Chronic Obstructive Pulmonary Disease and ICU management.pptx

COPD and how can it be managed in the ICU

1. Copd and its icu management Presented by - Smrithi Rajeev M.Sc. Respiratory Therapy

2. definition Chronic obstructive pulmonary disease can be defined as a disease characterized by progressive airflow limitation that is not fully reversible The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. COPD frequently results in significant activity limitation, permanent disability and frequent utilization of costly medical resources,.

3. Gold definition The Global Initiative for Chronic Obstructive Lung Disease (GOLD) now provides the following working definition: “ Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lung to noxious particles or gases. “

4. The most widely used definition evaluates the severity of exacerbation based on three symptoms Worsening dyspnea Increased sputum production Increase in sputum purulence

5. etiology Cigarette smoking Alpha 1 antitrypsin deficiency Childhood respiratory illnesses Outdoor indoor air pollution (cooking with coal, wood, charcoal) Occupational dust and chemical exposure

6. Pathophysiology Structural (excessive mucus production, mucus gland hypertrophy, inflammatory oedema) and functional airway narrowing (bronchoconstriction, loss of elastic recoil, and destruction of alveoli) causes expiratory airflow limitation. Consequences of severe, chronic airflow obstruction. 1. Reduced flow rates, limiting minute ventilation. 2. Ventilation/perfusion (V/Q) mismatch. 3. Air trapping, hyperinflation, and increased airway resistance place elevated workloads on the respiratory muscles and can result in muscle fatigue 4. CO 2 retention due to increased dead space and a shift of the haemoglobin oxygen binding curve.

7. Reference - Marin Kollef , Warren Issakow , The Washington Manual of Critical Care; 2nd edition; Chapter 12; Acute Exacerbations of Chronic Obstructive Pulmonary Disease , pg. no 76

8. Diagnosis – Chest radiograph

9. Abg findings Respiratory acidosis with worsening hypoxemia (worsening hypercapnia)

10. Pulmonary function test

11. Laboratory findings Emphysema Chronic Bronchitis

12. Management – for acute exacerbation Bronchodilator therapy Short acting beta 2 agonists – Albuterol, Levalbuterol, Pirbuterol Anticholinergic agents – Ipratropium and Tiotropium bromide Oxygen therapy – oxygen therapy should be given through nasal prongs or simple face mask to target saturation between 88% - 92% and PaO 2 > 60mmHg Systemic corticosteroids Antibiotics Nutritional support Identifying and treating the underlying cause

13. Treatment of acute exacerbation of COPD with antibiotics has shown to be beneficial in patients with moderate to severe exacerbation Streptococcus pneumoniae, moraxella catarrhalis and heamophilis influenza

14. Reference - Marin Kollef , Warren Issakow , The Washington Manual of Critical Care; 2nd edition; Chapter 12; Acute Exacerbations of Chronic Obstructive Pulmonary Disease , pg. no 77

15. Indications for Icu admission Severe dyspnea with inadequate response to initial resuscitative treatment Altered mental status Persistent or worsening hypoxemia or respiratory acidosis despite medical therapy Need for invasive or non invasive mechanical ventilation Hemodynamic instability

16. Reference - Marin Kollef , Warren Issakow , The Washington Manual of Critical Care; 2nd edition; Chapter 12; Acute Exacerbations of Chronic Obstructive Pulmonary Disease , pg. no 78

17. Noninvasive positive-pressure ventilation (NIPPV). The favored mode of assisted ventilation in patients with respiratory acidosis and/or severe dyspnea with clinical signs of respiratory muscle fatigue. Effectively reduces intubation rate, relieves dyspnea, improves acid- base status, decreases hospital length of stay, and reduces in hospital mortality and longer-term mortality at 1 year.

18. Pressure support ventilation, often begun at an inspiratory positive airway pressure (IPAP) of 8 cm H 2 O an expiratory positive airway pressure (EPAP) of 5 cm H 2 O and titrated according to patient comfort up to a goal inspiratory to expiratory pressure difference of 10 cm H 2 O to ensure adequate unloading of respiratory muscles. Can begin at maximal pressure (i.e., 15 IPAP, 5 EPAP) if in severe distress and tolerated. Contraindications to NIV : respiratory arrest, cardiovascular instability, severely impaired mental status/excessive agitation, recent craniofacial surgery, inability to clear secretions or to protect the airway.

19. Intubation and mechanical ventilation. a . Indications. i . Failure of NIPPV: unchanging dyspnea/respiratory distress or worsening ABG within 2 hours. ii. Severe acidosis (pH < 7.2) and worsening hypercapnia (Paco, > 60 mm Hg). iii. Life-threatening hypoxemia (Pao/ Fio , < 200 mm Hg). iv. Altered mental status or inability to clear secretions and to pro- tect the airway. v. Hemodynamic instability. b . Objectives: support of gas exchange and to rest the respiratory muscles .

20. Ventilator settings Mode – Volume/Pressure Mode with assist control Rate – 18-20 breaths/ minute Tidal volume – 8ml/kg PEEP – 0-5 cmh20 FiO2 to maintain saturation between 88% – 92% High flows should be maintained in order to allow for an inspiratory to expiratory ratio I:E – 1:4

21. There are other medical therapies that have been used to treat acute exacerbations of COPD like Mucolytic medications, chest physiotherapy and use of methylxanthine bronchodilators DVT and stress ulcer prophylaxis Nutritional support is vital in these patients but excessive carbohydrates must be avoided as it can increase the level of CO 2 production.

22. Dynamic hyperinflation or auto PEEP (positive end expiratory pressure) is a dangerous consequence of inadequate ventilators and can result in hypotension and cardiovascular collapse. Lower tidal volumes, respiratory rate, and higher inspiratory flow will increase time spent in exhalation and decrease auto PEEP must be titrated carefully to also not worsen respiratory acidosis and hypoxemia. AutoPEEP is measured on the ventilator with an expiratory hold maneuver and should be suspected in any patient who develops hypotension on mechanical ventilation for an exacerbation of COPD.

23. Smoking Cessation Vaccinations – Pneumococal and Influenza vaccines Pulmonary rehabilitation (PR) Prevention

24. 1. Assessment 2. Exercise Training Aerobic Exercise : Such as walking or cycling to improve cardiovascular health and increase stamina. Strength Training : Focusing on major muscle groups to improve overall strength. Breathing Exercises : Techniques like diaphragmatic breathing or pursed-lip breathing to improve ventilation and make breathing easier 3. Education Patients receive education about COPD, its management, and how to cope with the symptoms and limitations it imposes. Topics might include medication management, nutritional advice, and strategies to conserve energy. 4. Self-Management and Behavioral Intervention . Pulmonary rehabilitation

25. 5. Nutritional Counseling 6. Psychosocial Support

26. GOLD Guidelines – Updated The 2023 GOLD guidelines for COPD exacerbations include: Short-acting inhaled beta2-agonists, with or without short-acting anticholinergics, as the initial bronchodilators Triple therapy reduces mortality and exacerbations in patients with moderate-to-very-severe COPD and a prior history of exacerbations More emphasis is placed on exposure to indoor biomass smoke and air pollution in low- and middle-income countries as a risk factor

27. references Marin Kollef , Warren Issakow , The Washington Manual of Critical Care; 2nd edition; Chapter 12; Acute Exacerbations of Chronic Obstructive Pulmonary Disease , pg. no 76 Irwin and Rippe’s Manual of Intensive Care medicine ; 6 th edition ; Chapter 42 ; Chronic Obstructive Pulmonary Disease – pg. no. 312