CONGESTIVE HEART

FAILURE

Congestive Heart Failure

Inadequate pump function of the heart,
which leads to congestion resulting from
fluid in the lungs and peripheral tissues,
is a common end result of many cardiac
disease processes.

Left Ventricular Failure

CLINICAL PRESENTATION
Breathlessness (Dyspnea) : Orthopnea,
Paroxysmal nocturna dyspnea
Hemoptysis
Chest pain
Fatique
Nocturia
Confusion

Breathlessness (Dyspnea) : Orthopnea,

Paroxysmal nocturna dyspnea
Rise in pulmonary capillary pressures as a
consequence of elevated left ventricular
and atrial pressures
Causes fluid to move into the interstitial
spaces of the lung (pulmonary edema)
edema

Etiology
Inappropriate workloads placed on heart,
such as volume overload or pressure
overload
Restricted filling of the heart
Myocyte loss
Decreased myocyte contractility

Hemodynamic Changes
Systolic Dysfunction
Isovolumic systolic
pressure curve of
the pressurevolume
relationship is
shifted downward
This reduces stroke volume reduces
cardiac output

To maintain cardiac
output, heart respond
with three compensatory
mechanisms: First,
increased return of
blood to the heart
(preload) can lead to
increased contraction of
sarcomeres (FrankStarling relationship).
In the pressure-volume relationship, the heart
operates at a' instead of a, and stroke volume
increases,

Second, increased
release of
catecholamines can
increase cardiac
output by both
increasing the heart
rate and shifting the
systolic
isovolumetric curve
to the left

Finally, cardiac muscle can

hypertrophy and
ventricular volume can
increase, which shifts the
diastolic curve to the right.

Although each of these compensatory

mechanisms can temporarily maintain cardiac
output, each is limited in its ability to do so, and
if the underlying reason for systolic dysfunction
remains untreated, the heart ultimately fails.

Diastolic Dysfunction
In diastolic dysfunction, the
position of the systolic
isovolumic curve remains
unchanged (contractility of
the myocytes is preserved).
The diastolic pressure-volume
curve is shifted to the left,
with an accompanying
increase in left ventricular
end-diastolic pressure and
symptoms of congestive
heart failure

NEUROHUMORAL CHANGES
Initially, increased activity of the adrenergic
system and the renin-angiotensin system
provides a compensatory response that
maintains perfusion of vital organs.
Over time these changes can lead to
progressive deterioration of cardiac function.
Increased sympathetic activity occurs early in
the development of heart failure.

 Elevated plasma norepinephrine levels cause

increased cardiac contractility and an increased
heart rate that initially help maintain cardiac
output.
Continued increases lead to increased preload
(as a result of venous vasoconstriction) and
afterload (from arterial vasoconstriction), which
can worsen heart failure.

 Reduced renal blood pressure stimulates

the release of renin and increases the
production of angiotensin II.
II
Both angiotensin II and sympathetic
activation cause efferent glomerular
arteriolar vasoconstriction, which helps
maintain the glomerular filtration rate
despite a reduced cardiac output.
Angiotensin II stimulates aldosterone
synthesis, which leads to sodium
resorption and potassium excretion by the
kidneys.

 A vicious circle is initiated as continued

hyperactivity of the renin-angiotensin
system leads to severe vasoconstriction,
increased afterload, and further reduction
in cardiac output and glomerular filtration
rate.

 Heart failure is associated with the release

of cytokines and other circulating peptides.
The interleukins (ILs) and tumor
necrosis factor- (TNF- ) are the two
major groups of cytokines that may have
an important pathophysiologic role in heart
failure.
TNF- appears to have an important role in
the cycle of myocyte hypertrophy and cell
death (apoptosis)
IL-1 may accelerate myocyte hypertrophy.

CELLULAR CHANGES
delivery of Ca2+ to the contractile apparatus
and reuptake of Ca2+ by the sarcoplasmic
reticulum are slowed.
levels of 1 adrenergic receptors are
slightly increased myocardial hypertrophy
significant -adrenergic receptor
desensitization as a result of chronic
sympathetic activation.

Right Ventricular Failure

Patophysiology
Patients with isolated right ventricular failure
(pulmonary hypertension, cor pulmonale) can
have a mechanical reason for left ventricular
failure
When right ventricular pressure increases
relative to the left, the interventricular septum
can bow to the left and prevent efficient filling of
the left ventricle, which may lead to pulmonary
congestion.