, whichever occurs first.
The study enrolled 1000 patients and showed no benefit with PAC guided fluid therapy over the less invasive CVC guided therapy.
ARDS  FACTTPatients were treated with the specific fluid management strategy (to which they were randomized) for

Слайд 19ARDS FACTT
The Use of Conservative fluid management strategy was

associated with
Significant improvement in oxygenation index
Significant improvement in

Lung Injury score
increase in the number of ventilator- free days
ARDS  FACTT The Use of Conservative fluid management strategy was associated with Significant improvement in oxygenation

Слайд 20 ARDS Mechanical Ventilation
Ventilator associated lung injury
Volutrauma
Atelectotrauma
Biotrauma
Barotrauma
Air

embolism/translocation

ARDS Mechanical Ventilation  Ventilator associated lung injury Volutrauma Atelectotrauma BiotraumaBarotrauma Air embolism/translocation

Слайд 21NHLBI ARDS Network
Compared low tidal volumes (6ml/kg of ideal body

weight ) against conventional tidal volumes (12ml/kg ideal body weight

)

Significant decrease in mortality associated with the use of low tidal volumes (39.8% versus 31%, P= 0.007)
NHLBI ARDS NetworkCompared low tidal volumes (6ml/kg of ideal body weight ) against conventional tidal volumes (12ml/kg

Слайд 22NHLBI ARDS Network Improved Survival with Low VT


NHLBI ARDS Network  Improved Survival with Low VT

Слайд 23NHLBI ARDS Network Main Outcome Variables

NHLBI ARDS Network  Main Outcome Variables

Слайд 24NHLBI ARDS Network Main Organ Failure Free Days

NHLBI ARDS Network  Main Organ Failure Free Days

Слайд 25 ARDS Mechanical Ventilation
Initial tidal volumes of 8 mL/kg predicted body weight in

kg, calculated by:
 [2.3 *(height in inches - 60) + 45.5 for

women or + 50 for men].
Respiratory rate up to 35 breaths/min
 expected minute ventilation requirement (generally, 7-9 L /min)
Set positive end-expiratory pressure (PEEP) to at least 5 cm H2O (but much higher is probably better)
FiO2 to maintain an arterial oxygen saturation (SaO2) of 88-95% (paO2 55-80 mm Hg).
Titrate FiO2 to below 70% when feasible.
Over a period of less than 4 hours, reduce tidal volumes to 7 mL/kg, and then to 6 mL/kg.

ARDS  Mechanical VentilationInitial tidal volumes of 8 mL/kg predicted body weight in kg, calculated by: [2.3

Слайд 26ARDS Mechanical Ventilation

ARDS  Mechanical Ventilation

Слайд 27ARDS Mechanical Ventilation
Plateau pressure (measured during an inspiratory hold of 0.5

sec) less than 30 cm H2O,
High plateau pressures vastly

elevate the risk for harmful alveolar distension ( volutrauma).
If plateau pressures remain elevated after following the above protocol, further strategies should be tried:
Reduce tidal volume, to as low as 4 mL/kg by 1 mL/kg stepwise increments.
Sedate the patient to minimize ventilator-patient dyssynchrony.
Consider other mechanisms for the increased plateau pressure
ARDS Mechanical VentilationPlateau pressure (measured during an inspiratory hold of 0.5 sec) less than 30 cm H2O,

Слайд 28Potential benefits of hypercapnia in patients with ARDS
Decrease in

TNF-alpha release by alveolar macrophages
Decrease in PMNL-endothelial cell adhesion
Decrease

in Xanthine oxiedase activity
Decrease in NOS activity
Reduction of IL-8
Potential benefits of hypercapnia in patients with ARDS Decrease in TNF-alpha release by alveolar macrophages Decrease in

