basic concepts in neonatal ventilation - safe ventilation of neonate

Muhammad Ezzat Abdel-Shafy

MB.BCh, M.Sc PediatricsNeonatology Sp. , Benha Children Hospital

Physiology of Respiration

INFLUX OF FRESH AIR IN THE LUNG

Inspiration++++

Expiration

++++

Spontaneous Inspiration

Volume Change

Gas Flow

Pressure Difference

Mechanical Ventilation

Pressure Difference

Volume Change

Gas Flow

EQUATION OF MOTION

Force = (E x distance) + (R x speed) + (M x acceleration)

M

E

R

Force

What does the pressure do?

OVERCOMES AIRWAYAND

TISSUE RESISTANCE

.P(resist) = RRS x (V)

where R = resistance

• RRS is the feature of the tube

• Energy lost as heat


OVERCOMES INERTIA

..P(inert) = I x (V)

where I = inertance

• Work done to accelerate

gas and tissue

• Negligible in most instances


INDUCES CHANGE IN

LUNG VOLUME

P(vol) = 1/C x (V)

where C = compliance

Work done to overcome

the viscoelastic forces of

the lung and chest wall

EQUATION OF MOTION APPLIED TO THE LUNG

(single compartment model)

R

Pressure = (1/C x volume) + (R x flow) + (I x acceleration)

P

CRS = V/P

I

Law of LaPlace P = 2 x T/r

T = Surfactant

PEEP PIP

Vo

lum

e Surfactant

The Respiratory Equation of Motion

Pressure = Raw x Flow + CL/Volume

Airways ET tube Lung Chest Wall

C=D V

D P

R =D P

D F

Compliance and Resistance

Airway resistance describes the ability of the conducting part of the lung or the respiratory system to resist air flow

P1 P2

Pressure (P1-P2)

Resistance = P1 P2

Flow

Airway resistance in normal lungs = 25-50 cm H2O/L/sec

In Intubated infants it might be 50-100 cm H2O/L/sec

A B

It is determined by

1- Flow

2- Length of the conductive air way

3- Viscosity of the gases

4- Diameter of the airways

Airway Resistance

R=

8nL/r4

Airway Resistance

P1 P2

Laminar Flow

Turbulent Flow

Compliance describes the elasticity or distensiblility of the respiratory system

(lung and + chest wall)

Compliance

•Tidal volume is only a small

fraction of the total volume of

gas present in the lung during

normal breathing.

•The effect of breathing is to

replenish O2 and to wash out

CO2, but there is not complete

replacement of air in the

lungs or even the alveoli with

each breath.

•RV and FRC cannot be

measured with a spirometer.

•The FRC acts as a buffer

against extreme changes in

the alveolar PO2 and PCO2 with

a single breath.

Pulmonary volumes

and capacities

• Minute respiratory volume (V, minute ventilation)

V = VT * f (respiratory rate)

• Dead space volume (VD)

• Alveolar ventilation (VA): VA = (VT - VD) * f

B. Mechanical Properties of the lung

• Lung Distensibility

• Pressure-volume curve

• Compliance (CL= DV/DP)

• Pulmonary surfactant

surface tension

Laplace Law: P = 2T/r

atelectasis

FUNCTIONS OF SURFACTANT

TLCg = 30 mN/m

FRCg < 5 mN/m

• The distance between alveolar gas and alveolar capillary

lumen is on the order of 1 m

• Even though blood spends less than 1 sec in an alveolar

capillary, CO2 completely equilibrates between alveolar

gas and capillary blood and

• O2 normally equilibrates completely

The Alveolar-

Capillary

Diffusion Path

Length is Very

Short

Ventilator Settings

• Physiological Oxygenation Determinants:

1. Concentration gradient.

2. Surface area of gas exchange.

3. Ventilation perfusion matching

4. Diffusion efficency

Volume

Compliance =

Pressure

Air filed lung: hysteresis

Compliance

Mechanical Response to PPVCompliance, CRS

Resistance, RRS

Inspiratory Flow = constant

ΔVL

ΔPLPAO AcDve InspiraDon

Resistance, RRS

Inspiratory Flow

Compliance, CRS

ΔVL

ΔPLPAO = 0 Passive ExpiraDon

Pressure – Flow – Time -Volume• P = (1/CRS) x V + (RRS x Flow)

• VMAX = P x CRS

• Volume change requires time to take place

• When a step change in pressure is applied (P)

volume increases exponentially towards a plateau

Time Constant: (tau) = CRS x RRS

Describes the slope of the exponenDal curve

Volumetric behavior of the lung when exposed to pressure

Salazar & KnowlesJ Appl Physiol 1964

Vmax = maximum lung volume P = applied pressureh = half opening pressure

Time Constant of the Lung


= Dme required for a 63.2% stepwise change in a measured quanDty (eg volume)

How much of maximum VT

is delivered depends on Ti

How rapidly VT is achieved is determined by and FLOW

Time constants


Normal lung:

τ 3 mL/cm H2O x 0.04 cm H2O/mL/sec

0.12 sec (insp and exp)

Parenchymal disease:

τ 0.5 mL/cm H2O x 0.04 cm H2O/mL/sec

0.02 sec (insp and exp)

Airway disease:

τ 2 mL/cm H2O x 0.1 cm H2O/mL/sec

0.2 sec (exp > insp)

Effect of varying Time Constants

Understanding Time Constants at

the bedside

• All about the FLOW wave form

Time Constants

What would you do here?

Ti

Te

Zero flow Zero flow Zero flow

Total insp

time

Total insp

time

Total insp

time

Aim for zero flow condition being less than

⅓ of total insp time

How long should you set theTi?

Alveolar Plateau

Leak

Leak

The only true soluDon in the presence of a larger leak is to assess chest wall movement

Expiration is important

Premature flow terminaDon during expiraDon = gas trapping

Auto-PEEP

Functional Residual capacityresidual capacity

Tidal Volume

Inspiratoryreserve volume

Reserve volume

EExpiratoryReserve volume

Vital capacity

Total Lung Capacity

Lung Capacity and Volumes

FRC

FRC

Optimal Lung Inflation

Effect of Lung Volume on PVR

Lung Volume

PVR

Total PVR

Large VesselsSmall Vessels

Atelectasis

Overexpansion

FRC

PVR is the lowest at FRC

Overexpansion of

small vessels PVR

Atelectasis of large

vessels PVR

OxygenaDon

Lung Volume+ Diffusion and perfusion

Goals of mechanical ventilation

Maintain acceptable gas exchange with a minimum of:

lung injury

hemodynamic impairment

other adverse events (i.e. neurologic injury)

Minimize work of breathing

Surfactant deficiency

Alveolar atelectasis

Tidal breathing

High distending

pressure

Stretch and distorsion

Cellular membrane disruption

Protein rich oedema ( hyaline membranes)

Higher [ O2 ] and pressure

Barotrauma PIE, BPD

Need for high [ O2 ]

O2 toxicity

PULMONARY INJURY SEQUENCE

Acute

Lung

inflammation

CNN Rocourt

Ventilator Associated Lung Injury

All forms of positive pressure ventilation (PPV)

can cause ventilator associated lung injury

(VALI).

