Respiratory failure types and management.pptx

Respiratory failure

1. RESPIRATORY FAILURE PRESENTED BY: DR MUHSINA K. MODERATOR : DR PRIYANKAR SARKAR.

2. RESPIRATORY FAILURE Introduction Hypoxemia and hypercapnia Causes Classifications pathophysiology Signs and symptoms Investigations Management of acute respiratory failure Chronic and acute on chronic respiratory failure

3. INTRODUCTION Respiratory system has 2 primary functions 1.To facilitate O 2 uptake and delivery to vital organs and peripheral tissues. 2. Eliminate CO 2 and maintain pH balance. Respiratory failure is defined as the failure of these 2 main functions. Can be a primary problem or secondary complication.

4. HYPOXEMIA AND HYPERCAPNIA HYPOXEMIA: PaO 2 <60mmhg Any pulmonary disease which causes ventilation perfusion mismatch results in acute hypoxemia. Extreme levels of mismatch is caused by shunt –when an area of lung is not ventilating at all, eg : consolidation or collapse. HYPERCAPNIA: PaCO 2 <50mmhg Hypercapnia is caused by alveolar hypoventilation. central depression of respiratory drive impaired nerve transmission between CNS and muscles. esp,diaphragm reduced chestwall movements Redused alveolar ventilation due to pathology within lungs.

5. Causes of acute hypoxemia 1. HYPOVENTILATION Occurs when minute ventilation is less than 4-6 l/min Causes Depression of CNS from drugs Neuromuscular disease of respiratory muscles Increased PaCO 2 and decreased PaO 2 Alveolar –arterial PO 2 gradient is normal COPD Mostly corrected by additional O 2 supply. But hypercapnia is not corrected.

6. 2, VENTILATION PERFUSION MISMATCH Most common cause of hypoxemia Low V/Q ratio, may occur either from Decrease of ventilation secondary to airway or interstitial lung disease Overperfusion in the presence of normal ventilation e.g. PE Administration of 100% O2 eliminate hypoxemia.

7. 3. SHUNT The deoxygenated blood bypasses the ventilated alveoli and mixes with oxygenated blood → hypoxemia Persistent of hypoxemia despite 100% O2 inhalation Hypercapnia occur when shunt is excessive > 60%

8. CAUSES OF SHUNT Intracardiac Right to left shunt Fallot’s tetralogy Eisenmenger’s syndrome Pulmonary A/V malformation Pneumonia Pulmonary edema Atelectasis/collapse Pulmonary Hemorrage Pulmonary contusion

9. 4 . DIFFUSION ABNORMALITY Less common Due to abnormality of the alveolar membrane Reduction in the number the number of the alveoli Causes ARDS Fibrotic lung disease

10. 5.LOW INSPIRED O 2 TENSION At high altitude Improves with supplemental O 2 6.OXYGEN DELIVERY-CONSUMPTION MISMATCH Demand by peripheral tissues exceeded by supply. Eg:hypermetabolism , low cardiac output, low oxygen carrying capacity. Give supplemental O 2 and manage cause.

11. CLASSIFICATION TYPE 1 RESPIRATORY FAILURE Hypoxemia on breathing room air (PaO 2 <60 mmhg ) without hypercapnia (PaCO 2 <50 mmhg ) TYPE 2 RESPIRATORY FAILURE Hypoxemia (PaO 2 <60 mmhg ) with hypercapnia(PaCO 2 >50 mmhg ) Both type has acute and chronic conditions.

