1) Other names
2) Definition
a) "Congestive" means fluid is building up in the body because the heart isn't pumping the way it should. Despite the way it sounds, the term "heart failure" doesn't mean your heart has stopped working completely. It simply means that your heart isn't pumping blood through the body as well as it should.
b)
3) Pathophysiology
a) Arterial underfilling activates baroreceptors in the left ventricle, aortic arch, and carotid sinus, which then stimulate the vasomotor regulatory centers in the medulla [4]
b) The result is activation of the sympathetic nervous system, the renin-angiotensin-aldosterone system, and the arginine-vasopressin system, which leads to increased heart rate, myocardial contractility, peripheral vasoconstriction, and sodium and water retention. [4]
i) Have plasma aldosterone levels that are 20 times higher than normal [4]
ii) Aldosterone has multiple effects that promote progression of heart failure, including sodium retention, sympathetic activation, parasympathetic inhibition, baroreceptor dysfunction, and myocardial and vascular fibrosis [4]
c) Endothelin [4]
i) A neurohormone elevated in patients with heart failure [4]
ii) Induces release of atrial natriuretic peptides, arginine-vasopressin, and aldosterone [4]
iii) It is a potent long-acting vasoconstrictor [4].
d) Natriuretic peptides, which promote sodium excretion and diuresis, are secreted from the atria and ventricles in response to volume overload and increasing intramyocardial pressure [4].
4) Epidemiologic
a) Incidence
i) The incidence of heart failure in patients older than 80 years is 9 percent [7]. 2
b) Risk factors
i) Extreme obesity [16]
5) Etiology
a) Coronary artery disease (narrowing of the blood vessels to the heart)
b) Past heart attack
c) Problems with the heart muscle (also known as cardiomyopathy)
d) High blood pressure
e) Heart valve problems resulting from disease, infection or a congenital (present from birth) defect
i) Aortic stenosis [14]
f) Abnormal heart rhythms (also known as arrhythmias)
g) Damage to the heart caused by substances, such as alcohol or drugs
h) Congenital heart disease
6) Symptoms
a) Shortness of breath (perhaps when walking or climbing stairs)
b) Shortness of breath when lying down
c) Breathlessness that wakes you up suddenly in the night
d) General tiredness or weakness
e) Swelling of the legs (usually just the feet or ankles)
f) Rapid weight gain (1 to 2 pounds a day for three days in a row).
7) Test
a) Blood tests
i) B-type natriuretic peptide [15] (BNP)[13]
(1) First blood test to be approved in the United States as an aid in the diagnosis of congestive heart failure [13]
(2) Levels by themselves were more accurate than any historical or physical findings or laboratory values in identifying congestive heart failure as the cause of dyspnea. [15]
(3) The diagnostic accuracy of B-type natriuretic peptide at a cutoff of 100 pg per milliliter was 83.4 percent. [15]
(4) The negative predictive value of B-type natriuretic peptide at levels of less than 50 pg per milliliter was 96 percent. [15]
b) Urine tests
c) Chest x-ray
d) Electrocardiogram (EKG)
e) Echocardiography
i) A probe that sends out sound waves is moved across the surface of your chest.
ii) All patients with heart failure should undergo echocardiography or radionuclide ventriculography to confirm systolic dysfunction and determine the ejection fraction [1]
iii) This shows pictures of your heart that show how well it is pumping.
f) Radionuclide ventriculography
i) Involves injecting very low doses of a radioactive substance into your blood.
ii) This substance travels to your heart and helps your doctor get pictures showing how well it is pumping.
iii) The radioactive substance is safe and leaves your body completely after the test is finished.
8) How is CHF classified?
a) New York Heart Association (NYHA) classification for chronic heart failure symptoms [5]
i) Class I [5]
(1) Symptoms cause no limitation of physical activity. Ordinary physical activity does not lead to undue fatigue, palpitations, or dyspnea [5]
ii) Class II [5]
(1) Symptoms cause slight limitation of physical activity. Patient is comfortable at rest, but ordinary physical activity results in fatigue, palpitations, or dyspnea [5].
iii) Class III [5]
(1) Symptoms cause marked limitation of physical activity. Patient is comfortable at rest, but even slight physical activity causes fatigue, palpitations, or dyspnea [5].
iv) Class IV [5]
(1) Symptoms of cardiac insufficiency are present at rest, and discomfort is increased with any physical activity [5].
