Transcript Teaching at the Bedside Using CHF as the Model

Objectives
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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
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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
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Discuss diagnostic options for evaluation of the patient and the role of echo-cardiographic
evaluations, angiograms, BNP, etc.
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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
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Discuss how pre-load and post-load agents differ and the influences they have on the
outcome of patients
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Discuss the role of surgical interventions, utilization of pacemakers and defibrillators, etc. in
the treatment and their effect on the outcome of the patient
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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
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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
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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
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The condition is diagnosed with echocardiography and blood tests.
Treatment commonly consists of lifestyle measures +
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smoking cessation
light exercise including breathing protocols
decreased salt intake and other dietary changes)
Medications
devices or surgery.
Common causes of heart failure include
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shortness of breath
leg swelling
exercise intolerance.
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:10.1016/S0140-6736(05)66621-4. PMID 15924986.
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:10.1093/eurheartj/ehn309. PMID 18799522.
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]
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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 "preheart 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:10.1161/CIRCULATIONAHA.105.167586. PMID 16160202.
Pathophysiology
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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.
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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:10.1093/eurheartj/ehi492. PMID 16204268.
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:10.1291/hypres.30.439. PMID 17587756.[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:10.1074/jbc.M308134200. PMID 12939263.
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 (460-370 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 (1849-1920), 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;126:217-20.
• 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.
• http://www.oucom.ohiou.edu/fd/monographs/bedside.ht
m
Congestive Heart Failure Physical Examination
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BP 108/52
P 140, irreg.
R 30 and labored
Temp 99°F
Ht: 5'8"
Wt: 210.
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General: Breathless, moderately obese male in acute distress sitting upright complaining "I am going to die. Please help me."
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Neck: Distended neck veins with visible cannon waves, JVD to 12cm. Carotids without bruits.
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Chest: Scattered rhonchi throughout, rales bilateral one third lower bases. Cough is productive and frothy.
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Heart: Tachycardia and irreg. Grade 3/6 systolic murmur at LSB, S3 gallop noted.
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Abdomen: Liver palpable three centimeters below right costal margin. HJR+. Non-tender to palpation, +Bowel sounds 4 quadrants.
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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.
• http://content.onlinejacc.org/cgi/content/full/j.jacc.2008.11.009#SEC8
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 thyroidstimulating 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;138:285290.[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;7:183-193.[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;350:647654.[CrossRef][Web of Science][Medline]
•
31. Wang TJ, Larson MG, Levy D, et al. Impact of obesity on plasma natriuretic
peptide levels Circulation 2004;109:594-600.[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;43:1590-1595.[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 followup, 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;335:1933-40.
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 -- 1997. J Heart Lung Transplant 1997;16:691-712.
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.[123-125]
•
•
•
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;34:155-62.
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;94:3184-9.
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 (GISSI3),[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;327:669-77.
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;37:1022-36.
30.Waagstein F, Bristow M, Swedberg K. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy.
Lancet 1993;342:1441-6.
31.The Cardiac Insufficiency Bisoprolol Study (CIBIS) Investigators and Committees. A randomized trial of ßblockade in heart failure: the Cardiac Insufficiency Bisoprolol Study (CIBIS). Circulation 1994;90:1765-73.
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;353:2001-7.
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;334:1349-55.
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;24:1678-87.
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;92:212-18.
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 costeffectiveness of CRT remains uncertain.
• http://www.ahrq.gov/clinic/tp/resyntp.htm
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 30-88 years) or
coenzyme Q10 (n = 319, mean age 67 years, range 26-89 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. [email protected]
•
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: 12165115 [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 92668-3298, 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: 8800040 [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] Lowdose 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;345:669-85.
• 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 leftventricular dysfunction after recent myocardial
infarction: EMIAT. Lancet 1997;349:667-74.
Palliative care/Hospice
• Palliative care
– 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:10.1016/S1388-9842(01)00198-2. PMID 12034163.
38.^ Rosamond W, Flegal K, Furie K, et al. (January 2008). "Heart disease and stroke statistics--2008
update: a report from the American Heart Association Statistics Committee and Stroke Statistics
Subcommittee". Circulation 117 (4): e25–146. doi:10.1161/CIRCULATIONAHA.107.187998. PMID
18086926.
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:10.1136/heart.87.3.235. PMC 1767036. PMID
11847161.
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:10.1053/euhj.2002.3255. PMID 12445536.
41.^ Neubauer S (2007). "The failing heart — an engine out of fuel". N Engl J Med 356 (11): 1140–
51. doi:10.1056/NEJMra063052. PMID 17360992.
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:10.1016/S0002-8703(00)90311-9. PMID 10618565.
43.^ Heart Failure Information, Retrieved on 2010-01-21.
• 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/monograph
s/bedside.htm
• http://www.medscape.com/viewarticle/40957
7_2
• http://en.wikipedia.org/wiki/Heart_failure#M
anagement