12. Type 1 Hypoxemic RF PaO2 < 60 mmHg with normal or ↓ PaCO2 Associated with acute diseases of the lung Pulmonary edema (Cardiogenic, noncardiogenic (ARDS), pneumonia, pulmonary hemorrhage, and collapse Type 2 Hypercapnic RF PaCO2 > 50 mmHg Hypoxemia is common Drug overdose, neuromuscular disease, chest wall deformity, COPD, and Bronchial asthma

13. Acute RF Develops over minutes to hours pH decreases quickly to <7.2 Example; Pneumonia Chronic RF Develops over days increase in HCO3 pH decreases slightly Polycythemia, Corpulmonale Example; COPD

14. PATHOPHYSIOLOGY – TYPE 1 Impairment of ventilation of part of lung and perfusion ( eg:asthma , pneumonia) Hypoxia and CO 2 laden blood enter pulmonary veins Increased ventilation of neighboring normal lung increases CO 2 excretion Corrects alveolar CO 2 to normal

15. Normal neighboring area cannot augment O 2 uptake ( hb is already saturated) Admixture of blood from hypoventilated and normal area Hypoxia and normocapnia

16. PATHOPHYSIOLOGY –TYPE 2 Severe generalised ventilation perfusion mismatch Or disease that reduses total ventilation Insufficient normal lung to correct PaCO 2. Hypoxia and hypercapnia

17. CAUSES 1 – CNS Depression of the neural drive to breath Brain stem tumors or vascular abnormality Overdose of a narcotic, sedative, Myxedema, chronic metabolic alkalosis Acute or chronic hypoventilation and hypercapnia 2 - Disorders of peripheral nervous system, Respiratory muscles, and Chest wall Inability to maintain a level of minute ventilation appropriate for the rate of CO 2 production Guillian -Barre syndrome, muscular dystrophy, myasthenia gravis, Kyphoscoliosiss , morbid obesity Hypoxemia and hypercapnia

18. 3 - Abnormities of the airways Upper airways Acute epiglotitis Tracheal tumors Lower airway COPD, Asthma, cystic fibrosis Acute and chronic hypercapnia 4 - Abnormities of the alveoli Diffuse alveolar filling hypoxemic RF Cardiogenic and noncardiogenic pulmonary edema Aspiration pneumonia Pulmonary hemorrhage Associate with Intrapulmonary shunt and increase work of breathing

19. APPROACH TO RESPIRATORY FAILURE Take a brief history of course of disease, past history of respiratory diseases and comorbidities Look for signs and symptoms Assess respiratory function Assess conscious level Record vitals Pulse oximetry less than 94% arterial hypoxemia Bedside capnography ABG

20. ABG gold standard of diagnosing respiratory failure pH 7.35-7.45 PaO2 >70 mmHg PaCO2 35-45 mmHg HCO3 22-28 mmol /l ↓ pH Acidosis ↑ pH Alkalosis ↓ PaO2 Hypoxemia ↑ PaCO2 Hypercapnia ↓ pH+ ↑ PaCO2 R. acidosis ↑HCO3 ↑ pH+ ↓ PaCO2 R.Alkalosis ↓HCO3

21. ABG CHANGES IN RESPIRATORY FAILURE pH PaO 2 PaCO 2 BICARBONATE Type 1 RF Normal/high low Normal/low normal Acute type 2 RF Normal/low low high Normal/rising Acute on chronic type2 RF Normal/low low high raised

22. SIGNS AND SYMPTOMS Hypoxemia Dyspnea, Cyanosis Confusion, somnolence, fits Tachycardia, arrhythmia Tachypnea (good sign) Use of accessory muscles Nasal flaring Recession of intercostal muscles Polycythemia Pulmonary HTN, Corpulmonale , Rt. HF Hypercapnia ↑Cerebral blood flow, and CSF Pressure Headache Asterixis Papilloedema Warm extremities, collapsing pulse Acidosis ( respiratory/metabolic ) ↓pH, ↑ lactic acid

23. INVESTIGATIONS ABG- gold standard , need regular serial monitoring throughout. CBC, Hb Anemia → tissue hypoxemia Polycythemia → chronic RF Urea, Creatinine LFT → clues to RF or its complications Electrolytes (K, Mg, Ph ) → Aggravate RF ↑ CPK, ↑ Troponin 1→ MI ↑CPK, normal Troponin 1→ Myositis TSH → Hypothyroidism

