Sympathet

ic
activation
Decreased
parasympath
etic activity
Coronary
artery
disease

Hypertensio
n

Barorecept
or
dysfunction
Structural
and/or
function
cardiac
abnormality

Neurohormo
nal changes

RAAS
system
activation
Releasing
ANP and
BNP
Increased
vasopressin
and
endothelin
Other effect by
PGE, bradykinin,
NO

Vascul
ar
tone
Electrolyt
es
balance
Hemodyna
mic effects

Myocard
contractilit
y
Heart
rate
Cardia
c
output

ESC Guidelines for the diagnosis and treatment of acute and chronic heart
failure, 2016

In this case, patient had:

1. History of myocard infarction
2. High blood pressure (150/100 mmHg)
3. Orthopnoea, PND, dyspnoea on effort
4. Low EF (31%)
5. Structural cardiac abnormality (chambers and valve)
6. Minimal rales
7. Bilateral ankle oedema
8. Pansystolic murmur
9. Widened cardiac left border
10.Accelerated junctional rhythm, LAD, ST elevation in I, aVL,
V2-V5, Q wave on ECG

Clinical reason in using medication:

1. Captopril inhibits ACE in RAAS system
2. Aspilet prevents new thrombus formation
3. Furosemide increases sodium and water excretion
oedema
4. Spironolactone prevents hypokalaemia and
hypomagnesemia
5. Simvastatin reduces rate of cardiovascular events and
mortality by preventing plaque formation