Heart Failure power point slide for Medical students

This PowerPoint presentation provides a comprehensive overview of heart failure, detailing its causes, symptoms, and treatment options. Designed for educational purposes, it includes visually engaging slides that present complex medical information in an accessible format. Ideal for healthcare professionals, students, and educators, this resource aims to enhance understanding of heart failure and promote informed discussions in clinical settings.

1. CHAPTER: 18 DRUGS FOR HEART FAILURE BY ALI RAZA

2. ہے معاملہ کا دل یہ کیونکہ فرمائیں توجہ

3. HEART FAILURE it is complex , progressive disorder in which the heart is unable to PUMP sufficient blood to meet the need of body. Definition:

4. CARDINAL SYMPTOMS dyspnea fatigue fluid retention

5. CAUSES : Atherosclerosis Hypertensive heart disease Vavular heart disease Cogenital heart disease

6. Physiological COMPENSATORY mechanisms in HF Goals of pharmacologic intervention in HF

7. Physiology of Muscle Contraction Stimulus depolarization of membrane shortening of contractile Protein relaxation repolarization ACTION POTENTIAL Cardiac Contraction

8. ACTION POTENTIAL Cardiac myocyte are electrically excitable Rhythm Generated by SA node & AV Nod e have Long action potential; divided into 5 phases: Phase 0: FAST UPSTROKE Phase 1: PARTIAL REPOLARIZATION Phase 2: PLATEAU Phase 3: REPOLARIZATION Phase 4: FORWARD CURRENT

9. Cardiac Contraction: Force of Contraction ∝ Conc. of free cytosolic Calcium DRUGS increase intracellular Ca 2+ increase sensitivity to Ca 2+ increase Force of contraction

10. COMPENSATORY PHYSIOLOGICAL RESPONSES: Increase Sympathetic activity Renin-angiotensin-aldosterone-system (RAAS) Activation of Natriuretic peptides Myocardial hypertrophy

11. Sympathetic Activity: Baroreceptors sense decrease in BP activates Sympathetic Nervous System HR & Force of contraction

12. In addition, vasoconstriction enhance venous return increase Preload increase Stroke volume increase Cardiac Output Sympathetic Activity: but in long term , contribute to decline in Function

13. Renin-angiotensin-aldosterone-system (RAAS) Decrease Blood flow to Kidney release Renin angiotensin-II & Aldosterone increase peripheral resistance & Na-H 2 O retension Blood volume increase

14. If heart is unable to pump this extra volume Peripheral and Pulmonary edema increase workload Decline cardiac function

15. Natriuretic Peptide (hormone) : increase preload release of Atrial Natriuretic peptide & B-type Natriuretic Peptide vasodilation Natriuresis inhibtion of Renin & aldosterone

16. Myocardial Hypertrophy: Diastolic Heart Failure: Hypertrophy of Ventricles Ability to relax & accept Blood impaired Diastolic Heart Failure: Hypertrophy of Ventricles Ability to relax & accept Blood impaired

17. systolic HF: intially stretching of heart leads to stronger contraction However, excessive elongation cause weaker contraction diminished Ability to eject blood

18. Acute ( Decompensated) HF: if compensating mechanism FAILS to maintain Cardiac output, HF is decompensated sign & symptoms worsen

19. THERAPEUTIC Strategies IN HF:

20. Renin-angiotensin-aldosterone-system (RAAS) inhibitors: RAAS compensatory mechansim leads to increase Workload on heart and decline in cardiac function. ACE inhibitors ARBs aldosterone receptor Antagonist

21. Angiotensin-I Angiotensin-II vasoconstriction inactivate Bradykinin ACE

22. ACE inhibtors: Action: decrease vascular resistance ( preload & after-load) increase Cardiac output. Therapeutic uses: systolic HF start with Low doses and increase to maximal tolerated doses

23. P harmacokinetics: Oral administration ( but food may decrease absorption) except CAPTOPRIL and ENALAPRILAT all ACE inhibitor activated by hepatic enzyme all ACE inhibitor eleiminated through Urine except FOSINOPRIL.

24. adverse affect: Hyperkalemia (k+ level must be monitored) Dry cough Angio-edema postural hypottension