community acquired pneumonia ventilatory strategies · ventilator - induced lung injury barotrauma...
TRANSCRIPT
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