12/20/13

1
12/20/13

2

ACUTE RESPIRATORY
DISTRESS SYNDROME
Dr RAHUL ARORA
12/20/13

3

ETIOLOGY
&
PATHOGENESIS
ARDS- Definition
Acute Respiratory Distress Syndrome
is diffuse pulmonary parenchymal
injury associated with :
Non Cardiog...
Distinguishing cardiogenic from noncardiogenic pulmonary oedema.

CARDIOGENIC

NON- CARDIOGENIC

 Heart disease.
 Third ...
History of ARDS

 Petty Ashbaugh Severe Dyspnea, Tachypnea

et. al ,1971

12/20/13

Cyanosis refractory to O2
Decreased P...
History contd….

 Murray et al

1988

Preexisting Lung injury
Mild to moderate or
severe lung injury
Non pulmonary organ
...
History contd….
 Bernard et

al 1994

Acute onset
Bilateral infiltrates on
chest x-ray
PAWP <18 Mm Hg
Absence of clinical...
Synonyms
 Adult hyaline membrane disease
 Congestive atelectasis
 Progressive pulmonary consolidation
 Hemorrhagic ate...
DAD(Diffuse Alveolar Damage )
 DAD is a series of consistent although non

specific pathological change in the lung that ...
Inflammatory reaction

12/20/13

11
components of DAD
 Initiating Agents
 activation of inflammatory cascade
 Lung sequestration of neutrophils
 Release o...
AETIOLOGY

PULMONARY

12/20/13

EXTRA-PULMONARY

13
Etiology (contd….)
Direct lung injury(pulmonary)









12/20/13

Pneumonia ( most common )
Aspiration
Pulmonar...
Etiology (contd….)
Indirect lung injury
( Extra-pulmonary)

12/20/13











Sepsis (most common) – bacterial/...
TRALI :
Sudden onset of non-cardiogenic
pulmonary edema
 Often with systemic hypovolemia and
hypotension occuring during ...
ARDS
A : ASPIRATION
R : ROAD TRAFFIC ACCIDENTS
D : DIFFUSE ALVEOLAR DISEASE
S : SEPSIS

12/20/13

17
Pathogenesis of ARDS
Focus of infection
Endotoxin

Complement
Activation

direct cellular
injury

Clotting cascade

Cellul...
Inflammatory mediators
 Cytokines
 Complement proteins
 Coagulation proteins
 Prostaglandins
 Vaso-active peptides
 ...
12/20/13

20

PATHOPHYSIOLOGY
& DIAGNOSIS
Dr Siva Krishna Kota
Definition
Acute onset life threatening respiratory
failure with characteristic

Physiological
features

Pathological
feat...
Pathophysiology
Profound inflammatory response secondary to a
pulmonary or extrapulmonary insult.
Diffuse alveolar damage
...
(a) Exudative phase
 Basement membrane disruption
--Type I pneumocytes destroyed
--Type II pneumocytes preserved

 Surfa...
Exudative phase

12/20/13

24
Exudative phase

12/20/13

25
Exudative phase (contd….)
 Microatelectasis / alveolar collapse

-- interstitial edema
-- necrosed capillary endothelial
...
Exudative phase (contd….)

12/20/13

27
(b) Fibroproliferative phase
 Type II pneumocyte proliferate
-differentiate into Type I cells
-reline alveolar walls
-Reg...
Fibro-proliferative phase

12/20/13

29
(c) Fibrotic phase
 Characterized by:
– local fibrosis
– vascular obliteration
 Repair process:
– resolution or fibrosis...
Clinico-pathological
correlation

12/20/13

Stage I : unless direct lung injury is there
clear on auscultation
CXR unremar...
ARDS : Physiological features
A. Decreased lung compliance and volumes
microatelectasis
altered surfactant production & fu...
Physiological features (contd….)
C. Alteration in gas exchange (hypoxia)
- perfusion of underventilated lung
- perfusion o...
ARDS: Radiological feature
Vascular pedicle
< 55mm
No distention of UL
zone vessels
Peripheral shadows
No pleural effusion...
Criteria for diagnosis
Clinical setting
Chest Xray findings
Physiological parameters
Pathological features

DIAGNOSIS
12/2...
Criteria for diagnosis
A. Clinical Settings :

(i) pulm/extrapulm catastrophe
(ii)exclusion of chronic pulmonary &
left he...
Criteria for diagnosis ( cont..)
C. Physiologic parameters :
(i) ABG :PaO2< 50 with FiO2 of > 0.6
(ii)Compliance < 50 ml/ ...
ALI (MURRAY) SCORE :
A. Chest Xray findings
(alveolar consolidation)
B. Oxygenation status
(PaO2 / FiO2 )
C. Pulmonary com...
ALI score (MURRAY-score)

1.

Chest X film finding

Alveolar consolidation
One quadrant
Two quadrant
Three quadrant
Four q...
ALI score (MURRAY-score)

3. Pulmonary compliance

4. PEEP settings

Compliance
(ml/cmH2O)

PEEP
(cmH2O)

cont…..

> 80
60...
ALI score (contd….)

Score:
0
0.1-2.5
> 2.5

12/20/13

= none,
= mild - moderate
= severe

41
12/20/13

42

VENTILATORY
MANAGEMENT OF ARDS
Dr Pallavi Marghade
Treatment Strategies



Rx underlying cause

 Respiratory therapy for adequate

oxygenation/ventilation

 Adjunctive th...
Aims of Respiratory therapy
 to attempt to avoid tracheal intubation
 to reduce maximum pulmonary pressures

generated
...
Conventional ventilation
 Consists of large tidal volume of 10-

15ml/kg
 Arterial oxygenation supported by
raising Fio2...
Ventilator-Induced Lung
Injury(VALI)
Conventional ventilation
In injured lungs
High peak inflation and plateau pressure
Ov...
VALI : Volutrauma
Direct physical damage to A-C membrane
stress failure
sudden & rapid increase in permeability
Gattinoni ...
Flow L/min

60

0

60

Paw - Time

20

0

Volume - Time

600

VT ml

Paw cmH2O

VCV

Flow - Time

0
12/20/13

Time

48
VALI (contd…..)
Barotrauma Application of excessive pressure to the alveoli
Air passes from damaged A-C membrane into
the ...
Flow - Time
Flow L/min

