++
The main functions of the respiratory system are to replenish
the venous blood’s content of O2 while removing
its excess CO2. Respiratory failure describes the inability
to carry out this function commensurate with the needs of the organism.
This definition may be misleading. For example, to state that respiratory
failure exists when the partial tensions of O2 (PO2)
and CO2 (PCO2) in the arterial blood remain persistently
outside the range found in normal humans (values of PO2 <
50 mm Hg or PCO2 > 45 mm Hg are often cited). However,
this definition ignores the fact that breathing O2-enriched gas
can by itself restore the arterial PO2 to the normal range,
even though the gas-exchanging mechanism is faulty and may not sustain
the needs of the individual while breathing air. Conversely, the
same definition would categorize children with congenital cyanotic
heart disease (who are hypoxemic) or with diuretic-induced metabolic
alkalosis (who, as a compensatory mechanism, are hypercapnic) as
suffering from respiratory failure, even though their respiratory system
may be perfectly functional.
++
For these reasons, rather than detecting specific aberrations
in blood-gas content, the clinician’s primary concern should
be whether the respiratory system can support metabolic demands
under all the circumstances the patient is likely to encounter.
Fever or exercise often unveil otherwise compensated anomalies of
gas exchange by adding to the ventilatory load of the respiratory
muscles or by increasing demand for pulmonary blood flow. Hypoxemia
and hypercapnia interfere most noticeably with the function of the
central nervous and cardiovascular systems. Agitation, somnolence,
apathy, combativeness, or even stupor in an infant or child with
respiratory distress or decreased respiratory effort should at least
prompt the administration of O2, even if blood-gas analysis
is unavailable. Increasing tachycardia, arterial hypertension, or,
by way of progression, decreased perfusion, arterial hypotension,
and bradycardia are worrisome signs in a patient with a respiratory
derangement and, under most circumstances, constitute an immediate
indication to institute artificial ventilatory support.
+++
Disruption of
Gas Exchange
++
Understanding the mechanisms that lead to blood-gas aberrations
in infants and children with respiratory failure is essential to
interpreting clinical information and to planning treatment.8 Basic
to such understanding is the notion that the exchange of gases between
the inspired gas and the blood in the lungs produces two products:
the expired gas and the arterial blood (Fig. 102-4).
Each of these products is a composite of the contributions of millions
of alveolar-capillary units, weighted by the amount of oxygen or
carbon dioxide in blood or gas from each unit. In every one of these
units, and in the lung as a whole, the gas contents of the alveolar
gas and the capillary blood are linked reciprocally by relatively
simple laws that establish a framework for understanding the gas-exchanging
process and its abnormalities. Moreover, in alveolar-capillary units
where there is an exchange of gas, it is generally assumed that
the pressure of O2 and CO2 develop equilibrium
between the blood and gas phase.
++
++
Oxygen and CO2 are highly diffusible gases. Diffusion
impairments across the alveolar-capillary membrane play little role
in the genesis of hypoxemia or hypercapnia in children with respiratory
disease. Accordingly, it is safe to assume that the PO2 and
PCO2 of the blood exiting a given pulmonary capillary reflects
the PO2 and PCO2 of the gas contained in the corresponding
alveolus. The composition of the alveolar gas is determined by the rate
at which gases are exchanged across the alveolar-capillary membrane
(diffusion and perfusion), and the turnover rate of fresh air entering
the alveoli (ventilation). Mathematical modeling of the relationship
between alveolar PO2, ventilation, and O2 uptake
is relatively complicated,9 because O2 is
present in both the inspired and the expired gas. In contrast, modeling
of the relationship between PCO2, ventilation, and CO2 elimination
is relatively simple, because the inspired gas does not contain
CO2. For the whole lung, the average alveolar PCO2 is
directly proportional to the amount of CO2 produced by
the body and is inversely proportional to the volume of gas that
participates in alveolar gas exchange per unit of time. The latter
is known as alveolar ventilation (as opposed to minute
ventilation, which is the total amount of gas that exits
the lungs per unit of time or the product of tidal volume by breathing
frequency).
