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Heart Failure- II prognosis And Management

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1 Heart Failure- II prognosis And Management
Dr Hanan ALBackr 10/11/1429 (8/11/2008)

2 DEFINITION Heart failure (HF) is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.


4 Pathophysiology

5 Prevalence Prevalence 0.4-2% overall, 3-5 % in over 65s, 10% of over 80s Commonest medical reason for admission Annual mortality of 60% over 80s > 10% also have AF Progressive condition - median survival 5 years after diagnosis Common condition Prevalence above – one new case per 1000 population per annum, up to 10 per 1000 in elderly Readmission rates as high as 50% over 3 months Loss of cardiac reserve with age and HF may often complicate the presence of other conditions in the elderly If AF and HF - risk of thromboembolic complications esp. stroke - risk 2% in pts in SR but may > 10%/year in pts with AF, no anticoag + other risk factors Mortality varies according to aetiology and severity - prognosis can often be predicted according to the severity of the disease - annual mortality rate 10% Most deaths occur due to progressive pump failure, sudden cardiac death and recurrent MI

6 Rates of Sudden Cardiac Death

7 Typical Presentations Of Heart Failure
Syndrome of decrease exercise tolerance Syndrome of fluid retention No symptoms but incidental discovery of LV dysfunction

8 HISTORY Underlying causes –CAD, valvular disease, hypertension, family history etc. Aggravating factors –arrhythmias (AF), anaemia etc. Co-morbidities/differential diagnoses –COPD, obesity, chronic venous insuff etc.

9 Examination Raised JVP, peripheral oedema, ascites
Signs of poor tissue perfusion Pulse –tachycardia, irregular, thready, pulsus alternans Added heart sounds, murmurs, bibasal inspiratory crackles

10 TESTS 12leadECG CXR •BNP •Echocardiogram
Low sensitivity and specificity


12 EKG


14 CXR

15 Echocardiogram


17 Classification of severity
Class I - symptoms of HF only at activity levels that would limit normal individuals Class II - symptoms of HF with ordinary exertion Class III - symptoms of HF with less than ordinary exertion Class IV - symptoms of HF at rest

18 I No limitation of activities; They suffer no symptoms from ordinary activities
II Slight, mild limitation of activity; They are comfortable with rest or with mild exertion III Marked limitation of activity; They are comfortable only at rest IV Confined to bed or chair; Any physical activity brings on discomfort and symptoms occur at rest

19 Stages of HF  Stage A — High risk for HF, without structural heart disease or symptoms Stage B — Heart disease with asymptomatic left ventricular dysfunction Stage C — Prior or current symptoms of HF Stage D — Advanced heart disease and severely symptomatic or refractory HF


21 Etiology

22 The major causes of heart failure in the developed world are ischaemic heart disease and hypertension

23 Diagnostic Work-up In all cases History, exam, ekg Echo etiology
MR? LVEDD, RV fxn Labs TSH, ferritin, Na, Cr Exercise testing Prognosis, VO2Max Assessment of CAD One of few reversible causes In selected cases Labs Metanephrines Catheterization CAD Hemodynamics Endomyocardial biopsy If infiltrative disease considered



26 Therapy Aims for therapy Reduce symptoms & improve QOL
Reduce hospitalization Reduce mortality Pump failure Sudden cardiac death

27 The Donkey Analogy Ventricular dysfunction limits a patient's ability to perform the routine activities of daily living…

28 Management of Heart Failure
Overview Diagnosis and Evaluation Therapies Diuretics ACE-Inhibitors Digoxin Beta Blockers Recent non-Pharmacological Advances Sudden Death & ICD’s Contractile Dysynchrony and Biventricular Pacing Diastolic Dysfunction

29 Diuretics in Heart Failure
Benefits Improves symptoms of congestion Can improve cardiac output Improved neurohormonal milieu No inherit nephrotoxicity Limitations Oral absorption unpredictable Excessive volume depletion Electrolyte disturbance Unknown effects on mortality Ototoxicity

