ARDS acute respiratory distress syndrome.ppt

Updates in ARDS, feature, management in icu

1. DR.Syed Asreff
FCCCM
ARDS

2. INTRODUCTION

Acute respiratory distress syndrome (ARDS),
previously known as respiratory distress
syndrome (RDS), acute lung injury, adult
respiratory distress syndrome, or shock lung, is
a severe, life-threatening medical condition
characterized by widespread inflammation in
the lungs.

3. ARDS IS ALSO REFERRED AS

STIFF LUNG
SHOCK LUNG
WET LUNG
POST TRAUMATIC LUNG
ADULT RESPIRATORY DISTRESS SYNDOME
ADULT HYALINE MEMBRANE DISEASE
CAPILLARY LEAK SYNDROME
CONGESTIVE ATELECTASIS

4. old DEFINITION
Asbaugh,Bigelow & petty described ARDS as
“A syndrome of acute respiratory failure in adults
characterized by Non cardiogenic pulmonary
edema manifested by severe hypoxemia
caused by right to left shunting through
collapsed or fluid filled alveoli

5. the berlin definition(2011)
ARDS is an acute diffuse, inflammatory lung
injury, leading to increased pulmonary vascular
permeability, increased lung weight, and loss of
aerated lung tissue…[with] hypoxemia and
bilateral radiographic opacities, associated with
increased venous admixture, increased
physiological dead space and decreased lung
compliance.

6. Berlin definition key components
Timing: Within 1 week of a known clinical insult or
new or worsening respiratory symptoms
Chest imaging: Bilateral opacities — not fully
explained by effusions, lobar/lung collapse, or nodules
Origin of edema : Respiratory failure not fully
explained by cardiac failure or fluid overload.Need
objective assessment (e.g., echocardiography) to
exclude hydrostatic edema if no risk factor present.
(cont)

7. Oxygenation:   
Mild 200 mmHg < PaO
2/FIO
2
≤300 mmHg with PEEP or CPAP ≥5 cmH
2O  
 Moderate100 mmHg < PaO
2/FIO
2
≤200 mmHg with PEEP ≥5 cmH
2O    
 Severe PaO
2
/FIO
2
≤100 mmHg with PEEP ≥5
cmH
2O

10. CAUSES OF ARDS
DIRECT CAUSES:
Breathing in smoke or poisonous chemicals
Aspiration
Near drowning
Pneumonia
Severe acute respiratory syndrome (SARS), a
lung infection

11. Severe Sepsis
26%
Aspiration
15%
Trauma
11%
Other
13%
Pneumonia
35%

12. INDIRECT CAUSES :
 Bacterial blood infection (sepsis)
Drug overdose
Having many blood transfusions
Heart-lung bypass
Infection or irritation of the pancreas(pancreatitis)
Severe bleeding from a traumatic injury (such as a car
accident)
Severe hit to the chest or head

13. PATHOPHYSIOLOGY OF ARDS

17. . Direct or
indirect injury
to the
alveolus
causes
alveolar
macrophages
to release
pro-
inflammatory
cytokines

18. . Cytokines
attract
neutrophils into
the alveolus
and interstitum,
where they
damage the
alveolar-
capillary
membrane
(ACM).

19. ACM
integrity is
lost,
interstitial
and alveolus
fills with
proteinaceo
us fluid,
surfactant
can no
longer
support
alveolus

22. PATHoPHYSIOLOGY
Consequences of lung injury include:
Impaired gas exchange
Decreased compliance
Increased pulmonary arterial pressure

23. IMPAIRED GAS EXCHANGE
V/Q mismatch
Related to filling of alveoli
Shunting causes hypoxemia
Increased dead space
Related to capillary dead space and V/Q mismatch
Impairs carbon dioxide elimination
Results in high minute ventilation

24. DECREASED COMPLIANCE
Hallmark of ARDS
Consequence of the stiffness of poorly or non
aerated lung
Fluid filled lung becomes stiff/boggy
Requires increased pressure to deliver Vt

25. DECREASED PULMONARY ARTERY
COMPLIANCE
Occurs in up to 25% of ARDS patients
Results from hypoxic vasoconstriction
Positive airway pressure causing vascular
compression
Can result in right ventricular failure
Not a practice we routinely measure

26. CLINICAL FEATURES

28. HOW TO DETERMINE ARDS BY CHEST XRAY : ?

29. IT IS DIFFICULT TO DO SO
DIAGNOSIS SHOULD ALWAYS BE MADE BY
CLINICAL DIAGNOSIS.
NEED TO DETERMINE CARDIOGENIC VS NON
CARDIOGENIC EDEMA

