PHYSIOLOGY ORAL REVALIDA CVS

Cardiac Failure Case 10

OUTLINE
I. Background of the case The symptoms are classified under which side of the heart has the
II. Physiology dysfunction
III. Alignment: Left

BACKGROUND OF THE CASE

HEART FAILURE
→ Condition in which the heart can't pump enough blood to
meet the body's needs.
→ In some cases, the heart can't fill with enough blood. In
other cases, the heart can't pump blood to the rest of the
body with enough force.

SOME CASES OF HEART FAILURE INCLUDE

CORONARY HEART DISEASE

→ Plaque narrows the arteries and reduces blood flow to your
heart muscle.
• The buildup of plaque also makes it more likely that
blood clots will form in your arteries.
→ Blood clots can partially or completely block blood flow.
Coronary heart disease can lead to chest pain or
discomfort called angina, a heart attack, and heart
damage.

DIABETES
→ In diabetes, the body doesn’t make enough insulin or
doesn’t use its insulin properly.
→ Over time, high blood sugar levels can damage and
weaken the heart muscle and the blood vessels around the
heart, leading to heart failure.
HIGH BLOOD PRESSURE
→ Blood pressure is the force of blood pushing against the
walls of the arteries.
• If this pressure rises and stays high over time, it can
weaken your heart and lead to plaque buildup.
ISCHEMIA
→ It deprives the heart cells of oxygen and leads to acidosis
from the accumulation of lactic acid.
• This leads to cellular death and eventually necrosis of
the heart muscle thus reducing the ability of that
muscle to contract and expand whenever filled with
blood.
CARDIOMYOPATHY
→ It is a disease of the myocardium which can be classified
into three:
1. Dilated
2. Hypertrophic, and
3. Restrictive
→ This disease contributes to the inability of the heart to
distend and contract properly.
PHYSIOLOGY
ANATOMY
RIGHT SIDE OF THE HEART
→ Made up of the right atrium and the right ventricle
→ Distributes venous blood to the lungs through the
pulmonary artery for oxygenation
→ Right atrium receives blood returning from the superior
vena cava, inferior vena cava and coronary sinus.
LEFT SIDE OF THE HEART
→ Composed of the left atrium and left ventricle
→ Distributes oxygenated blood to the body via the aorta.
→ The left ventricle and two and a half times more muscular
than the right ventricle.
CARDIAC CYCLE
→ Refers to the events of one complete heart beat, during
which both atria and ventricles contract and then relax.
→ pumping action of the heart is accomplished by the rhythmic
relaxation and contraction of the muscular walls of its
chambers.
LENGTH
→ The average heart beats approximately 75 times per
minute, so the length of the cardiac cycle is normally
about 0.8 second.

VALVULAR HEART DISEASE

→ The valves ensure that blood flows into one direction.
1. Mid-to-late diástole
→ With valvular disease, blood has increased difficulty
moving forward, increasing pressure to the heart and The cycle starts with the heart in complete relaxation; the
increasing cardiac workload. pressure in the heart is low, and blood is flowing passively into
and through the atria into the ventricles from the pulmonary and
systemic circulations; the semilunar valves are closed, and the
CLINICAL MANIFESTATION
1B 2021 Garcia, Gironella, Go Lopez Aldana 1 of 4


AV valves are open; then the atria contract and force the blood
remaining in their chambers into the ventricles.
2. Ventricular systole.
Shortly after, the ventricular contraction begins, and the
pressure within the ventricles increases rapidly, closing the AV
valves; when the intraventricular pressure is higher than the
pressure in the large arteries leaving the heart, the semilunar
valves are forced open, and blood rushes through them out of
the ventricles; the atria are relaxed, and their chambers are
again filling with blood.
3. Early diastole
At the end of systole, the ventricles relax, the semilunar
valves snap shut, and for a moment the ventricles are
completely closed chambers; the intraventricular pressure drops
and the AV valves are forced open; the ventricles again begin
refilling rapidly with blood, completing the cycle.
FIRST HEART SOUND
→ “lub”
→ is caused by the closing of the AV valves.
SECOND HEART SOUND
→ “dub”
→ occurs when the semilunar valves close at the end of
systole.
DIASTOLIC DYSFUNCTION
→ Refers to the diastolic properties of the ventricle and occurs
when the ventricle becomes less compliant (i.e., "stiffer"),
that impairs ventricular filling.
→ Reduced filling of the ventricle results in less ejection of
blood. Diastolic dysfunction will result to higher ventricular
end-diastolic pressure, which serves as a compensatory
mechanism by utilizing the Frank-Starling mechanism to
augment stroke volume. In some types of heart failure
(e.g., dilated cardiomyopathy), the ventricle dilates
anatomically, which helps to normalize the preload
pressures by accommodating the increase in filled volume.
PATHOPHYSIOLOGY
→ In heart failure, a decreased stroke volume results in reduced
chamber emptying, with higher than normal diastolic volume
• This induces a greater stroke volume for the subsequent
contraction to help empty the ventricle and preserve
forward cardiac output
→ Resultant increase in blood volume helps to maintain cardiac
output; however, the increased volume can be deleterious
because it raises venous pressures, which can lead to
pulmonary and systemic edema. When edema occurs in the
lungs, this can result in exertional dyspnea (shortness of
breath during exertion).
→ Neurohumoral responses occur during heart failure. These
include activation of sympathetic nerves and the renin-
angiotensin system, and increased release of antidiuretic
hormone(vasopressin) and atrial natriuretic peptide. The net
effect of these neurohumoral responses is to produce arterial
CASE 10 Cardiac Failure
vasoconstriction (to help maintain arterial pressure), venous
constriction (to increase venous pressure), and
increased blood volumeto increase ventricular filling. In
general, these neurohumoral responses can be viewed as
compensatory mechanisms, but they can also aggravate heart
failure by increasing ventricular afterload (which depresses
stroke volume) and increasing preload to the point where
pulmonary or systemic congestion and edema occur.
CLINCAL MANIFESTATIONS BASED ON THE CASE:
v Shortness of breath/ Rapid respirations (20/min)
→ Excess fluid in the lung interstitium thus making the
lungs unable to expand fully, which means less air
will enter the lungs
→ Also fluid in the alveoli of the lung bases interferes
with gas exchange, especially the diffusion of oxygen
from alveoli to pulmonary capillaries.
v Severe fatigue and weakness
→ Since the heart is unable to pump enough blood to
the systemic circulation less oxygen and nutrients will
be distributed to the tissues. Another reason is there
is also a decrease ability of the lungs to oxygenate
the blood due to accumulation of fluid in the lungs.
v Abdominal distention
→ Since the pressure in the heart increases, it will be
difficult for the venous blood to return to the right
atrium because supposedly the pressure in the right
atrium is 0mmHg for the blood to easily be received
from the systemic circulation.
→ Blood will now build to the vessels, an increase in
capillary hydrostatic pressure promotes filtration and
thus leads to third space fluid shift.
→ Fluid now shifts from the capillaries to the peritoneum
and now leads to fluid accumulation known as
ascites.
v Angina pectoris
→ Chest pain due to cardiac disease. The heart muscle
doesn’t get blood as much as it needs.
v Cyanosis
→ Due to lack of blood being pumped to the circulatory
system, there will be low levels of oxygen in the blood
causing the skin look blue.
v Distention of the neck veins
→ The blood cannot enter the right atrium efficiently
because of increased pressure in the heart.
→ Since the pressure in the heart increases, it will be
difficult for the venous blood to return to the right
atrium because supposedly the pressure in the right
atrium is 0mmHg for the blood to easily be received
from the systemic circulation.
→ Fluid accumulates in the systemic circulation causing
the distention.
v Rales (crackling sounds) at the lung bases bilaterally
2 of 4


