d1
10
Respiratory Failure in
Childhood
Gregory 1. Redding, Jeffrey P. Morray,
and Catherine Rea
DEFINITION
Respiratory failure occurs when the lung
does not maintain normal gas exchange between alveoli and blood. By convention,
respiratory failure exists when plco~ is
greater than 50 mm Hg or the Pa02 is less
than 50 10m Hg when the patient breathes
room air. J An exception to this definition is
the child with arterial hypoxemia due to extrapulmonary
right-to-left shunt, usually
associated with eon genital heart disease.
INCIDENCE
The incidence of respiratory failure among
children is unknown. Epidemiologic studies
have been limited to surveys of patients in
IeUs. In 1972, Downes et al3 reported the
age-related disease entities most often associated with respiratory failure in their leU
(Table 10-1). Respiratory failure among
newborns occurred predominantly among
premature infants and those with eongeni-
tal heart or lung disease. Respiratory Infections and heart disease produced respiratory
failure most often in infants 1 to 24 months
of age. In children 2 to 12 years of age,
asthma was the most frequent underlying
condition associated with respiratory failure. More recent surveys have not been conduoted to determine if these conditions remain the leading cause of respiratory failure
in children.
Respiratory failure accounts for more
deaths in children than any oondition other
than accidents and congenital anomalies. I
Two thirds of the deaths from respiratory
failure in children occur in the first year of
life. The death rate from respiratory illness
is .approximately 12.5 per 1000 infants ~e.<iS
than 1 year of age. Among children 1 to 16
years of age, the death rate is 1/12 as frequent." The tendency of the newborn to develop respiratory failure more often than the
older child Is due Iu part to the inefficiency
of the developing respiratory system immediately after birth. During the neonatal
period and infancy, the upper and lower
117
lIB
III. RESPIRATORY DISEASE:
TABLE 10-1.
COMMON CAUSES OF ACUTE RESPIRATORYFAILURE IN CHILDREN
(1 MONTH TO 12 YEARS)
1-24 Months
2-12 Years
Bronchopneumonia
Bacterial
Viral (bronchiolitis)
Aspiration
Status asthmaticus
Upper airway obstruction
Congenital heart disease
Status asthmaticus
Septicemia
Foreign body aspiration
Intrathoracic anomalies
Diaphragmatic lesions
Vascular rings
Encephalitis
Congenital heart disease
Bronchopneumonia
Encephalitis
Peripheral polyneuritis
Septicemia
Poisoning
Trauma
Thoracic injury
Head injury
Traumatic shock
Drowning
Renal failure
Poisoning
Cystic fibrosis
From Downes JJ or al: Pediatr Clin North Am 19:423, 1912.2
airways are smaller and more unstable, the
chest wall is compliant, and the respiratory
muscles may be more prone to Fatigue." In
addition, collateral channels of ventilation
including pores of Kohn and canals of Lambert and Martin are poorly developed,
thereby predisposing infants with airway
obstruction to atelectasis and hypoxemia due
to ventilation-perfusion mis.rpatching. The
inefficient immune system or the newborn
may also predispose young patienls to severe
respiratory infections more often than the
older child."
the lower airways, the lung parenchyma
(including the alveoli, interstitium and pulmonary vasculature), the pleural space, and
the skeletal and muscular surroundings of
the thorax including the thoracic cage, respiratory muscles and the abdomen (Fig ..
10-1). The physical examination and chest
radiograph are the most useful means of immediately identifying which parts of the res- .
(~~I}?I~1lIO~
OF RESPffiATORY FAILURE
Classification schemes which identify the
anatomic site or the physiologic mechanism
of respiratory failure are most useful in the
management of individual patients.
Anatomic Classification
The respiratory system can be divided into
six compartments, each of which can male
function to' the point that respiratory failure
occurs. These include the CNS, the upper
airways (located above the thoracic outlet),
Figure 10- 1. Six compartments which, if compromised, can lead to respiratory failure.
119
10. RESPIRATORY FAILURE IN CHILDHOOD
piratory system are responsible for respiratory failure. 7
Central Nervous System. Disorders of the
CNS alter respiratory patterns and depth of
ventilation. Patients with brainstem disease
may present with hyperventilation, periodic
breathing, or intermittent apnea." Respiratory failure accompanies CNS depression
due to narcotics, anesthetics, metabolic encephalopathy (e.g., Reye's syndrome), infectious encephalitides, and intracranial
masses such as tumors and hematomas.
Most often these disorders lead to hypoventilation as a result of irregular breathing
or reduced tidal volume. The presence of
diffusely diminished breath sounds and an
irregular breathing pattern should prompt
further evaluation on the CNS. Changes in
mental status such as somnolence or restlessness may reflect primary CNS disease or
may result from hypoxemia or hypercapnia.
Similarly, changes in blood pressure and
heart rate may reflect primary CNS disease,
abnormal blood gas tensions, or both. Except for neurogenic pulmonary edema, the
chest radiograph is usually normal. when
only the CNS compartment is involved.