VALI is the result of a combination of the

following processes:

Barotrauma

Volutrauma

Atelectrauma

Biotrauma

Slutsky, Chest, 1999

Open Lung Ventilation Strategy

Volume

Pressure

Zone of Overdistention

Safe

window

Zone of

Derecruitment

and

atelectasis

Goal is to avoid injury zones

and operate in the safe window

Froese, CCM, 1997

Avoidance of mechanical ventilation

Surfactant replacement

Avoidance of excessive VT (Volume-targeted

ventilation)

Optimization of lung volume/ avoidance of atelectasis

Permissive hypercapnia/ lower SPO2

High-frequency ventilation

(?) Nitric oxide

(?) Liquid ventilation

Lung Injury: Strategies for Prevention

Oxygenation

MAP

PIP

PEEPI/E

ratio

Flow

FIO2

IT ET Time

Base line pressure

MAP

Mean Airway Pressure and How to Increase it

1. Increase PIP

2. Increase PEEP3. Increase IT

4. Increase Flow

4 3

2

Pressure

Cm H2O

I Time E Time I Time

Time (sec)

MAP= K(PIP-PEEP) {IT/(IT+ET)}+PEEP

1

Ventilator Settings

• MEAN AirWay Pressure (Paw)

In retrospect, the simplifying but reductionist elegance that focused upon a single unitary number [P AW ] may have misled the field. (Monkman and Kirpalani 2003).

Ventilator Settings

• Physiological Oxygenation Determinants:

1. Concentration gradient.

2. Surface area of gas exchange.

3. Ventilation perfusion matching

4. Diffusion efficency

Ventilator Settings

• The open lung approach makes the oxygenation improvement by increasing

mean airway pressure a matter of the past.

• The mean airway pressure is to be considered a monitoring tool and a

marker for severity of lung affection (with FiO2 requirements).

CO2 Elimination

MV

FrequencyResistance

Time constant

Tidal Volume

Pressure Gradient Compliance

PEEPPIP

ETI T

I/E ratio

Lung Protective Strategy

Low VT and P makes it possible to use higher PEEP without

high PIP. Ventilation on the expiratory limb of the P-V loop, once

recruitment occurs.

Ventilatory Volumes

VT = 4- 7 ml/kg

VD = 2-2.5 ml/kg

F= 40 -60 breath /minute

MV= 200-480 ml/kg/min

VA= 60-320 ml/kg/min

VT = VD + V A

Minute Ventilation = RR X VT

Minute alveolar ventilation= RR X V A (VT -VD)

Static Lung Volumes

RV= 10-15 ml/kg

FRC= 25-30ml/kg

TLC=50-90 ml/kg

VC= 35-80 ml/kgBaby Lung Concept!!!!

Patient Ventilator Interaction

Patient ventilator interaction can be simplified to three distinct phases:

Patient triggering

Ventilator breath delivery

Ventilator must deliver a sufficient amount of flow to mach or exceed the spontaneously breathing patient’s inspiratory demand

Deliver an adequate tidal volume

An adequate rise to pressure time (in pressure breath only)

The process of cycling the ventilator from inspiration to expiration

Patient-Ventilator AsynchronyPatient ventilator asynchrony will result in

# Impaired gas exchange

#Increased work of breathing

#Increased load to the respiratory muscles

# Increased intrathoracic pressures.

#Increased need for sedation and paralysis.

#Inconsistent tidal volume delivery

#Increased risk of IVH and fluctuations of BP

Neonatal synchrony should aim at preventing ineffective, delayed and double or auto triggering which may impair lung mechanics, gas exchange which in turn can lead to increase use of sedation and prolong the duration of recovery.

Discontinuation from the ventilatory support could be delayed, resulting in more complications.

Variation in tidal volume due to asynchrony in a patient on IMV. b Reduced variation in tidal volume by changing to SIMV Mode. c Improvement in tidal volume by changing to Assist Mode.

Assisted Ventilation of the Newborn 3/e, Goldsmith and Karotkin, Elsevier 2003.

Patient-Ventilator Asynchrony

How to Synchronize:II-Qualitative

Type of trigger

Pressure

Flow

NAVA

Pressure support

The device auto-regulates the PIP (“working pressure”) within preset limit (“pressure limit”) to achieve VT that is set by the user. Regulation of PIP is in response to exhaled VT to minimize artifact due to ETT leak.

Delivery room resuscitation

• The ventilation management efficacy starts in the delivery room.

