Heart failure is a clinical syndrome caused by the
inability of the heart to pump sufficient blood to
meet the metabolic needs of the body. Heart failure
can result from any disorder that reduces ventricular
filling (diastolic dysfunction) and/or myocardial
contractility (systolic dysfunction).
The incidence: 1 in 1000 population per year;
increasing by about 10% every year. In >85y incidence
is 10 cases per 1000.
The prevalence ranges from 3-20 cases per 1000
population, increasing to at least 80 cases per 1000 in
people aged 75 years and over.
The male to female ratio is about 2:1.
The median age of presentation is 76 years.
INTRINSIC PUMP FAILURE :The important cause of heart failure is the weakening of ventricular
muscle due to disease so that the heart fails to act as an efficient pump
Ischaemic heart disease (35-40%)
Cardiomyopathy (dilated) (30-34%)
Metabolic disorders like beri beri
INCREASED WORKLOAD ON THE HEART : It is due to either increased pressure load or volume
Increased pressure load
Chronic lung disease
Increased volume load
Hypoxia due to lung disease
IMPAIRED FILLING OF CARDIAC CHAMBERS:Cardiac failure may also result from defects in filling
Heart failure is associated with complex
neurohormonal changes including activation of
the renin angiotensin aldosterone system and
the sympathetic nervous system
Right sided heart failure
Right ventricle fails as effective pump
Right ventricle cannot eject blood returning through
Blood backs up into systemic circulation
The main causes are:
1. As a consequence of left ventricular failure
2. Pulmonary or tricuspid valvular disease
3. Congenital heart disease
4. Myocardial heart disease effecting right heart
Left sided heart failure
It is initiated by the stress to the left heart.
Left ventricle fails as effective pump
Left ventricle cannot eject blood delivered from right heart
through pulmonary circulation
Blood backs up into pulmonary circulation
The major causes are :
1. Systemic hypertension
2. Mitral or aortic valve disease
3. Ischemic heart disease
4. Cardiac myopathies
To understand the pathophysiologic processes
in heart failure, a basic understanding of
normal cardiac function is necessary. Cardiac
output (CO) is defined as the volume of blood
ejected per unit time (L/min) and is the product
of heart rate (HR) and stroke volume (SV): CO
= HR × SV. Stroke volume, or the volume of
blood ejected during systole, depends on
preload, afterload, and contractility.
TYPES OF HEART FAILURE
Heart failure may be classified into:
Acute heart failure
Chronic heart failure
Acute heart failure
Sudden and radip development of heart failure occurs in
1. Larger myocardial infarction
2. Valve rupture
3. Massive pulmonary embolism
4. Acute viral myocarditis
In this type there is sudden reduction in cardiac
output resulting in systemic hypotension but
edema does not take place
Chronic heart failure
It develops slowly as observed in following cases
1. Myocardial ischaemia
2. Multi valvular disease
3. Sytemic hypertension
4. Chronic disease
5. Progression of acute into chronic failure
In this type of failure there is a well maintained
arterial pressure and there is accumulation of
■ BNP (brain natriuretic peptide) >100 pg/mL
■ Electrocardiogram may be normal or it could show numerous abnormalities
including acute ST-T–wave changes from myocardial ischemia, atrial
fibrillation , bradycardia , left ventricular hypertrophy.
■ Serum creatinine may be increased because of hypoperfusion .
■ Complete blood count useful to determine if heart failure is a result of
reduced oxygen-carrying capacity
■ Chest radiography is useful for detection of cardiac enlargement
, pulmonary edema, and pleural effusions
■ Echocardiogram assesses left ventricle size, valve function, pericardial
effusion, and ejection fraction
■ Hyponatremia, serum sodium <130 mEq/L, is associated with reduced
survival and may indicate worsening volume overload and/or disease
TREATMENT OF HEART FAILURE
Rest, salt restriction, stop smoking
Removal of the cause:
This deserves top priority in all cases and
includes surgical measures correcting valvular
lesions or congenital malformations and medical
measures for treating hypertension or
infective endocarditis when Present
Removal of precipitating causes of heart
General lifestyle advice
Education:Effective counselling of patients and family emphasizing weight
monitoring and dose adjustment of diuretics may prevent hospitalization.
Obesity control:Maintain desired weight and body mass index.
Smoking: Smoking should be stopped, with help from anti-smoking clinics if
Physical activity, exercise training and rehabilitation
Dietary modification: Large meals should be avoided and if necessary
weight reduction instituted. Salt restriction is necessary and foods rich in
salt or added salt in cooking and at the table should be avoided. A low-
sodium diet is unpalatable and of questionable value. In severe heart failure
fluid restriction is necessary. Alcohol has a negative inotropic effect and
heart failure patients should moderate consumption.
Diet/weight reduction recommendations-individualized and culturally
Dietary Approaches to Stop Hypertension (DASH) diet
Sodium- usually restricted to 2.5 g per day
Potassium encouraged unless on K sparing diuretics (Aldactone)
Loop diuretics,thiazide diuretics and
potassium sparing diuretics
These act by promoting the renal excretion
of salt and water by blocking tubular
reabsorption of sodium and chloride. The
resulting loss of fluid reduces ventricular
filling pressures (preload), produces
consistent haemodynamic and symptomatic
benefits and rapidly improves dyspnoea and
Inhibit active exchange of Cl-Na
in the cortical diluting segment of
ascending loop of Henle
Inhibit reabsorption of Na in the
distal convoluted and collecting
Inhibit exchange of Cl-Na-K in
the thick segment of the ascending
loop of Henle
Drugs such as furosemide and
Have a rapid onset of action (i.v. - 5 min;
oral - 1-2 h) and generally short-lived (4-6
h) diuresis as the concentrating power of
the kidney is reduced.
