Acute vs. chronic Heart Failure and Systolic vs.
Diastolic Heart Failure
A
patient that present with an acute anterior wall MI
leading to acute Heart Failure. This is different than
an elderly patient with a 35 year history of HTN who
has Chronic Heart Failure. The treatment, causes, and
outcomes for each will be different. Acute can be
treated surgically and fixed.
Acute systolic dysfunction- Ischemia and MI
Chronic systolic dysfunction - HTN, DM, ischemic
myopathy and MI
Diastolic Dysfunction: Diastole
is the energy consumption part of the cardiac cycle so
it requires the most amount of oxygen. So an occluded
coronary artery will lead to diastolic dysfunction
Causes:
Acute diasytolic dysfunction – ischemia, MI,
tamponade
Chronic diastolic dysfunction- constriction,
restriction, hypertrophic, HTN, DM
Heart Failure Abnormalities
-
Impaired pump function / contractility
best looked at in a pressure volume loop
Normal pressure volume loops

1.
Start 30ml initial diastolic volume and ventricle
begins to fills.
2.
At
end diastolic volume = 90 ml
3.
LV
pressure increases until you begin systole and
contract ventricles
4.
At
end systole- volume is 30 ml
5.
Normal ejection fraction (60/90) = 66 %
2.
Mild to moderate Systolic dysfunction

1. Early diastolic volume is going to be 50ml. So
you can only pump out 40 ml
à
ejection fraction is decreased to 40/90 = 40% = mild
Heart Failure.
2.
To compensate to maintain CO, there is
an increase in end diastolic volume to 110ml
and there is a slight here is an increase in LV end
diastolic pressure. There is a normal 60 ml stroke
volume ejected to leave you with 50ml LV
volume. This is basically Starling’s law, where
you try to maintain CO by increasing end diastolic
volume.
3.
Severe dysfunction

The contractility is so compromised that early
diastolic volume 70ml so you can only compensate with
a little increase in end diastolic volume. There is
impaired CO because there will be a decrease in
ejection volume= SV
Starling curves

Relates filling of ventricle to contractility.
Normally as in exercise, as you fill the ventricle furtherà
increased contractility
àincreased
CO.
With impaired pump function you may get the same end
diastolic volume but can’t increase contractility to
increase CO. With severely impaired contractility you
can’t even get to the normal CO.
But
these alone do not explain all the mortalities and
exercise limitation in Congestive Heart Failure

Diastolic dysfunction
heart failure it is relaxation problem. In the
pressure -volume curve there normally is an increase
in pressure with increase in volume. But with
increased chamber stiffness- the same volume
increases there is a greater increase pressure.
So at low diastolic volumes you have high
end diastolic pressure in the ventricles. This
high pressure gets transmitted back to the pulmonary
vasculature, leading to congestions and edema.
B. CHRONIC Heart Failure
Acute Heart Failure clinical syndrome is generally a
hemodynamic problem that is isolated and severity is
related to myocardial dysfunction . Whereas,
chronic Heart Failure is LV
dysfunction but also with the following underlying
problems.
Chronic Heart Failure is not only explained by pump
function alone because if it were, then a CO vs
Exercise capacity graph would be linear. However it is
not linear, so there are more reasons to explain the
clinical problems.
Other causes of Chronic Heart Failure
1.
Neurohormonal abnormalities-
The consequences of a decrease in CO are
equally important as myocardial dysfunction in causing
symptoms.
1.
Decrease in CO sensed by kidney by decreased renal
perfusion
àincrease
renin secretion
à
increase Angiotensin II
à
increases release of Aldosterone, Endothelin
and ADH.
2.
These mediators increase water and Na retention (ADH,
Aldosterone) and cause vasoconstriction (Angiotensin
II and endothelin)
à
increase in afterload = wall stress
increase, which aggravates the underlying pump
dysfunction.
3.
Normally if you had a major hemorrhage and
intervascular volume is decreased, these would be
protective mechanism to conserve blood volume.
4.
Endogenous vasodilators and natriuretics exist but not
enough to compensate for these elevated levels (ANF,
NO, PG, dopamine)
2.
Adrenergic dysfunction –
elevated NE levels
3.
Cytokine abnormalities
a.
TNFα
is elevated and mediates apoptosisà
myocyte dysfunction but no current useful drug
treatments available.
b.
IL-6
c.
IFN-g
4.
Impaired electrical
function
Treatments
-
1. ACE inhibitor (Enalipril) improves
survival of Heart Failure seen in hundreds of
trials.
-
But clinical trials show that there is still high
mortality with use of ACE inhibitors.
à
Other drugs also needed at the same time a super
complex diagram of Heart Failure came about.
-
Aldosterone inhibitor
- added benefit in survival if used with ACE
inhibitors.
-
ADH inhibitors
now being looked at
-
*** Beta blockers --
MOST important development of therapy are now
used to greatly improves survival b/c elevation
of NEpi levels in Congestive Heart Failure
correlates with mortality