causes of respiratory failure i
DESCRIPTION
Lung tissue Pneumonia Pulmonary hemorrhage Pulmonary edema Respiratory distress syndrome (hyaline membrane disease). Causes of Respiratory Failure I. wet lung. HMD. meconial aspiration. congenital pneumonia. Adults and children: Acute respiratory distress syndrome (ARDS). - PowerPoint PPT PresentationTRANSCRIPT
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Causes of Respiratory Failure I
• Lung tissue– Pneumonia– Pulmonary
hemorrhage– Pulmonary edema– Respiratory distress
syndrome (hyaline membrane disease)
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HMD wet lung
congenital pneumoniameconial aspiration
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Adults and children: Acute respiratory distress syndrome (ARDS)
Newborn: Infant respiratory distress syndrome (iRDS)
Mortality: 25 - 35%
CLD: 15 - 25%
Ventilator induced lung
injury
Mechanical ventilation
Oxygenation
Lung volumes
Pulm. compliance
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4-day-old, 26-week gestation infant 2-day-old, 38-week gestation infant
MRI signal intensity from non-dependent to dependent regionsThe water burden of the lung makes the lung of the preterm infant,
despite surfactant treatment,vulnerable to VILI
Adams EW AJRCCM 2002; 166:397–402
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Nonhomogeneous Lung Disease
A strategy that is effective in opening damaged areas may result in overinflation and trauma to more normal areas of the lung.
The pathophysiology shared by these diseases is nonuniform lung involvement where certain lung units are nearly normal while other areas are markedly abnormal.
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Diffuse “Homogeneous” Lung Disease
The goals of assisted ventilation in this
group of patients are to improve lung inflation,
compliance and ventilation/perfusion matching while
avoiding barotrauma or compromise of cardiac output.
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The best approach = The extended sigh (stepwise increase and decrease of PEEP using the lowest VT possible)
Required Monitoring: SaO2, PaO2PaCO2 and/or endtidal CO2 Hemodynamics
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"static" compliance:
static PIP (Pplat) - PEEP
tidal volumeCst =
PEEP titration
The oxygenation response: Can it be used?
Recruitment Overdistension
Burns D J Trauma 2001;51:1177-81
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20/5
Steps of 5 cmH2O to 35/20 20/5
Pressure control ventilation
PEEP 5
PEEP 10
PEEP 15
PEEP 20
PEEP titration: O2 and CO2 response in a lung injury model of surfactant depletion
ETT disconnection
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O2-improvement = Shunt improvement =
PaO2
VA
PaCO2
a) recruitment
PaO2
PaCO2
VA
b) flow diversion
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PEEP 5
2
1
–
2
1
–
PEEP 15
1
1
1
1
1
1
O2-improvement does not exclude overinflation
Gattinoni L (2003)
Prevalent overinflation = dead space effect
PaO2 and PaCO2 increase
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Airway pressure (cmH2O)
Vo
lum
e (l
)(surfactant depleted
lung)
ALI
severe(A)RDS
Allowable Vt and disease severity
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Transition from CMV to HFOV
1) Pplat approaching 25 cmH2O after PEEP trial (recruitment) and / or PEEP > 12 cmH2O
2) Reduction of Vt < 5 required to match Pplat limits
3) “uncomfortably” high pCO2 or low pH (level dependent from additional pathologies)
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1. HFOV uses very small VTs. This allows the use of higher EELVs to achieve greater levels of lung recruitment while avoiding injury from excessive EILV.
CMVHFOV
CMVHFOV
Rationale for HFOV-based lung protective strategies
2. Respiratory rates with HFOV are much higher than with CV. This allows the maintenance of normal or near-normal PaCO2 levels, even with very small Vts.
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Suzuki H Acta Pediatr Japan 1992; 34:494-500
The concept of volume recruitment during HFO
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Continuous blood gas monitoring during HFO
CDP: 13
CollapseOverdistention
12 11 10 9 11
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Causes of Respiratory Failure II
Lung hypoplasia syndromes– Congenital diaphragmatic hernia– Potter syndrome– prolonged rupture of membranes– Hydrops fetalis
The common variable in this group of infants is small, often abnormal lungs. This is associated to:
- Difficult CO2 elimination
- Pulmonary hypertension (PPHN)
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Congenital diaphragmatic hernia
iNO HFO ECMO
Gentle ventilation (peak pressure limitation)
“Permissive” hypercapnia resp acidosis
May worsen PPHN
“Versus” VILI (baro- volutraumatisme)
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Congenital diaphragmatic hernia
Bohn D Am J Respir Crit Care Med 2002; 166: 911–915
Accept ductal shunting as long as RV function is not impaired!