60

PCV

0

60

Paw cmH2O

20

Paw - Time

0

Volume - Time

VT ml

600

0
12/20/13

Time

50
VALI (contd….)
Cyclical airway closure –
Repeated opening & closing of airways with each tidal
volume
Atelectrauma
Surfact...
How does PEEP work?
20

0

12/20/13

52
Mechanism of PEEP

12/20/13

53
PEEP Vs Fio2 : A Dilemma

 PEEP reduces intrapulmonary shunt and improves

arterial oxygenation at lower Fio2
 PEEP
card...
“Open-Lung ” Approach to PEEP
 “Open-lung” approach
– Not practical
– Does not improve
outcomes
 Optimal PEEP
– ???
– Mo...
Fio2
 No detectable oxygen toxicity Fio2<

50%
 Diseased lungs more prone to injury
due to hyperoxia
 Fio2 < 0.6 consid...
Optimal PEEP
 Maximize O2 delivery

DO2 = 10 x CO x (1.34 x Hb x SaO2)
 Maximize lung compliance
Crs = Vt/(Pplateau – PE...
ARDS Network protocol

FIO2 - 0.3 0.4 0.5 0.6
0.3
0.4 0.5 0.6

0.7 0.8 0.9 1.01.0
0.7
0.8
0.9

PEEP -

10-14

12/20/13

5
...
Lung-Protective Ventilation
 VT = 6 mL/kg
 Limit plateau pressures < 30 cmH2O
– Volume controlled ventilation

 Limit p...
Outcome

12/20/13

60
Lung-Protective Ventilation

 Complications: (derecruitement)
– Elevated PaCO2
• Limit: pH > 7.20 –7.25

– Worsening hypo...
Alternate Modes of
Mechanical Ventilation
 Non invasive ventilation
 Inverse-ratio ventilation
 Airway pressure-release...
Non Invasive
Positive Pressure Ventilation
 Tight fitting face

mask as a interface
between the ventilator
and patient.
...
NIPPV (contd….)
ADVANTAGES
 Can maintain verbal communication

 Can eat during therapy
 Decreased incidence of nosocomi...
Proportional-Assist ventilation
 Elevates airway pressure during inspiration
 Inspiratory airway pressure varies directl...
Inverse Ratio Ventilation
 Atelectatic alveoli are recruited and stabilised by

increasing the duration of inspiration
 ...
Normal ventilation
Flow L/min

60

I

E

I

E

0

60

12/20/13

Flow - Time

67
Inverse ratio ventilation
I

E

I

E

I

E

Flow L/min

60

0

60

12/20/13

Reduce auto-PEEP by reducing I-time
- Decreas...
Airway Pressure
Release Ventilation
 Similar to IRV but Pt. can breath

spontaneously during prolonged period of
increase...
TRACHEAL GAS INSUFFLATION
(TGI)
In ARDS/ALI
1. Increase physiological dead space
2. permissive hypercapnia
DURING CONVENTI...
TGI (contd…..)
IN TGI
Stream of fresh air (4 to 8 L/min)
insufflated through a small catheter or
through small channel in ...
HIGH FREQUENCY VENTILATION
Utilizes small volume (<VD) and high RR (100 b/min)
 Avoids over distention (VALI).
 Alveolar...
Prone Ventilation
Proposed mechanism – how it improves oxygenation
1) Increase in FRC
2) Improved ventilation of previousl...
Prone ventilation (contd….)
c)
c)
1.
2.
3.

Decrease chest wall compliance in p.p
Redistribution of tidal volume to atelac...
Prone Ventilation (contd…)

12/20/13

75
PRONE VENTILATION (contd….)
CONTRAINDICATION
Unresponsive cerebral hypertension
Unstable bone fractures
Left heart failure...
PRONE VENTILATION (contd….)
NO. OF PERSONS 3-5
POSITION OF ABDOMEN
allowed to protrude ; partial/complete restriction
POSI...
EXTRACORPOREAL
MEMBRANE OXYGENATION
Adaptation of conventional cardiopulmonary bypass technique.
Oxygenate blood and remov...
ECMO (contd….)
TYPES
1.

High-flow venoarterial bypass system.

2.

Low-flow venovenous bypass system.

Criteria for treat...
ARDS study : KEM Hospital
Statistics:
 study done over 2 years,
 mortality – 46.2%
 commonest etiology – pneumonia &
tr...
ARDS study : KEM Hospital (contd….)

 60% of pts required mechanical ventilation
 survivors spent less no. of days than ...
12/20/13

82

ADJUNCTIVE THERAPY
IN ARDS
Dr Prashant Pawar
Adjunctive therapies
1.
2.
3.
4.
5.
6.

7.
8.
9.
12/20/13

Treatment of infective complications/inciting cause
Hemodynamic...
Treatment of infective
complications
Most common complication is nosocomial
infection due to gram negative organisms and i...
HEMODYNAMIC MANAGEMENT
 Controversial
 Restrictive Fluid management
 Benefits shown by studies

∀ ↓pulmonary edema form...
Fluid management (contd..)
Detrimental effects
Ineffective Circulatory Volume (Sepsis).
Reduced cardiac output and decreas...
Vasopressors
Vasopressors
 Following restoration of intravascular volume to

euvolemic levels
(CVP:4-8cm of H2O, PCWP:6-1...
Nutritional support
Goals of nutritional support
 nutrients as per pt’s metabolic demand
 Treatment & prevention of macr...
Selective pulmonary
vasodilators
1.
2.
3.
4.
5.

