3. • Heart failure describes the clinical syndrome that develops when the heart cannot maintain
adequate output, or can do so only at the expense of elevated ventricular filling pressure.
• In mild to moderate forms of heart failure, symptoms occur only when the metabolic demand
increases during exercise or some other form of stress.
• In severe heart failure, symptoms may be present at rest.
• In clinical practice, heart failure may be diagnosed when a patient with significant heart disease
develops the signs or symptoms of a low cardiac output, pulmonary congestion or systemic
venous congestion
at rest or on exercise.
4. EPIDEMIOLOGY
•
Heart failure predominantly affects older people; the prevalence is 1.6% in the UK adult population but
affects more than 10% in those aged 80–89 years.
• untreated heart failure generally carries a poor prognosis; approximately 50% of patients with severe
heart failure due to left ventricular dysfunction will die within 2 years because of either pump failure or
malignant ventricular arrhythmias.
• The most common causes are coronary artery disease and myocardial infarction but almost all forms of
heart disease can lead to heart failure.
• An accurate diagnosis is important because treatment of the underlying cause may reverse heart failure
or prevent its progression.
5. PATHOGENESIS
• Heart failure occurs when cardiac output fails to meet the demands of the circulation.
Cardiac output is determined by preload (the volume and pressure of blood in the
ventricles at the end of diastole), afterload (the volume and pressure of blood in the
ventricles during systole) and myocardial contractility,
10. • The NewYork Heart Association (NYHA) Functional Classification:
• Class I HF: no limitations of ordinary physical activity (no HF symp.).
• Class II HF: slight limitations of ordinary physical activity (HF symp.); comfortable at
rest.
• Class III HF: marked limitations of less than ordinary physical activity (HF symp.);
comfortable at rest.
• Class IV HF: unable to carry on any physical activity without HF symp. or have symp.
at rest
11. • The American College of Cardiology Foundation & American Heart
Association (ACCF/AHA) Staging System:
Classifies pts either as being at risk for HF or as having the clinical $ of HF.
• Stage A HF: pts with RFs for HF (HTN, obesity, atherosclerotic dis. & the metabolic $).
• Stage B HF: pts with struct. heart dis. (previous MI, asympt. valvular dis. & LVH) but
without symptoms of HF.
• Stage C HF: pts with struct. heart dis. with symp. of HF.
• Stage D HF: pts with refractory or end-stage HF
12. HF SHOULD FURTHER BE CHARACTERIZED BY CAUSE :
(E.G.,ISCHEMIC, NON-ISCHEMIC,VALVULAR).
IT CAN BE CLASSIFIED AS PREDOMINANTLY:
•
A-Left, Right & Biventricular HF:
•Left-sided HF (LHF): ↓LV output →↑LAP →↑pulmonary venous pressure
o Ac. ↑LAP (e.g.AF) → pulm. congestion or oedema .
o Chr. ↑LAP (e.g. MS) → impair RV func.
•Right-sided HF (RHF): ↓RV output →↑RAP→ ↑systemic venous pressure
Isolated RHF: chr. lung dis. (?), PE & PS
•Biventricular HF (CHF): Dilated CMP or IHD; LHF → RHF
13. B- Diastolic & Systolic Dysfunction HF: assessed by echocardiography with Doppler
o Systolic dysfunc.:ABNL contraction with reduced ejection fraction <40%. (HFrEF) →CMP
o Diastolic dysfunc.:ABNL relaxation with preserved ejection fraction >50%. (HFpEF) →LVH
N.B: Systolic & diastolic dysfunction often coexist (e.g. CAD)
C- Acute & Chronic HF:
o Ac. (sudden): MI
o Chr. (gradual): progressiveVHD
D-High-Output & Low-Output HF:
o High-Output:uncommon disorder
o Low-Output:much more common
14. CLINICAL PRESENTATION :
• S/S of ↓C.O, pulm. congestion or systemic venous congestion.
•Acute HF:
o Hx: Dyspnoea .
o O/E:Agitated, pale, clammy, cold peripheries; P.R=↑(common)/ ↓; BP=variable.
•Chronic HF:
o Hx:
• Dyspnoea, fatigue, poor effort tolerance, edema, abd. distention,chest discomfort.
• Medical & Family Hx: DM, HT, dyslipidemia,sudden cardiac death, CAD & CMP.
• Drug Hx: .
• Social Hx: past & current use of tobacco products, alcohol & illicit drugs.
o O/E:
15. ON EXAMINATION :
General:
• Cold peripheries • ↑P.R, pulsus alternans → pathognomonic for severe LV
dysfunc.
• ↓B.P, narrow pulse press. • Stage D HF may exhibit Cheyne-Stokes respirations
(poor prognosis).
• Cardiac cachexia (wt. loss) • Oliguria. • ↑JVP
• Bilateral pitting L.L oedema (?) (not specific for HF)
Local:
• Precordium:
• S₃, S₄ (not specific for HF) • Accentuated P₂ of S₂ (pulm.HT)
• Murmurs of MR & TR (common in HF) worse in ac. decompensation.
• Chest Auscultation: Crackles are
a specific finding for HF.
• Abdominal Examination: tender hepatomegaly
18. INVESTIGATION :
•Blood Tests: Hb; RFT; LFT; S. Electrolytes;TFT; Brain (B-type) natriuretic peptide
(BNP) (NL<100pg/mL) differentiates cardiac from pulm. causes of dyspnea (↑ in
the former).
•CXR
•ECG: Ischaemia; HT;Arrhythmia
•Echocardiography
•Cardiac Catheterization
•Cardiac Biopsy
19.
20. MANAGEMENT OF HF:
•
A) Acute Decompensated HF (Pulmonary Oedema):This is an ac. medical ER
• Sit the pt up.
• O₂: high-flow,high-conc.
• Nitrates: (I.V GTN/ buccal) ↑every 10mins.
• Loop diuretic: (Furosemide or torsemide I.V)
• Rest & continuous monitoring: of cardiac rhythm, BP & pulse oximetry.
• Opiates: I.V in distressed pts.
• Inotropic agents: in hypotensive pts.
• Intra-aortic balloon pump insertion in pts with shock.
23. II-MEDICAL RX:
• ↑contractility, ↓preload, ↓afterload.
• Diuretics: Loop diuretics;Thiazides; Mineralocorticoid receptor antagonists
• ACEIs or ARBs: standard initial CHF therapy→ prolong life in pts with symp. CHF.
• β-blockers: gradual augmented dose→ improve symp. & prolong survival in pts with
HF & reduced EF <40%.
•Vasodilators:Venodilators (nitrates) & Arteriodilators (hydralazine)
• Ivabradine: acts on SAN & ↓HR; ↓hospitalizations in HF.
• Digoxin: controls HR in pts with systolic HF & AF. Unlike ACEIs & β-blockers, it does
not prolong SR in HF pts but ↓ hospitalizations.
• Amiodarone: anti-arrhythmic.
