Teaching at the Bedside Using CHF as the Model

Teaching at the Bedside Using CHF as the Model

Objectives • Demonstrate how the physician can teach the student/resident at the bedside or during rounds in a time- efficient and effective manner while addressing the clinical condition and needs of the patient • Introduce the bedside physical examination of the patient with CHF and how findings such as Rales/Rhonchi, a positive S-3 or S-4, tachycardia or arrhythmia’s, edema, hepatic congestion or ascites, mental aberrations, and hypertension correlate with the underlying patho-physiology, response to treatment and prognosis • Discuss diagnostic options for evaluation of the patient and the role of echo-cardiographic evaluations, angiograms, BNP, etc. • Utilize the presence of hemodynamically stable and unstable cardiac arrhythmias, Left Ventricular dysfunction or diminished cardiac output to demonstrate treatment choices for the patient and the outcomes • Discuss how pre-load and post-load agents differ and the influences they have on the outcome of patients • Discuss the role of surgical interventions, utilization of pacemakers and defibrillators, etc. in the treatment and their effect on the outcome of the patient • Discuss how co-existing conditions such as renal failure, CAD, COPD, D.M., and end- of -life choices of the patient influence treatment and patient outcomes • Discuss how social economic factors play a role in the treatment and outcome of the patient; genetics, race, diet, insurance, social habits such as alcohol and smoking, etc. how they influence the treatment and outcomes of the patient

Heart failure Heart failure (HF) often called congestive heart failure (CHF) is generally defined as the inability of the heart to supply sufficient blood flow to meet the needs of the body.[1][2][3] Heart failure can cause a number of symptoms including shortness of breath leg swelling exercise intolerance. The condition is diagnosed with echocardiography and blood tests. Treatment commonly consists of lifestyle measures + smoking cessation light exercise including breathing protocols decreased salt intake and other dietary changes) Medications devices or surgery. Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease Hypertension valvular heart disease cardiomyopathy. [4] The term "heart failure" is sometimes incorrectly used to describe other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest, which can cause heart failure but are not equivalent to heart failure. Heart failure is a common, costly, disabling, and potentially deadly condition.[4] In developed countries, around 2% of adults suffer from heart failure, but in those over the age of 65, this increases to 6–10%.[4][5] 1.^ "heart failure" at Dorland's Medical Dictionary 2.^ mayoclinic.com > Heart failure Dec. 23, 2009 3.^ medterms.com > Definition of Heart failure Last Editorial Review: 6/18/2002 4.^ a b c McMurray JJ, Pfeffer MA (2005). "Heart failure". Lancet 365 (9474): 1877–89. doi: /S (05) PMID 5.^ Dickstein K, Cohen-Solal A, Filippatos G, et al. (October 2008). "ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)". Eur. Heart J. 29 (19): 2388–442. doi: /eurheartj/ehn309. PMID

New York Heart Association Functional Classification
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.

American College of Cardiology/American Heart Association working group introduced four stages of heart failure:[11] Stage A: Patients at high risk for developing HF in the future but no functional or 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. The ACC staging system is useful in that Stage A encompasses "pre-heart failure" - a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV. Hunt SA, Abraham WT, Chin MH, et al. (2005). "ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult" (PDF). Circulation 112 (12): e154–235. doi: /CIRCULATIONAHA PMID

Pathophysiology The general effect is one of reduced cardiac output and increased strain on the heart. This increases the risk of cardiac arrest (specifically due to ventricular dysrhythmias), and reduces blood supply to the rest of the body. In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process: Arterial blood pressure falls. This destimulates baroreceptors in the carotid sinus and aortic arch which link to the nucleus tractus solitarius. This center in the brain increases sympathetic activity, releasing catecholamines into the blood stream. Binding to alpha-1 receptors results in systemic arterial vasoconstriction. This helps restore blood pressure but also increases the total peripheral resistance, increasing the workload of the heart. Binding to beta-1 receptors in the myocardium increases the heart rate and make contractions more forceful, in an attempt to increase cardiac output. This also, however, increases the amount of work the heart has to perform. Increased sympathetic stimulation also causes the hypothalamus to secrete vasopressin (also known as antidiuretic hormone or ADH), which causes fluid retention at the kidneys. This increases the blood volume and blood pressure. Reduced perfusion (blood flow) to the kidneys stimulates the release of renin – an enzyme which catalyzes the production of the potent vasopressor angiotensin. Angiotensin and its metabolites cause further vasoconstriction, and stimulate increased secretion of the steroid aldosterone from the adrenal glands. This promotes salt and fluid retention at the kidneys, also increasing the blood volume. The chronically high levels of circulating neuroendocrine hormones such as catecholamines, renin, angiotensin, and aldosterone affects the myocardium directly, causing structural remodeling of the heart over the long term. Many of these remodeling effects seem to be mediated by transforming growth factor beta (TGF-beta), which is a common downstream target of the signal transduction cascade initiated by catecholamines[19] and angiotensin II,[20] and also by epidermal growth factor (EGF), which is a target of the signaling pathway activated by aldosterone[21] Reduced perfusion of skeletal muscle causes atrophy of the muscle fibers. This can result in weakness, increased fatigueability and decreased peak strength - all contributing to exercise intolerance.[22] 19.^ Shigeyama J, Yasumura Y, Sakamoto A, et al. (December 2005). "Increased gene expression of collagen Types I and III is inhibited by beta-receptor blockade in patients with dilated cardiomyopathy". Eur. Heart J. 26 (24): 2698–705. doi: /eurheartj/ehi492. PMID 20.^ Tsutsui H, Matsushima S, Kinugawa S, et al. (May 2007). "Angiotensin II type 1 receptor blocker attenuates myocardial remodeling and preserves diastolic function in diabetic heart" (– Scholar search). Hypertens. Res. 30 (5): 439–49. doi: /hypres PMID [dead link] 21.^ Krug AW, Grossmann C, Schuster C, et al. (October 2003). "Aldosterone stimulates epidermal growth factor receptor expression". J. Biol. Chem. 278 (44): 43060–6. doi: /jbc.M PMID 22systemic pathophysiology in heart failure at GPnotebook

Osler’s words: ‘‘To study the phenomenon of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all’’ (Osler, 1903).

History The importance of bedside teaching has been discussed throughout the history of medicine. Like the modern preceptor, Hippocrates ( BC) was not only a teacher but also an itinerant practitioner. The first two principles of his Hippocratic method are: Observe all, and Study the patient rather than the disease. Although his exact methods of teaching are not known, it is difficult to imagine how the importance of these principles could be communicated unless patients were not present during these teaching encounters. The importance or observation and considering the patient and not just the disease are as relevant today and are still best taught in the presence of the patient.