++
The dead space, or wasted ventilation (Fig. 102-4) is the portion of the total minute
ventilation that does not participate in CO2 exchange.
This generally represents the gas that is expired from the lungs
that remains in the large airways during expiration, until re-inspired
into the alveoli during the next inspiration. Since this gas still
contains CO2, it does not contribute to elimination of
CO2 from the lungs and therefore is shown in Figure
102-4 as not contributing to CO2 gas exchange. Disorders
that increase the dead space usually do not cause hypercapnia because
the individual is able to increase minute ventilation sufficiently
to restore alveolar ventilation to the needed level to maintain
CO2 within a normal range (as occurs when breathing through
a short piece of tubing). Alveolar CO2 levels determine
the pulmonary arterial blood CO2 concentrations.
++
Arterial blood gas concentrations can be conceptualized as the
product of two idealized components. One consists of systemic venous blood
that bypasses (or is shunted away from) the alveoli
and hence does not participate in gas exchange. The other arises
from blood that undergoes perfect exchange with alveolar gas. The
mixture of these two components determines the actual arterial blood
gas concentrations.
++
For simplicity, the source of the blood that bypasses alveoli
(or venous admixture in the physiological parlance) has conventionally been viewed
as arising from several discrete pathways. First, true anatomic
shunt follows anatomic communications between the venous and
arterial side of the circulation. Some of these communications are
found in normal individuals (eg, thebesian veins, which connect the
coronary circulation to the left ventricle, or the bronchial vessels,
which direct venous blood into the pulmonary veins); others result from
cardiac malformations (see Chapter 484) or
lung disease resulting in alveolar collapse or consolidation (ventilation-perfusion
ratio of 0). Second, diffusion defects, whether caused by true alterations
of the alveolar capillary membrane or, more frequently, by blood being
forced through the capillaries at a rate that does not permit equilibration
with the alveolar gas, reduce the end-capillary PO2 and have
an effect similar to mixing venous blood with fully oxygenated blood.
Finally, ventilation-perfusion inequality results primarily from
incomplete oxygenation of blood circulating through lung units with
a low ventilation-perfusion ratio. Diffusion abnormalities and ventilation-perfusion
inequality create only a virtual shunt, which decreases
if the inspired oxygen concentration is increased. In contrast,
when a true anatomic shunt exists, O2 administration can
only increase the oxygen content of the arterial blood by raising
the volume of O2 dissolved in the pulmonary capillary blood;
thus, the calculated size of the shunt is affected minimally by
O2 administration.
++
Ventilation-perfusion inequality is by far the most common mechanism
of hypoxemia and hypercapnia,10 both in children
and adults with respiratory disease (Fig. 102-5).
Ventilation-perfusion differences are a natural consequence of the
parallel organization of the bronchial and arterial networks of
the lungs, which permits an infinite combination of ventilation-perfusion
ratios to coexist in the same lung. Gravity causes a certain degree
of ventilation-perfusion inequality in normal lungs by directing
a larger share of blood flow to dependent areas. Bronchial obstruction,
consolidation or collapse of alveolar spaces, and abnormalities
in pulmonary vascular function greatly exaggerate this inequality.
The cause of hypoxemia in ventilation-perfusion inequality lies
primarily with the alveolar-capillary units that have a low ventilation-perfusion
ratio. Because renewal of the alveolar gas through ventilation cannot
keep up with O2 uptake by the blood, these units have a
low alveolar PO2, usually in a range where the O2-hemoglobin
dissociation curve is steep. As a result, the end-capillary blood
is not fully loaded with O2, and when mixed with blood
from other units, it creates a substantial venous admixture. Units
with high ventilation-perfusion ratios have a high alveolar PO2.
However, these units cannot compensate for the venous admixture caused
by units with low ventilation-perfusion ratios, because at high
PO2 levels, the O2-hemoglobin dissociation curve
is flat, and the blood cannot increase its O2 content substantially.
