SlideShare une entreprise Scribd logo
1  sur  68
Télécharger pour lire hors ligne
Acute Respiratory Distress
Syndrome
Dr. Maged Abulmagd
Consultant intensivist,EBGH
Synonyms of ARDS
• Shock lung
• Pump lung
• Traumatic wet lung
• Post traumatic atelectasis
• Adult hyaline membrane
disease
• Progressive respiratory distress
• Acute respiratory insufficiency
syndrome
• Haemorrhagic atelectasis
• Hypoxic hyperventilation
• Postperfusion lung
• Oxygen toxicity lung
• Wet lung
• White lung
• Transplant lung
• Da Nang lung
• Diffuse alveolar injury
• Acute diffuse lung injury
• Noncardiogenic pulmonary
edema.
• Progressive pulmonary
consolidation
Timeline
• In 1967 – Ashbaugh, Bigelow, Petty, Levine - described Acute
Respiratory Distress Syndrome in adults
• In 1971, Petty and Ashbaugh modified its name from ‘acute’ to ‘adult’
Respiratory Distress Syndrome; to differentiate it from its newborn
counterpart
• In 1974, Webb and Tierney confirmed the existence of ventilator
associated lung injury
Timeline
• In 1992, American European Consensus Conference (AECC) gave
standardized definition for ARDS
• In 1997, Tremblay et al introduced the concept of biotrauma
• In 1998, Amato et al, conducted RCT - decrease in mortality using
low tidal volume ventilation and high PEEP (open lung strategy)
• In 2000, ARDS network trial demonstrated the benefits of low tidal
volume and PEEP ventilation
Definitions of ARDS
Ashbaugh and colleagues, 1967
• Severe dyspnea
• Tachypnea
• Cyanosis refractory to oxygen therapy
• Decreased pulmonary compliance
• Diffuse alveolar infiltrates on chest radiograph.
 Loosely defined criteria
 Definition of hypoxemia inconsistent
Bernard and colleagues, 1992
(American European Consensus conference definition)
A three-criteria system including chest radiograph, oxygenation score,
and exclusion of cardiogenic causes:
• Acute onset, bilateral infiltrates on chest radiography,
• Acute lung injury ~ PaO2/FIO2 ≤ 300
ARDS subset~ PaO2/FIO2 ≤ 200
• Pulmonary-artery wedge pressure of <18 mm Hg or the absence of
clinical evidence of left atrial hypertension
Bernard and colleagues, 1992
(American European Consensus conference definition)
Problems
• Acute onset : arbitrary; <1 week
• Bilateral infiltrates: inter observer variation, b/l pneumonia,
atelectasis, cardiogenic pulmonary edema
• PAOP of <18 mm Hg /absence of clinical evidence of left atrial
hypertension : PAOP: poor estimate of PVH, falsely raised with high
airway pressures
• Acute lung injury present if PaO2/FIO2 is 300 : new and arbitrary
value
BERLIN DEFINITION
Acute respiratory distress syndrome
Precipitating Factors
Direct Lung Injury
• Pneumonia
• Aspiration of gastric contents
• Pulmonary contusion
• Near-drowning
• Toxic inhalation injury
Indirect Lung Injury
• Sepsis
• Severe trauma
Multiple bone fractures
Head trauma
Burns
• Multiple transfusions
• Drug overdose
• Pancreatitis
• Post-cardiopulmonary bypass
Pathophysiology in ARDS
Based on the histological appearance -
Exudative phase (0-4 days)
• Alveolar and interstitial edema
• Capillary congestion
• Destruction of type I alveolar cells
• Early hyaline membrane formation
Proliferative Phase (3-10 days)
• Increased type II alveolar cells
• Cellular infiltration of alveolar septum
• Organisation of hyaline membranes
Fibrotic Phase (>10 days)
• Fibrosis of hyaline membranes and alveolar septum
• Alveolar duct fibrosis
Pathology in ARDS
Mechanisms in early phase -
• Release of inflammatory cytokines – TNF alpha, IL- 1,6,8
• Failure of alveolar edema clearance, epithelial and endothelial damage
• Increased permeability of alveolo – capillary membrane
• Neutrophil migration and oxidative stress
• Procoagulant shift – fibrin deposition
• Surfactant dysfunction
Mechanism in late (repair) phase –
• Fibroproliferation -TGF beta, MMPs, thombospondin, plasmin, ROS
• Remodelling - matrix and cell surface proteoglycans, MMP, imbalance of
coagulation and fibrinolysis.
Pathophysiology of ARDS
D/D : Hydrostatic pulmonary edema
 PCWP ≥ 18 mmHg
 Causes :
• Cardiogenic – LVF (eg. MI, myocarditis)
cardiac valvular disease (aortic, mitral)
• Vascular – systemic HTN, pulmonary embolism
• Volume overload - excessive iv fluids, renal failure
Cardiogenic vs Non-cardiogenic edema
1.1. Prior h/o cardiac diseasePrior h/o cardiac disease
22.Third heart sound.Third heart sound
3.3. CardiomegalyCardiomegaly
44. Infiltrates : Central distribution. Infiltrates : Central distribution
55. Widening of vascular pedicle No widening of vascular pedicle. Widening of vascular pedicle No widening of vascular pedicle
( ↑ width of mediastinum)( ↑ width of mediastinum)6.6. PA wedge pressurePA wedge pressure
7.7. Positive fluid balancePositive fluid balance
Cardiogenic
Absence of heart diseaseAbsence of heart disease
No third heart soundNo third heart sound
Normal sized heartNormal sized heart
Peripheral distributionPeripheral distribution
N orN or ↓↓ PA wedge pressurePA wedge pressure
Negative fluid balanceNegative fluid balance
Non-cardiogenic
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management - protective lung ventilation strategy
- role of ‘open lung approach’
 Adjuncts to core ventilation -
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Management contd.
• Non conventional/Salvage interventions
a. High frequency ventilation
b. Airway pressure release ventilation
c. Tracheal gas insufflation
d. Inverse ratio ventilation
e. Inhaled nitric oxide
f. Inhaled prostacyclin
g. Corticosteroids
h. Surfactant administration
i. Liquid ventilation
j. Extracorporeal membrane oxygenation
• Supportive therapy – nutrition, prevention of infection
Concept of VALI
 Mechanical ventilation - Basic care in critically ill ICU patients
 May cause or worsen lung injury – ventilator induced/associated lung
injury
 Components –
• Barotrauma
• Volutrauma
• Atelectrauma
• Biotrauma
VALI and MODS
Concept of ‘baby lung’
• Put forward by Gattinoni and colleagues first in 1987
• Lung injury in ARDS - non homogenous, basal
• Edema and consolidation > dependent lung regions - ↑ density of dorsal
regions
• Aerated ventral regions – ‘baby lung’ (300-500gms) – high compliance
• Ventilation of baby lung with normal tidal volumes and pressures – alveolar
over distension – injury to functional lung tissue
Management
Lung protective ventilation ARDS network protocol
• Goals
 Oxygenation : PaO2 55-80 mmHg, or SpO2 88 – 94% (excluding
pregnancy, intracranial hypertension or stroke where SaO2
goal>94%)
 Ventilation :
 Tidal volume : 4-6 ml/kg ideal body weight
 Plateau pressure : <30cmH2O
 Ph: 7.25-7.35
 I:E ratio of 1:1 – 1:3
Management contd.
Oxygenation
• Initially high Fio2 given (1.0) to correct hypoxia
• Fio2 and PEEP adjusted to the lowest level compatible with the
oxygenation goals
• Fio2 and PEEP adjusted in the following fixed combinations
{fio2/PEEP(mmHg)}
0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0
5 5 8 8 10 10 10 12 14 14 14 16 18 20-
24
FIO2
PEEP
Management contd
Initial ventilator set up and adjustments
STEP 1- Calculation of ideal body weight(IBW):
 For males, IBW(kg) = 50+2.3{height(inch)– 60}
Or IBW(kg)=50 + 0.91{height(cm)–152.4}
 For females, IBW(kg) = 45.5+2.3{height(inch)– 60}
Or IBW(kg)=45.5 + 0.91{height(cm)–152.4}
Management contd
STEP 2 - Volume assist control selected as ventilator mode
 Initial tidal volume (TV) set at 8ml/kg IBW
 TV reduced by 1ml/kg IBW 2 hourly until TV = 6ml/kg IBW
 Initial ventilator rate set to maintain baseline minute ventilation( not
>35/min)
 TV and respiratory rate adjusted to achieve the pH and plateau
pressure goals
 Inspiratory flow rate set above patients demand (usually >80L/min)
Open Lung Approach
• Introduced by Amato et al in 1998 – use of low tidal volume + high
PEEP+ recruitment (Open lung strategy) – reduce mortality in ARDS
• Maintaining inflation & deflation between 2 inflection points during entire
respiratory cycle
• Ventilatory settings - PEEP >Pflex & TV reduced so that Pplat < UIP
• Advantages- avoids repetitive opening and closing of alveoli (VALI)
- minimizes shear injury
Open Lung Approach
Pressure-Volume Curve
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management – protective lung ventilation strategy
role of ‘open lung approach’
 Adjuncts to core ventilation –
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Fluid restriction in ARDS
• Rationale – alveolar flooding depends on :
1. Capillary hydrostatic pressure
2. Oncotic pressure
3. Alveolar–capillary permeability
• Capillary permeability increased in ARDS
• ↓ hydrostatic pressure and ↑ oncotic pressure may help.
Fluid therapy in ARDS
Recommended :
• Central venous pressure guided therapy – 10-14 mmHg
( ARDS Network Trial 2003)
• Restricted fluid intake
• Increased urine output – Diuretics or RRT
Not recommended :
• Vasodilators
• Albumin
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management - protective lung ventilation strategy
- role of ‘open lung approach’
 Adjuncts to core ventilation –
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Permissive Hypercapnia
• Hickling and colleagues 1990
• “Degree of hypercapnia permitted in patients subjected to lower tidal
volumes”
• Upper limit – not defined; >100 mmHg avoided
 Advantages
• Increased surfactant secretion (animal models) – improved V/Q match,
oxygenation (improved compliance)
• Increased cardiac output and oxygen delivery (sympathoadrenal effects
predominate over cardiodepressant effects)
• Increased cerebral blood flow and tissue oxygenation
Permissive Hypercapnia
 Concerns
• Increase in pulmonary vascular resistance
• Impaired diaphragmatic function (impairs afferent transmission)
• Decrease in cardiac contractility
• Raised intracranial tension
 Individualize and treat
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management - protective lung ventilation strategy
- role of ‘open lung approach’
 Adjuncts to core ventilation –
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Prone Position Ventilation
 First suggested by Piehl and Brown in 1976
 Offers improved oxygenation by:
• Increased FRC
• Change in regional diaphragm motion
• Distribution of perfusion
• Better clearance of secretions
Prone Position Ventilation
• Sud and colleagues conducted – meta-analysis of 13 RCTs (1559
patients) on supine and prone position ventilation in ARDS/ALI
patients
 Median MV of 12 hours ( 4-24hrs) for 4 days( 1-10 days)
 Conclusion -cannot be recommended for routine Mx
-no evidence of improved survival
• Gattinoni et al suggested no overall reduction in mortality except in
very sick patients ( SAPS II Score >50)
• No decrease in ventilator associated pneumonia
Problems of prone position
• Facial edema
• Airway obstruction
• Difficulties with enteral feeding
• Transitory decrease in oxygen saturation
• Hypotension & Arrhythmias
• Vascular and nerve compression
• Loss of venous accesses and probes
• Loss of chest drain and catheters
• Accidental extubation
• Apical atelectasis d/t incorrect positioning of the tracheal tube
• Increased need for sedation
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management - protective lung ventilation strategy
- role of ‘open lung approach’
 Adjuncts to core ventilation –
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Recruitment maneuvers
• High pressure inflation maneuver aimed at temporarily raising the
transpulmonary pressure above levels typically obtained with
mechanical ventilation