History Sir William Osler ( ), a renowned clinician and teacher in Canada, England and the United States, became a strong proponent of teaching on rounds and stressed the importance of teaching at the bedside. In 1903 he stated, "How can we make the work of the student…practical…? The answer is, take him from the lecture room, take him from the amphitheater — put him in the outpatient department — put him in the wards." He also expounded that there should be "no teaching without a patient for a text, and the best is that taught by the patient himself." (Whitman, 1990)

History With this historical support for bedside teaching, where are we now? A study in 1964 indicated that less than 75% of teaching on rounds was done in the presence of the patient. In 1978 a similar study demonstrated a decline to 16% of teaching done at the bedside. Given the challenges of modern medicine with shortened hospital stays, increased acuity of illness in the patients and new requirements for oversight and documentation, it is doubtful that the amount of teaching at the bedside has increased. The conference room, nurse’s station or corridor have become the de facto location for teacher/learner interactions at the hospital. History makes it clear that teaching at the bedside has been a vital component of medical training. We should strive to make it as productive and valuable as possible and to convey the energy and excitement of these past shapers of the profession.

Some doctors believe that patients might object or feel uncomfortable with bedside teaching.
An article published by the BMJ in 1968, however, said that 93% of patients did not object to students being taught at the bedside. In fact, the patients love the attention and even feel that the doctors are communicating with them and are interested in them.[1][13] La Combe MA. On bedside teaching. Ann Int Med 1997;126: Bedside teaching. BMJ 1968;1:591.

Learners feel that the bedside is an excellent place to learn a wide variety of skills and often value this teaching more highly than their teachers (Nair et al., 1998). Many teachers may feel uncomfortable in the role of bedside teacher. Lack of experience, unrealistic expectations and discomfort with teaching in the presence of the patient can lead to a reluctance to teach at the bedside. There are techniques and approaches that help make bedside teaching more efficient, fun and effective.

Teaching at the Bedside: Obstacles to Bedside Teaching
If bedside teaching is valuable and important, why does it appear to be declining? A study of potential obstacles (Nair, Coughlan, & Hensley, 1998) revealed that time was considered to be the most significant factor interfering with bedside teaching. Pressures to see more patients, shortened hospital stays and competing demands for increased documentation are contributing to this decline. Preceptors may avoid beside teaching because of concern for patient comfort, yet research has shown that a majority of patients enjoy and benefit from bedside teaching (Nair, Coughlan, & Hensley, 1997; Simons, Bailey, & Zwillich, 1989; Wang-Cheng, Barnas, Sigmann, Riendl, & Young, 1989). When conducted with sensitivity and respect, teaching in the presence of patients can add to rapport and communication.

Preceptors may avoid beside teaching because of concern for patient comfort, yet research has shown that a majority of patients enjoy and benefit from bedside teaching (Nair, Coughlan, & Hensley, 1997; Simons, Bailey, & Zwillich, 1989; Wang-Cheng, Barnas, Sigmann, Riendl, & Young, 1989). When conducted with sensitivity and respect, teaching in the presence of patients can add to rapport and communication.

Actual teaching at the bedside during attending rounds, with emphasis on history taking and physical diagnosis, has declined from an incidence of 75% in the 1960s to an incidence of less than 16% today. Profound advances in technology, in imaging, and in laboratory testing and our fascination for these aspects of patient care, account for part of this decline, but faculty must also assume responsibility for the present lack of bedside teaching.

The Many Tasks of Rounding
The bedside is an important location for teaching, but it is not appropriate for all rounding functions. There are numerous functions that need to occur during rounds. Detailed discussion of differential diagnosis or care plan options is best done in a more confidential location. Administrative details and chart work will go more smoothly in a comfortable location away from interruptions. Presenting patients is usually best performed away from the bedside. Presentations done in the presence of the patient need to be sensitive to the patient and understandable by the patient. The typical format of patient presentation with its medical jargon may intimidate or confuse a patient. Mini-lectures or detailed discussions of differential diagnosis will almost always include terminology or information that may be confusing or difficult for the patient to understand. As attending you will be visiting all patients and this is a prime opportunity for role-modeling and bedside teaching. Although there is additional opportunity for teaching and role modeling in interactions with families this can disrupt a more formal planned teaching experience. Judgment is needed on how to incorporate discussions with family members into teaching.

Preparation is a key element to conducting effective rounds and increasing teacher comfort at the bedside. For those teachers planning bedside rounds especially if unfamiliar or uncomfortable with the technique, a preparatory phase would be of invaluable help in raising their comfort level. The following advices could be carried out: • The teachers need to familiarize themselves with the clinical curriculum that needs to be taught (Cox, 1993). • It is important to investigate the knowledge and the actual clinical skill levels of all the learners to be taught. • Teachers need to improve their own history taking, exam and clinical problem-solving skills by reading, learning from senior expert clinicians as well as use of multimedia such as CD-ROMs, tapes, videotapes etc. on specific areas of clinical examination (LaCombe, 1997). • An ideal adjunct to this stage of preparation would be faculty training on clinical skills and teaching methods.

Introduce yourself and the team to the patient; emphasize the teaching nature of the encounter. In large teaching hospitals patients are usually confused about who their real physicians are, as physician teams tend to make rounds in large groups and patients may see several different physicians in any given day. Physician teams are sometimes lax about introducing themselves and their team of physicians to the patient and explaining what their roles are in their healthcare. • Introduce yourselves to the patient. • It would also be helpful to orient the patients during the bedside encounter as to what is being planned (LaCombe, 1997). This is often a neglected step and leaves patients very puzzled during and after the encounter. • Patients need to be told that the encounter is primarily intended for teaching and that certain theoretical discussions may not be applicable to their illness. • Family need not be asked to leave if the patient wishes them to stay.

Draw a road map of what you plan to achieve at the bedside
For each encounter it is worth investing some time and energy in planning bedside rounds (Ende, 1997). Even if this plan is not strictly followed, as is often the case during bedside encounters, a rough road map would enable the teacher to walk into the encounter with some confidence. Some of the following strategies might help raise teacher confidence levels: • Decide what particular system is to be taught at the bedside. • What specific aspects are to be emphasized?: history taking, physical examination, patient counseling, delivering bad news etc. • What is the main theme for the day?: observation of trainees' performance or demonstration of history taking, exam etc. • Plan activities to keep everyone engaged and involved in the teaching and learning. • Select patent's who would make for good bedside teaching, preferably with the input of the learners. • Decide how much time is to be spent with a given patient.

Orient the learners to your plans for the session and negotiate goals and objectives for the session. Tell the learners what is to be taught. If the teacher has a plan or a road map of the intended teaching exercise, it would be wise to orient the learners to this plan (Cox, 1993). The following activities could be carried out during this orientation phase: • Orient the learners to the objectives of the exercise and activities planned. • Assign roles to each of the team member—this can prevent the utter chaos that sometimes invades a bedside teaching exercise and will also minimize the boredom felt by learners who may otherwise not feel fully engaged. • Learners need to be informed of the teacher's expectations and be educated about appropriate bedside manner. • Team ground rules need to be established. • Any sensitive discussions need to be postponed and the entire team needs to be aware of this.

