you learn how to approach acute respiratory failure

1. ACUTE RESPIRATORY FAILURE
Presenter: Dr. Abinet(MD, pediatric
resident)

2. Outline
• Objective
• Introduction
• Definition
• Epidemiology
• Etiology
• Pathophysiology
• Monitoring
• Management
• prognosis
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3. Objectives
• At the end of this presentation we should able to:
– Recognize clinical parameters of respiratory failure
– Describe respiratory developmental difference
between children and adults
– List clinical causes of respiratory failur
– Review the pathophysiologic mechanisms of
respiratory failure
– Evaluate and diagnose respiratory failure
– Discuss clinical intervention
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4. INTRODUCTION
• The main function of the respiratory system is
to:
– Supply sufficient O2 to meet metabolic demands
and
– Remove CO2
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5. Definition
• Respiratory failure is defined as inability of the
lungs to provide sufficient oxygen or remove
carbon dioxide to meet metabolic demands.
– Type I Hypoxic respiratory failure
– Type II Ventilatory failure
• Traditionally defined as Pao2 <60 torr with
breathing of room air and Paco2>50 torr
• The patient’s general state are more important
indicators than blood gas values.
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6. • Respiratory distress is a clinical impression,
• Respiratory distress can occur in patients
without respiratory disease,
• Respiratory failure can occur in patients
without respiratory distress
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7. Epidymology
• Acute Respiratory failure is a common problem in
infants and young children
• 50% seen in neonatal period
• 17% of children admitted to the PICU required
mechanical ventilator support for a minimum of
24 hours.
• Type 1 account 16%
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8. Developmental difference between
children and adults
• Soft thoracic cage
• Poorly developed intercostal muscles
• lack of “bucket-handle” motion in the rib cage
• Shorter diaphragm and decreased numbers of
type I muscle fibers
• Smaller airway
• Fewer air-exchanging units
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9. Cause
• Any component of respiratory system
– Airways
– alveoli
– chest wall and muscles of respiration
– Central and peripheral chemoreceptors
• Hypoperfusion secondary to:
– Hypovolemia
– Cardiogenic shock
– Septic shock
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10. SITE OF PATHOLOGY SYMPTOM
Lung and Airways Nasal flaring, retractions, tachypnea,
wheezing stridor, grunting
Chest wall and muscles
of respiration
Nasal flaring, tachypnea,
paradoxical respirations
Respiratory control Shallow or slow respirations,
abnormal respiratory patterns,
apnea
Clinical manifestations depend largely on the site of
pathology
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11. • Lung
– Central Airway Obstruction
– Peripheral Airway Obstruction
– Alveolar-interstitial Disease
• Respiratory Pump
– Thoracic Cage
– Brainstem
– Spinal Cord
– Neuromuscular
Anatomic Sites of Lesions Causing
Respiratory Failure
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12. • Cardiovascular
– Left-to-right shunt
– Congestive heart failure
– Cardiogenic shock
• Central nervous system
– Increased intracranial pressure
– Encephalitis
– Neurogenic pulmonary edema
– Toxic encephalopathy
Non pulmonary Causes of Respiratory
Distress
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13. • Metabolic
– Diabetic ketoacidosis
– Organic acidemia
– Hyperammonemia
• Renal
– Renal tubular acidosis
– Hypertension
• Sepsis
– Toxic shock syndrome
– Meningococcemia
Cont…
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14. • Ventilatory capacity(VC): The maximal
spontaneous ventilation that can be maintained
without development of respiratory muscle
fatigue
• Ventilatory demand(VD): the spontaneous
minute ventilation that results in an stable PaCO2
– VC >> VD
• Respiratory failure arise from decrease in VC or
increase in VD(or both)
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Pathophysiology of Respiratory Failure

