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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).

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Causes of respiratory failure i

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)

Mortality: 25 - 35%

Newborn: Infant respiratory distress syndrome (iRDS)

CLD: 15 - 25%

Oxygenation

Lung volumes

Pulm. compliance

Mechanical

ventilation

Ventilator induced lung injury


MRI signal intensity from non-dependent to dependent regions (ARDS)

The water burden of the lung makes the lung of the preterm infant,

despite surfactant treatment,vulnerable to VILI

2-day-old, 38-week gestation infant

4-day-old, 26-week gestation infant

Adams EW AJRCCM 2002; 166:397–402


Nonhomogeneous Lung Disease (ARDS)

The pathophysiology shared by these diseases is nonuniform lung involvement where certain lung units are nearly normal while other areas are markedly abnormal.

A strategy that is effective in opening damaged areas may result in overinflation and trauma to more normal areas of the lung.


Diffuse “Homogeneous” Lung Disease (ARDS)

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.


The best approach = The extended sigh (ARDS)

(stepwise increase and decrease of PEEP using the lowest VT possible)

Required Monitoring:

SaO2, PaO2

PaCO2 and/or endtidal CO2 Hemodynamics


Recruitment (ARDS)

Overdistension

tidal volume

"static" compliance:

static PIP (Pplat) - PEEP

Cst =

PEEP titration

The oxygenation

response: Can it

be used?

Burns D J Trauma 2001;51:1177-81


20/5 (ARDS)

ETT disconnection

PEEP 20

PEEP 15

PEEP 10

PEEP titration: O2 and CO2 response

in a lung injury model of surfactant depletion

Steps of 5 cmH2O to 35/20

Pressure control ventilation

20/5

PEEP 5


b) flow diversion (ARDS)

VA

VA

PaO2

PaO2

PaCO2

PaCO2

O2-improvement = Shunt improvement =

a) recruitment


Prevalent overinflation = dead space effect (ARDS)

1

1

2

2

1

1

1

1

1

1

PEEP

5

PEEP

15

PaO2 and PaCO2 increase

O2-improvement does not exclude overinflation

Gattinoni L (2003)


Allowable V (ARDS)t and disease severity

ALI

(surfactant depleted lung)

Volume (l)

severe

(A)RDS

Airway pressure (cmH2O)


Transition from CMV to HFOV (ARDS)

  • 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)


CMV (ARDS)

CMV

HFOV

HFOV

Rationale for HFOV-based lung protective strategies

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.

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.


The concept of volume recruitment during HFO (ARDS)

Suzuki H Acta Pediatr Japan 1992; 34:494-500


12 (ARDS)

11

10

9

11

Continuous blood gas monitoring during HFO

CDP: 13

Overdistention

Collapse


Causes of respiratory failure ii

Lung hypoplasia syndromes (ARDS)

Congenital diaphragmatic hernia

Potter syndrome

prolonged rupture of membranes

Hydrops fetalis

Causes of Respiratory Failure II

  • The common variable in this group of infants is small, often abnormal lungs. This is associated to:

  • Difficult CO2 elimination

  • Pulmonary hypertension (PPHN)


Congenital diaphragmatic hernia (ARDS)

Gentle ventilation (peak pressure limitation)

“Permissive” hypercapnia  resp acidosis

May worsen PPHN

iNO HFO ECMO

“Versus” VILI (baro- volutraumatisme)


Congenital diaphragmatic hernia (ARDS)

Accept ductal shunting as long as RV function is not impaired!

Bohn D Am J Respir Crit Care Med 2002; 166: 911–915


Survival rates in CDH (ARDS)

Total

Survivors

ECMO

Bohn D Am J Respir Crit Care Med 2002; 166: 911–915


“Geneva” attitude (ARDS)

Surfactant (-)

NO +/- (Cardiac US!)

HFOV +++ (early)

ECMO (-)

The Scandinavian Experience with CDH

Sakri H Pediatr Surg Int (2004) 20: 309–313


Causes of respiratory failure iii

Conducting airways (ARDS)

Aspiration (before or after birth)

Congenital malformation

Tracheal fistula

Causes of Respiratory Failure III


+ (ARDS)

+

Extra- and intrathoracic airway obstruction

Stridor

From Pérez Fontán JJ, 1990


No PEEP (ARDS)

PEEP 10cmH2O

Classical pathological conditions that may lead to a difficult to ventilate situation

Severe airway compression / malacia

courtesy from Quen Mok, Great Ormond Street Hospital for Children, London


Severe airway compression (ARDS)

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)


External PEEP in obstructive lung disease (PEEP-trial) (ARDS)

Caramez MP Crit Care Med 2005; 33:1519 –1528


External PEEP in obstructive lung disease (PEEP-trial) (ARDS)