Challenge the learners' minds without humiliating, augmented by gentle correction when necessary. Do the teaching. Expert educators have written several recommendations on the actual teaching at the bedside (LaCombe, 1997; Kroenke, 2001). Some of the suggestions are listed below: • Avoid asking the trainees impossible questions and 'read my mind' types of questions. Gentle corrections can be made when needed. • Actively discourage one-upmanship among the learners. • Admitting one's own lack of knowledge might set the tone for trainees to admit their limitations and engender a willingness to ask questions. • Teach professionalism and observation. • Keep all learners engaged to avoid boredom. • Emphasize that you are willing to learn from the trainees as well as the patient. • Demonstration of clinical skills can only be done at the bedside. • Avoidance of lengthy didactic discussions keeps learners engaged and involved during the session.

Bedside Teaching Pearls
Establish rules of conduct for bedside presentation early in the rotation. For example: Residents should not whisper in the patient’s room Calls should be made discreetly outside the room Laughing at a patient and the patient’s responses is never appropriate Describing the patient’s sex and race in front of the patient is awkward. Behavior should be proper and respectful - never flippant.

Make appropriate introductions between the patient and the learners.
Insure that the setting of the room is suitable for learning. Pull the patient’s bedside curtain Shut the patient’s door for privacy Invite family members and friends to wait in the lobby Ask the patient for permission to shut off the television

Teach in the presence of the patient.
This gives the patient the opportunity to learn about his/her disease and the patient receives confirmation that the team is actually considering every aspect of the case. It may also prompt new information from the patient.

Patient Comfort Issues
Provide advance notice of visit Limit length of time for patient comfort Explain all examinations and procedures to the patient All discussions and communications should be explained and understandable to the patient Avoid or modify presentations at the bedside Visit the patient is after rounds to answer questions and thank the patient

Teaching at the Bedside: The Office Setting
There are significant opportunities for teaching in the presence of the patient in the office or ambulatory setting. In the typical interaction, the learner sees the patient first, presents the patient to the preceptor outside of the exam room and then both return to the room to complete the visit. One can vary this order and of these components allows chances for bedside teaching. Although typically the learner sees the patient first, seeing the occasional patient together can allow an opportunity for significant role modeling. Although shadowing is usually considered a technique for early learners, it may be judiciously employed with more higher level learners to demonstrate advanced techniques of managing the visit, advanced questioning and dealing with multiple problems presented by the patient. The out-patient preceptor can often predict the challenges that certain patients will offer and can discuss in advance the goals and strategies planned for the encounter so that the learner can be actively analyzing the interaction.

Teaching at the Bedside: Conclusion
Bedside teaching has a long and venerable history and with good reason. Teaching in the presence of patients provides unique and valuable opportunities to integrate the knowledge and skills of medicine for the direct benefit of the patient. The teacher is able to role model skills and attitudes which are vital, but which are hard to communicate with words. Modern medicine has placed additional demands on all parties involved, but that is insufficient reason to abandon a teaching tradition that spans several millennia. We must renew and increase our efforts to pass on this tradition of medical education.

Congestive Heart Failure Physical Examination
BP 108/52 P 140, irreg. R 30 and labored Temp 99°F Ht: 5'8" Wt: 210. General: Breathless, moderately obese male in acute distress sitting upright complaining "I am going to die. Please help me." Neck: Distended neck veins with visible cannon waves, JVD to 12cm. Carotids without bruits. Chest: Scattered rhonchi throughout, rales bilateral one third lower bases. Cough is productive and frothy. Heart: Tachycardia and irreg. Grade 3/6 systolic murmur at LSB, S3 gallop noted. Abdomen: Liver palpable three centimeters below right costal margin. HJR+. Non-tender to palpation, +Bowel sounds 4 quadrants. Extremities: 4+ pitting edema of lower extremities to the knees. Nail beds minimally cyanotic, no clubbing. Pulses intact.

CLINICAL SIGNS: A. Acute failure - During the acute phase of heart failure the time honored clinical signs of acute heart failure reliably identify patients with fluid overload: • S3 if systolic, S4 if diastolic failure. • Terminal inspiratory crackling ralés in the right, then both lungs. • Abnormally prominent venous pulsations. • Peripheral edema. The presence of these signs is solely dependent on fluid overload. Without fluid overload they do not occur. Their presence indicates the need for diuresis. B. Chronic failure5 – The S3 gallop & other signs of CHF do not persist after fluid overload is corrected. There is therefore often no correlation between clinical signs of CHF and objective hemodynamic measures of cardiopulmonary status such as ejection fraction, cardiac output & cardiac index. C. Valsalva maneuver6: (Sensitivity 0.73, specificity 0.65 for CHF), is performed by inflating a BP cuff to 15 mmHg above the systolic pressure, then asking the patient to perform the Valsalva maneuver by holding the breath & contracting the diaphragm while holding the epiglottis closed. In normals the Korotkoff sounds disappear after a few beats. In CHF they persist as long as the breath is held with the diaphragm contracted. A decrease in the ratio of the systolic pressure at which the sound occurs before the Valsalva to the value during Valsalva to 80% or less is a positive test. A positive test is predictive of increased diastolic filling pressures, neurohumeral activation, CHF & all-cause mortality. D. Hepatojugular reflux: (0.24 sensitivity, 0.96 specific). Place a partially inflated BP cuff over the liver. Push on it to a pressure of 33 mmHg. If jugular-venous distention increases ≥3 cm with the patient in a 45o position, it's positive. E. The Proportional Pulse Pressure is said to predict cardiac index (CI) & pulmonary wedge pressure (PAWP). It is calculated by dividing pulse pressure by systolic BP. A value < 25% indicates a CI <2.2 & PAWP >18 mm Hg.

Laboratory Testing Laboratory testing may reveal the presence of disorders or conditions that can lead to or exacerbate HF. The initial evaluation of patients with HF should include a complete blood count, urinalysis, serum electrolytes (including calcium and magnesium), glycohemoglobin, and blood lipids, as well as tests of both renal and hepatic function, a chest radiograph, and a 12-lead electrocardiogram. Thyroid function tests (especially thyroid-stimulating hormone) should be measured, because both hyperthyroidism and hypothyroidism can be a primary or contributory cause of HF. A fasting transferrin saturation is useful to screen for hemochromatosis; several mutated alleles for this disorder are common in individuals of Northern European descent, and affected patients may show improvement in LV function after treatment with phlebotomy and chelating agents.

The single most useful diagnostic test in the evaluation of patients with HF is the comprehensive 2-dimensional echocardiogram coupled with Doppler flow studies to determine whether abnormalities of myocardium, heart valves, or pericardium are present and which chambers are involved. Three fundamental questions must be addressed: 1) Is the LV ejection fraction (EF) preserved or reduced? 2) Is the structure of the LV normal or abnormal? 3) Are there other structural abnormalities such as valvular, pericardial, or right ventricular abnormalities that could account for the clinical presentation? This information should be quantified with a numerical estimate of EF, measurement of ventricular dimensions and/or volumes, measurement of wall thickness, and evaluation of chamber geometry and regional wall motion.

