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Chronic Care Programme Treatment guidelines Cardiac Failure Chronic condition Alternative names Consultations protocols Preferred treating provider Notes preferred as indicated by option referral protocols apply Provider General Practitioner Physician Paediatrician Cardiologist Cardiology Paediatrician Surgeon Thoracic Surgeon New Patient Maximum consultations per annum Initial consultation Follow-up consultation Tariff codes Option/plan GMHPP Gold Options G1000, G500 and G200. Blue Options B300 and B200. GMISHPP Existing patient Stable Unstable Controlled Uncontrolled 1 1 3 1 0183; 0142; 0187; 0108 1 5 Investigations protocols Type Provider Treating doctor Urine dipstick (per stick, irrespective of the number of tests on stick) Blood glucose: quantitative Blood glucose: strip test with Pathologist or as per treating doctor Pathologist or as per treating doctor Any Maximum investigations per annum Mild Moderate to severe 1) Patient with cardiac disease but 1) Patient comfortable at no limitation on ordinary rest, less than ordinary physical activity eg can climb activity results in stairs / walk uphill without symptoms (marked symptoms. limitation) eg can walk < 2) Patient comfortable at rest, 1 – 2 blocks: can climb < ordinary activity results in 1 flight of stairs: symptoms (slight limitation) eg intolerant of walking can walk > 2 block on level uphill ground: can climb 1 flight of stairs at normal pace: 2) Patient symptomatic at symptomatic on walking uphill. rest, increases discomfort with any physical activity New Existing New & Existing patient patient Patient Tariff code 4188 4 2 4 4057 1 1 1 photometric reading ECG without effort ECG without and with effort Multistage treadmill test Cardiac examination: (M mode) Cardiac examination: 2 dimensional Cardiac examination + Doppler: Add Haemoglobin estimation Packed cell volume: Haematocrit Platelet count Chol / HDL / LDL / Trig Serum urea Serum creatinine Serum potassium Serum sodium Digoxin level (Drug level – biological fluid: quantitative) Digoxin level (Drug concentration: quantitative) Gamma glutamyl transferase (ggt) TSH Protein: total Aspartate aminotransferase (AST) Alanine aminotransferase (ALT) Lactate dehydrogenase (LD) Albumin INR / Pro-thrombin index CXR ICD 10 coding preferred provider Any preferred provider General Practitioner Specialists (see list) Specialists (see list) Specialists (see list) 4050 1 1 1 1232; 1233 1 1 2 1233 1 1 1 1235 1 1 1 3621 1 0 1 3622 1 1 1 Specialist (see list) Pathologist or as per treating doctor Pathologist 3625 1 1 2 3762 1 1 2 3791 1 1 2 Pathologist Pathologist Pathologist Pathologist Pathologist Pathologist Pathologist 3797 4025 4151 4032 4113 4114 4081 1 1 1 1 3 1 0 1 1 1 1 2 1 0 2 1 2 2 4 2 3 Pathologist 4493 0 0 3 Pathologist 4134 1 0 1 Pathologist Pathologist Pathologist 4507 4117 4130 1 0 0 0 0 0 1 1 1 Pathologist 4131 0 0 1 Pathologist Pathologist Pathologist Radiologist 4133 3999 3805 3445 0 0 0 1 0 0 0 1 1 1 6 2 I111.- I113.- I150. General Congestive heart failure (CHF), congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood through the body. It is not to be confused with "cessation of heartbeat", which is known as asystole, or with cardiac arrest, which is the cessation of normal cardiac function with subsequent hemodynamic collapse leading to death.[citation needed] Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" (ICD-9 428.9) is preferred over the older term "congestive heart failure".[citation needed] Other related terms include ischemic cardiomyopathy (implying that the cause of heart failure is coronary artery disease) and dilated cardiomyopathy (which is a description of echocardiographic findings characteristic of heart failure but which does not suggest any specific etiology.) Congestive heart failure exacerbation or decompensated heart failure (DHF) refer to episodes in which a patient with known chronic heart failure acutely develops symptoms. Congestive heart failure is often undiagnosed due to a lack of a universally agreed definition and difficulties in diagnosis, particularly when the condition is considered "mild". Even with the best therapy, heart failure is associated with an annual mortality of 10%.[1] It is the leading cause of hospitalization in people older than 65.