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To
tal
Su
rviv
ors
E
CM
O
Bohn D Am J Respir Crit Care Med 2002; 166: 911–915
Survival rates in CDH
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Sakri H Pediatr Surg Int (2004) 20: 309–313
The Scandinavian Experience with CDH
Surfactant (-)
NO +/- (Cardiac US!)
HFOV +++ (early)
ECMO (-)
“Geneva” attitude
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Causes of Respiratory Failure III
Conducting airways • Aspiration (before or
after birth)• Congenital
malformation• Tracheal fistula
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Extra- and intrathoracic airway obstruction
Stridor
From Pérez Fontán JJ, 1990
+
+
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Classical pathological conditions that may lead to a difficult to ventilate situation
Severe airway compression / malacia
No PEEP PEEP 10cmH2O
courtesy from Quen Mok, Great Ormond Street Hospital for Children, London
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Severe airway compression
Once you can ventilate these patients (with high PEEP) they are usually difficult to extubate
My advice: Keep a high PEEP on spontaneous ventilation, reduce pressure support and extubate from a high PEEP (ev. to CPAP or NIV)
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External PEEP in obstructive lung disease (PEEP-trial)
VT = 6 mL/kgRR = 6/min
VT = 6 mL/kgRR = 9/min
VT = 9 mL/kgRR = 6/min
VT = 9 mL/kgRR = 9/min
Caramez MP Crit Care Med 2005; 33:1519 –1528
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External PEEP in obstructive lung disease (PEEP-trial)
“paradoxical” response
Biphasic response Classical overinflation response
Caramez MP Crit Care Med 2005; 33:1519 –1528
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Duval E Pediatric Pulmonology 2000: 30:350–353
HFOV in severe airway obstruction
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Causes of Respiratory Failure IV
Air leak syndromes
• Pneumothorax• Bronchopulmonary
fistula• PIE
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CMVHFOV
CMV HFOV
PIP
PEEP
Tracheal pressure (cmH2O)
Endinspiration Endexpiration
Classical indication for HFV - because of small pressure swings
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PIE, bronchopleural fistula, pneumothroax
Recruit to improve oxygenation and in order to lower the FiO2 needed – then reduce the airway pressures to the lowest level needed (air leak will often cease)
References: Shen Chest 2002;121;284-6Mayes Chest. 1991; 100:263-4
Rubio Intensive Care Med. 1986;12:161-3
One sided intubation or airway blocking by inserted balloon catheters is almost never required even in severe airleak
(this was just a nice idea to get a case report)
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Causes of Respiratory Failure V
Pulmonary perfusion• Congenital heart
disease• Persistent fetal
circulation
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31 6/7 wks GA, 1000 g GA (small for GA)
1 course of prenatal steroids 12 hours before delivery
Presents with respiratory distress at birth:RR 64, indrawing, SO2 84% at RA
CPAP trial with fast increasing O2 requirements (> 60%) Venous and arterial umbilical catheter
First art BGA: pH 7.09, PCO2 11 kPa (83 mmHg), pO2 4.36
Intubation
Vent settings: TCPL, RR 60, PEEP 5, PIP 18Poor sats persists: SO2 78% under FiO2 80%
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PIP 24, PEEP 8, RR 60 no real change in SO2(SaO2 82 % , FiO2 100%)
Art BGA: pH 7.11, pCO2 10 kPa, pO2 3.33, BE –3.6
A: Surfactant? B: HFOV? C: Other?
Switch to HFOV: CDP 19, Pressure Ampl 46, Freq 12 Hz
SO2 80 %, FiO2 100%Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
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A: Surfactant? B: Increase CDP?C: Other?
CDP 19, Pressure Ampl 46, Freq 12 Hz
SO2 80 %, FiO2 100%Art BAG: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
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CDP 19, Pressure Ampl 46, Freq 12
SO2 80 %, FiO2 100%Art BGA: pH 7.31, pCO2 6.1, pO2 3.56, BE –2.8
CDP 14, Pressure Ampl 34, Freq 15
SO2 92 %, FiO2 can be lowered fast to 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
Diagnosis and what next?
