Respiratory failure

Weiss niemand.

Aber Modi, die Spontanatmung ermöglichen sind eher von Vorteil (zb. airway pressure related ventilation)

-> Spontanatmung so schnell wie möglich

Relexation kann manchmal von Vorteil sein

6 ml/kg

Bei kleinen inflamierten Lungen eher noch kleiner, bei grossen wenig inflamierten Lungen eher mehr Tidals

28-30 mbar

Transpulmonaler Druck steht im Vordergrund. Deswegen:

bei dehnbarer(hohe Compliance)  Thoraxwand (z.B.Kind) ist 30 mbar viel

bei weniger dehnbarer Thoraxwand (z.b. adipöser Patient) ist 30 mbar zu wenig

Leichte Hyperkapnie wird deswegen akzeptiert =permissive Hyperkapnie
 

lower inflection point

Zur Findung des best peep eher nicht geeigent, weil er zwar den Mindestdruck zur Eröffung der Alveolen anzeigt aber nicht die PEEP, der Derecruitement verhindert

1. PEEP should ideally be set at a high level (18-20 cm H₂O) immediately after a lung recruitment manoeuvre, then be titrated downwards towards the lowest possible value that prevents de-recruitment ('decremental PEEP'). This pressure (collapse pressure) may be found on the expiratory limb of a static pressure-volume

2. The 'best arterial oxygenation' method: Th PEEP is titrated from a high towards a lower level, arterial oxygenation will suddenly deteriorate when de-recruitment occurs.

3. The 'best breath-by-breath compliance' method: PEEP is lowered from a high value towards a lower value, breath-by-breath compliance will increase to a maximal value and then decrease again. The pressure at 'best compliance' is similar to the collapse pressure.

it is possible to use a reduced expiratory time without causing intrinsic PEEP (auto-PEEP).

The longer inspiratory time increases the intraalveolar mixing of gases and thereby improves CO₂ removal, and the shorter expiratory time decreases the tendency for time-dependent alveolar collapse.

However, it is seldom useful to increase the I:E-ratio to more than 1:1.

inverse I:E-ratio  is an increased risk of significant circulatory compromise (mean intrathoracic pressure will be higher) and of producing an intrinsic PEEP. This could produce overdistension of lung regions with long time constants while lung units with short time constants collapse. The only consistently demonstrated beneficial effect  of inverse I:E-ratio is enhanced CO₂ removal.

Recruitement-Manoever, dann PEEP um Aleolar-Kollaps zu vermeiden

Verhindert oft ECMO bei Hypoxie, aber niemand weiss ob es einen Effekt auf das outcome hat und ob es lungenschonend ist.

In early ALI/ARDS inflammation with the extravasation of fluid and cells are prominent features.

The wet, heavy, inflamed lungs during this early phase compress basal regions, causing dependent compression atelectasis, which later organise and consolidate. For this reason it is important to open up the collapsed lung early in the disease process, if possible within a few days of the diagnosis. Later attempts to recruit lung volume, when the collapsed parts of the lungs are organised and consolidated, are usually less successful and may also increase the risk of lung injury.

Transpumonaler Druck!

Druch Thorax-Wandcompliance (meistens durch hohen intraabd. Druck beinflusst)

40-55 cmH2O

Kann zu kreislaufkollaps bei hypovolämen Patienten führen!

Wenn möglich enteral

Whs. sind immunmodulatorische Zusätze hilfreich (Omega-3-Fettsäuren)

Keine schnellen, fetthaltigen Infusionen vor allem langkettige Lipide

Wichtig wegen schnellem Muskelabbau und hohem Energieumsatz

• Inhaled NO and inhaled prostacyclin act as selective pulmonary vasodilators, improving ventilation–perfusion ratio and oxygenation and reducing increased pulmonary artery pressure.
• Inhaled NO has a limited duration of action of one to two days and has no effects on outcome.
• Almitrine, a vasoconstrictor, may improve oxygenation in selected cases by augmenting hypoxic pulmonary vasoconstriction. There are no data on outcome.
• There are additive effects on oxygenation with combinations of inhaled NO, inhaled prostacyclin, almitrine and prone positioning.

Besserer Gasaustausch, schnellere Reduktion der Infektparameter, kürzere Beatmungsdauer und IPS-Liegezeit, Reduktion des relativen Risikos bzgl. Mortalität in zwei kleineren Studien (Meduri-Studie).

1-2mg/kg KG/d Methylprednisolon (SoluMedrol) bis 32 Tage

Murray-Score (aus Cecar-Trial) >3.0

oder gemäss Horowitz-Index <100 Verlegung in ECMO-Zentrum

50-70: ECMO-Indikation

-The frequency of nosocomial pneumonia is greater in patients with ARDS than in ventilated patients without ARDS.
-The risk of VAP increases with ventilator time in the ICU, at a rate of approximately 3% per day in the first week, 2% per day in the second week and 1% after the second week.
-VAP is associated with an increased length of stay and perhaps an additional mortality of 20-30%.
-Selective digestive decontamination and subglottic drainage are associated with decreased incidence of VAP in the general ICU population. There are too few data, however, to recommend SDD in ALI/ARDS.

-High transpulmonary pressures
-Large distending lung volumes
- Tidal opening or closed lung units inducing high shear forces in the interface between open and closed lung units.

high transpulmonary pressure (barotrauma)

overdistension (volutrauma)

-> lesions in the alveo-bronchiolar interfaces with air-leak into the peri-vascular sheath = on the chest radiograph as interstitial emphysema.