→ Oxygenated blood on the left side of the heart
regurgigates back to the pulmonary circulation due to
the increased pressure on the left side of the heart.
Accumulation of fluid in the lungs will make a
crackling sound as it is filled with air. It is heard best
at the base because fluid is heavier the air thus it will
stay at the base more likely rather than the apices .
v Tachycardia (110 beats/ min)
→ Since the body does not receive enough
oxygenated blood which is needed for normal
functioning, the body will do actions to
compensate the hypoxia and now stimulate the
symphathetic nervous system and one of the
effects is tachycardia.
POSSIBLE TREATMENTS
Specific objectives of medical management include the following:
1. Eliminate and reduce any etiologic contributory factors
such as uncontrolled hypertension and atrial fibrillation
2. Optimize pharmacologic and other therapeutic regimens
3. Reduce the workload on the heart by reducing the
preload and afterload
4. Promote a lifestyle conducive to cardiac health
Prevent episodes of acute decompensated heart failure.
PHARMACOLOGICAL THERAPY

v Diastolic gallop rhythm

→ also called S3, etected on auscultation. It is ANGIOTENSIN-CONVERTING ENZYME INHIBITORS
caused by a large volume of fluid entering the
ventricle at the beginning of the diastole. → Promotes vasodilation and dieresis by decreasing
preload and afterload. It prevents the secretion of
aldosterone thus prevents the reabsorption of water and
v Enlarged liver
sodium and promotes dieresis thus decreasing the blood
→ Severe heart failure causes blood to back up from volume and decreasing the workload of the heart.
the heart into the inferior vena cava. Such
congestion increases pressure in the inferior vena ANGIOTENSIN II RECEPTOR BLOCKER
cava and other veins that carry blood to it,
including the hepatic veins (which drain blood → It blocks the effects of Angiotensin II to its receptors. It
from the liver). can be prescribed as an alternative sa ACE inhibitors.
→ If this pressure is high enough, the liver becomes
engorged (congested) with blood and BETA-BLOCKERS
malfunctions; also an indication of how severe the
heart failure the patient is experiencing. → Such as Carvedilol have been found to reduce mortality
and morbidity in patients with HF by reducing the
v Edema at the ankles and over the lower tibias adverse effects from constant stimulation of the
→ The ankles edema is caused by the increased symphathetic nervous system.
hydrostatic pressure in the capillaries and venules
in the ankles. The large blood volume and high DIURETICS
venous pressure cause the hydrostatic pressure
to exceed the oncotic pressure, particularly in the → They are pressscribed to reeemove excess extracellular
dependent parts of the body. fluid by increaaasing the rate of urine produced in
patients with sign and symptoms of fluid overload.
v Chest x-ray
→ enlarged heart and diffuse density (fluid in the
lungs)- [Enlarged heart] Because of prolonged
inadequate blood supply, the myocardial fibers
REFFERENCES
contract less effectively. In addition, an increase
in blood volume caused by salt and water
retention by the kidneys, in response to a low
http://www.cvphysiology.com/Heart%20Failure/HF003
→ cardiac output, contributes to the dilation of the
heart. Since there is an increase workload of the
https://www.msdmanuals.com/home/liver-and-gallbladder-
heart, the cardiac muscles will exert more force to
disorders/blood-vessel-disorders-of-the-liver/congestive-
pump the blood, this increase in the load will lead
hepatomegaly
to hypertrophy of the cardiac muscle.
http://www.pathophys.org/heartfailure
v Normal sinus rhythm, q waves and left axis
deviation.
→ Due to left ventricular hypertrophy there is a left
axis deviation.

CASE 10 Cardiac Failure 3 of 4



CASE 10 Cardiac Failure 4 of 4