12/20/13

Inhaled Nitric oxide (iNo)
iv almitrine with/without iNo.
Aeros...
Inhaled nitric oxide
Mechanism : Endothelial derived relaxing factor
Smooth muscle vasodilation through
activation of cycl...
Inhaled nitric oxide

 DOSAGE:

Effect
Increase PaO2
decrease PAP

Dose
1-2 ppm to <10 ppm
10-40 ppm

 Time of Response ...
Inhaled nitric oxide
Side effects :
Usually Minimal
1. Rebound pulmonary hypertension & hypoxemia
2. Methemoglobinemia
3. ...
Almitrine

 Given iv : in low doses
 Potentates hypoxic pulmonary vasoconstriction
 Decreases shunt and thus improved o...
Pulmonary vasodilators(contd…)
Prostacyclins:




iv prostacyclin decreases pulmonary arterial pressure non
selectively...
Surfactant replacement
therapy






12/20/13

Deficiency and functional abnormality of surfactant
1. Decreases produc...
Surfactant Delivery Techniques
Instillation
• Rapid

Lavage
• May remove toxic

volume
•Homogenous
distribution

substance...
Anti inflammatory therapy
Glucocorticoids:
 No evidence of benefit in early sepsis/ARDS
 Methyl prednisolone in late sta...
Anti infl. Therapy(contd….)
Lisophylline & Pentoxifyline


Phosphodiesterase inhibitor
-Inhibit neutrophil chemotaxis & a...
Cycloxygenase inhibitors






12/20/13

TxA2 and Prostaglandin produced from AA by
Cyclooxygenase pathway.
Cause
1. N...
Antioxidants therapy
 Reactive oxygen metabolites derived from neutrophils,







12/20/13

macrophages and endothel...
ANTICOAGULANT THERAPY
IN ARDS
In ARDS – Fibrin deposition intra-alveolar and interstitial.
Local procoagulant activity and...
Activated Protein- C







12/20/13

Protein-c :Naturally occuring anticoagulant
1.Inactivates Va & VIIa – limit thro...
ARDS and β-agonists
ENHANCED RESOLUTION
ALVEOLAR EDEMA
Alveolar clearance of edema depends on
active sodium transport acro...
Partial Liquid Ventilation
In ARDS there is increased surface tension which can be
eliminated by filling the lungs with li...
Partial Liquid Ventilation (contd.. ..)
Mechanism of action





A.
B.

12/20/13

Reduces surface tension
Alveolar rec...
Partial Liquid Ventilation (contd..)

Total Liquid
Ventilation

Partial Liquid
Ventilation

1. Ventilator

Liquid

Convent...
Partial Liquid Ventilation (contd..)
Recommended dose of PFC
20ml/kg
-Beyond this dose – decrease
cardiac output
-More cli...
Mystery Unsolved

12/20/13

THRIVE FOR THE BEST

108
12/20/13

109

What have we learnt?
ALI- Syndrome of
pulmonary inflammation,
 vasoconstriction,
greater permeability of...
ARDS
 Not a single disease but rather a

pathophysiologic syndrome
 Catastrophic acute respiratory failure of
diverse et...
ARDS
 Associated with triggering events.
 Lungs bear the brunt of the injury as it

receives entire C O with exposure to...
ARDS
Dysregulated inflammatory-reparative processes  lung
injury & repair
 Important to understand the initiators & medi...
ARDS- notions about fluid
therapy
 Hypovolemia – major pathophysiologic factor of

ARDS
 Pulmonary edema – an effect, no...
ARDS: Lung Protection
Evidence supports a volume and pressure
limited approach
 In majority of patients with ARDS lung
re...
ARDS: Lung Protection




12/20/13

Use of high PEEP and
Recruitment maneuvers
may not help when low
potential for recru...
The Future
 Quantify the degree of primary v secondary

