Heart failure

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Slide 1 : Heart Failure Dr. Wafa Hammoud 1 Dr.wafa Hammoud
Slide 2 : 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. HF can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or myocardial contractility (systolic dysfunction). 2 Dr.wafa Hammoud
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Slide 4 : Epidemiology Large health problem in the US –5 million patients have HF –Over ½ million cases diagnosed each year •Most common discharge diagnosis in patients > 65 years of age 4 Dr.wafa Hammoud
Slide 5 : Etiology of HF HF results from any disorder which prevents: –The heart from contracting (Systolic Dysfunction) and/or –The ventricles from relaxing and filling with blood (Diastolic Dysfunction) •Systolic dysfunction is more prevalent •Systolic and diastolic dysfunction may coexist 5 Dr.wafa Hammoud
Slide 6 : Causes of Heart Failure Systolic Dysfunction (EF <40%) –Reduction in muscle mass e.g. MI •Degree of dysfunction is dependent on size of infarction –Dilated cardiomyopathies (CM) •Leads to systolic contractile dysfunction –Ventricular hypertrophy (HTN, aortic or pulmonic valve stenosis) •Diastolic Dysfunction –Myocardial infarction may slow ventricular relaxation and increase ventricular stiffness –Ventricular hypertrophy The leading causes of HF are CAD and HTN 6 Dr.wafa Hammoud
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Slide 8 : Normal Heart Function –What is Cardiac Output (CO)? •Volume of blood ejected per unit time. •CO = Heart Rate X Stroke Volume •SV dependent upon: –Preload: SV increase with ? in preload –Afterload: SV decrease with ? in afterload –Contractility 8 Dr.wafa Hammoud
Slide 9 : Compensatory Mechanisms Sympathetic Nervous System (SNS) Activation –Tachycardia and increased contractility •Increased preload by activating renin-angiotensin-aldosterone system (RAAS) –Na and water retention •Vasoconstriction –Helps shunt blood away from non-essential organs •Ventricular Hypertrophy and Remodeling Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression 9 Dr.wafa Hammoud
Slide 10 : Compensatory Mechanisms The neurohormonal model of HF recognizes that an initiating event (e.g., acute MI) leads to decreased cardiac output but that the HF state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors. These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin, proinflammatory cytokines (e.g., tumor necrosis factor a, interleukin-6 and interleukin-1ß), and endothelin-1. 10 Dr.wafa Hammoud
Slide 11 : HF Decompensation Exacerbation of symptoms requiring hospitalization •Common factors which precipitate HF –Noncompliance (fluid intake, medications or diet) –Inappropriate medications(negative inotropic, Cardiotoxic, Na- and water-retaining properties). –Cardiac events (MI, atrial fibrillation) –Non-cardiac events (pulmonary infections), anemia 11 Dr.wafa Hammoud
Slide 12 : Drugs may precipitate or exacerbate HF Nonselective ß- blockers CCB (verapamil) various antiarrhythmic agents, especially disopyramide, quinidine, and other class IA drugs anthracycline cancer chemotherapeutic agents (daunomycin and doxorubicin) amphetamine-like drugs and cocaine. NSAID (induce Na and water retention are via PG inhibition) glucocorticoids, androgens, estrogens, pioglitazone and rosiglitazone 12 Dr.wafa Hammoud
Slide 13 : Clinical Presentation of HF The patient presentation may range from asymptomatic to cardiogenic shock Left-sided failure –Blood not effectively pumped from the left ventricle to the peripheral circulation •Right-sided failure –Blood not effectively pumped from the right ventricle into the lungs 13 Dr.wafa Hammoud
Slide 14 : Signs and Symptoms of HF Symptoms: –Dyspnea –Orthopnea –Tachypnea –Fatigue –Cough –Exercise intolerance –Peripheral edema and ascites •Signs: •Pulmonary edema •Cardiomegaly •Hepatomegaly •B-type natriuretic peptide (BNP) >100 pg/ml 14 Dr.wafa Hammoud
