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Heart failure

Heart failure. Laszlo L. Tornoci Inst. Pathophysiology Semmelweis University. Definition.

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Heart failure

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  1. Heart failure Laszlo L. Tornoci Inst. Pathophysiology Semmelweis University

  2. Definition A clinical syndrome characterized by progressive weakening of the heart as a pump, causing complex changes in processes at systemic, organ and cellular levels, finally leading to premature myocardial cell death.

  3. Demography • Prevalence of symptomatic HF 0.4-2.0%, 6-10% in people over 65 years • Disease of the elderly (mean age > 70 years) • Prevalence is rising • Bad prognosis: 5-year survival rate < 50% • Mortality (even if age adjusted) is increasing

  4. Classification • Acute/chronic HF • Forward/backward failure • Systolic/diastolic dysfunction • Left/right sided HF

  5. Complaints • Left heart, backward failure • dyspnea • orthopnea • paroxysmal nocturnal dyspnea • Left heart, forward failure • weakness, fatigue • nycturia

  6. Physical findings • Right heart, backward failure • edema, hydrothorax • congestive hepatomegaly • distension of neck veins • Left heart, backward failure • pulmonary rales • Miscellaneous • cyanosis • S3 gallop

  7. Causes of heart failure • Underlying (true) causes • Precipitating causes (which make the clinical condition worse, ‘decompensate’ the patient)

  8. Underlying causes • Ischemic heart disease • Hypertension • Valvular heart disease • Cardiomyopathies • Other

  9. Precipitating causes 1. Increased workload • Increased cardiac output • metabolic need (fever, infection, hyperthyroidism) • volume overload (renal failure, high sodium intake) • Pressure overload • high BP • pulmonary embolism

  10. Precipitating causes 2. • Cardiac ischemia • Decreased efficiency (arrhythmias) • Drug effect • Endocarditis, myocarditis Same workload, but weaker heart

  11. Terms • Inotropy (contractility) • Lusitropy (capability to relax or be filled) • Preload • Afterload

  12. Frank-Starling law isometric contractions

  13. Contractility (inotropy)

  14. Pressure-volume (PV) loop

  15. Increasing inotropy

  16. Decreasing inotropy(systolic dysfunction)

  17. Decreasing lusitropy (diastolic dysfunction)

  18. Cardiac output vs. right atrial pressure

  19. Effect of contractility on cardiac output

  20. sympathetic stimulation hypertrophy ischemia, AMI valvular heart disease high BP parasympathetic stimulation sympathetic inhibition myocarditis Some of the factors affecting contractility increase decrease

  21. Venous return curve

  22. Venous return curves

  23. Determinants of MCFP

  24. Cardiac output – venous return

  25. Effect of sympathetic stimulation

  26. Fluid retention in chronic HF

  27. Neurohormonal response to HF Overview • Hemodynamic defense reaction • Salt and water retention • Vasoconstriction • Cardiac stimulation • Inflammatory reaction • Hypertrophic response

  28. torlasz: more examples are needed Neurohormonal response Effects by levels • Systemic • Organ • Cellular Fluid retention, fatigue, cachexia Hypertrophy, remodeling Change of myosin isoforms, Ca++

  29. Neurohormonal response to HF Overview • Hemodynamic defense reaction • Salt and water retention • Vasoconstriction • Cardiac stimulation • Inflammatory reaction • Hypertrophic response

  30. Hemodynamic defense reaction

  31. Hemodynamic defense reaction Effects: • Salt and water retention • Vasoconstriction • Cardiac stimulation: contractility , faster relaxation, HR  • Cell growth and proliferation Mediators: Stimulatory Inhibitory catecholamines (per. eff.) angiotensin II ADH endothelin ANP NO bradykinin dopamine cathecolamines (central eff.)

  32. Hemodynamicdefense reaction Adaptive (beneficial), short term responses

  33. Hemodynamicdefense reaction Maladaptive (not beneficial), long term responses

  34. Neurohormonal response to HF Overview • Hemodynamic defense reaction • Salt and water retention • Vasoconstriction • Cardiac stimulation • Inflammatory reaction • Hypertrophic response

  35. Inflammatory reaction • Adaptive (beneficial), short term results • not known (heat shock proteins?) • Maladaptive (not beneficial), long term results • cardiac cachexia • apoptosis • necrosis

  36. Neurohormonal response to HF Overview • Hemodynamic defense reaction • Salt and water retention • Vasoconstriction • Cardiac stimulation • Inflammatory reaction • Hypertrophic response

  37. Hypertrophic response • Gene expression in myocardial cells will change as a result of: • cell stress • hemodynamic defense reaction • inflammatory reaction Changes of growth factor expressions: TGF- , IGF-1 , FGF  adaptive hypertrophy maladaptive hypertrophy • sarcomere number • cardiac output • remodeling • energy demand • cell death

  38. Concentric hypertrophy

  39. Eccentric hypertrophy

  40. contradiction is possible! Therapy • Emergency setting • keep the patient alive! • Usual setting • alleviate symptoms (improve QOL) • prolong survival Goals of therapy in general

  41. Classical approaches in drug therapy • Circulation • decrease fluid retention (diuretics) • decrease afterload, preload (vasodilators) • Heart • positive inotropic agents (digitalis)

  42. Diuretic therapy

  43. Maladaptive features of the vasoconstrictor response vasoconstriction   afterload myocardial energy expenditure arrhythmias, sudden death myocardial cell death cardiac output   worse symptoms survival

  44. Expected response to vasodilators vasoconstriction  afterload  myocardial energy expenditure  arrhythmias, sudden death  myocardial cell death  cardiac output    better symptoms survival

  45. Actual response to vasodilators vasoconstriction   BP  afterload  myocardial energy expenditure  hemodynamic defense reaction arrhythmias, sudden death  myocardial cell death  cardiac output  hypertrophy   better symptoms survival 

  46. kallikrein, cathepsin G Renin-angiotensin system angiotensinogen (1-14) renin angiotensin I (1-10) ACE, chymase angiotensin II (1-8) peptidase angiotensin III (2-8) peptidase angiotensin IV (3-8) ACE: angiotensin converting enzyme

  47. Actions of ACE • Converts angiotensin I to angiotensin II • Breaks down kinins (bradykinin) So ACE inhibitors not only decrease angiotensin II levels, but increase bradykinin concentration. This is beneficial, but may cause coughing as a side effect.

  48. Summary of drug therapy *: long term effects are in parentheses

  49. Availability The heart failure lectures (in .ppt file format) can be downloaded from inside the university local area network (e.g. Students’ Center) at this address: http://xenia.sote.hu/depts/pathophysiology

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