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Clinical syndrome that can result from a structural or functional cardiac disorder
that impairs the ability of the ventricle to fill with or eject blood.
The syndrome may result from disorders of the pericardium, myocardium,
endocardium or great vessels, but majority of patients with HF have symptoms due to
LV dysfunction
The abnormality in cardiac function causes the failures of the heart to pump the
blood at a rate that is satisfactory for the requirements of metabolizing tissues.
Presentation of patients with HF
Decreased exercise tolerance
- dyspnea and fatique occurring at rest or during exercise
Fluid retention
- complaint of leg or abdominal swelling as primary symptoms
- impaired exercise tolerance not noticed by patient as it occurs gradually
No symptoms of symptoms of another disease
- cardiac enlargement or dysfunction may noted on usual routine evaluation or that
for another disease
Development stages of HF
Stage A
at risk for HF but without structural heart disease or symptoms of HF
- hypertension,atherosclerotic disease, diabetes, obesity, metabolic syndrome
- use of cardiotoxins
- family history of cardiomyopathies
Stage B
Structural heart disease but without signs or symptoms of HF
- previous myocardial infarction (MI), LV remodeling including LVH and low
fraction (EF), asymptomatic valvular disease.
Stage C
Structural heart disease with prior or current symptoms of HF
- known structural disease
- shortness of breath (SOB), fatique and reduced exercise tolerance
Stage D
Refractory HF
- marked symptoms at rest despite maximal medical therapy
- required specialized interventions

The full evaluation of HF requires consideration of the underlying abnormality of the
heart, the severity of the syndrome, the etiology, precipitating and exacerbating factors,
identification of concomitant diseases relative to the management and estimation of
determine predisposition to risk factors especially in lifestyle (eg smoking, diet,
alcohol comsumption, substance abuse etc)
prior or current evidence of MI, valvular disease or congenital heart disease
Review patients history of hypertension, DM, dyslipidemia, valvular, coronary or
peripheral artery disease (PAD), exposure to cardiotoxic agents, rheumatic fever,
chest irradiation, illicit drug use, STDs, malignancies etc.
Detailed family history to determine familial predisposition to atherosclerotic
disease or cardiomyopathy.
Possible causes of HF that need to be investigated:
- coronary artery disease (CAD)
- cardiomyopathies (alcoholic and idiopathic)
- congenital heart disease
- chronic arrhythmias
- endocrine disorders (esp thyrotoxicosis)
- inflammatory/immunological
- genetic conditions
- Hypertension
- Infections
- Malignancies
- Valvular heart disease
Identify and treat precipitating or exacerbating factors of HF:
- anemia
- arrhythmias, esp A-fib
- drugs (eg NSAIDs, calcium antagonists, corticosteroids, liquorice)
- excess salt intake
- infection
- pulmonary embolism
- renal dysfunction, renal artery stenosis
- silent MI
Physical exam
Abnormal physical findings in HF :
- presence of 3rd heart sound, S1<S2
- elevated jugular venous pressure
- irregular pulse, tachycardia
- positive hepato-jugular reflex

peripheral edema
pulmonary rales that do not clear with coughing
laterally displaced apical impulse

Assess Volume Status :

- this determines the need for diuretic therapy and detects limitation to use of
certain drug
- JVP is the most reliable sign of volume overload
- At each visit, record patients weight, BP (sitting and standing) and other
abnormal physical finding
Diagnostic test/Lab test :
lab testing will confirm the presence of HF and may show the presence of
disorders that can lead to exacerbate HF
initial evaluation should include, but is not limited to the following :

CBC, urinalysis, serum electrolytes, blood lipids

test renal and liver function
thyroid function tests should be done
myocardial specific enzyme analysis will be needed in acute exacerbations to exclude MI

- ECG changes are frequently found in HF patients
- will detect A-fib or flutter and ventricular arrhythmias as the cause or contributing factor of HF
- normal ECG suggests that HF may not be the cause of the patients symptoms

- Chest x-ray
- useful to detect cardiac enlargement and pulmonary congestion

- if available, test for natriuretic peptides (brain natriuretic peptide/BNP)

- BNP is elevated in HF; it is released from the heart response to left ventricular wall
stretch changes
- the diagnosis of HF is unlikely in a asymptomatic patient with a normal BP

Identification of Structural Abnormality

Transthoracic Doppler 2D echocardiography is the most useful diagnostic test in the
evaluation of HF.

this test allows the physician to establish whether the abnormality is

myocardial, pericardial or valvular

if abnormality is myocardial this test can distinguish between primary

systolic or diastolic disease

left ventricular ejection fraction (LVEF) can be determined and those

patient swith LVEF <40% are usually considered to have systolic dysfunction
Other tests
may be appropriate if diagnostic doubts or if clinical features suggest reversible cause of
- exercise test
- pulmonary function test

invasive investigation and angiography (should be performed if CAD is suspected

and patient may benefit from revascularization)
cardiac output
left atrial pressure