34. MANAGEMENT OF ARDS

35. EVIDENCE BASED MANAGEMENT OF
ARDS
• Treat the underlying cause
• Low tidal volume ventilation
• Use PEEP
• Monitor Airway pressures
• Conservative fluid management
• Reduce potential complications

36. MANAGEMENT GOALS
Diagnose & treat precipitating cause
Maintain oxygenation
Prevent Ventilator Induced Lung Injury(VILI)
Keep PH in normal range
Enhance Pt-Ventilator synchrony
sedation, analgesics, if necessary paralytics
Weaning

37. 1) DIAGNOSIS AND TREATMENT OF UNDERLYING
CAUSE :

39. 2.MAINTAIN TISSUE OXYGENATION:

40. 2.MAINTAIN TISSUE
OXYGENATION:The fractional concentration of inspired oxygen
(FiO2) should be kept at 50% or lower
to minimize the risk of oxygen toxicity
 An SaO2 above 90% should be sufficient to
maintain oxygen delivery to peripheral tissues
 If the FiO2 cannot be reduced to below 60%
external PEEP is added to help reduce the FiO2 to
nontoxic levels
(CONT)

41. 2.MAINTAIN TISSUE
OXYGENATION: The goal of O2 therapy is to administer the lowest
possible oxygen concentration to sustain a mixed
venous oxygen > 40 mm Hg
 Positive end expiratory pressure (PEEP) is
indicated for use in patients who are being
ventilated mechanically with high FiO2 (>0.50) and
who have a PaO2 of less than 65 mm Hg
 The purpose of PEEP in ARDS is to minimize
alveolar collapse and small airway closure and
reduce interstitial edema and total extravascular
lung water

42. 2.MAINTAIN TISSUE
OXYGENATION:
The goal of O2 therapy is to administer the lowest
possible oxygen concentration to sustain a mixed
venous oxygen greater than 40 mm Hg

43.  KEY POINTS

44. Fi O2 SHOULD BE < 60%
SpO2 SHOULD BE <90%
INDIC OF PEEP:
 PT WHO IS MECHANICALLY VENTILATED
WITH PaO2 <65%
 FiO2 >50%
GOAL :PROVIDE MIXED VENOUS O2 CONC OF >40%

45. 3.MECHANICAL VENTILATION

52. VENTILATOR ASSOCIATED LUNG INJURY

58. REDUCING VENTILATOR INDUCED
LUNG INJURY
1)LOW TIDAL VOLUME MECH VENTILATION

2) PEEP

59. PEEP

60. HYPOTHESIS:
In patients with ALI ventilated with 6 mL/kg, higher levels of
PEEP will result in better clinical outcomes than lower levels
of PEEP.

61. PEEP
•Positive End Expiratory Pressure
•Every ARDS patient needs it
•Goal is to maximize alveolar recruitment and
prevent cycles of recruitment/derecruitment

62. PEEP
Higher levels of PEEP/FiO2 does not improve
outcomes
may negatively impact outcomes:
Causing increased airway pressure
Increase dead space
Decreased venous return
Baro trauma

63. Multicenter randomized trial:
. Set a PEEP aimed to increase alveolar recruitment while limiting hyperinflation.
-Randomly assigned two groups: moderate PEEP (5-9cm H2O) vs. level of PEEP to reach a
plateau pressure of 28-30cm H2O
-Found that it didn’t significantly reduce mortality; however, it did improve lung function and
decreased days on ventilator and organ failure duration.

64.  Positive end expiratory pressure (PEEP) is
indicated for use in patients who are being
ventilated mechanically with high FiO2 (>0.50)
and who have a PaO2 of less than 65 mm Hg
 The purpose of PEEP in ARDS is to minimize
alveolar collapse and small airway closure and
reduce interstitial edema and total extravascular
lung edema.

65. Initial levels of PEEP should be in the range of 5-10
cm H2O
 Small increments of PEEP are added until the
optimal level is reached.
The best meaurement available for evaluating tissue
oxygenation at the bedside are 1) systemic oxygen
uptake (VO2 [oxygen

consumption]), 2)venous
lactate level, and 3)gastric intramucosal PH ( measure
directly by gastric tonometry)

66. PEEP
As FiO2 increases, PEEP should also increase

68. AUTO PEEP

69. Airway Pressures in ARDS
Plateau pressure is most predictive of lung injury
Goal plateau pressure < 30, the lower the better
Decreases alveolar over-distention and reduces risk of lung strain
Adjust tidal volume to ensure plateau pressure at goal
It may be permissible to have plateau pressure > 30 in some
cases
Obesity
Pregnancy
Ascites