Caramez MP Crit Care Med 2005; 33:1519 –1528


HFOV in severe airway obstruction (ARDS)

Duval E

Pediatric Pulmonology

2000: 30:350–353


Causes of respiratory failure iv

Air leak syndromes (ARDS)

Pneumothorax

Bronchopulmonary fistula

PIE

Causes of Respiratory Failure IV


CMV (ARDS)

HFOV

Tracheal pressure (cmH2O)

Endinspiration

Endexpiration

CMV

HFOV

PIP

Classical indication for HFV

- because of small pressure swings

PEEP


PIE, bronchopleural fistula, pneumothroax (ARDS)

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;284-6

  • Mayes 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)


Causes of respiratory failure v

Pulmonary perfusion (ARDS)

Congenital heart disease

Persistent fetal circulation

Causes of Respiratory Failure V


31 6/7 wks GA, 1000 g GA (small for GA) (ARDS)

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 18

Poor sats persists: SO2 78% under FiO2 80%


PIP 24, PEEP 8, RR 60 no real change in SO2 (ARDS)

(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


A: Surfactant? (ARDS)

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


CDP 19, Pressure Ampl 46, Freq 12 (ARDS)

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?


CDP 14, Pressure Ampl 34, Freq 15 (ARDS)

SO2 92 %, FiO2 40%

Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6


CDP 14, Pressure Ampl 34, Freq 15 Hz (ARDS)

SO2 92 %, FiO2 can be lowered fast to 40%

Art BGA: pH 7.37, pCO2 5.3, pO2 3.58, BE –1.6

SO2 78 %

CDP 13, Pressure Ampl 30, Freq 15 Hz

SO2 74 %

SO2 91 %, FiO2 can be furter lowered to 25%

Art BGA: pH 7.42, pCO2 4.4, pO2 3.50, BE –2

iNO 8 ppm

CDP 13, Pressure Ampl 25, Freq 15 Hz

Echo cardiac

SO2 94 %, FiO2 can be furter lowered to 21%

Art BGA: pH 7.39, pCO2 4.87, pO2 3.59, BE –2.3


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)

  • Increase in airway pressures for recruitment?

  • Surfactant

  • Increase iNO concentration

  • Other

BGA:


CDP 13, Pressure Ampl 25, Freq 15 Hz saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)


CDP 13, Pressure Ampl 25, Freq 15 Hz, FiO2 100%, iNO 12 ppm saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

Lactate:

2.2

4.5

Stepwise increase in CDP up to 20

SO2 72% pre and postductal

Art 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 ppm

Art BGA: pH 7.1, pCO2 5.0, pO2 2.36, BE - 5


CDP 20, Pressure Ampl 48, Freq 10 Hz, FiO2 100%, iNO 12 ppm saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

SO2 varies around 55 to 75%

Art BGA: pH 6.97, pCO2 10.0, pO2 2.86, BE – 12, Lactate 8.6

  • Increase iNO, B) switch to CMV

  • C) change HFO settings, D) second dose of surfactant


CDP reduction from 20 to 14 saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

Sat immediately improves to 90%,

allowing to reduce FiO2 to 60 then 40 %

Anticipate! A) I have to reduce iNO

B) I lower further CDP

C) 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%


  • R-L shunt across the FO saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

  • severe hypoxemia

  • RV dilatation and failure

  •  poor CO

  • Moderate mainly

  • postductal hypoxemia

  • + ev R-L shunt FO

    2) In general good CO

NO yes

NO may lead to L-R shunt

with pulmonary flooding

PPHN with:

Open ductus

Closed ductus


R-L shunt and RV dilatation before iNO saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)


Shunt inversement under iNO saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)


RDS and PPHN in the newborn infant: Nitric oxide effect saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

Right to left shunt without iNO

Left to right shunt on iNO

PA

PA

Duct

Duct

Ao

Ao

Indication: not poor postductal oxgygenation but signs of poor cardiac output


Take home messages saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

It is not always iRDS that causes hypoxemia in the preterm infant

If you don’t know what to do next with your ventilator settings

reduce your airway pressures first

Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator


Pressure – Flow – Time - Volume saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

Time constant: T = 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


Take home messages saturation to values around 60 to 65% under FiO2 of 100%, hemodynamic stable (BP 49 / 30)

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

When you try to recruit a lung you need to have appropriate monitoring (CO2!)

If you don’t know what to do next with your ventilator settings

reduce your airway pressures first

Try to anticipate changes in respiratory mechanics and gas exchange before turning knobs on your ventilator


  • 1) What are the characteristics of airway or lung disease?

  • - type (etiology) of disease

    • - stage of disease, history

    • - mechanical behaviour

2) Is the problem “physician”-induced?

3) Which bedside method (monitoring) might be helpful during a PEEP trial?


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