Nigerian Journal of Paediatrics 2012;39(1): 35 - 43
SYMPOSIUM
Ahmed G,
Ventilatory support of the newborn
Mohammed SS,
Abdulkadir MB,
Adesiyun OO
DOI: http://dx.doi.org/10.4314/njp.v39i1.8
Received: 3rd November 2011
Abstract
Respiratory disorders
The goal of treatment is safe and
Accepted: 3rd November 2011
are a frequent cause of admission
effective assistance to oxygen
in the newborn. Respiratory
delivery and carbon dioxide
Adesiyun OO
( )
diseases have unique physiologic,
removal from the tissues. Inspired
Ahmed G,
a n a t o m i c
a n d
c l i n i c a l
oxygen should be administered in a
Mohammed SS,
characteristics during this period
controlled manner to provide
Abdulkadir MB,
necessitating special management.
adequate but not excessive blood
K n o w l e d g e
o f
t h e
oxygen tension levels. Mechanical
Department of Paediatrics and
pathophysiology of pulmonary
ventilation may be required to treat
Child Health, University of Ilorin
diseases and their differential
metabolic abnormalities. There is
Teaching Hospital,
impact on the lungs of differing
the need for continuous monitoring
P.M.B.1459, Ilorin, Nigeria.
stages of maturity is essential to the
and re- evaluation. This article is
Email: omotayoadesiyun@yahoo.com,
safe and efficacious applications of
intended to present an overview of
Tel: +2347087621125
special techniques of treatment.
the embryology of the respiratory
P r i n c i p l e s o f r e s p i r a t o r y
system, pulmonary physiology in
m a n a g e m e n t
i n c l u d e
the newborn, the principles of
establishment of the airway,
oxygen therapy and mechanical
ensuring oxygenation, assisted
ventilation. It also discusses the
ventilation, assessing adequacy of
complications that can follow.
ventilation, correction of
metabolic abnormalities and
Key words: Ventilatory support,
alleviation of cause of distress.
oxygen delivery, newborn
Introduction
The development of the lung is divided into 5
overlapping stages.
Embryology of the Respiratory System
Embryonic stage (3-7week) branching of
the
primitive bud to form terminal
The respiratory system is an outgrowth of the ventral
bronchioles.
wall of the foregut. While the epithelium of the
Pseudo glandular stage (5-17weeks) further
larynx, tracheal, bronchi, and the alveoli originate in
division of the terminal bronchiole into 2 or
the endoderm, the cartilaginous, muscular, and
more respiratory bronchioles.
connective tissue component are mesodermal in
Canalicular stage (16-26week) terminal sacs
origin. By the 4
th
week of gestation, the
are form and the capillaries establishes close
tracheoesophageal septum separates the tracheal
network. The type II alveoli cells are well
from the foregut, with the foregut gut dividing as the
delineated.
lung bud anteriorly and the esophagus posteriorly.
Saccular stage (26-36week) thinning of the
Contact between the two is maintain through the
interstitium and fusion of type I cells, and the
larynx, which is formed by the tissues of the 4 and
th
capillary basement in preparation for the lung
6 pharyngeal arches.The lung bud develop into 2
th
function as an organ of gas exchange.
main bronchi, while the right forms 3 secondary
Alveolar stage (36week -3-8yrs of age)
bronchi and 3 lobes, the left forms 2 bronchi and 2
secondary septal formation, further sprouting of
lobes.
the capillary network & development of true
alveoli.
36
Towards the end of the 6 month, type II alveoli
th
of the air inside the lung alveoli. When no air is
cells produce surfactant a phospholipids rich fluid
flowing into or out of the lungs, the pressures in all
capable of lowering surface tension at the alveoli
parts of the respiratory tree, all the way to the alveoli,
surface.
are equal to atmospheric pressure, that is, 0 cmH O
2
pressure. Transpulmonary pressure is the difference
Clinical importance
between the alveolar pressure and the pleural
pressure. It is the pressure difference between that in
Abnormalities in stage I
lung aplasia,
the alveoli and that on the outer surfaces of the lungs,
tracheoesophageal fistula and pulmonary cysts.
and it is a measure of the elastic forces in the lungs that
Abnormalities in stage II - pulmonary
tend to collapse the lungs at each instant of respiration,
s e q u e s t r a t i o n ,
c y s t i c
a d e n o m a t o i d
called the recoil pressure .
malformations, congenital diaphragmatic
hernia.
