Respiratory Failure.pptx and managements

respiratory failure

1. Respiratory Failure Presenter: Dr. Nisha Thakur (PGY II) Moderator: Dr. Manisha Pradhan

2. Objectives To learn about: Definition of Respiratory failure Types of Respiratory failure Pathophysiology Diagnosis Management

3. Definition Inability of respiratory system to meet one or both of its gas exchange functions Oxygenation Carbon dioxide elimination

4. Types Type I respiratory failure Type II respiratory failure Type III respiratory failure Type IV respiratory failure

5. TYPE I RESPIRATORY FAILURE

6. Type I respiratory failure Hypoxaemic failure Low level of oxygen in the blood without increase level of CO2 in the blood Basic defect: failure of oxygenation characterized by- PO2 decreased: < 60 mm Hg PCO2 normal or decreased (< 45 mm Hg )

7. Causes Ventilation/perfusion (V ̇/Q̇ ) mismatch Shunt Alveolar hypoventilation Diffusion impairment Perfusion/diffusion impairment Decreased inspired O2

8. 1. V/Q mismatch Normal lungs, minor V/Q mismatch Overall V/Q = 0.8 Ranges between 0.3 and 3.0 Upper zone – non dependent has higher > 1 Lower zone – dependent area has lower <1

9. Pathologic V̇ /Q̇ mismatch --- disrupts the balance and hypoxemia results Ventilation is decreased despite adequate blood flow Causes Bronchospasm, mucous plugging, inflammation, and premature airway closure due to asthmatic or emphysematous exacerbations Infection, heart failure, and inhalation injury may lead to partially collapsed or fluid-filled alveoli

10. Clinical presentation Dyspnea, tachycardia and tachypnea Auscultation and percussion Bilateral wheezing --- bronchospasm Breath sounds diminished bilaterally with increased resonance on percussion --- emphysema Absence of breath sounds and decreased resonance on one side of the chest --- collapse, infection, edema, or effusion P(A-a) O2 --- elevated PaCO2 --- normal

11. 2. Shunt extreme version of V ̇/Q̇ mismatch in which there is no ventilation to match perfusion (V ̇/Q̇ = 0) Normal anatomical shunt --- 2% to 3% of the blood supply is shunted via the bronchial and thebesian veins

12. Pathologic anatomic shunt occurs Right-to-left blood flow through cardiac openings (ASD and VSD) Physiologic shunt ---- atelectasis, pulmonary edema, and pneumonia P(A-a) O2 --- elevated PaCO2 --- normal

13. Differentiating the Causes of Acute Hypoxemic Respiratory Failure V/q mismatch: A- a gradient increased Shunting: A- a gradient increased

14. 3. Diffusion Impairment Diffusion --- movement of gas across the alveolar-capillary membrane along a pressure gradient Causes Interstitial lung disease (e.g., pulmonary fibrosis, asbestosis, sarcoidosis)- thickening and scarring of the interstitium – prevents normal gas exchange Pulmonary vascular abnormalities Anemia, pulmonary hypertension, and pulmonary embolus

15. Clinical presentation Interstitial lung disease:- dyspnea, with a dry cough and fine, basilar crackles on auscultation, and clubbing of the nail beds Rheumatologic manifestations:- Joint abnormalities, Raynaud disease and telangiectasia Pulmonary hypertension:- signs of right-sided heart failure (edema, jugular venous distension) P(A-a) O2 -- elevated PaCO2 -- normal

16. 4. Perfusion/Diffusion Impairment Seen in liver disease complicated by the hepatopulmonary syndrome:- reduced arterial oxygen saturation due to dilated pulmonary vasculature in the presence of advanced liver disease or portal hypertension

17. Pathophysiology increased hepatic production of ET1 and pulmonary ETB due to stress pulmonary endothelial nitric oxide synthetase ( eNOS ) stimulation Pulmonary vascular dilatation  Translocation of intestinal bacteria and endotoxemia in liver disease patients massive accumulation of macrophages and monocytes in lungs macrophages release TNF-alpha and VEGF angiogenesis