• Types – Elevated sustained pressures : 40 cm H2O for 40 seconds
Sigh breaths : ↑ tidal volume / PEEP for one or several breaths
Extended sigh breath : VCV with PEEP well above LIP for a longer
time
• More effective in early ALI and those with more homogenous
disease; atelectasis > consolidation.
Recruitment maneuvers
Adverse effects
• Hypotension
• Barotrauma
• Raised ICP
• Haemodynamic instability
Management contd.
• Non conventional/Salvage interventions
a. High frequency ventilation
b. Airway pressure release ventilation
c. Tracheal gas insufflation
d. Inverse ratio ventilation
e. Inhaled nitric oxide
f. Inhaled prostacyclin
g. Corticosteroids
h. Surfactant administration
i. Liquid ventilation
j. Extracorporeal membrane oxygenation
• Supportive therapy – nutrition, prevention of infection
High Frequency Ventilation
• Mechanical ventilatory support using higher than normal breathing
frequencies
• Smaller tidal pressure swings (within inflection points) along with apt mpaw
• Smaller tidal volumes and higher mean pressure utilized for lung protection
• Special ventilators required
• Types - High Frequency Jet Ventilation (HFJV)
High Frequency Oscillatory Ventilation (HFOV)
HFV
HFJV
• A nozzle/injector creates high velocity ‘jet’ of gas directed into the
lung
• Injectors – 1-3mm diameter
• Expiration is passive
• Frequencies available – upto 600 breaths/min
• Available for neonatal and paediatric use only
HFOV
• Characterized by rapid oscillations of a diaphragm (at 3 to 10 hertz i.e
180 to 160 breaths/min) driven by a piston pump
• Frequencies available – 300-3000 breaths/min
• Expiration is also active – risk of air trapping minimal
HFV contd
Advantages
• Better oxygenation and ventilation
• Aids lung recruitment (high mpaw)
• Reduces oxygen toxicity (high mpaw)
• Minimizes VILI
Disadvantages
• Delivered tidal volumes difficult to monitor
• Deep sedation and/or paralysis required
• Inadequate humidification
• Direct physical airway damage
Airway Pressure Release Ventilation
• Alternative mode of ventilation that applies a form of CPAP that is
released periodically, augmenting CO2 release.
• Pressure limited, time cycled mode
• Permits spontaneous ventilation throughout the respiratory cycle
• Based on the ‘open lung’ concept – maximize and maintain
recruitment throughout the respiratory cycle
APRV contd
• Uses 2 airway pressures – P high and P low; 2 set time periods – T high
and T low, usually T high>T low
• P high is set above the closing pressure of recruitable alveoli (lower
inflection point)
• Set T high maintains the P high for several seconds
• T low helps remove CO2
APRV contd
Potential benefits :
• ↑ V/Q match
• ↓ diaphragmatic atrophy during critical illness
• ↑ cardiac output and oxygen delivery
• ↑ splanchnic perfusion
• ↑ renal and hepatic function
• Fewer days on mechanical ventilation
• Fewer days in ICU
Tracheal Gas Insufflation
• Normal ventilatory cycle - bronchi and trachea filled with alveolar gas
at end expiration
• In the next inspiration, CO2 laden gas forced back into alveoli.
• TGI - stream of fresh gas (at 4-8L/min) insufflated through a small
catheter/channels in the wall of endotracheal tube into the lower
trachea
• CO2 laden gas flushed out of the trachea before next inspiration
Tracheal Gas Insufflation contd.
Disadvantages
• Dessication of secretions
• Inadequate humidification
• Airway mucosal injury
• Accumulation of secretions in the TGI catheter
• Creation of auto PEEP from expiratory flow and resistance of the
ventilator-exhalation tubes and valve
Inverse Ratio Ventilation
• Alternative mode of ventilation
• Entails use of prolonged inspiratory times (I:E>1) using volume or
pressure cycled mode of mechanical ventilation
• Proposed mechanism of action – alveolar recruitment at lower airway
pressures, optimal distribution of ventilation
• Concerns – generation of auto PEEP
reduced cardiac output ( ↑ MAP)
Inhaled Nitric Oxide
 NO – endogenous vasodilator, from endothelium
 Vasodilatation of alveolar circulation reduces shunt and pulmonary
hypertension
 Problems:
• toxic nitrogen compounds
• methemoglobinemia
• pulmonary edema, acute RHF (interrupted flow)
• rebound pulmonary hypertension
• expensive
 Routine use not recommended
Inhaled Prostacyclin
• Cause vasodilation, inhibit platelet aggregation, reduction of
neutrophil adhesion and activation, ↓ pulmonary hypertension,
improved oxygenation
• Minimal systemic effects, harmless metabolites, no requirements for
monitoring
• Both positive and negative results obtained in various trials
• Presently not recommended
Corticosteroids
• Established ARDS – characterized by alveolar fibrosis
• Anti-inflammatory and antifibrotic properties of steroids – probable
role in ARDS
• No role in preventing but may help in treating ARDS
Surfactant Therapy
• Reduces alveolar surface tension
• Prevents alveolar collapse
• Anti inflammatory properties
• Anti microbial properties
• Exogenous surfactant – successful in neonatal respiratory distress
syndrome (reduced surfactant production)
• ARDS in adults – increased surfactant removal, altered composition,
reduced efficacy, reduced production
• Surfactant therapy not recommended in adults
Liquid Ventilation
• Involves filling the lung with liquid
• Removes the air liquid interface and supports alveoli, prevents
collapse
• Perfluorocarbons – have low surface tension, dissolve oxygen and
carbon dioxide readily, non toxic, minimally absorbed, eliminated by
evaporation though lungs
• Lowered surface tension may improve alveolar recruitment, arterial
oxygenation, increased lung compliance
• Can recruit dependent alveoli (advantage over PEEP)
Liquid Ventilation contd.
Types :
• Total – filling the entire lung with liquid, ventilated with a special
ventilator
- Expensive
• Partial - filling the lung to FRC with liquid, ventilated with
conventional ventilator
- Appropriate dose of PFC still to be determined
- ↑ chances of pneumothoraces, hypoxic episodes, hypotensive
episodes
• PFC radiodense – impossible to detect infection or follow the
progress of healing in a chest radiograph
• Liquid ventilation is not FDA approved
Extracorporeal Membrane Oxygenation
• Invasive, complex form of cardiopulmonary bypass
• Provides temporary gas exchange and blood circulation outside the
body
• Severe but potentially reversible respiratory failure
• Such periods of “lung rest” allow the lungs to recover
• Used when conventional strategies fail
• No good evidence available over conventional management
ECMO contd.
Types
• Veno - arterial – a catheter placed in both vein and artery. Provides
support both for heart and lungs
• Veno - venous – single double lumen catheter placed in the vein.
Provides support only for lungs
• ECMO allows ventilator pressures and volumes to be decreased to
prevent further VILI
• Reduction in intra - thoracic pressure allows fluid removal from lungs
with less risk of cardiovascular instability
ECMO contd
Complications :
• Haemorrhage
• Renal failure
• Haemolysis
• Hypotension/ hypertension
• Pneumothorax
• Infections
Management contd.
• Salvage interventions
a. High frequency oscillatory ventilation
b. Airway pressure release ventilation
c. Tracheal gas insufflation
d. Inverse ratio ventilation
e. Inhaled nitric oxide
f. Inhaled prostacyclin
g. Corticosteroids
h. Surfactant administration
i. Liquid ventilation
j. Extracorporeal membrane oxygenation
• Supportive therapy – nutrition, prevention of infection
Nutrition
• Enteral over parenteral
• High fat – low carbohydrate diet advocated - ↓ CO2
• Immuno modulatory nutrients
-amino acids - arginine and glutamine
-ribonucleotides
-omega-3 fatty acids
• Diet rich in fish oil, γ-linolenic acid, and antioxidants
• Standard nutritional formulations recommended
Antibiotics
• Infection - present initially : nonpulmonary sepsis
• Develop later - nosocomial infections : pneumonia and catheter-
related sepsis.
• Aim : identify, treat, and prevent infections.
• Most pneumonia > 7 days
• Prompt initiation of appropriate empiric therapy.
• Hand washing by medical personnel
• New areas :
- continuous suctioning of subglottic secretions to prevent their
aspiration
-development of new endotracheal tubes - resist formation of
bacterial biofilm that can be embolized distally with suctioning.
Management
• Treatment of the precipitating cause
• Mechanical ventilation –
 Core ventilator management - protective lung ventilation strategy
- role of ‘open lung approach’
 Adjuncts to core ventilation -
1. Fluid restriction
2. Permissive hypercapnia
3. Prone positioning
4. Recruitment maneuvers
Management contd.
• Non conventional/Salvage interventions
a. High frequency ventilation
b. Airway pressure release ventilation
c. Tracheal gas insufflation
d. Inverse ratio ventilation
e. Inhaled nitric oxide
f. Inhaled prostacyclin
g. Corticosteroids
h. Surfactant administration
i. Liquid ventilation
j. Extracorporeal membrane oxygenation
• Supportive therapy – nutrition, prevention of infection
Complications associated with ARDS
• Pulmonary: barotrauma ,volutrauma, pulmonary embolism, pulmonary
fibrosis, ventilator-associated pneumonia (VAP), Oxygen toxicity
• Gastrointestinal: haemorrhage (ulcer), dysmotility, pneumoperitoneum,
bacterial translocation
• Cardiac: Arrhythmias, myocardial dysfunction
• Renal: acute renal failure (ARF), fluid retention
• Mechanical: vascular injury, tracheal injury/stenosis (result of intubation
and/or irritation by endotracheal tube)
• Nutritional: malnutrition, anaemia, electrolyte deficiency
Long term sequelae of ARDS
• Pulmonary function – mild impairment, improves over 1 year
• Neurocognitive dysfunction
• Post traumatic stress disorder
• Physical debilitation
Infantile Respiratory Distress Syndrome
• Hyaline membrane disease
• Deficiency of surfactant : insufficient production in immature lungs,
immature babies
• Genetic mutation in one of the surfactant proteins, SP-B – rare, full
term babies
• Prevention : avoidance of premature birth, corticosteroids
• Treatment : surfactant replacement
References
• Harrison’s Principle of Internal Medicine, 16th
ed.
• Christie JD, Lanken PN. Acute lung injury and the acute respiratory distress
syndrome. Critical Care – Hall
• Foner BJ, Norwood SH, Taylor RW. Acute respiratory distress syndrome.
Critical Care, 3rd
ed. Civetta
• Wiener-Kronish JP, et al. The adult respiratory distress syndrome : definition
and prognosis, pathogenesis and treatment. BJA 1990; 65: 107-129.
• Clinical Anaesthesia. Barash, 6th
ed.
• Egans Respiratory Care, 7th
e
References
• Acute respiratory distress syndrome network. Ventilation with lower tidal volumes
as compared with traditional tidal volumes for acute lung injury and the acute
respiratory distress syndrome. N Engl J Med. 2000;242:1301-1308
• Brower RG, Morris A, MacIntyre N, et al. Effects of recruitment maneuvers in
patients with acute lung injury and acute respiratiry distress syndrome ventilated
with high positive end expiratory pressure. Crit Care Med.2003;31:2592-2597
• Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume
pressure limited ventilationwith permissive hypercapnia in severe adult respiratory
distress syndrome. Intensive care med. 1990;16:372-377
• Hickling KG, Walsh J,Henderson S, Jackson R. Low mortality rate in acute
respiratiry distress syndrome using low volume pressure limited ventilation with
permissive hypercapnia: a prospective study. Crit Care Med.1994;22:1568-1578

