NURS 487 MIDTERM 1 QUESTIONS WITH COMPLETE SOLUTIONS
Nurs 487 Midterm 1
SCORED A+
Study online at https://quizlet.com/_a5dizp
1. Cardiac Output •what's coming out of the heart in one minute (5 L/min)
2. Stroke volume •amount of blood in one beat in ml) (preload, afterload, contractility) x
HR bpm
•Ventricles fill with blood (end diastolic volume), the ventricles don't
eject out all the blood during systole, some amount is always left in the
ventricle after contraction (end systolic volume). The amount ejected is
the stroke volume (EDV - ESV).
3. Preload •EDV or how much fluid is going in, also described as how stretched the
myocytes are when the ventricle is full of blood (think of a balloon full of
air - when its full of air it has a lot of force, when its not full of air, not as
much force)
4. Afterload the resistance the ventricle must overcome to eject blood. If there is a
lot of pressure it takes a lot of force to open valves. This may reduce
the amount of blood ejected. Stenotic (narrowed) valves reduces blood
output = low CO.
5. contractility •how much squeeze the heart has, the more force the more it ejects
•Heart rate is increased if CO is reduced; if heart rate is decreased this
may also decrease CO if the SV doesn't increase
6. Fatty Streak lipids accumulate and migrate into smooth muscle cells
7. fibrous plaque - collagen covers the fatty streak
- vessel lumen is narrowed
- blood flow is reduced
- fissures can develop
8. complicated lesion - plaque rupture
- thrombus formation
-further narrowing or total occlusion of vessel
, Nurs 487 Midterm 1
Study online at https://quizlet.com/_a5dizp
9. collateral circulation circulation by secondary channels after obstruction of the principal chan-
nel supplying the heart (grows new vessels to bypass blockage)
10. Embolus travelling clot that occludes an artery (atrial fibrillation, infective endo-
carditis, PCI)
11. Vasculitis inflammation of blood vessel- Kawasaki disease, aneurysm
12. Vasospasm vessels constricts, reduces blood flow
13. ventricular fibrillation * the rapid, irregular, and useless contractions of the ventricles (quivering)
- need to start CPR
14. angiogram The radiographic visualization of blood vessels after the injection of
radiopaque substance. - shows you blocked vessels
15. Angina •Ischemia from not enough oxygen
•Angina = Chest pain
16. Chronic Stable Angina chest pain that occurs intermittently over a long period with the same
pattern of onset, duration, and intensity of symptoms - occurs when
oxygen demand increases (demand ischemia)
-** goes away at rest
17. What causes pain with anaerobic metabolism creates lactic acid = pain
angina?
18. Ischemia Lack of blood supply
19. unstable angina rupture of thickened plaque, exposing thrombogenic surface •UA: New
onset, occurs at rest (different from stable angina that goes away at rest),
worsening pattern
•Unpredictable and requires immediate attention
•Easily provoked (minimal to no exertion)
, Nurs 487 Midterm 1
Study online at https://quizlet.com/_a5dizp
•Common symptoms in females include fatigue, SOB, indigestion, anxi-
ety
•Remember in UA there is no ST elevation and cardiac enzymes are
normal
(There may be ST depression or T wave inversion which indicates is-
chemia but not infarct)
20. A 65 y/o female pre- myocardial oxygen supply has fallen below the demand
sents with chest pain
with activity and is di-
agnosed with chronic
stable angina. The pain
occurs when
21. Acute Coronary Syn- sudden symptoms of insufficient blood supply to the heart indicating
drome unstable angina or acute myocardial infarction
22. Myocardial Infarction •Interruption of blood supply to the cardiac muscle resulting in sustained
(NSTEMI or STEMI) ischemia and irreversible myocardial cell death
•Location of the infarction correlates with the involved coronary circula-
tion
•The longer the area is deprived of oxygen the greater chance of cell
death
•Causes altered contraction and heart function
•Sub-endocardium is affected first and necrosis will progress through
entire thickness of the heart muscle in 4-6 hrs
23. NSTEMI non-ST elevation myocardial infarction
- partial occlusion to vessel
24. STEMI ST elevation MI, real-time ongoing death of heart tissue due to ischemia
- complete occlusion to heart vessel
- reflected by reduced CO ECG changes and ruse in troponins
Nurs 487 Midterm 1
SCORED A+
Study online at https://quizlet.com/_a5dizp
1. Cardiac Output •what's coming out of the heart in one minute (5 L/min)
2. Stroke volume •amount of blood in one beat in ml) (preload, afterload, contractility) x
HR bpm
•Ventricles fill with blood (end diastolic volume), the ventricles don't
eject out all the blood during systole, some amount is always left in the
ventricle after contraction (end systolic volume). The amount ejected is
the stroke volume (EDV - ESV).
