Respiratory failure
- 1. BASICS OF RESPIRATORY FAILURE DR. BIPUL BORTHAKUR (PROFESSOR) DEPT OF ORTHOPAEDICS, SMCH
- 2. DEFINITION The inability of the respiratory system to adequately oxygenate the blood with or without a concurrent alteration in carbon dioxide elimination
- 3. Acute and Chronic Depending on underlying cause Acute eg: drug overdose, pneumonia, pneumothorax Chronic eg: severe COPD
- 4. TYPES Type I hypoxemic respiratory failure Type II hypercapneic respiratory failure
- 5. Type I - Hypoxemic Failure Oxygenation failure PaO2 < 60 mmHg OR < 8 kpa PaCO2 normal or < 35 mmHg pH normal or elevated
- 6. Type I - Hypoxemic Failure ventilation (VA) and perfusion (Q) mismatching is the most common cause of hypoxemia. Either by increasing the dead space or by wasted ventilation
- 7. Causes of Type I - RespiratoryFailure COPD Asthma Pneumonia Pulmonary embolism Pneumothorax Pulmonary edema ARDS Pulmonary fibrosis Obesity Lymphatic carcinamatosis Pnueumoconiosis Granulomatous lung disease Cyanotic cong heart disease Bronchiectasis Crush lung injury FAT embolism
- 8. Type II hypercapneic respiratory failure Ventilation failure PaO2 < 60 mmHg PaCO2 > 45 mmHg OR >6.7 kpa pH < 7.35
- 9. CAUSES OF Type II hypercapneic respiratory failure COPD Asthma Drug overdose/Poisoning Myasthenia gravis Polyneuropathy Poliomyelitis Myopathy,Porphyria Head/ cervical cord injury Primary alveolar hypoventilation Sleep apnoea syndrome Pulmonary edema ARDS Myxedema Laryngeal edema Tetanus Foreign body
- 10. Type III respiratory failure (perioperative respiratory failure) commonly in the perioperative period, due to lung atelectasis. After general anesthesia, decreases in functional residual capacity lead to collapse of dependent lung units. treated by frequent changes in position, chest physiotherapy, upright positioning aggressive control of incisional and/or abdominal pain. Noninvasive positive-pressure ventilation
- 11. Type IV respiratory failure due to hypoperfusion of respiratory muscles in patients in shock. Normally, respiratory muscles consume <5% of the total CO and O2 delivery. Patients in shock often suffer respiratory distress due to pulmonary edema, lactic acidosis, and anemia. then, up to 40% of CO may go to respiratory muscles.
- 12. Intubation and mechanical ventilation can allow redistribution of the CO away from the respiratory muscles and back to vital organs while the shock is treated
- 14. Patient Presentation Neurological Hypercapnoea also produce tremor,myoclonic jerks, asterexis etc. Increased CNS blood flow causes raised ICT- headache and papilloedema. Headache on waking up is common in chronic hypercapnia, may be due to increased CO2 retention in sleep
- 15. Patient Presentation Cardiovascular Tachycardia Elevated blood pressure early Eventual hypotension. Cardiac dysrythmias
- 16. Patient Presentation Skin Hypercarbia – warm,flushed skin with a bounding pulse, wet. Hypoxemia -cold and wet
- 17. Patient Presentation Respiratory Increased rate and depth (hyperpnea) Central cyanosis, due to hypoxemia Dyspnea - subjective feeling of difficult breathing
- 18. Patient Presentation Renal Decreased UOP Erythropoietin release with hypoxemia Excretion of H+ and retention of HCO3 - with respiratory acidosis
- 19. Patient Presentation Gastrointestinal Decreased bowel sounds Reduced gastric pH with tissue hypoxia , leads to gastric erosions and bleeding
- 20. Immediate determination of upper airway patency Examination for central and peripheral cyanosis Measurement of the respiratory rate Observation of the depth and pattern of respiration Initial Assessment and Stabilization of Respiratory Failure
- 21. Assess the configuration of the chest wall and its movement during the respiratory cycle Palpation and auscultation over each hemithorax Signs of respiratory distress including flaring of nostrils, pursed-lip breathing, and use of accessory muscles of respiration
- 22. Above observations allow an initial assessment of respiratory drive, pump function, and delivery of gas to the lungs
- 23. INVESTIGATIONS ARTERIAL BLOOD GAS MEASUREMENT PULSE OXIMETRY NON INVASIVE, BUT NO INFORMATION REGARDING Va ,PCO2
- 24. PULSE OXIMETRY There is a relationship between the amount of oxygen dissolved in the blood and the amount attached to the hemoglobin. Normal Oxyhemoglobin Dissociation Curve 97% saturation = 97 PaO2 (normal) 90% saturation = 60 PaO2 (danger) 80% saturation = 45 PaO2 (severe hypoxia)
- 25. MANAGEMENT Initial therapy be implemented before the specific DIAGNOSIS Adequate airway protection, oxygenation, and ventilation should be assured and stabilize the Patient Hypoxemia and hypercarbia can rapidly lead to circulatory failure and death THEN, if possible treat the primary condition.
