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