A comprehensive echocardiographic evaluation is important, because it is common for patients to have more than 1 cardiac abnormality that contributes to the development of HF. Furthermore, the study may serve as a baseline for comparison, because measurement of EF and the severity of structural remodeling can provide useful information in patients who have had a change in clinical status or who have experienced or recovered from a clinical event or received treatment that might have had a significant effect on cardiac function.

Supraventricular tachyarrhythmias may exert adverse effects via 4 different mechanisms: 1) the loss of atrial enhancement of ventricular filling may compromise cardiac output; 2) the rapid heart rate may increase demand and decrease coronary perfusion (by shortening ventricular filling time); 3) the rapidity of ventricular response may diminish both cardiac contraction (by aggravating abnormalities of the force-frequency relation) (316,317) and cardiac relaxation (318,319); and 4) the stasis of blood in the fibrillating atria may predispose patients to pulmonary or systemic emboli. In most patients with an ischemic or nonischemic dilated cardiomyopathy, the rapidity of ventricular response is more important than the loss of atrial support, because restoration of sinus rhythm does not result in predictable clinical benefits

Common Factors That Precipitate Hospitalization for Heart Failure
• Noncompliance with medical regimen, sodium and/or fluid restriction • Acute myocardial ischemia • Uncorrected high blood pressure • Atrial fibrillation and other arrhythmias • Recent addition of negative inotropic drugs (e.g., verapamil, nifedipine, diltiazem, beta blockers) • Pulmonary embolus • Nonsteroidal anti-inflammatory drugs • Excessive alcohol or illicit drug use • Endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism, hypothyroidism) • Concurrent infections (e.g., pneumonia, viral illnesses)

Three classes of drugs can exacerbate the syndrome of HF and should be avoided in most patients:
1 Antiarrhythmic agents (146) can exert important cardio depressant and proarrhythmic effects. Of available agents, only amiodarone and dofetilide (147) have been shown not to adversely affect survival. 2 Calcium channel blockers can lead to worsening HF and have been associated with an increased risk of cardiovascular events (148). Of available calcium channel blockers, only the vasoselective ones have been shown not to adversely affect survival (139,149). 3 Nonsteroidal anti-inflammatory drugs can cause sodium retention and peripheral vasoconstriction and can attenuate the efficacy and enhance the toxicity of diuretics and ACE inhibitors

Treatment In addition, moderate sodium restriction, along with daily measurement of weight, is indicated to permit effective use of lower and safer doses of diuretic drugs, even if overt sodium retention can be controlled by the use of diuretics.

Treatment Patients with marked volume overload will require intravenous diuretic therapy with up titration of diuretic dose and/or addition of synergistic diuretic agents. It should be noted that up titration of ACE inhibitors or beta blockers during decompensation may reduce the efficacy of the acute interventions to relieve congestion. Although it is important to ensure that evidence-based medications are instituted prior to the patient leaving the hospital, it is equally as critical to reassess medications on admission and to adjust their administration in light of the worsening HF.

Aldosterone Antagonists
Recommendations Concerning Aldosterone Antagonists. The addition of low-dose aldosterone antagonists is recommended in carefully selected patients with moderately severe or severe HF symptoms and recent decompensation or with LV dysfunction early after MI. These recommendations are based on the strong data demonstrating reduced death and rehospitalization in 2 clinical trial populations (155,161). The entry criteria for these trials describe a broader population than was actually enrolled, such that the favorable efficacy/ toxicity ratio may not be as applicable to patients at the margins of trial eligibility. For both of these major trials, patients were excluded for a serum creatinine level in excess of 2.5 mg per dL, but few patients were actually enrolled with serum creatinine levels over 1.5 mg per dL. In the trial of patients after MI, there was a significant interaction between serum creatinine and benefit of eplerenone. The average serum creatinine of enrolled patients was 1.1 mg per dL, above which there was no demonstrable benefit for survival.

Natriuretic peptides Natriuretic peptides are sensitive to other biological factors, such as age, sex, weight, and renal function (28). Elevated levels lend support to a diagnosis of abnormal ventricular function or hemodynamics causing symptomatic HF (29). Trials with these diagnostic markers suggest use in the urgent-care setting, where they have been used in combination with clinical evaluation to differentiate dyspnea due to HF from dyspnea of other causes (4), and suggest that its use may reduce both the time to hospital discharge and the cost of treatment (30). BNP levels tend to be less elevated in HF with preserved EF than in HF with low EF and are lower in obese patients (31,32). Levels of natriuretic peptides may be elevated meaningfully in women and in people over 60 years of age who do not have HF, and thus these levels should be interpreted cautiously in such individuals when distinguishing between cardiac and noncardiac causes of dyspnea. Elevated natriuretic peptide levels may lend weight to a suspected diagnosis of HF or trigger consideration of HF when the diagnosis is unknown but should not be used in isolation to confirm or exclude the presence of HF (30,33).

References 28. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal dysfunction during intensive therapy for advanced chronic heart failure Am Heart J 1999;138: [CrossRef][Web of Science][Medline] 29. Maisel A. B-type natriuretic peptide levels: a potential novel "white count" for congestive heart failure J Card Fail 2001;7: [CrossRef][Web of Science][Medline] 30. Mueller C, Scholer A, Laule-Kilian K, et al. Use of B-type natriuretic peptide in the evaluation and management of acute dyspnea N Engl J Med 2004;350: [CrossRef][Web of Science][Medline] 31. Wang TJ, Larson MG, Levy D, et al. Impact of obesity on plasma natriuretic peptide levels Circulation 2004;109: [Abstract/Free Full Text] 32. Mehra MR, Uber PA, Park MH, et al. Obesity and suppressed B-type natriuretic peptide levels in heart failure J Am Coll Cardiol 2004;43: [Abstract/Free Full Text]

Surgical treatment for congestive heart failure with autologous adult stem cell transplantation: A prospective randomized study Amit N. Patel, MD, MS a , b , c , * , Luis Geffner, MD b , Roberto F. Vina, MD b , Jorge Saslavsky, MD b , Harold C. Urschel, Jr, MD c , Robert Kormos, MD a , Federico Benetti, MD b a Department of Cardiothoracic Surgery, University of Pittsburgh, Pittsburgh, Pa b Department of Cardiovascular Surgery, Benetti Foundation, Rosario, Argentina c Department of Cardiothoracic Surgery, Baylor University Medical Center, Dallas, Tex

The combination of digoxin and beta blockers may be more effective than beta blockers alone for rate control. Although both verapamil and diltiazem can also suppress the ventricular response during exercise, they can depress myocardial function and increase the risk of worsening HF, especially in patients with HF and low EF, in whom these drugs should be avoided (329,330). If beta-blockers are ineffective or contraindicated in patients with atrial fibrillation and HF, amiodarone may be a useful alternative

