Diagnosis and Management of Respiratory Failure



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,  tracheo- or bronchomalacia), foreign body


Restrictive Lung Disease

1.       Pulmonary Fibrosis

Parenchymal Lung Disease

1.    Acute Respiratory Distress Syndrome

2.    Pneumonia:  infectious, aspiration

2.       Pulmonary Hypertension (primary or secondary)

3.       Congestive Heart Failure


1.        CNS impairment, drug ingestion

2.        Disorders with Respiratory Muscle Weakness:  SMA, Guillaume-Barre, etc





Pathophysiology of ARF



Hypoxic respiratory failure can result from various abnormalities in oxygen delivery:


1.      Decreased environmental O2 tension as is seen with altitudes

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.  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. 



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 = DV / DP   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.



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





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





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



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 6-10cc/kg depending on the patient’s disease process

            3.  Dead Space – may be manipulated with PEEP, bronchodilators, etc.