Chap253-Heart Failure Management
Chap253-Heart Failure Management
Chap253-Heart Failure Management
FAILURE:
Management
BY: PGI Czarine P. Castillon
What is Heart Failure?
Defined as a complex clinical syndrome that results from
structural or functional impairment of ventricular filling
or ejection of blood, which in turn leads to the cardinal
clinical symptoms of dyspnea and fatigue and signs of
HF, namely edema and rales.
01 HFpEF
HF with preserved EF
(40-50%) 02 ADHF
Acute Decompansated
Heart Failure
03 04
HFrEF Mgt of Selected
Heart Failure with Co-morbidity
reduced EF (40%)
Management:
Cardiac
05 Resynchronization
Therapy 06 SCD Prevention
07 08
Surgical Disease Mgt and
Therapy Supportive Care
01
HFpEF
Therapeutic targets: control of congestion,
stabilization of heart rate and blood pressure,
and efforts at improving exercise tolerance.
02
ADHF
A heterogeneous clinical syndrome most often
resulting in need for hospitalization due to
confluence of interrelated abnormalities of
decreased cardiac performance, renal dysfunction,
and alterations in vascular compliance.
Parameters assoc with worse outcomes:
S. Creatinine
Elevated troponin I
>2.75 mg/dL
ADHF
ADHF
● It is generally advisable to continue diuresis until euvolemia has been achieved.
● CARDIORENAL SYNDROME, an increasing cpx of ADHF, it reflects the interplay
between abnormalities of heart and kidney function, with deteriorating function of one
organ while therapy is administered to preserve the other.
● ULTRAFILTRATION is an invasive fluid removal technique that may supplement the need
for diuretic therapy. Study argues against using UF as a primary strategy in patients with
ADHF who are nonetheless responsive to diuretics.
● Inotropic therapy in those with a low-output state augments cardiac output, improves
perfusion, and relieves congestion acutely.
● Studies are in universal agreement that long-term inotropic therapy increases mortality.
● Currently indicated as bridge therapy (to either left ventricular assist device support or to
transplant) or as selectively applied palliation in end-stage heart failure.
03
HFrEF
RAAS blockers and betablockers form the
cornerstone of pharmacotherapy
RAAS blockers and beta blockers lead to attenuation of decline
and improvement in cardiac structure and function with
consequent reduction in symptoms, improvement in QOL,
decreased burden of hospitalizations, and a decline in mortality
from both pump failure and arrhythmic deaths
Neurohormonal Antagonism
Neurohormonal Antagonism
● Meta-analyses suggest a 23% reduction in mortality and a 35% reduction in the
combination endpoint of mortality and hospitalizations for heart failure in patients
treated with ACEIs.
● Patients treated with beta blockers provide a further 35% reduction in mortality on
top of the benefit provided by ACEIs alone.
● Optimally titrated doses of both ACEIs and beta blockers should be established in a
timely manner
Mineralocorticoid Antagonists
● The combination of hydralazine and nitrates has been demonstrated to improve survival
in HFrEF.
● Hydralazine - reduces systemic vascular resistance and induces arterial vasodilatation by
affecting intracellular calcium kinetics.
● Nitrates - transformed in smooth muscle cells into nitric oxide, which stimulates CGMP
production and consequent arterial-venous vasodilation.
NOVEL NEUROHORMONAL
ANTAGONISM