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Respiratory Failure in Children. Maa’n Idrees,MD. Definition:. Respiratory failure exists when the patient has hypoxia while breathing 50% oxygen with or without hypercapnia. Hypoxic R.F(type 1): PaO2<60mmHg with FiO2>0.6(cyanotic heart disease excluded)

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Respiratory Failure in Children

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Respiratory failure in children l.jpg

Respiratory Failure in Children

Maa’n Idrees,MD

Definition l.jpg


Respiratory failure exists when the patient has hypoxia while breathing 50% oxygen with or without hypercapnia.

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Hypoxic R.F(type 1):

PaO2<60mmHg with FiO2>0.6(cyanotic heart disease excluded)

Hypercapnic or ventilatory failure R.F(type 2):


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Clinical features:

Pulmonary features:


Chest retractions

Nasal flaring




Altered depth & pattern of respiration

Decreased air movement

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Cardiac features:





Cardiac arrest

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Neurologic features:






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The most sensitive clinical indicator of increasing resp. difficulty is a rising resp. rate.

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Impending respiratory failure due to lung disease:



Nasal flaring


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Impending respiratory failure due to resp. pump failure:

Decrease resp. rate

Shallowness of the breathing

No S & S of distress

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The severity is judged by the accompanying acedemia.

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Clinical respiratory physiology:

Perfusion distribution.

Alveolar physiology:LaPlaceLaw,surfactant.

Ventilation distribution.

Concept of shunting& dead space.


Work of breathing.

Ventilatory reserve.

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Physiological classification of pulmonary diseases:

1)Dead space producing dis.:

A.Anatomic:rapid shallow breathing&+ve pressure breathing.

B.Alveolar:acute pulmonary embolus & uneven distribution.

C.Ventilation in excess of perfusion:alveolar septal defects,mechanical hyperventilation.

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2)Shunt producing dis.:

A.Anatomic:CHD,fistula,vascular tumor.


C.Perfusion in excess of ventilation:hypoventilation,uneven distribution of ventilation,diffusion defects.

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A. Assessment of ventilatory status :

i.PaCO2 < 30mmHg - vent. Insufficiency:

Acute : pH > 7.5

Chronic :pH 7.4 –7.5

Completely compensated metabolic acidosis

:pH 7.3 –7.4

Partially compensated met.acidosis

:pH< 7.3

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ii.PaCO2 30 –50 mmHg - normal :

Metabolic alkalosis : pH >7.5

Normal : pH 7.3 –7.5

Metabolic acidosis : pH <7.3

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iii.PaCO2 >50 mmHg - ventilatory failure :

Partly compensated metabolic alkalosis

: pH >7.5

Chronic ventilatory failure

: pH 7.3 –7.5

Acute ventilatory failure

: pH <7.3

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Ventilatory insufficiency: is the presence of alveolar hyperventilation.Hyperventilation leads to alkalemia (high pH) ; this in acute ventilatory insufficiency.

Chronic ventilatory insufficiency: is hyperventilation with normal pH. Acute respiratory failure: is high arterial CO2 with acidemia.Respiratory failure occur due to inability to increase alveolar ventilation

Chronic respiratory failure:When there is metabolic compensation.

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B.Assessment of hypoxemic status:

Mild hypoxemia < 80 mmHg

Moderate < 60 mmHg

Sever < 40 mmHg

O2 therapy

Uncorrected below room air minimal

Correcred below 100 mmHg

Excessively >100 mmHg;below predicted

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C.Assessment of tissue oxygenation

Cardiac output.

Peripheral circulation.

Blood O2 transport mechanism:


-Bd O2 content

-Hb O2 affinity

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ABGs mistakes:

1)Mixed with room air



4)Delay in running

5)Heparin addition

6)Plastic syringe

7)Machine error

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Supplemental O2 by mask

Aerosolized treatment

If failed go ahead & intubate

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Therapy Depends on:

-Degree of hypoxemia


-underlying pathophysiology

Treatment toward:

*correction of the underlying cause.

*respiratory failure recover

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Oxygen therapy:

Why O2 therapy:

Rx hypoxia.

Decrease work of breathing.

Decrease myocardial work.

*Dangerous hypoxia should never be tolerated through a fear of O2 toxicity.

*Should be at the ,lowest conc. That provide an adequate PaO2.

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Methods of oxygen administration:

1)High flow oxygen systems:

Exact O2 conc. Delivered.

Given atmosphere is completely controlled.

Inspired O2 conc. does not vary.

2)Low flow oxygen systems:

Depends upon existence of reservoir of O2 & its dilution with room air.

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O2 toxicity:

Retrolental fibroplasia



Hyaline mem. formation in the lungs.

Fibrosis & interstitial edema ( in lungs ).


Alveolar cell Hyperplasia.

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! ! !

In sever distress Rx before Dx .

But majoritycan tolerate performing ABGs & pulse oximetry .

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Mechanical ventilation for:

*Respiratory arrest.

*Repeated apnea.

*Sever shock.

*Acute neurological compromise.

*Therapeutic hyperventilation.

*Sever distress despite maximal therapy.

*High PaCO2.

*Prophylactic postop.


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Institution of invasive respiratory support:




Death,surgical complications,misplacement.


Cartilaginous erosion,fatal hemorrhage,stomal infection,pn.


