Respiratory Failure in Children

1. Respiratory Failure in Children Maa’n Idrees,MD

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

3. Hypoxic R.F(type 1): PaO2<60mmHg with FiO2>0.6(cyanotic heart disease excluded) Hypercapnic or ventilatory failure R.F(type 2): PaCO2>50mmHg

4. Clinical features: Pulmonary features: Tachypnea Chest retractions Nasal flaring Cyanosis Diaphoresis Grunting Altered depth & pattern of respiration Decreased air movement

5. Cardiac features: Tachycardia Hypertension Bradycardia Hypotension Cardiac arrest

6. Neurologic features: Headache Restlessness Irritability Seizures Coma

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

8. Impending respiratory failure due to lung disease: Tachypnea Retractions Nasal flaring Grunting

9. Impending respiratory failure due to resp. pump failure: Decrease resp. rate Shallowness of the breathing No S & S of distress

10. The severity is judged by the accompanying acedemia.

11. Clinical respiratory physiology: Perfusion distribution. Alveolar physiology:LaPlaceLaw,surfactant. Ventilation distribution. Concept of shunting& dead space. Hypoxemia&hypoxia. Work of breathing. Ventilatory reserve.

13. 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.

14. 2)Shunt producing dis.: A.Anatomic:CHD,fistula,vascular tumor. B.Capillary:atelectasis,fluid. C.Perfusion in excess of ventilation:hypoventilation,uneven distribution of ventilation,diffusion defects.

15. 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

16. ii.PaCO2 30 –50 mmHg - normal : Metabolic alkalosis : pH >7.5 Normal : pH 7.3 –7.5 Metabolic acidosis : pH <7.3

17. 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

18. 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.

19. 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

20. C.Assessment of tissue oxygenation Cardiac output. Peripheral circulation. Blood O2 transport mechanism: -PaO2 -Bd O2 content -Hb O2 affinity

21. ABGs mistakes: 1)Mixed with room air 2)CBGs 3)VBGs 4)Delay in running 5)Heparin addition 6)Plastic syringe 7)Machine error

22. Rx: Position Supplemental O2 by mask Aerosolized treatment If failed go ahead & intubate

23. Therapy Depends on: -Degree of hypoxemia -pH -underlying pathophysiology Treatment toward: *correction of the underlying cause. *respiratory failure recover

24. 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.

25. 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.

26. O2 toxicity: Retrolental fibroplasia R.O.P. Convulsion Hyaline mem. formation in the lungs. Fibrosis & interstitial edema ( in lungs ). Atelectasis Alveolar cell Hyperplasia.

27. ! ! ! In sever distress Rx before Dx . But majoritycan tolerate performing ABGs & pulse oximetry .

28. Mechanical ventilation for: *Respiratory arrest. *Repeated apnea. *Sever shock. *Acute neurological compromise. *Therapeutic hyperventilation. *Sever distress despite maximal therapy. *High PaCO2. *Prophylactic postop. *Trauma.

29. Institution of invasive respiratory support: ??Tracheostomy. Complications: Early: Death,surgical complications,misplacement. Intermediate: Cartilaginous erosion,fatal hemorrhage,stomal infection,pn. Late: Heal failure,ring stenosis or collapse,cosmetic.

30. ETT: Complications: Immediate: Tube in or other bronchus,in esophagus. Early: Migration,leak,obstruction. Late: Laryngeal injury,mucosal ulceration,tracheomalacia, Tracheal narrowing & fibrosis.

31. Mechanical ventilation dangers: Airway complications. CVS complications. Respiratory complications. Infections. GIT complications. Salt & water retention.

32. Positive pressure ventilators: Mask C-PAP vent. Bag mask vent. Mask BiPAP Either ET tube or treacheostomy canula.

33. 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.

34. Component of ventilator breath: • Inspiratory time ( I ). • Expiratory time ( E ). • Vent. Frequency. • Vt ( tidal volume ). Either sets the I or the I:E ratio .

35. 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.

36. 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 .

37. 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.

38. Safety : Rule: What is not controllable is monitored . -Pop-off limits to the peak airway pressure . -O2 analyzer for FiO2.

39. 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.

40. 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 ).

41. Initial settings :

42. 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.

43. 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.

44. *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.

45. 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 .

46. Complications: a.Barotraumas. 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.

47. -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 ).

48. Newborn vulnerability to resp. failure : -Immaturity . -High chest wall compliance. -Malnutrition. -Hypo perfusion. -Electrolyte disturbances . -Hypophosphatemia .

49. Nitric oxide

50. ECMO