respiratory failure in children l.
Skip this Video
Download Presentation
Respiratory Failure in Children

Loading in 2 Seconds...

play fullscreen
1 / 53

Respiratory Failure in Children - PowerPoint PPT Presentation

  • Uploaded on

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)

I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
Download Presentation

PowerPoint Slideshow about 'Respiratory Failure in Children' - pancho

Download Now An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.

- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

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)

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


clinical features
Clinical features:

Pulmonary features:


Chest retractions

Nasal flaring




Altered depth & pattern of respiration

Decreased air movement

Cardiac features:





Cardiac arrest

Neurologic features:






impending respiratory failure due to lung disease
Impending respiratory failure due to lung disease:



Nasal flaring


impending respiratory failure due to resp pump failure
Impending respiratory failure due to resp. pump failure:

Decrease resp. rate

Shallowness of the breathing

No S & S of distress

clinical respiratory physiology
Clinical respiratory physiology:

Perfusion distribution.

Alveolar physiology:LaPlaceLaw,surfactant.

Ventilation distribution.

Concept of shunting& dead space.


Work of breathing.

Ventilatory reserve.

physiological classification of pulmonary diseases
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.

2)Shunt producing dis.:

A.Anatomic:CHD,fistula,vascular tumor.


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

a assessment of ventilatory status
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

ii.PaCO2 30 –50 mmHg - normal :

Metabolic alkalosis : pH >7.5

Normal : pH 7.3 –7.5

Metabolic acidosis : pH <7.3

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

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.

b assessment of hypoxemic status
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

c assessment of tissue oxygenation
C.Assessment of tissue oxygenation

Cardiac output.

Peripheral circulation.

Blood O2 transport mechanism:


-Bd O2 content

-Hb O2 affinity

abgs mistakes
ABGs mistakes:

1)Mixed with room air



4)Delay in running

5)Heparin addition

6)Plastic syringe

7)Machine error



Supplemental O2 by mask

Aerosolized treatment

If failed go ahead & intubate

therapy depends on
Therapy Depends on:

-Degree of hypoxemia


-underlying pathophysiology

Treatment toward:

*correction of the underlying cause.

*respiratory failure recover

oxygen therapy
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.

methods of oxygen administration
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.

o2 toxicity
O2 toxicity:

Retrolental fibroplasia



Hyaline mem. formation in the lungs.

Fibrosis & interstitial edema ( in lungs ).


Alveolar cell Hyperplasia.

! ! !

In sever distress Rx before Dx .

But majoritycan tolerate performing ABGs & pulse oximetry .

mechanical ventilation for
Mechanical ventilation for:

*Respiratory arrest.

*Repeated apnea.

*Sever shock.

*Acute neurological compromise.

*Therapeutic hyperventilation.

*Sever distress despite maximal therapy.

*High PaCO2.

*Prophylactic postop.


institution of invasive respiratory support
Institution of invasive respiratory support:




Death,surgical complications,misplacement.


Cartilaginous erosion,fatal hemorrhage,stomal infection,pn.


Heal failure,ring stenosis or collapse,cosmetic.




Tube in or other bronchus,in esophagus.




Laryngeal injury,mucosal ulceration,tracheomalacia,

Tracheal narrowing & fibrosis.

mechanical ventilation dangers
Mechanical ventilation dangers:

Airway complications.

CVS complications.

Respiratory complications.


GIT complications.

Salt & water retention.

positive pressure ventilators
Positive pressure ventilators:

Mask C-PAP vent.

Bag mask vent.

Mask BiPAP

Either ET tube or treacheostomy canula.

o2 applied to the bd gas exchange membrane due to
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.

component of ventilator breath
Component of ventilator breath:
  • Inspiratory time ( I ).
  • Expiratory time ( E ).
  • Vent. Frequency.
  • Vt ( tidal volume ).

Either sets the I or the I:E ratio .

pressure controlled vs volume controlled vent
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.

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 .

s i m v
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.

Safety :


What is not controllable is monitored .

-Pop-off limits to the peak airway pressure .

-O2 analyzer for FiO2.

lung diseases
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.

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 ).

initial settings42
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.

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.

*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.

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 .



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.

-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 ).

newborn vulnerability to resp failure
Newborn vulnerability to resp. failure :

-Immaturity .

-High chest wall compliance.


-Hypo perfusion.

-Electrolyte disturbances .

-Hypophosphatemia .

monitoring of respiratory failure
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.
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 .