CHRONIC HEART FAILURE

CHRONIC HEART FAILURE

2005 Canadian Hypertension Education Program Recommendations

Heart FailureWhat is Heart Failure?


Basic DefinitionHeart failure is a medical term that describes an inability of the heart to keep up its work load of pumping blood to the lungs and to the rest of the body.http://danilhammoudimd_1.tripod.com/cardio1/id57.htm


StatisticIt is estimated that as many as two million Americans suffer from congestive heart failure and that up to 29, 000 die annually from this chronic disorder.

Cannobio, Mary. Cardiovascular Disorders. Missouri: C.V. Mosby Company, 1990.


Symptoms(involving gravity/exhaustion of heartSwelling of the ankles, legs, and handsOrthopnea, or the shortness of breath when lying flat Shortness of breath during exertion


Symptoms(involving circulation)Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygenFatigue or weaknessRapid or irregular heart beatChanges of behavior such as restlessness, confusion, and decreased attention span


Symptoms(involving congestion)Unexplained or unintentional weight gainChronic coughIncreased urinationDistended neck veinsLoss of appetite or indigestion


Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such as:Congenital heart diseaseAtherosclerosisRheumatic feverCardiomyopathyValve disordersVentricular failureLeft or right-sided failureHypertensionProlonged alcohol or drug addictionPrevious heart attackDiabetesChronic rapid heartbeats


Congenital Heart DiseaseCHD affects one out of every one thousand babies. In these babies the marvelously intricate combination of chambers, valves, and vessels making up the heart and circulatory systems fails to form properly before birth. Septal, atrial, and ventricular defects are the most common.Heart. The World Book Encyclopedia. 1996 ed.


Rheumatic FeverStrep throat from the streptococcal infection begins a disease process where the heart valves are damaged. This condition is called rheumatic fever and it affects the connective tissues of the body.


CardiomyopathyCardiomyopathy is the stretching and enlarging of the heart cavity that occurs making the heart weak so it does not pump correctly


Ventricular FailureVentricular failure occurs when there are weak spots in the ventricular walls causing a bulge, or an aneurysm.


AtherosclerosisAtherosclerosis is the gradual clogging of the arteries by fatty, fibrous deposits. A tiny lump of fibrous tissue grows as the artery tries to repair the damage. Cholesterol accumulates and more tissue builds up. The arteries are thickened and hardened making a loss of elasticity causing congestion.http://danilhammoudimd_1.tripod.com/cardio1/id57.htm





KEY ISSUES IN CHRONIC HEART FAILURECommon

1-3 % of the population, rising to 6-10 % of people aged >65 yearsIncidence x2 in the last 10 years

Dangerous high mortality (>50% over 5 yrs, 50% of these deaths occur suddenly)Disabling high morbidity (on average, 1 in 5 patients is readmitted within 12 months)Costly 1.5-2.5% of health care budget


Contributors to Increased IncidenceImprovements in:- Survival post-MI- Technologies (i.e.. Laser, stents etc.)- Medical Treatments for ischemic heart disease- Overall survival


DEFINITION OF HEART FAILURE


DEFINITION OF HEART FAILURESymptoms of heart failure, typically breathlessness or fatigue, either at rest or during exercise, or ankle swelling

Objective evidence (preferably by echocardiography) of cardiac dysfunction (systolic and/or diastolic) at rest

Response to treatment directed towards heart failure

Criteria I. and II. should be fulfilled in all casesESC HF guidelines 2005


Qs to be answered while facing a patient with suspected heart failure

Are the patients symptoms cardiac in origin?

If so, what kind of cardiac disease is producing these symptoms

HEART FAILURE should never be the only diagnosis !