++
++
Alveolar-capillary units with low ventilation-perfusion ratios
cannot decrease their alveolar PCO2 much below the mixed-venous level;
thus, their ability to remove CO2 from the blood is impaired.
However, units with a high ventilation-perfusion ratio may lower their
alveolar PCO2 considerably. This establishes an efficient
mechanism of compensation, which makes hypercapnia less prominent than
hypoxemia, provided that the infant or child has sufficient respiratory
muscle reserve to support the necessary increase in ventilation.
++
By envisioning that each breath is a mixture of gas from dead
space (PCO2 = 0) and the alveolar space (PCO2 = PACO2),
the ratio of the dead space ventilation to the tidal volume (VT) can
be calculated as
++
VD/VT = (PACO2 – PECO2)/PACO2
++
where PECO2 is the PCO2 of the mixed expired
gas. Alveolar PCO2 cannot be measured directly but can
be estimated using widely available monitoring tools. The end-tidal PCO2,
for instance, measures the PCO2 of the gas exhaled at end-expiration
on the assumption that it contains only alveolar gas. The arterial
PCO2 is similar to the end-capillary PCO2, and
barring any shunting of venous blood into the arterial circulation,
it should be similar to the alveolar PCO2 (in clinical
practice, the end-tidal PCO2 is monitored as a surrogate
of the arterial PCO2; see Chapter 106). However, the end-tidal
PCO2 and the arterial PCO2 may be quite different,
especially in the presence of lung disease. The reason is that alveoli,
which are relatively underperfused, have very low alveolar PCO2 values;
thus, the gas that exits these alveoli lowers the end-tidal PCO2 considerably.
In contrast, alveoli that are relatively underventilated cannot
have PCO2 values greater than the mixed-venous blood (which
is only a few mm Hg greater than the arterial PCO2); thus,
they are underrepresented in the end-tidal PCO2. It follows that
substituting the end-tidal or the arterial PCO2 for the
alveolar PCO2 in the equation above yields two different
values of the dead space. When the end-tidal PCO2 is used,
the result estimates the volume of gas contained in the conducting
airways (fresh gas during inspiration and a mixture of fresh gas
and alveolar gas during expiration), away from the gas-exchanging
regions of the lung (anatomic or series
dead space).
++
On the other hand, when the arterial PCO2 is used, the
resulting value (physiological dead space) is greater,
because it includes the anatomic dead space and all the gas that
enters the alveoli without undergoing CO2 exchange (alveolar or parallel
dead space). Dead-space calculations are impractical in
clinical practice, because they require cumbersome collection of
the expiratory gas. However, the difference between arterial and
end-tidal PCO2 can be used as a simple bedside tool to assess
disease or treatment-related changes in the distribution of perfusion
in the lungs. Pulmonary emboli, for example, can be detected as
a conspicuous decrease in the end-tidal PCO2 relative to
the arterial PCO2 when the expired PCO2 is monitored
continuously (see Chapter 106). Similarly, redistribution of pulmonary
blood away from overinflated areas of the lung during the application
of positive end-expiratory pressure (PEEP) widens the difference
between arterial and end-tidal PCO2 in a fashion that can
be used to adjust the therapy.
++
Another factor that contributes to the complex relationship between
PO2, ventilation, and oxygen uptake is that O2 and
CO2 are often exchanged at an uneven rate; this creates
a volume deficit that must be filled with O2-containing
fresh gas (typically O2 consumption exceeds CO2 production
by 20%). Physiologists have circumvented these difficulties
by recognizing that the reduction in PO2 as gas equilibrates
with blood in the alveolus is directly related to the increase in
CO2. The alveolar PO2 can then be calculated by determining
the PO2 of the inspired gas and by subtracting the PO2 decline
produced by the CO2-O2 exchange between alveolus
and pulmonary capillary. The resultant expression is the alveolar
gas equation, in which the inequality of the CO2-O2 exchange
is represented by the respiratory exchange ratio (R),
or the result of dividing the CO2 production by the O2 consumption:
++
PAO2 = FIO2 (PB – PH2O) – PACO2 [FIO2 + (1 – FIO2)/R]
++
where FIO2 is the fractional concentration of O2 in
the inspired gas, PB is the atmospheric pressure,
and PH2O is the partial pressure of water vapor at body
temperature. This formulation illustrates well the point that alveolar PO2 and
PCO2 are linked to each other in such a way that, when
one of them is specified, only one value can exist for the other
in any particular alveolus. The alveolar gas equation can also be
used to take a global view of the lung as if gas exchange were homogeneous.
