Diagnosis and Management of Respiratory Failure
Objectives
1. Definitions, Classifications, and Causes of Respiratory Failure in Pediatrics
2. Pathophysiology of Acute Respiratory Failure
3. Recognition of ARF in Pediatric Patients
4. Multiple Techniques/Devices for the Delivery of Oxygen
5. Mechanical Ventilation
Definitions/Classification of Respiratory Failure
Acute Respiratory Failure is defined as the inability of the respiratory system to maintain
gas exchange at a sufficient rate to meet the body’s metabolic demands. The diagnosis
based on blood gas abnormalities is arbitrary but can be summarized by one of the
following values:
1. PaCO2 > 55 mm Hg
2. PaO2 < 60 mm Hg
3. SaO2 < 90% (in the absence of cyanotic congenital heart
disease)
ARF, as seen in the above parameters, can be broken down into hypoxic respiratory
failure and hypercapnic respiratory failure
Causes of ARF
Causes of ARF in Pediatric Patients Include:
Obstructive Lung Disease
1. Asthma
2. Bronchiolitis
3. Upper/Lower Airway Obstruction: anatomic (i.e. croup, epiglottitis, tracheoor bronchomalacia), foreign body
Restrictive Lung Disease
1. Pulmonary Fibrosis
2. Pneumothorax or other pleural diseases
Parenchymal Lung Disease
1. Acute Respiratory Distress Syndrome
2. Pneumonia: infectious, aspiration
3. Pulmonary Hypertension (primary or secondary)
4. Congestive Heart Failure
Other
1. CNS impairment, drug ingestion
2. Disorders with Respiratory Muscle Weakness: SMA, Guillaume-Barre, etc
Pathophysiology of ARF
Hypoxia:
Hypoxic respiratory failure can result from various abnormalities in oxygen delivery:
1. Decreased environmental O2 tension as is seen with altitudes (people in
Denver have lower O2 saturations than people on Long Island)
2. Decreased gas entry into the lungs: hypoventilation, airway obstruction, etc.
3. Problems with diffusion of gas from alveoli to pulmonary capillaries: fibrosis,
edema, etc.
4. V/Q mismatching (including the most severe form – shunt)
The most prevalent underlying problem in hypoxic respiratory failure in pediatrics is
mismatch of alveolar ventilation and pulmonary perfusion (V/Q mismatching).
Diseases that cause progressive atelectasis of the alveoli, like pneumonia or edema, will
limit the amount of O2 available for uptake. Although pulmonary blood flow to an
atelectatic segment will decrease as a response to a decrease in alveolar O2, it does not
decrease as much as oxygen availability. More unoxygenated blood will then circulate.
The most severe form of V/Q mismatching is called “shunt effect” wherein unoxygenated
blood will pass alveoli without undergoing gas exchange. This shunting can occur within
the heart (as is seen in congenital heart disease) or in the lung.
A good way to determine the degree of hypoxia involves using the alveolar gas equation.
This equation describes the relationship between the amount of oxygen in the lung (the
alveolar PO2 or PAO2) and the amount of oxygen that gets into the blood (PaO2). This
equation can also be used to determine if the hypoxia is secondary to an excess of CO2 in
the alveolus.
PAO2 = FIO2 (PB – PH20) – (PCO2 / R)
PAO2 = alveolar oxygen partial pressure (as opposed to PaO2 = arterial O2 pressure)
FIO2 = fraction of inspired oxygen (room air is .21)
PB = barometric pressure (at sea level, it is 760 mm Hg)
PH2O = partial pressure of water vapor (usually equal to ~47)
PCO2 = partial pressure of CO2 (this will be found on an arterial blood gas)
R = respiratory quotient; tells you how much CO2 is made for each O2 used: usually ~ 0.8
So on room air at sea level, a normal lung should have a PAO2 = .21(760-47) – (40 / .8) =
100. On 100% oxygen the normal lung should have a PAO2 = 1.0 (760-47) – (40 / .8) =
663
The difference between the amount of oxygen in the alveolus and amount that diffuses
into the blood is called the P(A-a)O2 gradient and should be less than 20.
Treatment of V/Q mismatching within the lung should be directed at increasing alveolar
oxygen (PAO2). Typically therapies are directed at reopening atelectatic alveoli (this is
called “recruitment”) and preventing reclosure (“derecruitment”). Other therapies can
include diuretics to move fluid out of the alveoli, prone positioning to remove the weight
of the mediastinum off of the lung, steroids to decrease inflammation, etc.
A second, less common cause of hypoxia is V/Q mismatching secondary to impaired
pulmonary blood flow that cannot exchange gas with normal alveoli. An example of this
is primary or secondary pulmonary hypertension.