Compliance describes the elasticity or distensibility
Abnormalities in stage III - Respiratory distress
(e.g., of the lungs, chest wall, respiratory system) and
syndrome (RDS) and lung hypoplasia.
is calculated from the change in volume per unit
Before birth, the lungs are filled with fluid that
change in pressure as follows:
has a high chloride content, little protein, some
Compliance =
! Volume
mucus from bronchi gland. Fetal breathing
! Pressure
movement begins before birth and these
movements are important for stimulating the
The higher the compliance, the larger the delivered
development and conditioning of respiratory
volume per unit changes in pressure. Normally, the
muscles.
chest wall is compliant in newborns and does not
impose a substantial elastic load compared to the
Pulmonary Physiology in the Newborn
lungs. The range of total respiratory system
compliance (lungs + chest wall) in newborns with
The goals of respiration are to provide oxygen to the
healthy lungs is 0.003-0.006 L/cm H O, while
2
tissues and to remove carbon dioxide. To achieve
compliance in babies with RDS may be as low as
these goals, respiration occurs through four major
0.0005-0.001 L/cm H O. The alveolar surface tension
2
functions:
is an important factor affecting the compliance of the
lungs is the surface tension of the film of fluid that
Pulmonary ventilation which involves the inflow
lines the alveoli. If the surface tension is not kept low
and outflow of air between the atmosphere and
when the alveoli become smaller during expiration,
the lung alveoli;
they collapse in accordance with the law of Laplace.
Diffusion of oxygen and carbon dioxide between
the alveoli and the blood gas exchange.
The law states that in spherical structures like the
Transport of oxygen and carbon dioxide in the
alveoli, the distending pressure equals 2 times the
blood and body fluids to and from the body's
tension divided by the radius (P = 2T/r). The low
tissue cells.
surface tension when the alveoli are small is due to the
Regulation of ventilation and other facets of
presence in the fluid lining the alveoli of surfactant, a
respiration.
lipid surface-tension-lowering agent. Surfactant is a
mixture of dipalmitoylphosphatidyl-choline (DPPC),
Mechanics of Pulmonary Ventilation
other lipids, and proteins. Surfactant also helps to
prevent pulmonary edema.
The lungs can be expanded and contracted in two
ways: Either by downward and upward movement
Resistance describes the inherent capacity of the air
of the diaphragm to lengthen or shorten the chest
conducting system (e.g, airways, endotracheal tube
cavity or via elevation and depression of the ribs to
[ETT]) and tissues to oppose airflow and is expressed
increase and decrease the anteroposterior diameter
as the change in pressure per unit change in flow as
of the chest cavity.
Normal quiet breathing is
follows:
accomplished almost entirely by the first method
Resistance =
! Pressure
while the second method occurs during heavy
! Flow
breathing and involves the use of muscles of
Airway resistance depends on the radii of the
inspiration and expiration.
airways (total cross-sectional area), the length of
airways, the flow rate, and the density and viscosity
Pleural pressure is the pressure of the fluid in the thin
of gas. Resistance is governed by Poiseuille's law
space between the lung pleura and the chest wall
stated as:
pleura. This is normally a slight negative pressure.
R = 8 l η ÷ π r ( where R - resistance, η - viscosity, l
4
On the other hand, alveolar pressure is the pressure
- length, and r - radius).
37
Thus, airway resistance is inversely proportional to
Volumes and Capacities
its radius raised to the 4 power. If the airway lumen
th
is decreased in half, the resistance will increase 16-
Tidal volume (V T ) is the amount of air moved in
fold. Newborns and young infants with their
and out of the lungs during each breath. At rest, it
inherently smaller airways are especially prone to
is usually 67 mL/kg body weight.
marked increase in airway resistance from inflamed
Inspiratory capacity (IC) is the amount of air
tissues and secretions. In diseases in which airway
inspired by maximum inspiratory effort after tidal
resistance is increased, flow often becomes
expiration.
turbulent. Distal airways normally contribute less to
Expiratory reserve volume (ERV) is the amount of
airway resistance because of their larger cross-
air exhaled by maximum expiratory effort after
sectional area, unless bronchospasm, mucosal
tidal expiration.
edema, and interstitial edema decrease their lumen.
