ARDS - ISAKanyakumari

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ARDS
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g.k.kumar
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ARDS
• Definition
• Epidemiology
• Patient presentation and
diagnosis
• Pathophysiology
• Treatment
• Complications
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Historical background
• First described in 1967 by Ashbaugh
et al
Consensus after 1994
• In 1994 a new definition was
recommended by the AmericanEuropean Consensus Conference
Committee.
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Definition
ARDS is characterized by
• Acute onset
• Bilateral infiltrates on chest
radiograph
• Pulmonary artery wedge pressure
< 18 mmHg; if unavailable, then
lack of clinical evidence of left
ventricular failure suffices
• PaO2:FiO2 < 200 mmHg
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Epidemiology
Epidemiology
• The annual incidence of ARDS 1.5 to 13.5
people per 100,000 in the general
population. In mechanically ventilated
population is much higher.
• (ALI) of 16.1% in ventilated patients
admitted for more than 4 hours.
• More than half these patients may develop
ARDS
- Brun-Buisson et al. (2004)
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Risk factors
• Mechanical ventilation, sepsis, pneumonia, shock,
aspiration, trauma (especially pulmonary contusion),
major surgery, massive transfusions, smoke
inhalation, drug reaction or overdose, fat emboli and
reperfusion pulmonary edema after lung
transplantation or pulmonary embolectomy. Pneumonia
and sepsis are the most common triggers, and
pneumonia is present in up to 60% of patients.
• Elevated abdominal pressure of any cause is also
probably a risk factor for the development of ARDS,
particularly during mechanical ventilation
.
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Predisposing Factors
Predisposing Factors
Pulmonary conditions
• Severe pneumonia.
• Aspiration
• Near drowning.
• Inhalation of toxins and other irritants
such as smoke.
• Lung injury and bruising.
• Oxygen toxicity.
• Fat embolism- Where bubbles of fat
travel through the bloodstream and block
off airways.
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Predisposing Factors
Systemic conditions
• Shock- Including septic shock and shock due to trauma.
• Septicaemia.
• Burns.
• Pancreatitis.
• Diabetic Ketoacidosis.
• Hypersensitivity reactions.
• Drugs reactions due to aspirin, heroin or paraquat.
• Multiple blood transfusions.
• Malaria.
• Acute liver failure.
• Obstetric complications- Problems during pregnancy or
delivery such as preeclampsia.
• Cardiac surgery and other complicated surgeries.
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Patient presentation
and diagnosis
Patient presentation and
diagnosis
• ARDS usually occurs within 24 to 48
hours of the initial injury or illness.
• The patient usually presents with
shortness of breath, tachypnea, and
symptoms related to the underlying
cause, i.e. shock
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Patient presentation and
diagnosis
• Arterial blood gas analysis
• Chest X-ray
• Pulmonary artery catheter for
measuring the pulmonary artery
wedge pressure.
• CT scanning
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Pathophysiology
Pathophysiology
• Diffuse inflammation of lung
parenchyma
• Typical histological presentation
involves diffuse alveolar damage and
hyaline membrane formation in
alveolar walls.
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Pathophysiology
• Endothelial dysfunction, fluid
extravasation from the capillaries and
impaired drainage of fluid from the lungs.
• This pulmonary edema increases the
thickness of the alveolo-capillary space.
• This impairs gas exchange leading to
hypoxia, increases the work of breathing,
eventually induces fibrosis of the airspace.
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Pathophysiology
• Dysfunction of type II pulmonary
epithelial cells, with a concomitant
reduction in surfactant production.
• Edema and decreased surfactant
production by type II pneumocytes
may cause whole alveoli to collapse,
or to completely flood.
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Pathophysiology
• This loss of aeration contributes further
to the right-to-left shunt, resulting in
massive intrapulmonary shunting.
• The loss of aeration may follow
different patterns according to the
nature of the underlying disease, and
other factors
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Pathophysiology
• In pneumonia-induced ARDS,
infiltrates are usually distributed to
the lower lobes, in their posterior
segments, and they roughly
correspond to the initial infected
area.