Upper AinoaYIf. The upper airways.extend
from the mouth and nose to the subglottic
trachea above the thoracic outlet. Obstruction of the upper airways increases resistance to airflow and therefore the work of
breathing during inspiration. Pediatric' disorders which commonly produce upper airway obstruction. are choanal atresia, maoroglossia with micrognathia, epiglottitis,
vocal cord anomalies or paralysis, and
subglottic edema duc to Infection or trauma
(e.g., following extubation) (Table 10-2). In
all of these cases, physical findings Include
suprasternaland
sometimes intercostal retractions accompanied by stridor or snor~~g.The obstruction may be fixed in dirnension (e.g .~ subglottic stenosis) and,
therefore, produce increased airway resistance during both inspiration and expiration. Alternatively, the obstruction may be
dynamic, as occurs in viral croup, produc-
TASLE 10-2. MECHANISMS
OF AIRWAY OBSTRUCTION
Intraluminal occkrslon
Secretions
,
Foreign bodies
Endobronchial masses, e.o., adenomas,
webs
Vocal cord paralysis and paresis
cysts,
Mural abnonnalities
Ed~ma
Spasm (laryngospasm and bronchospasml
Congenital instability tlaryngonialacia and tracheornalaolal
Acquired instability (bronchiectasisl
Sclerosis
Hypoplasia
Extramural abnormalities
Compression (nodes, tumors, enlarged heart, andl
or pulmonary vessels)
Restriction (due to underdevelopment
of surrounding structures, e.g., micrognathia)
ing severe airway obstruction primarily
during inspiration. In airway obstruction
above the thoracic outlet, stridor may
worsen with increased efforts to breathe.
The chest radiograph does not evaluate the
upper airways completely; in most cases of
upper airway obstruction the chest radiof' graph is normal. Abnormalities of the chest
film in the presence of stridor reflect involvement of respiratory compartments
other than the upper airways. Complete diagnostic evaluation includes radiographs of
the upper airways and, in some cases, direct
. endoscopic visualization.
Louier Airways. 'I'he lower airways extend
from the trachea to the conducting bronchioles. Common diseases of the lower airways that produce respiratory failure include asthma, bronchitis and bronchiolitis,
aspiration and inhalation syndromes, bronchiectasis. and airway compression from tumors;nodes,
and vascular structures. In
contrast to the upper. airways. the intrathoracic airways tend to dilate during inspiration (with increasing lung volume) and
collapse during expiration. Obstruction of
the Intrathoracic airways produces the most
difficulties during exhalation when the air-
120
ways normally diminish in caliber. Physical
findings inel ude prolonged exhalation,
wheezing' and rhonchi, and significant use
of abdominal D\UScleswhich provide the
power to forcefully exhale. As with the upper airways, lower airway obstruction may
, have fixed dimensions (e.g., a foreign body
aspiration), or may change dimensions with
breathing (e.g., a mild to moderate bronchospasm). Fixed airway obstruction of
either the upper or lower airways increases
the work of breathing in both inspiration
and expiration. Dynamic obstruction of the
lower airways primarily impairs exhalation.
Radiographic abnormalities usually underestimate tile severity of respiratory Iailure
associated with lower airway disease because the airway dimensions are difficult to
discern on inspection of the chest radiograph. Common manifestations of lower
airway obstruction are hyperinflation, air-:
way wall thickening or "cuffing," atelectasis, and a shift of tile mediastinal struc-
Figure 10 - Z. Chest radiograph in
infant with lower airway obstruction
producing hyperaeration of the left
lung. mediastinal shift. end volume
loss of right lung.
Ill. IIESPlRATOHY DISEASE
tures when the airway obstruction is
localized to one side of the lung (Fig. 10-2).
The lung parenchyma
includes the respiratory bronchioles, alveoli, interstitium, and pulmonary vasculature. Disorders of the parenchyma include
pneumonitis, pulmonary edema, hemorrhage, fibrosis, and primary alveolar collapse. Atelectasis can also occur as a result
of hypoventilation, weak respiratory musculature, or complete airway obstruction
and should prompt careful evaluation of
other compartments' of the respiratory sys·
tern. Pulmonary vascular disease in the absence of congenital or acquired cardiac disease is insidious and occult, often presenting
with exercise intolerance, syncope, unexplained tachypnea, or right heart failure.
Diffuse alveolar and interstitial diseases diminish the distensibility of the lungs. Reduced lung compliance produces tachypnea. When severe, alveolar and interstitial
Lung Parenchyma.
122
trcatments are designed to assure adequate
gas exchange and avoid the complications of
hypoxemia and respiratory acidosis. They
can be employed quickly and rationally if
the anatomic compartments of the respiratory system are evaluated systematically.
Such treatments allow the physician time to
diagnose and treat the underlying disease
entity compromising lung function. .
Physiologic Classifioa tion
A second way to approach the individual
child with suboptimal gas exchange is to determine the mechanism responsible for hypoxemia and hypercapnia independent of
the specific site(s) of disease.
It is important to remember that respiratory failure is defined by abnormal
blood gas tensions as well as by physical
findings. Cyanosis is not a reliable sign of
hypoxemia and is not recognized consistently by physicians or other health care
professionals.!" Similarly, minute ventilation cannot be assessed clinically becausethe
depth of ventilation and effectiveness of
each breath cannot be quantitated usin$
physical examination techniques. Respiratory rate is the most sensitive indicator of
pulmonary disease as it increases ill response
to hypoxemia, hypercapnia, and abnormal
lung mechanics.'! Its lack of specificity,
however, precludes its use as an index of respiratory failure.
Hypercapnia.
Carbon dioxide retention
usually results from hypoventilation, although occasionally increased CO2 production plays a role. 12 Hypoventilation, in turn,
occurs in one of three ways. If the central
and peripheral neural receptors that control
respiratory drive do not function, a patient's
dcpth or rate of breathing diminishes, leading to diminished tidal volume and minute
volume with subsequent CO2 retention.