Residual volume (RV) is the volume of gas
Small endotracheal tubes that may contribute
remaining in the lungs after maximum expiration.
significantly to airway resistance also are important,
Vital capacity (VC) is defined as the amount of air
especially when high flow rates that lead to turbulent
moved in and out of the lungs with maximum
flow are used. The range for total airway plus tissue
inspiration and expiration.
respiratory resistance values for healthy newborns is
20-40 cm H O/L/s; in intubated newborns this range
Total lung capacity (TLC) is the volume of gas
2
occupying the lungs after maximum inhalation.
is 50-150 cm H O/L/s.
2
Functional residual capacity (FRC) is the amount
of air left in the lungs after tidal expiration.
Time constant , measured in seconds, is a product of
compliance and resistance.
The VC, IC, and ERV are decreased in lung pathology
but are also effort dependent. The FRC represents the
Time constant = Resistance X Compliance
environment available for pulmonary capillary blood
for gas exchange at all times. A decrease in FRC is
It is a measure of how quickly the lungs can inflate or
often encountered in alveolar interstitial diseases and
deflate, and also a measure of how quickly the
thoracic deformities.
The major pathophysiologic
alveoli get into equilibrium with the air passages.
consequence of decreased FRC is hypoxemia.
Thus, the time constant of the respiratory system is
Reduced FRC results in a sharp decline in P A O 2 during
proportional to the compliance and the resistance.
exhalation because a limited volume is available for
For example, the lungs of a healthy newborn with a
gas exchange.
compliance of 0.004 L/cm H O and a resistance of 30
2
cm H O/L/s have a time constant of 0.12 seconds.
2
Gaseous exchange in the respiratory system occurs
When a longer time is allowed for equilibration, a
only in the terminal portions of the airways. The gas
higher percentage of airway pressure equilibrates
that occupies the rest of the respiratory system that is
throughout the lungs. The longer the duration of the
not available for gas exchange with pulmonary
inspiratory (or expiratory) time allowed for
capillary blood dead space. This space can be divided
equilibration, the higher the percentage of
as the anatomic dead space (respiratory system
equilibration.
volume exclusive of alveoli) and the physiologic
(total) dead space (volume of gas not equilibrating
For practical purposes:
with blood, i.e, wasted ventilation). In healthy
individuals, the two dead spaces are identical; but in
One time constant = 63% equilibrium.
disease states, there may be no exchange between the
2 time constant = 86% equilibrium.
gas in some of the alveoli and the blood, and some of
3 time constant = 95% equilibrium.
the alveoli may be overventilated.
5 time constant = 100% equilibrium.
Ventilation
perfusion (V/Q) mismatch usually is
Lungs with decreased compliance (such as in RDS)
caused by poor ventilation of alveoli relative to their
have a shorter time constant. Lungs with a shorter
perfusion. A V/Q mismatch is a major cause of
time constant will complete inflation and deflation
hypoxemia in infants with respiratory distress
faster than normal lungs. Patients with shorter time
syndrome (RDS) and other causes of respiratory
constants are best ventilated with relatively smaller
failure.
tidal volumes and faster rates to minimize peak
inflation pressure. In patients with increased airway
Gas exchange
resistance, a fast respiratory rate (and, therefore, less
time) does not allow enough pressure equilibration
The minute volume is a product of V T and respiratory
to occur between the proximal airway and the
rate. Alveolar ventilation is the volume of
alveoli.
atmospheric air entering the alveoli and is calculated
as:
38
(V T - dead space) × respiratory rate
the affinity of hemoglobin for O . The greater affinity
2
Gas exchange occurs by the process of diffusion and
of fetal hemoglobin (hemoglobin F) than adult
equilibration of alveolar gas with pulmonary
hemoglobin (hemoglobin A) for O 2 facilitates the
capillary blood.
movement of O 2 from the mother to the fetus.
Diffusion depends on the alveolar capillary barrier
O 2 Hb dissociation curve
and amount of available time for equilibration. In
health, the equilibration of alveolar gas and
pulmonary capillary blood is complete for both
oxygen and carbon dioxide. In diseases in which
alveolar capillary barrier is abnormally increased
(alveolar interstitial diseases) and/or when the time
available for equilibration is decreased (increased
blood flow velocity), diffusion is incomplete.
Because of its greater solubility in liquid medium,
carbon dioxide is 20 times more diffusible than
oxygen. Significant elevation of CO 2 does not occur
as a result of a diffusion defect unless there is
coexistent hypoventilation.
