INTRODUCTION
Heart failure is a disease in which there are multiple definitions and
the concept is adopted arbitrarily by each author, in such a way that the
terminology is so confusing now the authors of the mega trials in medical treatment
of heart failure, avoid thus refer to the disease to be treated and are only
set to indicate that the value of the ejection fraction is <40 or 35%. In
this paper, the goal is the promptly revise the concepts of contractility,
ventricular function, preload, afterload and heart failure, compensation
mechanisms. These definitions and concepts are based on the original
contributions of recognized researchers, in an attempt to clarify the concepts,
which was born the niomination of heart failure and thus avoid an erroneous
interpretation, almost always motivated by inadequate simplification of terms,
in order to scientifically explain the concept of ventricular function and
heart failure.
Heart function: “The
heart is a muscular pump that generates pressure and move volume, whose
function is the supply of oxygenated blood to the tissues of the body and send
unsaturated blood to oxygenate the lungs to Life sustaining” [1,2].
In the 20th century, there are hundreds of papers of basic
and clinical research on left ventricular function and heart failure, made by
great Scientist men. At this review, is intended to analyse those studies that
can clarify and give scientific support to achieve an understanding of the
concept of heart failure.
Contractility: “It
is the intrinsic capacity of the myofibril to shorten its length and its
shortening speed independent of the pre and afterload” [1].
In the isolated myofibril contractility can be measured by quantifying
degree and speed of shortening to stimulate it directly to a constant initial
length and without resistance to its shortening (no-load). The intact heart
contractility is very difficult to quantify in its function is always subject
to a diastolic load (preload) and a force that has to overcome during his emptying
(afterload).
Today the
closest way to meet the heart's intrinsic contractile State is the end systolic
relationship stress/volume or pressure/volume at which generates a curve that
is extrapolated to pressure 0 mmHg, this curve has been called “End systolic
elastanse” (Emax). This implies that a ventricle has more
contractility when reduce the systolic volume higher magnitude to one greater
afterload than another whose systolic volume is higher for the same afterload,
unfortunately the method is little practical and difficult to achieve in
clinical settings but has been very useful for basic and clinic research.
It's common
for the term “Contractility” is erroneously used interchangeably to refer to
the "ventricular function": ventricular function refers to the
relationship between contractility and instantaneous hemodynamic load (preload
and afterload) and do not mean intrinsic contractile State (heart
contractility) [3].
Preload: It is the length of the myofibril at rest,
immediately before ventricular contraction. In the intact heart is represented
by the diastolic volume than in normal conditions generates a force that
increases the area of the myofibril immediately before contraction (diastolic
wall stress) [1].
Afterload: is defined as the force per unit sector area
that opposes the ventricular contraction during the emptying of the heart
towards the great vessels and obeys to Laplace law, so it is quantified by
calculating the systolic wall stress.
S=P × r/ 2h3
Systolic left ventricular function: “Left ventricular function is the result of the
simultaneous interaction of contractility with
load (preload or afterload) and is quantified by ejection fraction (EF)” [3].
The normal values of EF: 67 ± 8%.
Diastolic function: It is
the ability of the heart to receive the systemic and pulmonary venous return
and that it is represented by the diastolic volume. This capacity is dependent
on isovolumic relaxation and ventricular distensibility (compliance) [2].
Cardiac reserve: “Is the ability of
the heart to increase cardiac output”.
A. Chronotropic reserve: “is the ability of the heart
to increase the cardiac output by increasing heart rate”.
B. Diastolic reserve: “is the ability of the heart to
increase cardiac output through the Frank-Starling mechanism, and its limit is
pulmonary edema”.
C. Systolic reserve: “is the ability of the heart to
increase cardiac output through increasing its contractility, which depends on
the anatomofunctional integrity of the myofibril (shifts upward Starling curve)”.
Heart failure: In 1967, Braunwald
et al. defined heart failure: “When the heart loses its ability to supply
enough blood to meet the metabolic needs of the tissues of the body in a normal
physical activity” [1]. This condition in 1970, Mason et al. [4], called “Decompensated
Heart Failure”. This definition conceptualized with clarity that heart is not
able when it ceases to fulfil its vital role, (tissue perfusion) that is why,
if it is not corrected in a period of hours or days, ensues death; and they
noted that when this picture appears, the organism avoid this lethal condition,
using mechanisms that attempt to restore cardiac output and tissue perfusion;
these mechanisms they call "compensatory mechanisms"; Which try to
restore the vital function of the heart: tissue perfusion.
Compensatory mechanisms
The Frank Starling
mechanism increases ventricular diastolic volume and normalises cardiac output.