Second, when respiratory muscle weakness
or paralysis occurs, the patient cannot de.velop the necessary negative intrathoracic
pressures to inhale effectively. Respiratory
muscle weakness occurs in response to myopathic disorders such as poliomyelitis,
Ill. RESl'J1IATORY DISEASE
myasthenia gravis, and Landry-CulllainBarre syndromes. 13 Respiratory muscle
strength may also be compromised by several metabolic derangements including
hypokalemia, hypomagnesemia, and hypophosphatemia.I" The most common condition to weaken the respiratory muscles in the
rcu L5 probably poor nutrition. This occurs
as a result of loss of muscle mass as well as
.primary loss of muscle contractile force per
unit of muscle cross-sectional area. 13.15 Respiratory muscle dysfunction can also occur
as a result of tonic-clonic seizures, and from
chest wall pain and splinting following surgery or trauma.
The third and most common reason for
hypoventilation is abnormal lung rnechanies so severely deranged that the patient
cannot sustain the work necessary to
breathe. In these cases, respiratory muscle
fatigue as a secondary event occurs as a result of progressive or intractable airway obstruction or restrictive lung disease. Obstructive lung disease occurs when either the
upper or lower airway caliber is reduced.
The mechanisms for airway obstruction cnn
be classifled as intraluminal occlusions, airway wall disease, and airway compression
or restriction by surrounding structures.
More specific mechanisms that reduce airwny dimensions arc listed in Table 10-2 in
accordance with this classification. In all
cases, resistance to air flow in inspiration
and expiration increases inversely with the
fourth power of the airway radius. N arrowing of the radius of the normal newborn trachea from 6 to 4 mm increases airway resistance by 500 percent. Obstructive lung
disease may initially· produce expiratory
muscle fatigue. However, with ineffective
exhalation and progressive air trapping, inspiratory muscles also function less efficiently and eventually fatigue as well.
Restrictive changes in lung mechanics
increase respiratory work by reducing the
distensibility of the respiratory system. As
mentioned above, parenchymal lung disease, pleural disorders, and abnormalities of
the chest wall and abdomen can all impede
inflation of thc lungs to the point that hy-
123
10. RESPIRATORY .-AILURE IN CIIILDIlOOD
percapnia develops. Restrictive lung disease
primarily fatigues the inspiratory muscles.
All three reasons for hypoventllation
(abnormal respiratory neural control, muscle weakness, or abnormal lung mechanics)
can be exacerbated by increased production
of carbon dioxide in peripheral tissues, Increased metabolic rate due to fever, severe
burns, and hyperalimcntation with high
concentrations of dextrose'> require increased minute ventilation iu patients with
norma/lung function. In all patients with
respiratory disease and minimal ventilatory
reserve, increased carbon dioxide production may lead to hypercapnia and respiratory acidosis.
Hypoventilation regardless of its etiology is also exacerbated by an increase ill anatomic or physiologic dead space (that proportion of tidal volume that does not
participate in alveolar ventilation despite
movements of air through the airways).
When dead space is increased, minute ventilation must increase to maintain normal
alveolar ventilation and arterial PC02' Increases in ventilation in response to increased dead spacc in the presence of abnormal lung mechanics increase respiratory
muscle work and further predispose respiratory muscles to fatigue. In general, increased dead space is associated with air
trapping and overdistentlon (e.g., asthma),
or by a loss of pulmonary capillary surface
area (e.g., vasculitis or pulmonary embolism). Patients with reduced tidal volume as
a result of muscle weakness or restrictive
lung disease may demonstrate improved gas
exchange following tracheostomy placement because the anatomic dead space
above the glottis has been reduced.
Hypoxemia.
Hypoxemia can result from
severe hypoventllation (Fig. 10-.3) or can be
seen with eucapnia or hypocapnia. The
mechanisms by which hypoxemia without
hypoventilation develops include ventilation-perfusion mismatching, abnormal diffusion
gases, and extrapulmonary shunting of blood from the venous to the arterial
circulation. Ventilation-perfusion
imbal-
or
200
-a
J:
E 150
..s
~N
a: 100
:5
e>
<t
50
o
o
2
4
6
ALVEOLAR VENTILATION
Figure 10-3.
In an adult breathing
,
,-,
8
10
12
(Umln)
21 percent
ygen, progressive hypoxemia occurs when
ventilation falls below 4 Urnin. (After Nunn
ygen. In Nunn JF led): Applied Respiratory
ogy, 2nded. London, Butterworttis,
1977,
ox-
alveolar
JF: OxPhysiolp 385.1
ance is by far the most common reason for
inefficient oxygenation. Whether impaired
diffusion actually occurs in the clinical setting is controversial. Normally, gas in the alveoli and red blood cells equilibrates in onethird the time required for blood to traverse
the pulmonary capillaries. 16 Except for conditions of high pulmonary blood flow, such
f'asexercise and severe anemia, impaired gas
diffusion is unlikely to produce significant
hypoxemia.
Ventilation and perfusion are evenly
matched in the normal lung. Imbalance can
occur when ventilation is greater than perfusion and when ventilation is reduced relative to pulmonary perfusion. When extreme, the former condition represents
physiologic dead space and the latter con. dition represents intrapulmonary
shunt
(Fig. 10-4). Hypoxemia occurs when perfused regions of the lung ventilate poorly.