30 Diuretics, ACE Inhibitors
Reduce the number of sacks on the wagon

31 ACE Inhibitors Reduce mortality, MI, Symptoms
Decrease preload and afterload CONSENSUS 1987 – enalapril vs. placebo – 31% reduction mortality in enalapril group Confirmed by SOLVD, AIRE, SAVE, TRACE 1995 meta-analysis showed 23% reduction total mortality, 35% in combined mortality/hosp admission Should be considered in all Consider in all including asymptomatic esp if EF < 40%. Generally well tolerated Reduce preload and afterload there by inc. CO Act on renin-angiotensin-aldosterone system and reduce afterload by reducing production of angiotensin II Indirect effect on Na and water retention by inhibiting the release of aldosterone and vasopressin thereby reducing venous congestion and preload Inc CO leads to inc renal perfusion which helps alleviate oedema CONSENSUS (cooperative new scandinavian enalapril survival study – landmark study in 253 NYHA class IV patients – benefits seen in 1 yr – red mortality and improvement in NYHA class in TX group enal up to 40mg/day SOLVD enalapril up to 20mg/day, AIRE ramipril, TRACE trandolapril Extensively investigated in large numbers of pts and found to reduce morbidity and mortality, improve NYHA class. This extends to different pt groups eg elderly, women, pts with or without CAD, with differing degrees of functional impairment and history of use of diuretics and dig In absence of clear CI the should be used as first line Rx in all with LVSD who do or do not have Sx – recommeded as 1st line by NICE, european society of cardiology, ACC/AHA

32 Practical ACEI prescribing
Test dose Titrate to higher end of range Continue indefinitely Caution in impaired renal function RAS / Aortic stenosis May cause hypotension may produce hypotension - most pronounced after 1st dose and sometimes severe - pts on high doses of loops and those with low circulating blood volume may be at highest risk options - short acting eg captopril test dosing Give at night May be lessened by longer acting agents associated with lower risk signif BP drops eg ram, perin Important to ensure that dose is titrated upwards to target dose that represents clinical trial data or represents the maximum tolerated by the patient ? Double dose slowly at not less than 2 weekly intervals In clinical practice many patients may be being treated with sub optimal doses hence outcomes may not be as good as expected. However, some is better than none (ATLAS 1999 study lisinopril mg od vs 2.5-5mg od – fewer hosp admissions with higher doses Potentially hazardous in pre-existing renal disease but mild to mod renal imp is not c/I - blockage of renin-angiotensin-aldosterone system may lead to reversible deterioration of renal function (renal perfusion lower in HF and glomerular filtration dependant upon angiotension mediated arterial vasoconstriction) Most are cleared by the kidney so other forms of dose related toxicity are more likely in renal imp Generally small increases in creatinine are acceptable, monitor for progressive increase – european guidelines 2005 suggest specialist input when Cr > 266micromol/L or 50% above baseline (whichever is smaller) ACEI C/I in RAS where activated R-A-A system maintains renal perfusion and in AS as use can dec CO due to decreased filling pressure in the LV Tolerate systolic 90mmHg

33 Potential problems with ACEI
Hyperkalaemia Hypotension Cough Hepatic and renal dysfunction Angiodema Hyperkalaemia due to red circulating aldosterone – care with K supplements / K sparing agents (25-50mg spironolactone generally well tolerated however) Cough due to impairment in bradykinin breakdown - develops in approx 10% pts and more common in women - difficult to attribute to ACEI as CCF also causes dry cough Encourage pts to tolerate if poss / change to different ACEI Rashes, loss or disturbances in taste, mouth ulcers and proteinuria may occur Many are prodrugs – monitor in hepatic dysfunction as this could reduce benefits Most depend upon kidney for excretion Can cause renal dys Need to individualise Tx to gain max benefit with min adverse FX

34 ß-Blockers Limit the donkey’s speed, thus saving energy

35 Beta-blockers US Carvedilol studies 1996
65% decrease mortality in carvedilol group 27% reduction in hospitalisations, reduction in progression of CCF CIBIS-II – Bisoprolol vs. placebo 34% reduction mortality (42% reduction in sudden death 32% hospitalisations Us carvedilol studies 1996 – 4 separate studies 1094 class II to IV pts CIBIS-II 1999 (coronary insufficiency bisoprolol study) – 2,647 class III and IV Sub group analysis suggested that benefits of bisoprolol higher in high risk groups eg diabetics, elderly, renal imp

