Community acquired pneumonia Ventilatory strategies · Ventilator - Induced Lung Injury Barotrauma...

Community acquired pneumonia

Simpósio de Infecção e Sepsis14ºA DIVERSIDADE DA SÉPSIS/SÉPSIS’ DIVERSITY

Community acquired pneumoniaVentilatory strategies

Teresa Honrado

Unidade de Cuidados Intensivos Polivalente da Urgência

Hospital de São João

Common and serious illness

9 - 16 % of patients who need hospitalization require ICU

Community acquired pneumonia

9 - 16 % of patients who need hospitalization require ICU

High mortality rate >20% (23 to 50%) in patients with severe CAP

Risk factors for mortality

SAPS II > 45ShockAcute renal failure

Community acquired pneumonia

Patients who need Intensive Care Unit

Focal/unilateral pneumonia

Difuse lung injury/bilateral infiltrates

Intubation and mechanical ventilation

Acute Lung Injury (ALI)Acute Respiratory Distress Syndrome (ARDS)

Acute onsetPresence of bilateral infiltrates on chest radiographyPaO2/FiO2 >200 e < 300 (ALI) PaO2/FiO2<200 (ARDS)PCWP<18 mmHg or clinical absence of left atrial hypertensio n

American - European Consensus Conference on ARDS ,1994

Direct insult-PneumoniaPulmonary contusionAspirationNear drowningReperfusion Pulmonary Edema

Inflamatory response of the lung, characterised by severehipoxemia, reduced compliance and radioghraphic infiltra tes

Acute Respiratory Distress Syndrome (ARDS)

Pathogenesis

Reperfusion Pulmonary Edema

Indirect insult - Systemic processSepsisAcute pancreatitisMultiple transfusion

The Host’ pulmonary Inflamatory response is a Key i n progression of ALIand is characterized by acute and difuse alveolar d amage

Inflammatory Mechanisms of Acute Lung Injury

Elevated concentration of inflammatory mediators

Disruption of the alveolar epithelial endothelial b arrier

VILI Ventilator - Induced Lung Injury

Barotrauma

Volutrauma and atelectrauma

Biotrauma

Ventilator induced release of proinflammatory mediators

Cells Stretching and Stress failure of cell membran e

High alveolar and microvasculature pressures Inflammatory response of endotothelial cells

MechanotransductionActivation of stretch – sensitive channels Proinflammatory mediators production

Disruption of the Extracellular Matrix

Ventilator induced release of proinflammatory mediators systemic damage to end organs

VILI Ventilator Induced Lung Injury ARDS

Contribution of injurious mechanical ventilation

Inadequate inflammatory response

MODS

Inflammatory response elicited by injurious MV is d irectly linked to multiorgan failuredue to cell apoptosis in distal organs…

[Imai et al.2003][Ranieri t al.1999]

Protective ventilatory strategies attenuate this in flammatory response

Patients who need mechanical ventilation

Protective Ventilation

Ventilatory strategies?

New treatments ?

Protective Ventilation

Physiologic approaches to minimize VILI

Pressure /Volume Curves

Computed tomography

Stress IndexImage

Monitoring

Computed tomography

Electrical impedance tomography

HFVNeurally adjusted ventilatory assist (NAVA)

Positioning

Extra corporal support

Ventilatory management

iLA- Interventional Lung Assist

NIH, ARDS network, NEJM 2000NIH, ARDS network, NEJM 2000

Lower tidal volumes - 22% reduction in mortality

P/V Curve in ALI/ARDS

Volume

UIP

Pressure

LIP

RCTs in ARDS : MortalityRCTs in ARDS : Mortality

1

10NIHNIH AmatoAmato

0,01

0,1

1

StewartStewart BrochardBrochard BrowerBrower

LL 95% CILL 95% CI

OROR

UL 95% CIUL 95% CI

30

40

502O

Is there a Is there a limitlimit for Pplat?for Pplat?