Oxygen transport
Control of Respiration
Oxygen (O 2 ) diffuses through the respiratory
membrane from the alveoli to the blood from where
The control and maintenance of normal breathing
it is transported to the tissues for utilization. O 2 is
largely reside within the respiratory control centers
transported in the blood combined with the O -
2
of the bulbopontine region of the brainstem.
carrying protein- hemoglobin. O 2 delivery to a
Neurons within this area of the brain efferent output
particular tissue depends on the amount of O 2
to the respiratory control muscles. Multiple afferent
entering the lungs, the adequacy of pulmonary gas
inputs induce modulation of the central respiratory
exchange, the blood flow to the tissue, and the
center efferent outputs to the respiratory and airway
capacity of the blood to carry O 2. The reaction is
muscles and lungs.
rapid, requiring less than 0.01 s. The deoxygenation
(reduction) of Hb O
4
8
is also very rapid. The
Among these inputs are signals from central and
transition from one state to another (i.e deoxyHb →
peripheral chemoreceptors, pulmonary stretch
OxyHb → deoxyHb) has been calculated to occur
receptors, and cortical and reticuloactivating system
about 10 times in the life of a red blood cell.
8
neurons. Theophylline and caffeine have been shown
to increase the central chemoreceptor ventilatory
2
The oxygen-hemoglobin dissociation curve, the
response to CO and decrease the number of apneic
curve relating percentage saturation of the O -
spells in premature babies.
2
carrying power of hemoglobin to the PO 2 has a
Physiologic Response to Respiratory Diseases
characteristic sigmoid shape. Combination of the
first heme in the Hb molecule with O 2 increases the
Tachypnea (RR > 60/min): Rapid and shallow
affinity of the second heme for O , and oxygenation
2
respirations are characteristic of parenchymal
of the second increases the affinity of the third, etc,
pathology, in which the elastic work of breathing is
so that the affinity of hemoglobin for the fourth O 2
increased disproportionately to the resistive work of
molecule is many times that for the first.
breathing.
Retractions: Subcostal, intercostal, and suprasternal
Three important conditions affect the oxygen-
are most striking, with increased negative
hemoglobin dissociation curve: the pH, the
intrathoracic pressure during inspiration. This occurs
temperature, and the concentration of 2, 3-
in extrathoracic airway obstruction as well as diseases
diphosphoglycerate (DPG; 2, 3-DPG). A rise in
of decreased compliance.
temperature or a fall in pH shifts the curve to the
right. When the curve is shifted in this direction, a
Inspiratory stridor is a hallmark of extrathoracic
higher PO 2 is required for hemoglobin to bind a
airway obstruction .
given amount of O . A convenient index of such
2
shifts is the P , the PO at which hemoglobin is half
50
2
Expiratory wheezing is characteristic of intrathoracic
saturated with O .Thus, the higher the P , the lower
2
50
airway obstruction, either extrapulmonary or
intrapulmonary.
39
Grunting is produced by expiration against a
is needed to prevent CO 2 build up.
partially closed glottis and is an attempt to maintain
Non-rebreather face mask: Delivers highest FiO 2
positive airway pressure during expiration for as
at 70-100%
long as possible. Such prolongation of positive
pressure is most beneficial in alveolar diseases that
Venturi mask: This works based on the Venturi
produce widespread loss of FRC, such as in
principle. It is the best method for delivering a
pulmonary edema, RDS and pneumonia.
specific and consistent FiO . The mask can deliver
2
Respiratory Support in the Neonate
FiO 2 of 24-55% at flow rate of 4-10L. The masks
are usually colour coded at 24%, 28%, 31%, 35%,
The aim of respiratory support in the neonate is to
40% and 50%
maintain adequate gas exchange, minimize risk of
Oxygen hood/ tent: has the added advantage of easy
lung injury, minimize haemodynamic impairment,
visualization.
avoid injury to other organs, and to reduce work of
breathing.
Monitoring Oxygen Therapy
Oxygen and issues regarding use
Clinical indices used include:
Oxygen saturation (spO )
2
Oxygen as a drug provided in the neonate can be
Transcutaneous PO2(tcPO )
2
used to improve arterial oxygenation, cause
Transcutaneous CO2(tcPCO )
2
pulmonary vasodilation, and to enhance systemic
Arterial blood gases
oxygen delivery.
