Cor Pulmonale & Respiratory Failure

1. Cor Pulmonale&Respiratory Failure Dr M Prins With acknowledgement to: Dr S R Dawadi

2. Please note These slides are complimentary to the information in Davidson’s and does not replace the textbook!

3. Cor pulmonale = Pulmonary heart disease = Right ventricular enlargement ( hypertrophy and / or dilatation) secondary to abnormality of Respiratory System.

4. Components of Respiratory system - • Gas exchanging organ - Lungs and its circulatory system • Pump that operates the ventilation of lungs - Thoracic cavity and related respiratory muscles • Controller - Areas in brain and related nerve tracts & fibers

5. Causes leading to Cor pulmonale - • Gas exchanging organ • COPD • Interstitial lung diseases • Thrombo-embolic diseases • Pump • Kyphoscoliosis • Guillian-Barre syndrome • Myasthenia gravis • Controller • Sleep apnea syndrome • Primary alveolar hypoventilation • Post encephalitis

6. Sequence of events - AcidemiaHypoxia Pulmonary Vessels Viscous Idiopathic Vasoconstriction Obliteration Blood PAH Pulmonary Hypertension RV Hypertrophy / Dilatation Rt. Heart Failure

7. Classification - • Acute–massive pulmonary embolism COPD – acute decompensation after resp. infection * acute dilatation without prior hypertrophy • Chronic –COPD, ILD recurrent PE * slow development of hypertrophy and dilatation

8. Symptoms & signs - • Loud P2, Parasternal heave • 3/6 pan systolic murmur over LSB increasing with inspiration • Raised JVP, Pedal edema, • Tender, smooth, pulsating hepatomegaly • + Ascitis

9. Respiratory Failure = Condition in which Respiratory System fails in one or both of its gas exchanging functions Oxygenation of - mixed CO2 elimination from - venous blood Development - Acutely = rapid and life threatening - Chronically = slow and may be unapparent

10. Components of Respiratory system - Gas exchanging organ - Lungs and its circulatory system Pump that operates the ventilation of lungs - Thoracic cavity and related respiratory muscles Controller - Areas in brain and related nerve tracts & fibers

11. Types of Respiratory Failure - • Type I = Hypoxemic respiratory failure * PO2 < 60 mmHg * PCO2 Low or Normal Ventilation perfusion mismatch / shunts • Type II = Hypercapnic respiratory failure * PO2 < 60 mmHg * PCO2 > 45 mmHg Hypoventilation

12. Hypoxia : Dyspnoea Central cyanosis Agitation Restlessness Confusion Hypercapnia : Headache Peripheral Vasodilatation Tremor / flap Bounding pulse Drowsiness Coma Clinical features

13. Classification - Respiratory Failure Acute Chronic Type I Type II Type I Type II Po2 - Pco2 - pH - HCO3 -

14. Acute Respiratory Failure - Type I Type II CausesPneumonia Acute asthma Pulmonary embolus Acute foreign body Pulmonary edema Narcotic drugs Pneumothorax Muscle paralysis ARDS Brainstem lesion TherapyMaintain Airway Maintain airway Treat the disease Treat the cause High-concentration O2 Mechanical ventilation Mechanical ventilation or tracheostomy

15. Chronic Respiratory Failure - Type IType II CausesEmphysema COPD Lung fibrosis Primary alveolar hypovent. Right –to-Left shunt Kyphoscoliosis Anemia Ankylosing spondylitis Therapy -Treat the disease - Treat the disease - Controlled long-term - Controlled long-term oxygen oxygen - Ventilatory support if necessary

16. Acute on Chronic Type II respiratory failure • Further insult on stable chronic condition • Acidemia, worsening hypercapnea, drowsiness and coma. • Causes(precipitating events) – Airway infections Bronchospasm Pneumothorax Sedative drugs Pulmonary embolus Cardiac failure Retention of secretions Trauma ( head injury, rib fracture )

17. Case studyPatient’s History • 76 year old male patient • 40 pack year smoking history • Diagnosed 4 years ago with COPD • Now complaining of – worsening SOB - increased sputum - swollen legs - RUQ pain • No orthopnoea or PND

18. Physical Examination • Plethoric, Central cyanosis, resp. distress • Raised JVP, Bilateral pedal edema, • Hyper inflated chest, Reduced breath sounds, Diffuse end expiratory wheezes • Parasternal heave, Loud P2, 3/6 pan systolic murmur over LSB increasing with inspiration • Tender, smooth, pulsating 6 cm hepatomegaly • No spleen palpable, No ascitis

19. Investigations • FBC – Hb 20,2; Hct 0,614; WCC 8,3; Plt 215 • Arterial blood gas – pH 7,34 (N) Pco2 52 mmHg ( ) Po2 54 mmHg ( ) Hco3 32 mmol / l ( ) O2Sats 86% ( )

22. Symptoms & signs - • Hyper inflated chest, Reduced breath sounds, Diffuse end expiratory wheezes • Plethoric, Central cyanosis, resp. distress • Parasternal heave, Loud P2, 3/6 pan systolic murmur over LSB increasing with inspiration • Raised JVP, Pedal edema, • Tender, smooth, pulsating 6cm hepatomegaly • No spleen palpable, No ascitis