ARDS, to optimise ventilation strategy.
 Monitor Real Time chang...
The
End

12/20/13

117
12/20/13

118
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ARDS

  1. 1. 12/20/13 1
  2. 2. 12/20/13 2 ACUTE RESPIRATORY DISTRESS SYNDROME Dr RAHUL ARORA
  3. 3. 12/20/13 3 ETIOLOGY & PATHOGENESIS
  4. 4. ARDS- Definition Acute Respiratory Distress Syndrome is diffuse pulmonary parenchymal injury associated with : Non Cardiogenic Pulmonary Edema resulting in severe respiratory distress and hypoxemic respiratory failure 12/20/13 4
  5. 5. Distinguishing cardiogenic from noncardiogenic pulmonary oedema. CARDIOGENIC NON- CARDIOGENIC  Heart disease.  Third heart sound  Absence of heart  Central distribution of infiltrates  Widening of vascular pedicles. 12/20/13 disease  No third heart sound  Peripheral distribution  Normal width of vascular pedicle 5
  6. 6. History of ARDS  Petty Ashbaugh Severe Dyspnea, Tachypnea et. al ,1971 12/20/13 Cyanosis refractory to O2 Decreased Pulmonary compliance Atelectasis, vascular congestion, hyaline membrane at autopsy. 6
  7. 7. History contd….  Murray et al 1988 Preexisting Lung injury Mild to moderate or severe lung injury Non pulmonary organ dysfunction 12/20/13 7
  8. 8. History contd….  Bernard et al 1994 Acute onset Bilateral infiltrates on chest x-ray PAWP <18 Mm Hg Absence of clinical evidence of left atrial hypertension 12/20/13 8
  9. 9. Synonyms  Adult hyaline membrane disease  Congestive atelectasis  Progressive pulmonary consolidation  Hemorrhagic atelactasis  Pump lung  Shock lung  Wet lung  White lung 12/20/13 9
  10. 10. DAD(Diffuse Alveolar Damage )  DAD is a series of consistent although non specific pathological change in the lung that result from any injurious factor that damage ENDOTHELIUM or ALVEOLAR EPITHELIUM 1) BRONCHIOLITIS OBLITERANS ORGANISING PNEUMONIA 2) ACUTE INTERSTITIAL PNEUMONIA DAD follows known catastrophic event that result in ARDS Sudden idiopathic Respiratory failure without history of catastrophic event seen in AIP 12/20/13 10
  11. 11. Inflammatory reaction 12/20/13 11
  12. 12. components of DAD  Initiating Agents  activation of inflammatory cascade  Lung sequestration of neutrophils  Release of neutrophilic cytotoxic products ALVELOAR WALL INJURY 12/20/13 12
  13. 13. AETIOLOGY PULMONARY 12/20/13 EXTRA-PULMONARY 13
  14. 14. Etiology (contd….) Direct lung injury(pulmonary)          12/20/13 Pneumonia ( most common ) Aspiration Pulmonary contusion Fat emboli Near drowning Inhalation injury Oxygen Transthoracic radiation Reperfusion pulmonary oedema after Lung Transplantation 14
  15. 15. Etiology (contd….) Indirect lung injury ( Extra-pulmonary) 12/20/13          Sepsis (most common) – bacterial/viral/parasitic Sever Trauma with Shock Cardio Pulmonary Bypass Drug overdose Acute Pancreatitis Transfusion of blood products Hypothermia Eclampsia Embolism 15
  16. 16. TRALI : Sudden onset of non-cardiogenic pulmonary edema  Often with systemic hypovolemia and hypotension occuring during or within few hours of transfusion  Thought to be resulting from interaction of specific leucocyte antibodies with leucocytes  12/20/13 16
  17. 17. ARDS A : ASPIRATION R : ROAD TRAFFIC ACCIDENTS D : DIFFUSE ALVEOLAR DISEASE S : SEPSIS 12/20/13 17
  18. 18. Pathogenesis of ARDS Focus of infection Endotoxin Complement Activation direct cellular injury Clotting cascade Cellular activation cytokine act. And proteolytic enzymes MODS 12/20/13 (lung, heart, GI, kidney, brain ) 18
  19. 19. Inflammatory mediators  Cytokines  Complement proteins  Coagulation proteins  Prostaglandins  Vaso-active peptides  Platelet Activating Factor  Neutrophil products 12/20/13 19
  20. 20. 12/20/13 20 PATHOPHYSIOLOGY & DIAGNOSIS Dr Siva Krishna Kota
  21. 21. Definition Acute onset life threatening respiratory failure with characteristic Physiological features Pathological features Radiological features ALI : PaO2/FiO2 < 300 ARDS : PaO2/FiO2 < 200 12/20/13 21
  22. 22. Pathophysiology Profound inflammatory response secondary to a pulmonary or extrapulmonary insult. Diffuse alveolar damage – acute exudative phase (1-7days) – proliferative phase (3-10 days) – chronic/fibrotic phase (> 1-2 weeks) 12/20/13 22
  23. 23. (a) Exudative phase  Basement membrane disruption --Type I pneumocytes destroyed --Type II pneumocytes preserved  Surfactant deficiency -- inhibited by fibrin --decreased type II cell production -- impaired surfactant funtion 12/20/13 23
  24. 24. Exudative phase 12/20/13 24
  25. 25. Exudative phase 12/20/13 25
  26. 26. Exudative phase (contd….)  Microatelectasis / alveolar collapse -- interstitial edema -- necrosed capillary endothelial cell -- alveolar cell + fibrin + plasma protein together form hyaline membrane 12/20/13 26
  27. 27. Exudative phase (contd….) 12/20/13 27
  28. 28. (b) Fibroproliferative phase  Type II pneumocyte proliferate -differentiate into Type I cells -reline alveolar walls -Regeneration of capillary endothelial cells  Fibroblast proliferation -interstitial/alveolar fibrosis -Lymphocytic infiltration -Collagen deposition 12/20/13 28
  29. 29. Fibro-proliferative phase 12/20/13 29
  30. 30. (c) Fibrotic phase  Characterized by: – local fibrosis – vascular obliteration  Repair process: – resolution or fibrosis depending on timing of intervention and management 12/20/13 30
  31. 31. Clinico-pathological correlation 12/20/13 Stage I : unless direct lung injury is there clear on auscultation CXR unremarkable Stage II : Hemodynamically stable no respiratory distress only mild tachypnea ( > 20/min ) ABG may show mild hypoxia Stage III:worsening hypoxemia dyspneic and cyanotic pt. ed work of breathing ed insp. pressure requirement in a patient 31 on ventilator
  32. 32. ARDS : Physiological features A. Decreased lung compliance and volumes microatelectasis altered surfactant production & function FRC causes distal air trapping B. Increased work of breathing in spontaneously breathing pts, increased ratio of Vd/Vt ratio. 12/20/13 respiratory failure unless assisted 32