9)
a) Correction of any underlying problems, such as high blood pressure. Treatment may also include lifestyle changes and medicine. Here are some important things you should talk about with your doctor:
b) Diet
i) A low-salt diet (2 to 3 g of sodium per day) is a basic component in the treatment of heart failure [7]
c) Alcohol. You will be advised to avoid alcohol or strictly limit your use of it.
d) Exercise. Most people with heart failure can still exercise, but your doctor will help you decide how much and what kind of exercise is right for you.
e) Another cornerstone of therapy is frequent measurement of body weight, preferably daily. Every patient should have a calculated target weight. Weight gain of 1.5 to 2.0 kg (3 to 5 lb) per week or new symptoms or signs may signal the need for a change in therapy and should precipitate a call to the physician [7]
f) Standing blood pressure needs to be followed closely. Many patients with heart failure are elderly and are prone to orthostatic hypotension, especially when treated with diuretics and vasodilators [7]. 6,7
g) Medication
i) Angiotensin-converting enzyme (ACE) inhibitors [4, 12]
(1) Most authorities agree that ACE inhibitors should remain first-line therapy for heart failure [4]
(2) Actions
(a) Modify neurohormonal activation in heart failure by inhibiting conversion of angiotensin I to angiotensin II (AII) through ACE [4]
(b) The reduction in AII, a potent myogenic agent, also may attenuate abnormal left ventricular remodeling [4]
(c) Cause down-regulation of the sympathetic nervous system and improve baroreceptor function. [4]
(3) Benefits
(a) Significantly improves survival [4,7, 12]
(i) The Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) [4]
1. 253 patients with NYHA class IV CHF [4]
2. Found that enalapril treatment reduced the mortality rate by 31% after 1 year compared with placebo [4] (27% all-cause mortality reduction) [4]
3. The patients who received the most benefit had the greatest neurohormonal activation as measured by norepinephrine levels [4].
(ii) Studies of Left Ventricular Dysfunction (SOLVD) [4]
1. 2,569 patients with class II, III, or IV CHF [4]
2. Enalapril vs placebo [4]
3. 16% all-cause mortality reduction [4]
i. © Vasodilator-Heart Failure Trial II (V-HeFT II) [4]
4. 804 patients with class II, III, or IV CHF [4]
5. Enalapril vs hydralazine HCl plus isosorbide dinitrate [4]
6. 28% all-cause mortality reduction after 2 years with enalapril [4]
(iii) Survival and Ventricular Enlargement Study (SAVE) [4]
1. 2,231 post-MI patients with ejection fraction of 40% or less [4]
2. Captopril vs placebo [4]
3. 19% all-cause mortality reduction [4]
(b) Improve symptoms [4,7, 12]
(c) Increase exercise capacity [4]
(d) Reduce the number of hospitalizations [4]
(e) Increase ejection fraction [4]
(f) Decrease recurrent myocardial infarction [4]
(4) Who benefits
(a) All stages [2]
(b) Ischemic and nonischemic cardiomyopathies [4]
(c) Symptomatic and asymptomatic left ventricular dysfunction [4]
(d) Enalapril therapy is associated with a significant reduction in the risk of hospitalization for heart failure among white patients with left ventricular dysfunction, but not among similar black patients [9]
(e)
(5) Dosage
(a) Have a high target dose for ACE inhibitor therapy independent of symptomatic relief or hemodynamic effect [4]
(i) High-dose versus standard-dose ACE inhibitors on mortality, morbidity and clinical status in patients with CHF [12]
1. Patients with moderate to severe symptoms of CHF [12]
2. Group 1 took the maximal tolerable dose of enalapril (up to 20 mg per day) [12]
3. Group 2 were titrated up to a maximum of 60 mg per day [12]
4. The enalapril dose was not increased if systolic blood pressure was less than 90 mm Hg or if the drug induced symptoms of hypotension. [12]