Heal failure,ring stenosis or collapse,cosmetic.

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Tube in or other bronchus,in esophagus.




Laryngeal injury,mucosal ulceration,tracheomalacia,

Tracheal narrowing & fibrosis.

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Mechanical ventilation dangers:

Airway complications.

CVS complications.

Respiratory complications.


GIT complications.

Salt & water retention.

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Positive pressure ventilators:

Mask C-PAP vent.

Bag mask vent.

Mask BiPAP

Either ET tube or treacheostomy canula.

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O2 applied to the Bd gas exchange membrane due to:

The airway opening pressure > alveolar pressure,

so inflation occur in inspiration & the reverse (i.e.airway opening pressure < alveolar pressure)occur in expiration.

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Component of ventilator breath:

  • Inspiratory time ( I ).

  • Expiratory time ( E ).

  • Vent. Frequency.

  • Vt ( tidal volume ).

    Either sets the I or the I:E ratio .

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Pressure controlled vs. volume controlled vent. :

i.Pressure controlled vent. :

Delivered pressure built up to achieve PIP ,since then it maintained during the whole I.

-Sets PIP & PEEP.

-Vt determined by dynamics &not sated.

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ii.Volume controlled vent. :

Vt is sated & pressure reached its max. at Vt.

perfused alveoli ventilated & intrapulmonary shunting is prevented.

So PIP is determined by Vt & pulmonary mechanics ; & not sated .

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S I M V :

-Either volume or pressure controlled.

-the determination of how long is too long is a function of vent. Frequency.

-Patient can inspire more often than the setting.

-Patient can’t control I time in assissted breaths.

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Safety :


What is not controllable is monitored .

-Pop-off limits to the peak airway pressure .

-O2 analyzer for FiO2.

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Lung diseases :

i)Decrease compliance : ARDS , Atelectasis, pneumonia , edema , intrapulmonary hemorrhage.

a-pressure controlled vent. :

increase MAP by increase PIP or PEEP.

Vt is low for a given PIP in normal lungs.

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b-volume controlled vent.:

PIP is higher than in normal lung.

ii)Increase airway resistance: Asthma , bronchiolitis , bronchopulmonary dysplasia, C.F.

Either lead to increase intrapulmonary shunting or increase dead space vent .

Dead space vent. Is due to traping phenomena.

Time constant is prolonged .

So prolongation of I : E ratio & decreasing the frequencu is ( or trapping will develop ).

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Initial settings :

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Initial settings :

i.Supporting normal lungs :

The vent.frequency is lower than normal frequency,but the Vt is larger than normal .

- (normal Vt :5 –7 mL/kg)

-So Vt setting at 10 –15 mL/kg to prevent atelectasis.

- Setting at 8 –10 mL is more suitable for prolonged vent.or diseased lung .

*This is for volume controlled vent.

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In pressure controlled :

Initial PIP :20 –25 cm H2O .

ii.Supporting diseases of decreased lung compliance:

Pressure controlled :

MAP need to be increased . Also PEEP needed to be titrated upward to achieve adequate oxygenation at FiO2 less than 0.6.

Initial PIP more than 30 cm H2O .

Pay attention to Vt.

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*In volume controlled pay attention to pressure alarms.

start with 100% O2 & then decrease to avoid O2 toxicity.

note : vent. Frequency can be set at higher rates than normal because T costant is decreased .

I time : 0.8 –1 sec.

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iii.Diseases of increase airway resistance:

Due to high T constant low vent. Frequency is needed(12 – 16 /min ).

Decrease PEEP To minimize trapping phenomena .

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b.O2 toxicity.

c.Volutrauma: manifested as pul.air leak (pneumothorax , pneumomediastinium , interstitial emphysema &bronchopleural fistula ).

mechanism of volutrauma :

- Over distension leads to increase Vt .

-If PEEP sated at low levels there will be cyclic collapse and re-expansion.

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-Volutrauma affects the healthier alveoli in diseases of decreased compliance .

  • In increase airway resistance diseases:

    over filling of healthy alveoli & over distension of (trapping ) in diseased alveoli .

    d.Decrease cardiac input .

    e.Decrease left ventricular SV & after load of Rt or Lt ventricle.

    (so patient may need fluid & inotrops .

    f.ET obstruction ( life threatening ).

    g.Subglottic stenosis.

    h.Nosocomial infection (leading cause of deathin resp. failure patients ).

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Newborn vulnerability to resp. failure :

-Immaturity .

-High chest wall compliance.


-Hypo perfusion.

-Electrolyte disturbances .

-Hypophosphatemia .

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Nitric oxide

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Etiology l.jpg


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Monitoring of respiratory failure:

  • Clinically.

  • Pulse oximetry.

    Acid-base balance disturbance.

  • Bd gas analysis:

    Alteration in oxygenation.

    1.analyzer malfunctioning

    2.incorrect sampling (WBC&air O2)

    3.inadequate anticoagulation

    (1000 i .u ./mL 0.1ml for 2 mL)

  • Capnography.

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Misleadings :

-PaO2 if inspire high FiO2 .

-PaO2 decrease due to intracardiac shunt without accompanying decrease in lung function .

-PaO2 increase in compensation for chronic metabolic alkalosis .

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