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Congestive Heart Failure

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Presentation on theme: "Congestive Heart Failure"— Presentation transcript:

1 Congestive Heart Failure
A Real Threat

2 Etiology Systolic Dysfunction(Decreased contractility):
Reduction in muscle mass(due to ishcemia&MI) Dilated cardiomyopathies(idiopathic,viral,alcoholic) Ventricular Hypertrophy: Pressure overload(systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) Volume overload(valvular regurgitation,high output states)

3 Etiology Diastolic Dysfunction(restriction in ventricular filling):
Increased ventricular stiffness Ventricular hypertrophy Infiltrative Myocardial disease (endomyocardial fibrosis) Myocardial ischemia and infarction Mitral or Tricuspid valve stenosis Pericardial disease(Pericarditis)

4 Compensatory mechanisms in heart failure
Compensatory response Benefecial effects of compensation Detrimental effects of compensation Increased preload(through Na&water retention) Optimize stroke volume Pulmonary and systemic congestion and edema formation Increased MVO2 Vasoconstrition Maintain blood pressure in face of reduced CO Shunt blood from nonessential organs to heart and brain Increased afterload Tachycardia (due to SNS activation) Helps maintain cardiac output Shortened diastolic filling time ß1-receptor downregulation &desensatization Arrhthemia Myocardial cell death Ventricular Hypertrophy and remodeling Helps maintain CO Reduces myocardial wall stress Decreased MVO2 Diastolic & systolic dysfunction Myocardial cell death &ischemia &arrhythemia



7 Classification(NYHA)
Functional Class Description I Patient w cardiac disease but wout limitation of physical activity.Ordinary activity does not cause undue fatigue, dyspnea or palpitation II Patient w cardiac disease that results in slight limitation of physical activity.Ordinary activity results in fatigue, dyspnea or palpitation III Patient w cardiac disease that results in marked limitation of physical activity.although patients are comfortable at rest, less than ordinary activity will lead to symptoms IV Patient w cardiac disease that results in an inability to carry on physical activity wout discomfort.symptoms are present even at rest with any physical activity, increased discomfort is experienced.

8 Classification(AHA) Stage Description A B C D
Patient is at high risk for the development of HF but has no apparent structural abnormality of the heart B Patient has structural abnormality of the heart but wout symptoms C Patient has structural abnormality f the heart & current or previous symptoms of HF D Patient has end-stage symptoms of HF that are refractory to standard treatment

9 Treatment

10 Treatment (Con,t) Stage A: Treat Risk factors: Control Glucose level
Control BP Dyslipidemia Thyroid disorder Valvular disease Avoid drugs which aggravate heart failure

11 Class II Wet Sx Diuretics (loop) + ACE Dry Sx
ACE  + B  (no diuretics) Sx resolve Sx don’t resolve improved didn’t improve give digoxin Spironolactone + B digoxin Spironolactone improved didn’t improve improved didn’t improved Give B Spironolactone Plan B Spironolactone Plan B

12  directly give ACE inh & Loop
Class III  directly give ACE inh & Loop Sx still exist Px responded Digoxin B & Spironolactone Didn’t respond Didn’t respond Plan B Plan B

13 (see if you hospitalize him or not)
Class IV (see if you hospitalize him or not) ACE  + Loop D + digoxin (don’t start B) If Px was already on B Did not respond optimize it Plan B Plan B Stage D worsening Stage C (II, III, IV)

14 if not improved Plan B Stage D or worsening Stage C
Hospitalize your Px. Optimize drug therapy if not improved wet dry Give aggressive diuretic therapy IV (thiazide and loop) to cause profound diuresis (give IV due to diuretic resistance Give iv high dose give combination Give positive inotropic agents (he is already on ACE inh, digoxin) improve Taper down +inotrop and go back to chronic Tx not improved Tissue hypoperfusion SBP < 80 Worsening renal function ↙Na  hypervolemia dilutional hyponatremia cyanosis Hemodynamic Monitoring (monitor BP, temp., CO, T0).