The enlargement of heart (cardiomegaly) and increased diastolic pressure with
increase left ventricular wall stress, triggers secretion of brain natriuretic peptide
(BNP); by other hand, the increase atrial wall stretching (stress) triggers ANP
secretion. These substances really are hormones that function as internal
diuretics and vasodilators allow relieve the congestion pulmonary and systemic
venous, which gets a hemodynamic State, that while the heart is in failure
(decreased EF), the patient maintains cardiac output and therefore tissue
perfusion (Compensated Heart Failure) and absence of systemic and pulmonary
congestion and this state, allow that the patient is in functional class I, so
in these conditions the patient has Asymptomatic Compensated Heart Failure
[2]. In these cases ACE Inhibitors have proven to be the most effective
treatment to prevent the progression to symptomatic heart failure. When heart
failure, appears and the Starling mechanism is not able for maintain cardiac
output, stimulates adrenergic system and catecholamine secretion increases the
heart rate (chronotropic reserve) and the positive inotropic effect increases
contractility, shifts upward the Starling curve (inotropic reserve), increasing
cardiac output; and also stimulates RAA system and these mechanism increase
cardiac output and tissue perfusion. By other hand, the secretion of
angiotensin II increase peripheral resistance and maintain the perfusion
pressure; aldosterone secretion retains renal Na+ and water increases the
intravascular volume, the preload and cardiac output and compensate heart
failure but produce clinical consequences: tachycardia, pallor, oliguria,
increases of heart size, dyspnea, edema, pulmonary congestion and hepatomegaly.
In conclusion, the patient's symptoms are not by themselves due to heart
failure, they are consequence to activation of the compensatory mechanisms, but
are those who maintain tissue perfusion and life, then this condition
corresponds to Symptomatic Compensated Heart Failure. That is,
compensation does not refer to the patients has symptoms, it refers to life
preservation [2,4].
When the
compensatory mechanisms fails to restore cardiac output appears tissue
hypoperfusion (the heart loses its vital functions), with corresponds to
cardiogenic shock (descompensated heart failure) [2,4].
Decompensated heart failure: “Is the
inability of the heart to eject sufficient amount of blood, to maintain an
adequate blood pressure, to perfuse oxygen to the tissues of the body. This
inability is due to ineffective myocardial contraction either by intrinsic
damage of the myofibril or excessive hemodynamic overload” [4].
When contractility
is depressed in potentially reversible (hibernating myocardium) systolic
reserve is lost until the cause (pharmacological, surgical or Interventional
coronary reperfusion) is solved and restores tissue perfusion and life is
preserved; but when there is extensive destruction of myofibrils by necrosis
(infarction) or inflammation (myocarditis), as in cardiogenic shock, systolic
reserve is lost and the application of inotropics is not follow of improvement
of EF; so it does not increase the cardiac output by this mechanism (loss of
the systolic reserve) and appears Decompensated Heart Failure [2,4]:
cardiogenic shock this concept, explains the reason for the reduction of
mortality of cardiogenic shock with early reperfusion, retrieving the viable
myocardial not functioning (hibernating myocardium) at risk of necrosis and
restores the systolic reserve, the cardiac output and life of the patient.
When there is
extensive myocardial damage and extreme downward deviation of ventricular
function curve occurs irreversible cardiogenic shock, without effective
treatment, leads to death. The clinical manifestations are: weak pulse, blood
systolic pressure <80 mm Hg, peripheral vasoconstriction, cold, wet and
bluish skin, oliguria (<50 cc/h), mental confusion, metabolic acidosis, are
the true symptoms of Decompensated Heart Failure in other words the
inability of the heart to maintain its vital function (tisular perfusion)
[2,4].
Diastolic dysfuction: “The
myocardial or extracardiac alterations that produce an impediment of variable
degree to the filling of the heart, which can cause to raise the
intraventricular diastolic pressure without increasing the diastolic volume and
which coincide with a normal ejection fraction” [2].
Patients who have
symptoms like shortness of breath and EF>50% (heart failure “with preserved
systolic function”) have a mortality rate of 7.6% at 10 years [5], while
patients who have heart failure in functional class I (40-50% FE) have a
mortality rate of 70%, 82% (FE<40%) and 90% in patients functional class II
to IV to 10 years; when the ejection fraction is <50% [6] and the difference
in mortality between two groups is explained because patients with heart
failure and “preserved systolic function” do not activate the neuroendrocrine
system.
CONCLUSION
1. Braunwald
E, Sonnenblick EH, Ross Jr (1992) Heart disease. A textbook of cardiovascular
medicine. 4th Edn. Saunders Co., p: 351.
2. Guadalajara-Boo
JF (2016) Understanding heart failure. Int J Cardiovasc Res 6: 1-8.
3. Braunwald
E (2013) Heart failure. J Am Coll Cardiol Heart Failure 1: 1-20.
4. Mason
DT, Spann Jr. JF, Zelis R, Amsterdam EA (1970) Alterations of hemodynamics and
myocardial mechanics in patients with congestive heart failure:
Pathophysiologic mechanisms and assessment or cardiac function and ventricular
contractility. Pro Cardiovasc Dis XII: 507-556.
5. Brogan
WC, Hillis LD, Flores ED, Lange RA (1992) The natural history of isolated left
ventricular diastolic dysfunction. Am J Med 92: 627-630.
6. Wang TJ,
Evans IC, Benjamin EJ, Levy D, Le Roy EC, et al. (2003) Natural history of
asymptomatic left ventricular systolic dysfunction in the community.
Circulation 108: 977-982.
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