• It is now well understood that the initial steps in resuscitation

significantly affects the outcome and may determine the pathway

of respiratory care of the patient.

• With good antenatal and delivery room management many

babies will be saved from the topic of this talk.

Adaptation Failure


• In full term infants, it is reasonable to initiate resuscitation with air.

Supplementary oxygen may be administered and titrated to achieve a

targeted pre-ductal oxygen saturation.

• In preterm babies <35weeks, it is more sophisticated.

• Several studies comparing low oxygen (21%-30%) with high oxygen (65% or

higher) showed no benefit or harm (PLoS One. 2012;7(12):e52033).


• In all studies most of the babies required about 30% at time of stabilization

irrespective to starting point.

• The current recommendation is to use low oxygen (21%-30%) for preterm

infants as a starting point for resuscitation.

• Like the full term babies, titration of oxygen to reach the targeted preductal

oxygen saturation.

• For good use of these recommendation it is of utmost importance to have a

pulse oximeter monitoring during resuscitation.


• The resuscitation of preterm babies is more challenging than full term

babies. The smaller the baby, the bigger the challenge.

• The early use of CPAP in delivery room have been showed to be beneficial

and may be superior to more aggressive intubation and ventilation.

• Early CPAP alone without prophylactic surfactant is the preferred option,

with selective surfactant treatment. (SUPPORT trial 2012, European consensus guidelines

for RDS 2013, AAP statement on Respiratory support in preterm infants at birth)


• T-Piece resuscitator is the preferred device for resuscitation especially in

preterm babies.

• Sustained Lung Inflation (SLI) is another alternative to fill the lung with

AIR. It showed a decrease in the need for mechanical ventilation in a

historical cohort. Lista G. et al, Neonatology 2011, 99(1):45-50.

• RCTs for SLI are not showing that much difference. SLI STUDY.


o Animal studies have suggested that a longer sustained inflation may be beneficial for establishing FRC during transition from fluid-filled to air- filled lungs after birth.

o Human studies showed reduction of the need for MV with sustained inflation. However, no benefit was found for reduction of mortality, bronchopulmonary dysplasia, or air leak.

Pediatrics Jan 2015, peds.2014-1692 (SLI study)


PPV and CPAP

• Administration of PPV is the standard recommended treatment for both preterm and term

infants who are apneic. Different devices can be used for PPV.

• The use of PEEP was speculated to be beneficial when PPV is administered to the newly born.

• Few RCTs showed no benefit for PEEP use in preterm infants regarding mortality, need for

cardiac drugs or chest compressions, or resuscitation stabilization at 5 min. However, the use of

PEEP decreased the intubation rate and the maximum pressures applied during PPV. J Pediatr.

2014 Aug;165(2):234-239.e3

• NRP recommends that, when PPV is administered to preterm newborns, use of approximately

5cm H2O PEEP is suggested, which will require the addition of a PEEP valve for self-inflating

bags.

PPV and CPAP

• For many years there have been a debate about early use of CPAP

prophylactically compared to intubation and ventilation for extremely

premature babies.

• Many studies tried to address this issue but there have been no good quality

studies to solve the issue. (Vermond Oxford DRM study).

• And to complicate things more there have been some conflicting data from

some trials. (COIN trial)

PPV and CPAP

• Now there is a good quality evidence that prophylactic CPAP improves many

outcomes compared to intubation and surfactant. It reduces need for MV,

reduces need for surfactant, decreases incidence of BPD and death or BPD,

decrease severe IVH and air leaks. N Engl J Med. 2010 May 27;362(21):1970-9

(SUPPORT study), Cochrane Database of Systematic Reviews 2016, Issue 6. Art. No.:

CD001243

• Based on this evidence, spontaneously breathing preterm infants with

respiratory distress should be supported with CPAP initially rather than

routine intubation for administering PPV.