Central mixed venous PO 2
2
Oxygen therapy works by increasing the fractional
End tidal CO
inspired concentration of oxygen (FiO ) and the
2
Complications of Oxygen Therapy: These include
oxygen flow rate. The FiO 2 determined by the
retinopathy of prematurity, bronchopulmonary
concentration of supplemental oxygen, the flow rate
dysplasia, absorption atelectasis, respiratory
of oxygen, oxygen delivery device, and the patient
acidosis, ventilatory depression, suppression of
respiratory effort.
erythropoeisis. Others are the complications related
to the delivery device.
The concentration of oxygen varies depending on
the source as follows: Room air 21%, oxygen tank
Continuous Positive Airway Pressure
100%, and oxygen concentrator >90% (varies with
the oxygen concentrator indicator).
The application of end-expiratory pressure is
intended to prevent alveoli and/or terminal airways
Oxygen delivery device that can be used include
from collapsing to airlessness. Continuous positive
nasal cannula, nasal catheter, face mask, oxygen
airway pressure (CPAP) may be applied during
hood, oxygen tent, endotracheal/nasotracheal
spontaneous breathing or as positive end-expiratory
tube/tracheostomy
pressure (PEEP) during mechanical ventilation. This
usually requires pressures between 4 to 6 cm H O for
2
Nasal cannula: This is a low flow device that can
CPAP and 3 to 8 cm H O for PEEP. The physiologic
2
deliver distending pressure. It is the least expensive
effects of CPAP/PEEP may vary depending on the
and the FiO 2 delivered is 24-40%.
underlying pulmonary pathology, although the
primary goal is to prevent alveolar collapse.
Nasal catheter: It is inserted into the oropharynx,
and delivers a FiO2 similar to nasal cannula
In the surfactant-deficient state, alveoli will collapse
It could easily be clogged by secretions.
at end-expiration unless a minimum distending
pressure is maintained. CPAP of 3 to 4 cm H O will
2
Face mask: There are various type which include
prevent alveolar collapse but will not recruit
the simple, partial rebreathing, non-rebreathing and
atelectatic alveoli. Opening pressures of 12 to 15 cm
theVenturi face mask.
H O are required to inflate collapsed alveoli. The
2
infant will need to create a large distending airway
Simple face mask: Allows unregulated flow of
pressure in the absence of CPAP. The shear forces
room air, and the FiO 2 delivered is 35-50%.
from opening and closing of small airways may
However an increase flow rate is needed to
contribute to alveolar epithelial damage. CPAP
prevent rebreathing.
theoretically could stimulate surfactant secretion.
Partial rebreather mask: Is a simple mask with an
Also, maintenance of alveolar volume will reduce
attached reservoir. Oxygen flow rate of 6-10L
right-to-left shunting of blood through atelectatic
required to deliver 40-70% FiO 2 and a high flow
alveoli, hence reducing oxygen needs.
40
Indications: Its initial use was directed at RDS.
S y n c h ro n i z e d
I n t e r m i t t e n t
M a n d a t o r y
However, can be used to reduce the need for
Ventilation (SIMV): Is a ventilatory mode in which
ventilatory care in extreme preterms, and is used for
the mechanically delivered breaths are synchronized
the INSURE technique. It is also useful in recurrent
to the onset of spontaneous patient breaths, but at a
apnoea of prematurity, and when weaning off
lower rate. The patient may breathe spontaneously
conventional ventilation.
between mechanical breaths from the continuous
flow in the ventilatory circuit.
Benefits:
It effectively maintains Functional
Residual capacity, helps reduce infant work of
Pressure Support Ventilation (PSV): It is a mode of
breathing, reduces the need for intubation and
ventilation that has no set rate and only supports the
mechanical ventilation, and reduces the incidence of
patient's own spontaneous effort. It is primarily a
chronic lung disease. It results in improved non-
weaning mode. The patient controls RR, Ti and peak
pulmonary outcomes (increase mean weight gain,
insp. Flow, while the ventilator controls only PIP.
mean length and head circumference at 36weeks
This system synchronizes inspiration by sensing
post menstrual age).
patient effort, and also synchronizes expiration by
terminating inspiration in response to a decline in
Complications: This includes overinflation leading
airway flow. This results in complete synchronization
to increased work of breathing, air leak syndromes,
of the functioning of the baby and the ventilator
carbon dioxide retention, decreased cardiac output
throughout the entire respiratory cycle.
with high values, complications from delivery
device, and gastric distension.