Слайд 29ARDS High versus Low PEEP
Higher PEEP along with low tidal

volume ventilation should be considered for patients receiving mechanical ventilation

for ARDS. This suggestion is based on a
2010 meta-analysis of 3 randomized trials (n=2,229) testing higher vs. lower PEEP in patients with acute lung injury or ARDS, in which ARDS patients receiving higher PEEP had a strong trend toward improved survival.
ARDS High versus Low PEEP Higher PEEP along with low tidal volume ventilation should be considered for

Слайд 30ARDS High versus Low PEEP
However, patients with milder acute lung injury

(paO2/FiO2 ratio > 200) receiving higher PEEP had a strong

trend toward harm in that same meta-analysis.
Higher PEEP can conceivably cause ventilator-induced lung injury by increasing plateau pressures, or cause pneumothorax or decreased cardiac output. These adverse effects were not noted in the largest ARDSNet trial (2004) testing high vs. low PEEP.

ARDS High versus Low PEEPHowever, patients with milder acute lung injury (paO2/FiO2 ratio > 200) receiving higher

Слайд 31ARDS Mechanical Ventilation

ARDS 	Mechanical Ventilation

Слайд 32ARDS Mechanical Ventilation

ARDS  	Mechanical Ventilation

Слайд 33ARDS Mechanical Ventilation
Neuromuscular blockers in early acute respiratory distress syndrome. 


N Engl J Med, 2010;363:1107-16. 
This multicenter RCT of 340 patients with severe ARDS found early use of 48 hours of neuromuscular blockade reduced mortality compared to placebo (NNT of 11 to prevent one death at 90 days in all patients, and a NNT of 7 in a prespecified analysis of patients with a PaO2:FiO2 less than 120).

ARDS 	Mechanical Ventilation Neuromuscular blockers in early acute respiratory distress syndrome. 

Слайд 34Basic management Strategies for patients with ALI/ARDS
Identify and treat underlying

causes
Ventilatory support
Lung protective ventilatory support strategy
Application of

PEEP
Restore and maintain hemodynamic function
Conservative fluid replacement strategy
Vasopressors and inotropics support
Prevent complications of critical illness
Ensure adequate nutrition
Avoid oversedation
Using weaning protocol with spontaneous breathing trials
Continous use of steroids for fibroproliferative phase,?questionable
Basic management Strategies for patients with ALI/ARDSIdentify and treat underlying causes Ventilatory support Lung protective ventilatory support

Слайд 35CASE #1
On admission to the ICU, the patient was

sedated and placed on volume control  mechanical ventilation with the

follow settings: FiO2: 0.6,  VT: 450 ml, RR:18,   PEEP:10 cm H2O, VΕ:8 L/min.
Additional supportive therapy included initial, empiric, broad-spectrum antibiotics and restrictive fluid management.
On Day 3, due to further impairment of oxygenation (SaO2 <80%) that did not improve with increases in both PEEP and FiO2, the patient was placed on high frequency oscillatory ventilation.
Although he had an initial improvement in oxygenation, his overall condition continued to decline and he died on Day 5 due to multiple organ failure.
CASE #1 On admission to the ICU, the patient was sedated and placed on volume control  mechanical

Слайд 36ARDS
Inhaled NO
Steroids
Prone Position
High Frequency Oscillatory Ventilation
ECMO

ARDSInhaled NOSteroids Prone Position High Frequency Oscillatory Ventilation ECMO

Слайд 37Inhaled Nitric Oxide
It is a bronchial and vascular smooth

muscle dilator
Decreases the Platelets Adherence and Aggregation
Improves Ventilation –Perfusion

ratio
Reduction in Pulmonary Artery Pressure and pulmonary Vascular Resistance
Inhaled Nitric Oxide It is a bronchial and vascular smooth muscle dilator Decreases the Platelets Adherence and

Слайд 38Inhaled Nitric Oxide
Two Prospective, Randomized, Placebo Controlled Clinical Trials

failed to demonstrate an improvement in the survival.
However, there

was improvement in the oxygenation…
Inhaled Nitric Oxide Two Prospective, Randomized, Placebo Controlled Clinical Trials failed to demonstrate an improvement in the

