Heart Failure:
It is a clinical syndrome in which an abnormality of cardiac structure or function
is responsible for the inability of the heart to eject or fill with blood at a
rate commensurate with the requirements of the metabolizing tissues.
HF results in a constellation of clinical manifestations, including in various
combinations, circulatory congestion, dyspnea, fatigue, and weakness.
The severities of the clinical manifestations are commonly described according
to criteria development by the Association. HF is frequently, but not always,
caused by a defect in myocardial contraction, and then the term myocardial failure
is appropriate.
The latter may result from a primary abnormally in heart
muscle, as occurs in the cardiomyopathies, or in viral myocarditis. HF also results
commonly from coronary atherosclerosis, which interferes with cardiac contraction
by causing myocardial infarction and ischemia.
HF may also occur in
congenital, valvular, and hypertensive heart disease in which the myocardium is
damaged by the long standing hemodynamic overload. In other patients with HF,
However a similar clinical syndrome is present but without any detectable
abnormality of myocardial function. In some as cases the normal heart is suddenly
presented with a mechanical load that exceeds its capacity.
Such as an
acute hypertensive crisis, rupture of an aortic valve leaflet, in endocarditis
or with a massive pulmonary emobilm.
HF in the presence of normal systolic
function also occurs in chronic conditions in which there is impaired filling
of the ventricles due to a mechanical abnormality such as tricuspis and mitral
stenosis without myocardial involvement, endocardial fibrosis, and some forms
of hypertrophic cardiomyopathy .
Type
of Heart Failure: It may be described as systolic or diastolic, high out put or
low out put acute or chronic right side or left side and forward or back ward.
These descriptors are often useful in a clinical setting, particularly
early in the patient’s course, but the differences often become blurred late
in the course of chronic HF.
Systolic
versus Diastolic Failure: The distinction between these two forms of HF Relates
to whether the principle abnormality is the inability of the ventricle to contract
normally and expel sufficient blood or to relax and fill normally.
The
man infestations of systolic failure related to an inadequate cardiac output with
weakness, fatigue, reduced exercises tolerance, and other symptoms of hypoperfusion,
while in diastolic.
HF the manifestations relate principally to the elevation
of filling pressures in the left and right ventricles. Diastolic HF is usually
defined as HF in patients with an ejection fraction > 50%. Diastolic HF may
be caused by increased resistance to ventricular.
Inflow and reduced ventricular diastolic capacity impaired ventricular relaxation
and myocardial fibrosis and frequently in women than men, especially elderly women
with hypertension. In most patient with HF, abnormalities both of contraction
and relaxation coexist.
Low
– Out Put Versus High Out put Heart Failure:
Low output HF
occurs secondary to ischemic heart disease, hypertension, dilated cardiomy opathy,
and valvular and pericardial disease, while high out put HF occurs in patients
with reduced systemic vascular resistance.
I.e. anemia, hyperthyroidism,
pregnancy, arteriovenous fistulas, beriberi, a paget’s disease. In clinical
practice, however, low-output high-output HF cannot always be readily distinguished.
The normal range of cardiac output is wide (2.2 to 3.5 l/min per m2).
In many patients with low-output HF, the cardiac output may actually be just above
the lower limit of normal range at rest (although lower than it had been previously),
but fails to rise normally during exertion. On the other hand, in patients with
so-called high-output HF,
The output may not exceed the upper limits
of normal (although it would have been above normally elevated had it been measured
before HF supervened); instead, it may have fallen to within normal limits with
HF.
The
hemodynamic burden placed on the myocardium by many forms of high-output heart
failure resembles that produced by chronic aortic regurgitation.
In
addition, thyrotoxicosis and beriberi may also impair myocardial metabolism directly,
while very severe anemia many interfere with myocardial function by producing
myocardial anoxia especially in the subendocardium and in the presence of underlying
obstructive coronary artery disease.
Acute
versus chronic heart failure
An
example of causes of acute HF is sudden rupture of a cardiac vale learlet secondary
trauma or infective endocarditis or a massive myocardial infarction a patient
who previously had no cardiac dysfunction.
In acute HF the sudden reduction
in cardiac output often results in systemic hypotension without peripheral edema.
Chronic HF is typically observed patients with dilated cardiomyopathy. Vascular
congestion is common chronic HF, but arterial pressure is ordinarily well maintained
until very late.
Right-sided
and left-sided heart failure
Many
of the clinic manifestations of HF results from the accumulation of fluid upstream
to (behind) the ventricles that is initially affected. For example.
Patients
in whom the left ventricle is hemodynamically overloaded (e.g. aortic regurgitation)
or weakened due to myocyte loss (e.g. post myocardial infarction) develop dyspnea
and orthopnea as a result of pulmonary congestion,
A affects the right
ventricle primarily (e.g. primary pulmonary hypertension secondary to chronic
pulmonary thronboembolism), symptoms resulting from pulmonary congestion hepatomegaly,
and systemic venoudistention, i.e. clinical manifestations of right-sided HF,
are prominent.
The muscle bundles composing both ventricles are continuous
and both ventricles share a common wall, the interventricular septure. The biochemical
changes that occur in the myocardium of HF (215).
Usually occur in the
myocardium of both ventricles. Therefore when HF has existed for months or years,
localization of excess flu behind one ventricle may no longer exist.
Backward
versus forward heart failure
A controversy has revolved around the
mechanism of the clinical manifestations resulting from HF. The concept of backward
HF contents that in HF, one or the other ventricle fails to discharge its contents
or fails to till normally.
As consequence, the pressure in the atrium
and venous system behind (upstream to) the failing ventricle rise, and retention
of sodium at water occurs as a consequence of the elevation of systemic venous
and capillary pressures and the resultant transudation of the fluid into the pulmonary
or systemic interstitial space.
On the other hand, proponents of the
forward HF hypothesis maintain that the clinical manifestations of HF result directly
from an inadequate discharge of blood into the arterial system.
According
to this concept, salt and water retention is a consequence of diminished renal
perfusion and excessive proximal and distal tubular reabsorption of sodium, the
latter through activation of the rennin-angiotensin-aldosterone system (RAAS)
.
The rate of onset of HF often influences the clinical manifestations.
For example, when a large portion of the left ventricle is suddenly destroyed,
as in myocardial infarction, the patients may succumb to acute pulmonary edema,
a manifestation of backward failure.
If the patient survives the acute
insult, clinical manifestations resulting from a chronically depressed cardiac
output, including the abnormal retention of fluid within the systemic vascular
bed, may develop, which is a manifestation of forward failure.
| Patho-physiology
in heart failures and the neuro-hormmal activation and compensatory mechanism
in heart failure | symptoms
/ clinical features of the heart failure |