StewartBrochard

AmatoNIH

Pplat (ttt) Pplat (st)0

10

20Cm

H2

Protective Ventilation – “Gold standard”

Tidal volume ≤≤≤≤ 6 ml/Kg

P. Plateau ≤≤≤≤ 30 cm H2O

To minimize shear stress injury due to overdistensi on and local and systemic inflammatory response

Acute Respiratory Distress Syndrome Network, N Engl J Med 2000

and local and systemic inflammatory response

And what about PEEP ?

P/V Curve in ALI/ARDS

Volume

UIP

Pressure

LIP

Zone ofOverdistention

“Safe”

Optimized lung volume : “safe window”Optimized lung volume : “safe window”

Injury

• Overdistension Edema fluid accumulationSurfactant degradationHigh oxygen exposureMechanical disruption

Volume

Pressure

“Safe”Window

Zone ofDerecruitmentand Atelectasis

Injury

• Derecruitment, Atelectasis

Repeated closure / re-expansionStimulation inflammatory responseInhibition surfactantLocal hypoxemiaCompensatory overexpansion

“Open Lung” approach

Ventilatory support - PEEP ?

Protective Ventilation “Gold standard”

PEEP higher than LIP – minimal peep

To prevent end expiratory collapse

High PEEP keeping the lung fully recruited

To avoid recruitement – derecruitment and shear stress forces

To minimize biotrauma

Higher versus Lower Positive End-Expiratory Pressures in Patients with the Acute Respiratory Distress Syndrome

The National Heart, Lung, and Blood Institute ARDS Clinical Trials Network* July 2004

Conclusions These results suggest that in patients with acute lung injury and ARDSwho receive mechanical ventilation with a tidal-volume goal of 6 ml per kilogram ofpredicted body weight and an end-inspiratory plateau-pressure limit of 30 cm of water,clinical outcomes are similar whether lower or higher PEEP l evels are used.

But…

Protective Ventilation – “Gold standard”

Tidal volume ≤≤≤≤ 6 ml/Kg

P. Plateau ≤≤≤≤ 30 cm H2O

To minimize shear stress injury due to overdistensi on and local and systemic inlammatory response

Acute Respiratory Distress Syndrome Network, N Engl J Med 2000

and local and systemic inlammatory response

PEEP – the optimal level and best method used to set it have not been definitively established

“Open Lung” approach

Electrical impedance tomography

Optimising ventilatory management

Monitoring regional lung recruitment and collapseduring incremental and decremental PEEP

Possibility of bedside titration of PEEP based on regional mechanics

Needs further development but seems to be useful fo r monitoring lung function

Assessing alveolar recruitment and lung colapse

High frequency oscillation ventilation - HFOV

Early improvement in PaO2/FiO2 ratio compared to pressure-control ventilation

Maintain acceptable gas exchange while ventilating with very small volumes and relatively high mean airway pressures

Optimising ventilatory management

Early improvement in PaO2/FiO2 ratio compared to pressure-control ventilationTrend to decreased 30-day mortality in the HFOV group

May be an effective rescue therapy?

Derdak S et al Am J Respir Crit Care Med 2002

Prone positioning in acute respiratory distress syn drome: a multicenter randomized clinical trial

Intensive Care Medicine 2008

Improvement in ventilation perfusion mismatchingRecruitment of atelectatic areasIncrease in end expiratory lung volume

Prone Position

Beneficial effect of early continuous prone positio ning

Optimising ventilatory management

The effect of prone positioning in acute respirator y distress syndromeor acute lung injury: a meta-analysis. Areas of uncertainty and recommendations for resear ch. Abroug F, Ouanes-Besbes L, Elatrous S, Brochard L. Intensive Care Medicine 2008

Studies with substancial clinical heterogeneityNo effects on mortalityNo differences in adverse airway complicationsSignificant improvement in oxigenation

Suggest beneffical effect More studies

Focal/unilateral pneumonia

Hipoxemia ⇐ Massive shunt across the diseased lobe

Optimizing V/Q – “ good lung down”

Positioning ?