  33. 33. Physiological features (contd….) C. Alteration in gas exchange (hypoxia) - perfusion of underventilated lung - perfusion of non ventilated lung - impaired diffusion - loss of HPV D. Pulmonary hypertension and RVF - pulmonary vasoconstriction - platelet aggregation and micro thrombosis - direct tissue damage & neurohormonal factors 12/20/13 33
  34. 34. ARDS: Radiological feature Vascular pedicle < 55mm No distention of UL zone vessels Peripheral shadows No pleural effusion No septal lines 12/20/13 34
  35. 35. Criteria for diagnosis Clinical setting Chest Xray findings Physiological parameters Pathological features DIAGNOSIS 12/20/13 35
  36. 36. Criteria for diagnosis A. Clinical Settings : (i) pulm/extrapulm catastrophe (ii)exclusion of chronic pulmonary & left heart diseases (iii)clinical respiratory distress B. CXRay : diffuse bilateral infiltrates sparing apex, cp- angle; with a narrow vascular pedicle 12/20/13 36
  37. 37. Criteria for diagnosis ( cont..) C. Physiologic parameters : (i) ABG :PaO2< 50 with FiO2 of > 0.6 (ii)Compliance < 50 ml/ cm of H2O (iii) shunt fraction (Qs/Qt>20%) (iv) dead space ventilation (Vd/Vt) D. Pathologically 12/20/13 -heavy lungs(>1kg), a post mortem finding -congestive atelectasis -hyaline membrane + fibrotic changes 37
  38. 38. ALI (MURRAY) SCORE : A. Chest Xray findings (alveolar consolidation) B. Oxygenation status (PaO2 / FiO2 ) C. Pulmonary compliance D. PEEP required to maintain oxygenation 12/20/13 38
  39. 39. ALI score (MURRAY-score) 1. Chest X film finding Alveolar consolidation One quadrant Two quadrant Three quadrant Four quadrant 12/20/13 Score 1 2 3 4 cont….. 2. Oxygenation status PaO2 / FiO2 > 300 mmHg 225-299 mmHg 175-224 mmHg 100-174 mmHg < 100 mmHg Score 0 1 2 3 4 39
  40. 40. ALI score (MURRAY-score) 3. Pulmonary compliance 4. PEEP settings Compliance (ml/cmH2O) PEEP (cmH2O) cont….. > 80 60-79 40-59 20-39 < 19 12/20/13 Score 0 1 2 3 4 <5 6-8 9-11 12-14 > 15 Score 0 1 2 3 4 40
  41. 41. ALI score (contd….) Score: 0 0.1-2.5 > 2.5 12/20/13 = none, = mild - moderate = severe 41
  42. 42. 12/20/13 42 VENTILATORY MANAGEMENT OF ARDS Dr Pallavi Marghade
  43. 43. Treatment Strategies  Rx underlying cause  Respiratory therapy for adequate oxygenation/ventilation  Adjunctive therapies 12/20/13 43
  44. 44. Aims of Respiratory therapy  to attempt to avoid tracheal intubation  to reduce maximum pulmonary pressures generated  avoid high Fio2 to prevent oxygen toxicity  maximise alveolar recruitment  finally at minimal cost to the cardiovascular system 12/20/13 44
  45. 45. Conventional ventilation  Consists of large tidal volume of 10- 15ml/kg  Arterial oxygenation supported by raising Fio2  Applying PEEP 12/20/13 45
  46. 46. Ventilator-Induced Lung Injury(VALI) Conventional ventilation In injured lungs High peak inflation and plateau pressure Overdistention of alveoli Volutrauma, Barotrauma, Induction of cytokines 12/20/13 MODS 46
  47. 47. VALI : Volutrauma Direct physical damage to A-C membrane stress failure sudden & rapid increase in permeability Gattinoni described three areas of lung on CT Can’t be ventilated at all 12/20/13 can be expanded in insp. but collapses during exp. Normal lung (baby lung) overdistention of alveoli with normal 47 Vt
  48. 48. Flow L/min 60 0 60 Paw - Time 20 0 Volume - Time 600 VT ml Paw cmH2O VCV Flow - Time 0 12/20/13 Time 48
  49. 49. VALI (contd…..) Barotrauma Application of excessive pressure to the alveoli Air passes from damaged A-C membrane into the interstitium,pleural space,mediastinum 12/20/13 49
  50. 50. Flow - Time Flow L/min 60 PCV 0 60 Paw cmH2O 20 Paw - Time 0 Volume - Time VT ml 600 0 12/20/13 Time 50
  51. 51. VALI (contd….) Cyclical airway closure – Repeated opening & closing of airways with each tidal volume Atelectrauma Surfactant loss high forces needed to open closed lung unit Epithelial damage 12/20/13 51
  52. 52. How does PEEP work? 20 0 12/20/13 52
  53. 53. Mechanism of PEEP 12/20/13 53
  54. 54. PEEP Vs Fio2 : A Dilemma  PEEP reduces intrapulmonary shunt and improves arterial oxygenation at lower Fio2  PEEP cardiac output pulmonary edema dead space resistance to bronchial circulation lung volume and stretch during inspiration 12/20/13 54 LUNG INJURY( more in direct lung injury)
  55. 55. “Open-Lung ” Approach to PEEP  “Open-lung” approach – Not practical – Does not improve outcomes  Optimal PEEP – ??? – Most cases: PEEP 15 – 20 cmH2O 12/20/13 55
  56. 56. Fio2  No detectable oxygen toxicity Fio2< 50%  Diseased lungs more prone to injury due to hyperoxia  Fio2 < 0.6 considered to be safe 12/20/13 56
  57. 57. Optimal PEEP  Maximize O2 delivery DO2 = 10 x CO x (1.34 x Hb x SaO2)  Maximize lung compliance Crs = Vt/(Pplateau – PEEP)  Lowest PEEP to oxygenate @ FIO2 < .60  Empiric approach: PEEP = 16 cmH2O and Vt = 6 ml/kg 12/20/13 57
  58. 58. ARDS Network protocol FIO2 - 0.3 0.4 0.5 0.6 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.01.0 0.7 0.8 0.9 PEEP - 10-14 12/20/13 5 5-8 8-10 10 14 14-18 18-22 58
  59. 59. Lung-Protective Ventilation  VT = 6 mL/kg  Limit plateau pressures < 30 cmH2O – Volume controlled ventilation  Limit peak airway pressures < 40 cmH2O – Pressure controlled ventilation 12/20/13 59
  60. 60. Outcome 12/20/13 60
  61. 61. Lung-Protective Ventilation  Complications: (derecruitement) – Elevated PaCO2 • Limit: pH > 7.20 –7.25 – Worsening hypoxemia • Correction: – Recruitement maneuver – increasing PEEP 12/20/13 61
  62. 62. Alternate Modes of Mechanical Ventilation  Non invasive ventilation  Inverse-ratio ventilation  Airway pressure-release ventilation  Bilevel airway pressure ventilation  Proportional-assist ventilation  High-frequency ventilation  Tracheal gas insufflation  ECMO 12/20/13 62
  63. 63. Non Invasive Positive Pressure Ventilation  Tight fitting face mask as a interface between the ventilator and patient.  Pressure controlled ventilation to prevent leaks  Pressure support ventilation  patient’s effort 12/20/13 63