The air follows the vascular sheath into the mediastinum, leading to mediastinal emphysema> the air can break through into the pleura (pneumothorax), into the subcutaneous tissue upwards (subcutaneous emphysema) or follow the main vessels downwards (retroperitoneal air) or the oesophagus (peritoneal air).

The incidence of overt pneumothorax is about 10% in patients with ARDS.

high transpulmonary pressure (barotrauma)

overdistension (volutrauma)

-> lesions in the alveo-bronchiolar interfaces with air-leak into the peri-vascular sheath = on the chest radiograph as interstitial emphysema.

The air follows the vascular sheath into the mediastinum, leading to mediastinal emphysema> the air can break through into the pleura (pneumothorax), into the subcutaneous tissue upwards (subcutaneous emphysema) or follow the main vessels downwards (retroperitoneal air) or the oesophagus (peritoneal air).

The incidence of overt pneumothorax is about 10% in patients with ARDS.

Overdistension + tidal opening and closing of lung units, inducing high shear forces in the interface between open and closed lung units

->produce small lesions in the airways and the alveolar compartments which trigger local inflammatory responses ('biotrauma').

The inflammation may become generalised and lead to multiple organ dysfunction.
Bacterial translocation from lungs to the pulmonary capillaries may augment the systemic inflammatory response.
(supported byanimal experiments, in three human studies ) 

Nein!

ALI/ARDS is an acute inflammatory condition in the lungs and is therefore always due to an underlying disease process.
The pulmonary inflammation may be caused by:

A direct (primary or pulmonary) injury to the lungs or

An indirect (secondary or extra-pulmonary) injury

ALI/ARDS due to a direct injury comprises 50-60% of all cases, with pneumonia as the most important single cause (40-50% of all cases). Other common direct causes are aspiration of gastric contents, pulmonary contusion, inhalation of toxic gases and near drowning.

Indirect ALI/ARDS is caused by systemic inflammation with generalised activation of mediators, inflammatory cells and endothelium due to infection (sepsis, peritonitis), tissue ischaemia or tissue damage (trauma, cardio-pulmonary bypass, pancreatitis, major surgery and some intoxications and overdoses).

old age, infection, neurological disease, alcohol abuse and multiple transfusions.

An initial acute first phase of some days to a week characterised by noncardiogenic pulmonary oedema due to capillary leak.

A second phase of one to two weeks with an inflammatory reaction and organisation of the oedema (hyaline membranes).

A third phase in which fibrosis and structural changes in lung tissues dominate.

However, fibrosis and organisation of the oedema may start very early in the process, so that the three phases overlap to some extent.

An initial acute first phase of some days to a week characterised by noncardiogenic pulmonary oedema due to capillary leak.

A second phase of one to two weeks with an inflammatory reaction and organisation of the oedema (hyaline membranes).

A third phase in which fibrosis and structural changes in lung tissues dominate.

However, fibrosis and organisation of the oedema may start very early in the process, so that the three phases overlap to some extent.

An initial acute first phase of some days to a week characterised by noncardiogenic pulmonary oedema due to capillary leak.

A second phase of one to two weeks with an inflammatory reaction and organisation of the oedema (hyaline membranes).

A third phase in which fibrosis and structural changes in lung tissues dominate.

However, fibrosis and organisation of the oedema may start very early in the process, so that the three phases overlap to some extent.

An initial acute first phase of some days to a week characterised by noncardiogenic pulmonary oedema due to capillary leak.

A second phase of one to two weeks with an inflammatory reaction and organisation of the oedema (hyaline membranes).

A third phase in which fibrosis and structural changes in lung tissues dominate.

However, fibrosis and organisation of the oedema may start very early in the process, so that the three phases overlap to some extent.

 increase in measured extravascular lung water (EVLW)

results in increased stiffness of the lungs (reduction of compliance)

decrease in functional residual capacity

increased intrapulmonary shunting.

+development of basal compression atelectasis produced by the weight of the wet lung.

+ increased intra-abdominal pressure, which is common in secondary ALI/ARDS.

delta V (tidalvolumen) / Delta p( Pmax-Peep) ml/mbar

50-100ml =Dehnbarkeit der Lunge

atemarbeit: Volumen x Druck

Extravaskuläres Lungenwasser

errechnet aus intrathorakalem Blutvolumen durch transpulmonaler Thermodilution

Macht Aussage über Volumenüberladung der Lungen

Funktionelle Residualkapazität

Expiratorisches Reservevolumen(forcierte Expiration) + Residualvolumen

Timing:

Within 1 week of a known clinical insult or new/worsening respiratory symptoms

Chest imaging:

a 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

PaO2/FiO2 <300

Früher: Echo oder PCWP <18 mmHg

300-200 ALI

<200 ARDS

PaO₂ >8 kPa

oxygen saturation of haemoglobin in arterial blood (SaO₂) >90%

pH 7.2-7.4

Pplateau <30mmHg

P mean<25mmHg

Vt 6ml/kg Kg

PEEP am "lower inflection point" der Druck-Volumen-Kurve 14-16mbar

Extrapulm.: bilateral symmetrisch dorsal und kaudale Verschattungen

Pulm.: dichte Regionen sind eher asymmetrisch und im Bereich des ursprünglichen Prozesses lokalisiert

Oxygen consumption and CO₂ production increase by 6-10% per °C.

This increased demand can exacerbate respiratory distress

• Fully conscious
• Cooperative
• Haemodynamically stable
• Tolerant of short periods without ventilatory support
• Able to take adequate tidal volumes
• Not fatigued

Immunkompromitierte (Vermeidung von nosokomialen Infektionen durch Intubation)

• Pronounced hypoxaemia
• Aspiration of gastric contents
• Misplacement of the endotracheal tube
• Haemodynamic compromise