18. Pathophysiology continues .. Pulmonary vasodilation and angiogenesis leads to: Arteriovenous (AV) shunt formation --- increases V/Q mismatch Increased perfusion secondary to vascular dilatation and collateralisation in the setting of preserved ventilation --- shunting of blood Increased pulmonary capillary wall thickness --- impaired diffusion of gases  

19. Clinical Presentation Signs of liver disease (e.g., ascites, jaundice, and spider nevi) Platypnea Orthodeoxia P(A-a) O2 – elevated , PaCO2- normal

20. 5 . Decreased Inspired Oxygen hypoxemia may develop when the inspired O2 is less than usual Causes higher altitude decrease in FIO2 accidental (anesthetist does not supply enough oxygen or improper installation of oxygen supply or leak in the breathing circuit) P(A-a) O2 -- normal, PaCO2 -- decreased

21. Arterial blood Veonous blood Increase in FiO2 -- increase PaO2 PO2 PCO2 PO2 PCO2 P(A-a) O2 Hypoventilation ↓  ↑ ↓  ↑ Normal Yes PiO2 ↓ ↓ ↓ ↓ normal Yes Shunt ↓ Normal ↓ Normal  ↑ No V/Q mismatch ↓ Normal ↓ Normal ↑ Yes Diffusion defect ↓ Normal ↓ Normal Increase during exercise Yes

22. TYPE II RESPIRATORY FAILURE

23. TYPE II RESPIRATORY FAILURE Hypercapnic RF pump, bellows, or ventilatory failure characterized by an elevated PaCO2, creating an uncompensated respiratory acidosis

24. PaCO2 and alveolar ventilation are inversely related alveolar and arterial PCO2 levels are doubled when alveolar ventilation is halved (illustrated by the metabolic hyperbola relationship)

25. Basic defect in type 2 respiratory failure is PaO2 --- decreased < 60 mm hg PaCO2 --- increased > 50 mm hg pH --- decreased

26. Causes Impaired central nervous system (CNS) drive to breathe Impaired strength with failure of neuromuscular function in the respiratory system Increased load(s) on the respiratory system Increased Carbon Dioxide Production

27. 1. Impairment in CNS drive Causes of Decreased ventilatory drive drugs (overdose or sedation) bilateral carotid endarterectomy with incidental resection of the carotid bodies brainstem lesions diseases of the CNS (multiple sclerosis, Parkinson disease, or elevated ICP) Hypothyroidism and sleep apnea P(A-a) gradient:- normal < 20mmHg

28. 2. Impaired strength with failure of neuromuscular function in the respiratory system Reduced strength can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis) respiratory muscle weakness (e.g., myopathy , electrolyte derangements, fatigue) P(A-a) gradient:- normal < 20mmHg

29. 3. Increase loads in respiratory system Subclassified into- resistive loads (bronchospasm) loads due to reduced lung compliance (e.g. alveolar edema, atelectasis, auto-PEEP) loads due to reduced chest wall compliance (e.g., pneumothorax, pleural effusion, abdominal distention) loads due to increased minute ventilation requirements (e.g., pulmonary embolus with increased dead-space fraction, sepsis) PA-a gradient – widened

30. 4. Increased Carbon Dioxide Production Causes Fever Agitation Exertion Shivering Hypermetabolism

31. CHRONIC RESPIRATORY FAILURE weeks to months to years and has become a chronic state, allowing compensatory adaptive mechanisms to develop Cause:- COPD or obesity-hypoventilation syndrome Compensation via kidney this compensatory metabolic alkalosis does not restore the pH all the way to normal

32. RULE OF THUMB:- Chronic and acute hypercapnic respiratory failure can be differentiated by the severity of change in pH Acute hypercapnic failure : pH decreases 0.08 for every 10 mm Hg increase in PaCO2 Chronic hypercapnic failure : pH decreases 0.03 for every 10 mm Hg increase in PaCO2

33. Acute-on-Chronic Respiratory Failure Chronic respiratory failure complicated by acute-on-chronic respiratory failure Precipitating factors include bacterial or viral infections, congestive heart failure, pulmonary embolus, pneumothorax , chest wall dysfunction