Assess Functional Capacity of HF patient

New York Heart Association (NYHA) Functional Capacity
Class I
- patient has no limitation of physical activity
- ordinary physical activity does not cause symptoms (eg palpitation, dypnea or

Class II
- patient has slight limitation of physical activity
- they are comfortable at rest but ordinary physical activity results in discomfort

Class III
- patient has a marked limitation of physical activity
- they are comfortable at rest but less than ordinary activity leads to discomfort

Class IV
- the patient is unable to carry out any physical activity without discomfort
- symptoms are present at rest and any physical activity will cause an increase in
Prognostic Parameters
- decreasing LVEF
- worsening NYHA functional status
- degree of hyponatremia
- decreasing peak exercise oxygen uptake
- decreasing hematocrit
- widened QRS on 12-lead ECG
- chronic hypertension
- resting tachycardia
- renal insufficiency of failure
- intolerance to therapy
- refractory volume overload
- changes in sensorium
Once HF is advanced, estimated survival guide is useful for the timing of transplantation,
other treatments reserved for severe disease, or hospice care.
dosing, side effects and precautions should be discussed along with the
importance of compliance
assist patients in dealing with complicated drug regimens
patients should be counseled to avoid taking NSAIDs
- emphasize that NSAIDs should not be taken to suppress cough caused by ACE

NSAIDs can cause Na retention, peripheral vasoconstriction and can decrease the
efficacy and increase the toxicity of ACE inhibitors and diuretics

- if in a stable condition, patients should be encouraged to carry out daily physical
activity and leisure time activities that do not induce symptoms
- strenuous exercises, competitive and tiring sports should be discouraged
- discuss patients concern about sexual activity
- advice, if appropriate, concerning use of sublingual nitrates prior to sexual
Lifestyle Modification
Diet modification

salt restriction
- moderate Na restriction is indicated to permit effective use of lower doses of
- if possible, dietary Na should be restricted to 2g (-1/2tsp)
- advise patient to restrict adding salt and soya sauce to cooking, not to add extra
salt or soya sauce at the table and to avoid foods which are very high in salt
- controlling the amount of Na intake is more relevant in advanced HF
- salt substitutes may contain K and when used in large quantities can lead

patient should avoid excessive fluids if suffering severe HF

Weight control

recommend that patients weigh themselves regularly (eg daily, 2x/wk)

patient should be instructed to contact healthcare professional if weight

gain of >2 kg in 3 days
- diuretic dose may need to be adjusted

- if patient is obese or overweight, then treatment should include weight loss
- goal BMI for Asian adult : 18.4 22.9 kg/m2, BMI for European adults : 18.5
24.9 kg/m2
- minimum reduction in overweight individuals is 5% reduction in body weight

abnormal weight loss

- many severe CHF patients suffer from malnutrition
- wasting of total body fat and lean body fat is referred to as cardiac cachexia and
this is an important predictor of reduced survival
- aim of cardiac cachexia treatment is to increase non-edematous body weight
ideally by increasing muscle mass through adequate physical exercise
- small, frequent meals may be beneficial if patient suffers nausea, dyspnea or
bloated feeling

Smoking cessation

primary goal : complete smoking cessation

assess patients tobacco use and strongly urge patient and family to stop

determine the patients degree of addiction and his/her readiness to quit

- identify which patient are willing to quit
- quit plan should be developed and pharmacotherapy (eg nicotine replacement,
Bupropion), counseling and formal cessation programs should be provided, if
Alcohol moderation

patients with alcoholic cardiomyopathy should not consume alcohol

moderate alcohol intake is permitted in other CHF patients (1 drink/day)

Control of risk and Preventing of Cardiovascular Events
Hypertension and Hyperlipidemia

ACE inhibitors or angiotensin II antagonists can prevent the development

end-organ disease, even in those who do not have hypertension

Long-term treatment with ACE inhibitors or angiotensin antagonists has

been shown to decrease the risk of renal disease

Prolonged therapy with Ramipril has been shown to lower the likelihood
of CV death, MI and HF

Angiotensin II antagonists reduce the incidence of 1 st hospitalization due

to HF
Atherosclerotic Disease

one large-scale trial showed that long-term treatment with an ACE

inhibitor decreased the risk of CV death, MI and stroke in patients with known
vascular disease

ACE inhibitors prevent HF in patients who are at risk of developing HF

and a history of atherosclerotic cardiovascular disease, DM or hypertension with
associated cardiovascular risk factors

Typically a patient with HF should be managed with a combination of :

diuretic, ACE inhibitor, beta-blocker and if required, Digoxin.
ACE Inhibitors
ACE inhibitors should be prescribed in all patients with HF due to LV
systolic dysfunction unless contraindicated or not tolerated

ACE inhibitors should also be given to patients with asymptomatic LV

systolic dysfunction
Action : interfere the rennin-angiotensin system by inhibiting the enzyme responsible for
conversion of angiotensin I to angiotensin II along with enhancing the action of kinins
and augmenting kinin-mediated prostaglandins
Effect : studies have shown that ACE inhibition improves survival, symptoms and
reduces hospitalization in patients with mild, moderate-severe CHF
If patient has recent or current history of fluid retention, diuretics should be started prior
to ACE inhibitors to ensure Na balance.
This will help prevent peripheral and pulmonary edema.