Contenu connexe

Tendances

Ards and ventilator management
Ards and ventilator managementArds and ventilator management
Ards and ventilator managementAmr Elsharkawy
 
ARDS 【A simplified evidence based approach】
ARDS 【A simplified evidence based approach】ARDS 【A simplified evidence based approach】
ARDS 【A simplified evidence based approach】Sherif Elbadrawy
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndromeKiran Bikkad
 
Ventilation strategies in ards rachmale
Ventilation strategies in ards   rachmaleVentilation strategies in ards   rachmale
Ventilation strategies in ards rachmaleDang Thanh Tuan
 
Pulmonary Oedema - Pathophysiology - Approach & Management
Pulmonary Oedema  - Pathophysiology - Approach & ManagementPulmonary Oedema  - Pathophysiology - Approach & Management
Pulmonary Oedema - Pathophysiology - Approach & ManagementArun Vasireddy
 
ARDS - Diagnosis and Management
ARDS - Diagnosis and ManagementARDS - Diagnosis and Management
ARDS - Diagnosis and ManagementVitrag Shah
 
12.Respiratory Failure
12.Respiratory Failure12.Respiratory Failure
12.Respiratory Failureghalan
 
Mechanical Ventilation for severe Asthma
Mechanical Ventilation for severe AsthmaMechanical Ventilation for severe Asthma
Mechanical Ventilation for severe AsthmaDr.Mahmoud Abbas
 
Management of Respiratory Failure
Management of Respiratory FailureManagement of Respiratory Failure
Management of Respiratory Failureyuyuricci
 
Ards 2018
Ards 2018Ards 2018
Ards 2018imran80
 
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGEACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGEmataharitimoer MT
 

Tendances (20)

Ards and ventilator management
Ards and ventilator managementArds and ventilator management
Ards and ventilator management
 
