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1. Chronic Obstructive Pulmonary Disease & Ischemic Heart Disease. Dr. Nadeem Sohail FM RTEH Muzaffargarh

2. Learning objectives of Chronic Obstructive Pulmonary Disease Basic Pathophysiology of COPD. Common Clinical Presentations of COPD. Diagnosis of COPD Treatment of COPD & complications.

3. Regarding Pathophysiology COPD all are true except: COPD is caused by cigarette smoking related to duration and pack per year smoking. COPD includes Chronic Bronchitis & Emphysema COPD is reversible after quitting smoking Maximal expiratory flow rate is reduced in COPD

4. All clinically seen in COPD patients except: Patients may have barrel shaped chest There may be tracheal tug during acute exacerbation of COPD. JVP may be raised. The aortic component is louder than pulmonic component of second heart sound. Heart sound may be barely audible.

5. Regarding Diagnosis of COPD all are true except? X-ray chest is Gold standard investigation to diagnose COPD. Forced Expiratory Volume in 1 second (FEV1) is reduced Total Lung Capacity (TLC) is increased. Xray chest may show flattening of diaphragm. Heart may be small in shape on Xray chest.

6. All are complications of COPD except Frequent chest infections Respiratory Failure Right Heart Failure Cirrhosis of liver Hepato-pulmonary syndrome

7. Chronic Obstructive Pulmonary Disease Chronic bronchitis and emphysema, which are two distinct pathologic conditions, share similar symptoms and frequently coexist. COPD is a chronic lung disease defined by persistent respiratory symptoms and airflow limitation or obstruction that is not fully reversible. COPD is a chronic, slowly progressive disease and is the fourth most common cause of death in US population.

8. Pathophysiology of COPD COPD is an inflammatory condition. Cigarette smoke and other irritants activate both macrophages and epithelial cells within the respiratory tract. Oxidative stress from irritants and inflammatory cells may lead to additional inflammation and tissue destruction. As the degree of inflammation increases, airflow obstruction worsens and the ability to fully exhale decreases. Inhalation is initiated before exhalation is completed, resulting in dynamic hyperinflation termed air trapping which is seen as an increased anteroposterior diameter of the chest and flattening of the diaphragm on chest radiographs.

9. Continued Pathophysiology of COPD The diaphragmatic flattening limits the ability to increase breath volume during exertion. compensatory use of accessory muscles to increase tidal volume and increased respiration rate increase minute ventilation. These changes increase the work of breathing and contribute to the sensation of dyspnea in patients with COPD.

10. Chronic Obstructive Pulmonary Disease Chronic Bronchitis Defined as a clinical diagnosis requiring patients to have a chronic cough productive of sputum for at least 3 months a year for at least 2 consecutive years in the absence of other diseases, such as asthma, bronchial/lung tumors, bronchiectasis, or chronic lung infections. Emphysema Whereas Emphysema is a pathologic diagnosis, consists of enlargement of the terminal air spaces due to destruction of alveolar walls.

11. Clinical Features of Chronic Obstructive Pulmonary Disease History: Smoking – Most important factor including duration, pack per smoking, Passive exposure is also risk factor. Exposure to irritants including biofuel gas, industrial fuel. Childhood respiratory Tract Infections. Family History particularly for Alphas 1 Trypsin deficiency. Shortness of breath at exertion is most important and initial symptom of COPD and should be suspected in a patient above age of 40 years if there is risk factor for COPD. Cough, can be dry or productive pointing towards Chromic Bronchitis or superadded infection.

12. Clinical Features of Chronic Obstructive Pulmonary Disease Shortness of breath in COPD is assessed by Modified Medical Council Dyspnea Scale

13. Clinical features of Chronic Obstructive Pulmonary Disease Other symptoms are non specific include: Orthopnea Generalized weakness/fatigue Wasting in advanced stage, loss of appetite Ascites/abdominal distension as complication of heart failure or cardiac cirrhosis Jaundice due to hepatic congestion

14. Clinical features Chronic Obstructive Pulmonary Disease Physical examination may have no signs on physical examination at all in early stages of COPD In advance cases: Inspection may show: Increased Respiratory Rate Barrel shaped chest ( Increased AP diameter of chest) in Emphysema Tracheal tug specially during acute exacerbation including using accessory muscle of respiration. There may be jugular venous distention during expiration when semirecumbent position. Edema feet due to impaired clearance of sodium & water by hypoxic kidneys in advance in COPD, not a sign of Right Heart Failure

15. Continued Clinical Features of Chronic Obstructive Pulmonary Disease On Auscultation of chest breath sounds: May be diminished only Prolonged expiration Inspiratory and expiratory wheezes and rhonchi There may be absent breath sounds in COPD patient with respiratory Failure. Vocal Fremitus reduced Cardiac sounds may be diminished or absent with loud Pulmonic component of second heart sound. Percussion note will be hyper resonant.

