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Acute respiratory distress syndrome

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ARDS , Respiratory failure , respiratory distress ,

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Acute respiratory distress syndrome

  1. 1. CUTE ESPIRATORY ISTRESS YNDROME Moderator : Dr. Mahesh Presenter : Dr. Vinaykumar S Appannavar A R D S
  2. 2. Learning objectives • Definitions • Calculations – Carrico index – P/F ratio • Signs and symptoms • Aetiology and pathogenesis • Non -pulmonary causes of ARDS • Respiratory failure • Basics • Monitoring • Management • Mechanical ventilation – Concepts, Phases, Modes , Settings
  3. 3. Definitions • It is often used to indicate signs and symptoms of abnormal respiratory pattern • New Berlin Definition of ARDS • Simplified Consensus Definition of ALI
  4. 4. New Berlin Definition criteria 1. Within 1 week of a known clinical insult or new or worsening respiratory symptoms 2. Bilateral opacities not fully explained by effusions lobar/lung collapse or nodules 3. Need objective assessment ( 2D Echo ) to exclude hydrostatic oedema , provided no risk factors 4. Carrico index – PaO2 / FiO2 ratio • </= 300 mmHg with PEEP >/= 5 cm H2O - MILD • </= 200 mmHg with PEEP >/= 5 cm H2O - MODERATE • < 100 mmHg with PEEP >/= 5 cm H2O - SEVERE
  5. 5. Simplified Consensus Definition of ALI • Acute onset – less than 7 days • Severe hypoxemia ( PaO2 / FiO2 < 300 for ALI and < 200 for ARDS ) • Diffuse bilateral pulmonary infiltrates on frontal radiograph consistent with pulmonary edema
  6. 6. Calculations – Carrico index – P/F ratio • To identify acute hypoxemic respiratory failure at any time while the patient is receiving supplemental O2 • Partial pressure of arterial oxygen – Pa02 - P • Fraction of inspired oxygen – FiO2 – F • A P/F Ratio less than 300 indicates acute respiratory failure , it also indicates what the pO2 would be on room air. 1. P/F ratio < 300 is equivalent to pO2 < 60 mm Hg on room air 2. P/F ratio < 250 is equivalent to pO2 < 50 mm Hg on room air 3. P/F ratio < 200 is equivalent to pO2 < 40 mm Hg on room air Ex – PaO2 is 90 mmHg on 40% Oxygen( FiO2 = 0.40). The P/F ratio is 90/0.40 = 225 The pO2 on room air = 45mmHg – less than the cut off.
  7. 7. • When the pO2 is unknown because an ABG is not available, the SpO2 measured by pulse oximetry can be used to approximate the pO2 Ex : Suppose a patient on 40% oxygen has a pulse oximetry SpO2 of 95%. Referring to the Table above, SpO2 of 95% is equal to a pO2 of 80mmHg. The P/F ratio = 80/0.40 = 200. The patient may be stable receiving 40% oxygen, but still has severe acute respiratory failure. If oxygen were withdrawn leaving her on room air, the pO2 would only be 40 mmHg
  8. 8. Relation : FIO2 (%) and litres per minute (O2) • Mask, Nasal Cannula (NC), Venturi mask (Venti-mask), NRB – mask • Venturi mask – delivers (FiO2) @ 24%, 28%,31%,35%,40% and 50% • NRB – mask delivers @ 100% oxygen • Ex : pO2 of 85mmHg on ABG while receiving 5 L/min of oxygen(40% oxygen) 40% 0f O2 - an FIO2 of 0.40 , the P/F ratio = 85 / 0.40 = 212.5.
