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CHRONIC HEART FAILURE.

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Presentation on theme: "CHRONIC HEART FAILURE."— Presentation transcript:

1 CHRONIC HEART FAILURE

2 Heart Failure What is Heart Failure?

3 Basic Definition Heart 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.

4 Statistic It 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.

5 Symptoms (involving gravity/exhaustion of heart
Swelling of the ankles, legs, and hands Orthopnea, or the shortness of breath when lying flat Shortness of breath during exertion

6 Symptoms (involving circulation)
Cyanosis, or a bluish color that is seen in the lips and fingernails from a lack of oxygen Fatigue or weakness Rapid or irregular heart beat Changes of behavior such as restlessness, confusion, and decreased attention span

7 Symptoms (involving congestion)
Unexplained or unintentional weight gain Chronic cough Increased urination Distended neck veins Loss of appetite or indigestion

8 Congenital heart disease Atherosclerosis Rheumatic fever
Congestive heart failure is a syndrome that can be caused by multiple underlying diseases such as: Congenital heart disease Atherosclerosis Rheumatic fever Cardiomyopathy Valve disorders Ventricular failure Left or right-sided failure Hypertension Prolonged alcohol or drug addiction Previous heart attack Diabetes Chronic rapid heartbeats

9 Congenital Heart Disease
CHD 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 ed.

10 Rheumatic Fever Strep 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.

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

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

13 Atherosclerosis Atherosclerosis 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.

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17 KEY ISSUES IN CHRONIC HEART FAILURE
Common 1-3 % of the population, rising to 6-10 % of people aged >65 years Incidence 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 – % of health care budget

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

19 DEFINITION OF HEART FAILURE
AHA / ACC HF guidelines 2001 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 Clinical symptoms / signs secondary to abnormal ventricular function ESC HF guidelines 2001

20 DEFINITION OF HEART FAILURE
Symptoms 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 cases ESC HF guidelines 2005

21 Q’s to be answered while facing a patient with suspected heart failure
Are the patient’s symptoms cardiac in origin? If so, what kind of cardiac disease is producing these symptoms

22 HEART FAILURE should never be the only diagnosis !

23 Etiology of Chronic Heart Failure
Coronary artery disease accounts for about 65% Non-ischemic Cardiomyopathy: Hypertension Valvular Heart Disease Idiopathic Thyroid Toxic or drug-induced

24 SYMPTOMS There 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

25 Electrocardiogram A 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

26 Types of Rhythms Associated with CHF

27 Types of CHF Left Ventricular Failure with Pulmonary Edema
Aka—systolic heart failure Right Ventricular Failure Aka—diastolic heart failure

28 The smooth, glistening pleural surface of a lung is shown here
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.

29 Left Ventricular Failure with PE
Occurs when the left ventricle fails as an effective forward pump back pressure of blood into the pulmonary circulation  pulmonary edema Cannot eject all of the blood delivered from the right heart. Left atrial pressure rises  increased pressure in the pulmonary veins and capillaries When 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

30 Signs and Symptoms of LVF
Severe resp. distress– Evidenced by orthopnea, dyspnea Hx of paroxysmal nocturnal dyspnea. Severe apprehension, agitation, confusion— Resulting from hypoxia Feels like he/she is smothering Cyanosis— Diaphoresis— Results from sympathetic stimulation Pulmonary congestion Often present Rales—especially at the bases. Rhonchi—associated with fluid in the larger airways indicative of severe failure Wheezes—response to airway spasm

31 Jugular Venous Distention—not directly related to LVF.
Comes from back pressure building from right heart into venous circulation Vital Signs— Significant increase in sympathetic discharge to compensate. BP—elevated Pulse rate—elevated to compensate for decreased stroke volume. Respirations—rapid and labored

32 ECHOCARDIOGRAPHY Assessment of LV systolic function (EF)
Assessment of LV diastolic function

33 Natriuretic peptides Plasma 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 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.