Under such ideal circumstances, the alveolar PO2 represents
the highest PO2 that could be expected in arterial blood.
Thus, any difference between the calculated alveolar PO2 and
the actual arterial PO2 (the alveolar-arterial
PO2 difference) is an important
means for detecting and understanding aberrations in gas exchange.
++
When alveolar ventilation decreases globally (hypoventilation),
alveolar PCO2 and, by extent, arterial PCO2 increase
with the reduction in alveolar ventilation. As shown by the alveolar
gas equation, alveolar and arterial PO2 decline, and the
decrease in arterial PO2 is proportional to the increase
in alveolar or arterial PCO2 (the proportionality constant
being R). While the alveolar-arterial PO2 difference is
useful for detecting an abnormality in gas exchange, its magnitude
changes considerably with the inspired O2 concentration,
which cannot always be controlled or known with precision. Thus,
physiologists have developed an alternative strategy to quantify
derangements in gas exchange. Just as dead space is an index of
the efficiency (or rather the inefficiency) of CO2 exchange
in the lungs, shunt or venous admixture provides
a similar quantitative index for the efficiency of O2 exchange
by dividing the pulmonary blood flow into two compartments. Shunt
is composed of pulmonary capillary blood that undergoes ideal O2 exchange
with the alveolar gas, and the venous admixture is composed of venous blood
that travels unaltered to the arterial side of the circulation.
Venous admixture (Q̇s) is usually expressed as a fraction
of the systemic blood flow (Q̇t), calculated by performing
an O2 mass balance across the pulmonary circulation:
++
Q̇s/Q̇•t = (Cc'O2 – CaO2)/(Cc'O2 – C⊢O2)
++
where Cc'O2, CaO2, and C⊢O2 are
the O2 contents (total volume of O2 per 100 mL
of blood) of the pulmonary capillary (estimated by the alveolar
gas equation), the arterial blood (measured directly in a systemic
artery), and the mixed venous blood (measured directly in the pulmonary
artery).
+++
Clinical Evaluation of
Respiratory Failure
++
The majority of infants and children who develop respiratory
failure suffer from some form of mechanical dysfunction of the lungs
or chest wall. Respiratory distress is then the leading manifestation
of the failure and the usual reason why medical attention is sought.
Careful assessment of the incumbent physical signs usually provides
helpful insight into the restrictive or obstructive character of
the dysfunction and into the exact nature of the disease causing
it (see above). Occasionally, however, an infant or child presents
with respiratory failure caused by a primary or secondary dysfunction
of the neural respiratory control. This circumstance may be difficult
to detect, unless the clinician suspects that the respiratory effort
is inadequate to support the patient’s ventilatory requirements
and analyzes the patient’s gas exchange function.
+++
Increased Respiratory
Effort and Mechanical Dysfunction
++
Severe respiratory disease inevitably interferes with both the
mechanical and gas-exchanging functions of the respiratory system.
Increased demands on the respiratory muscles combined with arterial
blood-gas abnormalities trigger a successful compensatory response
if two conditions are met: (1) the respiratory muscles must be able
to perform and sustain the necessary work, and (2) the gas-exchange
abnormalities must be correctable by an increase in ventilation.