16. Diagnosis of Chronic Obstructive Pulmonary Disease Radiological : X-ray Chest PA view. Not a sensitive investigation to diagnose COPD.

17. Diagnosis of Chronic Obstructive Pulmonary Disease

18. Diagnosis of Chronic Obstructive Pulmonary Disease Spirometry( Pulmonary Function Test) Gold standard investigation to Diagnose COPD. Showing Obstructive Pattern on flow volume curves. Total Lung Capacity is increased FEV1 is reduced. Other investigation also include Alpha1 anti trypsin levels if young patient having early onset COPD, Blood counts , ABGs in acute exacerbation to asses for respiratory failure, ECG, Echocardiography.

19. Chronic Obstructive Pulmonary Disease Key Points in COPD After a diagnosis of COPD has been established, the initial assessment focuses on disease severity, which is determined using a combination of symptoms, degree of airflow obstruction on spirometry, history of acute exacerbations, and presence of comorbid conditions. . Patients who have had two or more acute exacerbations within the last year, who have an FEV1 , of less than 50% of predicted, or who have ever been hospitalized for an acute exacerbation are considered to be at high risk for recurrent acute exacerbations.

20. Chronic Obstructive Pulmonary Disease

21. Complications of Chronic Obstructive Pulmonary Disease Acute Exacerbation , Most dangerous and frequent cause of mortality Recurrent respiratory tract Infections. Right Heart Failure Cardiac Cirrhosis Thromboembolism Complications related to steroid replacement including Iatrogenic Cushing as well suppression of Hypothalamic-Pituitary-Adrenal axis suppression.

22. Management of Chronic Obstructive Pulmonary Disease COPD not reversible , but certain measures stop the progression , worsening of lung functions Most important is to QUIT SMOKING, avoid biofuel gas exposure. For smoking cessation counselling, may need multiple cessations offering group counselling, explaining benefits of quitting smoking, offer nicotine replacement patches, gums, medications etc. Vaccinations including Influenzae & pneumococcal vaccination

23. Management of Chronic Obstructive Pulmonary Disease Pharmacological Management: Pharmacologic therapies in COPD are used to reduce symptoms, improve quality of life, and reduce the frequency and severity of exacerbations. Bronchodilators are mainstay of therapy in COPD irrespective of the severity of the disease. Bronchodilators or other inhalers are prescribed at any stage and the clinician should ensure that the patient receives education on proper inhaler technique.

24. Management of Chronic Obstructive Pulmonary Disease Inhaled bronchodilators include Beta agonists and anticholinergics/antimuscarinic agents. Both are available as short-acting and long-acting inhalers and improve symptoms and expiratory airflow. SABAs and muscarinic antagonists result in similar bronchodilation, and either can be used as monotherapy. However, dual treatment results in a greater degree of bronchodilation and expiratory airflow which may lead to symptom benefit in selected patients. If short acting bronchodilators are insufficient to control symptoms in patients with more severe disease, a long acting bronchodilator-either a LABA or a LAMA can be added. A second long-acting bronchodilator from the alternate bronchodilator class may be added in resistant cases/severe symptoms may result in clinical improvement.

25. Management of Chronic Obstructive Pulmonary Disease Inhaled Glucocorticoids Inhaled glucocorticoids are typically used only in combination with a long-acting bronchodilator for treatment of COPD. Inhaled glucocorticoids are not used alone unless a patient is not able to use long acting bronchodilators Inhaled glucocorticoids used alone and in combination with long-acting bronchodilators improve lung function and reduce symptoms and exacerbations in patients with moderate to severe COPD, but they are associated with an increased risk for pneumonia. In patients with severe COPD, triple inhaler therapy with a LABA, a LAMA, and an inhaled glucocorticoid may provide additional symptom benefit and reduced exacerbations.

26. Management of Chronic Obstructive Pulmonary Disease Other Pharmacological agents: Oral Glucocorticoids: given only during time of acute exacerbation. Oral methylxanthines (aminophylline and theophylline) are now rarely used to treat COPD. Theophylline has been shown to improve functional capacity and reduce the number of exacerbations. However. it has a narrow window between therapeutic and toxic dosages and is therefore only used for patients with advanced COPD who have refractory symptoms not controlled by standard therapy. Roflumilast is a selective phosphodiesterase 4 inhibitor that is used to reduce the frequency of exacerbations in patients with severe COPD who have primarily symptoms of chronic bronchitis.