[2] Classification There are many different ways to categorize heart failure, including: the side of the heart involved, (left heart failure versus right heart failure) whether the abnormality is due to contraction or relaxation of the heart (systolic dysfunction vs. diastolic dysfunction) whether the abnormality is due to low cardiac output or high systemic vascular resistance (low-output heart failure vs. high-output heart failure) the degree of functional impairment conferred by the abnormality (as in the NYHA functional classification Signs and symptoms Symptoms Symptoms are dependent on two factors. The first is based on the side of the heart, right or left, that is involved. The second factor is based on the type of failure, either diastolic or systolic. Symptoms and presentation may be indistinguishable making diagnosis impossible based on symptoms. Given that the left side of the heart pumps blood from the lungs to the organs, failure to do so leads to congestion of the lung veins and symptoms that reflect this, as well as reduced supply of blood to the tissues. The predominant respiratory symptom is shortness of breath on exertion (dyspnea, dyspnée d'effort) - or in severe cases at rest - and easy fatigueability. Orthopnea is increasing breathlessness on reclining, often measured in the number of pillows required to lie comfortably. Paroxysmal nocturnal dyspnea is a nighttime attack of severe breathlessness, usually several hours after going to sleep. Poor circulation to the body leads to dizziness, confusion and diaphoresis and cool extremities at rest. The right side of the heart pumps blood returned from the tissues to the lungs to exchange CO2 for O2. Hence, failure of the right side leads to congestion of peripheral tissues. This may lead to peripheral edema or anasarca and nocturia (frequent nighttime urination when the fluid from the legs is returned to the bloodstream). In more severe cases, ascites (fluid accumulation in the abdominal cavity) and hepatomegaly (painful enlargement of the liver) may develop. Heart failure may decompensate easily; this most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), arrhythmias, uncontrolled hypertension, and patient non-compliance with diet or medication.[3] Other classic precipitating factors are anaemia and hyperthyroidism. These place additional strain on the heart muscle, which may cause symptoms to rapidly worsen. Excessive fluid or salt intake (including intravenous fluids for unrelated indications, but more commonly from dietary indiscretion), and medication that causes fluid retention (such as NSAIDs and thiazolidinediones), may also precipitate decompensation.[4] Signs In examining a patient with possible heart failure, a health professional would look for particular signs. General signs indicating heart failure are a laterally displaced apex beat (as the heart is enlarged) and a gallop rhythm (additional heart sounds) in case of decompensation. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure. Predominant left-sided clinical signs are tachypnea and increased work of breathing (signs of respiratory distress not specific to heart failure), rales or crackles, which suggests the development of pulmonary edema, dullness of the lung fields to percussion and diminished breath sounds at the bases of the lung, which suggests the development of a pleural effusion (fluid collection in the pleural cavity) that is transudative in nature, and cyanosis which suggests hypoxemia, caused by the decreased rate of diffusion of oxygen from fluid-filled alveoli to the pulmonary capillaries. Right-sided signs are peripheral edema, ascites and hepatomegaly, an increased jugular venous pressure, which can be increased further by the hepatojugular reflux, and a parasternal heave. Causes Causes and contributing factors to congestive heart failure include the following:[12] Causes of heart failure Left-sided: hypertension (high blood pressure), aortic and mitral valve disease, aortic coarctation Right-sided: pulmonary hypertension (e.g. due to chronic lung disease), pulmonary or tricuspid valve disease. May affect both sides: Ischemic heart disease (due to insufficient vascular supply, usually as a result of coronary artery disease); this may be chronic or due to acute myocardial infarction (a heart attack), chronic arrhythmias (e.g. atrial fibrillation), cardiomyopathy of any cause, cardiac fibrosis, chronic severe anemia, thyroid disease (hyperthyroidism and hypothyroidism) Diagnosis Imaging Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction. In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the patient, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy. Chest X-rays are frequently used to aid in the diagnosis of CHF. In the compensated patient, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Electrophysiology An electrocardiogram (ECG/EKG) is used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Blood tests Blood tests routinely