The situation in which the respiratory muscles are no longer capable
of performing work commensurate with the organism’s ventilatory
needs is described as respiratory muscle fatigue, drawing
an obvious analogy with the behavior of skeletal muscle when subjected
to excessive work. Recognizing its imminence is fundamental to preventing
the development of life-threatening hypoxemia and hypercapnia, usually
via mechanical ventilatory support (see Chapter 109).
++
The ability of the respiratory muscles to assume an increased
mechanical load depends on the balance between the amount of energy that
the muscles can transform into physical work and the magnitude of
the work demands imposed by breathing.11 Increased
work requires that increased oxygen and energy substrate is supplied
to the respiratory muscles. Although these muscles, especially the
diaphragm, can increase their blood supply several fold,12 disorders
that decrease cardiac output may limit the capacity of the muscle
to respond.
++
The efficiency of the respiratory system13 describes
the proportion of energy consumed by the respiratory muscle for
pressure-volume work. In adults this is estimated not to exceed 15%,
whereas in infants values of 5% have been reported.14 Factors
that may affect the ability of the respiratory muscles to perform the
work of breathing include the respiratory pattern, the identity
and state of conditioning of the respiratory muscles, and the configuration
of the chest wall.
++
Breathing pattern is influenced by the nature and extent of the
mechanical derangements produced by the disease. Although the neural
mechanism has not been fully identified, the practical reality is
that infants and children modify their tidal volume and breathing
frequency in a manner that minimizes energy expenditure. Thus, any
conditions—external or internal—that interfere
with a patient’s ability to adopt an optimal pattern diminish
the respiratory system’s efficiency. Rapid breathing caused
by agitation, for example, may precipitate respiratory muscle fatigue
and failure in a child with croup or epiglottitis (see Chapter 510). Similarly, bradypnea caused by central nervous system depression
is a very disadvantageous breathing pattern in a child with pulmonary
edema or other form of restrictive lung disease.
++
Respiratory muscle fatigue appears to dictate respiratory pattern
requirements of its own. Patients who are experiencing a decrease in
the contraction force of their diaphragm often breathe rapidly and
shallowly, regardless of whether their disease is predominantly
restrictive or obstructive. It is also common for such patients
to alternate the respiratory load between several muscle groups
in a fashion that suggests that intermittent resting may make the
effort more sustainable.
++
Which specific muscles or muscle groups are activated in an effort
to overcome a mechanical impairment has substantial bearing on breathing
efficiency. The diaphragm can increase its work with only limited
increases of its O2 consumption and blood-flow requirements.
Other accessory inspiratory and expiratory muscles are much less
economical relative to the increase in ventilatory output that they
generate15; consequently, their energy demands
may quickly overburden the patient. Poor nutrition, atrophy from
lack of use (eg, in patients whose ventilation is fully supported
for long periods of time), and myopathy all decrease the efficiency
of the respiratory muscles by raising their energetic demands out
of proportion with the work that they perform.
++
Limited ossification of the rib cage and the short axial dimension
of the thorax make the newborn and small infant’s chest
wall particularly prone to distortion. This may affect respiratory
muscle efficiency by several mechanisms. First, all muscles achieve
their maximal ratio of work-to-energy consumption at an optimal
length. Overinflation of the lungs and abdominal distension flatten
the diaphragmatic dome and reduce the effective length of the phrenic
muscle fibers, degrading the maximal force that these fibers are
able to develop and the muscle’s overall energetic efficiency.
++
Second, developmental and disease-induced changes in the chest’s
geometry influence the area of contact between the lateral surface
of the diaphragm and the internal surface of the rib cage. This
area, known as the area of apposition of diaphragm
and the rib cage,16 facilitates lung inflation
by translating the increase in intra-abdominal pressure produced
by the diaphragmatic descent into an outward-directed force acting
on the ribs. Because infants have a relatively wide lower chest,
the costal insertions of the diaphragm are spread out, making their
area of apposition small. Overinflation of the lungs and abdominal
distention can further limit the lateral contact between diaphragm
and rib cage, thereby wasting the work that the diaphragm does on the
abdominal organs.