34. MANAGEMENT

35. Management of type I RF Treatment of hypoxaemia :- aim to maintain adequate oxygenation, achieved with an arterial oxygen pressure (PaO 2 ) of 60 mm Hg Oxygen delivered via nasal canula, simple face mask, nonrebreathing mask or high flow nasal canula In severe cases:- patient may require  invasive ventilatory support

36. Management of type II RF Correction of hypercapnia and respiratory acidosis: NIV Mechanical ventilation

37. 1. NIV mode of ventilatory support provided without endotracheal intubation CPAP alone or in combination with any mode of pressure-limited or volume-limited ventilation

38. Mechanisms that improve hypoxemia and hypercarbia: compensating for the inspiratory threshold load imposed by intrinsic PEEP supplementing a reduced tidal volume partial or complete unloading of the respiratory muscles reducing venous return and left ventricular afterload alveolar recruitment preventing intermittent narrowing and collapse in patients with obstructive sleep apnea/hypopnea syndrome by using pressure to splint the airway open during sleep

39. Indication of NIV

40. Settings in NIV Mode  Mostly on pressure-controlled NIV (e.g., bilevel positive airway pressure [BiPAP] Some can tolerance on volume-controlled NIV (e.g., patients with neuromuscular disease) Mask: oronasal mask tight fitting full-face mask, a nasal mask

41. Settings Bilevel positive airway pressure (BPAP):- 8 to 12 cm H2O (inspiratory pressure) and 3 to 5 cm H2O (expiratory pressure) Pressure support NIV (PSV-NIV):- 8 to 12 cm H2O (pressure support) and 3 to 5 cm H2O (positive end expiratory pressure) Volume-controlled NIV:- Tidal volume 6 to 8 ml/kg and 5 cm H2O positive end expiratory pressure; rate 10 to 12 breaths/minute.

42. Invasive ventilation Indications Hypoxaemia not corrected with NIPPV Severe acidosis ph <7.2 and Pa CO2 > 60 mmhg Impending respiratory arrest RR > 35 Low GCS Cardiovascular instablity Conditions – ARDS, raised ICP

43. Ventilator-specific strategies Low tidal volume (6 ml/kg ideal bodyweight) and avoidance of high inspiratory pressures ( P   plat  <30) to minimize the risk of volutrauma Reduced arterial oxygenation saturation (SaO 2 ) targets 88–95% and reduced partial pressure of arterial oxygen (PaO 2 ) 7.5–10.5 kPa – ‘permissive hypoxia’ Acceptance of mild to moderate respiratory acidosis – ‘permissive hypercapnia ’ Greater use of positive end-expiratory pressure (PEEP), particularly in more severe hypoxaemia

44. TYPE III RESPIRATORY FAILURE

45. TYPE III RESPIRATORY FAILURE Lung Atelectasis Residual anesthesia effects, post operative pain and abnormal abdominal mechanics contribute to decrease FRC and leads to collapse of dependent lung units

46. TYPE IV RESPIRATORY FAILURE

47. TYPE IV RESPIRATORY FAILURE Metabolic Demands Patients who are intubated and ventilated in the process of resuscitation for shock Due to hypoperfusion of respiratory muscles in patients in shock Normally, respiratory muscles consume <5% of total cardiac output and oxygen delivery Patients in shock experience respiratory distress- 40% of CO distributed to the respiratory muscles Intubation and mechanical ventilation allows redistribution of the cardiac output away from the respiratory muscles and back to vital organs

48. Summary Acute respiratory failure is identified by PaO2 less than 60 mm Hg or PaCO2 greater than 50 mm Hg, or both, in otherwise healthy individuals at sea level Hypoxemic respiratory failure is most commonly due to V ̇/Q̇ mismatch, shunt, or hypoventilation Hypercapnic respiratory failure, also known as ventilatory failure, results from decreased ventilatory drive, neurologic disease, or increased work of breathing The clinical condition of the patient is the most important factor in determining the need for ventilatory support

49. References Egan’s fundamentals of respiratory care Harrison’s principles of internal medicine

50. THANK YOU

51. References Egan’s fundamentals of respiratory care Harrison’s principles of internal medicine