These regions are said to have ventilation-perfusion ratios (V IQ) of less than 1
and are often described as "low VIQ" regions.!" Regions with low V (Q relationships
often result from airway, alveolar, or interstitial lung disease. The degree to which
these regions produce arterial hypoxemia
depends upon (1) the size of the lowV/Q regions, (2) the degree to which ventilation is
reduced in these regions, and (3) the degree
to which such regions are perfused. 17.19 For
example, airway obstruction due to foreign
124
Figure 10-4. In tho center is a
schematic of the "ideal" match between alveolar ventilation [V) and
perfusion (Q). To the left are progressive decreases in V, leading to
"shunt" on the far left. To the right
are progressive decreases in 0 leading to "dead space" on the far right.
III. RF.sPIRATORY DISEASE
Jlllooo
V/Q=O
"Shunt"
body aspiration produces alveolar hypoxemia and reduced ventilation in lung regions distal to the obstruction. If the foreign
body is lodged in the right malnstern bron-"
chus, it produces more hypoxemia than if it
is lodged in the segmental bronchus. If the
foreign body completely occludes the airway, Y/Q relations in the regions distal to
the occlusion will approach 0 (i.e., shunt associated with atelectasis), and produce more
hypoxemia compared to a foreign body
which partially occludes the airway,
Normally, blood is shunted away from
poorly ventilated to well-ventilated areas of
lung through active vasocoristriction of the
pulmonary vasculature in response to alveolar hypoxia. In the absence of any inhibiting
factor and in normal lung, a right mainstem
bronchus intubation" results in less than the
predicted 50 percent shunt due to regional f
hypoxic pulmonary vasoconstrtcnon.t? This"
mechanism can be overridden in the pre.~ence of pulmonary artery hypertension, 20
high positive airway pressure," or some
vasoactive drug~22 allowing blood to flow
through poorly ventilated regions, resulting
in decreased arterial oxygen tension.
In the presence ofY/Q mismatching,
arterial hypoxemia is made worse by any
situation which leads to increased oxygen
extraction and decreased mixed venous oxygen tension.F' This can occur as a result of
an increase in metabolic rate, as occurs with
fever and burns." Increased oxygen extraction also occurs as compensation for the decreased oxygen delivery seen with severe
anemia, low cardiac output states, and abnormal hemoglobin molecules. The rnechanism whereby reduced cardiac output exacerbates the hypoxemia of increased Qs/Qt
V/Q<1
V/Q=1
"ideal"
V/Q> 1
V/Qoo
"Dead space"
is shown in Figure 10-5. Treatment of complicating extrapulmonary factors that influence tissue oxygen delivery often improves
arterial hypoxemia without significantly
changingY/Q mismatching.
TREATMENT
FAILURE
OF RESPIRATORY
Oxygen Delivery
Hypoxemia due toY/Q mismatch is most effectively treated with supplemental oxygen
delivered by hood, mask, or endotracheal
tube. The patient who remains hypoxemic
despite increased Fi02 delivered by hood or
mask often requires intubation for delivery
of positive end-expiratory pressure (PEEP),
assisted ventilation, and pulmonary toilet.
A variety of systems are available for
delivery of oxygen to the nonintubated infant or child. For infants, the most commonly used system is a head hood made of
clear plastic, in conjunction with a humidjfjer or nebulizer to deliver warmed, humidified gas. 'Humidifiers are generally preferred over nebulizers, since the latter are
noisy and generate particulate water which
rains out in the tubing or hood. An oxygen
blender is used to deliver accurate concentrations, and Fi02 is monitored continuously. Because the hood is an open system,
the maximum Fio2 is 0.6 to 0.7.
The older child often tolerates nasal
cannulae or a face mask. Nasal cannulae are
low flow systems, delivering between 0.25
and 4.0 Llmin. The Fio2 depends on the flow
rate, and the child's minute volume and
ventilatory pattern; tachypnea usually results in entrainment of room air and a low
to.
125
RESPIRATORY FAILUlIE IN CIULDHOOD
With 50% Shunt
Plus Low Cardiac Output
WllhSO%
Normal,
Shunt
mixed
venous
blood
mIxed
arterial
blood
mixed
venous
blood
arterial
blood
venous
blood
II. '~
arterial
blood
,
9"
I
::~$
:::.
Py02
C.O.=4Umln
40
100
60
rnrnHg
75%
Figure 10-5.
C.O.=2Umln
28
mmHg
mmHg
Pa02
HgbSat
---
:.:;;
:f ,);,,:
~"~
C.O.=4Umin
II
I'"
99~~
75%
The effect of shunt fraction
(Pi7021 and arterial oxygen
40
mmHg
87%
(Qs/Qtl
al'd low
tension (P"do.l and hemoglobin
Fi02• The influence of flow rate on Fio , in
a patient breathing quietly is shown in Table 10-3. Flow rates in excess of 5 L/min are
poorly tolerated due to. irritation of nasal
mucosa and epistaxis.
Simple face masks deliver oxygen at a
fixed flow rate of 4 to 5 L/min to assure adequate washout of exhaled CO2, The Fio,
depends on the patient's inspiratory flow
rate, minute volume, and breathing pattern, and varies between 28 and 60 percent
(Table 10_3).25 A partial rebreathing mask
is a simple oxygen mask with a reservoir bag
attached.