++
Finally, inward distortion of the rib cage increases the shortening
the phrenic fibers must undergo in order to generate a certain volume change
in the lungs. In the absence of distortion, the volume displaced
by the diaphragmatic contraction is approximately the same as the
volume increase of the lungs. When inward distortion occurs, however,
the volume displaced by the diaphragm is divided between the volume
increase of the lungs and the volume created by the inward movement
of the rib cage (Fig. 102-6). Although the
diaphragm performs real work to distort the rib cage, the energy
used in the process is wasted in terms of ventilation. In this waste
lies one of the major disadvantages that the immature child faces
when developing lung disease: Chest-wall distortion can multiply
the work performed by the diaphragmatic muscle and may lead rapidly
to respiratory muscle fatigue, even in the absence of a serious
mechanical derangement of the lungs.7
++
+++
Decreased Ventilatory
Effort and Hypoventilation
++
Abnormal decreases in the respiratory effort lead to hypoventilation, a
condition in which the renewal of the alveolar gas is insufficient
to maintain normal CO2 and arterial O2 tensions. The
mechanisms underlying the ensuing blood-gas abnormalities are (1)
the dependence of alveolar PCO2 on alveolar ventilation
and (2) the combined effects of the poor renewal of the alveolar
gas and the continued uptake of O2 by the pulmonary capillaries
on the alveolar PO2. Hypoventilation may be difficult to
detect unless it occurs in a patient whose gas exchange is already
being monitored or unless it is accompanied by other clinical findings
such as upper-airway obstruction. Hypoxemia is not always evident
as cyanosis, especially if the patient has anemia or when the light
conditions are unfavorable. Hypercapnia produces nonspecific clinical
manifestations, somnolence usually being the most prominent.
++
The finding of a reduced respiratory effort, particularly when
the patient is hypercapnic and hypoxemic, should raise immediate
suspicion about the integrity of the central nervous system’s
function. Direct injuries to the brain, such as those caused by
ischemia, an expanding intracranial mass, or infection, can lessen
the brain stem’s response to chemoreceptor stimulation.
Metabolic toxins or exogenous pharmacological agents may have similar consequences.
Opioids, in particular, are effective inhibitors of the respiratory
drive, a property that is often exploited to reduce spontaneous breathing
and facilitate mechanical ventilation. However, their advantages
under such circumstances often turn to disadvantage when it comes
time to discontinue ventilatory support. Overdosing with opioids
and benzodiazepines is a frequent cause of persistent respiratory
failure in mechanically ventilated infants and children. Although
it is not always easy to distinguish medication-induced hypoventilation
from mechanical dysfunction and especially from muscle weakness, the
clinician should be alerted to this possibility whenever a patient
has a decreased arterial pH (acidemia) without signs of respiratory
distress.
++
The respiratory control appears to be under more dominant inhibitory
influences from supramedullary centers in newborn infants, especially
if they are born prematurely, than in older children and adults.17 This
developmental singularity explains why newborn infants may breathe
shallowly or even become apneic in response to alveolar hypoxemia.
It may also explain why these infants become apneic when their pulmonary
stretch receptors are activated by excessive lung inflation (the
basis of the Hering-Breuer reflex) or by stimuli that arise from
the lung interstitium and airway walls in the presence of lung disease.
An exaggerated inhibitory response to a combination of alveolar
hypoxemia and mechanoreceptor stimulation is likely to be responsible
for the frequency with which small infants have apnea as the first
manifestation of lung diseases such as viral pneumonitis.