These agents also produce potassium loss
and promote hyperuricaemia, and renal
function should be monitored.
Thiazides are less effective in patients with reduced
glomerular filtration rates.
Thiazide diuretics in combination with loop diuretics have
a synergistic action and greater diuretic effect.
Associated metabolic abnormalities are more likely and
close supervision is needed.
C.I:hepatic failure,renal impairment,electrolyte imbalance
Dose:25-75mg daily in divided doses
Spironolactone is a specific
competitive antagonist to
aldosterone, producing a weak diuresis
but with a potassium-sparing action.
Risk factors for developing
hyperkalaemia include spironolactone
dose > 50 mg/day, high-dose
inhibitor (ACEI) and renal impairment.
Actions of vasodilators in CCF:
Decrease in preload: preload is the amount of blood returning
to the heart which the heart has to pump. Two types of drugs
Venodilators: Nitrates, Na nitroprusside, ACE-
I, ARBs, prazosin.
Diuretics: Which reduce circulating volume.
Preload reduces the size of the ventricles, decreases
ventricular EDV/P, increases ejection fraction and efficiency of
Decrease in after load: After load is the resistance against
which the heart has to pump. Arterial dilators reduce the after
load. Nifedipine, minoxidil,hydralazine.
Balanced (mixed) vasodilators: ACE-I, ARBs, Na-
ACE-I: are mixed vasodilators, they dilate both arteries, and veins.
Arteriolar dilatation: This reduces after load. When load is
decreased, efficiency of the heart to pump the blood improves- there
is improvement in the ejection fraction. This is how, reduction in
after load helps a patient of CCF.
Venodilatation: This reduces preload. Preload means increased
capacity of the veins to hold blood: venous return decreases. In CCF
the ventricles are over stretched beyond the physiological limits.
Over stretched muscles do not produce sufficient power. Due to
reduction in venous return, ventricles size decreases and the length
return to with in physiological limits. This increases the force
generated by the ventricles. Thus reduction in preload is helpful in
patients with CCF.
Drugs such as α-adrenergic blockers (e.g.
prazosin) and direct smooth-muscle relaxants
(e.g. hydralazine) are potent arteriolar
vasodilators but are not very effective in
Calcium-channel blockers also reduce
afterload, but first-generation calcium
antagonists (diltiazem, nifedipine) may have a
detrimental effect on left ventricular
function in patients with heart failure.
Short- and long-acting nitrates act by reducing
preload and lowering venous pressure, with
resulting reduction in pulmonary and dependent
oedema but tolerance occurs.
Only combination therapy of nitrate with
hydralazine has been shown to improve
mortality and exercise performance, and may
be useful when ACEI are contraindicated.
10 mcg/min increased by 5-10 mcg/min q 5 min
β-Adrenoceptor blocking agents
There is considerable evidence to support the use of beta-blockers
in patients with chronic stable heart failure.
Initial doses should be low, e.g. carvedilol 3.125 mg twice daily.
Nebivolol is used in the treatment of stable mild–moderate heart
failure in patients over 70 years old
Beta blockers should not be used in the following conditions
Patients not receiving diuretics.
If iv ionotropic is required.
Amrinone- Ionodilator is an agent with both positive
inotropic and vasodilator effects. They inhibit phoshodiesteraeIII
enzyme. This increases the concentration of cAMP, -> more Ca++
This is responsible for for +ve ionotropic action. Vasodilator
effect of amrinone is the result of direct relaxant effect on
vascular smooth muscle. The drug reduces both the after load and
ADRS:Thrombocytopenia ,adominal pain,nausea,liver damage
Dobutamine, dopamine. Dobutamine is a selective β1
agonist. These drugs have positiv inotropic and vasodilator
properties through activation of adenylyl cyclase
Due to development of tolerance these drugs have a
C.I:acute myocardial infarction
ADRS:incresase in HR
SPIRANOLACTONE:It antagonises the effects of
Expansion of e.c.f
Fibrotic change in myocardium
Hypokalemia and hypomagnesemia
Contraindications :in renal insufficiency
Dose:25-200mg daily for adults
Digitalis glycosides have been used for many
years in patients with heart failure and atrial
Digoxin acts as a positive inotrope by
competitive inhibition of Na+/K+-
ATPase, producing high levels of intracellular
sodium. This is then exchanged for
extracellular calcium. High levels of
intracellular calcium result in enhanced actin-
myosin interaction and increased contractility.
Digoxin also improves baroreceptor
responsiveness, and reduces sympathetic
activity and circulating renin.
They have narrow safety margin
Anorexia, nausea, vomiting
abdominal discomfort or pain and diarrhea.
Headache, malaise, fatigue, drowsiness, confusion, delirium,
hallucination or rarely convulsions.
Blurred vision, mostly for yellow and green vision, diplopia.
Any type of arrhythmia may be produced including:
May be due to steroidal structure.
Treatment Of Digitalis Toxicitiy:
1) Stop the responsible drug.
2) KCl syrup or slow release or I.V. with ECG monitoring if plasma potassium is low or normal.
3) If due to calcium injection give disodium edetate I.V. which is chelating agent for calcium.
4) Cholestyramine binds to digitalis in gut, thus inhibit absorption and decreases the toxicity
5) In acute toxicity give specific digitalis antibodies (Fab fragment).
6) Treatment of associated arrhythmia:
Partial heart block is treated by atropine.
Ventricular arrhythmia without A-V block is treated by lidocaine I.V. or beta blockers.
Ventricular arrhythmia with A-V block & atrial arrhythmia is treated by Diphenylhydantoin