1. Heart failure Dr Rafat Mosalli

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

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

4. Cardiovascular - Basic

5. Preload Amount of volume filling ventricles during diastole Amount of volume filling ventricles during diastole Proportional to volume status Proportional to volume status Increasing preload=increases stroke volume (in general) 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 Dehydration Blood Loss Blood Loss Post-operative blood loss Post-operative blood loss Third Spacing due to Decreased oncotic pressure or Vascular leak. Third Spacing due to Decreased oncotic pressure or Vascular leak. Hyper dynamic circulation Hyper dynamic circulation

8. Back to Preload - treatment Crystalloidsvs.Colloids

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

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

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

12. Back to our diagram

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

15. How else can we affect contractility? Adrenergic Receptors

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

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

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

19. Adrenergic Agonists: drugs Dopamine Dopamine Dobutamine Dobutamine Epinephrine Epinephrine

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

21. Dobutamine  1 selective  1 selective Effect: increased inotropy and chronotropy Effect: increased inotropy and chronotropy Use: to increase contractility Use: to increase contractility

22. Epinephrine works at all receptors  >  works at all receptors  > 

23. Remember that diagram?

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

25. Afterload Reduction: drugs Nitroprusside Nitroprusside Nitroglycerin Nitroglycerin Nitric Oxide Nitric Oxide

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

27. Again back to the diagram:

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

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

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

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

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

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

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

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

36. diagnosis Hx Hx Clinical exam Clinical exam Investigations: Investigations: Blood work CXREKGECHO

37. Treatment Depend on the pathophysiology Depend on the pathophysiology Aim: Aim: Increase Preload Increase Preload Afterload reduction Afterload reduction Correct Myocardial depressants: Correct Myocardial depressants: enhance Myocardial contractility enhance Myocardial contractility

38. Treatment Underlying cause(sepsis,CHD) Underlying cause(sepsis,CHD) Rest Rest O2 O2 Diet and growth follow-up Diet and growth follow-up Medications: Medications:InotropesDigoxine Vasodilator therapy Diuretics (Furosemide)