Clinical syndrome that is
characterised by inability of
heart to maintain a CO that is
sufficient for the body's needs
Classification and corresponding causes
Low output most
common = low CO that
fails to increase w/
exertion
Pump failure
Systolic
dysfunction -
<40% EF
MI, IHD, CM
Diastolic
dysfunction
- EF >50%
Constrictive
pericarditis,
restrictive CM,
tamponade, HTN
Decreased HR
BB,
MI,
heart
block
-vely inotropic
drugs eg
antiarrhythmics
Excessive preload
AR, MS, MR or fluid overload
More likely if renal
impairment, or big
volumes involved, or
simultaneous cardiac
insult, or elderly
Excessive afterload
AS, HTN
NYHA
classification of
sx severity
high output =
CO
high/normal
but incr needs
Anaemia,
pregnancy,
paget's,
hyperthyroidism,
AVMs, beri beri
Investigations and diagnosis
If normal ECG and
BNP then diagnosis
unlikely
If either
AN then
echo
required
Can indicate a
cause ± presence of
LV dysfunction
>100 then
+ve, if <50
then -ve
Highest in
those w/ syst +
diastolic
dysfunction.
Sx of HF
and
objective
evidence of
dysfunction
at rest.
Framingham
criteria for CCF
2 majors or 1
major and 2
minors
Major
PND, creps, S3 gallop,
cardiomegaly, increased
CVP (>16cmH20 in RA),
>4.5kg w loss in 5/7 of
treatment, Neck vein
distension, acute
pulmonary oedema,
hepatojugular reflux
Minor
Bilateral ankle
oedema,
dyspnoea on
ordinary exertion,
tachycardia
(>120), dec vital
capacity by 1/3,
nocturnal cough,
hepatomegaly,
pleural effusion.
Loops reduce sx eg furos
40mg/day or bumet 1-2mg/day.
SE = low K, renal impairment
(requires large doses). ? thiazide
if refractory oedema eg
metolazone 5-20mg/day
Add K sparing if K<3.2,
predisposed to arrhythmia,
concurrent digoxin therapy
(hypoK increases risk of dix
toxicity), K losing condition.
ACEI
Dec mortality in
proportion to LV
dysfunction, dec risk
of hospitalisation,
provide sx relief in
1/52 approx.
AKI, K imbalances,
cough, 1st dose
hypotension,
angiooedema (non-allergic)
B blockers
Start after ACEI and
diuretic, start low and slow.
Cold peripheries, sleep
disturbance, fatigue, impotence
and loss of libido, loss of
warning signs of hypoglycaemia
can be lost
Sprinolactone (both)
In patients that are still
sx despite other max
therapy, prevents
remodelling, and
improves endothelial
function. Little risk of
hyperK even if taking
ACEI.
Vasodilators (equal)
Hydralazine (DI lupus) + ISDN
if intolerant to ACEI and ARBs.
Reduces mortality in black
people with HF, in combo w/
standard therapy.
Drugs for sx relief only
Digoxin
Helps even in SR. ?
if LV systolic
dysfunction + signs
and sx of HF despite
standard therapy inc
ACEI and BB. Or ? in
AF.
Maintain K 4-5.
HypoK increases
risk of toxicity.
Sx of toxicity
Dec cognition,
yellow/green
halos,
arrhythmias, N,
anorexia.
If serious arrhythmia,
correct hypokalaemia,
and give Digibind - dig
specific ab fragments
taken from immunised
sheep.
Diuretics
Surgical
ICD
Transplant
Mechanism of disease
Compensatory
mechanisms that
try to maintain
perfusion and CO
when the heart
begins to fail.
These
become
pathological
as the failure
progresses
SNS activation
Increased preload
through venoconstriction.
But increased after load
due to arteriolar
constriction.
RAAS activation
Increased
fluid
retention,
with
increased
after load
due to AII.
Natriuretic peptides
Released
by atria,
ventricles,
and vasc
endothelium
Water, salt
loss, relaxes
smooth muscle
(dec preload).
?Compensatory
mechanism but
inadequate.
Sensitivity
>90%, specificity
80-90%
Not raised in
acute HF
exacerbation.
Low if no LV
dysfunction or
HF.
Secretion inc by
glucocorticoids,
tachycardia, thyroid
hormones. Endothelin1
and AII influence
secretion.
LV dilatation
Decreased ejection of blood -
stretched ventricle. Over time
starling response flattened
and increased venous
pressure.
Hypertrophy, loss of
myocytes and
increased fibrosis
leading to irreversible
pump failure.