Слайд 1 JSC “Astana Medical University”
ACUTE RESPIRATORY
DISTRESS SYNDROME
Done by: Nessipbay A.
Group:433 GM
Checked by: Akhmetzhanova
Слайд 2ARDS
Objectives
Updated definition of ARDS
Briefly review Pathophysiology and Pathogenesis
Etiology/Risk factors
Clinical Presentation
Diagnosis, Differential Diagnosis
Management
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
Слайд 5ARDS, New Definition
All modifications were based on the principle that
syndrome definitions must fulfill three criteria:
Feasibility
Reliability
Validity
Слайд 6Acute Respiratory Distress Syndrome
The Berlin definition
JAMA. 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
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.
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
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
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
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
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
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
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.
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
Слайд 20
ARDS
Mechanical Ventilation
Ventilator associated lung injury
Volutrauma
Atelectotrauma
Biotrauma
Barotrauma
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)
Слайд 22NHLBI ARDS Network
Improved Survival with Low VT
Слайд 23NHLBI ARDS Network
Main Outcome Variables
Слайд 24NHLBI 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.
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
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
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.
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.
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).
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
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.
Слайд 36ARDS
Inhaled NO
Steroids
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
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…
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.
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.
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
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.
Слайд 46Enrollment, 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
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
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
Слайд 50Primary 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.
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
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.
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
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
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.