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)
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):
Altered depth & pattern of respiration
Decreased air movement
The most sensitive clinical indicator of increasing resp. difficulty is a rising resp. rate.
Decrease resp. rate
Shallowness of the breathing
No S & S of distress
The severity is judged by the accompanying acedemia.
Concept of shunting& dead space.
Work of breathing.
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.:
C.Perfusion in excess of ventilation:hypoventilation,uneven distribution of ventilation,diffusion defects.
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
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.
Mild hypoxemia < 80 mmHg
Moderate < 60 mmHg
Sever < 40 mmHg
Uncorrected below room air minimal
Correcred below 100 mmHg
Excessively >100 mmHg;below predicted
Blood O2 transport mechanism:
-Bd O2 content
-Hb O2 affinity
1)Mixed with room air
4)Delay in running
Supplemental O2 by mask
If failed go ahead & intubate
-Degree of hypoxemia
*correction of the underlying cause.
*respiratory failure recover
Why O2 therapy:
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.
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.
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 .
*Acute neurological compromise.
*Sever distress despite maximal therapy.
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.
Salt & water retention.
Mask C-PAP vent.
Bag mask vent.
Either ET tube or treacheostomy canula.
The airway opening pressure > alveolar pressure,
so inflation occur in inspiration & the reverse (i.e.airway opening pressure < alveolar pressure)occur in expiration.
Either sets the I or the I:E ratio .
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 ¬ 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 .
-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.
What is not controllable is monitored .
-Pop-off limits to the peak airway pressure .
-O2 analyzer for FiO2.
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 ).
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 .
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 .
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 ).
h.Nosocomial infection (leading cause of deathin resp. failure patients ).
-High chest wall compliance.
-Electrolyte disturbances .
Acid-base balance disturbance.
Alteration in oxygenation.
2.incorrect sampling (WBC&air O2)
(1000 i .u ./mL 0.1ml for 2 mL)
-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 .