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RESPIRATORY FAILURE-EVALUATION AND MANAGEMENT

RESPIRATORY FAILURE-EVALUATION AND MANAGEMENT. Dr Binila Chacko Associate Professor Medical ICU, CMC Vellore. DR THOMAS COGAN. DR WILLIAM HOWES. RESPIRATION. CELLULAR RESPIRATION. TRANSPORT OF GASES. VENTILATION. DEFINITION. Failure of the lung to maintain adequate gas exchange

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RESPIRATORY FAILURE-EVALUATION AND MANAGEMENT

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  1. RESPIRATORY FAILURE-EVALUATION AND MANAGEMENT Dr Binila Chacko Associate Professor Medical ICU, CMC Vellore

  2. DR THOMAS COGAN • DR WILLIAM HOWES

  3. RESPIRATION • CELLULAR RESPIRATION • TRANSPORT OF GASES • VENTILATION

  4. DEFINITION • Failure of the lung to maintain adequate gas exchange • Abnormalities of arterial blood gas tensions. • PaO2 < 60 mmHg with or without hypercarbia PaCO2 > 46 mmHg • Onset usually acute or sub-acute

  5. WHY IS THIS TOPIC IMPORTANT • Common problem • 360,000 cases per year United States • 36% die during hospitalization • Estimated that respiratory failure will become more common as the population ages, increasing by as much as 80 percent in the next 20 years

  6. PHYSIOLOGY • PACEAMAKER • Increased airway resistance • Decreased lung compliance • REDUCE PUMP EFFICIENCY • INCREASE WORK OF BREATHING • Resistance • Compliance • PUMP • GAS EXCHANGER

  7. FACTORS AFFECTING EFFICIENCY OF GAS TRANSFER • Alveolar capillary interface • Transit time of blood in the pulmonary capillaries • 0.7seconds

  8. PaO2 • PAO2 Alveolar partial pressure of oxygen • Diffusing capacity • Ventilation-perfusion matching

  9. PAO2 determinants • Alveolar pressure=PAO2+PACO2+PA(H20)+PA N2 • Alveolar pressure • Alveolar gas equation • PAO2=(FiO2 x713)-PACO2/R • FiO2 • PACO2

  10. PaO2 • PAO2 • Diffusing capacity • Transit time in the pulmonary capillaries-0.7seconds • Alveolar capillary interface • Increase in thickness • Since CO2 diffusion 20 times that of oxygen • usually hypoxemia unless there is ventilatory failure

  11. PaO2 • PAO2 • Diffusing capacity • Ventilation-perfusion matching • Normal alveolar ventilation (V) about 4 to 6 L, Perfusion (cardiac output, Q) about 5 L • Normal V/Q=0.8-1.2

  12. V/Q matching • Intracardiac/intrapulmonary • Predominant hypoxemia • Anatomical/ physiological • Predominant hypercarbia

  13. PaO2 quick recap • PAO2 • Alveolar pressure, FiO2 and the PaCO2 • Diffusing capacity • Alveolar capillary membrane and time across pulmonary capillaries • Ventilation-perfusion matching • Dead space and shunt effect

  14. Carbon dioxide outflow Respiratory rate Tidal volume Ventilation-perfusion matching • Dependent on alveolar ventilation • Resp rate x (VT-VD) • VT=Tidal volume • VD=Dead space • Again shows the importance of V/Q matching in carbon dioxide regulation

  15. TYPES • Physiological approach • Type 1 and 2 • Pathophysiological approach • Types 1 to 4

  16. Hypoxemic/type I respiratory failure • Hypercapnic/type II respiratory failure TYPES • SHUNT • Pathophysiological approach • Types 1 to 4