Autologous adult stem cell transplantation
A randomized study was conducted with a novel epicardial technique to deploy stem cells as an adjuvant to conventional revascularization therapy in patients with congestive heart failure. METHODS: After institutional review board and government approval, adult autologous stem cell transplantation (CD34+) was performed in patients with ischemic cardiomyopathy and an ejection fraction of less than 35% who were scheduled for primary off-pump coronary artery bypass grafting. Preoperatively, the patients underwent echocardiography, stress thallium imaging single photon emission computed tomography, and cardiac catheterization to identify ischemic regions of the heart and to guide in the selection of stem cell injection sites. The patients were prospectively randomized before the operative therapy was performed. Patient follow-up was 1, 3, and 6 months with echocardiography, single photon emission computed tomography, and angiography. RESULTS: There were 20 patients enrolled in the study. Ten patients had successful subepicardial transplantation of autologous stem cells into ischemic myocardium. The other 10 patients, the control group, only had off-pump coronary artery bypass grafting. There were 8 male and 2 female subjects in each group. The median number of grafts performed was 1 in both groups. On angiographic follow-up, all grafts were patent at 6 months. The ejection fractions of the off-pump coronary artery bypass grafting group versus the off-pump coronary artery bypass grafting plus stem cell transplantation group were as follows: preoperative, 30.7% ± 2.5% versus 29.4% ± 3.6%; 1 month, 36.4% ± 2.6% versus 42.1% ± 3.5%; 3 months, 36.5% ± 3.0% versus 45.5% ± 2.2%; and 6 months, 37.2% ± 3.4% versus 46.1% ± 1.9% (P < .001). There were no perioperative arrhythmias or neurologic or ischemic myocardial events in either group. CONCLUSIONS: Autologous stem cell transplantation led to significant improvement in cardiac function in patients undergoing off-pump coronary artery bypass grafting for ischemic cardiomyopathy. Further investigation is required to quantify the optimal timing and specific cellular effects of the therapy.

Devices and Surgical Interventions
Implantable Cardioverter Defibrillators A significant percentage of patients with heart failure die secondary to sudden cardiac death. Results of the Multicenter Automatic Defibrillator Implantation Trial (MADIT) confirmed the survival benefits of implantable cardiovascular defibrillators (ICDs) after myocardial infarction in patients with nonsustained ventricular tachycardia, inducible ventricular tachycardia, and low EF. Although remarkably effective in terminating ventricular tachycardia, some terminal electrical events in heart failure are due to bradyarrhythmias or electromechanical dissociation. In addition, the high cost of ICDs may limit their widespread application; however, patients who meet MADIT entry criteria will benefit from them. 91.Moss A, Hall W, Cannon D, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med 1996;335:

Transplantation Cardiac transplantation is a life-saving alternative for patients with end-stage heart failure. Survival rates at 1 and 5 years average 75-85% and 60-65%, respectively, which are remarkably better than figures for medically treated patients.[92] 92.Hosenpud J, Bennett L, Keck B, Fiol B, Novick R. Registry of the International Society of Heart and Lung Transplantation: fourteenth official report J Heart Lung Transplant 1997;16:

Nesiritide Nesiritide (b-type natriuretic peptide) is being studied for treatment of decompensated heart failure. Natriuretic peptides have several effects in the body. In the peripheral vasculature, nesiritide causes vasodilation and increased permeability, which in turn cause decreased intravascular volume and lower blood pressure. In the failing heart this decreases both preload and afterload. Nesiritide causes decreased release of renin and adrenal aldosterone, both of which are increased in heart failure. This allows the body to regain control of fluid and electrolyte imbalances. The glomerular filtration rate is increased because of vasodilation of afferent renal arterioles, providing good diuresis and decreasing the volume overload often seen with a decompensated heart. Nesiritide also has an effect on the central nervous system, causing decreased appetite for salt and water, and decreased release of catecholamines. This decrease in sympathetic outflow suppresses reflex tachycardia and vasoconstriction that often accompany decreases in preload, thus sustaining the decrease in blood pressure and increase in diuresis.

A study assessed the hemodynamic effects of nesiritide before, during, and after infusions in 103 patients with NYHA classes II-IV disease with left ventricular EF of less than 35%.[123] Dosages of 0.015, 0.03, and 0.06 µg/kg/minute were compared with placebo infusions given over 24 hours. During the infusion reductions were seen in pulmonary wedge pressure (27% to 39%) systemic vascular resistance right atrial pressure Stroke volume index and cardiac index increased, and heart rates remained stable. Hemodynamic effects were reflected in decreased symptoms within an hour or 2 of start of infusion. Nesiritide should not be given to patients experiencing significant hypotension since it further decreases blood pressure. It also should not be given to patients who are dehydrated because of its diuretic and natriuretic effects. The drug has potential to be good first-line therapy for symptomatic patients with decompensated congestive heart failure.[ ] 123.Mills R, LeJemtel T, Horton D, et al. Sustained hemodynamic effects of an infusion of nesiritide (human b-type natriuretic peptide) in heart failure: a randomized, double-blind, placebo-controlled clinical trial. Natrecor study group. J Am Coll Cardiol 1999;34: 124.Abraham W, Lowes B, Ferguson D, et al. Systemic hemodynamic, neurohormonal, and renal effects of a steady-state infusion of human brain natriuretic peptide in patients with hemodynamically decompensated heart failure. J Cardiol Failure 1998;4:37-43. 125.Marcus L, Hart D, Packer M, et al. Hemodynamic and renal excretory effects of human brain natriuretic peptide infusion in patients with congestive heart failure. Circulation 1996;94:

Left Ventricular Volume-Reduction Surgery
Ventricular volume reduction or remodeling has received extensive media publicity.[104] A portion of the dilated left ventricle is removed, with repair of the mitral and tricuspid valves. Although adequate follow-up data were not reported, the outcome of two series of patients undergoing the procedure were published. Fifty-three candidates for transplantation with dilated cardiomyopathy underwent partial left ventriculectomy and mitral valve repair.[105] Five patients died, one preoperatively and four at late follow-up. Eight patients required LVAD after the procedure. Survival at 11 months was 87%, with 72% of patients remaining off the transplant list. Twenty-five patients (47%) returned to functional class I or II during the year of follow-up. Results were viewed with skepticism as the cardiac index rose only from 2.2 to 2.4 L/min/m[2]. Fourteen patients who were not transplant candidates underwent the procedure.[106] Etiology of heart failure was mixed, with eight having cardiomyopathy, five ischemic heart disease, and one valvular disease. Three patients died during surgery and one died 3 months after the operation. Most important, cardiac index increased from 1.91 ± 0.4 to 2.27 ± 0.6 L/min/m2 (p=0.001). The investigators concluded that the procedure holds the greatest promises for patients not eligible for transplantation. As of this writing, many centers have abandoned the surgery due to increased mortality. The experience of the surgeon and type of patient who best tolerates this procedure affect mortality. Volume-reduction surgery may be an option for patients as a bridge to transplantation or to extend life if no other option is available. 104.Batista R, Santos J, Takeshita N, Bocchino L, Lima P, Cunha M. Partial left ventriculectomy to improve left ventricular function in end-stage heart disease. J Cardiol Surg 1996;11:96-7.