performed include electrolytes (sodium, potassium), measures of renal function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used. According to a meta-analysis comparing BNP and N-terminal pro-BNP (NTproBNP) in the diagnosis of heart failure, BNP is a better indicator for heart failure and left ventricular systolic dysfunction. In groups of symptomatic patients, a diagnostic odds ratio of 27 for BNP compares with a sensitivity of 85% and specificity of 84% in detecting heart failure. [5] Angiography Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery. Monitoring Various measures are often used to assess the progress of patients being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts). Diagnostic criteria No system of diagnostic criteria has been agreed as the gold standard for heart failure. Commonly used systems are the "Framingham criteria"[6] (derived from the Framingham Heart Study), the "Boston criteria",[7] the "Duke criteria",[8] and (in the setting of acute myocardial infarction) the "Killip class".[9] Functional classification is generally done by the New York Heart Association Functional Classification.[10] This score documents severity of symptoms, and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and doesn't reliably predict the walking distance or exercise tolerance on formal testing.[11] The classes (I-IV) are: Class I: no limitation is experienced in any activities; there are no symptoms from ordinary activities. Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion. Class III: marked limitation of any activity; the patient is comfortable only at rest. Class IV: any physical activity brings on discomfort and symptoms occur at rest. In its 2001 guidelines, the American College of Cardiology/American Heart Association working group introduced four stages of heart failure:[12] Stage A: a high risk HF in the future but no structural heart disorder; Stage B: a structural heart disorder but no symptoms at any stage; Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment; Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care. Treatment The treatment of CHF focuses on treating the symptoms and signs of CHF and preventing the progression of disease. If there is a reversible cause of the heart failure (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, or hypertension), that should be addressed as well. Treatments include exercise, eating healthy foods, reduction in salty foods, and abstinence from smoking and drinking alcohol. Modalities Diet and lifestyle measures Patients with CHF are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include:[16] Moderate physical activity, when symptoms are mild or moderate; or bed rest when symptoms are severe. Weight reduction – through physical activity and dietary modification, as obesity is a risk factor for heart failure and left ventricular hypertrophy. Monitor weight - this is a parameter that can easily be measured at home. Rapid weight increase is generally due to fluid retention. Weight gain of more than 2 pounds is associated with admission to the hospital for heart failure[17] Sodium restriction – excessive sodium intake may precipitate or exacerbate heart failure, thus a "no added salt" diet (60–100 mmol total daily intake) is recommended for patients with CHF. More severe restrictions may be required in severe CHF. Fluid restriction – patients with CHF have a diminished ability to excrete free water load. Hyponatremia frequently develops in decompensated heart failure due to the effects of excess circulating neuroendocrine hormones. While the activation of the reninangiotensin-aldosterone axis due to decreased renal perfusion promotes both sodium and water retention, the activation of atrial natriuretic peptide due to atrial stretch favors sodium excretion, and the activation of antidiuretic hormone due to peripheral baroreceptors that sense hypotension as well as due to the activation of the sympathetic nervous system favors water retention alone, leading to disproportionately more water retention than sodium retention. The severity of the hyponatremia during an episode of decompensated heart failure can be predictive of mortality. Generally water intake should be limited to 1.5 L daily or less in patients with hyponatremia, though fluid restriction may be beneficial regardless in symptomatic reduction. Pharmacological management There is a significant evidence–practice gap in the treatment of CHF; particularly the underuse of ACE inhibitors and β-blockers and aldosterone antagonists which have been shown to provide mortality benefit.