Red Book - ARDS

Question 1

Berlin definision of ARDS

Answer 1

Acute, diffuse inflammatory lung injury

Leads to increased vascular permeability
Increased lung weight and loss or aerated tissue

Causing hypoxaemia
bilateral radiographic opacities

Associated with: Increased venous admixture
Increased physiological dead space
Decreased lung compliance

Question 2

What as the problem with former definitions

Answer 2

No clarity of what ACUTE meant

No inclusion of risk factors for ARDS

Variability of CXR interpretation

Less PCWP being used (initially they wanted <18mmHg not due to LVF)

No PEEP given in the definition

Question 3

Oygenation criteria for ARDS

Answer 3

PF ratio:

Mild 200-300 (26.7 to 40 kPa)
Mode 100-200 (13.3 to 26.7)
Severe < 100 ( <13.3 kPa)

All with at least PEEP/CPAP 5cmH2O

Question 4

Diagnostic criteria

Answer 4

TIMING - develops in 1 week of insult/resp symptoms

RADIOLOGY - bilateral opacities not explained by effusion, collapse or nodules

Resp failure - not explained by LVF or fluid overload

Oxygenation (PF)

Has to be ventilated (invasive or non-invasive with PEEP > 5)

Question 5

Causes of ARDS

Answer 5

Pulmonary and Extra Pulmonary

Pulm Extra-pulm
Pneumonia Sepsis
Pulm Contusion Burns
Aspiration pneumonitis Major trauma
Inhalational injury TRALI
Pulm vasculitis Severe acute panc
Drowning Cario bypass (pump lung)

Question 6

Pathophysiology of ARDS

Answer 6

Three phases - Exudate, Proliferative, Fibrotic

Exudative - 2-4 days
   Inflammation to epithelium
  Leak protein rich fluid in alveoli and interstitium
  Destroy pulm vascular bed
  Microthrombus formation

VQ mismatch, hypoxia
Reduced lung compliance

Proliferative (4-7)
Type II pneumocytes and fibroblasts
Alveolar fibrin deposition
Exudate turns to scar formation

Fibrotic stage )7-14
Fibrosis and underlying structural damage

Question 7

Additional tests in ARDS

Answer 7

Bloods - FBC, U&E, LFT, CRP, Coag, Amylase/Lipase, Cultures

ABG - quantify PF

CXR/CT chest

Echo if no known risk factors for ARDS

Question 8

Name the mechanisms by which ventilator induced lung injury occurs

Answer 8

Volutrauma (overdistend alveloi)

Barotrauama (high pressure injury)

Atelectotrauma (shearing from collapse and re-expansion)

Biotrauma (inflammation from high volumes)

Question 9

List the various ventilatory strategies

Answer 9

Lung protective ventilation

Neuromuscular blocking agents

Recruitment manoeuvres

Decremental PEEP

Prone

ECMO

Oscilator

(Steroids and Nitric Oxide)

Question 10

Describe Lung protective vent

Answer 10

Low Tv - 5-7 ml/kg of IBW
High resp rate but less than 35/min

Permissive hypercapnoea - higher PaCO2 so long as pH >7.2 (except in TBI)

Aim SaO2 88-95%

Consider prolonged I:E or inverse ration ventilation

PEEP > 5cm

Find optimum PEEP - point of best compliance
Use FiO2/PEEP increments from tables

Maintain plateau pressure below 30cm455445

Question 11

Evidence for NMBD in ARDS

Answer 11

ACURASYS Trial

Cisatracurium versus placebo

Improved 90 day mortality when PF ratio<120
Increased vent free days

Question 12

Evidence for recruitment/decrimental peep

Answer 12

2016

In moderate-severe ARDS, recruitment improved oxygenation and lung mechanics
No mort benefit

Question 13

Evidence for proning

Answer 13

PROSEVA trial

50% reduction in mortality ventilated and proned for 16 hours a day

NNT = 6

Question 14

Evidence for oscilators

Answer 14

OSCAR - no mortality benefity

OSCILLATE - evidence of harm

Question 15

Evidence for steroids

Answer 15

Meta analysis 1995 - increased harms no benefits

Steinberg 2006 - methylpred - increased vent free days BUT no difference in 60 day mort

Increased myopathy

2007 - methylpred infusion - improved organ dysfunction, LOS, BUT many more vasopressor dependent patients in the placebo

ADRENAL trial - shocl resolved and less time on vent but NO difference in mortality

Question 16

Components of the Murrary Score

Answer 16

PF ratio
PEEP
Compliance
CXR (quadrants affected)

Question 17

What Murray score should prompt ECMO

Answer 17

Greater than or equal to 3

Question 18

Evidence for ECMO

Answer 18

CESAR trial - improved mortality

Many patients moved to tertiary centre didnt get ecmom

Question 19

Types of ECMO

Answer 19

V-V - facilitaties gas exchange, no haem support
V-A haem support and gas exchange
A-V - rare - uses own system as pump

ECCO2R removes CO2 whilst o2 is provided by ventilation

Question 20

Indications for ECMO VA

Answer 20

Cardiogenic shock of almost any cause
        Myocarditis
        Intractilbe arrhytmia
        Overdose with cardiac depression (LAs)
        PE
        Anaphylaxis

Weaning from CPB

Bridge to transplant
Primary graft failure

Chronic cardiomyopathy

Pulmonary hypertension AFTER endarterctomy

ECLS

Question 21

Indications for VV ECMO

Answer 21

Any REVERSIBLE cause of resp failure

ARDS with bacterial/viral pneumonia

Lung transplnt
Bridge
Primary graft failure
Intra-op

Lung rest
Contusion (trauma)
Smoke
Obstruction

Pulm Haemorrhage

Status asthmaticus

Question 22

Contraindications to ECMO

Answer 22

Absolute - irreversible organ damage, failure, not a transplant candidate

Advanced malignancy

Chronic severe pulmonary hypertension

Relative:
Age over 75
Polytrauam with many bleeding sites
CPR >60minutes

VA - Aortic regurg severe
Aortic dissection

VV - Unsupoortable cardiac failure
Severe pulm hypertension
Cardiac arrest

Question 23

Complications of ECMO

Answer 23

Cannula, Antocoag, Equipment

Cannula
    PTx
    Vascular disruption
    Infection
    Emboli
    Bleed

Anticoag - heparin, haemrrhahe
HIT

Equipment - pump and oxygenation failure
Exsanguination

Question 24

Equipment for ECMO

Answer 24

Cannulae
Tubing with heparin (systemic)
Pump - external pump with centrifuge or roller
Membrane oxygenator
Heat exchanger
Gas blender