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Heart failure

Heart failure. Dr Rafat Mosalli. Objectives. Definition Pathophysiology Age specific Causes Clinical pictures Investigations Treatment. Definition. Difficult to define It is not a diagnosis, but rather constellation of clinical symptoms and signs due to various causes

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Heart failure

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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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