Flow Sensitive Ventilation (FSV): Inspiration is
triggered by changes in flow and ends not according
Mechanical Ventilation
to time but according to airway flow changes. During
inspiration, the ventilator records the peak expiratory
This is an invasive life support procedure. The goal
flow rate and subsequently terminates inspiration
is to optimise both gas exchange and clinical status at
when the inspiratory flow decreases to 5-10% of peak
minimum FiO 2
and ventilatory pressures/ tidal
flow. This enables both inspiratory and expiratory
volumes.
synchrony. Benefits of FSV include total breath
synchronization, decreased work of breathing, less
Conventional Ventilation
sedation, more efficient tidal volume delivery,
improved gas exchange, and fewer complications.
Ventilatory modes: Untriggered or triggered.
Untriggered
Mode:
Consists of intermittent
Newer modalities of Mechanical Ventilation
mandatory ventilation (IMV) and intermittent
positive pressure ventilation (IPPV).
Volume guaranteed (VG)
Volume associated pressure support (VAPS)
Intermittent Mandatory Ventilation: Provides
Pressure regulated volume control (PRVC)
fixed rate of mechanical ventilation and allows
Proportional assist ventilation (PAV)
spontaneous breathing between mechanical breathes
from continuous flow of oxygen.
Volume Guaranteed (VG)
Triggered ventilation: Consists of flow trigger and
This is a pressure-limited, time or flowcycled,
pressure trigger
volume-targeted form of ventilation. The
microprocessor compares exhaled tidal volume of the
Triggered modes: Types are the assist/control
previous breath to the desired target and adjusts the
mode, synchronized intermittent mandatory
working pressure up or down to try to achieve the
ventilation, pressure support ventilation, flow
target tidal volume. There is limit of pressure
sensitive ventilation, and volume timed ventilation.
increment from one breath to the next to a maximum
of 3cm H O to avoid overcorrection. Thus, several
2
Assist/Control
(A/C):
This modality involves
breaths may be needed to reach the target tidal
either the delivery of a synchronized mechanical
volume after a sudden change. The VG mode cannot
breath each time a spontaneous patient breath is
increase pressure higher than set pressure limit.
detected (ASSIST), or in the event that the patient
Benefits of VG
fails to exhibit spontaneous resp. effort , the
ventilator delivers a mechanical breath at a regular
Maintenance of constant tidal volumes in the
rate (CONTROL).
face of changing compliance, resistance and
changing ET- tube leak
Prevention of overdistention and volutrauma
41
Automatic lowering of pressure support level
1. Ventilatory strategy in RDS Ensure an inspiratory
during weaning (auto-weaning). As the
flow rate 7-12 L/min, peak inspiratory pressure
patient's lungs improve and compliance
20-25cmH 2 O and positive end expiratory
increases, peak inspiratory pressure is weaned
pressure 4-5cmH O. The inspiratory time should
2
automatically.
be 0.5s while the expiratory time is set at 1.0s.
Trigger volume mode preferred. Alternative
Indications for VG: Virtually any infant requiring
strategy is with high frequency ventilation.
mechanical ventilation especially when lung
2. Ventilatory strategy in MAS
mechanics are likely to change, or in patients with
There is a high risk of pneumothorax because of
heterogenous lung disease because of differing time
ball valve effect, thus a low PEEP should be
constant throughout lung parenchyma
utilized to splint the airways. If airway resistance
is high, a slow rate, moderate pressure strategy
High Frequency Ventilation
should be utilized. If pneumonitis is more
prominent, more rapid rates can be utilized. HFV
HFV is a form of mechanical ventilation that uses
can be used with failed conventional ventilation
small tidal volumes, sometimes less than anatomic
or air leaks.
dead space, and extremely rapid ventilator rates.
3. Ventilatory strategy in air leaks
Goal is to reduce the mean airway pressure (MAP)
HFV in comparison to conventional IMV
to as low as possible and rely on FiO 2 to improve
HFV delivers at high frequency: 300-1200/min=5-
oxygenation. HFOV is the modality of choice.
20 HzU and utilizes very small tidal volumes and can
Maintain MAP, do not use sigh maneuver. Use
detect incomplete inspiration and expiration. Causes
low PEEP
dampening of the oscillations along the airways and
4. Ventilatory strategy in apnoea with normal lungs
2
ensures a nearly constant alveolar pressure. Also,
Ensure low gas flow, low PIP 10-18cmH O, low
HFV has the ability to independently manage
PEEP 3-4cmH 2 O, and normal rates 30-
ventilation and oxygenation, while ensuring the safe
40breaths/min
use of mean airway pressure that is higher than that
generally used during conventional mechanical
Oxygenation Index: This is an index of disease
ventilation.
severity
OI =
PAWx FiO2
Types of HFV
PaO2
An index greater than 15 indicates severe respiratory
HFFI (Higher-Frequency Flow interrupting
compromise, while an index greater than 40 on
Ventilation)
multiple occasions indicate mortality > 80%
HFJV(High- Frequency JetVentilation)
HFOV(High-Frequency OscillatoryVentilation)
Complications of Mechanical Ventilation
Indications for HFOV: Rescue therapy and air leak
syndromes.