27. Management of Chronic Obstructive Pulmonary Disease Other Agents: Macrolide antibiotics have inflammatory and antimicrobial effects. Long term macrolide therapy may reduce the frequency of exacerbations when prescribed for patients with severe COPD and a history of frequent exacerbations. Mucolytics and antitussives are not routinely used in the management of COPD but may provide some symptomatic relief in patients with significant sputum production.

28. Management of Chronic Obstructive Pulmonary Disease Nonpharmacologic Therapy: Pulmonary Rehabilitation is a comprehensive program that combines exercise training, nutritional support, education, and social support for patients with chronic lung conditions. It has been shown to relieve symptoms, improve quality of life, and decrease frequency of hospitalizations in patients with COPD. Oxygen Therapy as supplemental oxygen has been shown to improve quality of life and decrease mortality in patients with COPD and resting hypoxemia with an arterial Po, of 55 mm Hg or less or an oxygen saturation (as measured by pulse oximetry) of 88%, or less. Patients with cor -pulmonale, heart failure, or erythrocytosis should be offered the use of supplemental oxygen if their Po2 is 59 mm Hg or less or their oxygen saturation is 89% or less.

29. Non Invasive Positive Pressure Ventilation (NPPV), also termed noninvasive mechanical ventilation, can be used for acute and chronic respiratory failure and in patients with a COPD exacerbation and acute hypercapnic respiratory failure with acidosis. Surgery Transplant

30. Ischemic Heart Disease/Coronary Artery Disease Learning Objectives Risk Factors for IHD/CAD. Classification of IHD/CAD. Pathogenesis Clinical Manifestation and diagnosis Management strategies and referral Complications.

31. Ischemic Heart Disease/Coronary Artery Disease Risk Factors

32. Emerging risk factors for IHD/CAD -Metabolic syndrome -Triglyceride - Lp (a) -Lp-PLA2 -Fibrinogen -Homocysteine -Urine microalbuminuria/creatinine ratio -Hs CRP -Impaired fasting glucose (100-125 mg/dl per ADA)

33. Ischemic Heart Disease/Coronary Artery Disease Classification/Types of IHD/CAD

34. Pathogenesis of Ischemic Heart Disease/Coronary Artery Disease Atherosclerosis is a progressive disease The process begins in childhood and has clinical manifestations in late adulthood Advanced lesions are a result of three processes: Lipid accumulation Accumulation of intimal smooth muscle cells, macrophages, T-lymphocytes Formation of connective tissue matrix by proliferated smooth muscle cells

35. Ischemic Heart Disease/Coronary Artery Disease Evaluation for Angina includes a focused history eliciting information on the following characteristics of symptom of chest pain/discomfort: Quality Location Radiation Duration Aggravating factors (exertion, Anxiety, meals) Relieving factors Associated symptoms (shortness of breath. nausea. Diaphoresis) Some demographic groups including women, patients with diabetes mellitus. may present with atypical symptoms including exertional dyspnea. nausea. or worsening fatigue.

36. Ischemic Heart Disease/Coronary Artery Disease Evaluation for Angina Stable angina pectoris is reproducible angina (discomfort or pressure of the chest, neck, or arms) of at least 2 months duration that is precipitated by a stable level of exertion or emotional stress and is relieved with rest. Unstable angina is new onset angina or angina occurring at a relatively low level of exertion, occurring at rest or accelerating in frequency or severity. Unstable angina is associated with increased short term risk for acute myocardial infarction.

37. Ischemic Heart Disease/Coronary Artery Disease After initial evaluation of stable further testing will be to do ECG to search for ongoing ischemia. After excluding active cardiac ischemia patient having high probability of Angina/IHD/CAD will be assessed by Stress/Exercise ECG Stress Echocardiography Coronary Angiography/CTY angiogram for Coronary Vessels and will be decided by Cardiologist

38. Ischemic Heart Disease/Coronary Artery Disease General Approach to management of Anginal Patients will be: Address for risk factors, smoking cessions Cardioprotective Medications including Aspirin reduces the risk for Ml and cardiovascular death in patients with stable angina. Guidelines recommend low dose aspirin (75-162 mg/d) for secondary prevention because it is as effective as high-dose aspirin (325 mg) in preventing MI and confers a lower bleeding risk. In aspirin intolerant patients, clopidogrel, alternative. Statin therapy remains a cornerstone of secondary prevention because it has been shown to reduce the risk for MI, death, and stroke. High intensity statin therapy (atorvastatin, 40-80 mg/d, or rosuvastatin, 20-40 mg/d) decreases the LDL cholesterol level by 50%, or more. ezetimibe or proprotein convertase subtilisin/ kexin type 9 (PCSK) inhibitors can be add on therapy or alternate if side effects or intolerant to statin therapy.