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Pathophysiology
• In sepsis or trauma-induced ARDS,
infiltrates are usually more patchy
and diffuse. The posterior and basal
segments are always more affected,
but the distribution is even less
homogeneous.
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Treatment
Treatment
• Mechanical ventilation
• Antibiotic
• When sepsis is diagnosed,
appropriate protocols should be
enacted.
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Mechanical ventilation
• The overall goal is to maintain acceptable gas
exchange and to minimize adverse effects in its
application.
• Three parameters are used:
PEEP, to maintain maximal recruitment of
alveolar units.
Mean airway pressure (to promote recruitment
and predictor of hemodynamic effects)
Plateau pressure (best predictor of alveolar
overdistention).
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Mechanical ventilation
VARIABLES
NIH-ARDS NETWORK PROTOCALS
TIDAL VOLUME
≤6 ml/kg
PLEATAU PRESSURE
≤30 cm H2O
VENTILATION SET
RATE/ pH GOAL
6-35/ min to achieve pH ≥7.30
INSPIRATORY
FLOW,I:E RATIO
Flow to achieve I:E Ratio 1:1-1:3
OXYGENATION
GOAL
PaO2 ≥55mmHg,SpO2 ≥88%
FiO2/PEEP
0.3/5, 0.4/5-8, 0.5/8-10,
0.6/10,
0.7/10-14, 0.8/14, 0.9/14-18,1/18-24
WEANING
When FiO2/PEEP 0.4/8 ,with PSV
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Mechanical ventilation
• Low tidal volume ventilation
• Plateau pressure less than 30 cm
H2O was a secondary goal,
• APRVis the primary mode of choice
when ventilating a patient with ARDS
or ALI.
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AIRWAY PRESSURE RELEASE
VENTILATION(APRV)
• A CPAP circuit with release valve at
expiratory limb –driven by time
device
• APRV is a CPAP system causing
. alveolar ventilation by briefly
interrupting CPAP.
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APRV
• Release valve opens for 1-2sec.
• Pr drops to lower level-low CPAP(0to2cmH2O)
• Lung volume less than FRC in expiration
• alveolar ventilation & CO2 elimination
• Reapplication of CPAP by closing valveHigher CPAP(10to 12 cm H2O)
• FRC & oxygenation.
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APRV
• ADVANTAGES:
• Lesser PIP ,so less hemo dynamic
changes.
• To alveolar ventilation in ALI of
mild to moderate.
• A weaning mode.
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Mechanical ventilation
Advantages to APRV ventilation
• decreased airway pressures,
• decreased minute ventilation,
• decreased dead-space ventilation,
• promotion of spontaneous breathing, near
elimination of neuromuscular blockade
• almost 24 hour a day alveolar recruitment,
• decreased use of sedation,
• positive effect on cardiac output (due to the
negative inflection from the elevated baseline
with each spontaneous breath).
• A patient with ARDS on average spends 8 to 11
days on a mechanical ventilator; APRV may reduce
this time significantly.
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INVERSE RATIO
VENTILATION(IRV)
•I:E >1
•PC-IRV / VC-IRV
• Ti with set pr opening of stiff alveoli
units improved oxygenation
• Te
not allowing alveoli to collapse
development of intrinsic PEEP
reduction of shunting
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IRV……,
Improve oxygenation by
•Reducing intra pulmonary shunting
•Improvement of V/Q matching
•Decreased dead space ventilation
•Increased MAP & intrinsic PEEP
Useful when high FiO2 & high PEEP to be
avoided
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Inverse ratio ventilation
• Inverse ratio ventilation is reserved for severe cases when
it is impossible to oxygenate the patient adequately.
• Treatment involves increasing the amount of time that the
ventilator is inspiring versus expiring.
• Patients normally spend more time exhaling than inhaling, at
a ratio of about 3:1. Increasing the amount of time spent
inhaling re-expands more collapsed alveoli than positive
pressure alone.
• This is an uncomfortable technique and usually requires
sedation and a muscle-paralyzing drug that keeps the
respiratory muscles from resisting the unnatural inverse
ratio ventilation.
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Prone position
ventilation
• Distribution of lung infiltrates in
acute respiratory distress syndrome
is non-uniform.
• Repositioning into the prone position
(face down) might improve
oxygenation by relieving atelectasis
and improving perfusion.