24. Chest x ray → Pulmonary edema → ARDS Echocardiography→rule out Cardiogenic pulmonary edema → ARDS → PAP, Rt ventricular hypertrophy in CRF ■ PFT- (FEV1/ FVC ratio) Decrease → Airflow obstruction Increase → Restrictive lung disease

25. ECG→ cardiac cause of RF → Arrhythmia due to hypoxemia and severe acidosis ■ Right heart catheterization to measure ●Pulmonary capillary wedge pressure (PCWP) ● Normal → ARDS (<18 mmHg) ● Increased → Cardiogenic pulmonary edema

26. MANAGEMENT OF ACUTE RESPIRATORY FAILURE ACUTE TYPE 1(as in case of status asthmaticus ) Correction of hypoxemia O2 administration via nasal prongs, face mask, intubation and Mechanical ventilation Goal: Adequate O2 delivery to tissues PaO2 = > 60 mmHg Arterial O2 saturation >90% NIPPV Immediately reduce work of breathing Stall endotracheal intubation Patient education about fitting of mask Strap mask for proper seal

27. - Noninvasive Ventilatory support ( N IPPV ) Mild to moderate RF Patient with imminent need for intubation should be omitted Patient should have Intact airway, Alert, normal airway protective reflexes To start, EPAP of 3-5 mmhg , then pressure increased to patient comfort, ABG parameters, respiratory rate and use of accessory muscle use. EPAP is usually sufficient

28. Mechanical ventilation. Endotracheal intubation: Indications Severe Hypoxemia Altered mental status Worsening acidosis Importance precise O2 delivery to the lungs remove secretion ensures adequate ventilation The lowest FIO2 that produces SaO2 >90% and PO2 >60 mmHg should be given to avoid O2 toxicity Ventilator setting(to avoid hyperinflation) Tidal volume:5-7 ml/kg Respiratory rate:10-18/min Plateu pressure: <30 CMH2O

29. Neuromuscular blockers should be avoided after peri -intubation With corticosteroids , produce severe , occasionally irreversible myopathy. Sedation Preferred to manage patient agitataion , rather than paralysis Lesser doses used along with patient adjusted ventilator settings. Most patients- liberated from ventilator in 4-5 days

30. MANAGEMENT OF ACUTE TYPE 2 RESPIRATORY FAILURE As in case of acute COPD exacerbation. Respiratory load is high,with barely adequate neuromuscular compliance Hence patient becomes easily tired to maintain ventilation So trivial insult in COPD patients, ends up in respiratory failure. Emergency, need immediate airway intervention. NIPPV Setting adjusted to work of breathing (after assessing tidal volume, respiratory rate and use of accessory muscle tone)

31. ENTROTRACHEAL INTUBATION. Initial setting is assist control ventilation Tidal volue:5-7ml/kg Respiratory rate:20-24 /min External PEEP of 5-10 mmhg should be applied to counteract intrinsic PEEP(reduces work of breathing without hyperinflation) High inspiratory flow rate should be used to maximize time of expiration. Spontaneous breathing trial should started after 24-48 hours Sedation : patient needs less sedation as compared to asthma patients

32. Bronchodilators and corticosteroids: reduce airflow obstruction and dynamic hyperinflation restores balance between neuromuscular compatibility and respiratory load. Antibiotics : to treat infections. Manage hypokalemia, hypophosphatemia and hypomagnesemia (causes muscle fatigue and worsen ventilation)

33. Chest physiotherapy Treatment of the underlying causes After correction of hypoxemia, hemodynamic stability Antibiotics Pneumonia Infection Bronchodilators (COPD, BA) Salbutamol reduce bronchospasm airway resistance

34. Anticholinergics (COPD,BA) (cause secretions thick) Ipratropium bromide inhibit vagal tone relax smooth muscles Theophylline (COPD, BA) (causes arrhythmia) improve diaphragmatic contraction relax smooth muscles Diuretics (pulmonary edema) Frusemide Methyl prednisone (COPD, BA, acute esinophilic pneumonia) Reverse bronchospasm, inflammation Fluids and electrolytes Maintain fluid balance and avoid fluid overload IV nutritional support To restore strength, loss of muscle mass TPN via peripheral or central line.