[18] Treatment of CHF aims to relieve symptoms, maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g. spironolactone). It should be noted that while intuitive, increasing heart function with some drugs, such as the positive inotrope Milrinone, leads to increased mortality.[19][20] Angiotensin-modulating agents ACE inhibitor (ACE) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.[21][12][22] ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy (also referred to as AT1-antagonists or angiotensin receptor blockers), particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEI therapy.[23][24] ACEIs and ARBs decrease afterload by antagonizing the vasopressor effect of angiotensin, thereby decreasing the amount of work the heart must perform. It is also believed that angiotensin directly affects cardiac remodeling, and blocking its activity can thereby slow the deterioration of cardiac function. Diuretics Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure:[16] Loop diuretics (e.g. furosemide, bumetanide) – most commonly used class in CHF, usually for moderate CHF. Thiazide diuretics (e.g. hydrochlorothiazide, chlorthalidone, chlorthiazide) – may be useful for mild CHF, but typically used in severe CHF in combination with loop diuretics, resulting in a synergistic effect. Potassium-sparing diuretics (e.g. amiloride) – used first-line use to correct hypokalaemia. o Spironolactone is used as add-on therapy to ACEI plus loop diuretic in severe CHF. o Eplerenone is specifically indicated for post-MI reduction of cardiovascular risk. If a heart failure patient exhibits a resistance to or poor response to diuretic therapy, ultrafiltration or aquapheresis may be needed to achieve adequate control of fluid retention and congestion. The use of such mechanical methods of fluid removal can produce meaningful clinical benefits in patients with diuretic-resistant heart failure and may restore responsiveness to conventional doses of diuretics.9 Beta blockers Until recently (within the last 20 years), β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure.[22] As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, and extended-release metoprolol. The antagonism of β1 inotropic and chronotropic effects decreases the amount of work the heart must perform. It is also thought that catecholamines and other sympathomimetics have an effect on cardiac remodeling, and blocking their activity can slow the deterioration of cardiac function. Positive inotropes Digoxin (a mildly positive inotrope and negative chronotrope), once used as first-line therapy, is now reserved for control of ventricular rhythm in patients with atrial fibrillation; or where adequate control is not achieved with an ACEI, a beta blocker and a loop diuretic.[22] There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions.[25] It is contraindicated in cardiac tamponade and restrictive cardiomyopathy. The inotropic agent dobutamine is advised only in the short-term use of acutely decompensated heart failure, and has no other uses.[22] Phosphodiesterase inhibitors such as milrinone are sometimes utilized in severe cardiomyopathy. The mechanism of action is through the antagonism of adenosine receptors, resulting in inotropic effects and modest diuretic effects. Alternative vasodilators The combination of isosorbide dinitrate/hydralazine is the only vasodilator regimen, other than ACE inhibitors or angiotensin II receptor antagonists, with proven survival benefits. This combination appears to be particularly beneficial in CHF patients with an African American background, who respond less effectively to ACEI therapy.[26][27] Aldosterone receptor antagonists The RALES trial[28] showed that the addition of spironolactone can improve mortality, particularly in severe cardiomyopathy (ejection fraction less than 25%.) The related drug eplerenone was shown in the EPHESUS trial[29] to have a similar effect, and it is specifically labelled for use in decompesated heart failure complicating acute myocardial infarction. While the antagonism of aldosterone will decrease the effects of sodium and water retention, it is thought that the main mechanism of action is by antagonizing the deleterious effects of aldosterone on cardiac remodeling. Recombinant neuroendocrine hormones Nesiritide, a recombinant form of B-natriuretic peptide, is indicated for use in patients with acute decompensated heart failure who have dyspnea at rest. Nesiritide promotes diuresis and natriuresis, thereby ameliorating volume overload. It is thought that, while BNP is elevated in heart failure, the peptide that is produced is actually dysfunctional or non-functional and thereby ineffective. Vasopressin receptor antagonists Tolvaptan and conivaptan antagonize the effects of antidiuretic hormone (vasopressin), thereby promoting the specific excretion of free water, directly ameliorating the volume overloaded state, and counteracting the hyponatremia that occurs due to the release of neuroendocrine hormones in an attempt to counteract the effects of heart failure. The EVEREST trial, which utilized tolvaptan, showed that when used in combination with conventional therapy, many symptoms of acute decompensated heart failure were significantly improved compared to conventional therapy alone[30] although they found no difference in mortality and morbidity when compared to conventional therapy.