- 26. Type I respiratory failure GOAL: to increase the oxygen saturation to 85 to 90 % by giving oxygen at increasing FiO2. Maintain adequate cardiac output and correct anemia. Treat contitions like fever, agitation, overfeeding, vigorous respiratory activity & sepsis which increase O2 demand
- 27. Type I respiratory failure prolonged exposure to high FiO2(>50%)/prolonged duration of treatment is avoided, due to pulmonary toxicity.
- 28. Type I respiratory failure Indications of mechanical ventilation are: 1. Inadequate oxygenation despite of high FiO2 2. Increasing PaCO2 associated with altered mental status or increasing fatigue 3. Failure to control secretions
- 29. Type II respiratory failure Most commonly COPD, there is some degree of c/c resp failure leading to hypercapnea. Acute on c/c: acidemia and increase in bicarbonate in ABG
- 30. Type II respiratory failure 1. Relief of hypoxia By giving supplemental O2. by nasal prongs at flow of 1 to 3 L/ min Or by venturi mask with flow set to 24 to 28 %. Recheck arterial blood gases/O2 saturation to look for improvement. PaO2 of > 50 mmHg is considered as adequate
- 31. Type II respiratory failure Avoid sedatives, as they decrease ventilatory drive To improve acidosis and hypercapnea and oxygenation respiratory stimulants like doxapram can be tried, by close monitoring of ABG.
- 32. Type II respiratory failure Non invasive positive pressure ventilation. Advantage : avoiding intubation Aims at improving ventilation and gas exchange and reduces work of respiratory muscles
- 33. Mechanical Ventilation in respiratory failure Indications 1. Failure to attain PaO2 of 60 mmHg despite of FiO2 of 0.6 2. Rapidly increasing hypercapnea, producing uncompensated acidosis 3. Mental confusion either due to hypoxemia/hypercapnea 4. Tachypnoea(>35/min) 5. Clinical judgement of impending exhuation of the patient
- 34. Airway acsess Nasotracheal/ orotracheal intubation dis adv: laryngeal/ tracheal trauma, used only up to 72 hrs Tracheostomy: complications; hemorrhage, infection erosion of tube to esophagus, tracheal stenosis, tube blockade and respiratory infection
- 35. Ventilator settings Tidal volume of approx 10 ml/kg RR of 10 to 20/ min So minute ventilation is 100 to 150 ml/kg
- 36. In COPD/asthma In COPD tidal volume is kept at a little lower level(7 – 9 ml/kg) to avoid auto PEEP and to prevent high inflation pressures to already over inflated lungs to prevent barotrauma. I:E ratio is kept at 1:4 or 1:5 to minimise air trapping Peak inflation pressures are kept under 30 – 35 cm H2O FiO2 is kept at 35%
- 37. In COPD/asthma Regular monitoring of blood gases is needed. Adjust inspired O2 and level of PEEP to PaO2 and minute ventilation against PaCO2
- 38. Auto PEEP/ intrinsic PEEP Develops in COPD due to decreased elastic recoil, decreased expiratory flow and expiratory time due to tachypnoea- air trapping and positive alveolar pressure at end of breathing. Can impede venous return and decrease cardiac output. Increase chance of barotrauma
- 39. In ARDS.. Tidal volume is kept low to prevent barotruama and pnuemothorax and maintaining CVP at a lower range; PEEP is maintained at a higher range to minimise FiO2 and prevent alveolar collapse I:E ratio is kept >1:1 This results in better survival than conventional ventilation strategies.
- 40. Managenment of patient on ventilator Monitor ECG, heart rate, BP, oxygenation, ABG, urine output Do not lower PaCO2 suddenly in a patient whom the resting level is known to be high. Better to aim at treating acidosis Adeqaute sedation Regular suction of airways Adequate nutrition : enteral/ parenteral
- 41. Weaning.. Some times difficult with COPD Can be tried when underlying condition/ infection has subsided, SaO2>90% with FiO2 < 0.4 and PEEP<5,alveolar ventilation is adequate with pH normal, cardiovascular function is stable, upper airway function is normal, Weaning index; ratio of beathing frequency to tidal volume(breaths/min/L) <105 in spont ventilation thru tube, succesful Extubation is likley
- 42. Weaning modes T piece and CPAP Weaning: best tolerated by patients with mechanical ventilation for brief periods SIMV & PSV modes best for intubated for extended periods &require gradual respiratory-muscle reconditioning
- 43. complications Barotrauma(1 – 8%) more common with ARDS Assc with high peak airway pressures, High levels of external and auto PEEP, High tidal volumes GI bleeding due to gastric erosions Nosocomial pneumonia Cardiac arrhythmias, pulmonary embolism etc
- 44. Prognosis Best predictor of mortality in patients with acute on chronic respiratory failure is degree of acidemia. pH< 7.26 is assc with higher mortality. Long term mortality of patients who survive an episode of acute respiratory failure depends on underlying illness. Eg: COPD, 50% survival at end of 3 years
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