Download Pathogenesis of cardiac failure

MODULE 11:
Cardiology
More people in Ireland die from diseases of the circulatory
system than from any other condition. Ireland is still above the
EU average for premature deaths from coronary heart disease
and three out of four deaths in those under 65 are the result of
heart attack, stroke or another disease of the circulatory
system.
The WIN Continuing Education module for 2005 is focusing on
various aspects of cardiac nursing. The articles are aimed at
assisting nurses to understand, care for and educate patients
who present with cardiac conditions.
To date this module has addressed the pathogenesis of
coronary heart disease, and the in-hospital management of
patients who present with conditions including STEMI, NSTEMI
and unstable angina.
This month we focus on the pathophysiology of heart failure.
It is intended as a precursor to the upcoming article on the
management of patients with heart failure.
At the end of the module you will have the opportunity to
complete some self-test questions to enable you to identify
what you have learned each month.
It is therefore advisable that you keep the entire series of
articles for reference.
Table 1
PART 6
Pathogenesis of
cardiac failure
New York classification of heart failure3
l Class I: No limitations during ordinary activity (asymptomatic)
l Class II: Slight limitation during ordinary activity
l Class III: Marked limitation in ordinary activity, without
symptoms at rest
l Class IV: Inability to carry out any physical activity without
dyspnoea +/- rest symptoms
by Mary Mooney and Lisa Browne
THE INCIDENCE, prevalence and morbidity associated with congestive heart failure should not be underestimated. Epidemiological
studies have demonstrated the enormity of this problem within
society. The implications of this syndrome include immeasurable
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economical and psychological consequences.
This article focuses of the pathophysiology of heart failure and
is intended as a precursor to the upcoming article on the management of patients with heart failure. It is essential to understand the
pathophysiology of heart failure, as the rationale for the management, particularly the drug therapy, is based on this. To maximise
understanding, it is advisable to review, if necessary, the anatomy
and physiology of the heart in conjunction with this article.
Heart failure is a complex clinical syndrome comprising a constellation of signs and symptoms resulting in cardiac dysfunction. It
is classically characterised by abnormalities in left ventricular function and neurohormonal regulation, often caused by damage or
insult to the myocardium. The dysfunctional myocardium fails to
pump effectively and thus fails to meet the metabolic needs of the
body. The person classically presents with dyspnoea, oedema and
fatigue, which contribute to several other symptoms associated
with heart failure. The greatest majority of patients who present
with heart failure are elderly and most have serious co-existing disease.2
Within the clinical setting there are various models used to classify the presence and degree of heart failure in patients.The model
most frequently adopted in Ireland is the New York classification,
which comprises four grades of failure (see Table 1).
Causes of heart failure
Heart failure is a manifestation of another clinical pathology.The
clinical causes include problems with restricted filling, increased
intra-cardiac pressure, volume loading, contractile impairment and
dysrhythmias.
Contractile impairment
Myocardial infarction is one of the primary causes of cardiac failure. In this situation the myocardium has been damaged, resulting
in an inability to pump efficiently and effectively. Ischaemic heart
disease also contributes to heart failure by similar mechanisms.
Restricted filling
If the heart is unable to fill properly during the cardiac cycle then
heart failure can ensue. This can happen if, for example, there is
stenosis of the tricuspid or bicuspid valves or in the presence of
constrictive pericarditis, where the heart cannot fill at ease.
Increased pressures
Any obstruction or disease which increases the contractile pressures during the cardiac cycle can precipitate heart failure. Such
causes include hypertension, aortic or pulmonary stenosis or pulmonary embolism, for example.
Volume loading
If the heart is overloaded with volumes of fluid, it can compensate efficiently (within physiological limits) in the short term. Heart
failure will develop however, if the problem is prolonged. Issues
related to volume loading include regurgitation from any of the
four main cardiac valves.
Dysrhythmias
Severe bradycardia and severe tachycardia may cause heart failure and filling where ejection times are delayed or augmented.
This module is supported by MSD Ireland (Human Health) Ltd.
continuing education/41+42
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Continuing Education
Systolic and diastolic heart failure
Traditionally it was considered that heart failure was caused by
impaired left ventricular function. However, with advances in imaging modalities, it is now well recognised that heart failure may occur
in people with normal left ventricular systolic function. Hence the
differentiation between systolic and diastolic heart failure have been
delineated. While the presentation of symptoms is the same in both
systolic and diastolic heart failure, the pathogenesis is different.
Diastolic congestive heart failure
Within this condition there is impaired diastolic relaxation of the
left ventricle. In other words, the ventricle becomes less compliant
or stiffer, which impairs ventricular filling.This impairment results in
reduced ventricular compliance, which in turn causes inadequate
left ventricular filling. As a consequence of this, left atrial pressure
rises and the increased pressure is often transmitted to the pulmonary system, leading to pulmonary congestion and dyspnoea.
This compensatory mechanism occurs in an effort to enhance ventricular filling and to maintain cardiac output.
The predisposing conditions associated with diastolic heart failure
are those which impact negatively on left ventricular filling. The
main cause is hypertension.4 Blood pressure elevation can precipitate the development of left ventricular hypertrophy, which reduces
both wall stress and compliance within the ventricle. In addition,
coronary artery disease, cardiomyopathy and valvular heart disease
(aortic stenosis and bicuspid regurgitation) may contribute to wall
stiffness, increased pressures and diastolic heart failure.