ACE Inhibitors Over the last decade, ACE inhibitors have been studied extensively in patients with heart failure. A series of large-scale clinical trials, starting with the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS)[11] in 1987 and continuing through the Acute Infarction Ramipril Efficacy (AIRE) study[12] in 1994, provide data to support their use. They improve symptoms, decrease disease progression, and lengthen survival. The Survival and Ventricular Enlargement study (SAVE),[13] and more recently, the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico (GISSI-3),[14] and the fourth International Study of Infarct Survival (ISIS-4),[15] indicate that ACE inhibitors also reduce the risk of recurrent myocardial infarction in patients with left ventricular dysfunction. 12.The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators. Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. Lancet 1993;342:821-8. 13.Pfeffer M, Braunwald E, Moye L. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. N Engl J Med 1992;327: 14.Gruppo Italiano per lo Studia della Sopravvivenza nell'Infarto Miocardico. GISSI-3: effects of lisinopril and transdermal glyceryl trinitrate singly and together on 6-week mortality and ventricular function after acute

ß-Adrenergic Antagonists
Whether or not sustained activation of the sympathetic nervous system can be deleterious to an already failing heart has been debated for years. The clinical benefit of ß-adrenergic blockers in these patients was first demonstrated in 1975.[29] Since that time, several studies showed improved left ventricular ejection fraction (EF) and reduction in hospitalizations, but failed to demonstrate a significant mortality benefit.[30,31] Further studies, the second Cardiac Insufficiency Bisoprolol Study (CIBIS II)[32] and the Metoprolol CR/XL Randomized Intervention Trial in Heart Failure (MERIT-HF),[33] with greater numbers of patients, showed mortality reductions of 32% and 34%, respectively. The most convincing evidence in favor of ß-blockers comes from various carvedilol studies in which the overall reduction in mortality was 65%.[34]

Beta Blockers references
29.Waagstein F, Hjalmarson A, Varnauskas E, Wallentin I. Effect of chronic ß-adrenergic receptor blockade in congestive cardiomyopathy. Br Heart J 1975;37: 30.Waagstein F, Bristow M, Swedberg K. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Lancet 1993;342: 31.The Cardiac Insufficiency Bisoprolol Study (CIBIS) Investigators and Committees. A randomized trial of ß-blockade in heart failure: the Cardiac Insufficiency Bisoprolol Study (CIBIS). Circulation 1994;90: 32.CIBISIIInvestigators and Committees. The Cardiac Insufficiency Bisoprolol Study II (CIBIS II): a randomized trial. Lancet 1999;353:9-13. 33.Merit-HF Study Group. Effect of metoprolol CR/XLin chronic heart failure: Metoprolol CR/XL Randomized Intervention Trial in Congestive Heart Failure (MERIT-HF). Lancet 1999;353: 34.Packer M, Bristow M, Cohn J. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med 1996;334: 35.Metra M, Nardi M, Goibbomo R, Dei Cas L. Effects of short- and long-term carvedilol administration on rest and exercise hemodynamic variables, exercise capacity and clinical conditions in patients with idiopathic dilated cardiomyopathy. J Am Coll Cardiol 1994;24: 36.Australia-New Zealand Heart Failure Research Collaborative Group. Effects of carvedilol, a vasodilator-ß-blocker, in patients with congestive heart failure due to ischemic heart disease. Circulation 1995;92: 37.Colucci W, Packer M, Bristow M. Carvedilol inhibits clinical progression in patients with mild heart failure [abstr]. Circulation 1995;92:I-395. 38.Bristow M, Gilbert E, Abraham W. Multicenter Oral Carvedilol Heart Failure Assessment (MOCHA): a six-month dose-response evaluation in class II-IV patients [abstr]. Circulation 1995;92:I-142. 39.Packer M, Colucci W, Sackner-Bernstein J. Prospective randomized evaluation of carvedilol on symptoms and exercise tolerance in chronic heart failure: results of the PRECISE trial [abstr]. Circulation 1995;92:I-143. 40.Cohn J, Fowler M, Bristow M. Effect of carvedilol in severe chronic heart failure [abstr]. J Am Coll Cardiol 1996;27:170A.

Hydralazine and Isosorbide Dinitrate
In a large-scale trial that compared the vasodilator combination with placebo, the use of hydralazine and isosorbide dinitrate reduced mortality but not hospitalizations in patients with HF treated with digoxin and diuretics but not an ACE inhibitor or beta blocker (136,137). However, in another large-scale trial that compared the vasodilator combination with an ACE inhibitor, the ACE inhibitor produced more favorable effects on survival (52), a benefit not evident in the subgroup of patients with Class III to IV HF. In both trials, the use of hydralazine and isosorbide dinitrate produced frequent adverse reactions (primarily headache and gastrointestinal complaints), and many patients could not continue treatment at target doses. Of note, a post hoc retrospective analysis of both vasodilator trials demonstrated particular efficacy of isosorbide dinitrate and hydralazine in the African American cohort (119). A confirmatory trial has been done. In that trial, which was limited to the patients self-described as African American, the addition of hydralazine and isosorbide dinitrate to standard therapy with an ACE inhibitor and/or a beta blocker was shown to be of significant benefit (120). The benefit was presumed to be related to enhanced nitric oxide bioavailability. Accordingly, this combination is recommended for African Americans who remain symptomatic despite optimal medical therapy.

Thiamin As many as 20% of patients on long term loop diuretic therapy exhibit biochemical evidence of thiamin deficiency because of increases urinary thiamin excretion, even if dietary thiamin is adequate. Since ethanol inhibits GI absorption of thiamin uptake this is especially important among ETOH drinkers. Severe thiamin deficiency may produce peripheral vasodilation and 2o high output failure ("wet" beriberi) and in more advanced cases may produce low output biventricular failure. Thiamin supplements cure these patients.

Non-Pharmaceutical and Ancillary Treatments: CPAP and BiPAP
Positive pressure breathing: CPAP and BiPAP redistribute fluid within the lung, reduces both preload and afterload, increases cardiac output by increasing intrathoracic pressure and increases ejection fraction. It also reduces endothelin-1 (the systemic and pulmonary vasoconstrictor) faster than O2 by mask. BiPAP reduced the need for intubation for pulmonary edema in one study. Aerobic Exercise16 improves exercise tolerance and stamina, improving left ventricular volume and stroke volume. As fitness improves, heart rate, blood pressure, sympathetic tone and exercise induced platelet activation are also improved. There are no cardiac contraindications to graded exercise training in patients with stable CHF caused by left ventricular systolic dysfunction.