ARDS
ARDSARDS
ARDS
 
ards.pptx
ards.pptxards.pptx
ards.pptx
 
Ards
ArdsArds
Ards
 
ARDS 【A simplified evidence based approach】
ARDS 【A simplified evidence based approach】ARDS 【A simplified evidence based approach】
ARDS 【A simplified evidence based approach】
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndrome
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndrome
 
ARDS
ARDSARDS
ARDS
 
Ventilation strategies in ards rachmale
Ventilation strategies in ards   rachmaleVentilation strategies in ards   rachmale
Ventilation strategies in ards rachmale
 
Pulmonary Oedema - Pathophysiology - Approach & Management
Pulmonary Oedema  - Pathophysiology - Approach & ManagementPulmonary Oedema  - Pathophysiology - Approach & Management
Pulmonary Oedema - Pathophysiology - Approach & Management
 
Ards m ibrahim
Ards m ibrahimArds m ibrahim
Ards m ibrahim
 
ARDS - Diagnosis and Management
ARDS - Diagnosis and ManagementARDS - Diagnosis and Management
ARDS - Diagnosis and Management
 
12.Respiratory Failure
12.Respiratory Failure12.Respiratory Failure
12.Respiratory Failure
 
Mechanical Ventilation for severe Asthma
Mechanical Ventilation for severe AsthmaMechanical Ventilation for severe Asthma
Mechanical Ventilation for severe Asthma
 
Management of Respiratory Failure
Management of Respiratory FailureManagement of Respiratory Failure
Management of Respiratory Failure
 
Prone Ventilation In ARDS
Prone Ventilation In ARDSProne Ventilation In ARDS
Prone Ventilation In ARDS
 
Ards 2018
Ards 2018Ards 2018
Ards 2018
 
ARDS
ARDSARDS
ARDS
 
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGEACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
ACUTE RESPIRATORY DISTRESS SYNDROME AND HOW TO MANAGE
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndrome
 

En vedette

Updates on Acute respiratory distress syndrome
Updates on Acute respiratory distress syndromeUpdates on Acute respiratory distress syndrome
Updates on Acute respiratory distress syndromeHamdi Turkey
 
Respiratory distress syndrome in neonates
Respiratory distress syndrome in neonates Respiratory distress syndrome in neonates
Respiratory distress syndrome in neonates Mohammed Abdul Raheem
 
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)ghalan
 
Nasal drugdeliverysystem
Nasal drugdeliverysystemNasal drugdeliverysystem
Nasal drugdeliverysystemuttam_aswal
 
Pulmonary trauma
Pulmonary traumaPulmonary trauma
Pulmonary traumaWan Adam
 
Chapter 19-respiratory-distress-syndr
Chapter 19-respiratory-distress-syndrChapter 19-respiratory-distress-syndr
Chapter 19-respiratory-distress-syndrHellen Kyakuwaire
 
Ventilator associated pneumonia
Ventilator associated pneumoniaVentilator associated pneumonia
Ventilator associated pneumoniadrcsaravind89
 
Recent advances in pulmonary drug delivery
Recent advances in pulmonary drug deliveryRecent advances in pulmonary drug delivery
Recent advances in pulmonary drug deliverySamiksha Sawant
 
Nasal Injuries
Nasal InjuriesNasal Injuries
Nasal Injuriespdhpemag
 
Acute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromeMekelle Universty
 
Nasal & Pulmonary Drug Delivery System
Nasal & Pulmonary Drug Delivery SystemNasal & Pulmonary Drug Delivery System
Nasal & Pulmonary Drug Delivery SystemAmrutaSambrekar
 
Complications of 3rd Stage of Labor
Complications of 3rd Stage of LaborComplications of 3rd Stage of Labor
Complications of 3rd Stage of Laborhanisahwarrior
 
Respiratory distress syndrome in a premature baby
Respiratory distress syndrome in a premature babyRespiratory distress syndrome in a premature baby
Respiratory distress syndrome in a premature babyvissalini Jayabalan
 
Respiratory distress of the newborn
Respiratory distress of the newbornRespiratory distress of the newborn
Respiratory distress of the newbornsnich
 
Abdominal trauma
Abdominal traumaAbdominal trauma
Abdominal traumaFaiz Hmoud
 
Thoracic trauma presentation
Thoracic trauma presentationThoracic trauma presentation
Thoracic trauma presentationMazin Eragat
 

En vedette (20)

Updates on Acute respiratory distress syndrome
Updates on Acute respiratory distress syndromeUpdates on Acute respiratory distress syndrome
Updates on Acute respiratory distress syndrome
 
Respiratory Distress Syndrome
Respiratory Distress SyndromeRespiratory Distress Syndrome
Respiratory Distress Syndrome
 
Respiratory distress syndrome in neonates
Respiratory distress syndrome in neonates Respiratory distress syndrome in neonates
Respiratory distress syndrome in neonates
 
Respiratory distress syndrome
Respiratory distress syndromeRespiratory distress syndrome
Respiratory distress syndrome
 
Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)Respiratory Distress Syndrome (Rds)
Respiratory Distress Syndrome (Rds)
 
Nasal drugdeliverysystem
Nasal drugdeliverysystemNasal drugdeliverysystem
Nasal drugdeliverysystem
 
Pulmonary trauma
Pulmonary traumaPulmonary trauma
Pulmonary trauma
 
Chapter 19-respiratory-distress-syndr
Chapter 19-respiratory-distress-syndrChapter 19-respiratory-distress-syndr
Chapter 19-respiratory-distress-syndr
 
Ventilator associated pneumonia
Ventilator associated pneumoniaVentilator associated pneumonia
Ventilator associated pneumonia
 
Recent advances in pulmonary drug delivery
Recent advances in pulmonary drug deliveryRecent advances in pulmonary drug delivery
Recent advances in pulmonary drug delivery
 
Nasal Injuries
Nasal InjuriesNasal Injuries
Nasal Injuries
 
Acute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome
 
Nasal & Pulmonary Drug Delivery System
Nasal & Pulmonary Drug Delivery SystemNasal & Pulmonary Drug Delivery System
Nasal & Pulmonary Drug Delivery System
 
Complications of 3rd Stage of Labor
Complications of 3rd Stage of LaborComplications of 3rd Stage of Labor
Complications of 3rd Stage of Labor
 
Respiratory distress syndrome in a premature baby
Respiratory distress syndrome in a premature babyRespiratory distress syndrome in a premature baby
Respiratory distress syndrome in a premature baby
 
Trauma in pregnancy
Trauma in pregnancyTrauma in pregnancy
Trauma in pregnancy
 
Respiratory distress of the newborn
Respiratory distress of the newbornRespiratory distress of the newborn
Respiratory distress of the newborn
 
Respiratory Distress in The Newborn
Respiratory Distress in The NewbornRespiratory Distress in The Newborn
Respiratory Distress in The Newborn
 
Abdominal trauma
Abdominal traumaAbdominal trauma
Abdominal trauma
 
Thoracic trauma presentation
Thoracic trauma presentationThoracic trauma presentation
Thoracic trauma presentation
 

Similaire à Acute respiratory distress syndrome

Dr. Radhey Shyam (presentation)
Dr. Radhey Shyam (presentation)Dr. Radhey Shyam (presentation)
Dr. Radhey Shyam (presentation)rsd8106
 
Presentasi text book reading.pptx
Presentasi text book reading.pptxPresentasi text book reading.pptx
Presentasi text book reading.pptxdr. andrea wahyu
 
Presentasi text book reading.pptx
Presentasi text book reading.pptxPresentasi text book reading.pptx
Presentasi text book reading.pptxdr. andrea wahyu
 
Ventilotry managemant of ards
Ventilotry managemant of ardsVentilotry managemant of ards
Ventilotry managemant of ardsDrAvinashKumar6
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndromeAsraf Hussain
 
Acute Respiratory Distress Syndrome ARDS
Acute Respiratory Distress Syndrome ARDSAcute Respiratory Distress Syndrome ARDS
Acute Respiratory Distress Syndrome ARDSvijay mundhe
 
Acute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromePriyaRamalingam6
 
Acute respiratory distress syndrome by dr md abdullah saleem
Acute respiratory distress syndrome  by  dr md abdullah saleemAcute respiratory distress syndrome  by  dr md abdullah saleem
Acute respiratory distress syndrome by dr md abdullah saleemsaleem051
 
ARDS Acute Respiratory Syndrome
ARDS Acute Respiratory SyndromeARDS Acute Respiratory Syndrome
ARDS Acute Respiratory SyndromeDee Evardone
 