  9. 9. Signs and symptoms • Restlessness • Dyspnoea • Tachypnoea • Cough • Chest wall retractions • Nasal flaring • Fever • Stridor , wheeze, grunting • Extreme tiredness • Disorientation • Shortness of breath • Tachycardia • Laboured/rapid breathing • Cyanosis • Thick frothy sputum • Acidotic breathing • Abnormal breath sounds ; crackles • Decreased PaO2 LateEarly
  10. 10. Aetiology and Pathogenesis
  11. 11. Non-pulmonary causes of RD EXAMPLES MECHANISMS CARDIOVASCULAR • Left to right shunt • CCF • Cardiogenic shock • Pulmonary blood/water content • Metabolic acidosis • Baroceptor stimulation CENTRAL NERVOUS SYSTEM • Raised ICP • Encephalitis • Toxic encephalopathy • Stimulation of brainstem respiratory centres METOBOLIC • DKA • Organic acidaemia • Hyperammonaemia • Stimulation of central and peripheral chemoreceptors RENAL • RTA • HTN • Stimulation of central and peripheral chemoreceptors • Left ventricular dysfunction SEPSIS • Toxic shock syndrome • Meningococcaemia • Cytokine stimulation of RS centres • Baroceptors stimulation • Metabolic acidosis
  12. 12. Respiratory failure • It occurs when oxygenation and ventilation are insufficient to meet the metabolic demands of the body • Abnormality in A. lung and airways B. Chest wall and muscles of respiration C. Central and peripheral chemoreceptors • It is traditionally defined as respiratory dysfunction resulting in PaO2 < 60 torr with breathing of room air and PaCO2 >50 torr resulting in acidosis • General condition of the patient to be considered • ALI ARDS
  13. 13. Clinical manifestation of Respiratory failure Site of pathology Symptoms Lung and airways Nasal flaring , retractions, tachypnoea, wheezing stridor , grunting Chest wall and muscles of respiration Nasal flaring , tachypnoea , paradoxical breathing Respiratory control Shallow or slow respirations , abnormal respiratory pattern , apnoea
  14. 14. Pathophysiology of RF 1. Hypoxic respiratory failure- failure of oxygenation 2. Hyper carbic respiratory failure- failure of ventilation • Hypoxic respiratory failure results from intra pulmonary shunting, venous admixture and inadequate diffusion of oxygen RF Alveolar ventilation Pulmonary capillary perfusion Diffusion capacity Composition of inspired gas Arterial gas Small airway obstruction Collapsed/fluid in alveoli • Interstitial oedema • fibrosis • ARDS, Pneumonia • Atelectasis, pulmonary oedema
  15. 15. • Ventilation – perfusion Mismatch (V/Q) - For exchange of O2 and CO2 to occur alveolar gas must be exposed to blood in pul. Capillaries • Intrapulmonary shunting • Dead space ventilation • VD/VT = 0.33
  16. 16. • Diffusion - Gas exchange requires diffusion across the interstitial space b/w alveoli and pulmonary capillaries -Presence of hyper carbia in disease that impair diffusion is indicative of alveolar hypoventilation. Ex – Interstitial pneumonia, ARDS and airway obstruction
  17. 17. Basics – Hb-O2 dissociation curve
  18. 18. Monitoring • Clinical examination - Pulse oximetry - Respiratory rate - Progression with time - abnormal clinical findings, CXR , CT scan • Blood gas abnormalities(ABG) - Metabolic acidosis with respiratory compensation - Respiratory acidosis with Metabolic compensation • Assessment of oxygenation and ventilation deficits - A-aO2 gradient, P/F Ratio, PaO2/PAO2 ratio
  19. 19. Management The goal is to ensure a patent airway and provide necessary support . 1. Oxygen administration - FiO2 % O2 delivered = 21% + [(nasal cannula flow (L/Min) * 3)] - simple mask, Venturi mask, Partial Rebreather and NRB’s with reservoir bags
  20. 20. 2. Airway Adjuncts - Maintaining of a patent airway is a critical step [A] – Oropharyngeal airway [B] – Nasopharyngeal airway [A] [B] 3. Inhaled gases - It helps > airway obstruction and improving ventilation [A] – Heliox(60%) - viscous, less dense, laminar flow - laryngotracheobronchitis, subglottic stenosis [B] – Nitric oxide (5-20ppm) – pulmonary vasodilator, - improves pul. Blood flow and V/Q mismatch
  21. 21. 4. Positive pressure respiratory Support • Non-invasive , is useful in treating both hypoxemic and hypo ventilatory RF. • Helps to aerate partially atelectatic, prevent alveolar collapse and increases FRC • It improves pulmonary compliance and reduces intra pulmonary shunting • CPAP – FiO2 can be adjusted through an Oxygen blender. The delivery of O2 through high flow nasal cannula helps to wash out CO2 from naso-pharynx & prevents rebreathing • Benefits –extrathoracic airway obstruction, < lung compliance • Potential risk – nasal irritation, hyperinflation &abdominal distention