Optimising ventilatory management

Optimizing V/Q – “ good lung down”

Differencial lung ventilation

Neurally adjusted ventilatory assist (NAVA)

Optimising ventilatory management

Is NIV effective and safe in CAP/ARDS patients ?

Not the same benefit for all

Non Invasive Ventilation for Acute Respiratory Fail ure?

Efficacy of NIV depends on the cause of the hypoxemia

NPPV 30% failure ARDS 51% failurePneumonia 50% failure

Cardiogenic pulmonary edema 10% failure

n = 354 pts;

Multivariate analysis

NIV failure :

• Age > 40• SAPS II ≥ 35• ARDS/CAP

• PaO2/FIO2 1h ≤ 146

Independent risk factors for death

Need for caution Closely monitoring Closely monitoring Not delay intubation

Without significant benefit unless hypercapnic

PaO2 persistently (more than 6 to 8 hours) < 60mmHg orArterial oxygen saturation (SpO2) persistently < 90 % with Venturi oxigen at maximal concentration (50% )

Severe hypoxemic respiratory failure :

NIV in Hypoxemic patients without pulmonary diseas e

-Hypercapnic PaCO2> 45mmHg on admission-Emergency intubation-Recent esophageal, facial or cranial trauma or surg ery -Decreased consciousness-Severe hemodynamic instability-Lack of cooperation-Tracheotomy or other disease from upper airway-Severe ventricular arrhytmia or ischemia-Active upper gastrointestinal bleeding-More than one organ dysfunction

Excluded

..Based on the above evidence, the initiation of NPPV therap y is warranted in appropriate

COPD patients with pneumonia, but the benefit of NPPV therap y in pneumonia patients

without COPD has not been established .

..NPPV therapy should be used with caution in such patients

Acute applications of Noninvasive Positive Pressure VentilationTimothy Liesching et al. Chest 2003; 124:699-713

No RCT specifically designed to determine the effectiveness of NIV in ARDS Results reported by subgroupsVery small number of patients

Lack properly powered RCT evidence

3 highly experienced centers admitted 479 ARDS pati ents

70% ARDS patients ventilated at admission147 pts (31%) patients eligible for study - NIV as f irst line intervention

46% patients failed and intubated

54% of ARDS patients avoided intubation

Predictors of the need for intubationGreater ageHigher SAPS Higher levels põf PEEP

Multivariable analysisSAPS II > 34PaO2/ FIO2 ≤ 175 at 1 hour

were independent predictors of the need of intubati on

Higher levels põf PEEPLower PaO2/ FIO2

The dilemma: to whether or not to use NIV in these patients?

More challenging to support noninvasivelySeverely deranges ventilatory mechanics and gas exchangeHigher levels of pressure support and PEEPFrequently with Sepsis or MODS

The results require caution

There is good results in highly experienced centers in NIV

No evidence that establishes the NIV efficacy to treat ARDS

Cannot even exclude the possibility of NIV was deleterious

NIV failure is associated with higher mortality in patients with de novorespiratory failure

The dilemma: to whether or not to use NIV in these patients?

It remains unanswered

NIV in CAP/ARDS patients? Keys to management

Early screened to determine need for intubation – 1 h

Look for prediction of NIV failure

Highest severity scoresLow tolerance to NIVSeverity of hipoxemiaInability to correct hypoxemia 1-h

Patients require very close monitoring in special units staffed with experienced caregivers

Delayed intubation - increases morbility and mortality

Early screened to determine need for intubation – 1 h

In CAP/ARDS patients, an early improvement in oxigenation is clearly important to justify continuation

Community acquired pneumonia - Ventilatory strategie sConclusions

Protective Ventilation – “Gold standard”

Tidal volume ≤≤≤≤ 6 ml/Kg

P. Plateau ≤≤≤≤ 30 cm H2O

PEEP – the optimal level and best method used to set it ha ve not

Use of NIV - It remains unanswered – use with caution

PEEP – the optimal level and best method used to set it ha ve not been definitively established

Prone Position - beneffical effect suggested