Systolic congestive heart failure
Within this condition there is a loss of intrinsic contractility within
the ventricle. Symptoms are related to a decrease in cardiac output
and the effect of an altered load on a failing ventricle. The ventricle,
in this situation, is unable to contract and expel the blood supply.
The result is a reduced ejection fraction, an enlarged left ventricle
and a remodelling of the cardiac chamber. The process of remodelling induces an altered ventricular shape which in turn distorts the
bicuspid valve causing regurgitation and increased volume overload
in the failing ventricle. This overloading contributes further to the
remodelling process and disease progression.
Both systolic and diastolic heart failure result in decreased stroke
volume (amount of blood ejected from each ventricle during systole – normally 60ml-100ml.) This reduction in output initiates a
cascade of events in the body.
Neurohormonal responses
The decrease in stroke volume causes activation of central and
peripheral chemo and baro-reflexes, which elicit increases in sympathetic nerve stimulation.5
When the sympathetic nervous system is activated there is an
increase in heart rate, myocardial contractility and vasoconstriction
of veins and arteries in an effort to maintain blood pressure. The
arteriolar vasoconstriction is most evident in the skin, gut and kidney, as blood is diverted to the vital organs.
Due to reduced renal perfusion and increased sympathetic activity, there is a release of renin from the kidney. Renin, an enzyme,
responsible for the conversion of angiotensin I to angiotensin II, is a
potent vasoconstrictor. The already overwrought heart is placed
under further strain as it must now pump against increased afterload (tension developed by ventricle to expel blood), which
worsens contractile dysfunction.
Furthermore, renin stimulates the secretion of aldosterone from
the distal nephron, which promotes the retention of salt and water.
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WIN June 2005
This increases ventricular filling and in the short term helps maintain cardiac output. In the failing heart however, the retention of
salt and water serves only to exacerbate the condition.
Natriuretic peptides
On a more positive note, these endogenously generated amino
acids (ANP, BNP, CNP) are found in human atria and ventricles in
increased quantities in heart failure. They contribute to salt and
water balance. Their beneficial role in heart failure is seen in their
promotion of vasodilation and natriuresis.They mediate a decrease
in cardiac preload, afterload and in neuro-hormonal compensatory
mechanisms.
Oedema formation
Blood volume is augmented through a number of mechanisms in
heart failure. As referred to above, salt and water retention arise from
reduced renal perfusion, reduced urinary output and increased levels of aldosterone and renin levels. Levels of arginine vasopressin
(anti-diuretic hormone) are also elevated in heart failure and this too
promotes the retention of fluid. The increase in fluid volume secondary to compensatory mechanisms can be deleterious in heart
failure because it increases preload and raises venous pressures,
leading to pulmonary and systemic oedema. Pulmonary oedema
occurs when left atrial pressure rises, usually above 18mmHg20mmHg, causing an increase in pulmonary capillary pressures.
Systemic oedema occurs when failure is evident in the right side
of the heart, due largely to salt and water retention and overloading. If the right ventricle is unable to cope with the venous return
then systemic ‘flooding’ occurs. Oedema of abdominal viscera can
result in ascites. Oedema arises from impaired synthesis of plasma
proteins because of hepatic engorgement, which reduces capillary
osmotic pressure and exacerbates oedema formation.
Ventricular remodelling
Ventricular hypertrophy and ventricular dilatation are features of
myocardial responses to heart failure. The responses stem from
myocyte hypertrophy, mechanical distension, myocardial fibrosis
and cardiomyocyte apoptosis. These maladaptive changes cause
adverse ventricular remodelling6. In addition, angiotensin II mediates cellular hypertrophy within the myocardium, which may lead
to further loss of myocardial function.
Understanding pathophysiology
An understanding of the pathophysiology of heart failure is
essential to the correct management of the condition. The pathophysiology involves changes in cardiac function, neuro-hormonal
states, systemic vascular function and blood volume. The compensatory mechanisms that arise in heart failure may be beneficial in
the short term but lead to adverse clinical conditions in the long
term. The presenting symptoms are manifestations of the failure
itself, which is inevitably caused by an underlying pathology.
Lisa Browne is a chest assessment nurse at the Mater Hospital, Dublin and Mary
Mooney is lecturer in cardiovascular nursing at TCD
References
1. Guazzi M. Alveolar-capillary membrane dysfunction in chronic heart failure:
pathophysiology and therapeutic implications. Clinical Science 2000; 98: 633-641.
2. Charanjit S, Sabharwal J. Heart failure: current concepts. MJAFI 2003; 59(4): 283-285.
3. Fonarow G. Heart failure: recent advances in prevention and treatment. Rev in
Cardiovascular Med 2000; 1(1): 25-33.
4. Levy D, Larson MG,Vasan R et al.The progression from hypertension to congestive heart
failure. JAMA 1996; 20: 1557-1562.
5. Shah M,Vagar A, Sumant L, Abraham W. Pathophysiology and clinical spectrum of
acute congestive heart failure. Rev in Cardiovascular Med 2 2001; (supplement 2), S2-S6.
6. Baig M, Mahon N, McKenna W.The pathophysiology of advanced heart failure. Am
Heart J 1998; 135: S216-S230.