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Exam (elaborations)

UTA NURS 5315 MOD 6 PULM AND SHOCK FINAL PAPER QUESTIONS AND SOLUTIONS

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UTA NURS 5315 MOD 6 PULM AND SHOCK FINAL PAPER QUESTIONS AND SOLUTIONS

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UTA NURS 5315 MOD 6 PULM AND
SHOCK FINAL PAPER QUESTIONS AND
SOLUTIONS

◉ Mitral Valve Regurgitation
Answer: -Characterized by INCOMPLETE CLOSURE of mitral valve
-Caused by MITRAL VALVE PROLAPSE (flaps don't close together
properly, leaving valve ajar); more common in WOMEN; STICKING
CHEST PAIN
-Blood in left ventricle backs up to left ventricle during systole
(mitral valve should be closed during systole/contraction of
heart)
-Leads to atrial dilation/hypertrophy, increased pulmonary
vascular pressure/volume, PULMONARY EDEMA
-S/sx: Dyspnea, rales, pansystolic murmur, S3 & S4 heart sounds


◉ Aortic Valve Stenosis
Answer: -Most common valvular disease
-Most common causes are aortic valve CALCIFICATION
(stiffening) in people over 60; congenital aortic valve stenosis in
people less than 30
-Normal valve 3 cm; symptoms seen when valve less than 1 cm;
severe when valve is less than 0.5 cm

,-Narrowed valve prevents outflow from left ventricle to aorta.
This backs up blood to the left atrium and ultimately floods the
lung causing PULMONARY EDEMA
S/Sx: Pulmonary hypertension/edema, poor outflow of aorta to
body (aorta sends out oxygenated blood to body), causing fainting
or chest pain
Simplified: Aorta is stiff and can't send out oxygenated blood
properly to the body, depriving tissues of oxygen. Blood gets
backed up into lungs, causing pulmonary edema.


◉ Aortic Valve Regurgitation
Answer: -Valve is TOO WIDE or TOO NARROW, blood doesn't pass
through effectively, causing back flow of blood into the left
ventricle


-Marked by EARLY DIASTOLIC MURMUR (on systole, heart
contracts and pushes blood up the aorta, but on diastole, heart
relaxes and ineffective aortic valve is not able to hold blood up in
aorta, so blood falls and makes a swish sound, which is the
murmur)
-Most commonly caused by AORTIC ROOT DILATION(starting
point of aorta is too wide)
-Other causes: infective endocarditis, rheumatic fever, aortitis
from syphilis, coarctation (congenital narrowing of aorta), aortic
dissection (tear), ankylosing spondylitis (inflammatory arthritis)


-Acute: increases left ventricular end-diastolic pressure (LVEDP)
(increased blood back down in the left ventricle increases

,pressure), decreased stroke volume (not much blood is being
pushed from left ventricle because blood's backed up and
overwhelming left ventricle), normal or decreased pulse pressure,
decreased cardiac output (aorta is not effectively pumping blood
from heart)


Chronic: Body adjusts; LVEDP normalizes, systolic bp increases
(compensation: harder contraction to push blood out of aorta
before it falls back down to left ventricle), diastolic bp decreases
(compensation: decreased relaxation of heart to stop blood from
seeping back out of aorta), cardiac output is normal, pulse
pressure is increase. Blood ultimately is backed up into the left
atrium and pulmonary circulation.


◉ Atherosclerosis Causes
Answer: -Begins with tissue injury
Sources of injury:
CIGARETTES (toxins)
Hypertension (increased force of the blood hitting the blood
vessel can weaken it)
Diabetes
Hyperlipidemia (lipids take place of endothelial cells lining the
blood vessel, initiating an inflammatory response)


◉ Patho of Atherosclerosis r/t Hyperlipidemia - Inflammatory
Response

, Answer: 1. Tissue injury to endothelial cells lining the blood
vessel.
2. Endothelial cells become inflammed and unable to produce
sufficient antithrombotic and vasodilating cytokines, increasing
risk for clot formation and creating a tighter space for plaques and
clots to grow.
3. Macrophages and platelets are called to the area of injury,
further congesting the growing plaque area.
4. LDL replaces endothelial cells in the lining of the blood vessel.
5. Macrophages engulf the LDL particles.
6. Macrophages eat too much LDL, causing them to burst and
become foam cells (under a microscope they look like sea foam)
7. Accumulation of foam cells causes a fatty streak. Fatting streak
further triggers inflammatory responses, repeating the whole
cycle, and growing the fatty streak.
8. Smooth muscle hyperplasia from all the inflammation grows,
produces collagen, and covers the fatty streak to create a fibrous
plaque.
9. The plaque may calcify, protrude into the vessel, and occlude
blood flow, resulting in ischemia or infarction.


◉ Hyperlipidemia
Answer: Leading cause of coronary artery disease


Most commonly affects promximal portions of coronary arteries,
larger branches of carotid arteries, circle of Willis (base of brain),

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