Etiology of Chronic Heart FailureCoronary artery disease accounts for about 65%Non-ischemic Cardiomyopathy:HypertensionValvular Heart DiseaseIdiopathicThyroidToxic or drug-induced


SYMPTOMSThere is a poor relationship between symptoms and the severity of cardiac dysfunction. Mild symptoms should not be equated with minor cardiac dysfunction

Symptoms may be related to prognosis particularly if persisting after therapy

Once a diagnosis of heart failure has been established, symptoms may be used to classify the severity of heart failure and should be used to monitor the effects of therapy


ElectrocardiogramA normal electrocardiogram (ECG) suggests that the diagnosis of CHF should be carefully reviewed

The presence of pathological Q-waves may suggest myocardial infarction as the cause of cardiac dysfunction.

A QRS width >120 ms suggests that cardiac dyssynchrony may be present and a target for treatment


Types of Rhythms Associated with CHF


Left Ventricular Failure with Pulmonary EdemaAkasystolic heart failure

Right Ventricular FailureAkadiastolic heart failure


The smooth, glistening pleural surface of a lung is shown here. This patient had marked pulmonary edema, which increased the fluid in the lymphatics that run between lung lobules. Thus, the lung lobules are outlined in white.


Occurs when the left ventricle fails as an effective forward pumpback pressure of blood into the pulmonary circulation pulmonary edemaCannot eject all of the blood delivered from the right heart.Left atrial pressure rises increased pressure in the pulmonary veins and capillariesWhen pressure becomes to high, the fluid portion of the blood is forced into the alveoli. decreased oxygenation capacity of the lungs AMI common with LVF, suspect


Severe resp. distress Evidenced by orthopnea, dyspneaHx of paroxysmal nocturnal dyspnea.Severe apprehension, agitation, confusionResulting from hypoxiaFeels like he/she is smotheringCyanosis

DiaphoresisResults from sympathetic stimulationPulmonary congestionOften presentRalesespecially at the bases.Rhonchiassociated with fluid in the larger airways indicative of severe failureWheezesresponse to airway spasm


Jugular Venous Distentionnot directly related to LVF. Comes from back pressure building from right heart into venous circulation Vital SignsSignificant increase in sympathetic discharge to compensate.BPelevatedPulse rateelevated to compensate for decreased stroke volume.Respirationsrapid and labored


ECHOCARDIOGRAPHYAssessment of LV systolic function (EF)Assessment of LV diastolic function


Natriuretic peptidesPlasma concentrations of BNP and NT-proBNP are helpful in the diagnosis in HF

A low-normal concentration in an untreated patient makes HF unlikely as the cause of symptoms

BNP and NT-proBNP have considerable prognostic potential. Their role in treatment monitoring remains to be determined


The value of BNP in HF diagnosisA. Is well established in the general populationB. Is well established in persons at risk of heart failureC. Is well established in patients with suggestive symptomsD. Has an overall accuracy of 100%E. Is based on a high negative predictive value


The value of BNP in HF diagnosisA. Is well established in the general populationB. Is well established in persons at risk of heart failureC. Is well established in patients with suggestive symptomsD. Has an overall accuracy of 100%E. Is based on a high negative predictive value


NYHA classification of HFClass I No limitation: ordinary physical exercise does not cause undue fatigue, dyspnea, or palpitations

Class II Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations, or dyspnea

Class III Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

Class IV Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity


Heart disease(any)HypertensionDiabetes, Hyperchol.Family HxCardiotoxinsAsymptomaticLV dysfunctionSystolic / DiastolicMarked symptomsat rest despitemax. therapyDyspnea, FatigueReduced exercisetoleranceStages in the Evolutionof Heart FailureClinical CharacteristicsABCD


ACE-i blockersTreat risk factorsAvoid toxicsACE-i in selected p.In selectedpatientsPalliative therapyMech. Assist deviceHeart TransplantACE-i blockersDiuretics / DigitalisStages in the Evolutionof Heart Failure TreatmentABCD


Goals of treatment in CHF


Prolong survival

ACE inhibitorsBeta blockersSpironolactoneAngiotensin receptor blockersImplantable cardioverter-defibrillators


Symptom reduction and improvedactivity tolerance

Exercise trainingDiureticsACE inhibitorsDigoxinBeta blockers


Prevent progression (remodeling)

ACE inhibitorsBeta blockersSpironolactoneAngiotensin receptor blockersCardiac resynchronization (biventricular pacing)