This includes ventilation induced lung injury,
ventilation induced pneumonia, air leak syndromes,
Clinical Applications of Mechanical Ventilation
traumatic injury to large airways and endotracheal
tube complications.
CPAP: Mildly affected neonates with RDS: start
at 4-6cm H O and increase gradually to a maximum
Ventilator Induced Lung Injury (VILI)
2
of 7-8cm H O. It is titrated by: clinical assessment of
2
retractions, respiratory rates, and oxygen saturation.
There are four mechanisms of VILI: Barotrauma
(high airway pressure), volutrauma (large tidal
Neonatal Pulmonary Physiology By Disease State.
volume), atelectotrauma (alveolar collapse and re-
expansion), and biotrauma (increased inflammation).
Strategies need to be developed for the various
disease states requiring ventilation in the neonate.
Volutrauma caused by mechanical overdistension
leads to alveolar epithelial cell damage, alveolar
Setting parameters are required for the inspiratory
protein damage, altered lymphatic flow, hyaline
flow rate, peak inspiratory pressure, positive end
membrane formation, and inflammatory cell influx in
expiratory pressure, oxygen concentration,
the lungs. The precise tidal volume required to
inspiratory time, expiratory time, trigger volume.
minimize volutrauma is not known. Therefore efforts
Derived parameters are the FiO2, mean airway
to limit tidal volume may be a beneficial practice in
pressure, flow parameters, tidal volume, and the
the neonatal intensive care unit.
respiratory rate.
42
Ventilator Associated Pneumonia (VAP)
Retinopathy of prematurity is a vaso-proliferative
retinal disorder that decreases with gestational age.
This is defined as pneumonia in mechanically
Approximately 65% of infants with a birth weight
ventilated patients that develops ≥ 48 h after the
less than 1250g and 80% of those with a birth weight
patient has been placed on mechanical ventilation.
less than 1000g will develop some degree of
VAP is the second most common hospital acquired
retinopathy of prematurity.
infection among neonatal intensive care unit (NICU)
patients. This is often caused by organisms such as
Extracorporeal Membrane Oxygenation
Pseudomonas aeruginosa (the most common),
Staphylococcus aureus, Enterobacter species, and
This can be defined as a mechanical means of
Klebsiella pneumoniae
providing oxygen delivery and carbon dioxide
removal for patients who have cardiac and/or
Diagnostic criteria forVAP
respiratory failure. May be veno-arterial or veno-
Worsening gas exchange (oxygen desaturation or
venous.
increased oxygen or ventilatory requirements)
and 3 of the following:
Indication
Temperature instability with no obvious cause.
Critically ill term and late preterm newborns with
Leukopenia or leukocytosis with left shift.
reversible respiratory and/or cardiac failure who
Increased pulmonary secretions or greater need
have failed appropriate maximal medical
for suctioning.
management.
In conditions such as meconium aspiration
Examination reveals apnea, tachypnea, nasal flaring
syndrome, respiratory distress syndrome,
with chest retractions, grunting. Wheezing, rales,
persistent pulmonary hypertension of the
rhonchi may be present, with either bradycardia or
newborn, pneumonia, sepsis, severe rhythm
tachycardia.
disturbances, neonatal cardi0myopathies
Strategies to reduce VAP will include to prevent
Specific indications
contamination of equipment, ensure endotracheal
Respiratory criteria: OI >30-40 for 4 hours, acute
tube care, and to minimize duration of intubation.
deterioration with intractable hypoxaemia,
barotrauma with severe air leak not responsive to
Air-leak syndromes
HFOV
Cardiovascular/oxygen delivery criteria:Cardiac
T h e s e
i n c l u d e :
P n e u m o t h o r a x ,
arrest, plasma lactate >45mg/dl with metabolic
pneumomediastinum, pneumopericardium,
acidosis not improving or escalating with despite
pulmonary interstitial emphysema, and
adequate medical care, mixed venous saturation
subcutaneous emphysema.
