Heart failure ppt

Heart failure: definition,signs,symptoms,lab values, tests, pharmacological therapy

1. CONGESTIVE CARDIAC FAILURE PRESENTED BY THUSHARA. C 1 st YEAR M.PHARM GRACE COLLEGE OF PHARMACY

2. CONTENTS DEFINITION CLASSIFICATION ETIOLOGY CLINICAL MANIFESTATION PATHOPHYSIOLOGY DIAGNOSIS MANAGEMENT

3. DEFINITION Heart failure is defined as a chronic and progressive condition where the heart muscle is unable to pump enough blood through the body to meet the body’s need for blood and oxygen

4. Classification Systolic heart failure Diastolic heart failure Acute heart failure Chronic heart failure Left side heart failure Right side heart failure

5. ETIOLOGY Arrythmias Myocardial infraction Hypertension Anemia Atherosclerosis Infection Obesity Alcohol and tobaco use

6. CLINICAL MANIFESTATIONS SYMPTOMS SIGNS Fatigue Weakness Shortness of Breath on exertion Shortness of Breath at Rest Cough and wheezing Anorexia / loss of appetite Paroxymal nocturnal dyspnea Nausea Abdominal pain Nocturia Pulmonary edema Pleural effusion Tachycardia Narrow pulse pressure Cardiomegaly Peripheral edema Jugular vein distension

7. LABORATORY TESTS BNP > 100g/ml Electrocardiogram may be normal., or it could show numberous abnormalities include ST-T wave changes Serum creatinine increased due to hypoperfusion Complete blood count is useful to determining heart failure is due to a reduced oxygen carrying capacity Chest x-ray useful for detecting cardiac enlargement,, pulmonary edema and pleural effusion Hyponatremia : Serum sodium <130mEq/L is associated with reduced survival and indicating worsening volume overload and/or disease progression

8. Pathophysiology

9. Diagnosis Electrocardiogram (ECG) Chest x-ray Echocardiography (“Echo”) Heart catheterization Angiography Blood tests

10. MANAGEMENT NON PHARMACOLOGICAL MANAGEMENT Bed rest Consuming small but frequent meals Moderate sodium restriction (2-4g/day) Smoking cessation Avoid alcohol intake

11. Treatment (Medication) ACE Inhibitors Diuretics Inotropic Agents Beta Blockers Calcium Channel Blockers Vasodilators Digitalis glycosides Aldosterone antagonist Angiotensin receptor blockers PHARMACOLOGICAL MANAEMENT

12. DIURETICS

13. Thiazides Hydrochlorothiazide, metolazone , chlorthalidone . Block sodium reabsorption in the cortical diluting segment at the terminal portion of the loop of Henle and in the proximal portion of the distal convoluted tubule Thiazides are ineffective when the GFR falls below 30–40 mL /min . Decrease preload and improve ventricular efficiency by reducing circulating volume Remove peripheral edema and pulmonary congestion ADR: Hypokalaemia , hearing loss, Hypercalcaemia , Mg depletion GIT and CNS disturbances

14. Loop diuretics Furosemide , bumetanide and torsemide . Rapid onset and a relatively short duration of action Two or more doses are preferable to a single larger dose. Inhibit chloride reabsorption in the ascending limb of the loop of h enle , which results in natriuresis , and metabolic alkalosis . Increases systemic venous capacitance and produce rapid symptomatic relief ADR: Hpokalaemia , alkalosis

15. Potassium sparing diurestics Spironolactone, triamterene, and amiloride Spironolactone is a specific inhibitor of aldosterone.

16. INHIBITORS OF THE RENIN–ANGIOTENSIN–ALDOSTERONE SYSTEM

17. ACE Inhibitors Captoprill, enalaprill, isnoprill it inhibit angiotensin converting enzyme ACE inhibitors causes feed back increase in renin release resulting in over production of Ang1, since its conversion to Ang2 is blocked. Ang1 divert to Produce more Ang (1-7) which produce vasodilation, Decrease in Ang2 and aldosterone attenuates many of the deleterious effects this neurohormones , including ventricular remodeling, myocardial fibrosis, cardiac hypertrophy , norepinephrine release, sodium and water retention ADR : Hypotension, renal insufficiency, dizziness, lightheadedness, blurred vision, syncope, hyponatremia , hypovolemia , dry cough, Angioedema Contraindicated during second and third trimester of pregnancy due to increased risk of fetal renal failure.

18. Angiotensin Receptor blockers Losartan , candesartan,valsartan Angiotensin 2 ,a vasocontrictor is concerned with ventricular remodelling and fluid retention. These drugs inhibit the binding of angiotensin 2 to its AT₁ receptor. Thus they preclude the a bove mentioned effects of angiotensin 2. These agents do not exert any action on bradykinin and thus do not produce cough. Has comparable effect to ACE I Can be used in certain conditions when ACE I are contraindicated 18 Adverse drug reactions Hypotension Impariment of renal functioning Dose Candesartan Initial: 4-8mg Targeted dose -32mg Valsartan Initial:40mg Targeted dose -160mg

19. Inotropes Increase force of contraction All increase intracellular cardiac Ca ++ concentration Eg : Digitalis (cardiac glycoside) Dobutamine ( β -adrenergic recepter agonist ) Amrinone (PDE inhibitor) 19