ARDS Anaesthesia seminar 2023.pptx
ARDS Anaesthesia seminar 2023.pptxARDS Anaesthesia seminar 2023.pptx
ARDS Anaesthesia seminar 2023.pptxdrsandeepsinghjadon
 
ARDS (acute respiratory distress syndrome) ppt SlideShare
ARDS (acute respiratory distress syndrome) ppt SlideShareARDS (acute respiratory distress syndrome) ppt SlideShare
ARDS (acute respiratory distress syndrome) ppt SlideSharesonam
 
Pediatric Acute Respiratory Distress Syndrome
Pediatric Acute Respiratory Distress Syndrome Pediatric Acute Respiratory Distress Syndrome
Pediatric Acute Respiratory Distress Syndrome Owais Mohd
 

Similaire à Acute respiratory distress syndrome (20)

Dr. Radhey Shyam (presentation)
Dr. Radhey Shyam (presentation)Dr. Radhey Shyam (presentation)
Dr. Radhey Shyam (presentation)
 
Presentasi text book reading.pptx
Presentasi text book reading.pptxPresentasi text book reading.pptx
Presentasi text book reading.pptx
 
Presentasi text book reading.pptx
Presentasi text book reading.pptxPresentasi text book reading.pptx
Presentasi text book reading.pptx
 
Ventilotry managemant of ards
Ventilotry managemant of ardsVentilotry managemant of ards
Ventilotry managemant of ards
 
Acute respiratory distress syndrome
Acute respiratory distress syndromeAcute respiratory distress syndrome
Acute respiratory distress syndrome
 
Acute Respiratory Distress Syndrome ARDS
Acute Respiratory Distress Syndrome ARDSAcute Respiratory Distress Syndrome ARDS
Acute Respiratory Distress Syndrome ARDS
 
Acute Respiratory Distress Syndrome
Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
Acute Respiratory Distress Syndrome
 
Ards and ALI
Ards and ALIArds and ALI
Ards and ALI
 
Acute respiratory distress syndrome by dr md abdullah saleem
Acute respiratory distress syndrome  by  dr md abdullah saleemAcute respiratory distress syndrome  by  dr md abdullah saleem
Acute respiratory distress syndrome by dr md abdullah saleem
 
Ards rahul
Ards rahulArds rahul
Ards rahul
 
ARDS Acute Respiratory Syndrome
ARDS Acute Respiratory SyndromeARDS Acute Respiratory Syndrome
ARDS Acute Respiratory Syndrome
 
ARDS Anaesthesia seminar 2023.pptx
ARDS Anaesthesia seminar 2023.pptxARDS Anaesthesia seminar 2023.pptx
ARDS Anaesthesia seminar 2023.pptx
 
ARDS
ARDSARDS
ARDS
 
Ards
ArdsArds
Ards
 
ARDS (acute respiratory distress syndrome) ppt SlideShare
ARDS (acute respiratory distress syndrome) ppt SlideShareARDS (acute respiratory distress syndrome) ppt SlideShare
ARDS (acute respiratory distress syndrome) ppt SlideShare
 
Ards
ArdsArds
Ards
 
ARDS
ARDSARDS
ARDS
 
ARDS- Satya.pptx
ARDS- Satya.pptxARDS- Satya.pptx
ARDS- Satya.pptx
 
Pediatric Acute Respiratory Distress Syndrome
Pediatric Acute Respiratory Distress Syndrome Pediatric Acute Respiratory Distress Syndrome
Pediatric Acute Respiratory Distress Syndrome
 
Ards
ArdsArds
Ards
 

Dernier

Thyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptxThyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptxRajendra Dev Bhatt
 
Neurological Evaluation of Acute Ischemic stroke in Emergency Room
Neurological Evaluation of Acute Ischemic stroke in Emergency RoomNeurological Evaluation of Acute Ischemic stroke in Emergency Room
Neurological Evaluation of Acute Ischemic stroke in Emergency RoomSudhir Kumar
 
Human Skeletal System_By Anupam Das......
Human Skeletal System_By Anupam Das......Human Skeletal System_By Anupam Das......
Human Skeletal System_By Anupam Das......anupamdas2143
 
(IDE)and(IVD),QMS,21 CFR part820 , 801)
(IDE)and(IVD),QMS,21 CFR part820  , 801)(IDE)and(IVD),QMS,21 CFR part820  , 801)
(IDE)and(IVD),QMS,21 CFR part820 , 801)chahattyagi200
 
Derma Pharmaceutical Franchise Company - Solace Biotech Limited
Derma Pharmaceutical Franchise Company - Solace Biotech LimitedDerma Pharmaceutical Franchise Company - Solace Biotech Limited
Derma Pharmaceutical Franchise Company - Solace Biotech LimitedSBL DIGITAL
 
Problems associated with the production of recombinant protein.pdf
Problems associated with the production of recombinant protein.pdfProblems associated with the production of recombinant protein.pdf
Problems associated with the production of recombinant protein.pdfNetHelix
 
Reproductive and Child Health Services ppt.pptx
Reproductive and Child Health Services ppt.pptxReproductive and Child Health Services ppt.pptx
Reproductive and Child Health Services ppt.pptxVeereshDemashetti
 
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptx
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptxANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptx
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptxsiddharthroy26587
 
Methicillin-resistant Staphylococcus Aureus (MRSA)
Methicillin-resistant Staphylococcus Aureus (MRSA)Methicillin-resistant Staphylococcus Aureus (MRSA)
Methicillin-resistant Staphylococcus Aureus (MRSA)Ahmad Thanin
 
Basic of Thyroid Hormone:- An In-depth Analysis
Basic of Thyroid Hormone:- An In-depth AnalysisBasic of Thyroid Hormone:- An In-depth Analysis
Basic of Thyroid Hormone:- An In-depth AnalysisAshishMaletha2
 
SMA Implementation science seminar (Day 1).pptx
SMA Implementation science seminar (Day 1).pptxSMA Implementation science seminar (Day 1).pptx
SMA Implementation science seminar (Day 1).pptxAbdirahmanWaseem
 
clean rooms and its classification .pptx
clean rooms and its classification .pptxclean rooms and its classification .pptx
clean rooms and its classification .pptxushakiranmai4
 
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...Genesis Institute of Pharmacy, Radhanagari.
 
Ovarian tumors Lecture notes for MBBS.pptx
Ovarian tumors Lecture notes for MBBS.pptxOvarian tumors Lecture notes for MBBS.pptx
Ovarian tumors Lecture notes for MBBS.pptxSizan Thapa
 
INTRODUCTION TO THE FORENSIC SCIENCE.ppt
INTRODUCTION TO THE FORENSIC SCIENCE.pptINTRODUCTION TO THE FORENSIC SCIENCE.ppt
INTRODUCTION TO THE FORENSIC SCIENCE.pptKavitha Krishnan
 
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdf
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdfEMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdf
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdfMayuriGamit2
 
Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptxCholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptxRajendra Dev Bhatt
 
SGK VIÊM KHỚP DẠNG THẤP YHN .pdf
SGK VIÊM KHỚP DẠNG THẤP YHN              .pdfSGK VIÊM KHỚP DẠNG THẤP YHN              .pdf
SGK VIÊM KHỚP DẠNG THẤP YHN .pdfHongBiThi1
 
airway management recorded for S2.pptx
airway management  recorded  for S2.pptxairway management  recorded  for S2.pptx
airway management recorded for S2.pptxnakera38
 

Dernier (20)

Thyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptxThyroid function tests for MBBS, LAB. MED & BDS.pptx
Thyroid function tests for MBBS, LAB. MED & BDS.pptx
 
Neurological Evaluation of Acute Ischemic stroke in Emergency Room
Neurological Evaluation of Acute Ischemic stroke in Emergency RoomNeurological Evaluation of Acute Ischemic stroke in Emergency Room
Neurological Evaluation of Acute Ischemic stroke in Emergency Room
 
Human Skeletal System_By Anupam Das......
Human Skeletal System_By Anupam Das......Human Skeletal System_By Anupam Das......
Human Skeletal System_By Anupam Das......
 