Слайд 40ARDS Steroid
A protocol for steroids in late ARDS, based

on the Meduri paper*
The patient must have no demonstrable infection
broncho-alveolar

lavage may be necessary to confirm this. This includes undrained abscesses, disseminated fungal infection and septic shock
Steroids should not be started less than 7 days, or more than 28 days, from admission
The patient should not have a history of gastric ulceration of active gastrointestinal bleeding
Patients with burns requiring skin grafting, pregnant patients, AIDS, and those in whom life support is expected to be withdrawn, are unsuitable

*Meduri GU, Kohler G, Headley S, Tolley E, Stentz F, Postlethwaite A. Inflammatory cytokines in the BAL of patients with ARDS. Persistent elevation over time predicts poor outcome. Chest 1995; 108(5):1303-1314. (2) Meduri GU, Headley AS, Golden E, Carson SJ, Umberger RA, Kelso T et al. Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial. JAMA 1998; 280(2):159-165.

ARDS  	Steroid A protocol for steroids in late ARDS, based on the Meduri paper*The patient must

Слайд 41ARDS Steroids
The patient should have evidence of ARDS and require

an FiO2 >/= 50%
The steroid regimen:
Loading dose 2mg/kg
Then 2mg/kg/day from

day 1 to 14
Then 1mg/kg/day from day 15 to 21
Then 0.5mg/kg/day from day 22 to 28
Then 0.25mg/kg/day on days 29 and 30
Finally 0.125mg/kg on days 31 and 32.

ARDS  	SteroidsThe patient should have evidence of ARDS and require an FiO2 >/= 50%The steroid regimen:

Слайд 42Prone Positioning
Relieves the cardiac and abdominal compression exerted on the

lower lobes
Makes regional Ventilation/Perfusion ratios and chest elastance more uniform
Facilitates

drainage of secretions
Potentiates the beneficial effect of recruitment maneuvers

Prone PositioningRelieves the cardiac and abdominal compression exerted on the lower lobesMakes regional Ventilation/Perfusion ratios and chest

Слайд 45Study Overview
Placing patients who require mechanical ventilation in the prone

rather than the supine position improves oxygenation.
In this trial, the

investigators found a benefit with respect to all-cause mortality with this change in body position in patients with severe ARDS.
Study OverviewPlacing patients who require mechanical ventilation in the prone rather than the supine position improves oxygenation.In

Слайд 46Enrollment, Randomization, and Follow-up of the Study Participants.
Guérin C et

al. N Engl J Med 2013;368:2159-2168

Enrollment, Randomization, and Follow-up of the Study Participants.Guérin C et al. N Engl J Med 2013;368:2159-2168

Слайд 47Characteristics of the Participants at Inclusion in the Study.
Guérin C

et al. N Engl J Med 2013;368:2159-2168

Characteristics of the Participants at Inclusion in the Study.Guérin C et al. N Engl J Med 2013;368:2159-2168

Слайд 48Ventilator Settings, Respiratory-System Mechanics, and Results of Arterial Blood Gas

Measurements at the Time of Inclusion in the Study.
Guérin C

et al. N Engl J Med 2013;368:2159-2168
Ventilator Settings, Respiratory-System Mechanics, and Results of Arterial Blood Gas Measurements at the Time of Inclusion in

Слайд 49Kaplan–Meier Plot of the Probability of Survival from Randomization to

Day 90.
Guérin C et al. N Engl J Med 2013;368:2159-2168

Kaplan–Meier Plot of the Probability of Survival from Randomization to Day 90.Guérin C et al. N Engl

Слайд 50Primary and Secondary Outcomes According to Study Group.
Guérin C et

al. N Engl J Med 2013;368:2159-2168

Primary and Secondary Outcomes According to Study Group.Guérin C et al. N Engl J Med 2013;368:2159-2168

Слайд 51Conclusions
In patients with severe ARDS, early application of prolonged prone-positioning

sessions significantly decreased 28-day and 90-day mortality.

ConclusionsIn patients with severe ARDS, early application of prolonged prone-positioning sessions significantly decreased 28-day and 90-day mortality.