5. The results from the study showed no difference in mortality or morbidity rates between the standard-dose and high-dose enalapril groups. [12]
6. There was no difference between the two groups in hospital admission rates for CHF exacerbations [12]
(b) The trend in treating mild to moderate heart failure is to maximize the use of ACE inhibitors and minimize or possibly stop the use of loop diuretics [7]
(c) Low-dose ACE inhibitor therapy should be used if high doses are not tolerated because of hypotension, renal insufficiency, or hyperkalemia. [4]
(d) Lisinopril
(i) Assessment of Treatment with Lisinopril and Survival (ATLAS) trial [4]
1. Designed to define the optimal dosing of ACE inhibitors [4]
2. 3,164 patients with NYHA class II, III, or IV heart failure and an ejection fraction of 30% or less were assigned [4]
3. Receive either a low dose (2.5 to 5 mg/day) or a high dose (32.5 to 35 mg/day) of lisinopril for 3 1/2 to 5 years [4]
4. Both treatment groups experienced similar improvements in symptoms and functional class, but those who received the high dose had a 12% lower relative risk of death or hospitalization and 24% fewer hospitalizations for heart failure [4]
(ii) 20 mg per day [2]?
(e) Captopril 150 mg per day [2,7]
(f) Enalapril 20 mg per day [2,7, 12]
(g) Quinapril 40 mg per day [2]
ii) Beta blockers [4]
(1) First-line therapy [5]
(2) Indications
(a) CHF due to left ventricular systolic dysfunction [4, 5]
(b) Ejection fraction less than 40% [5]
(c) Mild to moderate heart failure as judged by New York Heart Association (NYHA) (10) class II or III symptoms [5]
(i) Therapy probably should be considered in patients with NYHA class I or IV symptoms, despite limited data supporting its benefits at this time [5]
1. The authors conclude that the 29 percent relative risk reduction seen in these class IV CHF patients with beta blockade compares favorably with the overall 32 percent relative risk among all patients with symptomatic heart failure [8].
(3) Contraindications
(a) Signs of clinically unstable heart failure in the previous 2 weeks [5]
(i) Weight gain [5]
(ii) Increased diuretic dosage [5]
(iii) Worsening functional class [5]
(iv) Hospitalization for worsening symptoms [5]
(v) Need for intravenous diuretics or inotropic agents [5]
(b) Bronchial asthma or emphysema sensitive to beta agonists [5]
(c) Bradycardia (heart rate <60 beats per minute) [5]
(d) Hypotension (systolic blood pressure <100 mm Hg) [5]
(e) Second- or third-degree heart block [5]
(4) Options: Until further studies are available, treatment should be limited to use of those agents with proven benefits [5]
(a) Carvedilol [5]
(i) Currently, it is the only beta blocker that has earned US Food and Drug Administration approval for treatment of CHF [5]
(ii) A third-generation beta blocker [5]
(iii) A nonselective beta-receptor antagonist that also blocks alpha1 receptors and has unique antioxidant properties [5]
(iv) The benefit of carvedilol was apparent and of similar magnitude in both black and nonblack patients with heart failure [10]
(b) Extended-release metoprolol [5]
(i) Second-generation, beta1-selective adrenoreceptor blocker [5]
(c) Bisoprolol [5]
(i) A second-generation beta1-selective adrenoreceptor blocker [5]
(5) Dosage
(a) Started at low doses [5]
(i) Patients should first be stable on standard therapy for CHF, including ACE inhibitors, diuretics, and digoxin [5]
(ii) Carvedilol therapy is usually started at 3.125 mg twice daily for 2 weeks [5]
(iii) Bisoprolol is started at 1.25 mg once daily [5]
(iv) Metoprolol CR/XL is usually started at 25 mg once daily [5]
1. For patients with relatively severe symptoms (NYHA class III or IV), a starting dose of 12.5 mg once daily may be appropriate [5].