(IDE)and(IVD),QMS,21 CFR part820 , 801)
(IDE)and(IVD),QMS,21 CFR part820  , 801)(IDE)and(IVD),QMS,21 CFR part820  , 801)
(IDE)and(IVD),QMS,21 CFR part820 , 801)
 
Derma Pharmaceutical Franchise Company - Solace Biotech Limited
Derma Pharmaceutical Franchise Company - Solace Biotech LimitedDerma Pharmaceutical Franchise Company - Solace Biotech Limited
Derma Pharmaceutical Franchise Company - Solace Biotech Limited
 
Oral disorders .pptx
Oral disorders .pptxOral disorders .pptx
Oral disorders .pptx
 
Problems associated with the production of recombinant protein.pdf
Problems associated with the production of recombinant protein.pdfProblems associated with the production of recombinant protein.pdf
Problems associated with the production of recombinant protein.pdf
 
Reproductive and Child Health Services ppt.pptx
Reproductive and Child Health Services ppt.pptxReproductive and Child Health Services ppt.pptx
Reproductive and Child Health Services ppt.pptx
 
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptx
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptxANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptx
ANATOMY OF THE CEREBRUM WITH CLINICAL ANATOMY.pptx
 
Methicillin-resistant Staphylococcus Aureus (MRSA)
Methicillin-resistant Staphylococcus Aureus (MRSA)Methicillin-resistant Staphylococcus Aureus (MRSA)
Methicillin-resistant Staphylococcus Aureus (MRSA)
 
Basic of Thyroid Hormone:- An In-depth Analysis
Basic of Thyroid Hormone:- An In-depth AnalysisBasic of Thyroid Hormone:- An In-depth Analysis
Basic of Thyroid Hormone:- An In-depth Analysis
 
SMA Implementation science seminar (Day 1).pptx
SMA Implementation science seminar (Day 1).pptxSMA Implementation science seminar (Day 1).pptx
SMA Implementation science seminar (Day 1).pptx
 
clean rooms and its classification .pptx
clean rooms and its classification .pptxclean rooms and its classification .pptx
clean rooms and its classification .pptx
 
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...
HDT Unit 2: Nutraceuticals Global Market Overview And Growth Of Nutraceutical...
 
Ovarian tumors Lecture notes for MBBS.pptx
Ovarian tumors Lecture notes for MBBS.pptxOvarian tumors Lecture notes for MBBS.pptx
Ovarian tumors Lecture notes for MBBS.pptx
 
INTRODUCTION TO THE FORENSIC SCIENCE.ppt
INTRODUCTION TO THE FORENSIC SCIENCE.pptINTRODUCTION TO THE FORENSIC SCIENCE.ppt
INTRODUCTION TO THE FORENSIC SCIENCE.ppt
 
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdf
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdfEMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdf
EMBRYOLOGY AND FOETAL DEVELOPMENT-mayu.pdf
 
Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptxCholesterol Biosynthesis  and catabolism for MBBS, Lab. MEd. BDS.pptx
Cholesterol Biosynthesis and catabolism for MBBS, Lab. MEd. BDS.pptx
 
SGK VIÊM KHỚP DẠNG THẤP YHN .pdf
SGK VIÊM KHỚP DẠNG THẤP YHN              .pdfSGK VIÊM KHỚP DẠNG THẤP YHN              .pdf
SGK VIÊM KHỚP DẠNG THẤP YHN .pdf
 
airway management recorded for S2.pptx
airway management  recorded  for S2.pptxairway management  recorded  for S2.pptx
airway management recorded for S2.pptx
 