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Slide 16 : Diagnosis Laboratory tests identifying disorders that may cause or worsen HF: CBC Serum electrolytes (including Ca, Mg ) Renal, hepatic, thyroid function tests Urinalysis lipid profile A1C. Chest x-ray or ECG Ventricular hypertrophy Chest x-ray may also show pleural effusions or pulmonary edema. The echocardiogram: is the single most useful evaluation procedure because it can identify abnormalities of the pericardium, myocardium, or heart values and quantify the left ventricular ejection fraction (LVEF) to determine if systolic or diastolic dysfunction is present. 16 Dr.wafa Hammoud
Slide 17 : Classifying and Categorizing the HF Patient New York Heart Association Functional Classification Class I: No limitation of physical activity Class II: Slight limitation of physical activity Class III: Marked limitation of physical activity Class IV: Unable to carry on any physical activity w/o discomfort 17 Dr.wafa Hammoud
Slide 18 : Goals of Therapy Relieve symptoms and improve quality of life •Remove or mitigate underlying cause •Prevent hospitalization and prolong life •Preventing the development of the disease 18 Dr.wafa Hammoud
Slide 19 : 19 TREATMENT OF CHRONIC HEART FAILURE GENERAL APPROACH The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. Nonpharmacologic interventions cardiac rehabilitation and restriction of fluid intake (maximum 2 L/day from all sources) and dietary sodium (approximately 2 to 3 g of sodium per day). Dr.wafa Hammoud
Slide 20 : Stages of Heart Failure •Stage A –High risk for developing HF; no structural abnormalities •Stage B –Structural abnormalities; no symptoms •Stage C –Structural abnormalities; current or previous symptoms •Stage D –End stage symptoms refractory to treatment 20 Dr.wafa Hammoud
Slide 21 : Stage A •Patients do not have structural heart disease or symptoms •High risk due to the presence of risk factors •Emphasis is on identification and modification of risk factors to prevent development of structural heart disease 21 Dr.wafa Hammoud
Slide 22 : Stage A: Goals and Therapy •Goals: –Treat hypertension –Encourage smoking cessation –Treat lipid disorders –Encourage regular exercise –Discourage alcohol intake, illicit drug use –Control metabolic syndrome •Therapy: –ACEI or ARB in appropriate patients for vascular disease or diabetes 22 Dr.wafa Hammoud
Slide 23 : Stage B Structural heart disease present, but no symptoms –At risk for development of HF –Treatment is targeted at reducing further injury and preventing (or slowing) remodeling 23 Dr.wafa Hammoud
Slide 24 : Stage B: Goals and Therapy •Goals: –All measures under Stage A •Therapy: –ACEI or ARB –Beta-blockers 24 Dr.wafa Hammoud
Slide 25 : Stage C Patients with structural disease and previous (or current) symptoms •Goals –All measures under Stage A and B –Dietary sodium restriction •Therapy –Medications for routine use: ACEI, beta blockers, diuretics (if clinical evidence of fluid retention) If diuresis is initiated and symptoms improve once the patient is euvolemic, long-term monitoring can begin. If symptoms do not improve –an aldosterone receptor antagonist, ARB (in ACEI intolerant patients), digoxin, and/or hydralazine/isosorbide dinitrate (ISDN) may be useful in carefully selected patients. - Other general measures include moderate sodium restriction, daily weight measurement, immunization against influenza and pneumococcus, modest physical activity, and avoidance of medications that can exacerbate HF 25 Dr.wafa Hammoud
Slide 26 : Stage D •Patients who are symptomatic at rest despite maximal medical therapy •Goals –All measures under A, B and C (as appropriate) •Therapeutic Options –Treat acute HF decompensation –Compassionate end of life care/hospice –Extraordinary measures e.g. Heart transplant 26 Dr.wafa Hammoud
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Slide 28 : ACE Inhibitors for HF Decrease angiotensin II and aldosterone (reducing ventricular remodeling, myocardial fibrosis, cardiac hypertrophy, norepinephrine release, vasoconstriction, and sodium and water retention) •Clinical benefits of ACE-I in HF: –Symptoms improvement, improved exercise tolerance –Frequency of acute CHF exacerbations are reduced –Improvement of EF with long term use •Decrease mortality & the combined risk of death and hospitalizations •Many trials have documented reductions in mortality of 25% 28 Dr.wafa Hammoud