  22. 22. BiPAP – Bilevel positive airway pressure • This device allows to set an expiratory PAP and inspiratory PAP • The additional iPAP during inspiration helps augment tidal volume and improve alveolar ventilation in low compliance & obstructive lung disease • Benefits – Children with neuromuscular weakness, diseases of intrathoracic airway obstructions
  23. 23. 5. Endotracheal intubation and mechanical ventilation • ID = [Age(in years)/4] + 4 • Indications A. Primary respiratory disorder 1.Severe Hypoxemia (PaO2 <60 mmHg on 60% FiO2) 2.Severe Hypoventilation ( PaCO2 > 50 mmHg ) B. Primary Neuromuscular disorder - Myopathy, lack of airway protection, Need for sedation C. Tight control of PaCO2 and pH - Raised ICP , Severe pulmonary hypertension
  24. 24. • Administration of sedative and analgesic followed by a paralytic agent – facilitates intubation • Midazolam, Lorazepam, ketamine, propofol are commonly used sedatives • Vecuronium, Rocuronium are paralytic agents • CXR should also be obtained to confirm proper placement of tracheal tube. Which should lie roughly halfway b/w the glottis and carina.
  25. 25. Mechanical ventilation • The need to assist lung function , supporting left ventricular performance and treating intra cranial hypertension • Mechanical ventilation is also used in patients whose respirations are unreliable – unconscious patients, neuromuscular dysfunction, and when deliberate hyperventilation is desired • The goals are to maintain sufficient oxygenation and ventilation to ensure tissue viability • Aim is to protect lungs from damage due to O2 toxicity, Barotrauma, atelectrauma , volutrauma , and biotrauma
  26. 26. Basic concepts of Ventilator management • Equation of motion • Baby lung concept • Open lung concept / Critical opening pressure • Functional Residual Capacity
  27. 27. 1. Equation of Motion • A pressure gradient is required for air to move from one place to another • Normal and Ventilation • Pressure necessary to move air requires 2 factors 1. Lung elastance 2. Chest wall elastance • Elastance = P/ V • Compliance = 1/Elastance [Static process] • Resistance = P/ Flow [Dynamic process] • Pressure gradient = V/C + (Flow * R)
  28. 28. 2. Baby lung concept • This concept originated when multiple CT scan examinations that the aerated tissue has the dimensions of the lung of a 5-6 yr old child (300-500gm of aerated tissue) • ARDS lung is not only stiff but also small • Functional – Gentle lung ventilation is needed • The smaller the baby lung <the potential for damage and VILI
  29. 29. 3. Open lung concept • Collapsed or atelectatic alveoli require a considerable amount of pressure to open • Recruitment • In disease condition alveoli tend to collapse • The minimum pressure required to keep open the lung may cause 1.Barotrauma 2. Volutrauma • Tidal recruitment – injurious to the lung
  30. 30. • Safe zone of ventilation • Keeping tidal ventilation b/w the upper and lower Inflection points [PFLEX] • PEEP – 6ml/kg of tidal volume
  31. 31. 4. Functional Residual Volume • During inspiration – O2 enters alveoli • During expiration - O2 is being removed by pulmonary capillary circulation • FRC – Volume of gas left at the end of the expiration • In diseases that decreases FRC – Hypoxia • Application of PEEP • Increasing the inspiratory time [Ti]
  32. 32. Ways to increase MAP
  33. 33. Phases of Mechanical ventilation • The planning of a ventilatory strategy must consider the 4 phases of respiratory cycle 1. Initiation of respiration and a variable that is controlled – MODE 2. Inspiratory phase characteristics – pressure and volume delivered 3. Termination of inspiration – CYCLE 4. Expiratory phase characteristics
  34. 34. 1. Mode • The initiation of inspiration may be set to occur at a predetermined rate and interval regardless of patient effort • Control mode – breath control is entirely by ventilator • Support mode – supports the patient inspiratory effort based on set t . trigger values • Triggers – flow triggered and pressure triggered