[31]. Devices Patients with NYHA class III or IV, left ventricular ejection fraction (LVEF) of 35% or less and a QRS interval of 120 ms or more may benefit from cardiac resynchronization therapy (CRT; pacing both the left and right ventricles), through implantation of a bi-ventricular pacemaker, or surgical remodeling of the heart. These treatment modalities may make the patient symptomatically better, improving quality of life and in some trials have been proven to reduce mortality. The COMPANION trial demonstrated that CRT improved survival in individuals with NYHA class III or IV heart failure with a widened QRS complex on an electrocardiogram.[32] The CARE-HF trial showed that patients receiving CRT and optimal medical therapy benefited from a 36% reduction in all cause mortality, and a reduction in cardiovascular-related hospitalization.[33] Patients with NYHA class II, III or IV, and LVEF of 35% (without a QRS requirement) may also benefit from an implantable cardioverter-defibrillator (ICD), a device that is proven to reduce all cause mortality by 23% compared to placebo. This mortality benefit was observed in patients who were already optimally-managed on drug therapy.[34] Patients with severe cardiomyopathy are at high risk for sudden cardiac death due to ventricular dysrhythmias. Another current treatment involves the use of left ventricular assist devices (LVADs). LVADs are battery-operated mechanical pump-type devices that are surgically implanted on the upper part of the abdomen. They take blood from the left ventricle and pump it through the aorta. LVADs are becoming more common and are often used by patients who have to wait for heart transplants. Surgery The final option, if other measures have failed, is heart transplantation or (temporary or prolonged) implantation of an artificial heart. These remain the recommended surgical treatment options. However, the limited number of hearts available for transplantation in a growing group of candidates, has led to the development of alternative surgical approaches to heart failure. These commonly involve surgical left ventricular remodeling. The aim of the procedures is to reduce the ventricle diameter (targeting Laplace's law and the disease mechanism of heart failure), improve its shape and/or remove non-viable tissue.[35] These procedures can be performed together with coronary artery bypass surgery or mitral valve repair. If heart failure ensues after a myocardial infarction due to scarring and aneurysm formation, reconstructive surgery may be an option. These aneurysms bulge with every contraction, making it inefficient. Cooley and coworkers reported the first surgical treatment of a left ventricular aneurysm in 1958.[36] The used a linear closure after their excision. In the 1980s, Vincent Dor developed a method using an circular patch stitched to the inside of the ventricle (the endoventricular circular patch plasty or Dor procedure) to close the defect after excision.[37] His approach has been modified by others. Today, this is the preferred method for surgical treatment of incorrectly contracting (dyskinetic) left ventricle tissue, although a linear closure technique combined with septoplasty might be equally effective.[38][39] The multicenter RESTORE trial of 1198 participants demonstrated an increase in ejection fraction from about 30% to 40% with a concomitant shift in NYHA classes, with an early mortality of 5% and a 5-year survival of 70%.[40] As of yet, it remains unknown if surgery is superior to optimal medical therapy. The STICH trial (Surgical Treatment for IschemiC Heart Failure) will examine the role of medical treatment, coronary artery bypass surgery and left ventricle remodeling surgery in heart failure patients. Results are expected to be published in 2009 and 2011.[41] The Batista procedure was invented by Brazilian doctor Randas Batista in 1994 for use in patients with non-ischemic dilated cardiomyopathy. It involves removal of a portion of viable tissue from the left ventricle to reduce its size (partial left ventriculectomy), with or without repair or replacement of the mitral valve.