1
Bio
BIO 669 QUIZ 4 QUESTIONS & VERIFIED
ANSWERS| GRADE A| 100% CORRECT
(NEW 2024/ 2025 UPDATE)
myocardial ischemia - ANS ✓local, temporary deprivation of coronary blood
supply
-need O2 >50% to not decrease function of heart
3 types of myocardial ischemia - ANS ✓stable angina-specific amount of
exercise ppl can do before noticing chest pain, chronic, know how far they can go
before symptoms start. tx w/NTG to vasodilate
-prizmetal angina-occurs unpredictably & at rest, while sleeping. transient
ischemia that doesn't follow any pattern
-silent iscemia-have ischemia w/out the detectable symptoms like angina
acute coronary syndromes - ANS ✓include unstable & stable angina, transient
ischemia, sustained ischemia, MI, myocardial inflammation & necrosis
unstable angina - ANS ✓results from reversible myocardial ischemia
-presents as new onset angina, angina occurring at rest, or angina that increases
in severity or frequency
-is a sign of impending MI or rupture so will need treated
sustained ischemia - ANS ✓can lead to changes in myocardium
-stunning the myocytes=ischemia leading to damage of myocardium & makes
cells hypocontractible, lasting hours-days (temporary)
-hibernating myocardium=myocytes adapt & stop working to prolong their
survival, reversible
-myocardial remodeling=mediated by RAAS that leads to myocyte hypertrophy &
permanent loss of contractile function
MI - ANS ✓stemi & nonstemi
-nonstemi=affects only the area under endocardium & not thru entire myocardial
wall (subendocardail MI) will see ST depression & T wave inversion w/out Q
waves
Bio 669
, 2
Bio
-stemi=affects entire myocardial wall (transmural MI) will see ST elevation,
sudden & extended obstruction of myocardial blood supply, leads to death of
cells
S&S of MI - ANS ✓sudden severe chest pain that may radiate, n/v, diaphoresis,
dyspnea,
complications=cardiac arrest due to ischemia, L ventricular dysfunction, &
electrical instability
acute pericarditis - ANS ✓acute inflammation of pericardium
-occurs w/anything that increases friction like an increase in proteins,
transudate, or anything that causes inflammation of pericardial fluid
-leads to friction rubs
pericardial effusions - ANS ✓accumulation of fluid in the pericardial cavity
-if it occurs slowly over time the pericardium can stretch & accommodate w/out
compressing the heart
-if it occurs rapidly it causes compression of heart known as cardiac tamponade-
which leads to decreased blood flow & can stop it completely
constrictive pericarditis - ANS ✓addition of connective tissue that leads to
compression of the heart & decreased cardiac output
-seen w/TB patients
-as you increase metabolic demands the heart can't increase to meet those needs
because its restricted
-develops gradually
hypertropic cardiomyopathy - ANS ✓can be hypertropic
obstructive/asymmetrical septal cardiomyopathy OR hypertensive/valvular
cardiomyopathy
-both increase afterload, decrease EF, & cardiac output
hypertropic obstructive cardiomyopathy - ANS ✓thickening of septal wall
which causes outflow obstruction of LV tract
hypertensive/valvular hypertropic cardiomyopathy - ANS ✓occurs b/c of
increased resistance to ventricular ejection, myocytes hypertrophy trying to
compensate for increased workload
restrictive cardiomyopathy - ANS ✓normal systolic BP but increased diastolic
BP & normal wall thickness
Bio 669
Bio
BIO 669 QUIZ 4 QUESTIONS & VERIFIED
ANSWERS| GRADE A| 100% CORRECT
(NEW 2024/ 2025 UPDATE)
myocardial ischemia - ANS ✓local, temporary deprivation of coronary blood
supply
-need O2 >50% to not decrease function of heart
3 types of myocardial ischemia - ANS ✓stable angina-specific amount of
exercise ppl can do before noticing chest pain, chronic, know how far they can go
before symptoms start. tx w/NTG to vasodilate
-prizmetal angina-occurs unpredictably & at rest, while sleeping. transient
ischemia that doesn't follow any pattern
-silent iscemia-have ischemia w/out the detectable symptoms like angina
acute coronary syndromes - ANS ✓include unstable & stable angina, transient
ischemia, sustained ischemia, MI, myocardial inflammation & necrosis
unstable angina - ANS ✓results from reversible myocardial ischemia
-presents as new onset angina, angina occurring at rest, or angina that increases
in severity or frequency
-is a sign of impending MI or rupture so will need treated
sustained ischemia - ANS ✓can lead to changes in myocardium
-stunning the myocytes=ischemia leading to damage of myocardium & makes
cells hypocontractible, lasting hours-days (temporary)
-hibernating myocardium=myocytes adapt & stop working to prolong their
survival, reversible
-myocardial remodeling=mediated by RAAS that leads to myocyte hypertrophy &
permanent loss of contractile function
MI - ANS ✓stemi & nonstemi
-nonstemi=affects only the area under endocardium & not thru entire myocardial
wall (subendocardail MI) will see ST depression & T wave inversion w/out Q
waves
Bio 669
, 2
Bio
-stemi=affects entire myocardial wall (transmural MI) will see ST elevation,
sudden & extended obstruction of myocardial blood supply, leads to death of
cells
S&S of MI - ANS ✓sudden severe chest pain that may radiate, n/v, diaphoresis,
dyspnea,
complications=cardiac arrest due to ischemia, L ventricular dysfunction, &
electrical instability
acute pericarditis - ANS ✓acute inflammation of pericardium
-occurs w/anything that increases friction like an increase in proteins,
transudate, or anything that causes inflammation of pericardial fluid
-leads to friction rubs
pericardial effusions - ANS ✓accumulation of fluid in the pericardial cavity
-if it occurs slowly over time the pericardium can stretch & accommodate w/out
compressing the heart
-if it occurs rapidly it causes compression of heart known as cardiac tamponade-
which leads to decreased blood flow & can stop it completely
constrictive pericarditis - ANS ✓addition of connective tissue that leads to
compression of the heart & decreased cardiac output
-seen w/TB patients
-as you increase metabolic demands the heart can't increase to meet those needs
because its restricted
-develops gradually
hypertropic cardiomyopathy - ANS ✓can be hypertropic
obstructive/asymmetrical septal cardiomyopathy OR hypertensive/valvular
cardiomyopathy
-both increase afterload, decrease EF, & cardiac output
hypertropic obstructive cardiomyopathy - ANS ✓thickening of septal wall
which causes outflow obstruction of LV tract
hypertensive/valvular hypertropic cardiomyopathy - ANS ✓occurs b/c of
increased resistance to ventricular ejection, myocytes hypertrophy trying to
compensate for increased workload
restrictive cardiomyopathy - ANS ✓normal systolic BP but increased diastolic
BP & normal wall thickness
Bio 669
