2007 Engleza Heart Failure

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    CHRONIC CONGESTIVE

    HEART FAILURE

    2004 - 2005

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    BACKGROUND:

    HF PREVALENCE o from 3 - 20 at 45 years

    to 80-160 over75 years

    N.Sharpe, 1998

    MORTALITY o with aging

    5% deaths throughHF

    below 45 years1/3 deaths through HF to 75 years

    2/3 deaths through HF above 75 years

    Chignon J, 1998

    PHARMACOLOGICAL APPROACH

    a. medication: intake / abuse / drug associations

    b. changes in: - pharmacokinetics- pharmacodinamics

    - social, economic, mental context.

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    DEFINITION

    (after ESC)

    SUBJECTIVE:

    HF symptoms:

    dyspnea/ortopnea/ nocturnal paroxysmal d.

    edema

    tachycardia

    rales

    LV gallop

    distended neck veins

    OBJECTIVE: systolic/diastolic dysfunction

    RETROSPECTIVE: response to correct HF treatment

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    HF DIAGNOSIS: STEPS

    Recognize HFpicture

    Etiology

    Pathogenesis: systolic/diastolic dysfunction

    Recognize decompensation: edema, dyspnea

    Assess morbidity/mortality predictive factors

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    LV FAILURE

    LV FAILURE: asymptomatic at rest, symptomatic at effort

    edema

    Cardiac asthma

    Rest symptomatic LV failure

    RV FAILURE

    1. RECOGNIZE HF

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    2. ETIOLOGY

    CORONARY ARTERY DISEASE

    - MYOCARDIAL INFARCTION

    - CHRONIC ISCHEMIA

    Systemic HYPERTENSION

    CARDIOMYOPATHIES

    - DILATIVE, HYPERTROPHIC, RESTRICTIVE- ACUTE MYOCARDITIS

    - OTHER: METABOLIC, ENDOCRINE, NEUROMUSCULARE, TOXIC, etc.

    VALVE DISEASES

    - SEVERE AORTIC STENOSIS

    - MITRALREGURGITATION

    - AORTIC REGURGITATION

    - MITRALSTENOSIS

    OTHER

    - ARRHYTHMIAS / BLOCKS

    - INCREASED CARDIAC OUTPUT

    - CONGENITAL CARDIAC DISEASES

    - COR PULMONALE

    - CONSTRICTIVE PERICARDITIS

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    adapted LV insufficient LV

    * dilation

    * remodelling

    * hemodynamic factors;

    neurohumoral factors

    3. LV DYSFUNCTION

    * POPULATION AT RISK

    * CAD

    * Hypertension* valvular disease

    * cardiomyopathies at onsetLV DYSFUNCTION

    DIASTOLIC

    -LVHc + EFn

    -distensibility

    -relaxation

    -E/A

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    DIASTOLIC DYSFUNCTION

    = LV can not be filled at low pressure

    Consequences * congestive syndrome pulmonary

    peripheral

    * EndD LV P > 12 mmHg

    CLINIC signsofcongestive HF

    cardiac silhouette normal

    normal EF

    Asymptomatic diastolic dysfunction ECHO

    angiography/scintigraphy

    Symptomatic: LV failure pulmonary HT right HF congestive syndrome chronic

    low cardiac output

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    DIASTOLIC DYSFUNCTION

    ETIOLOGY:

    * PERICARDITIS

    * ENDOMYOCARDIALF

    IBROSIS* Relaxation and ventricularcompliance deterioration:

    concentric LV hypertrophy

    CAD

    RESTRICTIVE CARDIOPATHIES

    * Pulmonary venousreturn decrease: HYPOVOLEMIA

    * Secondary tosystolic dysfunction: MITRAL STENOSIS

    AGGRAVATING FACTOR: ATRIAL FIBRILLATION

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    DYSFUNCTION

    SYSTOLIC DIASTOLIC

    HISTORY OF

    * MI ++ +/-* HTN + + +

    ANAMNESIS

    * BRUTAL ONSET +/- ++

    X-RAY

    * CARDIOMEGALY + + -

    ECG* Q WAVE ++ +/-

    * LV H +/- + +

    ECHO EF q EF n

    E/A < 1

    DIASTOLIC DYSFUNCTION

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    4. INVESTIGATIONS

    1. HF detection

    - Chest X-ray: cardio-thoracic index, pulmonary stasis

    - Echocardiography: LV dysfunction- Ergospirometry: VO2 max

    2. HF etiology

    - ECG: ischemia / infarction, hypertrophy, arrhythmia

    - Echocardiography: valve disease, systolic / diastolic dysfunction

    - Rare causes: - thyroid dysfunction

    - anemias- amiloidosis, sarcoidosis

    - Cardiac catheterization

    - PBM (myocardial biopsy)

    3. HFseverity

    - Isotopic ventriculography

    - Myocardial scintigraphy- Ergospirometry

    4. HFprognosis

    - Holtermonitoring

    - Assess - renal function

    - liverfunction

    - hydro-electrolitic equilibrium

    - plasma NA peptide (> 900ng/ml)

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    Establish diagnosis

    Assessments in all cases

    Necessary Supports Opposes

    History with symptoms +++ Ifabsent

    Objective evidence +++ Ifabsent

    Response to treatment ++

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    Testsfordiagnosis

    Test

    Necessary Supports Opposes

    Electrocardiogram ++ Ifnormal

    Echocardiography +++ Ifnormal

    Chest x-ray Ifcongestion Ifnormal

    Blood count Ifnormal

    Blood chemistry Ifnormal

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    Aditional tests

    Test

    Necessary Supports Opposes

    Exercise test Ifnormal

    Natriuretic peptide Ifelevated Ifnormal

    Cardiac cath. Ifnormal

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    CLASS I: no activity limitation patients have cardiac

    dysfunction, had before HF symptoms and are under medication

    for HF

    CLASS II: moderate limitation of physical activity:

    asymptomatic in resting, but usual effort leads to dyspnoea,

    fatigue, palpitations or angina

    CLASS III: important limitation of physical activity :

    asymptomatic at rest, but an effort below the usual intensity

    leads to symptoms.

    CLASS IV: HF symptoms are present at rest and aggravated at

    minimal effort. The patient is not able to perform any physical

    activity without symptoms.

    NYHA Classification

    ( New York Heart Association) 1964

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    CLASA A VO2 max > 20 ml/min/kg

    CLASA B VO2 max = 16-20 ml/min/kgCLASA C VO2 max = 10-15 ml/min/kg

    CLASA D VO2 max < 10 ml/min/kg

    CLASA E VO2 max < 6 ml/min/kg

    Weber andJanicki Classification 1985

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    * HYPERVOLEMIA

    * PRIMARY CARDIOMYOPATHY

    * CAD + ATRIAL ARRHYTHMIA

    * DYSELECTROLYTEMIAS

    - alcalosis with hypo-K+

    - hypo-Na+

    *ALCOHOL

    * INADEQUATE TREATMENT

    -digitalic toxicity-dysfunction -systolic

    -diastolic - diuretics !!!

    - antiarrhythmics

    5. POTENTIAL REVERSIBLE CONDITIONS

    THAT AGGRAVATE HF

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    1. ACE inhibitors

    - first-line therapy in patients with reduced EF < 45%, with orwithoutsymptoms

    - in all HFstages.- fluid retention: ACE-i + Diuretic.

    Recommendations:

    - avoid excessive diuresis before treatment

    - start with a low dose and build up tomaintenance dosage with

    weekly monitoring creatinine and plasma ions- avoid potassium-sparing diuretics during therapy initiation

    - avoid NSAIDs

    If no satisfying response:

    - change with anotherACE-i or

    - Choose an AT1-receptorinhibitor

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    2. Beta-blockade in HF

    Indications

    -stable mild, moderate and severe HFof ischemic and non-ischemicorigin (ifno contraindications)

    -patients with LV dysfunction with/without HFpost-MI forsurvivalbenefit

    Initiation and uptitration ofbeta-blockade in HF:

    - stable patient on a background therapy with ACE-i + DiureticDigoxin

    - nofluid retention

    - no hypotension ( SBP < 90 mmHg)

    - no bradycardia (HR < 55 / min)

    - titrate slowly and carefully from low initial dose to target doses

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    BETA-BLOCKERS in HF

    -BLOCKER INITIAL DOSE (mg) TITRATION (mg) MAX DAILY DOSE(mg)

    BISOPROLOL 1,25 2,5/3,75/5/7,5/10 10CARVEDILOL 3,125 6,25/12,5/25/50 50

    METOPROLOL

    Succinate CR 12,5/25 25/50/100/200 200

    Tartrate 5 10/15/30/50/75/100 150

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    Patientsshould be addressed to a specialist if:

    Severe HF class III/IV Unknown etiology

    Relative CI: bradicardia, low blood pressure

    Low dose intolerance

    Previous beta-blockeruse with treatment cessation because of

    symptoms Suspicion ofasthma orCAD

    Beta-blockers: contraindications in HF

    Asthma

    Severe bronchitis

    Symptomatic bradicardia orhypotension

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    3. DIURETICS

    Loop-diuretics or thiazides

    Always togetherwith an ACE-i

    If GFR < 30 ml/min (glomerular filtration rate) then nothiazides (exception: if thiazides are adjuvant to loop-diuretics)

    Insufficient response:

    1. Increase diuretic dose2. Associate loop-diuretics and thiazides

    3. Persistent fluid retention: loop-diuretics twice a day

    4. Severe HF: monitorcreatinine and electrolytes

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    Potassium-sparing diuretics: triamteren, amiloride,

    spironolactone

    Only if hypo-K+ persists after therapy initiation with ACE-I

    and diuretics

    Initiate with low dose for 1 week, then assess plasma K+

    and creatinine after 5 - 7 days and increase correctly the

    dose. Monitor K+ and creatinine every 5 7 days till K+ is

    constant.

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    MEDICATION INITIAL

    DOSE

    (mg)

    MAX

    DOSE

    (mg)

    SIDE EFFECTS

    l.POTASSIUM-SPARING D.

    * SPIRONOLACTONE 25 100

    * AMILORID 5 40 HYPER-K +

    * TRIAMTEREN 50 100

    2.THIAZIDES

    * HYDROCHLOROTHIAZID 25 50 DYSELECTROLYTEMIA

    * METOLAZONE 2,5 10 THIAZIDIC DIABETES

    METABOLIC

    DISORDERS

    3.LOOP-DIURETICS

    * FUROSEMID 10 240

    * BUMETANID 0,5 10 DYSELECTROLYTEMIA

    * TORASEMID 5 100 METABOLIC

    DISORDERS

    * ETACRINIC ACID 50 200

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    4. DIGITALIS GLYCOSIDES are indicated in:

    -atrial fibrillation

    -any symptomatic HFstage

    -sinusrhythm, ifpersistent HF (systolic LVdysfunction) even if treated with ACE-i + Diuretic

    Digoxin + Beta-blocker: superiorassociation vs. monotherapy

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    5. Vasodilators

    May be used as adjunctive therapy in HFforthe reliefof

    angina oracute dyspnea (nitrates) orconcomitant

    hypertension (DHP calcium antagonists) AT1 bl betterchoice than nitrates /hydralazine when

    intolerance to ACE-I

    Alpha-blockers are not recommended in HF

    DHP calcium antagonists have no effect on survival inHF due to LV systolic dysfunction

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    HF WORSENING imposesfollowing associations:

    -Spironolactone and / or-Loop-diuretic + thiazide

    HF class IV NYHA despite ofoptimal therapy and correct diagnosis

    -Continue with mentioned measures

    -Add palliative therapy in final stages (opioids)

    LV DIASTOLIC DYSFUNCTION

    Recommendations

    -Beta-blockers

    -Calcium antagonists (Verapamil)

    -ACE-i

    -Diuretics (caution!)-Arrhythmias control sustained VT Amiodarone

    Symptomatic A.F. Digitalis

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