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Back to Cardiovascular Diseases
Heart failure
Definition
The heart cannot produce enough
blood flow to satisfy the body’s needs or can
do so only with difficulty.
Aetiology
Heart dysfunction may be either systolic or diastolic.
Systolic dysfunction: systole
is the act of contraction by the heart and is
governed by 2 cardiac properties (1)
contractility (the ability of the muscle to
contract) and (2) afterload
(the force against which the heart is pumping).
Decreased
contractility: myocardial infarction,
valvular heart disease, hypertension, cardiomyopathy.
Increased afterload such as hypertension,
aortic valve stenosis.
Diastolic dysfunction:
diastole is the phase of relaxation of the heart muscles after
pumping and is governed by active and passive properties.
Active relaxation occurs early in diastole when Ca++ is pumped outside
the myocardium. It is active because it utilizes energy
and is impaired by ischemia. Passive relaxation occurs
when the mitral and tricuspid valves open thus letting the blood
pooled in the atria enter the ventricles. It is impaired
by increased stiffness of the ventricles as occurs in concentric hypertrophy
and in infiltrative diseases of the heart.
Clinical suspicion
Heart failure is suspected by clinical presentation. Symptoms include
shortness of breath on effort, palpitations, syncope,
cough, swelling
of the legs. Radiographic evidence of large heart size and pulmonary vasculature
redistribution strengthens the suspicion.
Diagnosis
The diagnosis should be confirmed by echocardiography, radionuclide
ventriculography, or cardiac catheterization with left ventriculography.
Treatment
The ideal treatment would be to remove the cause,
if not then attempt at removing the precipitating cause however most of
the time this is not possible.
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Systolic heart failure
General strategy of management
if patient's blood pressure >90/60
Vasodilators
These dilate the vessels in the body.
Angiotensin - converting enzyme inhibitors (ACE inhibitors)
1st line therapy for
the entire spectrum of congestive heart failure, whether asymptomatic
or severe; unless contraindicated.
Rationale: heart failure
is accompanied by compensation mechanisms one
of which is vasoconstriction. This increases venous return and arterial
tone which maintains blood pressure and perfusion. However, it also increases
impedance to ventricular ejection (afterload).
This results in a vicious cycle in which decreased stroke volume results
in more intense vasoconstriction which further decreases stroke volume.
Hence vasodilator therapy breaks the cycle. vasodilator therapy was the
only therapy in congestive heart failure found to prolong survival associated
with improved quality of life.
Contraindications: not
given in patients with predominant diastolic failure or with those in
which heart failure results from aortic stenosis / mitral stenosis. Not
given in patients with impaired renal function or with bilateral renal
artery stenosis. Do not give concomitant potassium sparing diuretic with
angiotensin converting enzyme and monitor blood pressure carefully when
initially instituted in combination with a diuretic.
ACE inhibition should be started
72 h after any acute myocardial infarction with symptoms or echocardiographic
evidence of systolic dysfunction.
ACE inhibition should not be started
within the first 24 h of an acute myocardial infarction.
Dose and type: start with small
doses (1/4 to 1/2 a tablet) of ACE inhibitors and give in sitting position
to avoid first dose hypotension. Gradually titrate the dose every other
dosing schedule to reach 3 tablets daily (maximum dose is 50mg tds).
Isosorbide dinitrate – hydralazine:
The combination of these two drugs
also improves survival. They are given as a 2nd line in patients
who do not tolerate ACE inhibitors.
Diuretics
If congested
diuretics are beneficial.
Digoxin
If uncontrolled
by above or concomitant supraventricular arrhythmias.
other inotropics.
Dose:
0.25mg
daily maintenance dose to be monitored by
serum levels. It is reduced in the elderly and in individuals with
short stature and those with renal insufficiency.
If the patients is hypotensive
Sympathomimetic amines and amrinone
(see below).
Refractory heart failure
When the response to ordinary treatment is inadequate,
heart failure is considered to be refractory. Before assuming that this
condition simply reflects advanced, perhaps preterminal, myocardial depression,
careful consideration must be given to several possibilities: (1) an underlying
and overlooked cause of the heart disease that may be amenable to specific
surgical or medical therapy, such as silent aortic or mitral stenosis,
constrictive pericarditis, infective endocarditis, hypertension, or thyrotoxicosis,
(2) one or a combination of the precipitating causes of heart failure,
such as pulmonary or urinary tract infection, recurrent pulmonary emboli,
arterial hypoxemia, anemia, or arrhythmia, and (3) complications of overly
vigorous therapy, such as digitalis intoxication, hypovolemia, or electrolyte
imbalance.