  17. IN AN UNWELL PATIENT • CLINICAL EXAMINATION • MANAGEMENT • HAPPEN IN PARALLEL

  18. Clinical assessment TO ASSESS SEVERITY TO DETERMINE THE CAUSE

  19. Clinical assessment • RESPIRATORY COMPENSATION • SYMPATHETIC STIMULATION • TACHYCARDIA • HYPERTENSION • SWEATING • TISSUE HYPOXIA • HEMOGLOBIN DESATURATION • RESPIRATORY COMPENSATION • SYMPATHETIC STIMULATION • TISSUE HYPOXIA • HEMOGLOBIN DESATURATION • RESPIRATORY COMPENSATION • TACHYPNEA • USE OF ACCESSORY MUSCLES • SYMPATHETIC STIMULATION • TISSUE HYPOXIA • HEMOGLOBIN DESATURATION • RESPIRATORY COMPENSATION • SYMPATHETIC STIMULATION • TISSUE HYPOXIA • HEMOGLOBIN DESATURATION • CYANOSIS • RESPIRATORY COMPENSATION • SYMPATHETIC STIMULATION • TISSUE HYPOXIA • ALTERED MENTAL STATUS • SHOCK-DECREASED ORGAN PERFUSION • HEMOGLOBIN DESATURATION • WORRY IF • RR >30/MIN • CAN’T SPEAK IN FULL SENTENCES • AGITATED/CONFUSED • DETERIORATING DESPITE THERAPY • TO ASSESS SEVERITY

  20. To determine the cause… • APPLYING PHYSIOLOGY TO PATHOLOGY

  21. Approach to Type I respiratory failure • Hypoxemia • reduction in oxygen in the blood-low PaO2 • Hypoxia • reduction in oxygen in the tissues

  22. LOW PaO2 =HYPOXEMIA • Low PAO2 • Overdistended alveoli(Intrinsic/extrinsic-PEEP) • Decreased blood supply-Pulmonary embolism/Shock • Alveolar capillary • Alveolar disease (fluid/pus/protein/blood) • Intra-pulmonary shunting - collapsed lung (atelectasis) • tasis)

  23. MUST REMEMBER • More than one pathophysiological process may co-exist. • Pure diffusion abnormalities are uncommon.

  24. WHAT’S THE NEXT STEP? • Find out where the abnormalty is • Pa CO2 • A-a gradient

  25. A-a gradient

  26. Is the A-a gradient increased ? • No • Increased • A-a gradient • No • No • Shunt • Low PaO2 • Yes • Is the CO2 increased ? • Response to oxygen therapy • Yes • Yes • Normal - pure hypoventilation • Low inspired FiO2 • V/Q mismatch • Alveolar disease • Interstitial disease • Diffusion problems • Pulmonary embolism

  27. Approach to hypercapnic respiratory failure • Increased CO2 production • Increased muscle activity (spasms, convulsions) • Hyper metabolic states (fever, sepsis) • Carbohydrate rich feeds. • HYPERCAPNIA OCCURS ONLY IF CO2 ELIMINATION CANNOT KEEP PACE WITH PRODUCTION • Reduced CO2 elimination • Increased CO2 production • Reduced CO2 elimination • CONTROLLER-BRAIN/SPINAL CORD/NMJ • PUMP • ALVEOLOCAPILLARY UNIT Increased CO2 production Reduced CO2 elimination

  28. Shunt • Low • Is the A-a gradient increased? • V/Q mismatch • Alveolar disease • Interstitial disease • Diffusion problems • Pulmonary embolism • Yes • Neuromuscular problem • Increased production • No • Response to oxygen therapy • Pure hypoventilation • Reduced elimination • High CO2 • No • PI Max • Normal • Yes • Central hypoventilation syndrome

  29. Don’t forget to look at the pH • PaCO2 must always be considered in relation to the pH. • Acute hypercapnic respiratory failure • Shift in the pH, • Compensatory mechanisms take time • Chronic hypercapnic respiratory failure • pH is usually close to normal,

  30. Management of hypoxemic respiratory failure • treatment of the underlying cause (specific treatment) • improving oxygen delivery to the tissues • limiting potentially damaging therapies • reducing tissue oxygen demand.