The mask should fit tightly
enough so the bag fills and remains inflated
with flow rates of 6 liters per minute or
more. The patient inspires a mixture of fresh
gas and gas from the bag that is roughly 30
percent expired gas (primarily anatomic
dead space gas, high ill oxygen). This system
provides concentration of oxygen up to 60
to 80 percent (Table 10-3).25,26
mmHg
50%
75"10
cardIac output on mixed venous
saturation
(stippled areal.
Nonrebreathing masks include one-way
valves over the exhaled gas ports, and a oneway valve between the mask and a reservoir
bag. With a good fit and high fresh gas flow
sufficient to keep the bug distended, this system can deliver close to 100 percent oxygen
in the nonintubated patient.
Venturi masks utilize the Bernoulli
principle to entrain room air at a constant
proportion to oxygen and deliver a fixed
Flo, at high fresh gus flows equal to or
above the patients' spontaneous minute ventilation.27,28 The Fio2 is adjustable from 24
to 50 percent depending on the oxygen flow
rate (from 4 to 12 liters per minutej.P" A
Venturi device can also be used in conjunction with a hood. The aerosol mask is used
with a nebulizer, and utilizes a Venturi system to entrain room air to deliver a fixed
Fio2 at high flow. 26
An oxygen tent can be used for the child
who does not tolerate a mask but is too large
126
III. RESrmUORY DISEASE
TABLE 10-3.
EXPECTED INSPIRED
o,
concentrations
AT VARIOUS
System
Nasal cannula
Venturi
mask
Simple mask
M asks with reservoirs
Partial
Nonrebroathing
1'leonates
and small children
(Floz) FOR COMMONLY
USED EOUIPMENT
FRESH GAS FLOWS
02 Flow Rate. lImln
1
2
3
4
5
4-6
total flow 105
4-6
total flow 45
8- 10 total flow 45
8 -10 total flow 33
8 -12 total flow 33
A02
Range Adult
Population"
0.21·0.24
0.23-0.28
0.27-0.34
0.31-0.38
0.32-0.44
0.24
0.28
0.35
0.40
0.60
5-6
7-8
0.30-0.45
0.40-0.60
5
7
0.35-0.50
0.35-0.75
0.65-1.0
10
4-15
0.40-1.0
with low n~l1utt! veutitaucn orten have higher Fioz for all devicos except
for a hood. The Fio2 delivered changes
markedly each time the tent is opened, and
can reliably deliver only about 30 percent
oxygen.
Regardless of the delivery system used,
it is appropriate to deliver the least amount
of oxygen nCCf'_'>Sary
to keep the child welt
oxygenated. The inspired oxygen concentration should be analyzed and documented
throughout each day of treatment. Arterial
oxygcn tension or hemoglobin saturation
should be analyzed to establish thc optimum dose of supplemental oxygen. Noninvasive estimates of oxygenation such as oximetry and transcutaneous 1'02 monitoring
can be used to reduce the need for repeated
sampling of arterial blood (see Chapter 11).
A variety of complications can arise
from oxygen therapy including:
1. Pulmonary toxicity (see Chapter 15)
2. CNS toxicity (with hyperbaric exposures)
3. Alteration in tracheal clearance of seoretions and bacteria
'4. Retinopathy of prematurity
5. Diminished respiratory drive in patients
with chronic CO2 retention
6. Absorption atelectasis from denltrogen-
the Venturi
mask.
ation of alveoli ill patients with airway obstruction breathing 100 percent
oxygerr"
7. Bacterial contamination of aerosols and
heated rnist'°
B. Water intoxication with ultrasonic nebulizers'"
9. Thermal injury from overheated inspired gas
Mechanical Ventilation
Selection of appropriate treatment depends.
on both the site and mechanism of respiratory failure. The decision to intervene is
based upon the clinical examination; the
absolute values of Paco., Pao-, and pH; the
rate at which these values change; and
knowledge of the underlying disease producing the respiratory failure. Elevated
PaC02 is common in chronic respiratory failure due to severe bronchopulmonary dysplasia, end stage cystic fibrosis, and progressive muscular dystrophy. Hypercapnia
in these entities is usually associated with a
normal arterial pH as n result of compensatory renal conservation of bicarbonate.
Such cases do not demand immediate intervention with assisted ventilation. The ab-
10. RESP1RATORY FAILURE IN CHILDHOOD
solute value of Paco, which dictates immediate therapy, therefore, varies with a
patient's ability to compensate as hypercapnia develops. Administration of high
concentration oxygen without mechanical
ventilation to a patient with chronic hypercapnia may produce further hypoventilation by abolishing hypoxic drive.
The child with acute hypoventilation
causing severe hypercarbia and acidosis,
with or without hypoxemia, usually requires intubation and mechanical ventilation with positive pressure and increased inspired oxygen concentration. The mechanical ventilator can predictably improve
ventilation to insure effective excretion of
carbon dioxide.