Slide 29 : ACE Inhibitors for HF •Benefits are observed in mild, moderate or severe HF •All patients with LV dysfunction should receive an ACE I (unless intolerant) –Symptomatic improvement may take several weeks. 29 Dr.wafa Hammoud
Slide 30 : ACE Inhibitors for HF ACE Inhibitors approved for the treatment of HF Captopril, enalapril, lisinopril, quinapril, fosinopril, ramipril, trandolapril •Initiation of ACE I therapy –Start with low dose & increase every 1-4 weeks. –Target dose? –Monitoring parameters: K, Scr, blood pressure 30 Dr.wafa Hammoud
Slide 31 : Beta Blockers for HF •Best studied beta blockers in HF are carvedilol, metoprolol extended/controlled release and bisoprolol The ACC/AHA guidelines recommend use of ß-blockers in all stable patients with HF and a reduced LVEF in the absence of contraindications or a clear history of ß-blocker intolerance. Patients should receive a ß- blocker even if symptoms are mild or well controlled with ACE inhibitor and diuretic therapy. 31 Dr.wafa Hammoud
Slide 32 : Beta-Blockers for HF •Benefits of beta-blockers in HF: –Prevent progression of disease –Decrease mortality by decreasing myocyte death (from catecholamine-induced necrosis) –Will increase EF with chronic therapy –improving LV systolic function, decreasing heart rate and ventricular wall stress and thereby reducing myocardial oxygen demand, and inhibiting plasma renin release. –Reverse remodeling (antiarrhythmic effects) •Symptomatic improvement may occur after several months. 32 Dr.wafa Hammoud
Slide 33 : Beta Blockers for HF •Initiation of beta-blocker therapy –When HF symptoms are stable and patient is euvolemic –Start low and go slow double dose every 2-4 weeks (to avoid symptomatic worsening or acute decompensation) •Initial doses –bisoprolol 1.25 mg qd, carvedilol 3.125 bid, metoprolol succinate CR/XL 12.5 mg qd •Target doses –Bisoprolol 10 mg qd, carvedilol 25 mg bid, metroprolol XL 200 mg qd •Monitoring parameters: –BP, HR, edema & fluid retention 33 Dr.wafa Hammoud
Slide 34 : Diuretics for HF •Reduce symptoms •No effect on disease progression (never use as the only therapy) •Adjust treatment to result in 1-2 pounds of weight loss per day (more aggressive inpatient) •Na & fluid restriction is important. •Monitor and replace K & Mg (goal: K=4.0 mEq/L, Mg=2.0 mEq/L) 34 Dr.wafa Hammoud
Slide 35 : Diuretics for HF To restore and maintain euvolemia in HF In addition to acting in the thick ascending limb of the loop of Henle, they induce a prostaglandin-mediated increase in renal blood flow that contributes to their natriuretic effect. •Loops are strong diuretics even with decreased renal function. •Available loop diuretics: 1. furosemide 2. bumetanide 3. torsemide 4. ethacrynic acid •Initiation of diuretic therapy –Initiate therapy with low doses of diuretic (i.e. lasix 20-40 mg/day) and increase dose until patient maintains stable dry weight without dyspnea •Typical furosemide dose in HF 20-160 mg/day Doses of loop diuretics above the recommended ceiling doses produce no additional diuresis in HF. Thus, once those doses are reached, more frequent dosing should be used for additional effect, rather than giving progressively higher doses. 35 Dr.wafa Hammoud
Slide 36 : Digoxin Aldosterone Antagonists Angiotensin II Receptor Blockers ARBs Nitrates and Hydralazine Drug Therapies to Consider for Selected Patients 36 Dr.wafa Hammoud
Slide 37 : 1. Digoxin in HF •Positive inotropic effect. •DIG trial: –Double blind, randomized, placebo controlled trial (n=6800 patients) –Primary endpoint: all-cause mortality –Randomized to digoxin or placebo •Conclusions: –Mortality was the same in both groups –Hospitalizations for worsening HF was reduced by 28% by digoxin compared to placebo (p<0.001) 37 Dr.wafa Hammoud
Slide 38 : Digoxin for HF Place in therapy: –Early in therapy for patients with HF and atrial fibrillation to help control ventricular response –For HF patients in normal sinus rhythm, used with other standard HF therapies (ACEI’s, beta-blockers, diuretics) in patients with symptoms •Initiation: 0.125 mg-0.25 mg qd •Target serum concentration: 0.5 1.0 ng/mL , no benefit of higher plasma levels. Blood samples should be collected at least 6 hours, and preferably 12 hours or more, after the last dose •Monitoring parameters: digoxin toxicity 38 Dr.wafa Hammoud