(b) Gradually increased [5]
(i) The increases in dose should generally occur at 2- to 3-week intervals [5]
(ii) Patients should undergo reevaluation before any adjustments are made [5]
(iii) Carvedilol dose is doubled at 2-week intervals until the target level is achieved [5]
(iv) Bisoprolol dose is increased by 1.25 mg every 1 to 2 weeks [5]
(v) Metoprolol CR/XL dose is doubled at 2-week intervals [5]
(c) Target goals established through major clinical trials [5]
(i) Carvedilol 25 mg twice daily for patients who weigh less than 85 kg and 50 mg twice daily for patients who weigh 85 kg or more [5]
(ii) Bisoprolol: 10 mg once daily [5]
(iii) Metoprolol CR/XL: 200 mg once daily is reached [5]
(6) Benefits
(a) Improve left ventricular function [4,5]
(i) In one meta analysis, the ejection fraction was 23% ± 4% in the placebo group and 31% ± 4% in the beta-blocker group, representing a 29% increase in ejection fraction in patients treated with beta blockers [5]
(b) Reduced hospilizations [5]
(i) In one meta analysis, the number of hospitalizations for worsening of CHF decreased by 41% (95% CI, 26%-52%, P<. 001) in the patients assigned to beta-blocker therapy [5]
(c) Improve symptoms [4]
(d) Improve functional class [4,5]
(i) In a Meta analysis, treated patients were 32% more likely to show improvement in NYHA functional class (95% CI, 1%-74%, P=. 04) and 30% less likely to have a worsening of NYHA functional class (95% CI, 4%-50%, P=. 03) than patients given placebo [5].
(e) Prolong survival [4,5]
(i) Reduction in mortality rates with beta blockers appears to be dose-related [4]
(ii) US Carvedilol Heart Failure Study [4,5]
1. 1,094 patients {4,5]
a. With NYHA class II, III, or IV CHF [4,5
b. EF 23%[5]
2. Carvedilol (25-50 mg bid [5]) vs placebo [4]
3. 65% (395% CI9%-80% [5]) All-cause mortality reduction [4,5]
(iii) Cardiac Insufficiency Bisoprolol Study II (CIBIS-II) [4,5]
1. 2,647 patients
a. NYHA class III or IV CHF [4,5]
2. Bisoprolol (10 mg qd [5]) vs. placebo [4]
3. 34% (19-47% [5]) All-cause mortality reduction [4,5] over an average 6.5-month follow-up [5]
(iv) Metoprolol CR/XL Randomised Intervention Trial in Congestive Heart Failure (MERIT-HF) [4]
1. 3,991 patients with NYHA class III or IV CHF [4]
2. Metoprolol CR/XL (200 mg qd [5]) vs placebo [4]
3. 34% (19% to $7% [5]) All-cause mortality reduction [4]
iii) Aldosterone antagonists [4]
(1) Spironolactone therapy should be considered in all patients with severe symptomatic heart failure in the absence of significant renal insufficiency or hyperkalaemia [4]
(2) Randomized Aldactone Evaluation Study (RALES) [4]
(a) 1,663 patients [4]
(i) With NYHA class III or IV heart failure who were already being treated with ACE inhibitors [4]
(ii) Excluded patients with creatinine levels greater than 2.5 mg/dL and potassium levels greater than 5 micrograms/dL. [4]
(b) Assigned to receive either spironolactone (25 to 50 mg daily) or placebo [4]
(c) Demonstrated significant survival benefit in patients
(d) The incidence of hyperkalemia in both groups was low [4]
iv) Angiotensin II receptor blockers [4]
(1) ARBs can be considered an effective alternative therapy for patients who cannot tolerate ACE inhibitors because of side effects such as cough [4]
(2) Actions
(a) Currently available ARBs selectively block the AT1 receptor, producing vasodilatation and inhibiting muscle cell proliferation [4]
(3) Evaluation of Losartan in the Elderly (ELITE) study [4]
(a) 722 elderly patients with an ejection fraction of 40% or less and NYHA class II, III, or IV heart failure [4]
(b) Received either 50 mg captopril three times a day or 50 mg of losartan potassium once a day for 1 year {4]
(c) A secondary end point was death, hospitalization for heart failure, or both; this end point was reduced by 32% in the group that received losartan [4]
(4) ELITE II [4]
(a) 3,152 patients [4]