[42]. Although several studies showed benefits from this surgery, studies at the Cleveland Clinic concluded that this procedure was associated with a high early and late failure rate. At 3 years only 26 percent were event-free and survival rate was only 60 percent.[43] Most hospitals have abandoned this operation and it is no longer included in heart failure guidelines.[35] Newer procedures under examination are based on the observation that the spherical configuration of the dilated heart reduces ejection fraction compared to the elliptical form. Meshlike constraint devices such as the Acorn CorCap aim to improve contraction efficacy and prevent further remodeling. Clinical trials are underway.[44] Another technique which aims to divide the spherical ventricle into two elliptical halves is used with the Myosplint device.[45] Approach Acute decompensation In acute decompensated heart failure, the immediate goal is to re-establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are secure. Supplemental oxygen should be administered immediately to correct hypoxemia. Acute decompensation may be complicated by respiratory failure, which will require treatment with endotracheal intubation and mechanical ventilation. While heart failure is associated with a volume overloaded state, volume status should be adequately evaluated. Since heart failure patients are generally on chronic diuretics, overdiuresis can occur. In the case of diastolic dysfunction without systolic dysfunction, fluid resuscitation may in fact improve circulation by decreasing heart rate, which will allow the ventricles more time to fill. Even if the patient is edematous, fluid resuscitation may be the first line of treatment if the patient is hypotensive. The patient may in fact be intravascularly volume depleted, although if the hypotension is due to cardiogenic shock, additional fluid may make the situation worse. If the patient's circulatory volume is adequate but there is persistent evidence of inadequate end-organ perfusion, inotropes may be administered. In certain circumstances, a left-ventricle assist device (LVAD) may be necessary. Certain scenarios will require emergent consultation with cardiothoracic surgery. Heart failure due to acute aortic regurgitation is a surgical emergency associated with high mortality. Heart failure may occur after rupture of ventricular aneurysm. These can form after myocardial infarction. If it ruptures on the free wall, it will cause cardiac tamponade. If it ruptures on the intraventricular septum, it can create a ventricular septal defect. Other causes of cardiac tamponade may also require surgical intervention, although emergent treatment at bedside may be adequate. It should also be determined whether the patient had a history of a repaired congenital heart disease as they often have complex cardiac anatomy with artificial grafts and shunts that may sustain damage, leading to acute decompensated heart failure. Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft. Once the patient is stabilized, attention can be turned to treating pulmonary edema to improve oxygenation. Intravenous furosemide is generally the first line. However, patients on longstanding diuretic regimens can become tolerant, and dosages must be progressively increased. If high doses of furosemide are inadequate, boluses or continuous infusions of bumetanide may be preferred. These loop diuretics may be combined with thiazide diuretics such as oral metolazone or intravenous chlorthiazide for a synergistic effect. Intravenous preparations are preferred because of more predictable absorption. When a patient is extremely fluid overloaded, they can develop intestinal edema as well, which can affect enteral absorption of medications. Another option is nesiritide, although it should only be considered if conventional therapy has been ineffective and the patient is extremely symptomatic. Provided that the patient has an adequate blood pressure and is not bradycardia, a β1 selective beta-blocker such as metoprolol should be started. In cases of more severe cardiomyopathy, a beta blocker with alpha antagonist effects such as carvedilol or labetalol may be preferred. An ACE inhibitor or angiotensin receptor blockers should be started as well. If the ejection fraction is poor, an aldosterone receptor antagonist should be started as well. The criteria for successful treatment of acute decompensated heart failure is the re-establishment of adequate oxygenation off of supplemental