  64. 64. NIPPV (contd….) ADVANTAGES  Can maintain verbal communication  Can eat during therapy  Decreased incidence of nosocomial pneumonia  Shorter requirement of ventilator assistance and ICU stay DISADVANTAGES Not feasible in obtunded and delirious patients  Additional time commitments from nurses and respiratory therapist  12/20/13 64
  65. 65. Proportional-Assist ventilation  Elevates airway pressure during inspiration  Inspiratory airway pressure varies directly with pt’s effort allowing breath to breath variation  Inspiratory assistance can be customised to the elastance and resistance properties  Best mode to use with NIPPV 12/20/13 65
  66. 66. Inverse Ratio Ventilation  Atelectatic alveoli are recruited and stabilised by increasing the duration of inspiration  I/E should be > 1 12/20/13 During PCV---- inspiratory time VCV---- using deccelerating flow or adding inspiratory pause Disdvantages : Auto PEEP Uncomfortable requiring sedation/paralysis 66
  67. 67. Normal ventilation Flow L/min 60 I E I E 0 60 12/20/13 Flow - Time 67
  68. 68. Inverse ratio ventilation I E I E I E Flow L/min 60 0 60 12/20/13 Reduce auto-PEEP by reducing I-time - Decrease respiratory rate - Decrease tidal volume - Increase Inspiratory flow rate 68
  69. 69. Airway Pressure Release Ventilation  Similar to IRV but Pt. can breath spontaneously during prolonged period of increased airway pressure  Potential lung protective effects of IRV  Air trapping occurs 12/20/13 69
  70. 70. TRACHEAL GAS INSUFFLATION (TGI) In ARDS/ALI 1. Increase physiological dead space 2. permissive hypercapnia DURING CONVENTIONAL VENTILATION : Bronchi and trachea are filled with alveolar gas at end exhalation which is forced back into the alveoli during next inspiration. 12/20/13 70
  71. 71. TGI (contd…..) IN TGI Stream of fresh air (4 to 8 L/min) insufflated through a small catheter or through small channel in wall of ET into lower trachea flushing Co2 laden gas. COMPLICATION 1) Dessication of secretions 2) Airway mucosal injury 3) Nidus for accumulation of secretions 4) Auto – PEEP 12/20/13 71
  72. 72. HIGH FREQUENCY VENTILATION Utilizes small volume (<VD) and high RR (100 b/min)  Avoids over distention (VALI).  Alveolar recruitment.  Enhances gas mixing, improves V/Q. APPLICATION : 1. Neonatal RDS. 2. ARDS. 3. BPF. 12/20/13 COMPLICATION : 1. Necrotizing trachebronchitis. 2. Shear at interface of lung. 3. Air trapping. Two controlled studies (113 and 309) no benefit. 72
  73. 73. Prone Ventilation Proposed mechanism – how it improves oxygenation 1) Increase in FRC 2) Improved ventilation of previously dependent regions. (a) Difference in diaphragmatic supine: dorsal and ventral portion move symmetrically prone :dorsal > ventral PPL at dorsal TP pressure Result Higher Lower Atelactasis Less More opening PPL -3.0 12/20/13 Supine PPL -1.0 +2.8 prone +1.0 73
  74. 74. Prone ventilation (contd….) c) c) 1. 2. 3. Decrease chest wall compliance in p.p Redistribution of tidal volume to atelactatic dorsal region. Weight of heart may affect ventilation. Improvement in Cardiac output Better clearance of secretions Improved lymphatic damage Effect on gas exchange Improves oxygenation – allows decrease Fio2; PEEP - Variable - not predictable response rate – 50-70% 12/20/13 74
  75. 75. Prone Ventilation (contd…) 12/20/13 75
  76. 76. PRONE VENTILATION (contd….) CONTRAINDICATION Unresponsive cerebral hypertension Unstable bone fractures Left heart failure Hemodynamic instability Active intra abdominal pathology TIMING ARDS > 24 hrs./ 2nd day FREQUENCY Usually one time per day DURATION 2 to 20 hrs/day. OUTCOME Improvement in oxygenation No improvement in survival POSITIONING ACHIEVED BY 12/20/13 Circ electric, bed (Late 1970s). Manual 2 step 76 Light weight portable support frame (Vollman prone positioner)
  77. 77. PRONE VENTILATION (contd….) NO. OF PERSONS 3-5 POSITION OF ABDOMEN allowed to protrude ; partial/complete restriction POSITION OF HEAD Head down/ Head up position. ADEQUATE SEDATION +/- NMBA COMPLICATIONS pressure sore Accident removal of ET; Catheters Arrhythmia Reversible dependent odema (Face, anterior chest wall) Gattinoni et al, in a MRCT evaluated the effect of 7 hr / day prone positioning x 10 day improvement in oxygenation, no survival benefit 12/20/13 77
  78. 78. EXTRACORPOREAL MEMBRANE OXYGENATION Adaptation of conventional cardiopulmonary bypass technique. Oxygenate blood and remove CO2 extracorporally. 12/20/13 78
  79. 79. ECMO (contd….) TYPES 1. High-flow venoarterial bypass system. 2. Low-flow venovenous bypass system. Criteria for treatment with extracorporeal gas exchange Fast entry criteria PaO2 <50 mmHg for >2 h at FiO2 1.0; PEEP > 5 cmH2O Slow entry criteria PaO2 <50 mmHg for >12 h at FiO2 0.6; PEEP > 5 cmH2O maximal medical therapy >48 h Qs /Qt > 30%; Cstat <30 ml/cmH2O 12/20/13 Gattinoni showed decreased mortality to 50% by using ECMO as compared to 90% mortality in historical control group, therefore 79 the results are encouraging
  80. 80. ARDS study : KEM Hospital Statistics:  study done over 2 years,  mortality – 46.2%  commonest etiology – pneumonia & tropical diseases  50% of pts with renal and hematologic complication didn’t survive  MODS, LIS, APACHE-II were the mortality predictors 12/20/13 80
  81. 81. ARDS study : KEM Hospital (contd….)  60% of pts required mechanical ventilation  survivors spent less no. of days than the non survivors on ventilator due to innate complication of mechanical ventilation  Use of steroids didn’t reduce mortality  PFT done in 7 survivors showed abnormality due to both ARDS & VALI  long term assessment was not possible because of non-compliance of patients to follow up. 12/20/13 81
  82. 82. 12/20/13 82 ADJUNCTIVE THERAPY IN ARDS Dr Prashant Pawar
  83. 83. Adjunctive therapies 1. 2. 3. 4. 5. 6. 7. 8. 9. 12/20/13 Treatment of infective complications/inciting cause Hemodynamic Management – Fluids, Vasopressors. Nutritional support Selective Pulmonary vasodilators. Surfactant replacement therapy. Anti-inflammatory Strategies. a) Corticosteroids. b) Cycloxygenase & lipoxygenase inhibitors. c) Lisofylline and pentoxifylline. Antioxidants – NAC : Procysteine Anticoagulants. Partial liquid ventilation. 83
