EXAM 3 NURS 5315 UTA CARDIAC AND
PULMONARY PREPARATION GUIDE WITH
TESTED QUESTIONS AND ANSWERS
◉ 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
PULMONARY PREPARATION GUIDE WITH
TESTED QUESTIONS AND ANSWERS
◉ 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