34 The value of BNP in HF diagnosis
A. Is well established in the general population B. Is well established in persons at risk of heart failure C. Is well established in patients with suggestive symptoms D. Has an overall accuracy of 100% E. Is based on a high negative predictive value

35 The value of BNP in HF diagnosis
A. Is well established in the general population B. Is well established in persons at risk of heart failure C. Is well established in patients with suggestive symptoms D. Has an overall accuracy of 100% E. Is based on a high negative predictive value

36 NYHA classification of HF
Class 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

37 Stages in the Evolution Clinical Characteristics
Hypertension Diabetes, Hyperchol. Family Hx Cardiotoxins A Stages in the Evolution of Heart Failure Clinical Characteristics B Heart disease (any) Asymptomatic LV dysfunction Systolic / Diastolic C Dyspnea, Fatigue Reduced exercise tolerance D Marked symptoms at rest despite max. therapy 4

38 Stages in the Evolution
Treat risk factors Avoid toxics ACE-i in selected p. A Stages in the Evolution of Heart Failure Treatment B ACE-i  blockers In selected patients C ACE-i  blockers Diuretics / Digitalis D Palliative therapy Mech. Assist device Heart Transplant 4

39 Goals of treatment in CHF
Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms Treatment of Heart Failure. Objectives The 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 patient’s 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.

40 Prolong survival ACE inhibitors Beta blockers Spironolactone
Angiotensin receptor blockers Implantable cardioverter-defibrillators Treatment of Heart Failure. Objectives The 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 patient’s 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.

41 Symptom reduction and improved activity tolerance
Exercise training Diuretics ACE inhibitors Digoxin Beta blockers Treatment of Heart Failure. Objectives The 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 patient’s 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.

42 Prevent progression (remodeling)
ACE inhibitors Beta blockers Spironolactone Angiotensin receptor blockers Cardiac resynchronization (biventricular pacing) Treatment of Heart Failure. Objectives The 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 patient’s 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.

43 Non-pharmacological management
Sodium and fluid restriction Alcohol Weight Smoking Rest and exercise

44 Dietary advice 2-2.5 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

45 Activity and exercise councelling
Encourage regular activity in all patients Exercise training/cardiac rehabilitation in stable, motivated patients

46 Activity and exercise councelling
Symptomatic 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

47 Pharmacologic Therapy
Treatment Pharmacologic Therapy Diuretics ACE inhibitors Beta Blockers Digitalis Spironolactone Other Treatment of Heart Failure. Drugs This is a simple and pragmatic classification of the vast numbers and types of medications in the pharmacopoeia for the treatment of heart failure.

48 Approach to the patient with HF
Assess LV function (EF < 40%) Assess volume status Fluid retention? Yes No Diuretic ACE inhibitor Digoxin Beta-blocker

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

50 Spironolactone. Indications
Recent or current symptoms despite ACE-i, diuretics, dig. and b-blockers AHA / ACC HF guidelines 2001 Recommended in advanced heart failure (III-IV), in addition to ACE-i and diuretics Hypokalemia ESC HF guidelines 2001

51 Angiotensin II Receptor Blockers (ARB)
Candesartan, Eprosartan, Irbesartan Losartan, Telmisartan, Valsartan Efficacy seems to be equal to ACE-I Indicated in patients intolerant to ACE-I Can be considered in combination with ACE-I in patients who remain symptomatic 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.

52 Nitrates. Clinical Use CHF with myocardial ischemia
Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency) Treatment of Heart Failure. Nitrates: Use in Heart Failure Through 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 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.

53 Positive Inotropic Therapy
May increase mortality Exception: Digoxin, Levosimendan Use only in refractory CHF NOT for use as chronic therapy 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.

54 Drugs to Avoid (may increase symptoms, mortality)
Inotropes, long term / intermittent Antiarrhythmics (except amiodarone) Calcium antagonists (except amlodipine) Non-steroidal antiinflammatory drugs (NSAIDS) Tricyclic antidepressants Corticosteroids Lithium ESC HF guidelines 2001

55 New Drugs (ongoing research)
1. New neurohormonal modulators Beta-blockers Aldosterone receptor antagonists Angiotensin II receptor antagonists Endothelin inhibitors Vasopresin inhibitors Natriuretic Peptides Endopeptidase inhibitors Vasopeptidase inhibitors

56 Diastolic Heart Failure
Treat as HF with low LVEF Control: Hypertension Tachycardia Fluid retention Myocardial ischemia Ongoing research

57 ICD Implantation 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 LVEF≤35% and QRS duration ≥ 120 msec ICD therapy is recommended to improve survival in patients after cardiac arrest or who have sustained ventricular tachycardia

58 Heart Transplant. Indications
Refractory cardiogenic shock Documented dependence on IV inotropic support to maintain adequate organ perfusion Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity

59 Thank you for attention!


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