Cardiac Resynchronization Therapy
Conclusions: In patients with NYHA Class III or IV CHF despite medical management, reduced ejection fractions, and prolonged QRS duration, CRT improves functional and hemodynamic markers and reduces morbidity/mortality. Given the moderate implantation success rates, biventricular pacemaker insertions should only be done by experienced providers. The cost-effectiveness of CRT remains uncertain.

CAM Treatment Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study. Morisco C, Trimarco B, Condorelli M. Facoltà di Medicina e Chiruriga, Università degli Studi di Napoli Federico II. Abstract The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range years) or coenzyme Q10 (n = 319, mean age 67 years, range years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.

CAM Treatment Pioneering trials of CoQ10 in heart failure involved primarily patients with dilated weak heart muscle CoQ10 was added to standard treatments for heart failure such as fluid pills (diuretics), digitalis preparations (Lanoxin), and ACE inhibitors. Several trials involved the comparison between supplemental CoQ10 and placebo on heart function as measured by echocardiography. CoQ10 was given orally in divided doses as a dry tablet chewed with a fat containing food or an oil based gel cap swallowed at mealtime. Heart function, as indicated by the fraction of blood pumped out of the heart with each beat (the ejection fraction), showed a gradual and sustained improvement in tempo with a gradual and sustained improvement in patients' symptoms of fatigue, dyspnea, chest pain, and palpitations. The degree of improvement was occasionally dramatic with some patients developing a normal heart size and function on CoQ10 alone. Most of these dramatic cases were patients who began CoQ10 shortly after the onset of congestive heart failure. Patients with more established disease frequently showed clear improvement but not a return to normal heart size and function.

CAM treatment The physiological benefit of ribose administration is clear. Ribose supplementation improves diastolic heart function, increases exercise tolerance and enhances patient quality of life. Given as D-ribose These benefits are provided by the role ribose plays in increasing cardiac energy reserves that become depressed during ischemia or hypoxia associated with coronary artery disease or congestive heart failure. A key molecule, called adenosine triphosphate (or ATP for short), is known as the energy currency of the cell because the amount of ATP we have in our tissues determines whether we will be fatigued, or will have the energy we need to live vital, active lives. Ribose provides the key building block of ATP, and the presence of Ribose in the cell stimulates the metabolic pathway our bodies use to actually make this vital compound. If the cell does not have enough Ribose, it cannot make ATP. So, when cells and tissues become energy starved, the availability of Ribose is critical to energy recovery.

CAM treatment Evaluation of the therapeutic efficacy of L-carnitine in congestive heart failure. Ghidini O, Azzurro M, Vita G, Sartori G. Source Reparto Medicina Interna, Ospedale Bussolengo, Verona, Italy. Erratum in Int J Clin Pharmacol Ther Toxicol 1989 Aug;27(8):418. Abstract To evaluate the therapeutic efficacy of L-carnitine in elderly subjects suffering from heart failure, secondary to ischemic and/or hypertensive heart disease, 38 patients (22 men, 16 women) were studied, aged from 65 to 82 years. In addition to traditional therapy (digitalis, diuretics, antiarrhythmic agents) given in all cases, 21 patients received oral L-carnitine on the basis of a randomized protocol in 1-g doses twice daily for 45 days (the other 17 received placebo). In the group treated with L-carnitine, a distinct improvement was observed in both subjective and objective conditions; reduced heart rate, edema and dyspnea, increased diuresis and a marked reduction in daily digitalis consumption. L-carnitine treatment also induced a significant reduction in serum cholesterol and triglyceride levels. No adverse reactions attributable to L-carnitine administration were observed in any of the patients.

Thyroid hormone metabolism in patients with congestive heart failure: the low triiodothyronine state. Ascheim DD, Hryniewicz K. Source Division of Circulatory Physiology, Department of Medicine, Columbia University College of Physicians & Surgeons, New York, New York 10032, USA. Abstract Thyroid hormone has multiple effects on the cardiovascular system, ranging from molecular and cellular effects to the consequent hemodynamic alterations. Consequently, thyroid function has been evaluated in small cohorts of patients with advanced heart failure that indicate a significant prevalence of morphologic or functional thyroid disorders. We sought to determine the prevalence of altered thyroid hormone metabolism in a broad spectrum of ambulatory heart failure patients. Thyroid function tests were evaluated in 132 ambulatory patients (98 males, 32 females, mean age, 67 years) with left ventricular systolic dysfunction (EF < 35%) and New York Heart Association (NYHA) class I-IV symptoms. Hypothyroidism was defined as serum thyroid-stimulating hormone (TSH) > 4.25 U/mL and low triiodothyronine (T3) state was defined as T3 levels < 80 ng/dL, with normal thyroxine (T4) and TSH level. Seven percent of patients were found to have primary hypothyroidism and 34% have a low T3 state. Of patients receiving amiodarone, 21% had elevated TSH levels and 76% had low T3 levels. The prevalence of abnormal thyroid function correlated with NYHA class. There is an unexpectedly high risk of hypothyroidism and low T3 syndrome in patients regardless of treatment with amiodarone, which appears to correlate with disease severity that requires further investigation. PMID: [PubMed - indexed for MEDLINE]

CAM treatment and thyroid hormone
Thyroid Hormone Metabolism in Advanced Heart Failure Michele A. Hamilton, MD Division of Cardiology, University of California at Los Angeles School of Medicine, Los Angeles, California Patients with advanced congestive heart failure are often severely ill and may experience substantial abnormalities in thyroid hormone metabolism. Thus, we examined this patient population to determine the prevalence and prognostic significance of altered thyroid hormone concentrations, the course of thyroid abnormalities in congestive heart failure survivors, and the potential relationship of thyroid abnormalities to overall metabolic rate. Our results indicate that thyroid hormone metabolism. (ie, the triiodothyronine to reverse triiodothyronine ratio) is altered in a majority of patients with advanced congestive heart failure and is an independent predictor of mortality. Currently a study is underway that will provide further evidence for the mechanisms involved in congestive heart failure and abnormal thyroid hormone metabolism. (Ann Thorac Surg 1993;56:S48-53)

CAM Treatment Gemmotherapy Hawthorn

Significance of magnesium in congestive heart failure.
Douban S, Brodsky MA, Whang DD, Whang R. Source Department of Medicine, University of California, Irvine Medical Center, Orange , USA. Abstract Electrolyte balance has been regarded as a factor important to cardiovascular stability, particularly in congestive heart failure. Among the common electrolytes, the significance of magnesium has been debated because of difficulty in accurate measurement and other associated factors, including other electrolyte abnormalities. The serum magnesium level represents < 1% of total body stores and does not reflect total-body magnesium concentration, a clinical situation very similar to that of serum potassium. Magnesium is important as a cofactor in several enzymatic reactions contributing to stable cardiovascular hemodynamics and electrophysiologic functioning. Its deficiency is common and can be associated with risk factors and complications of heart failure. Typical therapy for heart failure (digoxin, diuretic agents, and ACE inhibitors) are influenced by or associated with significant alteration in magnesium balance. Magnesium therapy, both for deficiency replacement and in higher pharmacologic doses, has been beneficial in improving hemodynamics and in treating arrhythmias. Magnesium toxicity rarely occurs except in patients with renal dysfunction. In conclusion, the intricate role of magnesium on a biochemical and cellular level in cardiac cells is crucial in maintaining stable cardiovascular hemodynamics and electrophysiologic function. In patients with congestive heart failure, the presence of adequate total-body magnesium stores serve as an important prognostic indicator because of an amelioration of arrhythmias, digitalis toxicity, and hemodynamic abnormalities. PMID: [PubMed - indexed for MEDLINE] Publication Types, MeSH Terms, Substances

