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Discussion
Diuretic consumption in normovolemic heart
failure paient will stimulate renin angiotensin
aldosterone system may lead into increased
angiotensin 2. Angiotensin 2 is a potent
peripheral
vasoconstrictor
with
increased
adrenergic activity would increase systemic
vascular resistance (SVR). The increased SVR
would decrease stroke volume and cardiac
output that would eventually lead to a vicious
cycle of worsening heart failure. Meanwhile, ACEinhibitors
would
reduce
Angiotensin
II,
diminished afterload and thereby elevated
cardiac output. The diuretic was stopped
because the patient was on a euvolemic state.
Optimization in ACE-inhibitor dosage leads to
Conclusion
improvement of patients
physical capabilities
Although
therapy
the main treatment
and morediuretic
controlled
heartisrate.
for heart failure with volume overload, however it
shouldnt be given in heart failure patient with
euvolemic state.