20. DIGOXIN 20 It inhibits the Functions in the exchange of Na⁺ for k⁺ ions. Such blockage results in intracellular accumulation of Na⁺ ions . These ions are then exchanged with Ca₂⁺ ions through N a⁺ - Ca₂⁺ exchange carries. These ca₂⁺ ions increase the contractility of the myocardium which is beneficial to the failing heart. Digoxin enhances the cholinergic activity which reduces the HR and AV conduction . Due to this the time required for diastolic filling gets enhanced while the myocardial o2 consumption is retarted . The sympathetic outflow comprising renin, aldosterone is also decreased by dioxin inhibit Na  + ,K  + ATPase , pump which

21. Drug reaction Bradycardia Nausea Vomiting Visual disturbances Non paroxysomal junctional tachycardia Supraventricular tachycardia Sexual dysfunction Neuralgic pain USES: For tachyarrhythmias For ventricular arrhythmias 21

22. Dopamine acts at a variety of receptors (dose dependant) Rapid elimination- can only be administered as a continuous infusion 22 Stimulates beta-adrenergic receptors and produces a positive inotropic response. Unlike the vasoconstriction seen with high doses of dopamine, dobutamine produces a mild vasodilatation β -Adrenergic Agonists DOPAMINE DOBUTAMINE

23. β Adrenergic Agonist 23

24. β1 Blockers MOA Heart failure is accompanied by an increase activation of sympathetic nervous system. This brings about structural & functional modification in the myocardium. β Blockers inhibit the sympathetic outflow of norepinephrine and counteract the changes produced. The ventricular remodelling in heart failure is also reversed by β Blockers Increases beta receptor sensitivity. Adverse drug reaction Hypotension Bradycardia Worsening of CHFsymptoms . 24 bisoprolol , carvedilol , metoprolol

25. Isosorbide dinitrate , isosorbide mononitrate , and hydralazine also used specially in patients who cannot tolerate ACE inhibitors. 25 VASODILATORS

26. Vasodilator( Hydralazine ) It directly relaxes the arterioles & arteries reducing the peripheral vascular reesistances & preload. It also help to reduce after load. Adverse drug reaction : Nausea Palpitation Tachycardia Salt & water retention on prolong therapy. 26

27. Bipyridines phosphodiesterase inhibitors Targets PDE -3 (found in cardiac and smooth muscle) Ex. Inamrinone , milrinone 27 alter the intracellular movements of calcium by influencing the sarcoplasmic reticulum increasing inward calcium flux in the heart during the action potential increase myocardial contractility Inhibition of PDE3 Increase in cAMP the conversion of inactive protein kinase to active form Protein kinases are responsible for phosphorylation of Ca channels increased Ca entry into the cell ↑ Vascular Permeability leads to ↓ in intravascular fluid Volume increase in contractility vasodilation

28. Nitrates & Nitrites Nitroglycerin is denitrated by glutathione S  - transferase in smooth muscle Free nitrite ion is released, which is then converted to Nitric Oxide   activation of guanylyl cyclase enzyme increase in cGMP dephosphorylation of myosin light chain , preventing the interaction of myosin with actin (Myosin light chain kinase essential for smooth muscle contraction). Results in vasodilation 28

29. CALCIUM CHANNEL BLOCKERS Verapamil , diltiazam , nefedipine It blocks the calcium channel and prevent the entry of calcium in to the cell There by prevent the contraction and arterial dialation occur

30. The beneficial effects of spironolactone derive from the direct and competitive blockade of specific aldosterone receptors. Aldosterone inhibitors therefore have three types of effects: - Diuretic effect, which is most noticeable when fluid retention and increased levels of aldosterone are present Antiarrhythmic effect, mediated by the correction of hypokalemia and hypomagnesaemia. Antifibrotic effect. This effect, demonstrated in animal models, can contribute to a decrease in the progression of structural changes in patients with heart failure. ALDOSTERONE RECEPTOR ANTAGONIST EG: SPIRONOLACTONE

31. Stage A At high risk of heart failure but without structural heart disease or symptoms of heart disease Stage B Structural heart disease, but without sign or symptoms of heart failure Stage C Structural heart disease with prior or symptoms of heart failure Stage D Refractory heart failure requiring specialized interactions Patient with: HTN, Atherosclerotic disease , DM,Obesity , family history of cardiomayopathy Patients with: Previous mayocardial infraction,left ventricl e remodelling , including left ventricular hypertrophy and low ejection factor,valvular disease Patient with: Known structural heart disease and shortness of breath and fatigue, reduced exercise tolerance Patients with: patient who are marked symptoms at rest despite maximal medical therapy,such as those who are currently hospitalised or cannot be safely discharged from the hospital without specialised intervention Structura l HF Devolepment of HF symptoms Therapy Goals Treat HTN, lipid disoders , encourage smoking cessation,discourage alcohol intake Drugs: ACE inhibitor or ARB in appropriate patients for vascular disease or DM Therapy Goals: All measures under stage A Drugs: ACE inhibitor or ARB in appropriate patients Β eta blocker in appropriate patient Therapy Goals: All measures under stage A , B, dietary salt restriction, drugs for routine use, Diuretics for fluid retention, ACE inhibitors, beta blockers, ARB, digitalis,hydrallazine or nitrates Therapy Goals: Appropriate measures under stages A,B,C Descion based on appropriate level of care options Compassionate end of life care Extraordinary measures: heart transpantation ,

32. Thank you…