oxygen, adequate perfusion of end-organs, and return to baseline symptomatology. A parameter frequently used is return to "dry" weight. As the test is becoming more easily available, return to baseline BNP can also serve as a measure of adequate treatment. Chronic management The goal is to prevent the development of acute decompensated heart failure, to counteract the deleterious effects of cardiac remodeling, and to minimize the symptoms that the patient suffers. In addition to pharmacologic agents (oral loop diuretics, beta-blockers, ACE inhibitors or angiotensin receptor blockers, vasodilators, and in severe cardiomyopathy aldosterone receptor antagonists), behavioral modification should be pursued, specifically with regards to dietary guidelines regarding salt and fluid intake. Exercise should be encouraged as tolerated, as sufficient conditioning can significantly improve quality-of-life. In patients with severe cardiomyopathy, implantation of an automatic implantable cardioverter defibrillator(AICD) should be considered. A select population will also probably benefit from ventricular resynchronization. In select cases, cardiac transplantation can be considered. While this may resolve the problems associated with heart failure, the patient generally must remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides. Palliative care and hospice Without transplantation, heart failure caused by ischemic heart disease is not reversible, and cardiac function typically deteriorates with time. (In particular, diastolic function worsens as a function of age even in individuals without ischemic heart disease.) The growing number of patients with Stage D heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines. Medicine formularies Plan or option GMHPP Link to appropriate Mediscor formulary [Core] Gold Options G1000, G500 and G200 Blue Options B300 and B200 GMISHPP Blue Option 100 n/a Epidemiology According to the American Heart Association, about 4.9 million Americans are living with congestive heart failure. Of these, 2.5 million are males and 2.4 million are females. Ten people out of every 1,000 people over age 65 have this condition. There are about 400,000 new cases each year. Prognosis Prognosis in heart failure can be assessed in multiple ways including clinical prediction rules and cardiopulmonary exercise testing. Clinical prediction rules use a composite of clinical factors such as lab tests and blood pressure to estimate prognosis. Among several clinical prediction rules for prognosing acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying patients and identifying those at low risk of death during hospitalization or within 30 days.[46] Easy methods for identifying low risk patients are: ADHERE Tree rule indicates that patients with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications. BWH rule indicates that patients with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or less breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications. A very important method for assessing prognosis in advanced heart failure patients is cardiopulmonary exercise testing (CPX testing). CPX testing is usually required prior to heart transplantation as an indicator of prognosis. Cardiopulmonary exercise testing involves measurement of exhaled oxygen and carbon dioxide during exercise. The peak oxygen consumption (VO2 max) is used as an indicator of prognosis. As a general rule, a VO2 max less than 12-14 cc/kg/min indicates a poorer survival and suggests that the patient may be a candidate for a heart transplant. Patients with a VO2 max<10 cc/kg/min have clearly poorer prognosis. The most recent International Society for Heart and Lung Transplantation (ISHLT) guidelines (http://www.jhltonline.org/article/PIIS1053249806004608/fulltext#sec1) also suggest two other parameters that can be used for evaluation of prognosis in advanced heart failure, the heart failure survival score and the use of a criteria of VE/VCO2 slope>35 from the CPX test. The heart failure survival score is a score calculated using a combination of clinical predictors and the VO2 max from the cardiopulmonary exercise test. References 1. Stefan Neubauer (2007). "The failing heart — an engine out of fuel". N Engl J Med 356 (11): 1140-51. PMID 17360992. 2. Krumholz HM, Chen YT, Wang Y, Vaccarino V, Radford MJ, Horwitz RI (2000). "Predictors of readmission among elderly survivors of admission with heart failure". Am. Heart J. 139 (1 Pt 1): 72-7. doi:10.1016/S0002-8703(00)90311-9. PMID 10618565. 3. Fonarow GC, Abraham WT, Albert NM, et al (April 2008). 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