35. WEANING FROM MECHANICAL VENTILATION Daily spontaneous breathing trial after 48 hours with a T-piece Gradual reduction to SIMV Assess breathing : slow deep breath rather than rapid shallow RAPID SHALLOW BREATHING INDEX(RSB) Unassisted RR/min divided by tidal volume/l If value<105  spontaneous breathing is expected to be successful Finally extubate when, Stable underlying respiratory status Adequate oxygenation Intact respiratory drive Stable cardiovascular status Patient is a wake, has good nutrition, able to cough and breath deeply

36. COMPLICATIONS OF ACUTE RESPIRATORY FAILURE Pulmonary Pulmonary embolism barotrauma pulmonary fibrosis (ARDS) Nosocomial pneumonia Cardiovascular Hypotension, ↓CO Arrhythmia MI, pericarditis GIT Stress ulcer, ileus, diarrhea, hemorrhage Infections Nosocomial infection Pneumonia, UTI, catheter related sepsis Renal ARF ( hypoperfusion , nephrotoxic drugs) Poor prognosis Nutritional Malnutrition, diarrhea hypoglycemia, electrolyte disturbances

37. Chronic and acute on chronic resp failure Most common type 2 chronic – COPD PaCO 2 is raised , academia absent (kidneys retain bicarbonate-arterial pH is normal) Exacerbation causes acute on chronic Clinical feature: failure with acidemia and initial respiratory distress followed by coma. These patients lose their chemosensitivity to elevated PaCO 2 So higher supplemental oxygen will cause respiratory depression.

38. Assessment and management. Signs of CO 2 retension Confusion Flapping tremor Bounding pulse ABG is mandatory Principal aim of management is to achieve safe PaCO 2 without increasing PaO 2 and acidosis. The risk of worsening hypercapnia and acidosis should be balanced against that of hypoxia.

39. NIV Conscious patients with adequate respiratory drive, Reduce need for intubation and short hospital stay. 2. INTUBATION AND VENTILATION: Drowsy patient Lower respiratory drive Weaning and extubation will be difficult. 3. DOXAPRAM Respiratory stimulant drug. Minor and transient improvement in ABG

40. HOME VENTILATION IN CHRONIC RESPIRATORY FAILURE. Indicated for—spinal deformities, CNS hypoventilation, neuromuscular diseases. Type 1 failure gradually develops type 2 failure Signs of CO 2 retension : early morning headache and fatigue Diagnosis : sleep study, morning ABG Initially compromised ventilation will be sufficient for night time metabolic needs. Then worsens Chronic CO 2 retention Night NIV  day time NIV.

41. Perioperative respiratory failure ATELECTASIS: collapse of lung tissue with loss of volume. Prevention and management Incentive spirometry Ensuring adequate analgesia for chest and abdominal incisions Upright position Early mobilization Nasogastriac suction to alleviate abdominal secretions Paracentesis to avoid tense ascites.

42. 2. HYPOPERFUSION Inadequate delivery of oxygen to respiratory muscles coupled with excess respiratory muscle load. Eg : sepsis, acidosis Management Adequate IV fluids Increase fio 2 . Acidosis correction

43. REFERENCES Davidson’s principles and practice of medicine, 22 nd edition. Harrison’s principles of internal medicine, 19 th edition. Paul marino’s the ICU book, 4 th edition. Diagnosis and management of acute respiratory failure, harward university, Elsevier.feb 2024 . Ventilatory failure.bhakti patel , university of Chicago reviewed, april 2024.

44. Thank you.