15. Type I (hypoxemic respiratory failure)
• Termed nonventilatory,or normocapnic,
respiratory failure,
• Characterized by abnormally low PaO2 with
normal to low PaCO2
• Results from
– Ventilation–Perfusion Mismatch
– Intrapulmonary shunt
– Venous admixture
– Insufficient diffusion of oxygen
– Dead space ventilation
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16. Cont…
• Intrapulmonary shunt: When an unventilated area of
the lung is perfused
• Shunt fraction(venous admixture): total amount of
pulmonary blood flow that perfuses nonventilated or
underventilated areas of the lung
• Can be calculated as:
Qs/Qt = (Cc′O2−CaO2)/(Cc′O2−CvO2)
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17. • Pathologic admixture can be caused by
– atelectasis
– Pulmonary edema
– pneumonia
– congenital heart disease
• In the normal lung, shunt fraction is less than 5%
• Shunt fraction of greater than 15% results in
significant impairment of oxygenation.
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Cont…

18. • Dead space ventilation: areas of the lung that are
ventilated but not perfused
• The fraction of tidal volume that occupies dead
space (Vd/Vt) is calculated
– Vd/Vt = [(PaCO2 – PECO2) /PaCO2]
– Normal Vd/Vt 0.33
• Increases in states that result in decreased
pulmonary perfusion, such as
– pulmonary hypertension
– hypovolemia
– decreased cardiac output
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Cont…

19. • Diffusion: diffusion capacity of CO2 is 20 times
greater than that of O2
• diffusion defects manifest as hypoxemia
rather than hypercarbia
• Examples
– interstitial pneumonia,
– ARDS,
– scleroderma
– pulmonary lymphangiectasia.
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Cont…

20. Type II Hypercarbic respiratory failure
• Decreased minute alveolar ventilation (TV x
RR).
– This can occur from centrally-mediated disorders
of respiratory drive,
– Increased dead space ventilation,
– Obstructive airway disease.
• The two entities may coexist as a combined
failure of oxygenation and ventilation
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21. Causes of Type I respiratory failure
Acute respiratory distress syndrome
Aspiration
Atelectasis
Bronchiolitis
Cardiogenic pulmonary edema
Cystic fibrosis
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22. Embolism (air, blood, fat)
Interstitial lung disease
pulmonary edema
Sepsis
Severe pneumonia
Toxin/toxic gas inhalation
Transfusion-related acute lung
injury
Trauma (pulmonary contusion)23 May 2020 22ARF

23. –Respiratory center
• Drugs
• Central alveolar hypoventilation
syndrome
–Upper motor neuron
• Cervical spinal cord trauma
• Syringomyelia
• Demyelinating diseases
• Tumors
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Causes of Type II respiratory failure

24. –Anterior horn cell
• Poliomyelitis
–Lower motor neuron
• phrenic nerve damage
• Guillain-Barré syndrome
–Neuromuscular junction
• Botulism, multiple sclerosis, myasthenia
gravis
• Neuromuscular blocking antibiotics
• Organophosphate poisoning
• Tetanus23 May 2020 24ARF

25. –Chest wall and pleura
•Contracted chest burn scars, flail
chest,
•kyphoscoliosis
•Massive pleural effusion, morbid
obesity
•Muscular dystrophy, pneumothorax
–Increased airway resistance
•Laryngeal obstructio
–Lower airway obstruction
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26. MONITORING A CHILD IN RD AND RF
• Clinical Examination
• Impending respiratory failure can present as:
– Dyspnea, Mood changes, Disorientation, Pallor
– Fatigue, flushing, agitation, restlessness,
headache, tachycardia
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27. • General
– Fatigue
– Excessive sweating
• Respiratory
– Tachypnea
– Altered depth and pattern of respiration (deep, shallow,
irregular, apnea)
– Retractions of the chest wall
– Flaring of the alae nasi
– Cyanosis
– Decrease or absence of breath sounds
– Expiratory grunting
– Wheezing or prolonged expiration
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Signs of respiratory failure

28. Cont…
• Cardiac
 Tachycardia
 Hypertension
 Bradycardia
 Hypotension
 Cardiac arrest
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•Cerebral
 Restlessness
 Irritability
 Headache
 Mental confusion
 Papilledema
 Seizures
 Coma