++
In rare circumstances, the anomaly of the respiratory control
is isolated to the respiratory premotor network. The only manifestation
of the disease is hypoventilation, usually during sleep, when supramedullary
excitatory influences on the respiratory control are at a minimum
(Ondine’s curse). More frequently, the decrease in respiratory
drive is part of a more extensive dysfunction of the central nervous system,
involving supratentorial areas of the brain or other centers in
the brain stem. Because the medullary neuronal networks that control
the inspiratory muscles (eg, diaphragm) and the muscles that dilate
the upper airway (eg, genioglossus or cricoarytenoid) are integrated functionally,
hypoventilation is usually associated with upper-airway obstruction
caused by decreased pharyngeal tone and glottic obstruction. This
is manifested as snoring (stertor), stridor, and reduced air entry
into the lungs during inspiration. The neuronal reflexes responsible
for airway-protective mechanisms such as coughing and gagging are
part of these networks, and they are also frequently impaired. In
such case, accumulation of mucus and saliva in the upper airway
and bronchi compounds the airway obstruction. Because the amplitude
of the respiratory excursions and absolute lung volume are decreased,
alveolar collapse becomes inevitable. Thus, it is not unusual to
find alveolar densities in chest radiographs of patients in whom
the primary alteration is a reduction of the respiratory drive,
a feature that may create confusion by leading the clinician toward
a diagnosis of primary lung disease.
+++
Management of Respiratory
Failure
++
Mechanical ventilation, whether provided through an endotracheal
tube or a mask, is often the only viable alternative to restore
gas exchange and to unload the respiratory muscles when respiratory
failure is imminent or already present. The physiological bases
and practical applications of the various techniques of ventilatory
support are discussed in Chapter 109.
++
Patients with respiratory dysfunction are best served when even
the initial treatment addresses the cause, or at least the mechanism,
of the dysfunction. For example, pulmonary edema in a child with
left-ventricular failure is best treated with diuretics and, if
appropriate, with inotropic medications. Bacterial pneumonia demands
the use of antibiotics selected for the causal organism. Life-threatening
upper-airway obstruction should be relieved by bypassing the obstructed
airway segment with an endotracheal tube or with another type of
artificial airway. However, etiologic or mechanistic approaches
require time and may not be possible if the cause of the disease
is not apparent. Under such circumstances, the goal of therapy is
to guarantee the adequacy of gas exchange with minimal discomfort,
pain, and complications for the patient. On occasion, this goal
can be achieved by simple measures that increase the efficiency
of the respiratory system, while avoiding interventions that may
render it inefficient. For example, lifting the head of the bed
in a patient with severe orthopnea may reduce upper-airway resistance
and increase the initial length of the diaphragmatic fibers, improving the
diaphragm’s ability to handle its load enough so as to
turn an unstable situation into a more stable one. Removing ascites
that are impinging upon diaphragmatic movement may also improve
the efficiency of the diaphragmatic contraction and increase lung
volume at end-expiration. Avoiding actions that may frighten or
upset a severely distressed child with croup or epiglottitis, on
the other hand, allows the child to continue using an advantageous
breathing pattern while physicians prepare for safe intubation of
the trachea.
++
Of all the alterations found in respiratory failure, hypoxemia
is by far the most life-threatening. Every clinician must remember that
administering O2 to a child with respiratory distress is
inherently safe and should be done immediately until the hypoxemia
is corroborated by blood-gas analysis. The only notable exceptions
are in patients for whom hyperoxia-induced pulmonary vasodilation may
divert systemic blood flow to the pulmonary circulation through
a large left-to-right shunt (eg, large ventricular septal defects,
hypoplastic left-heart syndrome) or in newborns with ductal-dependent
lesions whose ductus arteriosus may constrict in response to an
increasing PO2. Oxygen can be administered with a variety
of devices. Nasal prongs are widely used at all ages, because they
are comfortable and usually well tolerated by infants and toddlers.
Unfortunately, they provide only limited O2-enrichment
and humidification of the inspired gas and are not useful in patients who
breathe through their mouths. Hoods can raise the concentrations
of inspired O2 to close to 100%, but they are
cumbersome and threatening to small children. Masks and face tents are
best tolerated by older patients. When equipped with a bag reservoir
and a one-way exhalation valve (non-rebreathing masks), these two
types of devices approach the O2 delivery efficiency of
a hood.