Слайд 53
Vent settings to improve oxygenation
FIO2
Simplest maneuver to quickly increase PaO2
Long-term

toxicity at >60%
Free radical damage
Inadequate oxygenation despite 100% FiO2 usually

due to pulmonary shunting
Collapse – Atelectasis
Pus-filled alveoli – Pneumonia
Water/Protein – ARDS
Water – CHF
Blood - Hemorrhage





PEEP and FiO2 are adjusted in tandem

Vent settings to improve oxygenationFIO2Simplest maneuver to quickly increase PaO2Long-term toxicity at >60%Free radical damageInadequate oxygenation despite

Слайд 54
Vent settings to improve oxygenation
PEEP
Increases FRC
Prevents progressive atelectasis and

intrapulmonary shunting
Prevents repetitive opening/closing (injury)
Recruits collapsed alveoli and improves V/Q

matching
Resolves intrapulmonary shunting
Improves compliance
Enables maintenance of adequate PaO2 at a safe FiO2 level
Disadvantages
Increases intrathoracic pressure (may require pulmonary a. catheter)
May lead to ARDS
Rupture: PTX, pulmonary edema


PEEP and FiO2 are adjusted in tandem


Oxygen delivery (DO2), not PaO2, should be used to assess optimal PEEP.

Vent settings to improve oxygenationPEEP Increases FRCPrevents progressive atelectasis and intrapulmonary shuntingPrevents repetitive opening/closing (injury)Recruits collapsed alveoli

Слайд 55Vent settings to improve ventilation
Respiratory rate
Max RR at 35 breaths/min


Efficiency of ventilation decreases with increasing RR
Decreased time for alveolar

emptying
TV
Goal of 10 ml/kg
Risk of volutrauma
Other means to decrease PaCO2
Reduce muscular activity/seizures
Minimizing exogenous carb load
Controlling hypermetabolic states
Permissive hypercapnea
Preferable to dangerously high RR and TV, as long as pH > 7.15

Vent settings to improve ventilationRespiratory rateMax RR at 35 breaths/min Efficiency of ventilation decreases with increasing RRDecreased

Слайд 56
Vent settings to improve ventilation
Respiratory rate
Max RR at 35 breaths/min


Efficiency of ventilation decreases with increasing RR
Decreased time for alveolar

emptying
TV
Goal of 10 ml/kg
Risk of volutrauma
Other means to decrease PaCO2
Reduce muscular activity/seizures
Minimizing exogenous carb load
Controlling hypermetabolic states
Permissive hypercapnea
Preferable to dangerously high RR and TV, as long as pH > 7.15


RR and TV are adjusted to maintain VE and PaCO2

PIP
Elevated PIP suggests need for switch from volume-cycled to pressure-cycled mode
I:E ratio (IRV)
Increasing inspiration time will increase TV, but may lead to auto-PEEP
Maintained at <45cm H2O to minimize barotrauma
Plateau pressures
Pressure measured at the end of inspiratory phase
Maintained at <30-35cm H2O to minimize barotrauma

Vent settings to improve ventilationRespiratory rateMax RR at 35 breaths/min Efficiency of ventilation decreases with increasing RRDecreased

Слайд 57
Origins of mechanical ventilation
Negative-pressure ventilators (“iron lungs”)
Non-invasive ventilation first used

in Boston Children’s Hospital in 1928
Used extensively during polio outbreaks

in 1940s – 1950s
Positive-pressure ventilators
Invasive ventilation first used at Massachusetts General Hospital in 1955
Now the modern standard of mechanical ventilation


The era of intensive care medicine began with positive-pressure ventilation

The iron lung created negative pressure in abdomen as well as the chest, decreasing cardiac output.

Iron lung polio ward at Rancho Los Amigos Hospital in 1953.

Origins of mechanical ventilationNegative-pressure ventilators (“iron lungs”)Non-invasive ventilation first used in Boston Children’s Hospital in 1928Used extensively

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