Hypercarbia
Hypercapnic respiratory failure is caused by impaired minute ventilation. Minute
ventilation (or alveolar ventilation, VA) is defined as effective tidal volumes multiplied by
the respiratory rate, or:
VA = (VT – VD) f
VT = tidal volume or the size of the breath
VD = dead space or the volume of gas in areas that do not undergo gas exchange
f = respiratory rate
So, the minute ventilation, and subsequently carbon dioxide clearance, can be impaired
by decreasing the tidal volume or respiratory rate or by increasing the dead space in the
lung. Rarely, high carbon dioxide levels can be found in patients with excessive
nutritional calories or in excessive hypermetabolic states (i.e. burns) but this
overproduction of CO2 will not cause ARF by themselves.
It is important to realize that CO2 is a highly soluble gas and diffuses readily across the
alveolar-capillary membrane, so diffusion problems (pulmonary edema, pulmonary
fibrosis, etc) are NOT likely to be the primary etiologies of hypercapnic respiratory
failure. Things that will not allow the pulmonary blood to deliver CO2 to the alveoli or
allow the airways to expel the gas are more likely etiologies (see below)
Decreased Tidal Volume
1. Respiratory muscle fatigue (myasthenia gravis, SMA, poor nutrition, etc)
2. Excess sedation (opioids, etc.)
3. Lung hyperinflation
4. Pneumothorax
Decreased Respiratory Rate
1. Sedation
2. Fatigue
3. CNS dysfunction
Increased Dead Space
1. Airway abnormalities
a. Infectious etiologies: bronchiolitis, pneumonia
b. Asthma
c. Airway obstruction: intrinsic or extrinsic; primary (malacia) or
foreign body
2. Cardiac abnormalities
a. Hypovolemia
b. Pulmonary embolism
c. Severe cardiac dysfunction or excessive mean airway pressures
Another equation that is important when discussing hypercapnic respiratory failure is the
equation for compliance. Compliance describes how easily the lung expands:
C = V / P For any volume given, if the amount of pressure needed to achieve this
volume rises, then the lungs can be said to be less compliant or stiffer and
the ability to clear CO2 will be hindered. This is an important concept in
mechanical ventilation.
Combination:
It is important to realize that, although one should consider the separate
aspects of respiratory failure, these alterations in physiology and gas
exchange rarely appear by themselves. For example, bronchiolitis can
present with hypercarbia from increased dead space and decreased tidal
volumes because of impaired chest wall compliance as well as hypoxia
from V/Q mismatches and atelectasis
Recognition of ARF
1. Clinical presentation: includes work of breathing, respiratory rate, mental status,
cyanosis, etc
2. Laboratory Data:
a. CBC: elevated Hgb may suggest chronic hypoxemia
b. Bicarbonate: if elevated, may suggest chronic hypercarbia
c. Arterial blood gas: suggests the type of respiratory failure and the degree of
embarrassment
d. Chest xray: may help in determining the cause of ARF
CLINICAL APPEARANCE AND PHYSICAL EXAMINATION ARE THE MOST
IMPORTANT FACTORS IN DETERMINING THERAPIES
Oxygen Supplementation
In order for oxygen to travel from the alveolus to the pulmonary capillaries, it must move
down a pressure gradient. Therefore, if a patient is hypoxemic, supplemental oxygen,
which can increase this gradient, may be necessary as a temporizing intervention, until
the etiology of the abnormality can be treated. There are various ways and devices used
to deliver oxygen which will be addressed in this section. Oxygen-delivering devices can
be divided into high flow systems (O2 delivery is > patient’s minute ventilation) and low
flow systems (O2 delivery is < patient’s minute ventilation)
Nasal cannula: 100% FIO2 is delivered at flows of 0.25 – 5 L/min (this is a low flow
system); the actual FIO2 seen in the patient’s lungs is hard to estimate because it depends
on the patient’s minute ventilation and how much room air is entrained. Some people
have estimated that the maximal amount of oxygen that can be administered via this
technique is ~ 40%. Although this is a comfortable way of delivering oxygen, the flow
causes drying and irritation of the nasal mucosa.
Venturi and Aerosol Face Masks: These are high flow systems that can provide up to ~
50% FIO2 depending on the patient’s inspiratory flow demands and the amount of room
air that is let into the system. The amount of oxygen is more reliable than in the nasal
cannula and can be titrated more easily and the gas can be humidified thereby preventing
drying of the airways. Nebulized solutions can also be delivered via face masks.
Reservoir Face Masks: These are also high flow systems. The patient breathes gas from
a reservoir bag that is filled with 100% FIO2. The flow rate of oxygen is adjusted so that
this bag will be completely or partially distended during the breathing cycle. The FIO2 in
this system can reach up to 60 – 70%.