Mechanical ventilators can be classified
according to their method of control. Volume controlled ventilators (Dennell MA-I,
Engstrom, Emerson, Siemens-Servo, Bear)
deliver a preset tidal volume regardless of
the pressure required to do so. Pressure controlled ventilators (Bird, Bournes, HP-200,
Sechrist, Healthdyne) deliver breaths to a
predetermined positive pressure. The volume of each breath is determined by mechanical characteristics of the patient's
respiratory system, changes in airway resistance, or lung compliance. Regardless of
their method of control, all pediatric ventilators should be small, light-weight, and
compact. They should be-easy to understand and operate with clearly marked
knobs and a minimal number of adjustable
parts. Parts must be easy to clean and replace. Humidification of inspired gas must
be performed with a heated humidifier.P
Heated inspiratory and expiratory tubing
help minimize water condcnsation. All ventilators must be equipped with adequate
alarms, including a high pressure alarm to
detect excessive airway pressure (e.g., from
airway obstruction) and a low pressure
alarm to detect ventilator leaking or disconnect. Alarms for inspired oxygen concentration aod gas temperature are also desirable.
Pressure preset ventilators have several
advantages for use in infants and children
under 8 to 10 kg. Most often, infants and
127
young children are intubated with uncuffed
endotracheal tubes to prevent subglottic injury; a variable amount of air leak around
the endotracheal tube is often seen, which
makes the delivery of accurate tidal volumes
with volume preset machines difficult. 33
Additionally, time-flow and pressure preset
ventilators have a rapid response time and
can be used at rapid ventilator rates frequently useful in the management of small
infants. The disadvantage of pressure and
time-flow preset ventilators is that rapid
changes in airway resistance or lung complianoe result in the delivery of inconsistent
tidal volumes, potentially resulting in hyper- or hypoventilation.
. Volume preset machines deliver-a constant tidal volume, independent of thc pressure required. The delivered tidal volume
must be varied depending on the internal
compression volume of the circuit (including hoses, humidifier, water traps, and
alarm tubing). For very small children and
infants, compression volume of the mechanical ventilator Il}!lY consume all of the predicted tidal volume.P' As the size of the child
increases, the compression volume to delivered volume ratio becomes smaller, making
the volume preset determination more accurate. Frequent adjustments of ventilator
settings are usually not necessary. The peak
inspiratory pressure (PIl') generated by constant tidal volumes is a useful tool to monitor changes in lung mechanics. Increased
PIP may indicate a decrease in compliance
or increase in airway resistance (e.g., endotracheal
tube obstruction,
bronchospasm, excessive secretions, pneumothorax).
Decreasing PIP is usually seen as underlying
lung disease heals or as leaks develop around
endotracheal tubes, within the ventilation
system, or through chest tubes.
Modes of Ventilation.
Most ventilators,
whether they be volume or pressure preset,
allow multiple possible modes of ventilation. In the spontaneous breathing mode,
the patient breathes warm, humidified gas
without machine delivered mechanical
breaths. Frequently, continuous positive
128
III. RESPIRATORY DISEASE
airway pressure (Cl'AP) is delivered at a
minimum of 2 to 3 cm H20 to prevent alveolar collapse and resultant hypoxemia.
CPAP can be increased as necessary in order
to maintain arterial POz in children with
diffuse and evenly distributed alveolar collapse.
For patients who require mechanical
breaths in addition to their own spontaneous breaths to maintain adequate gas exchange, intermittent mandatory ventilation
(IMV) is most frequently used. With IMV,
the patient is abJe to breathe spontaneously
from a constant flow of gas streaming by the
endotracheal
tube in between mechanical
breaths
selected by the operator. IMV can
be synchronized
or unsynchronized.
With
synchronized IMV, the ventilator delivers a
predetermined
breath once every time frame
when the patient initiates a breath on his or
her own. With unsynchronized
IMV, the
patient breathes spontaneously
in between
controlled breaths, but receives a controlled
breath independently
of his or her own respiratory cyele. IMV has several advantages
over other modes of ventilation. Initially devised as a weaning teohnique.P IMV allows
a controlled and gradual reduction in ventilator support. However, IMV also has advantages during the acute phase of dn iJJness, Because the patient on IMV generates
negative pleural pressure during spontaneous breaths, mean intrathoracic
pressure
is reduced,
perhaps
resulting
in fewer
hemodynamic
alterations
and less barotrauma than with continuous positive pressure ventilation.j"
However, few appropriately controlled
prospective
studies have
been done comparing IMV and controlled
mechanical
ventilation;
none of the putative advantages of IMV have been proved,
despite the fad that the technique has become widely accepted.:"
Continuous
mandatory
ventilation
(CMV) refers to continuous machine-delivered mechanical
breaths without
interspersed,
patient-generated
spontaneous
breaths. CMV is indicated when the patient
is unable to generate spontaneous breaths as
a result of disease, sedatives, or the use of
paralytic agents.
as
In the assist-control
mode of ventilation, the patient initiates each inspiration,
but in so doing receives a full tidal volume
generated by the ventilator. Most pediatric
patients have rapid respiratory
rates and
tend to hyperventilate
while on assist-control mode, resulting in hypocapnia and respiratory alkalosis. With the exception of
those patients requiring mechanical ventilation because of eNS disease (e.g., ventilator-dependent
quadraplegics),
assist-control mode has not proved very useful in
infants and small children.
Initiation of Ventilation. To initiate
mechanical ventilation
with a volume preset
ventilator, a delivered Udal volume of 10 to
15 mllkg and a ventilator rate necessary to
deliver a total minute ventilation of 150 to
200 mllkg/min
are commonly
chosen.