Physiologic Effects of CPAP

Courtesy of Stewart Hooper

Atmospheric Pressure nCPAP 6 cmH20

Intubation and Surfactant

• The decision to intubate may be a life changer for the baby. The intubation

procedure itself carries many risks and potential complications.

• The intubation is a DE-Stabilizing maneuver.

• Unfortunately, the pre-medication is largely under-used although it is safe,

well tolerated, and decreases the adverse events with intubation plus

increasing chance of successful attempt.

• The most important component is analgesic (mostly opiate). Atropine and

muscle relaxant can be added.

Intubation and Surfactant

INSURESUR LISA

• Less Invasive Surfactant Administration:

• Small feeding tube placed in the trachea under vision using laryngoscope

while the baby is spontaneously breathing on CPAP.

• No baby will be intubated for surfactant administration only.

What about Surfactant

Property Effect

Surface Activity Essential for rapid adsorption and spreading Gravity Surfactant distributed with fluid by gravity in large

airways Volume The higher the volume, the better the distribution Rate of Administration Rapid administration results in a better distribution Ventilator Settings Pressure and positive end-expiratory pressure clear

airways of fluid Fluid Volume in Lung Higher volumes of fetal lung fluid or edema fluid

may result in a better distribution

• Exogenous Surfactant interacts with the type II cells. Surfactant

components are recycled from the airspaces back to type II cells

where lipids are diverted into lamellar bodies for re-secretion.

• Recycling is more efficient in preterm than adult lung, and

recycling rates as high as 80- 90% have been measured in the

newborn. The very long biologic half-life values for airspace

surfactant are explained by continued reuptake and resecretion.

How treatment works

• The treatment dose of surfactant functions as substrate for recycling in the uninjured preterm lung, partially explaining why surfactant treatment effects can persist for days. Surfactant treatment quickly increases the metabolic pool for endogenous metabolism.

• The second bit of magic is the effect that endogenous surfactant metabolism has on the surfactant used for treatment. All surfactants used to treat infants are far from “natural” in that the compositions and lipoprotein aggregate forms differ from the surfactant in the hypo- phase of the healthy lung.

• However, within hours of surfactant treatment, the preterm lamb lung transforms treatment surfactant into a surfactant that is more effective when recovered and used for a second treatment; that is, the surfactant is improved or activated by contact with the preterm lung.

• The presumption is that the lung contributes surfactant proteins and recycles the exogenous surfactant components for secretion in the lung saccules at the right place and time.

• Therefore, the persistence of a surfactant response after a single treatment results from the uninjured lung integrating the exogenous surfactant into endogenous surfactant metabolism, a process that continues over many days. A single treatment can cure the surfactant deficiency disease component of RDS in most infants.

• The crucial variable for the need for a second dose of surfactant is lung injury. The preterm infant who has RDS has a low surfactant pool size, and if lung injury results in edema, the proteins in the edema fluid can inhibit surfactant function. This concept can be illustrated by the inverse relationship between oxygenation and minimal surface tension in preterm lambs following a surfactant treatment

• The crucial variable for the need for a second dose of surfactant is lung injury. The preterm infant who has RDS has a low surfactant pool size, and if lung injury results in edema, the proteins in the edema fluid can inhibit surfactant function.

• The non-responders either have lung injury prior to birth (infection), lung injury after birth and prior to treatment, pulmonary hypoplasia, or a cardiovascular explanation for the lack of response (low blood pressure, congenital heart disease). The clinician should seek diagnoses other than RDS in the preterm infant who has respiratory failure and does not respond to surfactant.

Matching Ventilatory Setting with Pathophysiologic state

When using ventilation strategy you should pay attention to the

underlying lung condition. There is no one-size-fits-all strategy.

Consider the cause of ventilation, the course of the disease, and

the mechanical derangement.

Notice that with any strategy, the setting adjustment depends

mainly on the lung mechanics.

Normal Lung Ventilation

• Why to ventilate?

• What are mechanical characteristics of

the lungs?

