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Early Detection and

Interventions in Respiratory
Dr Nigam Prakash Narain

Definition: Respiratory Failure

Defined as inadequate gas exchange

due to pulmonary or non-pulmonary
causes leading to hypoxemia,
hypercarbia or both.
Documented by PaCO2 > 50 mm of Hg
or PaO2 < 50-60 mm of Hg.

Status of ABG
Arterial Blood Gas analysis: single
most important lab test for evaluation
of respiratory failure.

Respiratory Failure: Causes

1. Upper airways obstruction:
> Laryngomalacia
> Subglottic stenosis
> Laryngotracheobronchitis
> Tracheitis & Epiglottitis
> Retropharyngeal / Peritonsillar abscess
> Acute hypertrophic tonsillitis
> Diphtheria
> foreign body, trauma, vocal cord palsy

2. Lower airway obstruction:

> Bronchiolitis, Asthma, Foreign body
3. Alveolar and pleural disease:
> pneumonia, pulmonary edema, effusion
empyma, pneumothorax, ARDS
4. CNS causes:
> Infections, injury, trauma, seizures
> tetanus, SMA, Polio
> AIDP, Phrenic nerve injury
> Myasthenia gravis, botulism,
> Muscle dystrophies, Polymyositis
> Congenital myopathies, muscle fatigue

Respiratory failure:
clinical manifestations
Exaggerated use of accessory muscles
Intercostal, supraclavicular and subcostal
In neuromuscular disease, the signs of
respiratory distress may not be obvious
In CNS disease, an abnormally low
respiratory rate, and shallow breathing are
clues to impending respiratory failure

Three distinctive clinical profiles have
been suggested in children:
1. Mechanical dysfunction of airways
2. Neuromuscular dysfunction
3. Breathing control dysfunction
A rapid assignment to one of these profiles
facilitates early diagnosis and treatment

Profile 1: Mechanical dysfunction of

Most common type
Results from alterations in the mechanical
properties of the airways, lung parenchyma
or chest wall.
Present with typical signs of respiratory
increased effort, Tachypnea, retractions,
accessory muscle use, nasal flaring,
adventitious breath sounds, grunting

Profile 2: neuromuscular disease

Results from myopathies involving resp
muscles or polyneuropathies / phrenic nerve
Associated with an increased neural output,
but is not effectively translated into effective
Tachypnea, shallow respiratory efforts and
profound dyspnea are characteristic

Profile 3: Alteration in control of

Usually results from CNS injury /
developmental deficits
Ondines curse, Apnea of prematurity,
CNS injury / depression
Associated with decreased neural output
to resp muscles, thus signs of respiratory
distress are unusual, even with significant
respiratory compromise

Evaluation of Respiratory failure

The following parameters are important in
evaluation of respiratory failure:
1. PaO2
2. PaCO2
3. Alveolar-Arterial PO2 Gradient
P(A-a)O2 Gradient = PIO2 PaCO2 / R
where PiO2 = partial pressure of inspired air,
R = 0.8
4. Hyperoxia Test

PaO2 / PaCO2
Normal value depends on :
a. Position of patient during sampling
b. Age of patient
PaO2 (Upright) = 104.2 -- 0.27 x age (Yrs)
PaO2 (Supine) = 103.5 0.47 x age (Yrs)
PaCO2 : normal value= 35-45 mm of Hg
unaffected by age/ positioning

Alveolar-Arterial O2 gradient
Normal P(A-a)O2 gradient: 5-10 mm of Hg
A sensitive indicator of disturbance of gas
Useful in differentiating extrapulmonary
and pulmonary causes of resp. failure.
For any age, an A-a gradient > 20 mm of
Hg is always abnormal.

Causes of Hypoxemia
1. Low PiO2 ~ at high altitude
2. Hypoventilation ~ Normal A-a gradient
3. Low V/Q mismatch ~ A-a gradient
4. R/L shunt ~ A-a gradient

PaCO2 is always increased
A-a gradient is normal ( 10 mm of Hg)
Hyperoxia Test : dramatic rise in PO2

V/Q mismatch- Diagnosis

A-a gradient is
PaCO2 may or may not be elevated
Hyperoxia test : Dramatic rise in PaO 2

R-L shunt: diagnosis

PaO2 is
PaCO2 is usually normal
A-a gradient is
Hyperoxia Test : Poor / No response

Hypercapnia :
Severe low V/Q mismatch: major
mechanism of hypercapnia in intrinsic lung

Status of ABG
It is not possible to predict PaO 2 and
PaCO2 accurately using clinical criteria.
Thus, the diagnosis of Respiratory failure
depends on results of ABG studies.

Respiratory failure:
Supportive therapy
Specific therapy

Supportive therapy

Secure the airway

Pulse oximetry
Oxygen: by mask, nasal cannula, head box
Proper positioning
Nebulization if indicated
Blood sampling: Routine, electrolytes, ABG
Secure IV line
CXR: upright AP & lateral views

Hypoxemic / Non - Hypercapnic

respiratory failure
The major problem is PaO2.
If due to low V/Q mismatch; oxygen
If due to pulmonary intra-parenchymal
shunts (ARDS), assisted ventilation with
PEEP may be needed.
If due to intracardiac R-L shunt: O 2 therapy
is of limited benefit. Surgical t/t is needed.

Hypercapnic Respiratory failure

Key decision is whether mechanical
ventilation is required or not.
In Acute respiratory acidosis: Mechanical
ventilation must be strongly considered.
Chronic Resp acidosis: patient should be
followed closely, mech ventilation is rarely
In acute-on-chronic respiratory failure, the
trend of acidosis over time is a crucial factor.

Mechanical Ventilation: Indications

1. PaO2< 55 mm Hg or PaCO2 > 60 mm Hg
despite 100% oxygen therapy.
2. Deteriorating respiratory status despite
oxygen and Nebulization therapy
3. Anxious, sweaty lethargic child with
deteriorating mental status.
4. Respiratory fatigue: for relief of metabolic
stress of the work of breathing

Mechanical Ventilation: Strategies

Non-Invasive Ventilation: CPAP / BIPAP
Invasive Ventilation: SIMV, A/C, PAV
Other approaches to mechanical
a. High frequency ventilation (HFV)
b. Permissive Hypercapnia
c. Prone positioning

3 types: Oscillatory, Jet & Flow interruption
Very small tidal volumes are used
(<1ml/kg), very rapid rates (150-1000
bpm) and lower mean airway pressures
are used.
This approach is used to minimize the
possibility of barotrauma to airways.
Used if conventional ventilation fails to
improve gas exchange

Permissive Hypercapnia
Allows the PaCO2 to rise into the 60-70
mm of Hg range, as long as the patient is
adequately oxygenated (SaO2> 92%), and
able to tolerate the acidosis.
This strategy is used to limit the amount of
barotrauma and volutrauma to the patient.

Prone positioning
Positioning the patient in the prone
position has been shown to improve
oxygenation and reduce ventilator induced
lung injury.
However, the outcome may not be

Used in the treatment of newborns and
small infants with life threatening,
refractory respiratory failure, unresponsive
to mechanical ventilation.
Inhales nitric oxide may improve
oxygenation by reducing increased
pulmonary vascular resistance.
Inhaled NO is now being used in place of
ECMO in NICU in some centers.