  84. 84. Treatment of infective complications Most common complication is nosocomial infection due to gram negative organisms and it is the major cause of death Antibiotics to be chosen as per : • Initial insult of ARDS • Sputum culture best taken shortly after intubation • Bronchoalveolar lavage • Blood culture & sensitivity 12/20/13 84
  85. 85. HEMODYNAMIC MANAGEMENT  Controversial  Restrictive Fluid management  Benefits shown by studies ∀ ↓pulmonary edema formation ∀ ↑ compliance and lung function • Negative fluid balance is associated with improved survival • Net positive balance <1 litre in first 36 hrs. associated with improved survival • decrease length of ventilation, ICU stay and hospitalization. 12/20/13 . 85
  86. 86. Fluid management (contd..) Detrimental effects Ineffective Circulatory Volume (Sepsis). Reduced cardiac output and decreased tissue perfusion. Goal 1. 2. 3. 4. 12/20/13 5. Guidelines for management of tissue hypoxia International consensus conference (AJRCCM- 1996) Promote oxygen delivery Adequate volume CVP – 8-12 mmHg PAOP-14-16 mmHg (Optimal CO; less risk of Edema) Crystalloids vs Colloids:No clear evidence Blood Transfusion : Hb < 10 gm/dl Reduce oxygen demand : a) Sedation : Analgesia, NMBA b) Treat Hyperpyrexia c) Early institution of mech. vent. (shock). No role of supraphysiological. oxygen delivery. 86
  87. 87. Vasopressors Vasopressors  Following restoration of intravascular volume to euvolemic levels (CVP:4-8cm of H2O, PCWP:6-14 mmHg)  GOAL to achieve MAP 55 to 65 mmHg  No clear evidence that any vasopressor or combination of them is superior. 12/20/13 87
  88. 88. Nutritional support Goals of nutritional support  nutrients as per pt’s metabolic demand  Treatment & prevention of macro/micro nutrients deficiency.  Enteral mode is to be preferred ( less infection and low cost)  High fat, low carbohydrate diet es RQ, CO2 production and duration of ventilation  Immunomodulatory nutrition like amino acids, omega-3 fatty acids. ( no survival benefit) 12/20/13 88
  89. 89. Selective pulmonary vasodilators 1. 2. 3. 4. 5. 12/20/13 Inhaled Nitric oxide (iNo) iv almitrine with/without iNo. Aerosolized prostacyclins. Inhibition of cyclic nucleotide phosphodiesterase. Inhalation of Endothelin receptor antagonists 89
  90. 90. Inhaled nitric oxide Mechanism : Endothelial derived relaxing factor Smooth muscle vasodilation through activation of cyclic GMP Benefits in ARDs 1. Improves Oxygenation 2. Improves V/Q mismatch. 3. Reduction in pulmonary artery pressure 4. Inhibits platelet aggregation and neutrophil adhesion. 12/20/13 Selectivity of iNO Rapid inactivation on contact with hemoglobin. 90
  91. 91. Inhaled nitric oxide  DOSAGE: Effect Increase PaO2 decrease PAP Dose 1-2 ppm to <10 ppm 10-40 ppm  Time of Response : <10 min to several hours. Response to iNo is not static phenomenon.  Mortality Benefits : None  Possible role in severe refractory hypoxemia a/w PAH 12/20/13 91
  92. 92. Inhaled nitric oxide Side effects : Usually Minimal 1. Rebound pulmonary hypertension & hypoxemia 2. Methemoglobinemia 3. Toxic NO2 ; Nitrous & Nitric Acid Prevented by decreasing contact time & conc. of gas. 12/20/13 92
  93. 93. Almitrine  Given iv : in low doses  Potentates hypoxic pulmonary vasoconstriction  Decreases shunt and thus improved oxygenation Has additive effect with : iNo iNo + prone position 12/20/13 93
  94. 94. Pulmonary vasodilators(contd…) Prostacyclins:    iv prostacyclin decreases pulmonary arterial pressure non selectively, can increase shunt; worsen oxygenation. Inhaled prostacyclin selectively vasodilates the well ventilated areas Selectivity in dose of 17-50 ng/kg/min. PGI2- Not metabolized in lung so lost at higher doses. PGE1- 70-80% is metabolized in lung. PDE –5 Inhibitors: Dipyridamole ; Sildenafil Endothelin receptor antagonist Nonselective ET antagonist-bosentan Selective ETA 2 antagonist –LU-B1352 12/20/13 94
  95. 95. Surfactant replacement therapy     12/20/13 Deficiency and functional abnormality of surfactant 1. Decreases production 2. Abnormal composition 3. Inhibitors of surfactant function 4. Conversion of large to small surfactant aggregates 5. Alteration/Destruction caused by substances in alveolar space (plasma, fibrinogen, fibrin, alb; Hb) Impaired surfactant function: 1) Atelactasis / collapse 2) Increase edema formation Benefits : Improved lungs function., compliance, oxygenation. Mortality benefits: none 95
  96. 96. Surfactant Delivery Techniques Instillation • Rapid Lavage • May remove toxic volume •Homogenous distribution substances. •Can deliver large volume. •Homogenous distribution. • Techn. Not • Vol. recover can •Can deliver large standardized • Short term impairment in ventilation be poor • Short term impairment in ventilation. Aerosolization Continuous smaller volume. Non uniform distribution. Slow, no optimal device, Filters may plug.
  97. 97. Anti inflammatory therapy Glucocorticoids:  No evidence of benefit in early sepsis/ARDS  Methyl prednisolone in late stages associated 12/20/13 with improved LIS score & decreased mortality  Steroids -Inhibit transcriptional activation of various cytokines -Inhibit synthesis of phospholipase A2 -Reduced production of prostanoids, PAF -Decreases Fibrinogenesis  Increased Risk of Nosocomial Infection 97
  98. 98. Anti infl. Therapy(contd….) Lisophylline & Pentoxifyline  Phosphodiesterase inhibitor -Inhibit neutrophil chemotaxis & activation  Lisophylline inhibits release of FreeFattyAcids from cell membrane under oxidative stress  NIH ARDS trial shows no benefits. Ketoconazole  Potent inhibitor of thromboxane and LT synthesis  12/20/13 Reported to prevent ALI/ARDS in high risk surgical patients  NIH ARDS trial shows no benefits. 98
  99. 99. Cycloxygenase inhibitors     12/20/13 TxA2 and Prostaglandin produced from AA by Cyclooxygenase pathway. Cause 1. Neutrophil chemotaxis and adhesion 2. Broncho-constriction 3.↑ vascular permeability 4. platelet aggregation Animal studies shown that Cycloxygenase inhibitors attenuate lung injury ;and improve pulmonary hypertension and hypoxemia Clinical trials of ibuprofen : No proven benefits 99