15 Negative inotropic effect
cardiotoxic Sodium &water retention Antiarrhythmic (disopyramide,flecainide) Calcium channel blocker(verapamil…) Itraconazole Terbinafine Rosiglitazone Doxorubicine Daunomycin Cyclophosphamide NSAIDs Cox-2 inhibitor Glucocorticoids Androgens Estrogens Salicylate(high dose Na containing Drugs (carbenicillin, ticarcillin)

16 Treatment (Con,t) Stage B=Class I ACE inhibitors Or
Beta blocker if recent or previous MI& reduced ejection fraction due to remodeling Stage C Є class II,III,&IV ACE inhibitors & Beta blockers In all Px If Sx still exist Or EF still low Add Digoxin When symptoms resolves add aldactone

17 Role of drugs in CHF

18 Angiotensin converting enzyme inhibitors
Cardioprotctive effect Preload & Afterload RA system less Na/water retention bradykinin level vasodilation mortality, hypertrophy, & fibrosis


20 ACE inhibitor Approved for Use in HF
Generic Name Brand Name Usual daily dose(mg) Dosing frequancy Target dosing survival benefit Prodrug Elimination T1/2 Captopril Capoten tid 50tid No Renal 2 Enalapril Renitec 2.5-40 bid 10bid Yes 10 Lisinopril Zestril 5-40 qd 10qd 12 Ramipril Tritace qdorbid 5bid yes 9-18

21 BETA BLOCKERS Mortality Vasoconstriction
Carvidilol alpha+beta blocker &antioxidant effect Bisoprolol Metoprolol

22 DIGOXIN + inotropic effect sympathetic output from CNS(NE)
Not mortality but improve Sx Therapeutic level: 0.5-1ng/ml for CHF Max: 1-1.5ng/ml for A fib

23 Clinical Pharmacokinetics of Digoxin
Oral bioavailability: Tablets % Elixir % Capsules % Onset of action: Oral hr IV hr Terminal half –life: Normal renal function hr Anuric patient days Volume of distribution L/kg Fraction unbound in plasma % Fraction excreted unchanged in urine %

24 Diuretics Sx relief of edema & pulmonary congestion
Direct vasodilation , Preload DOC: Furosamide: Na excretion 20-25% Thiazide: Na Excretion 5-8% Dose: 20-40mg bid Up to 400mg as max dose If Clcr>30ml/min dose up to 1-3g/d

25 Loop Diuretics Used in HF
Furosemide Bumetanide Usual daily dose 20-160mg/day 0.5-4mg/day Normal renal function 80-160mg 1-2mg Clcr:20-25ml/min 160mg 2mg Clcr<20ml/min 400mg 8-10mg Bioavailability Average50% 80-90% Affected by food Yes T1/2 hr hr

26 Spironolactone Aldosterone, preload,ventricular remodeling
Morbidity &mortality(Rales study) Used if Scr<2.5mg/dl & K<5meq/L Aplerenone No gynecomastia Mortality & morbiity in acute MI

Persistent cough &angioedema due to ACE inhibitors If persistent HTN Add ARB or CaCh blocker (amlodepine) If concomitant angina: add nitrate or amlodepine

28 New Drug Investigation
Natriuretic Peptides: Atrial Natriuretic Peptides (ANP) Brain Natriuretic Peptides (BNP C-type Natriuretic Peptides (CNP) Neseritide: Recombinant BNP

29 New Drug Investigation
Omapatrilat: Vasopeptidase Inhibitor ACE inhibitor INH neutral endopeptidas Bradykinin & NP SE: Angiodema

30 Precipitating factors in Heart failure Decompensation
Noncompliance with drugs or diet Cardiac Ischemia Inadequate therapy at time of admission Cardiac arrhythmias Uncontrolled hypertension

31 Thank YOU

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