ards management

ARDS MANAGEMENT

SAMIR EL ANSARYICU PROFESSOR

AIN SHAMSCAIRO

Pulmonary capillary leak

Inactivation of surfactant

Interstitial& alveolar edema

Severe & refractory hypoxemia

SHUNTING - Stiff lungs

Alveolar atalectasis

Damage to alveolar capillary membrane

DIFFUSE lung injury

CAUSES

Early pathologic features of ARDS • Diffuse alveolar damage (DAD)

• There is minimal alveolar septal thickening, hyperplasia of pneumocytes

• Eosinophilic hyaline membranes present

Links Between VILI and MSOF

Biotrauma and Mediator Injuries

What does surfactant do?

Alveoliwithout

surfactant

Alveoliwith

surfactant

Cyanosis

Pao2 / Fio2 < 200REFRACTORY HYPOXEMIA

Gas ExtravasationBarotrauma

1

A Portal for Gas & Bacteria?

Microvascular Fracture in ARDS

Excessive PEEP, particularly in combination with hypovolemia, can decrease cardiac output and

oxygen delivery, and increase the risk of barotrauma

Subcutaneous emphysema

CT scan showed Severe surgical emphysema and pneumomediasteum

Diseased Lungs Do Not Fully Collapse,Despite Tension Pneumothorax

…and

They cannot always be fully “opened”

Dimensions of a fully Collapsed Normal Lung

Tension Cysts

Spectrum of Regional Opening Pressures(Supine Position)

Superimposed

Pressure Inflated 0

Alveolar Collapse(Reabsorption)

20-60 cmH2O

Small AirwayCollapse

10-20 cmH2O

Consolidation

Lung Units at Risk for Tidal Opening & Closure

=

Opening

Pressure

How Much Collapse Depends on the Plateau

R = 100%

20

60

100

Pressure [cmH2O]20 40 60

To

tal L

un

g C

apac

ity

[%]

R = 22%

R = 81%

R = 93%

00

R = 0%

R = 59%

Some potentially recruitable units open only at high pressure

More Extensive Collapse But Lower PPLAT

Less Extensive Collapse But Greater PPLAT

Mechanical Ventilator

PRESSURE VOLUME CURVE

Recruitment Maneuvers (RMs)

Proposed for improving

Arterial oxygenation

Enhancing alveolar recruitment

All consisting of short-lasting increases in intrathoracic pressures

Recruitment Maneuvers (RMs)

–Vital capacity maneuver

(inflation of the lungs up to 40 cm H2O, maintained for 15 - 26 seconds)

–Intermittent sighs

–Extended sighs

Recruitment Maneuvers (RMs)

–Intermittent increase of PEEP

–Continuous positive airway pressure (CPAP)

–Increasing the ventilatory pressures to a plateau pressure of 50 cm H2O for 1-2

minutes

Other manoeuvres

• Prone positioning ventilation

• Prolonged inspiration

• Inverse ratio ventilation

Limit of open lung strategy

• To minimise VILI

to the less damaged alveoli

Max insp pressure

(plateau pressure 30-32cm H20)

Limit of open lung strategy

Max pressure remains unchanged

TV will decreaseAlveolar ventilation will decrease

Alv V: dead space vent ratio

will decrease

Increasing PaCO2

• Management options

Increase resp rate

Minute

volume

Delivered TV TV ml/kg Resp rate

6.4 L 640 ml 8 10

6.4 L 480 ml 6 14

6.4 L 320 ml 4 20

6.4 L 160 ml 2 40

Anatomical dead space 150ml

Increasing PaCO2

• Permissive hypercapnia

• Tracheal gas insuflation

•Reduce

•dead space

Increasing PaCO2

As alveolar ventilation decreases

will require increasing FIO2

Otherwise will result

in alveloar hypoxia and arterial hypoxaemia

Liquid Ventilation

More clinical trials are req. to demonst.

efficacy.

• Inert

• No odor

• No color

• Low surface tension

• Carry large amount of O2 & CO2

Perfluorocarbon(PFC)

Medication: Morphine sulfate

(0.1mg/kg/dose), pavulon(0.1 mg/kg/dose)

Rimar (30 ml/kg)Ventilation settings:

Ti 5 sec, hold 10 sec, Te 5 sec (3-6 cycles/min)CO2 eleminated by

increase tidal volumeO2 managed by change O2

content and FRC

ON START OF GAS VENTILATION

ONE HOUR AFTER PLV

48 HOUR AFTER PLV 3 WEEKS AFTER PLV

Partial liquid ventilation with perflubron in premature infants with severe

respiratory distress syndrome

High-frequency Oscillatory Ventilation

• Active expiration Pressurised circuit

High-frequency Ventilation

35cm H20

90 cm

3-9 hz0.1-3ml/kg

42

Pressure transmission HFOV

P

T

proximal

trachea

alveoli

Due to the attenuation of the pressure wave

by the time it reaches the alveolar region

it is reduced down to .1 - 5 cmH2O

BRONCHOTRON

VENTILATOR

CONVENTIONAL( = LOW FREQUENCY )

VENTILATION UNIT

PULSATION

( = HIGH FREQUENCY )

VENTILATION UNIT

However …Risks of barotrauma and hemodynamic compromise with high frequency ventilation can approximate those of conventional ventilation

KINETIC THERAPY

MEDISCUS AIR CUSHION BED PULMONAIR

MEDISCUS TRAUMA BED ROTOREST

APPLICATION OF SURFACTANT

CUROSURF - SURVANTA

ALVEOLFACT

50 – 200 mg/kgBW

BY ENDOTRACHEAL OR ENDOBRONCHIAL ROUTE

APPLICATION OF SURFACTANT

• PREVENT END-EXPIRATORY COLLAPSE OF ALVEOLI

• RECRUITMENT OF ATELECTATIC LUNG AREAS

• IMPROVED COMPLIANCE

• IMPROVED OXYGENATION

• IMPROVED VENTILATION /PERFUSION RATIO

SECRETION ELEMINATIONVIA IPPB

• BETTER DISTRIBUTION OF MEDICATED AEROSOLS

• BRONCHOSPASMOLYTIC

• IMPROVED OXYGENATION

• SECRETOLYSIS

JET THERAPY

• SECRETOLYSIS ( SECRETION MOBILISATION )

• DISSOLUTION OF RESORPTIVE ATELECTASES

• IMPROVED OXYGENATION

• INTRACRANIAL PRESSURE REDUCTION

CLINI – JETHIGH FREQUENCY JET VENTILATION

HFJV

HANDY INSTRUMENT

PRODUCES SHORT GAS PULSES

FOR SECRETOLYSIS

DISSOLVE SECRETIONS

( KETCHUP EFFECT )

INCENTIVE SPIROMETRYSUSTAINED MAXIMAL INSPIRATION

• ALVEOLAR RECRUITMENT

• PREVENTION OF ATELECTASES

• MUSCLE TRAINING

• COUGH PROVOCATION

• IMPROVED OXYGENATION AND VENTILATION

Dilates pulmonary

blood vessels and

helps reduce

shunting

REDUCTION IN INTRAPULMONARY R-L SHUNT

Nitric Oxide

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

elansarysamir@yahoo.com