Slide 39 : 2. Aldosterone Antagonists for HF •Agents: spironolactone and eplerenone •Aldosterone is a neurohormone that plays a role in sodium and water retention and ventricular remodeling (collagen deposition and cardiac fibrosis) •ACEI or ARBS may not totally suppress aldosterone, therefore aldosterone antagonist needed 39 Dr.wafa Hammoud
Slide 40 : Aldosterone Antagonists for HF Recent evidence also suggests an important role in attenuating the systemic proinflammatory state and oxidative stress caused by aldosterone. Based on clinical trial results demonstrating reduced mortality, low-dose aldosterone antagonists may be appropriate for: (1) patients with moderately severe to severe HF who are receiving standard therapy; and (2) those with LV dysfunction early after MI. 40 Dr.wafa Hammoud
Slide 41 : Aldosterone Antagonists for HF •Place in therapy: –Clases III & IV HF –Left ventricular dysfunction immediately after MI •Initiation –spironolactone 25 mg qd, increased to 50 mg qd (same for eplerenone) •Monitoring parameters: Potassium within 1 week of treatment. •Gynecomastia interacts with androgen and progesterone receptors(Not with eplerenone-low affinity for androgen and progesterone receptors. ) 41 Dr.wafa Hammoud
Slide 42 : 3. Angiotensin Receptor Blockers (ARBs) for HF •Chronic administration of ACEI may lead to “ACE Escape” = increased circulating concentrations of ANG II, NE and aldosterone •ARBs considered in patients intolerant to ACEIs •Potential role of ARBs as adjunct therapy (controversial) 42 Dr.wafa Hammoud
Slide 43 : 4. Nitrates and Hydralazine Nitrates (e.g., ISDN) and hydralazine : combination treatment of HF because of their complementary hemodynamic actions. Nitrates : venodilators (reductions in preload) Hydralazine: direct vasodilator (acts on arterial smooth muscle to reduce systemic vascular resistance and increase stroke volume and cardiac output). This combination improves: - endpoint of mortality, hospitalizations for HF - quality of life 43 Dr.wafa Hammoud
Slide 44 : Nitrates and Hydralazine Practice guidelines recommend part of standard therapy in black ethnic with moderately severe to severe HF. may also be reasonable for patients of other ethnicities with persistent symptoms despite optimized therapy with an ACEI (or ARB) and ß-blocker. appropriate as first-line therapy in patients unable to tolerate ACEI or ARBs (renal insufficiency, hyperkalemia, or possibly hypotension). Obstacles to successful therapy with this drug combination include the need for frequent dosing (i.e., three times daily with the fixed-dose) a high frequency of adverse effects (e.g., headache, dizziness, GI distress) increased cost for the fixed-dose combination product. 44 Dr.wafa Hammoud
Slide 45 : 45 TREATMENT OF ACUTE DECOMPENSATED HEART FAILURE GENERAL APPROACH The term decompensated HF refers to patients with new or worsening signs or symptoms that are usually caused by volume overload and/or hypoperfusion and lead to the need for additional medical care, such as emergency. The goals of therapy to relieve congestive symptoms optimize volume status treat symptoms of low cardiac output minimize the risks of drug therapy so the patient can be discharged in a compensated state on oral drug therapy. Dr.wafa Hammoud
Slide 46 : 46 Reversible or treatable causes of decompensation should be corrected. Drugs that may aggravate HF should be evaluated carefully and discontinued when possible. The first step in managing decompensated HF is to ascertain that optimal treatment with oral medications has been achieved. If there is evidence of fluid retention, aggressive diuresis, often with IV diuretics, should be accomplished. Optimal treatment with an ACE inhibitor should be a priority. Although ß-blockers should not be started during this period of instability, they should be continued, if possible, in patients who are already receiving them on a chronic basis. Most patients should be receiving digoxin at a low dose prescribed to achieve a trough serum concentration of 0.5 to 1 ng/mL. Dr.wafa Hammoud
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