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Prone position
ventilation
• Improved V/P in previously atelectactic areas due
to uniform distribution of plural pr -Lamm etall
• Requires atleast more than 6 hrs/ day of prone
ventilation.
• A significant decrease in right ventricular
enlargement and a significant reduction in septal
dyskinesia, after 18 h of prone positioning.-Vielliard
etall ,CHEST-OCT-2007
• No improvement in mortality in clinical trials
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Fluid management
• Several studies have shown that
pulmonary function and outcome are
better in patients that lost weight or
wedge pressure was lowered by
diuresis or fluid restriction
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Corticosteroid
• Steroids cause a suppression of
inflammation during the fibroproliferative
phase of ARDS. The initial regimen
consists of mps 2 mg/kg daily. After 3-5
days a response must be apparent. In 1-2
weeks the dose can be tapered to mps 0.51.0 mg daily. In the absence of results
steroids can be discontinued.-Meduri et al
• ARDSnet LAZARUS study demonstrated
that they are not efficacious in ARDS.
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Nitric oxide
• Inhaled nitric oxide (NO) potentially acts as
selective pulmonary vasodilator. Rapid binding to
hemoglobin prevents systemic effects. It should
increase perfusion of better ventilated areas.
There are no large studies demonstrating positive
results.
• Almitrine bismesylate stimulates chemoreceptors
in carotic and aortic bodies. It has been used to
potentiate the effect of NO, presumably by
potentiating hypoxia-induced pulmonary
vasoconstriction. In case of ARDS it is not known
whether this combination is useful.
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Surfactant therapy
• To date no prospective controlled clinical
trial has shown a significant mortality
benefit of exogenous surfactant in ARDS
• IV N-Acetyl-Cysteine which may
increase the lung surfactants
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Newer /Near future
Treatment options
Anti-inflammatory
Strategies
• Antioxidant Therapy -N-acetylcysteine and procysteine,
oxygen free-radical scavengers and precursors for
glutathione, were efficacious in some experimental studies
• Prostaglandin Agonists/Inhibitors: Prostaglandin E1 is a
vasodilator that blocks platelet aggregation and decreases
neutrophil activation
• Ibuprofen- an inhibitor of the cyclooxygenase pathway
• Ketoconazole, a potent inhibitor of thromboxane and
leukotriene synthesis
• Pentoxifylline is a phosphodiesterase inhibitor that inhibits
neutrophil chemotaxis and activation in animal models of
ARDS
• Lisofylline inhibited release of TNF, IL-1, and IL-6,
•
Anti–IL-8 Therapy
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Enhanced Resolution of
Alveolar Edema
Alveolar fluid clearance depends primarily on active
sodium transport across the alveolar epithelium
• Salmeterol, a lipid-soluble ß2-agonist
• Intra-alveolar terbutaline administration
markedly increased alveolar fluid clearance
• Dobutamine, ß2-adrenergic agonist, markedly
increased alveolar and lung fluid clearance in an
experimental rat model
• Dopamine, when administered at 5 µg/kg/min IV,
increased alveolar fluid clearance in an isolated
perfused rat model by increasing the activity of
.
Na-K ATP pumps.
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Enhanced Repair of the
Alveolar Epithelial Barrier
• Studies suggest that hepatocyte
growth factor and keratinocyte
growth factor are major mitogens
for alveolar epithelial type II cells
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Complications
Complications
• Pulmonary: barotrauma (volutrauma),
pulmonary embolism (PE), pulmonary
fibrosis, ventilator-associated pneumonia
(VAP).
• Gastrointestinal: hemorrhage (ulcer),
dysmotility, pneumoperitoneum, bacterial
translocation.
• Cardiac: arrhytmias, myocardial
dysfunction.
• Renal: acute renal failure (ARF), positive
fluid balance.
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Complications
• Mechanical: vascular injury, pneumothorax
(by placing pulmonary artery catheter),
tracheal injury/stenosis (result of
intubation and/or irritation by
endotracheal tube.
• Nutritional: malnutrition (katabolic state),
electrolyte deficiency.
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Thank you
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ARDS
Dr.G.K.Kumar
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