70. ASSESS CAUSE OF HIGH PLATEAU PRESSURE:
ALWAYS REPRESENTS SOME PATHOLOGY:
STIFF NON COMPLIANT LUNG :ARDS,
HEART FAILURE
Pneumothorax
Mucus Plug
Right main stem intubation
Compartment syndrome
Chest wall fat / Obesity

71. LOW TIDAL VOLUME VENTILATION

72. Hypothesis:
In patients with ALI, ventilation with smaller tidal volumes (6 mL/kg) will result in
better clinical outcomes than traditional tidal volumes (12 mL/kg) ventilation

73. LOW TIDAL VOLUME VENTILATION
•When compared to larger tidal volumes, Vt of 6ml/kg of ideal
body weight:
•Decreased mortality
•Increased number of ventilator free days
•Decreased extrapulmonary organ failure
•Mortality is decreased in the low tidal volume group despite
these patients having:
•Worse oxygenation
•Increased pCO2 (permissive hypercapnia)
•Lower pH

74. LOW TIDAL VOLUME VENTILATION
ARDS affects the lung in a
heterogeneous fashion
Normal alveoli
Injured alveoli can
potentially participate in
gas exchange,
susceptible to damage
from opening and
closing
Damaged alveoli filled with
fluid, do not participate
in gas exchange

75. LOW TIDAL VOLUME
VENTILATION
Protective measure to avoid over distention of
normal alveoli
Uses low (normal) tidal volumes
Minimizes airway pressures
Uses Positive end-expiratory pressure (PEEP)

76. FLUID THERAPY

77. HYPOTHESIS : Diuresis or fluid restriction may improve
lung function but could jeopardize extrapulmonary organ
perfusion
CONCLUSION : Conservative fluid management improved
lung function and shortened mechanical ventilation times
and ICU days without increasing nonpulmonary organ
failures

78. FLUID THERAPY:
Hypoalbuminemic patients should receive coloids
whereas all other patients should receive crystalloid
fluids to decrease the pulmonary congestion
The patient´s pulmonary capillay wedge pressure
(PCWP) is kept as low as possible as long as the
cardiac output and tissue perfusion can be
maintained at normal levels
 Maintenance of the PCWP at 10-15 mm Hg
provides adequate, but not excessive intravascular
volumes

81. Hypothesis: Early application of prone positioning would improve
survival in patients with severe ARDS.
Conclusion: Early application of prolonged prone positioning
significantly decreased 28 day and 90 mortality in patients with
severe ARDS.

87. VENTILATORY WEANING

88. WEANING
Daily CPAP breathing trial
FiO2 <.40 and PEEP <8
Patient has acceptable spontaneous breathing efforts
No vasopressor requirements, use judgement
Pressure support weaning
PEEP 5, PS at 5cm H2O if RR <25
If not tolerated, ↑RR, ↓Vt – return to A/C
Unassisted breathing
T-piece, trach collar
Assess for 30minutes-2 hours

89. Tolerating Breathing Trial?
SpO2 ≥90
Spontaneous Vt ≥4ml/kg PBW
RR ≤35
pH ≥7.3
Pass Spontaneous Awakening Trial (SAT)
No Respiratory Distress ( 2 or more)
HR > 120% baseline
Accessory muscle use
Abdominal Paradox
Diaphoresis
Marked Dyspnea
If tolerated, consider extubation

90. PUTTING ALL TOGETHER
1) Calculate patient’s predicted body weight:
•Men (kg) = 50 + 2.3(height in inches – 60)
•Females (kg) = 45.5 + 2.3(height in inches – 60)
2)Set Vt = predicted body weight x 6cc
3)Set initial rate to approximate baseline minute
ventilation (RR x Vt)
4)Set FiO2 and PEEP to obtain SaO2 goal of >=88%
5)Diuresis after resolution of shock
6)Refer to ARDSnet guidelines

91. TROUBLE SHOOTING COMMON
PROBLEMS

92. -Randomized control trial, stopped with 548 of 1200
patients
-Found early initiation of HFOV does not reduce and
may increase hospital mortality

93. found there is no significant effect of 30 day
survival between patients who received HFOV
and conventional mechanical ventilation

94. Neuromuscular blocking agents may increase oxygenation and
decrease ventilator associated lung injury in severe ARDS
patients
-Multicenter double blind trial with 340 patients; received
48hrs of cisatracurium (Nimbex) or placebo
-Found that early administration of NBA improved 90 day
survival and increased time off vent without increase in muscle
weakness

95. OTHER METHODS

1)HIGH FLOW VENTILATION
2)ECMO
3)PARTIAL FLUID VENTILATION

96. EXTRA CORPOREAL MEMBRANE OXYGENATION

97. ECMO(EXTRA CORPOREAL MEMBRANE
OXYGENATION)