Acute respiratory distress syndrome

  • 1. Acute Respiratory Distress Syndrome Dr. Maged Abulmagd Consultant intensivist,EBGH
  • 2. Synonyms of ARDS • Shock lung • Pump lung • Traumatic wet lung • Post traumatic atelectasis • Adult hyaline membrane disease • Progressive respiratory distress • Acute respiratory insufficiency syndrome • Haemorrhagic atelectasis • Hypoxic hyperventilation • Postperfusion lung • Oxygen toxicity lung • Wet lung • White lung • Transplant lung • Da Nang lung • Diffuse alveolar injury • Acute diffuse lung injury • Noncardiogenic pulmonary edema. • Progressive pulmonary consolidation
  • 3. Timeline • In 1967 – Ashbaugh, Bigelow, Petty, Levine - described Acute Respiratory Distress Syndrome in adults • In 1971, Petty and Ashbaugh modified its name from ‘acute’ to ‘adult’ Respiratory Distress Syndrome; to differentiate it from its newborn counterpart • In 1974, Webb and Tierney confirmed the existence of ventilator associated lung injury
  • 4. Timeline • In 1992, American European Consensus Conference (AECC) gave standardized definition for ARDS • In 1997, Tremblay et al introduced the concept of biotrauma • In 1998, Amato et al, conducted RCT - decrease in mortality using low tidal volume ventilation and high PEEP (open lung strategy) • In 2000, ARDS network trial demonstrated the benefits of low tidal volume and PEEP ventilation
  • 5. Definitions of ARDS Ashbaugh and colleagues, 1967 • Severe dyspnea • Tachypnea • Cyanosis refractory to oxygen therapy • Decreased pulmonary compliance • Diffuse alveolar infiltrates on chest radiograph.  Loosely defined criteria  Definition of hypoxemia inconsistent
  • 6. Bernard and colleagues, 1992 (American European Consensus conference definition) A three-criteria system including chest radiograph, oxygenation score, and exclusion of cardiogenic causes: • Acute onset, bilateral infiltrates on chest radiography, • Acute lung injury ~ PaO2/FIO2 ≤ 300 ARDS subset~ PaO2/FIO2 ≤ 200 • Pulmonary-artery wedge pressure of <18 mm Hg or the absence of clinical evidence of left atrial hypertension
  • 7. Bernard and colleagues, 1992 (American European Consensus conference definition) Problems • Acute onset : arbitrary; <1 week • Bilateral infiltrates: inter observer variation, b/l pneumonia, atelectasis, cardiogenic pulmonary edema • PAOP of <18 mm Hg /absence of clinical evidence of left atrial hypertension : PAOP: poor estimate of PVH, falsely raised with high airway pressures • Acute lung injury present if PaO2/FIO2 is 300 : new and arbitrary value
  • 10. Precipitating Factors Direct Lung Injury • Pneumonia • Aspiration of gastric contents • Pulmonary contusion • Near-drowning • Toxic inhalation injury Indirect Lung Injury • Sepsis • Severe trauma Multiple bone fractures Head trauma Burns • Multiple transfusions • Drug overdose • Pancreatitis • Post-cardiopulmonary bypass
  • 11. Pathophysiology in ARDS Based on the histological appearance - Exudative phase (0-4 days) • Alveolar and interstitial edema • Capillary congestion • Destruction of type I alveolar cells • Early hyaline membrane formation Proliferative Phase (3-10 days) • Increased type II alveolar cells • Cellular infiltration of alveolar septum • Organisation of hyaline membranes Fibrotic Phase (>10 days) • Fibrosis of hyaline membranes and alveolar septum • Alveolar duct fibrosis
  • 12. Pathology in ARDS Mechanisms in early phase - • Release of inflammatory cytokines – TNF alpha, IL- 1,6,8 • Failure of alveolar edema clearance, epithelial and endothelial damage • Increased permeability of alveolo – capillary membrane • Neutrophil migration and oxidative stress • Procoagulant shift – fibrin deposition • Surfactant dysfunction Mechanism in late (repair) phase – • Fibroproliferation -TGF beta, MMPs, thombospondin, plasmin, ROS • Remodelling - matrix and cell surface proteoglycans, MMP, imbalance of coagulation and fibrinolysis.
  • 14. D/D : Hydrostatic pulmonary edema  PCWP ≥ 18 mmHg  Causes : • Cardiogenic – LVF (eg. MI, myocarditis) cardiac valvular disease (aortic, mitral) • Vascular – systemic HTN, pulmonary embolism • Volume overload - excessive iv fluids, renal failure
  • 15. Cardiogenic vs Non-cardiogenic edema 1.1. Prior h/o cardiac diseasePrior h/o cardiac disease 22.Third heart sound.Third heart sound 3.3. CardiomegalyCardiomegaly 44. Infiltrates : Central distribution. Infiltrates : Central distribution 55. Widening of vascular pedicle No widening of vascular pedicle. Widening of vascular pedicle No widening of vascular pedicle ( ↑ width of mediastinum)( ↑ width of mediastinum)6.6. PA wedge pressurePA wedge pressure 7.7. Positive fluid balancePositive fluid balance Cardiogenic Absence of heart diseaseAbsence of heart disease No third heart soundNo third heart sound Normal sized heartNormal sized heart Peripheral distributionPeripheral distribution N orN or ↓↓ PA wedge pressurePA wedge pressure Negative fluid balanceNegative fluid balance Non-cardiogenic
  • 16. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation - 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 17. Management contd. • Non conventional/Salvage interventions a. High frequency ventilation b. Airway pressure release ventilation c. Tracheal gas insufflation d. Inverse ratio ventilation e. Inhaled nitric oxide f. Inhaled prostacyclin g. Corticosteroids h. Surfactant administration i. Liquid ventilation j. Extracorporeal membrane oxygenation • Supportive therapy – nutrition, prevention of infection
  • 18. Concept of VALI  Mechanical ventilation - Basic care in critically ill ICU patients  May cause or worsen lung injury – ventilator induced/associated lung injury  Components – • Barotrauma • Volutrauma • Atelectrauma • Biotrauma
  • 20. Concept of ‘baby lung’ • Put forward by Gattinoni and colleagues first in 1987 • Lung injury in ARDS - non homogenous, basal • Edema and consolidation > dependent lung regions - ↑ density of dorsal regions • Aerated ventral regions – ‘baby lung’ (300-500gms) – high compliance • Ventilation of baby lung with normal tidal volumes and pressures – alveolar over distension – injury to functional lung tissue
  • 21. Management Lung protective ventilation ARDS network protocol • Goals  Oxygenation : PaO2 55-80 mmHg, or SpO2 88 – 94% (excluding pregnancy, intracranial hypertension or stroke where SaO2 goal>94%)  Ventilation :  Tidal volume : 4-6 ml/kg ideal body weight  Plateau pressure : <30cmH2O  Ph: 7.25-7.35  I:E ratio of 1:1 – 1:3
  • 22. Management contd. Oxygenation • Initially high Fio2 given (1.0) to correct hypoxia • Fio2 and PEEP adjusted to the lowest level compatible with the oxygenation goals • Fio2 and PEEP adjusted in the following fixed combinations {fio2/PEEP(mmHg)} 0.3 0.4 0.4 0.5 0.5 0.6 0.7 0.7 0.7 0.8 0.9 0.9 0.9 1.0 5 5 8 8 10 10 10 12 14 14 14 16 18 20- 24 FIO2 PEEP
  • 23. Management contd Initial ventilator set up and adjustments STEP 1- Calculation of ideal body weight(IBW):  For males, IBW(kg) = 50+2.3{height(inch)– 60} Or IBW(kg)=50 + 0.91{height(cm)–152.4}  For females, IBW(kg) = 45.5+2.3{height(inch)– 60} Or IBW(kg)=45.5 + 0.91{height(cm)–152.4}
  • 24. Management contd STEP 2 - Volume assist control selected as ventilator mode  Initial tidal volume (TV) set at 8ml/kg IBW  TV reduced by 1ml/kg IBW 2 hourly until TV = 6ml/kg IBW  Initial ventilator rate set to maintain baseline minute ventilation( not >35/min)  TV and respiratory rate adjusted to achieve the pH and plateau pressure goals  Inspiratory flow rate set above patients demand (usually >80L/min)
  • 25. Open Lung Approach • Introduced by Amato et al in 1998 – use of low tidal volume + high PEEP+ recruitment (Open lung strategy) – reduce mortality in ARDS • Maintaining inflation & deflation between 2 inflection points during entire respiratory cycle • Ventilatory settings - PEEP >Pflex & TV reduced so that Pplat < UIP • Advantages- avoids repetitive opening and closing of alveoli (VALI) - minimizes shear injury
  • 27. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management – protective lung ventilation strategy role of ‘open lung approach’  Adjuncts to core ventilation – 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 28. Fluid restriction in ARDS • Rationale – alveolar flooding depends on : 1. Capillary hydrostatic pressure 2. Oncotic pressure 3. Alveolar–capillary permeability • Capillary permeability increased in ARDS • ↓ hydrostatic pressure and ↑ oncotic pressure may help.
  • 29. Fluid therapy in ARDS Recommended : • Central venous pressure guided therapy – 10-14 mmHg ( ARDS Network Trial 2003) • Restricted fluid intake • Increased urine output – Diuretics or RRT Not recommended : • Vasodilators • Albumin
  • 30. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 31. Permissive Hypercapnia • Hickling and colleagues 1990 • “Degree of hypercapnia permitted in patients subjected to lower tidal volumes” • Upper limit – not defined; >100 mmHg avoided  Advantages • Increased surfactant secretion (animal models) – improved V/Q match, oxygenation (improved compliance) • Increased cardiac output and oxygen delivery (sympathoadrenal effects predominate over cardiodepressant effects) • Increased cerebral blood flow and tissue oxygenation
  • 32. Permissive Hypercapnia  Concerns • Increase in pulmonary vascular resistance • Impaired diaphragmatic function (impairs afferent transmission) • Decrease in cardiac contractility • Raised intracranial tension  Individualize and treat
  • 33. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 34. Prone Position Ventilation  First suggested by Piehl and Brown in 1976  Offers improved oxygenation by: • Increased FRC • Change in regional diaphragm motion • Distribution of perfusion • Better clearance of secretions
  • 35. Prone Position Ventilation • Sud and colleagues conducted – meta-analysis of 13 RCTs (1559 patients) on supine and prone position ventilation in ARDS/ALI patients  Median MV of 12 hours ( 4-24hrs) for 4 days( 1-10 days)  Conclusion -cannot be recommended for routine Mx -no evidence of improved survival • Gattinoni et al suggested no overall reduction in mortality except in very sick patients ( SAPS II Score >50) • No decrease in ventilator associated pneumonia
  • 36. Problems of prone position • Facial edema • Airway obstruction • Difficulties with enteral feeding • Transitory decrease in oxygen saturation • Hypotension & Arrhythmias • Vascular and nerve compression • Loss of venous accesses and probes • Loss of chest drain and catheters • Accidental extubation • Apical atelectasis d/t incorrect positioning of the tracheal tube • Increased need for sedation
  • 37. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation – 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 38. Recruitment maneuvers • High pressure inflation maneuver aimed at temporarily raising the transpulmonary pressure above levels typically obtained with mechanical ventilation • Types – Elevated sustained pressures : 40 cm H2O for 40 seconds Sigh breaths : ↑ tidal volume / PEEP for one or several breaths Extended sigh breath : VCV with PEEP well above LIP for a longer time • More effective in early ALI and those with more homogenous disease; atelectasis > consolidation.
