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ROBINA, Paulyn Crystal P.

SERDENIA, Marie Angelica S.


VEGA, Dianne Grace B.
 2% is the overall prevalence in adult population in developed
countries

 HF prevalence follows an exponential pattern: rising with age,


and affects 6–10% of people over the age of 65

 Relative incidence is lower in women than in men


 women constitute at least half of the cases of HF because of their
longer life expectancy
 The overall prevalence of HF is thought to beincreasing, in
part because current therapies for cardiac disorders, such as
 Myocardial infarction (MI),
 Valvular heart disease, and
 Arrhythmias

 HF patients are now broadly categorized into:


 HF with a reduced EF (HFrEF; formerly systolic failure)
 HF with a preserved EF (HRpEF; formerly diastolic failure)
 Heart failure begins after an
index event produces an
INITIAL DECLINE IN THE
HEART'S PUMPING
CAPACITY.
 Caused by
 the loss of cardiac myocyte’s
functionality or
 disruption in the generation of
force in myocardium.
 Onset of this index event may be abrupt(MI), gradual or
insidious(hemodynamic pressure or volume overloading), and
hereditary(genetic cardiomyopathies).
 Most of LV dysfunction remain asymptomatic because of the
variable compensatory mechanism that are being activated such
as:
 the renin-angiotensin-aldosterone (RAA) and
 adrenergic nervous systems, and
 increased myocardial contractility. In addition,
 activation of vasodilatory molecules including ANP and BNP,
prostaglandins (PGE2 and PGI2), and nitric oxide (NO)
 However, the sustained activation of these systems can lead to secondary
end-organ damage within the ventricle, with worsening left ventricular
remodelling and subsequent cardiac decompensation.

 Genetic background, sex, age, or environment may influence these


compensatory mechanisms. Patients may become symptomatic which
results in striking increase in morbidity and mortality rates.

 Transition to symptomatic HF is accompanied by increasing activation of


neurohormonal, adrenergic, and cytokine systems that leads to LV
remodelling.
heart pumping capacity

Stroke Volume

Cardiac Output

Compensatory mechanism

Adrenergic system activation Renin- angiotensin- aldosterone


myocardial contractility system activation
Renin- angiotensin- aldosterone
system activation

Renin + Angiotensinogen
Heart Rate Cardiac Workload
Angiotensin I

Ventricular hypertrophy /
Angiotensin II
dilation

Peripheral vasoconstriction Aldosterone secretion

afterload Na & H2O retention


edema
Plasma volume
Cardiac output
Preload

Cardiac workload
1. Increased circulating volume and preload
•Chronic ventricular dilation or hypertrophy

2. ventricular dilation or hypertrophy


3. Tachycardia
4. Continuous sympathetic activation
5. Increased total peripheral resistance
resulting in higher afterload
6. Chronic elevation of angiotensin II
and aldosterone trigger production
of cytokines
7. Edema