Prevention of Sudden Death.
Patients with previous cardiac arrest or documented sustained ventricular arrhythmias have a high risk of recurrent events. Implantation of an ICD has been shown to reduce mortality in cardiac arrest survivors. An ICD is indicated for secondary prevention of death from ventricular tachyarrhythmias in patients with otherwise good clinical function and prognosis, for whom prolongation of survival is a goal. Patients with chronic HF and a low EF who experience syncope of unclear origin have a high rate of subsequent sudden death and should also be considered for placement of an ICD

The role of ICD implantation for the primary prevention of sudden death in patients with HF and low EF and no history of spontaneous or inducible VT has been addressed by several large trials that used only readily available clinical data as entry criteria (93,97,98). The first of these demonstrated that ICDs, compared with standard medical therapy, decreased the occurrence of total mortality for patients with EF of 30% or less after remote MI

Antiarrhythmics Patients with chronic heart failure are at increased risk of sudden death due to ventricular arrhythmia. Statistics show that sudden arrhythmic death is the cause of approximately 40% of heart failure deaths.[15] Low-dose amiodarone was evaluated in two controlled studies of patients with heart failure[83,84] and in a study in patients with left ventricular dysfunction after myocardial infarction.[85] The Grupo de Estudio de la Sobrevida en la Insuficiencia Cardiaca en Argentina (GESICA) was a randomized, multicenter trial of low-dose amiodarone.[83] Eighty percent of the 516 patients had NYHA class III-IV disease, with evidence of cardiac enlargement and an EF of 35% or below. Patients received amiodarone 600 mg/day for 14 days, and then 300 mg/day for 2 years. Additional therapy included a low sodium diet, diuretics, digitalis, and vasodilators. Mortality was 41.4% in controls and 33.5% in the amiodarone group (RR=0.28, p=0.024). Fewer patients receiving amiodarone died or were hospitalized due to worsening heart failure (45.8% vs 58.2%, RR=0.31, p=0.0024). The beneficial effect was evident in all subgroups examined and was independent of the occurrence of nonsustained ventricular tachycardia. Side effects were reported in 6.1% of patients taking amiodarone, with 4.6% discontinuing therapy. The investigators concluded that low-dose amiodarone safely and effectively reduces mortality and morbidity in patients with severe heart failure.

References Antiarrhythmics
15.ISIS-4 (Fourth International Study of Infarct Survival) Collaborative Group. A randomized factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulfate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995;345: 83.Doval H, Nul D, Grancelli H, et al. Randomized trial of low-dose amiodarone in severe congestive heart failure. Lancet 1994;344:493-8. 84.Singh S, Fletcher R, Fisher S, et al. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. N Engl J Med 1995;333:77-82. 85.Julian D, Camm A, Frangin G, et al. Randomized trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. Lancet 1997;349:

Palliative care/Hospice
Patients with CHF often have significant symptoms, such as shortness of breath and chest pain. Both palliative care and cardiology are trying to get palliative care involved earlier in the course of patients with heart failure, and some would argue any patient with NYHA class III CHF should have a palliative care referral. Palliative care can not only provide symptom management, but also assist with advanced care planning, goals of care in the case of a significant decline, and making sure the patient has a medical power of attorney and discussed his or her wishes with this individual. Hospice Without transplantation, heart failure may not be reversible and cardiac function typically deteriorates with time. The growing number of patients with Stage IV 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.

Epidemiology Mostly as a result of the costs of hospitalization, it is associated with a high health expenditure; costs have been estimated to amount to 2% of the total budget of the National Health Service in the United Kingdom, and more than $35 billion in the United States.[37][38] Heart failure is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life.[39][40] With the exception of heart failure caused by reversible conditions, the condition usually worsens with time. Although some people survive many years, progressive disease is associated with an overall annual mortality rate of 10%.[41] Heart failure is the leading cause of hospitalization in people older than 65.[42] In developed countries, the mean age of patients with heart failure is 75 years old. In developing countries, two to three percent of the population suffers from heart failure, but in those 70 to 80 years old, it occurs in 20—30 percent. Heart failure affects close to 5 million people in the USA and each year close to 500,000 new cases are diagnosed. What is of more concern is that more than 50% of patients seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days. In tropical countries, the most common cause of HF is valvular heart disease or some type of cardiomyopathy. Moreover as underdeveloped countries become more affluent, there has also been an increase in diabetes, hypertension and obesity which has resulted in heart failure. In USA, HF is much higher in African Americans, Hispanics, Native Americans and recent immigrants from the eastern bloc countries like Russia. This high prevalence in these ethnic populations has been linked to high incidence of diabetes and hypertension. In many new immigrants to the USA the high prevalence of heart failure has largely been attributed to lack of preventive health care or substandard treatment.[43]

Epidemiology references
37.^ Stewart S, Jenkins A, Buchan S, McGuire A, Capewell S, McMurray JJ (June 2002). "The current cost of heart failure to the National Health Service in the UK". Eur. J. Heart Fail. 4 (3): 361–71. doi: /S (01) PMID 38.^ Rosamond W, Flegal K, Furie K, et al. (January 2008). "Heart disease and stroke statistics update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee". Circulation 117 (4): e25–146. doi: /CIRCULATIONAHA PMID 39.^ Juenger J, Schellberg D, Kraemer S, et al. (March 2002). "Health related quality of life in patients with congestive heart failure: comparison with other chronic diseases and relation to functional variables". Heart 87 (3): 235–41. doi: /heart PMC PMID 40.^ Hobbs FD, Kenkre JE, Roalfe AK, Davis RC, Hare R, Davies MK (December 2002). "Impact of heart failure and left ventricular systolic dysfunction on quality of life: a cross-sectional study comparing common chronic cardiac and medical disorders and a representative adult population". Eur. Heart J. 23 (23): 1867–76. doi: /euhj PMID 41.^ Neubauer S (2007). "The failing heart — an engine out of fuel". N Engl J Med 356 (11): 1140–51. doi: /NEJMra PMID 42.^ 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: /S (00) PMID 43.^ Heart Failure Information, Retrieved on

CHF is an expensive disease the inability of patients to obtain medicines can result in significant morbidly and mortality and results in a significant increase in the total medical expenses.

References http://www.oucom.ohiou.edu/fd/monographs/bedside.htm

Teaching at the Bedside Using CHF as the Model

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