23. Clinical problem - • COPD ( etiology – smoking) - Cor pulmonale, features of right heart failure - Secondary polycythaemia - Chronic Type II respiratory failure

24. Therapy - • Before RHF ensues - Decrease RV workload ( reduce PHT) - treatment of underlying cause - prompt achievement of arterial oxygenation • After RHF has developed - Cardio tonic measures – rest; diuretics - Oxygen

25. Long Term Oxygen Therapy • Continuous: = For > 16 hours / day - resting PO2 < 55 mmHg or O2 saturation < 88% - resting PO2 55 – 59 mmHg or O2 SATS. < 89% but with - pulmonary hypertension - Cor pulmonale - polycythaemia (Hct > 56%) • Non-continuous: - during exercise PO2 < 55mmHg or O2 SATS< 88% - during sleep if - hypoxia or- pulm hpt, daytime somnolence cardiac arrhythmia

26. Long-term O2 therapy Benefits : - improves survival - symptomatic improvement in effort tolerance - reduces polycythaemia - prevents progression of pulm. hypertension Aim : - PO2 > 60mmHg without worsening PCO2 - O2 saturation > 90%

27. Diuretics therapy Decrease RV filling volume Reduction of peripheral edema Improve function of both RV and LV Great caution required Volume depletion with reduced cardiac output Hypokalemic metabolic alkalosis ( reduce ventilatory drive) Cardiac arrhythmia ( electrolytes and acid base imbalance) Loop diuretic + spironolactone

28. Venesection Indication Polycythemia Aim Hkt 55

29. Conclusion • Development of Cor pulmonale indicates poor prognosis • Left heart diseases must be excluded prior to diagnosis • Varieties of diseases of respiratory system should be considered • Co-existence of multiple diseases possible • Oxygen and diuretics are mainstay of therapy

30. Oxygen Therapy Dr M Prins Div Pulmonology Dept of Internal Medicine

31. Clinical Significance of PaO2 and SaO2 values TE Oh. Intensive Care Manual

32. TE Oh. Intensive Care Manual

33. Oxygen Cascade

34. Ganong WF. Review of Medical Physiology

35. MRC 1981 87 patients 3 years No oxygen 45 patients 2 L/min: 15 hours/day 42 patients 19 died 30 died Lancet 1981

36. NOTT (USA) 1980 203 patients 12 hours 19 hours continuous • Follow-up for 19 months • Added one liter during sleep/exercise • Mortality • 12 hours 21% • 19 hours / continuous 11% Ann Intern Med 1982

37. Vital Air Home Heallthcare

38. Indications for Long Term Oxygen Therapy (1) • Chronic obstructive pulmonary disease: • Non-smokers with stable, severe COPD (FEV1<1,5l) • PaO2 < 55 mmHg • With or without hypercapnia (PaCO2>45mmHg) • Disease must be stable for 3 months after exacerbation

39. Indications for Long Term Oxygen Therapy (2) • Other lung disorders with respiratory failure: • Diffuse interstitial lung disease • Cystic fibrosis • Bronchiectasis • Primary or metastatic lung tumors

40. Indications for Long Term Oxygen Therapy (3) • Hypoxia-related symptoms / conditions that may improve with oxygen therapy: • Pulmonary hypertension • Congestive heart failure due to Cor pulmonale • Erythrocytosis • Impairment of the cognitive process

41. Guidelines for Long Term Oxygen Therapy The aim of long term oxygen therapy is to maintain oxygen saturation above 90%

42. Oxygen Delivery Methods • At least 15 hours per day • Start at • 24% • 1-2 l/min • Nasal cannulae • Increase gradually to avoid CO2 buildup • Aim: Saturation 90%

43. Dual-prong nasal Cannula • Standard in stable hypoxemic patient • Low flow of pure oxygen • Each litre per minute adds 3-4% to FIO2: • 1 L/min increase FIO2 to 24% • 2 L/min increase FIO2 to 28% • 3 L/min increase FIO2 to 32%

44. Face Masks Smith RA. Oxygen Therapy. Critical Care 3rd ed 1997

45. Oxygen delivery systems: 1. Oxygen Concentrators • Air 21% oxygen, 78% nitrogen, 0,9% argon, 0,1% other • Adsorbent material remove nitrogen from air • Deliver 95,5% oxygen into tank Picture: Afrox

46. Oxygen Concentrator Afrox

47. Oxygen Concentrators • ADVANTAGES • Safe, no fire hazard • Easy to operate • No inconvenience to replenish as with cylinders • Easy to move around in home with extended supply line • Easy to transport • Cost effective • Not unsightly A • DISADVANTAGES • Dangerous with power failure • When travelling a small cylinder or other equipment needed • Electricity needs to be paid • Electricity is essential National Guideline on LTOT: Dept Health

48. Medical Oxygen Cylinders Afrox

49. Oxygen Cylinders • Disadvantages • Costly • Dangerous fire hazard • Not easy to open flow meter • Can be damaged while transporting • Older and sick patients cannot handle the cylinders • Large cylinders are heavy and can cause damage or injury • Unsightly, many cylinders have to be accommodated • Patients try to save on oxygen and benefit is lost if used incorrectly • Advantages • Needs no electricity • Small cylinder is easy to handle when travelling

50. Medical Oxygen Cylinders VitalAir