(b) Received either 50 mg captopril three times a day or 50 mg of losartan potassium once a day for 1 year {4]
(c) Death as the primary end point [4]
(d) No statistically significant difference in mortality rate between the two groups (15.9% in the captopril group compared with 17.7% in the losartan group) [4]
(5) Valsartan Heart Failure Trial (Val-HeFT) [11]
(a) Randomized, double-blind, placebo-controlled trial that included 5,010 patients [11]
(b) Mild to severe chronic heart failure, an ejection fraction of at least 40 percent and left ventricular diastolic transverse diameter greater than 2.9 cm per m2, [11]
(c) Valsartan titrated to a target dosage of 160 mg twice daily (2,511 patients) or placebo [11]
(d) In patients receiving valsartan, combined mortality and morbidity from heart failure decreased by a significant 13.3 percent, and this benefit was especially significant in patients who were not receiving beta-blockers or ACE inhibitors.] 11]
(e) Patients receiving valsartan had a 27.5 percent reduction in the number of hospitalizations for heart failure, experienced a better quality-of-life as measured by the Minnesota Living with Heart Failure questionnaire, and showed a 22.9 percent improvement in their New York Heart Association (NYHA) classification, indicating favorable effects on disease progression. [11]
(6) Combination therapy with ARBs and ACE inhibitors [4]
(a) A disturbing trend toward increased mortality and morbidity rates was found in the subgroup of patients who received combination therapy with valsartan, ACE inhibitors, and beta blockers [4]
(b) Valsartan Heart Failure Trial (Val-HeFT) [4]
(i) 5,010 patients with an ejection fraction of less than 40% and NYHA class II, III, or IV heart failure who were receiving standard therapy for CHF, including ACE inhibitors (93%), beta blockers (36%), diuretics (86%), and digoxin (67%) [4]
(ii) Given either an ARB, valsartan (target dose, 160 mg twice a day), or placebo [4]
(iii) Treatment with valsartan had a neutral effect on the all-cause mortality rate but reduced hospitalizations for heart failure by 27.5% and the combined end point of morbidity and mortality by 13.3%. [4]
(iv) A disturbing trend toward increased mortality and morbidity rates was found in the subgroup of patients who received combination therapy with valsartan, ACE inhibitors, and beta blockers [4]
v) "Therapy with digoxin is associated with an improved mortality and morbidity of HF, including women and patients with non-systolic HF." (12/8/11)
vi) Estrogen [1]
(1) One study found that use among older women with congestive heart failure is associated with a decrease in the overall and cardiac death rates [1]
h) Although it is technically complex, atriobiventricular pacing significantly improves exercise tolerance and quality of life in patients with chronic heart failure and intraventricular conduction delay [3]
i) Surgical procedures [6]
i) Reduction ventriculoplasty [6]
(1) Also called the Batista procedure [6]
(2) Part of the left ventricular muscle that is dyskinetic is excised, resulting in an increase in contracting myocardium that maintains cardiac output [6]
(3) Offers a potential solution to a subset of patients with end-stage heart failure [6]
ii) Transmyocardial laser revascularization [6]
(1) Very small, diffusely diseased coronary arteries that are not amenable to most types of interventional therapy [6]
iii) Dynamic cardiomyoplasty [6]
(1) Consists of wrapping the latissimus dorsi muscle around the heart and stimulating the muscle to contract in synchrony with cardiac systole [6]
(2) Candidates for this procedure usually are not eligible for heart transplantation and have irreversible heart failure that is refractory to medical therapy [6]
iv) Insertion of partial or total heart assist devices; the patient's own heart continues to do some baseline work. [6]
(1) Insertion of partial assist devices [6]
(a) Intra-aortic balloon pump [6]