Non-pharmacological managementSodium and fluid restriction

Alcohol

Weight

Smoking

Rest and exercise


Dietary advice2-2.5 g sodium restriction (about 5-6 g of salt)

Fluid restriction (in patients with refractory fluid retention, significant hyponatremia or severely impaired renal function

Low fat diet and caloric restriction when indicated

Abstention from alcohol or restriction to 1 drink per day


Activity and exercise councellingEncourage regular activity in all patients

Exercise training/cardiac rehabilitation in stable, motivated patients


Activity and exercise councellingSymptomatic and psychologic benefits:Aerobic training results in increased exercise capacity (peak oxygen consumption), improved quality of life (questionnaires), reduced sympathetic nervous system activity

Possible beneficial effect on prognosis


TreatmentPharmacologic TherapyDiureticsACE inhibitorsBeta BlockersDigitalisSpironolactoneOther


Approach to the patient with HFAssess LV function(EF < 40%)

Assess volume statusFluid retention? ACE inhibitorBeta-blockerDiureticNoYesDigoxin


Digitalis. Indications When no adequate response to ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 AF, to slow AV conduction

Dose 0.125 to 0.250 mg / day


Spironolactone. IndicationsRecent or current symptoms despite ACE-i, diuretics, dig. and b-blockersAHA / ACC HF guidelines 2001Recommended in advanced heart failure (III-IV), in addition to ACE-i and diureticsHypokalemiaESC HF guidelines 2001


Candesartan, Eprosartan, IrbesartanLosartan, Telmisartan, ValsartanEfficacy seems to be equal to ACE-IIndicated in patients intolerant to ACE-ICan be considered in combination with ACE-I in patients who remain symptomaticAngiotensin II Receptor Blockers (ARB)


Nitrates. Clinical UseCHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspneaIn acute CHF and pulmonary edema:NTG sl / ivNitrates + Hydralazine in intoleranceto ACE-I (hypotension, renal insufficiency)


May increase mortality Exception: Digoxin, LevosimendanUse only in refractory CHF NOT for use as chronic therapyPositive Inotropic Therapy


Inotropes, long term / intermittentAntiarrhythmics (except amiodarone)Calcium antagonists (except amlodipine)Non-steroidal antiinflammatory drugs (NSAIDS)Tricyclic antidepressantsCorticosteroidsLithiumDrugs to Avoid (may increase symptoms, mortality) ESC HF guidelines 2001


1. New neurohormonal modulatorsBeta-blockersAldosterone receptor antagonists Angiotensin II receptor antagonistsEndothelin inhibitors Vasopresin inhibitorsNatriuretic PeptidesEndopeptidase inhibitorsVasopeptidase inhibitors New Drugs (ongoing research)


Diastolic Heart FailureTreat as HF with low LVEFControl: Hypertension Tachycardia Fluid retention Myocardial ischemiaOngoing research


ICDImplantation of an ICD in combination with biventricular pacing may be considered in patients who remain symptomatic with severe heart failure NYHA class III-IV with LVEF35% and QRS duration 120 msecICD therapy is recommended to improve survival in patients after cardiac arrest or who have sustained ventricular tachycardia


Heart Transplant. IndicationsRefractory cardiogenic shockDocumented dependence on IV inotropic support to maintain adequate organ perfusionPeak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularizationRecurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalitiesContraindications: age, severe comorbidity


Thank you for attention!