  • 39. Recruitment maneuvers Adverse effects • Hypotension • Barotrauma • Raised ICP • Haemodynamic instability
  • 40. Management contd. • Non conventional/Salvage interventions a. High frequency ventilation b. Airway pressure release ventilation c. Tracheal gas insufflation d. Inverse ratio ventilation e. Inhaled nitric oxide f. Inhaled prostacyclin g. Corticosteroids h. Surfactant administration i. Liquid ventilation j. Extracorporeal membrane oxygenation • Supportive therapy – nutrition, prevention of infection
  • 41. High Frequency Ventilation • Mechanical ventilatory support using higher than normal breathing frequencies • Smaller tidal pressure swings (within inflection points) along with apt mpaw • Smaller tidal volumes and higher mean pressure utilized for lung protection • Special ventilators required • Types - High Frequency Jet Ventilation (HFJV) High Frequency Oscillatory Ventilation (HFOV)
  • 42. HFV HFJV • A nozzle/injector creates high velocity ‘jet’ of gas directed into the lung • Injectors – 1-3mm diameter • Expiration is passive • Frequencies available – upto 600 breaths/min • Available for neonatal and paediatric use only HFOV • Characterized by rapid oscillations of a diaphragm (at 3 to 10 hertz i.e 180 to 160 breaths/min) driven by a piston pump • Frequencies available – 300-3000 breaths/min • Expiration is also active – risk of air trapping minimal
  • 43. HFV contd Advantages • Better oxygenation and ventilation • Aids lung recruitment (high mpaw) • Reduces oxygen toxicity (high mpaw) • Minimizes VILI Disadvantages • Delivered tidal volumes difficult to monitor • Deep sedation and/or paralysis required • Inadequate humidification • Direct physical airway damage
  • 44. Airway Pressure Release Ventilation • Alternative mode of ventilation that applies a form of CPAP that is released periodically, augmenting CO2 release. • Pressure limited, time cycled mode • Permits spontaneous ventilation throughout the respiratory cycle • Based on the ‘open lung’ concept – maximize and maintain recruitment throughout the respiratory cycle
  • 45. APRV contd • Uses 2 airway pressures – P high and P low; 2 set time periods – T high and T low, usually T high>T low • P high is set above the closing pressure of recruitable alveoli (lower inflection point) • Set T high maintains the P high for several seconds • T low helps remove CO2
  • 46. APRV contd Potential benefits : • ↑ V/Q match • ↓ diaphragmatic atrophy during critical illness • ↑ cardiac output and oxygen delivery • ↑ splanchnic perfusion • ↑ renal and hepatic function • Fewer days on mechanical ventilation • Fewer days in ICU
  • 47. Tracheal Gas Insufflation • Normal ventilatory cycle - bronchi and trachea filled with alveolar gas at end expiration • In the next inspiration, CO2 laden gas forced back into alveoli. • TGI - stream of fresh gas (at 4-8L/min) insufflated through a small catheter/channels in the wall of endotracheal tube into the lower trachea • CO2 laden gas flushed out of the trachea before next inspiration
  • 48. Tracheal Gas Insufflation contd. Disadvantages • Dessication of secretions • Inadequate humidification • Airway mucosal injury • Accumulation of secretions in the TGI catheter • Creation of auto PEEP from expiratory flow and resistance of the ventilator-exhalation tubes and valve
  • 49. Inverse Ratio Ventilation • Alternative mode of ventilation • Entails use of prolonged inspiratory times (I:E>1) using volume or pressure cycled mode of mechanical ventilation • Proposed mechanism of action – alveolar recruitment at lower airway pressures, optimal distribution of ventilation • Concerns – generation of auto PEEP reduced cardiac output ( ↑ MAP)
  • 50. Inhaled Nitric Oxide  NO – endogenous vasodilator, from endothelium  Vasodilatation of alveolar circulation reduces shunt and pulmonary hypertension  Problems: • toxic nitrogen compounds • methemoglobinemia • pulmonary edema, acute RHF (interrupted flow) • rebound pulmonary hypertension • expensive  Routine use not recommended
  • 51. Inhaled Prostacyclin • Cause vasodilation, inhibit platelet aggregation, reduction of neutrophil adhesion and activation, ↓ pulmonary hypertension, improved oxygenation • Minimal systemic effects, harmless metabolites, no requirements for monitoring • Both positive and negative results obtained in various trials • Presently not recommended
  • 52. Corticosteroids • Established ARDS – characterized by alveolar fibrosis • Anti-inflammatory and antifibrotic properties of steroids – probable role in ARDS • No role in preventing but may help in treating ARDS
  • 53. Surfactant Therapy • Reduces alveolar surface tension • Prevents alveolar collapse • Anti inflammatory properties • Anti microbial properties • Exogenous surfactant – successful in neonatal respiratory distress syndrome (reduced surfactant production) • ARDS in adults – increased surfactant removal, altered composition, reduced efficacy, reduced production • Surfactant therapy not recommended in adults
  • 54. Liquid Ventilation • Involves filling the lung with liquid • Removes the air liquid interface and supports alveoli, prevents collapse • Perfluorocarbons – have low surface tension, dissolve oxygen and carbon dioxide readily, non toxic, minimally absorbed, eliminated by evaporation though lungs • Lowered surface tension may improve alveolar recruitment, arterial oxygenation, increased lung compliance • Can recruit dependent alveoli (advantage over PEEP)
  • 55. Liquid Ventilation contd. Types : • Total – filling the entire lung with liquid, ventilated with a special ventilator - Expensive • Partial - filling the lung to FRC with liquid, ventilated with conventional ventilator - Appropriate dose of PFC still to be determined - ↑ chances of pneumothoraces, hypoxic episodes, hypotensive episodes • PFC radiodense – impossible to detect infection or follow the progress of healing in a chest radiograph • Liquid ventilation is not FDA approved
  • 56. Extracorporeal Membrane Oxygenation • Invasive, complex form of cardiopulmonary bypass • Provides temporary gas exchange and blood circulation outside the body • Severe but potentially reversible respiratory failure • Such periods of “lung rest” allow the lungs to recover • Used when conventional strategies fail • No good evidence available over conventional management
  • 57. ECMO contd. Types • Veno - arterial – a catheter placed in both vein and artery. Provides support both for heart and lungs • Veno - venous – single double lumen catheter placed in the vein. Provides support only for lungs • ECMO allows ventilator pressures and volumes to be decreased to prevent further VILI • Reduction in intra - thoracic pressure allows fluid removal from lungs with less risk of cardiovascular instability
  • 58. ECMO contd Complications : • Haemorrhage • Renal failure • Haemolysis • Hypotension/ hypertension • Pneumothorax • Infections
  • 59. Management contd. • Salvage interventions a. High frequency oscillatory ventilation b. Airway pressure release ventilation c. Tracheal gas insufflation d. Inverse ratio ventilation e. Inhaled nitric oxide f. Inhaled prostacyclin g. Corticosteroids h. Surfactant administration i. Liquid ventilation j. Extracorporeal membrane oxygenation • Supportive therapy – nutrition, prevention of infection
  • 60. Nutrition • Enteral over parenteral • High fat – low carbohydrate diet advocated - ↓ CO2 • Immuno modulatory nutrients -amino acids - arginine and glutamine -ribonucleotides -omega-3 fatty acids • Diet rich in fish oil, γ-linolenic acid, and antioxidants • Standard nutritional formulations recommended
  • 61. Antibiotics • Infection - present initially : nonpulmonary sepsis • Develop later - nosocomial infections : pneumonia and catheter- related sepsis. • Aim : identify, treat, and prevent infections. • Most pneumonia > 7 days • Prompt initiation of appropriate empiric therapy. • Hand washing by medical personnel • New areas : - continuous suctioning of subglottic secretions to prevent their aspiration -development of new endotracheal tubes - resist formation of bacterial biofilm that can be embolized distally with suctioning.
  • 62. Management • Treatment of the precipitating cause • Mechanical ventilation –  Core ventilator management - protective lung ventilation strategy - role of ‘open lung approach’  Adjuncts to core ventilation - 1. Fluid restriction 2. Permissive hypercapnia 3. Prone positioning 4. Recruitment maneuvers
  • 63. Management contd. • Non conventional/Salvage interventions a. High frequency ventilation b. Airway pressure release ventilation c. Tracheal gas insufflation d. Inverse ratio ventilation e. Inhaled nitric oxide f. Inhaled prostacyclin g. Corticosteroids h. Surfactant administration i. Liquid ventilation j. Extracorporeal membrane oxygenation • Supportive therapy – nutrition, prevention of infection
  • 64. Complications associated with ARDS • Pulmonary: barotrauma ,volutrauma, pulmonary embolism, pulmonary fibrosis, ventilator-associated pneumonia (VAP), Oxygen toxicity • Gastrointestinal: haemorrhage (ulcer), dysmotility, pneumoperitoneum, bacterial translocation • Cardiac: Arrhythmias, myocardial dysfunction • Renal: acute renal failure (ARF), fluid retention • Mechanical: vascular injury, tracheal injury/stenosis (result of intubation and/or irritation by endotracheal tube) • Nutritional: malnutrition, anaemia, electrolyte deficiency
  • 65. Long term sequelae of ARDS • Pulmonary function – mild impairment, improves over 1 year • Neurocognitive dysfunction • Post traumatic stress disorder • Physical debilitation
  • 66. Infantile Respiratory Distress Syndrome • Hyaline membrane disease • Deficiency of surfactant : insufficient production in immature lungs, immature babies • Genetic mutation in one of the surfactant proteins, SP-B – rare, full term babies • Prevention : avoidance of premature birth, corticosteroids • Treatment : surfactant replacement
  • 67. References • Harrison’s Principle of Internal Medicine, 16th ed. • Christie JD, Lanken PN. Acute lung injury and the acute respiratory distress syndrome. Critical Care – Hall • Foner BJ, Norwood SH, Taylor RW. Acute respiratory distress syndrome. Critical Care, 3rd ed. Civetta • Wiener-Kronish JP, et al. The adult respiratory distress syndrome : definition and prognosis, pathogenesis and treatment. BJA 1990; 65: 107-129. • Clinical Anaesthesia. Barash, 6th ed. • Egans Respiratory Care, 7th e
  • 68. References • Acute respiratory distress syndrome network. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med. 2000;242:1301-1308 • Brower RG, Morris A, MacIntyre N, et al. Effects of recruitment maneuvers in patients with acute lung injury and acute respiratiry distress syndrome ventilated with high positive end expiratory pressure. Crit Care Med.2003;31:2592-2597 • Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low volume pressure limited ventilationwith permissive hypercapnia in severe adult respiratory distress syndrome. Intensive care med. 1990;16:372-377 • Hickling KG, Walsh J,Henderson S, Jackson R. Low mortality rate in acute respiratiry distress syndrome using low volume pressure limited ventilation with permissive hypercapnia: a prospective study. Crit Care Med.1994;22:1568-1578