36 Beta-blockers MERIT-HF - metoprolol COPERNICUS
NYHA class IV, EF < 25% 35% reduction in mortality with carvedilol CAPRICORN - 23% reduction in mortality post MI Merit HF 1999 showed similar results with metop CR in class II to IV COPERNICUS 2001 carvedilol prospective randomised cumulative survival study safe and effective in severe HF with 74% pts achieving target dose CAPRICORN 2001– carvedilol post infarct survival control in left ventricular dysfunction – ef <33% post MI – indicating safe and effective post MI

37 Practical Beta blocker prescribing
“Start low, go slow” Bisoprolol 1.25mg od Carvedilol 3.125mg bd Not rescue therapy Contra indicated in PVD, severe bradycardia Cardioselective agents in mild to moderate reversible airways disease Symptoms likely to worsen before improve - start on low doses and titrate upwards – not more than 2 weekly intervals as per BNF recommendations Severe bradycardia - < 50bpm – consider also concurrent therapy e.g. antiarrythmics, diltiazem, digoxin Cochrane review 2001– no strong evidence to support withholding cardioselective BB in pts with reversible airways disease – use cardioselective agent and careful monitoring of resp function

38 Digitalis Compounds Like the carrot placed in front of the donkey

39 Implantable Cardioverter Defibrillator (ICD)
1-3 leads + pulse generator Sudden onset criteria Stability criteria Treatment zones Pacing Cardioversion Defibrillation Combined CRT-D available

40 Biventricular pacemaker
Resynchronise ventricles by simultaneous pacing NICE guidance published 2007

41 Recommendations An ACE inhibitor should be given to all patients with heart failure unless there are contraindications. In patients intolerant of ACE inhibitors, ARBs are an alternative (level of evidence, A). In symptomatic patients with heart failure, beta-blockers are recommended to reduce mortality rates (level of evidence, A). Aldosterone antagonists are recommended to reduce mortality rates in certain patients with heart failure. These include patients with current or recent history of dyspnea at rest, and patients with recent myocardial infarction who have systolic dysfunction with either clinically significant signs of heart failure or with concomitant diabetes mellitus (level of evidence, B).

42 Recommendations For persistently symptomatic black patients with heart failure, direct-acting vasodilators reduce overall mortality rates when added to background therapy with ACE inhibitors, beta-blockers, and diuretics (if needed). Direct-acting vasodilators are also an alternative for patients with heart failure who are intolerant of ACE inhibitors (level of evidence, B). For patients with heart failure and volume overload, diuretics are recommended (level of evidence, B).

43 Heart Failure: More than just drugs.
Dietary counseling Patient education Physical activity Medication compliance Aggressive follow-up Sudden death assessment

44 Treatment - general No added salt Treat / prevent BP, IHD, EtOH
Stop smoking Exercise and wt control Education Focus of heart failure management has changed significantly over the past 2 decades shifting from symptom management and palliation to improving prognosis and functional status NSF CHD lists general goals of treatment as - relieve Sx, delay progression of disease, reduce cardiac events reduce hopitalisation and mortality - effective Tx can considerable improve QOL and increase survival Pts often elderly with co-morbidities, other complications such as renal imp, polypharmacy/concordance may exist Careful monitoring reqd to detect ADRs, suboptimal Rx and poor concordance IHD – ca channel blockers such as amlodipine shown to be safe as more selective action on vascular tissue and less pronounced action on cardiac contractility than others

45 Patient education Understanding of need for treatment and it’s risks and benefits Timing of doses – diuretics, nitrates Side effects of medicines Self management - monitor weight, oedema Side effects – ACEI Signs of digoxin toxicity

46 Role of HF team Initiate, monitor and individualise therapy
Education and support for pts and carers Liaison with Consultant and GP Encourage and facilitate self management Close links with Community matrons Telephone support End of life care – involvement of palliative care teams

47 Take home message Heart failure is a clinical diagnosis
ACE- inhibitors should be titrated to highest doses tolerable Beta blockers should be used universally but must be titrated slowly Spironolactone should be used in III-IV patients but K+ needs to be monitored closely Digoxin can be used to reduce morbidity Role of ARB remains to be determined in patient tolerating BB & ACE-I Preventive therapy & patient education is the key to reduction of burden

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