29. Cont…
• Laboratory Findings
– Hypoxemia
– Hypercapnia
– Acidosis
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30. Cont…
• Pulse oximetry
– indirectly measures arterial Hb-O2 saturation by
differentiating oxyhemoglobin from deoxygenated
hemoglobin
– pulsatile circulation is required
– Spo2 90% = Pao2 60mmhg
– Spo2 value greater than 95% is a reasonable goal,
especially in emergency situations
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31. • Limitations:
– recognize all types of hemoglobin as either
oxyhemoglobin or deoxygenated hemoglobin
– dangerous levels of hypercarbia may exist in
patients with ventilatory failure, who have
satisfactory Spo2 if they are receiving supplemental
oxygen
– in patients with poor perfusion and poor pulsatile
flow to the extremities
• Exception in cardiac shunt lesions
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Cont…

32. Cont…
• Capnography(end-tidal CO2 measurement)
– helpful in determining the effectiveness of
ventilation and pulmonary circulation
– useful for monitoring the level of ventilation in
intubated patients
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33. Blood Gas Abnormalities in RD and RF
• CBG provides a good estimate of Paco2 and
arterial pH, but less so for Pao2
• venous blood gas sample provides reliable
estimate of arterial pH and Pco2 (PCO2 6torr
higher, PH 0.03 lower than arterial blood)
• Helpful for determining site of pathology
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34. Parameter newborn Infant and child
Tidal volume (mL/kg) 5–6 7–8
Arterial blood
PH 7.30–7.40 7.30–7.40 (≤2 yr)
7.35–7.45 (>2 yr)
PCO2(mm Hg) 30–35 30–35 (≤2 yr)
35–45 (>2 yr)
Standard HCO3(mEq/L) 20–22 20–22 (≤2 yr)
22–24 (>2 yr)
PO2(mm Hg) 60–90 80–100
Normal Values
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35. Assessment of Oxygenation and
Ventilation Deficits
• A-ao2gradient: PAo2 – PaO2
• PaO2/FIO2 ratio: In hypoxic respiratory failure, a
PaO2/FIO2 value <300 is consistent with acute lung
injury, and a value <200 is consistent with ARDS.
• the intent is to measure
– V/Qmismatch,
– intrapulmonary shunt, and
– diffusion defect
• PAo2/PaO2 indicative of V/Q mismatch and alveolar
capillary integrity.
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36. • Oxygenation index (OI): aimed at standardizing
oxygenation to the level of therapeutic
interventions.
OI = (MAP X FIO2) / PaO2
• Ventilation index (VI) is aimed at standardizing
alveolar ventilation to the level of therapeutic
interventions
VI = [ventilatory rate X (PIP-PEEP)X PaCO2]/1000
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37. • Goals are to anticipate and recognize
respiratory problems and to support those
functions that are compromised or lost.
• AHA rapid cardiopulmonary assessment
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MANAGEMENT OF ACUTE RESPIRATORY
FAILURE

38. 23 May 2020 38ARF
Cont…

39. • Restoration of airway patency
– Clearing of secretions or mechanical obstructions
– Artificial airways: oropharyngeal airway is useful in
an unconscious infant or child
– Nasopharyngeal airways
– Endotracheal tube(ETT)
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Cont…

40. • Institution of ventilation
– assisted ventilation may be necessary if adequate
air entry and breath sounds are not observed
– BVM
– Facemask
– A laryngeal mask airway (LMA
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41. • Nasal prong
– Flow rate < 5L/min
– FIO = 21% X (nasal canula flow(L/min) X 3)
– Provide 23% and 40% FIO
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Methods of oxygen administration
•Nasopharyngeal catheter
•Flow rate 5-10L/min
•Provide 50% FIO