The combination of an intravenously administered vasodilator,
such as sodium nitroprusside, along with a potent sympathomimetic amine,
such as dopamine or dobutamine, often results in an additive effect, raising
cardiac output and lowering filling pressure. Intravenous amrinone, sometimes
accompanied by the administration of a converting enzyme inhibitor, also
may be useful in patients with refractory heart failure.
Sympathomimetic amines
Dopamine, the naturally occurring immediate
precursor of norepinephrine, has a combination of actions which makes
it particularly useful in the treatment of a variety of hypotensive states
and congestive heart failure. At very low doses, i.e., 1 to 2 (ug/kg)/min,
it dilates renal and mesenteric blood vessels through stimulation of specific
dopaminergic receptors, thereby augmenting renal and mesenteric blood
flow and sodium excretion. In the range of 2 to 10 (ug/kg)/min, dopamine
stimulates myocardial beta receptors but induces relatively little tachycardia,
while at higher doses it also stimulates alpha-adrenergic receptors and
elevates arterial pressure.
Dobutamine is a synthetic catecholamine which
acts on beta1, beta2, and alpha receptors. It exerts a potent inotropic
action, has only a modest cardioaccelerating effect, and lowers peripheral
vascular resistance, but since it simultaneously raises cardiac output,
it has little effect on systemic arterial pressure. Dobutamine, given
in continuous infusions of 2.5 to 10 (ug/kg)/min, is useful in the treatment
of acute heart failure without hypotension. Like the other sympathomimetic
amines, it may be particularly valuable in the management of patients
requiring relatively short-term inotropic support--up to 1 week--in conditions
which are reversible, such as the cardiac depression which sometimes follows
open-heart surgery, or in patients with acute heart failure who are being
prepared for operation. Adverse effects include sinus tachycardia, tachyarrhythmias,
and hypertension.
A major problem with all sympathomimetics is the loss
of responsiveness, apparently due to "downregulation" of adrenergic receptors,
which becomes evident within 8 h of continuous administration. This problem
may be managed by intermittent therapy.
Cardiac transplantation: improved survival from
50% for 1yr to 50% 5yrs.
Diastolic heart failure
Diuretics if congested
Ca++ channel blockers in
some cases
NO ROLE for digoxin.
The rapid relief of acute myocardial ischemia is often
effective when diastolic dysfunction is secondary to this condition. The
reduction in heart rate caused by beta-blockers has several beneficial
on diastolic function, including a prolongation of the filling period
and an amelioration of ischemia. calcium channel blockers, especially
Verapamil, have been shown to accelerate ventricular relaxation in patients
with hypertrophic cardiomyopathy and have been reported to be useful in
the treatment of diastolic dysfunction characteristic of this condition.
Other beneficial mechanisms are reduction in heart rate, control of hypertension,
reduced microvascular ischemia and oxygen demand, amelioration of intracellular
calcium overload and regression of left ventricular hypertrophy.
Ventricular filling pressure and secondary venous congestion
may be reduced by restriction of sodium intake and the administration
of diuretics and venodilators. Even in the absence of ischemia, nitrates,
by reducing preload, are useful in managing diastolic dysfunction and
in the treatment and prevention of consequent severe pulmonary congestion.
Nitroglycerin may be administered intravenously or sublingually in emergency
situations, and long acting nitrates, such as isosorbide dinitrate, are
often effective in the long term. In the long term, however, excessive
preload reduction should be avoided because these patients often require
higher-than-normal filling pressures to maintain an adequate stoke volume.
The maintenance of heart rhythm and rate is of critical
importance. Tachycardia, whatever the underlying mechanism, must be controlled,
thereby increasing the fraction of each cardiac cycle available for ventricular
filling. Maintenance of sinus rhythm with synchronized atrioventricular
sequential pacing may be crucial in permitting atrial augmentation of
ventricular filling. Digoxin and other inotropic agents have no established
place in these patients with relatively well preserved ejection fraction,
and could, in principle, have an adverse effect in this group. Exercise
training induces significant improvement in exercise capacity in patients
with dilated cardiomyopathy and a pattern of abnormal left ventricular
relaxation. Finally, it has been shown that endogenous nitric oxide released
from the coronary microcirculation selectively enhances left ventricular
relaxation in the isolated ejecting guinea pig heart. These findings may
lead to a new therapeutic approach to diastolic heart failure, with treatments
aimed at the coronary microcirculation.
The American College of Cardiology / American Heart
Association task force divides pharmacologic treatment into three classifications
for the management of diastolic HF : Class I refers to drugs that are
always indicated, such as diuretics and nitrates, and drugs suppressing
atrioventricular conduction and anticoagulation if atrial fibrillation
is present. Class II agents are " acceptable "; however, their efficacy
is uncertain. These include calcium channel blockers, beta-blockers, ACE
inhibitors and anticoagulation in patients with intracardiac thrombus.
Class III drugs are not indicated and include drugs with positive inotropic
effects.
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