  35. 35. Control Modes 1. Intermittent mandatory ventilation [IMV] - The inspiration is initiated at the set frequency with timing independent of patient effort • In b/w machine delivered breaths, the patient can breathe spontaneously • Support – patient’s needs • To prevent asynchrony - SIMV
  36. 36. Assist-control Mode • In AC mode , each and every breath is triggered by pressure or flow generated by patient efforts and assisted with either preselected inspiratory pressure or volume • On AC mode with backup rate @ 20 breaths /min • Patient with 15 breaths /min will get 15 assisted + 5 additional breaths • Patient with 25 breaths / min will get all breaths assisted
  37. 37. Control Variable
  38. 38. Support Modes • Pressure- support ventilation(PSV) and volume support ventilation(VSV) are designed to support patients spontaneous respiration • With PSV initiation is by patient efforts , which is then “supported” by a rapid rise in ventilator pressure up to preselected level • SIMV+PSV will allow the patient to control the rate, Vt, and inspiratory time • Gentle mode of ventilation • VSV – inspiratory pressure to support spontaneous breath – preset Vt
  39. 39. 2. Inspiratory phase characteristics • Ti – Inspiratory flow waveform and pressure rise time can be adjusted • In PCV – Ti is set in seconds • IN VCV – TI is set in inspiratory flow ( Volume/ time) • With increase in Ti – Improves MAP, Higher level of PaO2 • In VCV – Inspiratory wave form [ ] is adjusted
  40. 40. 3. Cycle • The 2 most commonly used inspiratory terminating mechanisms in control modes are 1. Time cycled and 2. Volume cycled • Time cycled is always pressure limited • Volume cycled is made pressure limited to prevent barotrauma • In PSV – 25% of PIP – flow cycled
  41. 41. 4. Expiratory phase manures • The most useful – PEEP application • Benefits – 1. Recruit atelectatic lung 2. increase FRC • Auto PEEP/Air trapping • Salutary effects include redistribution of extravascular lung water away from gas exchanging areas, improved V/Q relationship and stabilisation of the chest wall
  42. 42. Conventional ventilator settings • Ti – Time given for inspiration • Te – Time given for expiration • I:E ratio – total of 1 sec • R – No. of breaths/ min • Tv- Tidal volume • FiO2 – Fraction of inspired O2 • PIP – Max. pressure used to inflate lungs at peak of inspiration • Trig – Amount of air pushed by baby to machine
  43. 43. Patient ventilator asynchrony 1. Triggering the ventilator 2. Selection of appropriate inspiratory time 3. Selection of inspiratory flow pattern 4. Use of support modes 5. Use of sedation and pharmacological paralysis
  44. 44. Complications 1. VILI • In attempting to recruit and maintain FRC, the clinician must be careful not to over distend alveoli • Excessive PIP and Vt has to be avoided • Decreased production and inactivation of surfactant results in atelectasis and impairment of gas exchange • Evidence – avoid Vt >/= 10ml/kg and Pplat >/= 30 cm H20 in severe acute hypoxemic respiratory failure • Insufficient PEEP
  45. 45. 2. Ventilator associated pneumonia [VAP] • Multifactorial • Aspiration • New onset of fever and leukocytosis • Demonstration of infiltrates by chest radiographs • How to reduce - Elevation of bed for 30degress and use of protocol for oral decontamination during mechanical ventilation • The regular assessment of extubation readiness and liberation from mechanical ventilation as soon as clinically possible
  46. 46. Conclusion and key messages • Pediatric ALI/ARDS is an illness with high mortality and requires excellent supportive care in PICU • Severe sepsis and pneumonia – Leading predisposing conditions • MV should be initiated early • Lung protective strategies – Low Vt and optimal PEEP • Recruitment maneuvers • The impact of prone positioning on mortality is uncertain , it does not improve oxygenation • Supportive care including invasive monitoring , restricted fluid management , attention to MODS and prevention of nosocomial infection are crutial to improve the outcome
  47. 47. References • Nelson textbook of Pediatrics – 01st South Asia edition • Nelson textbook of Pediatrics – 21St International edition • Medical emergencies in children- Meharban Singh – 05th edition • PALS guidelines • NCBI

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