Whatever tidal volume and ventilator rate
are chosen, the adequacy of chest expansion
and air entry is observed and alveolar ventilation is assessed by determining
the arterial PC02. Peak airway pressure is the net
result of airway resistance, total respiratory
compliance, inspiratory flow rate, and tidal
volume. With normal airway resistance and
lung compliance,
a tidal volume of 10 to 15
cc/kg, a peak flow rate of 30 to 40 L/min,
and an inspiratory to expiratory ratio of 1:2
to 1:3, a PIP of 20 to 30 em of water is usu- "
ally generated.
In the presence of severely
decreased lung compliance or increased airway resistance, peak airway pressure is significantly elevated, and may be associated
with barotrauma
or cardiovascular
compromise. In an attempt to reduce peak airway
pressure, peak: flow can be reduced, prolonging inspiratory time; alternatively tidal
volume can be reduced
(usually accompanied by an increase in a ventilator rate to
maintain minute ventilation
constant).
A
frequently used pattern for supporting ventilation in patients with alveolar disease appears to be one of a relatively large tidal volume (15 cclkg) with a prolonged inspirator)'
time (inspiration.expiration
of 1:1 to 1:2)
and low inspiratory
flow rate at a low ventilator frequency. This pattern may provide
adequate distribution
of ventilation
at the
1Il. RESPIRATORY DISEASE
130
Fluid Retention.
Positive intrathoracic
pressure decreases urine output and causes
sodium and water retention. This may result from increasing levels of circulating antidiuretic hormone or from changes in the
distribution of renal blood flow. 41 Hyponatremia and water intoxication can also be
seen in association with the use of ultrasonic
nebulizers,"! which produce particulate
water of small enough dimension to reach
the distal airway and to be absorbed into the
circulation. For this reason, ultrasonic
nebulizers cannot be recommenclerl in mechanically ventilated patients.
Infection. Infection and sepsis poses one.of
the major risks involved in the treatment of
respiratory failure. Gram-negative organisms are most commonly implicated in nosocomial respiratory infections. Transrnission of organisms is caused by compromised
pulmonary host defenses, gram-negative
colonization of the hospital environment
and inadequate handwashing technique.
The incidence of infection can be significantly reduced by a few simple practices:
careful handwashing with a bacteriocidal
agent prior to handling the patient, limited
examination of the patient by personnel not
Immediately
involved in care, and strict
aseptic technique when handling the airway and vascular catheters.
Weaning from Mechanical Ventilation
Absolute criteria for weaning from mechanical ventilation arc difficult to state definitively, given wide variability in both patients and disease processes. However, some
suggested guidelines are given in Table 10-4.
No single weaning technique has been
universally accepted. IMV was initially
conceived of as a weaning method;" a gradual reduction of IMV over time allows the
patient to generate an increasing proportion
of the minute ventilation. Alternatively, the
patient can be placed on a T-piece for increasing periods of time as he or she is able
to tolerate. The time required for weaning
depends on the nutritional status of the patient and the severity of the underlying
""."".• "".c..,.•••.•,......,., •.•••••••
.·_.·
.
TABLE 10-4.
SUGGESTED GUIDELINES
FOR INITIATION OF WEANING
fROM
MECHANICAL
VENTILATION
1. Poslttve nitrogen balance
2. Metabolic stablhtv
3. Cardiovascular stability
4. Maximum inspiratory force>
5. Vital capacity>
- 20 em water
10-15 ml/kg
6. Acceptable Po" with Fio. ~0.5
< 8-10 mm Hg
and PEEP
7. Absence of muscle relaxants or high dose sedatives/relaxants
pulmonary and extra pulmonary disease.
Weaning can be accomplished in periods
varying from minutes to weeks.
Regardless of whieh weaning technique
is chosen, the patient is watched closely for
signs of intolerance, including dyspnea,
tachypnea, hyper- or hypotension, bradyor tachycardia, pallor, cyanosis, anxiety,
hypoxemia, and hypercarbia.
Once the child has been weaned from
mechanical ventilation, spontaneous ventilation with 2 to 4 em H20 CPAP is continued before extubation is attempted. Extubation from CPAP or PEEP maintains
functional residual capacity and prevents
~distal airway collapse with resultant hypox.emia. 42 Once the child has demonstrated
stability with spontaneous ventilation and is
able to protect his or her airways, extubation can occur. In children who demonstrate rapid improvement, the CrAP trial
can be safely eliminated, and extubation can
occur from IMV rates of 2 to G breaths/min.
It is our 'custom to extubate children early
in the day, so that close observation is possible. Increased inspired oxygen concentrations (often increased 5 to 10 percent from
pre-extubation levels) are continued by mask
or hood.
High-Frequency Ventilation
Until recently, mechanical ventilation implied the administration of large tidal volumes at low frequencies. Most conventional
ventilators are used at frequencies under 60
cycles/minute (cpm), though some pediatric
131
10. RESPIRATORY FAILURE IN CHILDHOOD
ventilators with small compressible volumes
can generate 120 to 150 cpm. However,
there is no proof that low frequency, high
tidal volume ventilation is optimal. In fact,
it is theoretically possible that the circulatory depression and barotrauma associated
with conventional ventilation might be reduced if higher frequencies were used, assuming that adequate gas exchange could be
maintained. These principles were first applied by SjOstrand4.'lin 1967, in a study in
which dogs were ventilated through a tracheal catheter at a frcqucncy of 80 cpm. The
phasic fluctuations in arterial pressure,
which occur in association with large tidal
volume ventilation, were minimized and
adequate gas exchange was maintained.