  31. Management of hypoxemic respiratory failure • treatment of the underlying cause (specific treatment) • improving oxygen delivery to the tissues • DO2 = [1.39 x Hb x SaO2+ (0.003 x PaO2)] x Q • Hb • SaO2 • PaO2 • Cardiac index • Increase FiO2 • PEEP

  32. Improving oxygen delivery • Target is to maintain cerebral oxygenation • Increase FiO2 • FiO2 start with 100% (unless COPD) and reduce FiO2 based on ABG (P/F ratios) • Apply extrinsic PEEP - “Open lung ventilation” (can be done by invasive MV or NIV) • Physiological goal of preventing alveolar collapse

  33. Oxygen delivery devices • Flow • Performance • Performance • Variable • the oxygen concentration of the air-oxygen mix reaching the alveoli is not constant • Fixed • not influenced by respiratory rate, size of the reservoir or oxygen flow rate • Flow • Low flow • deliver oxygen less than PIFR • High flow • deliver oxygen at flow rates higher than PIFR

  34. Oxygen delivery devices

  35. Management of hypoxemic respiratory failure • treatment of the underlying cause (specific treatment) • improving oxygen delivery to the tissues • limiting potentially damaging therapies • Lung protective ventilatory strategies • reducing tissue oxygen demand. • control of fever, sepsis or seizures • ventilatory support offloads the respiratory muscles

  36. Alveolar recruitment • Increase tidal volumes (increase distending pressures) - keep alveoli open • Increase inspiratory time • Increase PEEP

  37. How much tidal volume? • Landmark NIH NHLBI ARDS network • Prospective, randomized, multi-center trial of 12 ml/kg vs 6 ml/kg tidal volume positive pressure ventilation for treatment of acute lung injury and acute respiratory distress syndrome • 861 patients • The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000, 342:1301–1308

  38. OPTIMAL PEEP SETTING • Defined as the lowest PEEP attainable without causing a significant drop (>10%) in PaO2 • No agreed upon method of determination • • • Staircase recruitment manouvre • ARDSNet protocol • Higher than the lower infection point on a pressure-volume loop • Thoracic tomography • Oesophageal balloon directed estimation of pleural pressures to calculate transpulmonary pressures and guide PEEP titration

  39. How do you set PEEP? • LIP is that point of the curve where the slope of the line changes significantly. • Believed to represent the opening of majority of alveoli

  40. How do you set PEEP?

  41. Benefits of PEEP • Increases transpulmonary distending pressures • Displaces edema fluid into interstitium • Decreases atelectasis • Decrease in right to left shunt • Improved compliance • Improved oxygenation

  42. Whom should I ventilate? • Decision to ventilate • Complex • Multifactorial • No simple rules • Severity of respiratory failure • Cardiopulmonary reserve • Adequacy of compensation • Ventilatory requirement • Underlying disease • Treatment already given • Risks of mechanical ventilation

  43. Always consider ..

  44. Different clinical situations • Mild hypoxemia (PaO2 60 – 70 mmHg on room air) • a nasal cannula or a simple mask may be sufficient. • Moderate hypoxemia (PaO2 50-60 mmHg) • a partial re-breather mask or venturi device • latter preferred for COPD patients. • Severe hypoxemia (PaO2 <50 mmHg) not responding to simpler devices • non-rebreather systems (e.g. CPAP, non-invasive ventilation, Ambu-bag, Bains) • Invasive mechanical ventilation

  45. Specific to management of hypercapnic respiratory failure • Reduce CO2 production • controlling fever and excess motor activity (convulsions) • Reducing carbohydrate intake. (R.Q Carbohydrates 1.0 and for fat is 0.7) • Particularly important for COPD

  46. IMPROVE LUNG MECHANICS To enhance CO2 elimination.. • Respiratory drive can be increased • Reducing the use of sedation • Drugs that increase respiratory drive (COPD) • acetazolamide, medroxy-progesterone acetate • Benefit not proven in randomized trials • Ventilation-GOAL TO INCREASE ALVEOLAR VENTILATION • Improve Lung mechanics • P ABCDE • P- propping up • A-Analgesics to reduce chest pain • B-Bronchodilators • C-Compliance-ventilatory/non-ventilatory strategies • D-Drugs such as xanthines • E-Electrolyte correction • PROGRESSIVE HYPERCARBIA DUE TO LOSS OF HYPOXIC DRIVE IS RARE • HYPOXIA KILLS!!

  47. Always consider ..

  48. NIV COPD • The number needed to be treated for benefit • N=8 patients to save one life • N=5 to avoid one invasive mechanical ventilation • N=3 to avoid “a” complication of ventilation • Milder exacerbations • Evidence not clear • Post hoc analysis suggest benefit below pH of 7.37 and PaCO2 of > 55 mm Hg

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