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CDP 14, Pressure Ampl 34, Freq 15SO2 92 %, FiO2 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
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CDP 14, Pressure Ampl 34, Freq 15 Hz
SO2 92 %, FiO2 can be lowered fast to 40%Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6
CDP 13, Pressure Ampl 30, Freq 15 Hz
SO2 91 %, FiO2 can be furter lowered to 25%Art BGA: pH 7.42, pCO2 4.4, pO2 3.50, BE –2
SO2 78 %
SO2 74 %
CDP 13, Pressure Ampl 25, Freq 15 Hz
SO2 94 %, FiO2 can be furter lowered to 21%Art BGA: pH 7.39, pCO2 4.87, pO2 3.59, BE –2.3
iNO 8 ppm
Echo cardiac
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6 hours later (after refixation of ETT) rapid drop in saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)
BGA: A) Increase in airway pressures for recruitment?B) SurfactantC) Increase iNO concentrationD) Other
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CDP 13, Pressure Ampl 25, Freq 15 Hz
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CDP 13, Pressure Ampl 25, Freq 15 Hz, FiO2 100%, iNO 12 ppm
Stepwise increase in CDP up to 20
SO2 72% pre and postductalArt BGA: pH 7.22, pO2 3.56, pCO2 8.0, BE - 3
Gradually increase in P-Ampl to 46 Surfactant
SO2 varies around 65 to 75% on FiO2 100%, iNO 12 ppmArt BGA: pH 7.1, pCO2 5.0, pO2 2.36, BE - 5
Lactate:
2.2
4.5
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CDP 20, Pressure Ampl 48, Freq 10 Hz, FiO2 100%, iNO 12 ppmSO2 varies around 55 to 75%Art BGA: pH 6.97, pCO2 10.0, pO2 2.86, BE – 12, Lactate 8.6
A) Increase iNO, B) switch to CMV C) change HFO settings, D) second dose of surfactant
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CDP reduction from 20 to 14
Sat immediately improves to 90%, allowing to reduce FiO2 to 60 then 40 %
Anticipate! A) I have to reduce iNOB) I lower further CDPC) I change other settings – which one?D) Excellent work, I need a coffee now!
Reduce pressure amplitude immediately when lowering CDP (coming of overdistension will render oscillation swings more effective!)
Pressure amplitude from 48 to 30 (visible wiggeling)Art BGA: pH 7.39, pCO2 3.4, pO2 6.26, BE – 10
CDP reduction from 14 to 10, P-amplitude to 24, FiO2 to 21%
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PPHN with:
1) R-L shunt across the FO severe hypoxemia
2) RV dilatation and failure poor CO
1) Moderate mainly postductal hypoxemia + ev R-L shunt FO
2) In general good CO
NO yes NO may lead to L-R shuntwith pulmonary flooding
Open ductusClosed ductus
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R-L shunt and RV dilatation before iNO
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Shunt inversement under iNO
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RDS and PPHN in the newborn infant: Nitric oxide effect
Right to left shunt without iNO Left to right shunt on iNO
PA
Ao
DuctPA
Ao
Duct
Indication: not poor postductal oxgygenation but signs of poor cardiac output
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Take home messages
It is not always iRDS that causes hypoxemia in the preterm infant
If you don’t know what to do next with your ventilator settingsreduce your airway pressures first
Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator
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Pressure – Flow – Time - Volume
Time constant: = Crs x Rrs
To short Ti and/or Te will lead to inefficient alveolar ventilation and risk of intrinsic PEEP
Adapt your respirator rate (Ti and/or Te) to the stage and mechanical characteristics of lung disease
The saying “ we ventilate at 60/min” is a testimony of no understanding
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Take home messages
In pulmonary disease lung volumes (functional for gas exchange) are usually reduced – the “need” for smaller VT than physiological VT is a logical consequence of this
If you don’t know what to do next with your ventilator settingsreduce your airway pressures first
Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator
When you try to recruit a lung you need to have
appropriate monitoring (CO2!)
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In situations of difficult ventilation an analytical approach is required
3) Which bedside method (monitoring) might be helpful during a PEEP trial?
2) Is the problem “physician”-induced?
1) What are the characteristics of airway or lung disease?
- type (etiology) of disease
- stage of disease, history
- mechanical behaviour