Such "high-frequency ventilation" (HFV)
tas been defined as ventilation of the lungs
It a frequency which is equal to or greater
.han four times the normal physiologic
:ange. H Three different techniques of proriding HFV have evolved during the last 15
fears: high frequency positive pressure venilation (HFPPV), high frequency jet venIlation (HFJV), and high frequency osoilation (HFO).
With HFPPV, Ircquencles of 60 to 100
'pm are generated by opening and closing
he outflow from a pressurized air-oxygen
;as source, using a fluidic, mechanical, or
Iectromagnetic valve. Tidal volumes are
-nly slightly larger than dead space, resultng in low airway pressure and decreased
hance of barotrauma and circulatory irn.airment, The' duration ot" inspiration is
isually fixed at 20 to 40 percent of each
ycle, expiration is passive. As inspiratory
ime is prolonged and expiratory time is
hortened, lung volume increases because
he lungs have less time to empty. This inrease in lung volume can be minimized by
sing the shortest inspiratory time which
rovides adequate gas exchange. This techique can be conceived of as positive pres.rre ventilation at increased rates,
HFJV was introduced by Klain and
mithiS in 1977. With this technique, fresh
as is injected into the trachea through a
nall orifice catheter (1.6 to 2.0 mm ID) at
frequencies of 8 to 600 cpm. Tidal volumes
approximate dead space volume. Because
gas enters the trachea at a high velocity, ambient gas is intrained according to Bcmoullli's principle. This has the advantage of augmenting the tidal volume (perhaps to
volumes in excess of dead space), but has the
disadvantage of changing the concentration
of the inspired gas mixture. Supplying both
the ventilator and the patient circuit with
gas from a common fresh gas source overcomes this disadvantage. At rates above 600
cpm, CO2 elimination may be inadequate.:" The driving pressure is the main
determinant of minute volume and can be
adjusted between 0 and 85 psi.
During HFPPV and HFJV, the tidal
volume decreases as the frequency of ventilation is Increased, assuming u constant
driving pressure and inspiratory to expiratory time (Fig: 10-6). As-tidal volume decreases, the dead space to tidal volume ratio
increases, resulting in an increasing need for
minute volume (10 to 40 L/min).
Hilth frequency oscillation (HFO) operates at 180 to 3000 cpm. Cyclic pressure
changes are generated by connecting a piston pump or the cone of a load speaker directly to the paticnt's cndotrncheul tube.
The gas in the airways is thus oscillated toand-Ire in a sinusoidal fashion. Expiration
is active, which distinguishes HFO from
either HFPPV or HFJV. Inspiration and exw
:=;:
:3g
oJ
0(
o
1=
ex:
a
g
~
w
>
FREQUENCY
Figure 10-6. Change in tidal volume dolivered by a
jet ventilator as the frequency is increased (a) at constant driving pressure and I:E ratio, (b) when the driving pressure is doubled, and (e) when the I:E ratio is
halved.
13!!
piration each occupy 50 percent of the cycle.
and this the inspiratory to expiratory time is
fixed at 1:1. Since tidal volumes are below
dead space volume, the exchange of carbon
dioxide and oxygen is a form of forced diffusion.
Unfortunately, measurement of tidal
ventilation during HFV is difficult. Direct
methods of volume measurement which are
used during conventional ventilation are not
applicable to HFV, because the frequency
response of most devices is too low and because any flow meter imposed would add
unacceptable resistance and dead space to
the patient's airway. Consequently,· most
patients receiving HFV have no volume
monitoring.
Clinical Uses for HFV
HFV has been used for intraoperative, postoperative, long-term, and emergency situations which require a low pressure airway.
Intraoperatively, HFV has been used during
laryngoscopy and bronchoscopy.f? during
microlaryngeal surgery." and thoracotomy.
HFV may be the method of choice for treatment of bronchopleural fistula. 49 It may also
be useful in patients with adult respiratory
distress syndrome to avoid excessive peak
pressures.P? though a prospective con/parative study with conventional ventilation has
not been done. HFV can be superimposed
upon conventional ventilation, which may
smooth and speed the transition from controlled ventilation to spontaneous breathing.51 Application of HFJY following upper
airway traurna'" and cardiopulmonary
resuscitatlon'f has also been described.
Complications of HFV.
Potential complications of UFY include the following: (1)
tracheal damage if humidification of fresh
gas is insufficient; (2) hypothermia, particularly in the pediatric patient if fresh gas is
not adequately preheated; (3) barotrauma
with lung rupture and tension pneumothorax if exhalation is impaired in any way;
(4) interstitial emphysema (with HFJV) possibly leading to tension pneumothorax or
Ill. RESPIRATORY DISEASE
pneumomediastinum if the percutaneous'
intratracheal catheter is dislodged.
The Future of HFV.
HFV has challenged
classic theories of gas exchange and has introduced the concepts of facilitated diffusion and other types of intrapulmonary gas'
distribution. In addition, it is clear that gas"
exchange can be maintained in certain cases
with HFV at lower peak and mean airway
pressures. Its use in selected circumstances,
such as bronchopleural fistula has been
demonstrated. Once well-controlled studies
comparing HFV to conventional techniques
have been done and adequate monitoring
teehntques have been developed to ensure
patient safety, HFY will likely play an increasingly important role in the treatment
of pedlatric respiratory failure. A national
multi-Institutional study is currently under
way to investigate the role of HFY in treatment of neonatal respiratory disease.
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