Routinely used in HF patients for the relief of congestive symptoms and

signs of fluid retention

Continue diuretic until patient is in euvolemic state and then continue at

maintenance dose to prevent recurrence

ACE inhibitors and beta-blocker should be used and maintained even once
the patient responds to the diuretic. Diuretics can cause activation of the renninangiotensin-aldosterone systemn in patients with mild symptoms of HF and
combination with ACE inhibitors counteract this neuro-hormonal activation.
Actions : increase urinary Na excretion and decrease physical signs of fluid retention
Effects : reduced jugular venous pressure, pulmonary congestion, peripheral edema and
body weight.
They are the only medications that can adequately control fluid retention of HF.
Thiazide Diuretics
thiazide diuretics may be sufficient for patients with mild HF
may be used in combination with loop diuretics for resistant edema
Loop diuretics :
*loop diuretics are usually necessary when HF worsens and as HF progresses higher
doses will be necessary especially if patient failed to respond to thiazide diuretics

thiazides or metolazone can be used in combination with loop diuretics for

a synergistic effect and these combination are useful for severe HF
Potassium-sparing diuretics

should only be used if patient suffer hypokalemia regardless of ACE


beta-blocker should be given to all patients with stable HF due to LV

systolic dysfunction unless contraindicated or not tolerated

as long as patient is not in ICU, does not have evidence of fluid

overload/volume depletion and has not recently received positive inotropic agents,
beta-blocker should be administered

patient with LV systolic dysfunction following MI with or without HF

symptoms should be started on beta-blockers in addition to ACE inhibitors
Actions : the adverse effects of the sympathetic nervous system are inhibited by betablockers in patients with HF
Effects : bisoprolol, carvedilol and metoprolol have been shown to reduce symptoms of
HF, improve clinical status of patients and reduce the risk of death and hospitalization

digoxin is indicated for patients with any degree of symptomatic HF and

A-fib regardless if LV systolic or diastolic dysfunction is the cause

in patients with sinus rhythm digoxin may be used to improved status and
relieve symptoms in patients whose symptoms are not relieved with diuretics, ACE
inhibitors and beta-blockers.

Digoxin may be used early to reduce symptoms in patients who have

started ACE inhibitors and beta-blockers but have not yet started to respond

Other authorities recommend using digoxin only if diuretics, ACE

inhibitors and beta-blockers fail to relieve symptoms
Actions : inhibit Na-K ATPase which results in an increase of the contractile state of the
heart (+ve inotropic action)
Benefit may also be related to this enzyme inhibition in noncardiac tissues
Effects : reduces symptoms and improves clinical status but has not been shown to
improve survival
Angiotensin II antagonists

angiotensin II antagonists can be used in patients who have been shown to

be intolerant to ACE inhibitors

may be considered in combination with ACE inhibitors in patient who

remain symptomatic in order to reduce mortality

when combination therapy is employed, careful monitoring of the patients

BP, renal function and K levels is necessary
Actions : inhibits the action of angiotensin II but does not inhibit kinase
Effects : angiotensin II antagonists have proven to be of benefit in HF patients intolerant
of ACE inhibitors
When sued in addition to ACE inhibitors in symptomatic patients has been shown to
improve morbidity and mortality
Hydralazine + Isosorbidedinitrate
may be considered for patients who cannot take ACE inhibitors because of
hypotension or renal insufficiency
angiotensin II antagonists are preferred as an alternative in patients who
cannot tolerate ACE inhibitors because of cough or angioedema

compliance with isosorbide + hydralazine is usually poor because of high

pill load and adverse effects
Actions : when combined, hydralazine and isosorbide have complimentary dilating
Isosorbide may also inhibit abnormal myocardial and vascular growth and therefore may
reduce ventricular remodeling
Hydralazine theoretically may interfere with molecular mechanisms responsible for
progression of HF
Effects : when used at recommended doses may have some beneficial effect on mortality,
but not hospitalization
consider low dose spironolactone in patients with recent or current
symptoms at rest despite digoxin, beta-blocker, ACE inhibitor and diuretic
patients serum K level should be <5 mml/L and serum Cr < 250
micromol/L (2.8 mg/dL) prior to the start of therapy
Actions : spironolactone inhibits aldosteron more effectively than ACE inhibitors or
angiotensin II antagonists
This inhibition is beneficial because aldosteron may exert adverse effects on the function
and structure of the heart
Effects : low dose spironolactone when combined with ACE inhibitor and diuretic
improved survival of patients with advanced HF.