Resuscitation Bag-Mask-Valve Units: These bags are high flow units that are to be used
in the resuscitation phase of ARF. If properly used, the patient can get close to 100%
FIO2 with this system
Noninvasive Positive Pressure Ventilation (NPPV)
In this high flow system, either nasal prongs or a tightly applied mask is used to deliver a
controlled FIO2 as well as positive pressure. There are two modes that can be used to
deliver the oxygen: continuous positive airway pressure (CPAP) or bilevel positive
airway pressure (tradename = BIPAP). CPAP provides a fixed continuous pressure,
regardless of respiratory phase. BIPAP provides an inspiratory pressure and an
expiratory pressure. In the PICU, a common starting pressure for BIPAP is 10 cm H2O
for inspiration and 5 cm H2O for exhalation.
This mode of respiratory support is best applied in an awake, cooperative patient who is
expected to improve in 48-72 hours. Infants that are very tachypneic and toddlers who
refuse the mask may not be suitable candidates. There are also questions about the ability
to deliver nebulized solutions (i.e. albuterol) via this system. That being said, NPPV has
been shown to decrease the need for mechanical ventilation in various illnesses.
The face masks may be nasal or cover the nose and mouth. The nasal masks are more
comfortable but require the patient to breathe more from the nose than mouth, or an air
leak will develop, diminishing the machine’s effectiveness.
Mechanical Ventilation
ALWAYS REMEMBER: BAG-MASK-VENTILATION CAN BE AN EFFECTIVE
METHOD TO OXYGENATE PATIENTS; IF CONDITIONS ARE NOT IDEAL
FOR INTUBATION, BMV SHOULD BE EMPLOYED UNTIL SUCH
CONDITIONS ARE MET
Indications for tracheal intubation:
1. airway protection
2. provide better gas exchange in respiratory failure
3. shock
4. reducing metabolic demand by decreasing a patient’s work of breathing
5. facilitation of suctioning/pulmonary toilet
6. mild hyperventilation for intracranial hypertension
Modes of Mechanical Ventilation (lectures by the attendings will provide more detailed
explanations)
The main modes of ventilation used in the PICU are:
1. SIMV Pressure Control with Pressure Support: in this mode, the
ventilator will give breaths in synchrony with the patient’s spontaneous
breaths; the size of the breath is determined by the pressure that is dialed into
the ventilator; the volume the patient receives depends on the lungs’
compliance (see above equation for compliance); the patient’s spontaneous,
self-generated breaths are supplemented by the pressure support
a. Set Values: Pressure Control, Pressure Support, PEEP, FIO2, Rate,
Inspiratory Time
b. Measured Values: Tidal Volume
c. Typical Settings: PC=20, PS=10, PEEP=5; Rate and IT depend on
patient’s age
d. Typical situations for PCPS use: poorly compliant lungs, airleak around
ETT, etc
2. SIMV Volume Control with Pressure Support: in this mode, the ventilator
will give breaths in synchrony with the patient’s spontaneous breaths; the size
of the breath is determined by the tidal volume that is dialed into the
ventilator; the pressure needed to deliver this volume depends on the lungs’
compliance; the patient’s spontaneous self-generated breaths are
supplemented by the pressure support
a. Set Values: Tidal Volume, Pressure Support, PEEP, FIO2, Rate,
Inspiratory Time
b. Measured Values: Peak Inspiratory Pressure
c. Typical Settings: TV< 10cc/kg, PS=10, PEEP=5, Rate and IT depend on
patient’s age
d. Typical Situations for VCPS use: head injury, airway issues, obstructive
lung disease, etc.
3. Pressure Support Ventilation: in this mode, the ventilator provides a preset
level of inspiratory pressure with each breath to help overcome the work of
breathing imposed by the endotracheal tube, the tubing of valves of the
ventilator, and the disease process; the set amount of pressure support that is
applied is delivered with each patient-generated breath; the volume of each
breath is determined by the lung compliance
4. Other
Other modes like High Frequency Oscillatory Ventilation (HFOV) and
Airway Pressure Release Ventilation (APRV) will be discussed during the
rotation
Gas Exchange During Mechanical Ventilation
Oxygenation: Primarily determined by the Mean Airway Pressure and FIO2
1. MAP – affected by PEEP, PIP, IT; PEEP primarily used for hypoxia
2. FIO2 -- >60% FIO2 has been shown to toxic to the lung
Ventilation: Primarily determined by the alveolar minute ventilation (see above)
1. Rate – based on the age and disease process; care should be taken with
obstructive lung diseases when exhalation, a passive process, may take longer
than expected
2. Tidal Volume – depends on the compliance of the lung; goal should be 610cc/kg depending on the patient’s disease process
3. Dead Space – may be manipulated with PEEP, bronchodilators, etc.