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Understanding Heart Failure: Pathophysiology, Causes, and Treatments

Heart failure is not merely a diagnosis but a collection of clinical symptoms arising from various causes leading to inadequate oxygen delivery by the heart. This guide explores the definition and pathophysiology of heart failure, age-specific causes, clinical presentations, and essential investigations. It outlines strategies for treatment, including preload and afterload management, along with the roles of adrenergic receptors and various medications. Understanding these concepts is crucial for an effective approach to managing heart failure in patients of all ages.

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Understanding Heart Failure: Pathophysiology, Causes, and Treatments

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  1. Heart failure Dr Rafat Mosalli

  2. Objectives • Definition • Pathophysiology • Age specific Causes • Clinical pictures • Investigations • Treatment

  3. Definition • Difficult to define • It is not a diagnosis, but rather constellation of clinical symptoms and signs due to various causes • Inadequate O2 delivery by the heart to meet the demand of the body • O2 delivery=O2 blood content +COP

  4. Cardiovascular - Basic

  5. Preload • Amount of volume filling ventricles during diastole • Proportional to volume status • Increasing preload=increases stroke volume (in general)

  6. Preload Problems Either there is not enough preload or The heart needs more than usual

  7. Too little or heart need more? • Dehydration • Blood Loss • Post-operative blood loss • Third Spacing due to Decreased oncotic pressure or Vascular leak. • Hyper dynamic circulation

  8. Back to Preload - treatment Crystalloids vs. Colloids

  9. Crystalloids Isotonic Fluid : • Normal Saline • 154 mEqNaCl/l • Lactated Ringers • 130mEq Na+ • 4mEq K+ • 3mEq Ca+2 • 109mEq Cl- • 28mEq Lactate

  10. Colloids • Oncotic properties • More likely to stay intravascular • Longer duration of action

  11. Commonly used colloids • 5% Albumin • 25% Albumin • Plasma - FFP • Packed Red Blood Cells (PRBC’s)

  12. Back to our diagram

  13. Contractility • Somewhat dependent on preload • Impaired Secondary to: • infection • metabolic • hypoxia, ischemia • surgery

  14. How else can we affect contractility? Adrenergic Receptors

  15. Alpha receptors • Peripheral vasculature • Stimulation causes vasoconstriction • Increase SVR and afterload

  16. Beta-1 receptors - Heart Stimulation leads to a cascade of activity • Activates adenylatecyclase • Increases cAMP production • This increases Ca+2 entry into the cell • Increases strength of contraction (inotropy) and rate of contraction (chronotropy)

  17. Beta-2 receptors - lungs • Located in the lungs and peripheral vasculature • Stimulation causes smooth muscle relaxation • Bronchodilation in the lungs • Vasodilation in peripheral vasculature

  18. Adrenergic Agonists: drugs • Dopamine • Dobutamine • Epinephrine

  19. Dopamine • Alpha, beta and dopaminergic agonist • Effects: • ‘renal’ dose • Middle range: more beta • Higher range: alpha starts to predominate • Use: inotrope, vasoconstriction

  20. Dobutamine • b1 selective • Effect: increased inotropy and chronotropy • Use: to increase contractility

  21. Epinephrine • works at all receptors b>a

  22. Remember that diagram?

  23. Afterload • Refers to work against which the heart is contracting • Either :an immediate obstruction such as valvular stenosis or hypertrophy Or related to systemic vascular resistance • As you might imagine decreasing the afterload will help the heart to contract

  24. Afterload Reduction: drugs • Nitroprusside • Nitroglycerin • Nitric Oxide

  25. Who needs afterload reduction? • Decreases force against which heart has to contract • Poor LV function or for patients with aortic insufficiency or mitral regurgitation

  26. Again back to the diagram:

  27. Heart Rate • We rarely manipulate heart rate(aside from arrhythmias) • heart block drug:Isoproteronol

  28. Back to the Diagram BP = CO x SVR • We’re finally on SVR - systemic vascular resistance

  29. Systemic Vascular Resistance • Remember SVR also contributes to afterload • In general, increasing SVR will increase afterload and decrease cardiac output • Since this patient population needs improved CO we usually avoid increasing afterload,

  30. Drugs that increase SVR • Alpha agonists, primarily • Epinephrine • We already talked about this • Norepinephrine • Phenylephrine

  31. causes • First week of life: • Obstructive lesion: COA,AS,HLHS, PS,TAPVR • Volume overload lesion: TR,PR,PDA ,AVM • Others( myocardial contractility dysfunction,arrythmia) • 1-4 weeks: • As Above + shunt lesions (VSD,PDA)

  32. Causes >4 weeks: Shunt lesions as above, coronary and myocardial diseases at any age: -Myocardial & pericardial diseases -Arrhythmia( SVT,heart block) -Sepsis,acidosis,hypoxia -Metabolic (endocrine,Glycogen storage type2) -Drugs -Severe anemia - Tumors

  33. Age specific causes: summary 1-Neonates • Obstructive and ductal dependant lesions 2-Post neonatal • Shunt lesions • Myocardial contractility diseases

  34. Signs and symptoms : • Impaired Myocardial performance: Shock, feeding problems, sweating, FTT, pallor, rhythm problems, Cardiomegaly, gallop rhythm • Pulmonary congestion: Dyspnea, cyanosis, wheezing, tachypnea, rales,cough Respiratory acidosis • Systemic venous congestions Edema ,hepatomegaly, neck vein distention • Specific cause

  35. diagnosis • Hx • Clinical exam • Investigations: Blood work CXR EKG ECHO

  36. Treatment • Depend on the pathophysiology • Aim: • Increase Preload • Afterloadreduction • Correct Myocardial depressants: • enhance Myocardial contractility

  37. Treatment • Underlying cause(sepsis,CHD) • Rest • O2 • Diet and growth follow-up • Medications: Inotropes Digoxine Vasodilator therapy Diuretics (Furosemide)

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