3. Preload •EDV or how much fluid is going in, also described as how stretched the
myocytes are when the ventricle is full of blood (think of a balloon full of
air - when its full of air it has a lot of force, when its not full of air, not as
much force)
4. Afterload the resistance the ventricle must overcome to eject blood. If there is a
lot of pressure it takes a lot of force to open valves. This may reduce
the amount of blood ejected. Stenotic (narrowed) valves reduces blood
output = low CO.
5. contractility •how much squeeze the heart has, the more force the more it ejects
•Heart rate is increased if CO is reduced; if heart rate is decreased this
may also decrease CO if the SV doesn't increase
6. Fatty Streak lipids accumulate and migrate into smooth muscle cells
7. fibrous plaque - collagen covers the fatty streak
- vessel lumen is narrowed
- blood flow is reduced
- fissures can develop
8. complicated lesion - plaque rupture
- thrombus formation
-further narrowing or total occlusion of vessel
, Nurs 487 Midterm 1
Study online at https://quizlet.com/_a5dizp
9. collateral circulation circulation by secondary channels after obstruction of the principal chan-
nel supplying the heart (grows new vessels to bypass blockage)
10. Embolus travelling clot that occludes an artery (atrial fibrillation, infective endo-
carditis, PCI)
11. Vasculitis inflammation of blood vessel- Kawasaki disease, aneurysm
12. Vasospasm vessels constricts, reduces blood flow
13. ventricular fibrillation * the rapid, irregular, and useless contractions of the ventricles (quivering)
- need to start CPR
14. angiogram The radiographic visualization of blood vessels after the injection of
radiopaque substance. - shows you blocked vessels
15. Angina •Ischemia from not enough oxygen
•Angina = Chest pain
16. Chronic Stable Angina chest pain that occurs intermittently over a long period with the same
pattern of onset, duration, and intensity of symptoms - occurs when
oxygen demand increases (demand ischemia)
-** goes away at rest
17. What causes pain with anaerobic metabolism creates lactic acid = pain
angina?
18. Ischemia Lack of blood supply
19. unstable angina rupture of thickened plaque, exposing thrombogenic surface •UA: New
onset, occurs at rest (different from stable angina that goes away at rest),
worsening pattern
•Unpredictable and requires immediate attention
•Easily provoked (minimal to no exertion)
, Nurs 487 Midterm 1
Study online at https://quizlet.com/_a5dizp
•Common symptoms in females include fatigue, SOB, indigestion, anxi-
ety
•Remember in UA there is no ST elevation and cardiac enzymes are
normal
(There may be ST depression or T wave inversion which indicates is-
chemia but not infarct)
20. A 65 y/o female pre- myocardial oxygen supply has fallen below the demand
sents with chest pain
with activity and is di-
agnosed with chronic
stable angina. The pain
occurs when
21. Acute Coronary Syn- sudden symptoms of insufficient blood supply to the heart indicating
drome unstable angina or acute myocardial infarction
22. Myocardial Infarction •Interruption of blood supply to the cardiac muscle resulting in sustained
(NSTEMI or STEMI) ischemia and irreversible myocardial cell death
•Location of the infarction correlates with the involved coronary circula-
tion
•The longer the area is deprived of oxygen the greater chance of cell
death
•Causes altered contraction and heart function
•Sub-endocardium is affected first and necrosis will progress through
entire thickness of the heart muscle in 4-6 hrs
23. NSTEMI non-ST elevation myocardial infarction
- partial occlusion to vessel
24. STEMI ST elevation MI, real-time ongoing death of heart tissue due to ischemia
- complete occlusion to heart vessel
- reflected by reduced CO ECG changes and ruse in troponins