42. • Mask
• Simple mask
– O2 flow rate 5-10L/min
– Provide 30-60% FIO
• Venturi mask
– O2 flow rate 5-10L/min
– Provide 30-50% FIO
• Partial rebreather
– O2 flow rate 15-20L/min
– Provide 30-60% FIO
• Nonrebreather
– Provide 95% FIO
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43. Inhaled Gases
• Helium-oxygen mixture(heliox) is useful in
overcoming airway obstruction and improving
ventilation.
• Helium is much less dense and slightly more
viscous than nitrogen
• associated hypoxemia may limit its use in
patients requiring more than 40% oxygen
• Nitric oxide (NO) is a powerful inhaled
pulmonary vasodilator.
• improve pulmonary blood flow and V/Q
mismatch
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44. Positive-Pressure Respiratory Support
• High-flow nasal cannula: delivers gas flow at
4-16 L/min
• providing significant continuous positive
airway pressure (CPAP) but not quantifiable
• Another benefit of a high-flow nasal cannula
system is the washout of CO2 from the
nasopharynx, which decreases rebreathing of
CO2 and dead space ventilation
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45. Cont…
• CPAP most useful in diseases of mildly
decreased lung compliance and low FRC, such
as atelectasis and pneumonia.
• Bilevel positive airway pressure (BiPAP)
provide positive airway pressure during
exhalation and inahalation
• augment tidal volume and improve alveolar
ventilation in low compliance and
obstructive lung disease
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46. Endotracheal Entubation
• Indicated in the patient with ARF
– who has continued severe hypoxemia despite
supplemental oxygen administration
– who has worsening hypercapnia with acidosis
– who requires airway protection
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47. • Clinical
– Respiratory:
• Apnea,
• decreased breath sounds despite rigorous chest wall
movement,
• weakening ventilatory effort
– Cardiac
• Asystole,
• peripheral collapse,
• severe bradycardia or tachycardia
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Criteria for intubation and mechanical ventilation

48. Cont…
– Cerebral
• Coma,
• lack of response to physical stimuli,
• uncontrolled restlessness
– General
• Limpness,
• loss of ability to cry
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49. Cont…
• Laboratory
– PaCO2
• Newborn: >60–65 mm Hg
• Older infant or child: >55–60 mm Hg
• Rapidly rising (>5 mm Hg/hr)
• PH < 7.25
– PaO2(FIO2=100%)
• Newborn: <40–50 mm Hg
• Older infant or child: <50–60 mm Hg
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50. • More than one episode of apnea with
bradycardia
• An episode of cardiac arrest is adequate
indication for initiating mechanical ventilation,
even in the absence of blood gas data.
• Laboratory values less extreme than those
indicated must be supplemented by clinical
evidence of severity to warrant initiating
mechanical ventilation.
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51. • Support pulmonary gas exchange
– Alveolar ventilation (PaCO2and pH)
– Arterial oxygenation (PaO2and SaO2)
• Increase lung volume
– End-inspiratory lung inflation
– Functional residual capacity
• Reduce work of breathing
– Unload respiratory muscles
Physiologic goals of mechanical ventilation
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52. 23 May 2020 ARF 52

53. Work up for underlying cause
• CBC
• Microbiology
• Chest radiography
• Electrocardiogram
• Echocardiography
• Pulmonary function tests
• Bronchoscopy
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54. • Varies according to the etiology
• For ARDS mortality 40-45% some patients
have some degree of pulmunary function
impairment after 1yrs
• Significant mortality occure in patient with
hypercapneic respiratory failure because such
patient have chronic respiratory disorder and
other comorbidities
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prognosis

55. Reference
• Emily L. Dobyns, MD • Todd C. Carpenter, MD •Anthony G. Durmowicz, MD
• Kurt R. Stenmark, MD. Kendig’s disorder of respiratory tract in children.
7th edn. Page 224-242
• Ashok P. Sarnaik, Jeff A. Clark, and Ajit A. Sarnaik. Nelson text book of
pediatrics, 20th edn. Page 528-544
• Julio Pérez, F ontán. Rudolph’s pediatrics, 22nd edn. Chapter 102
• Brochard L., Mancebo J., Elliott M.W. (2002). Noninvasive ventilation for
acute respiratory failure. European Respiratory Journal, Volume 19,
Number 4, p 712- 721
• Uptodate 21.6
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56. THANK YOU
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