Plasma B-type natriuretic peptide (BNP) is a cardiac neurohormone specifically secreted from the cardiac ventricles as a response to ventricular volume expansion, pressure overload, and resultant increased wall tension. Physiologic effects of BNP include diuresis, natriuresis, vasodilation, and anti-fibrotic activity, plus it inhibits the renin-angiotensin-aldosterone system and lowers endothelin levels.In healthy patients, BNP is produced primarily in the ventricles, but in patients with failing hearts, peptide production increases and becomes more generalized throughout the myocardium. Increased cardiac filling pressure is a potent stimulus for peptide secretion . The pro-peptide itself circulates and is cleaved into the biologically active fragment (C-BNP) and the N-terminal pro-B-type natriuretic peptide (NT-proBNP), both of which are measurable in plasma. 44Treatment of Heart Failure.ObjectivesThe objectives of treatment of the patient with heart failure are many, but they may be summarized in two principles: decrease symptoms and prolong life. In daily practice, the first priority is symptom control and the best plan is to adjust to the individual patients particular circumstances over the course of therapy. Nevertheless, the rest of the listed objectives should not be forgotten, as medical therapy now has the potential for decreasing morbidity (hospital admissions, embolism, etc.), increasing exercise capacity (all of the usually prescribed drugs), improve the quality of life, control neurohormonal changes (ACE-I, beta blockers), retard progression (ACEI) and prolong life.

Treatment of Heart Failure.ObjectivesThe objectives of treatment of the patient with heart failure are many, but they may be summarized in two principles: decrease symptoms and prolong life. In daily practice, the first priority is symptom control and the best plan is to adjust to the individual patients particular circumstances over the course of therapy. Nevertheless, the rest of the listed objectives should not be forgotten, as medical therapy now has the potential for decreasing morbidity (hospital admissions, embolism, etc.), increasing exercise capacity (all of the usually prescribed drugs), improve the quality of life, control neurohormonal changes (ACE-I, beta blockers), retard progression (ACEI) and prolong life.



Treatment of Heart Failure.DrugsThis is a simple and pragmatic classification of the vast numbers and types of medications in the pharmacopoeia for the treatment of heart failure.Treatment of congestive heart failure.Angiotensin II inhibitors

Drugs which create a selective and competitive block of the AT1 receptors include: losartan, valsartan, irbersartan and candersartan.Treatment of Heart Failure.Nitrates: Use in Heart FailureThrough venodilation, nitrates reduce LVEDP, PAD, and PCWP, thereby improving pulmonary congestion and exercise tolerance. The reduction in end-diastolic pressure and volume decrease wall tension and oxygen consumption. Cardiac output and arterial pressure are not significantly changed, although a decrease in the LVEDP of 12 mmHg can decrease cardiac output. Nitrates are particularly useful in patients with signs of pulmonary congestion (PCWP > 18 mm Hg) and normal cardiac outputs, or in patients with orthopnea and PND. Recommended doses are well tolerated and rarely cause reflex tachycardia or hypotension. In patients with acute heart failure accompanied by pulmonary edema nitroglycerine can be given sublingually or i.v. I.V. administration allows for immediate onset of action, and rapid disappearance of effect within 10-30 minutes of stopping the infusion. Patients receiving I.V. nitroglycerin should be monitored. In patients with low cardiac output, nitrates can be used in conjunction with arterial vasodilators, dopamine, or dobutamine. In the treatment of chronic heart failure preparations with long half-lives are used. Topical nitroglycerine and other nitrates administered qHS are effective in patients with orthopnea and PND.Treatment of heart failure.Inotropes: General problems

Positive inotropic drugs which increase cellular levels of cAMP have important proarrhythmic effects and seem to accelerate the progression of heart failure. Their hemodynamic effects decreased with prolonged treatment which suggests that they should not be used for chronic treatment. Safety and efficacy increases when they are used in low doses, with which the increase in contractility is slight. This points out that their beneficial effects probably do not depend on their positive inotropic action. The reduction in neurohumoral activation produced by digoxin and ibopamine, the antiarrhythmic action of Vesnarinone or the vasodilatory effects of dopamine, dobutamine or PDE III inhibitors may be more important than the increase in contractility that until recently was though to be their utility in the treatment of heart failure. With the exception of digoxin, chronic administration of these drugs increases mortality, so their use, in low doses, should be restricted to patients with refractory heart failure, with persistent symptoms despite treatment with combinations of other drugs. As it is precisely the sickest patients who manifest the increase in mortality, treatment with inotropic drugs is not likely to prolong the survival of these patients.

CHRONIC HEART FAILURE

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