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QOD Test 2 Patho Questions And Verified Solutions

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QOD Test 2 Patho Questions And Verified Solutions...

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  • October 24, 2024
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QOD Test 2 Patho Questions And Verified Solutions


How does hypertension affect afterload? What would be the consequences for the
heart? Why might someone with long-standing hypertension develop heart failure? -
ANSWER Afterload is the resistance the heart must overcome eject blood from a given
chamber. Hypertension increases afterload because the heart must generate more
force to overcome the increase in blood pressure. This could create afterload for the left
ventricle (if it is systemic hypertension) or the right ventricle (if it is pulmonary
hypertension). Another example of a process that could increase afterload would be
valve stenosis. For example, in aortic stenosis, the heart must generate more pressure
to push blood through the narrowed heart valve.

If the heart has to continually work against high blood pressure, the heart will
hypertrophy to compensate, just like any other muscle that has to work against
increased resistance. Unfortunately, this hypertrophy is pathologic and contributes to
ventricular wall stiffness and decreased chamber size. Both of these factors can
contribute to diastolic dysfunction and heart failure.

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A patient has been diagnosed with left sided heart failure and an ejection fraction of
33%. What is the significance of this EF? How would this patient's left ventricular
end-systolic volume (ESV) compare to someone with a healthy heart? Would the ESV be
increased or decreased? Explain your answer.

Start a New Thread - ANSWER Ejection fraction tells us what percentage of the EDV is
pumped out of the heart with each beat. Thus, ejection fraction is very much related to
cardiac output. A normal EF is somewhere between 55%-70%. So a person with a normal
EF who starts with an EDV of 100 mL will pump out between 55 and 70 mL of blood
during systole. A person with an EF of 33% has systolic dysfunction. If they start with
100 mL of blood, then they only pump out 33 mL of blood during systole, which results in
a subsequent drop in cardiac output.

ESV would then be increased because more blood would be remaining in the ventricle at
the end of systole. When the heart relaxes during diastole, the heart continues to fill as
normal, and the blood returning during diastole is added to the excess blood already in
the ventricle. This will lead to increased ventricular pressures, which cause excessive
stretch of the ventricle. The increased stretch of the myocardium will lead the atria and
ventricles to release ANP and BNP respectively, which increase sodium (and therefore
water) excretion in the kidneys.

, What is a valve stenosis and valve regurgitation (incompetence)? How could these valve
disorders lead to heart failure? - ANSWER Valve stenosis is a thickened, stiff, scarred,
or malformed valve that does not open fully. Regurgitation is an "incompetent" valve
that does not close fully (it can't make an effective seal when it is closed). Both of these
disrupt the normal one-way route of blood flow through the heart, leading to congestion
in the chambers and structures before the valve.

The last sentence is very important! For example, mitral stenosis or regurgitation will
lead to congestion in the left atria. This causes left atrial hypertrophy and an increase in
the left atrial ESV. The left ventricle, however, will have a decreased ESV. Why does the
left ventricle have a reduced ESV? Here is why:

1. With mitral stenosis, less blood makes it into the left ventricle during filling, which
decreases end diastolic volume. If you start with less blood at the beginning of systole,
you will have less at the end of systole as well.

2. Mitral regurgitation reduces left ventricular afterload. How? Because you essentially
now have two "doors" out of which blood can escape during systole (both the aortic
valve and the mitral valve are now allowing blood out during systole). Since blood is
escaping out of both valves, more blood is pumped out during systole, leading to a lower
left ventricular ESV.

Heart failure will eventually happen in valve stenosis/regurgitation because of blood
back up. For example:

Aortic stenosis --> blood backs up in to left ventricle--> ventricle dilates and
hypertrophies to compensate --> compensatory mechanisms eventually are inadequate
(remodeling of heart becomes pathologic) --> blood backs up into left atria --> blood
backs up into lungs, potentially leading to pulmonary edema and to signs of inadequate
organ perfusion (dizziness, possible fainting, chest pain, low urine output, diminished
pulses, etc.)



How could a pulmonary embolism lead to right-sided heart failure? - ANSWER The right
ventricle pumps deoxygenated blood through the pulmonary semilunar valve into the
pulmonary artery and into the lungs. A pulmonary embolism is a blockage in one of the
pulmonary arteries of the lungs. That blockage can thus cause blood to back up into the
right ventricle. The right ventricle then has to pump harder to overcome the increased
afterload in pulmonary circulation. However, if the PE is large enough, the pressure may
become too great for the RV to overcome, and it can lead to sudden, acute right
ventricular failure. It can be a rapidly developing situation that requires emergency care
to prevent cardiac arrest and respiratory failure.



How could myocardial infarction lead to low blood pressure and shock? What signs and
symptoms might you see and why would they be present? - ANSWER Myocardial

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