Ventilation Strategy for Normal Lung

Settings

1. Times: 1. Ti: good (0.4-0.5)

2. Rate: med 20-40/min.

2. Pressures:

1. CDP: Low-mod (4-5).

2. Inflating: least to have Vt 4-6

ml/kg (8-10-12).

Attention to cardiovascular interaction with ventilation.

Respiratory Distress Syndrome (RDS)

library.med.utah.edu/WebPath/PEDHTML/PED055.html

Using CPAP immediately after birth with subsequent selective surfactant administration may be considered as an alternative to routine intubation with prophylactic or early surfactant administration in preterm infants. If it is likely that respiratory support with a ventilator will be needed, early administration of surfactant followed by rapid extubation is preferable to prolonged ventilation

Surfactant: How and when

• Prophylactic Surfactant: any place yet??

• Rescue surfactant: early vs. late.

• What type of surfactant to use

animal or synthetic

what animal?

• Technique: no difference

• Stabilization before and after.

• Setting adjustment.

• Surfactant is a powerful recruitment tool

Guidelines for Surfactant Treatment of RDS

< 26 wk 29-31 wk > 32 wk

Early CPAP/NIPPV

Surfactant if intubated

for resuscitation

Early CPAP/NIPPV

Surfactant if intubated

for resuscitation

Observe

CPAP/NIPPV if

respiratory distress

Early Rescue with

100-200 mg/kg if FiO2 >

0.30 + white CXR.

•Start Caffeine

Early Rescue with

100-200 mg/kg if FiO2 >

0.40 + white CXR.

•Start Caffeine

Delayed Rescue with

100 mg/kg if FiO2 > 0.40

+ white CXR

•Caffeine if symptomatic

Redosing:

FiO2 > 0.30

How soon: 2-12 hrs

from the 1st dose

Redosing:

FiO2 > 0.40

How soon: 6-12 hrs

from the 1st dose

Redosing:

FiO2 > 0.40

How soon: 6-12 hrs

from the 1st dose

Ventilation Strategy for RDS

Settings

1. Times:

1. Ti: short (0.2-0.35 sec)

2. Rate: high >60/min.

2. Pressures:

1. CDP: good-high (4-6-8-10!!!!).

2. Inflating: least to have Vt 4-6

ml/kg (12-15).

Pressures need change after

surfactant.

Blood Gases

1. Permissive Hypercapnea

• pCO2 levels 45-65

• pH 7.25-7.3

2. Less Aggressive Oxygenation

Goals

• paO2 45-55

• Saturations 88-92%

Ventilator Settings

• The challenge is to detect the optimal PEEP.

• Failure to give appropriate PEEP will make the heterogeneous pathology of

the lung worse.

“Atelectotrauma”

Expiration

InspirationVentilated

Stable

Ventilated

Unstable Unventilated

Non-Homogenous Aeration in RDS

Recruitment/ de-recruitment injury

Shear forces

Adequate PIP, Insufficient PEEP

CCP COP

CCP = critical closing pressure; COP = critical opening pressure

VT

P

FRC

P

VInspiration

Expiration

Adequate PIP, Adequate PEEP

COP PCCP

FRC

V

VT

P

Good oxygenation, low FiO2, minimal lung injury

CCP = critical closing pressure; COP = critical opening pressure

Ventilator Settings

• The challenge is to detect the optimal PEEP.

• Failure to give appropriate PEEP will make the heterogeneous pathology of

the lung worse.

!

P

COPCCP

!!

VT

FRC

E I

Ventilator Settings

• Trials have been made to adjust PEEP according to P-V loop lower infliction

point. But in newborns with narrow ETT, the resistance of the tube will

distort the shape of P-V loop shifting the lower infliction point.

• It is better practice to titrate PEEP according to lung opening predicton by

oxygenation improvement (good saturation in FiO2<0.25).

basic concepts in neonatal ventilation - safe ventilation of neonate

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