Cardiac failure

• A state in which the heart cannot provide

sufficient cardiac output to satisfy the
metabolic needs of the body

• It is commonly termed congestive heart failure

(CHF) since symptoms of increase venous
pressure are often prominent
 Cardiac Failure
• The cause is usually:
1) Decreased contractility of the
myocardium resulting from diminished
coronary blood flow.
2) Failure can also be caused by damaged
heart valves
3) External pressure around the heart
4) Vitamin B deficiency
5) Primary cardiac muscle disease
6) Any other abnormality that makes the
heart a hypoeffective pump.
Circulatory Dynamics in Cardiac Failure

• Acute Effects of Moderate Cardiac Failure

•If a heart suddenly becomes severely damaged, such as

by myocardial infarction, the pumping ability of the
heart is immediately depressed.

•Two effects occur

a. Reduced cardiac output

b. Damming of blood in the veins, resulting in

increased venous pressure
 Circulatory Dynamics in Cardiac Failure

•Compensation for Acute Cardiac

Failure by Sympathetic Nervous
Reflexes

a. Baroreceptor reflex
b. Chemoreceptor reflex
c. CNS ischemic response
d. And other reflex mechanism
Parasympathetic nervous reflexes
are inhibited.

Fig. 22.1
•Chronic Stage of Failure-Fluid Retention and
Compensated Cardiac output
a. Retention of fluid by the kidneys-normal urine
output does not occur until the CO and arterial
pressure are back to normal. A low cardiac
output has a profound effect on renal function,
sometimes causing anuria when the cardiac
output falls to 50 to 60 percent of normal. urine
output does not return to normal after an acute
heart attack until the cardiac output and arterial
pressure rise to normal levels.
 Moderate Fluid Retention Can Be
Beneficial
Increased blood volume increases venous return in two
ways:
a. Increases the mean systemic filling pressure
which increases the pressure gradient for
causing venous flow toward the heart.
b. Distends the veins which reduces the venous
resistance and allows even more ease of flow
of blood to the heart.
If the heart is not too greatly damaged, this
increased venous return can often fully
compensate for the heart's diminished pumping
ability.
Detrimental Effects of Excess Fluid Retention
a. Increases the workload on the damaged heart

b. Overstretching of the heart causing further damage

c. Filtration of fluid into the lungs, causing edema and

deoxygenating of the blood

d. Development of extensive edema in other parts of

the body
 Recovery of the Myocardium after Myocardial
Infarction

a. New collateral blood supply penetrates the periphery of

the infarcted area

b. Undamaged musculature hypertrophies

c. Degree of recovery depends on the amount of damage.

After acute myocardial infarction, the heart recovers
rapidly during the first few days and weeks and achieves
most of its recovery within 5 to 7 weeks, although mild
degrees of additional recovery can continue for months.
Cardiac Output Curve After Partial Recovery
 Circulatory Dynamics in Cardiac Failure
• Decompensated Heart Failure

a. If severely damaged, no amount of compensation can

make the heart pump a normal output, the kidneys
will not excrete normal quantities of fluid, fluid
retains, develops edema, eventually leads to death.

Fig. 22.2
• Clinically, one detects this serious
condition of decompensating principally
by the progressing edema, especially
edema of the lungs, which leads to
bubbling rales (a crackling sound) in the
lungs and to dyspnea (air hunger). Lack
of appropriate therapy when this state
of events occurs rapidly leads to death.
 Circulatory Dynamics in Cardiac Failure

• Treatment of Decompensation

a. Strengthening the heart by cardiotonic drugs, such as

digitalis, so that the heart becomes strong enough to
pump adequate quantities of blood required to make
the kidneys function normally again.

b. Administering diuretic drugs to increase kidney

excretion
 Unilateral Left Heart Failure
•When the left side of the heart fails without failure of the
right side, Blood continues to be pumped by the right side
with usual vigor, so it is not pumped adequately out of the
lungs by the left heart into the systemic circulation, the
mean pulmonary filling pressure rises.
•Volume of blood in the lung increases, the pulmonary
capillary pressure increases, and if this rises above or equal
to the colloid osmotic pressure of the plasma, about 28 mm
Hg, fluid begins to filter out of the capillaries into the lung
interstitial spaces and alveoli, resulting in pulmonary edema.
•Left heart failure results in:
a. Pulmonary vascular congestion
b. Pulmonary edema
 Low-Output Cardiac Failure—
Cardiogenic Shock
• Circle of Cardiac Deterioration Leading to Shock
and Death

• Treatment

a. Surgically removing the clot in the coronary artery

b. Catheterizing the blocked coronary and infusion

with chemicals to dissolve the clot
 Edema in Patients with Cardiac Failure
• Inability of Acute Cardiac Failure to Cause Peripheral
Edema
•However, either left or right heart failure is very slow to cause
peripheral edema. When a previously healthy heart acutely
fails as a pump, the aortic pressure falls and the right atrial
pressure rises.
Long-Term Fluid Retention by the Kidneys-the Cause of
Peripheral Edema in Persisting Heart Failure

a. Decreased glomerular filtration rate

b. Activation of the renin-angiotensin system and increased
reabsorption of water and salt by the renal tubules
c. Increased aldosterone secretion
d. Activation of the sympathetic nervous system

a. Role of ANP to Delay Onset of Cardiac Decompensation

Atrial natriuretic peptide (ANP) is a hormone released by the atrial
walls of the heart when they become stretched, direct
effect on kidneys to increase excretion of salt and
water
 Acute Pulmonary Edema in Late-Stage Heart
Failure-Another Lethal Vicious Cycle

• Without new cardiac damage, it usually

is set off by some temporary overload of
the heart, such as might result from a
bout of heavy exercise, some emotional
experience, or even a severe cold. The
acute pulmonary edema is believed to
result from the following vicious cycle:
1. Because of limited pumping capacity of the left
heart, blood begins to dam up in the lungs
2. Elevates the pulmonary capillary pressure, and
a small amount of fluid begins to transude into
the lung tissues and alveoli.
3. diminishes the degree of oxygenation of the
blood
4. weakens the heart and also weakens the
arterioles everywhere in the body, thus
causing peripheral vasodilation.
5. increases venous return of blood from the
peripheral circulation still more
6. further increases the damming of the blood in
the lungs, leading to still more transudation of
fluid, more arterial oxygen desaturation, more
venous return, and so forth. Thus, a vicious
circle has been established.
 Cardiac Reserve

• Maximum percentage that the CO can increase

above normal

Fig. 22.4 Cardiac reserve in different conditions, showing less than zero reserve for two of the conditions
Splanchnic circulation
Cerebral circulation
Circle of willis