Page 251 - ACCCN's Critical Care Nursing
P. 251
228 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E
poorest five-year survival rate, with the exception of lung ● Diastolic heart failure (or heart failure with preserved
59
cancer. In Australia during 2001–2002, 41,874 patients systolic function [HFSF]): indicates normal systolic
were hospitalised with a primary diagnosis of CHF (0.7% function with a normal ejection fraction but impaired
60
of all hospitalisations). Internationally, heart failure is relaxation so there is a resistance to filling with increased
the most common cause of hospitalisation in patients filling pressures. Diastolic dysfunction usually occurs
55
aged over 70 years. Approximately 40% of patients in conjunction with systolic dysfunction and is more
admitted to hospital with heart failure will be readmitted common in the elderly.
or die within one year. 61 ● Low cardiac output syndrome: this occurs in response
to hypovolaemia and/or hypertension. Severe vasocon-
Over 50% of patients newly diagnosed with heart failure
have concurrent ischaemic heart disease, hypertension is striction further reduces the cardiac output.
present in 65% and idiopathic dilated cardiomyopathy ● High cardiac output syndrome is the result of an
55
(5–10% of cases). The causes of heart failure can be cate- increase in metabolic demands causing a decrease in
gorised according to (a) myocardial disease, (b) arrhyth- SVR leading to an increase in stroke volume and
mias, (c) valve disease, (d) pericardial disease and (e) cardiac output. Burns and sepsis are the main causes.
congenital heart disease. Myocardial disease may be ● Left sided heart failure: occurs when there is a reduced
62
caused by myocardial infarction and fibrosis from pro- left ventricular stroke volume resulting in accumula-
longed ischaemic heart disease which accounts for tion of blood in the pulmonary system.
approximately two-thirds of systolic heart failure causing ● Right sided heart failure: is the congestion of blood in
systolic dysfunction and a reduced ejection fraction. the systemic system due to the inability of the right
ventricle to expel its blood volume.
Arrhythmias, including both brady- and tachyarrhyth-
mias, may cause heart failure due to changes in filling RESPONSES TO HEART FAILURE
time affecting preload and resultant cardiac output. Myo- When heart failure occurs, several adaptive responses are
cardial oxygen demand is increased and if the heart is initiated by the body in an attempt to maintain normal
poorly perfused, muscle contraction will be affected. perfusion (see Figure 10.8). These mechanisms are suc-
Frequent premature contractions and atrial fibrillation cessful in the normal heart, but contribute to decreased
disturb mechanical coordination so that the ventricles effectiveness in the failing heart. The compensatory mech-
may not be adequately filled for efficient contraction. anisms include:
Heart failure patients are also at high risk of sudden
cardiac death due to ventricular fibrillation or tachycar- ● sympathetic nervous system response
dia. Valvular disease causing heart failure usually involves ● renin-angiotensin-aldosterone system (RAAS)
valves on the left side of the heart (mitral and/or aortic ● Frank-Starling response
valves). Aortic stenosis results in an increase in afterload ● neurohormonal response.
and ventricular hypertrophy develops with reduced dia- The sympathetic nervous system is the first response to
stolic compliance resulting in a reduced ejection fraction. be stimulated in heart failure. It occurs within seconds
Mitral stenosis is usually due to rheumatic heart disease. of a reduction in cardiac output and the parasympathetic
Valvular incompetence results in a dilated ventricle to system becomes inhibited. The baroreceptor reflexes
accommodate the regurgitant volume. Stroke volume are activated in response to a reduced arterial pressure.
increases in an attempt to empty its contents and ven- The beta-adrenergic receptors located in the heart are
tricular muscle mass increases. However, over time the activated resulting in an increase in heart rate and cont-
ventricle is unable to maintain the increased workload ractility to increase stroke volume and cardiac output.
and heart failure develops. Valvular heart disease and Sympathetic nervous system response in the peripheral
treatment is described in more detail in Chapter 12.
vascular system results in vasoconstriction which increase
There are several terms used to describe the pathology systemic venous return (SVR) and mean systemic filling
and signs and symptoms of heart failure. These include: pressures. This results in an increase in venous return,
preload and afterload (see Figure 10.8). The consequence
● Backward failure: refers to the systemic and pulmo- of this activation is increased myocardial oxygen demand.
nary congestion that occurs as a result of failure of Although blood flow to essential organs is maintained,
the ventricle to expel its volume. perfusion to the kidneys, gastrointestinal system and
● Forward failure: is due to an inadequate cardiac output skin is reduced and peripheral resistance increased.
and leads to decrease in vital organ perfusion. Chronic activation of vasoconstrictors contributes to the
● Acute heart failure: includes the initial hospitalisation progression of cardiac failure through increased resis-
for the diagnosis of heart failure and exacerbations tance and effects on cardiac structure, causing hypertro-
of chronic heart failure. phy and fibrosis and downregulation of beta-adrenergic
● Chronic heart failure: develops over time as a result of receptors and endothelial dysfunction. Chronic poor
the inability of compensatory mechanisms to maintain perfusion to skeletal muscles may contribute to changes
an adequate cardiac output to meet metabolic demands. in muscle metabolism, resulting in further reductions in
● Systolic heart failure: refers to the inability of the exercise tolerance.
ventricle to contract adequately during systole resulting
in a reduced ejection fraction and an increased The next compensatory mechanism to be activated is the
end-diastolic volume. This is the most common form RAAS. This is stimulated within minutes, in response to
of heart failure. a decrease in kidney perfusion resulting in a decrease in