(i) The most commonly used short-term assist device [6]
(ii) An inflatable balloon catheter is introduced percutaneously through the femoral artery into the descending aorta [6]
(iii) The balloon is timed to inflate during the diastole, increasing diastolic pressure and improving coronary perfusion [6]
(b) Permanent implantable balloon pump [6]
(i) The intra-aortic balloon pump is sutured into a portion of the descending aorta [6]
(2) Insertion of total assist devices [6]
(a) ABIOMED BVS 5000 [6]
(i) Can be used to augment left, right, or both left and right ventricular function [6]
(ii) Not portable and patients are confined to bed once it is placed. [6]
(iii) It is used for short-term assistance only, such as during treatment of postcardiotomy shock. [6]
(b) Thoratec Ventricular Assist Device [6]
(i) Used to assist the left, right, or both ventricles [6]
(ii) Pneumatically powered, and the movable console allows patients to walk around the hospital [6]
(c) HeartMate Vented Electric Left Ventricular Assist System
(i) Powered by an electric pneumatic pump and provides excellent cardiac output (>9 L/min) [6]
(ii) The least thrombogenic device currently available, and patients do not need to use anticoagulant medications [6]
(iii) Portable, and patients can be discharged from the hospital after the unit is installed [6]
(iv) Approved for use in patients who are awaiting heart transplantation [6]
(d) Novacor Left Ventricular Assist Device [6]
(i) Electrically driven [6]
(ii) Can be easily carried by the patient and thus allows patients to live at home and lead relatively normal lives while awaiting heart transplantation [6]
(iii) More thrombogenic than some of the other assist devices, and anticoagulation therapy is needed in patients who use it [6]
v) Heart replacement [6]
(1) Total artificial heart implantation [6]
(a) CardioWest Total Artificial Heart [6]
(i) Pneumatically driven by pipes that connect the ventricles [6]
(2) Orthotopic or heterotopic donor heart transplantation [6]
(a) Orthotopic, if the heart is placed in the same position as the recipient's normal heart [6]
(b) Heterotopic, if the donor heart is placed beside the recipient heart [6]
(c) Criteria
(i) General criteria [6]
1. End-stage heart disease (<50% survival after 1 yr) as determined by cardiopulmonary testing (maximum oxygen consumption <14 mL/kg/min) [6]
2. Malignant intractable arrhythmias [6]
3. Intractable ischemia [6]
4. Debilitated lifestyle [6]
5. Primary cardiac tumors [6]
(ii) Specific criteria [6]
1. Compliant patient (noncompliance is leading cause of death after transplantation) [6]
2. Freedom from cancer for at least 5 yr [6]
3. No HIV infection [6]
4. Age <70 yr [6]
5. Reversible pulmonary hypertension [6]
6. No significant liver, renal, or pulmonary disease that could decrease life span considerably [6]
7. No irreversible end-organ damage due to chronic diseases (eg, diabetes mellitus) [6]
(d) Priority for heart transplantation
(i) NYHA class IA if they are in the hospital and need circulatory support or mechanical ventilation, are receiving high doses of inotropic drugs, have a Swan-Ganz catheter in place, or have a life expectancy of less than 7 days [5]
(ii) Class IB, patients who have ventricular assist devices already in place or are being treated with intravenous inotropic medication are considered [5]
(iii) Class II, those waiting at home [5]
10) Prognosis
a) Mortality
i) The overall five-year mortality rate is 50 percent [7]. 1
ii) The annual mortality rate is 10% to 15% for patients with mild to moderate heart failure (New York Heart Association [NYHA] classes I and II) [4[
iii) The annual mortality rate is up to 50% for the sickest patients (NYHA class IV) [4]
11) Information for patients
12)
Reference:
1.Estrogen Improves Survival in Older Women with CHF - February 15, 2001 - American Family Physician
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