<55% for 1 hour
Risk factors for air-leak syndromes in neonates are
Contraindications
extreme low birth weight, endotracheal tube
These include: Gestational age less than 32 weeks
displacement, using long inspiratory time (> 0.5
and/ or birth weight less than1800g, mechanical
sec), ↑
PIP, ↑
Vt. Also, increase in clinical
ventilation beyond 10-14 days due to likely
interventions including suction procedures, chest
irreversible lung disease, intraventricular
radiography, reintubation, bag & mask ventilation
hemorrhage greater than grade I, and coagulopathy
and chest compressions are risk factors. Other risk
unlikely to resolve with transfusion. Others are
factors are MAS, RDS, pulmonary hypoplasia.
severe congenital anomalies, uncorrectable cardiac
lesions, CDH with OI>45, hypoxic ischaemic
Tracheal
injury
and
endotracheal
tube
related
encephalopathy, and plasma lactate >225mg/dl.
complications
Complications
These include subglottic stenosis, tracheal
These are acute renal failure, hypertension,
perforation, palatal deformities, vocal cord avulsion,
haemolysis, seizures, hypotension, CNS infarction,
laryngeal oedema, subglottic cysts, necrotizing
intracranial haemorrhages, sepsis, surgical bleeding,
tracheitis and septal injury.
pulmonary haemorrhage, disseminated intravascular
coagulopathy (DIC), and brain death. Others are
Chronic lung disease is defined as the need for
cannula problems, air embolism, pump failure, and
supplemental oxygen beyond 28days of postnatal
clot formation.
age or oxygen dependency at 36weeks
postmenstrual age.
Supportive Care: This involves the use of surfactant
therapy, inhaled nitric oxide, heliox, ensuring
43
adequate tissue perfusion by optimizing
Arterial blood gas analyzers, flow sensors, oxygen
cardiovascular function and total parenteral
sensors, surfactant, total parenteral nutrition (TPN),
nutrition.
and disposable supplies (endotracheal tubes,
catheters, chest tubes, etc).
To be more practical where do we stand?
There is the need to establish mechanical ventilatory
care in our centers. Requirements are:
Acknowledgement
Manpower: Nursing staff, doctors, laboratory staff,
radiographers, need for training.
Reproduced with kind permission of the department
of Paediatrics and Child Health of the University of
Materials: Functioning ventilators, regular oxygen
Ilorin Teaching Hospital, Ilorin Nigeria owners of the
supply, regular power supply, regular water supply, a
Ilorin Paediatric Digest 2010.
mobile x-ray machine, pulse oximeters, complete
patient monitors (BP, HR,Temp, O 2 saturation),
References
1. Gomella LT. Neonatology:
5. Chatburn RL. Fundamentals
9. Shouman B. Complications
st
of Mechanical Ventilation. 1
of mechanical ventilation.
Management, Procedures,
ed. Ohio: Mandu Press, 2003.
Text of a lecture delivered at
On-call Problems, Diseases,
6. Tobin MJ. Principles and
the Advanced Neonatology
Workshop in Mansoura,
and Drugs. 6 ed. New York:
th
Practice of Mechanical
Ventilation. 1 ed. New York:
st
Egypt, November 2010.
McGraw Hill, 2009.
McGraw Hill, 1994.
10. Ganong WF, editor. Review
2. Cloherty JP, Eichenwald EC,
7. El Sallab S. Modes of
of Medical Physiology. 21st
Stark AR. Manual of
conventional mechanical
ed. San Francisco: Lange
neonatal care. 6 ed.
th
ventilation. Text of a lecture
Medical Books/McGraw-
Philadelphia: Lippincott
delivered at the Advanced
Hill Medical Publishing
Williams, 2008.
Neonatology Workshop in
Division 2003.
3. Fox G, Hoque N, Watts T.
Mansoura, Egypt, November
11. Sadler TW. Langman's
Medical Embryology, 9
th
Oxford Handbook of
2010.
Neonatology. 1 ed. Oxford:
st
8. Khashaba M. Pulmonary
edition, 2004; 275 284.
Oxford University Press,
Physiology. Text of a lecture
2010.
delivered at the Advanced
4. Helfaer MA, Nichols DG.
Neonatology Workshop in
Rogers' Handbook of
Mansoura, Egypt, November
Pediatric Intensive Care. 4
th
2010.
ed. Philadelphia: Lippincott
Williams & Wilkins, 2009.