  100. 100. Antioxidants therapy  Reactive oxygen metabolites derived from neutrophils,     12/20/13 macrophages and endothelial cells OXIDANTS INCLUDE Super oxide ion (02-), hydrogen peroxide (H2O2) hypochlorous acid (Hocl), hydroxyl radical (OH..) Interact with proteins, lipid and DNA ENDOGENOUS ANTIOXIDANTS Superoxide dismutase, Glutathione, Catalase Vit E & Vit C ; Sulfhydryls Antioxidant therapy replenishing glutathione-cysteine derivatives : N-Acetyl Cysteine & procysteine Beneficial effects not proven 100
  101. 101. ANTICOAGULANT THERAPY IN ARDS In ARDS – Fibrin deposition intra-alveolar and interstitial. Local procoagulant activity and reduced fibrinolysis. ↑ Procoagulant ↓ Fibrinolysis ↑ TF (VIIa) Fibrinolytic inhibitors ↑ PAI–1 ; PAI-2, α2 antiplasmin ↓ urokinase and tPA ↑ Fibrin causes__ Inhibit surfactant → atelactasis with Fibrinonectin → Matrix on which fibroblast aggregation and fibroblast proliferation 12/20/13 Potent chemotactic (Neutrophil recruitment) 101
  102. 102. Activated Protein- C     12/20/13 Protein-c :Naturally occuring anticoagulant 1.Inactivates Va & VIIa – limit thrombin generation. 2.Inhibit PAI-1 activity - ↑ fibrinolysis. 3.Anti-inflam. - ↓ cytokines, inhibit apoptosis. APC administ. Improved survival. absolute risk reduction in mortality Faster resolution of respiratory dysfuntion. Adverse effects Risk of bleeding Efficacy proved in severe sepsis 102
  103. 103. ARDS and β-agonists ENHANCED RESOLUTION ALVEOLAR EDEMA Alveolar clearance of edema depends on active sodium transport across the alveolar epithelium β2 adrenergic stimulation : 1. 2. 3. 12/20/13 Salmeterol Dopamine Dobutamine 103
  104. 104. Partial Liquid Ventilation In ARDS there is increased surface tension which can be eliminated by filling the lungs with liquid (PFC). Perflurocarbon: Colourless, clear, odourless, inert, high vapour pressure Insoluble in water or lipids Most common used – perflubron ( Perfluoro octy bromide) Characteristics of PLV 1.Improved Compliance/ Gas exchange 2. Anti-inflam. properties 3.Decreased risk of nosocomial pneumonia. 4.Reduces pulmonary vascular resistance. 5.Little effect on hemodynamics 12/20/13 104
  105. 105. Partial Liquid Ventilation (contd.. ..) Mechanism of action     A. B. 12/20/13 Reduces surface tension Alveolar recruitment – liquid PEEP. Selective distribution to dependent regions. surfactant phospholipid synthesis and secretion. Anti Inflammatory properties Indirect : mitigation of VALI Direct a) endotoxin stimulated release of TNF; IL-1; IL8. b) decreases production of reactive oxygen species. c) Inhibit neutrophil activation and chemostaxis. d) Lavage of cellular debris. 105
  106. 106. Partial Liquid Ventilation (contd..) Total Liquid Ventilation Partial Liquid Ventilation 1. Ventilator Liquid Conventional 2. Tidal volume delivered of Oxygenated PFC Gas 3. Lungs are filled Completely by PFC Filled till FRC by PFC 4. Feasibility Experimental Yes 5. Disadvantage 12/20/13 Loss of gas by evap., cost. 106
  107. 107. Partial Liquid Ventilation (contd..) Recommended dose of PFC 20ml/kg -Beyond this dose – decrease cardiac output -More clinical trials are required to demonstrate efficacy.  Additive effect of PLV has been shown in combination with: -NO -Surfactant -HFOV -prone ventilation  Trials of PLV in ARDS confirmed safety but not efficacy. 12/20/13 107
  108. 108. Mystery Unsolved 12/20/13 THRIVE FOR THE BEST 108
  109. 109. 12/20/13 109 What have we learnt? ALI- Syndrome of pulmonary inflammation,  vasoconstriction, greater permeability of both alveolar capillary endothelium & epithelium, non-cardiogenic pulmonary oedema   arterial hypoxemia resistant to O2 therapy,  appearance of diffuse infiltrates on X-ray chest
  110. 110. ARDS  Not a single disease but rather a pathophysiologic syndrome  Catastrophic acute respiratory failure of diverse etiology & high mortality  No single test or marker to accurately diagnose or predict the outcome of ARDS  Represents the pulmonary expression of systemic inflammatory process 12/20/13 110
  111. 111. ARDS  Associated with triggering events.  Lungs bear the brunt of the injury as it receives entire C O with exposure to circulating agents and exposure to environmental insults during ventilation 12/20/13 111
  112. 112. ARDS Dysregulated inflammatory-reparative processes  lung injury & repair  Important to understand the initiators & mediators of immunochemical response of ARDS & its effects  O2 debt & tissue hypoxia , improper tissue O2 utilization  O2 debt from ↓ ed tissue perfusion organ failure ; monitoring O2 debt & optimizing peripheral tissue oxygenation imp; transcutaneous surface electrode for high risk surgical patients 12/20/13 112
  113. 113. ARDS- notions about fluid therapy  Hypovolemia – major pathophysiologic factor of ARDS  Pulmonary edema – an effect, not the cause of ARDS  Fluid restriction may ↓ CO & tissue perfusion & worsen non pulmonary organ function  ARDS – an end organ failure of an antecedent hypovolemic-hypoxemic event except for ARDS caused by direct lung injury 12/20/13 113
  114. 114. ARDS: Lung Protection Evidence supports a volume and pressure limited approach  In majority of patients with ARDS lung recruitment and overinflation occur simultaneously in different lung regions as seen on CT imaging • High PAP opens collapsed ARDS lung and partially opens oedematous ARDS lung. • High PEEP and Low Vt decrease lung cytokines and survival.  12/20/13 114
  115. 115. ARDS: Lung Protection   12/20/13 Use of high PEEP and Recruitment maneuvers may not help when low potential for recruitment. (consolidation) Improving oxygenation by itself does not equate with improved outcome 115
  116. 116. The Future  Quantify the degree of primary v secondary ARDS, to optimise ventilation strategy.  Monitor Real Time changes in ventilation 12/20/13 116
  117. 117. The End 12/20/13 117
  118. 118. 12/20/13 118
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