39. Ischemic Heart Disease/Coronary Artery Disease General Approach to management of Anginal Patients will be: ACE inhibitor therapy is indicated for stable angina if there is concomitant diabetes. chronic kidney disease. left ventricular (LV) dysfunction (ejection fraction less than 40%, Heart Failure or Prior H/O MI. Antianginal medications including beta blockers, calcium channel blockers and nitrates are all indicated. Coronary Revascularization by Cardiac Surgeon.

40. Acute Coronary Syndrome ( ACS) Presents , most commonly have chest pain that is more prolonged, severe, worse than anginal chest pain, described as more severe crushing/stabbing/squeezing/pressure like worst pain ever. In diabetes and elderly may be silent May present atypically as confusion, weakness, sweating, diaphoresis, arrythmias, heart blocks. First step will be ECG and cardiac blood markers to diagnose as:

41. Ischemic Heart Disease/Coronary Artery Disease Initial Medical Therapy for Acute Coronary Syndromes: All patients presenting with ACS should receive a loading dose of aspirin. supplemental oxygen for oxygen saturation less than 90%, to 92% therapy to relieve symptoms (nitrates) therapy to reduce infarct size (beta blockers. ACE inhibitors) high intensity statin therapy, and antithrombotic therapy (antiplatelet agents and anticoagulants)

42. Ischemic Heart Disease/Coronary Artery Disease Primary Percutaneous Coronary Intervention PPCI refers to the process by which an emergency medical provider activates a team of clinicians to initiate emergent coronary angiography and PCI in patients with STEMI. The goal time from first medical contact until PPCI is 9O-120 minutes or less. Because rates of achieving vessel patency are higher and more reliable with PPCI than with thrombolysis, PPCI is the preferred method of treating STEMI when the patient presents to a PCl -capable hospital. Thrombolytic Therapy. If primary percutaneous coronary intervention (PCI) is not available within 120 minutes of first medical con tact, patients with ST elevation myocardial infarction should receive thrombolytic therapy and be transferred urgently to a PCl -capable center

43. For NSTEMI , Risk calculation system TIMI

44. Ischemic Heart Disease/Coronary Artery Disease Complications can include: Arrythmias Acute Heart Failure Ventricular wall rupture Acute Mitral Regurgitation Pericarditis Chronic Heart Failure Post MI Anginal symptoms

45. Ischemic Heart Disease/Coronary Artery Disease Self Assessment Questions Atherosclerotic Plaque buildup can begin in childhood. True False

46. Ischemic Heart Disease/Coronary Artery Disease Self Assessment Questions Coronary artery disease is … A buildup of plaque in the arteries that carry blood to the heart The same thing as coronary heart disease Sometimes called hardening of the heart’s arteries All of the above

47. Ischemic Heart Disease/Coronary Artery Disease Self assessment What causes plaque to build up in the arteries? Smoking High Blood pressure High Cholesterol High Blood sugar All of the above

48. Ischemic Heart Disease/Coronary Artery Disease Self Assessment What are the noticeable symptoms of CAD? Chest Pressure or discomfort Shortness of Breath Fatigue Syncope All of the above

49. Ischemic Heart Disease/Coronary Artery Disease Self Assessment Which lifestyle change WON'T help treat CAD? Quitting smoking Eating a healthy, low-fat, low-sodium, high-fiber diet Getting regular exercise Managing stress Maintaining a healthy weight Following a gluten-free diet

50. Ischemic Heart Disease/Coronary Artery Disease Self Assessment A 45-year-old woman presents with ongoing chest pain. Immediate observations reveal BP 140/80 mmHg, heart rate 90 bpm, and saturations 99% on room air. What should you do next? Administer oxygen Administer analgesia Give aspirin 300 mg Perform a 12-lead ECG

51. Ischemic Heart Disease/Coronary Artery Disease Self Assessment A 60yo man presents to the ED with chest pain which started suddenly in the left chest whilst he was lifting a heavy box. The pain is difficult to localize but after 1 hour pain localized to the left side of the lower thoracic back. He has had H/O mid thoracic pain. He is sweating and anxious but has no shortness of breath. Blood pressure is 160/90 mmHg, heart rate is 100 bpm and saturations are 99% on room air. The ECG does not show acute ST change. D-dimer is 1700 ng/mL (normal < 500 ng/mL), and troponin is awaited. Based on the information available, what is the most likely diagnosis? Acute coronary syndrome Pulmonary embolism Acute aortic syndrome Musculoskeletal pain

52. Ischemic Heart Disease/Coronary Artery Disease Self Assessment 55-year-old woman in clinic who has been referred with recent c/o off & on chest pains. You feel that the nature of the pains is atypical for ischemia although they are reproduced with exertion. She has no identifiable risk factors for ischemic heart disease and the resting ECG is normal. What would you recommend? CT coronary angiogram Reassure—no further tests required Invasive coronary angiogram Exercise treadmill test