NURS 330 MIDTERM fully
solved & updated 2025-
2026(100% verified for
accuracy)
Stroke Volume - answer the volume of blood pumped out by a
ventricle with each heartbeat (normal is 70mLs) - how much enters
minus how much is leftover = how much leaves.
Affected by AL, PL, contractility
Cardiac Output - answer CO = Heart Rate x Stroke Volume. amount
of blood pumped out each minute (4-8 L/min)
What is preload affected by? - answer venous return, blood volume,
heart rhythm (atrial kick), heart rate
What is afterload affected by? - answer Valves, Vessels (BP, plaque),
Viscosity (hematocrit)
What is contractility affected by? - answer Calcium, ability of
myocytes, Starling's Law.
If we can improve contractility to the sweet spot, we can increase
CO
Ejection Fraction - answer Fraction of diastolic volume pumped with
each beat (normal is about 55-65%)
,S1/lub sound - answer closure of bicuspid and tricuspid valves
s2/dub sound - answer closure of pulmonary and aortic valve
s3 - answer tense chordinae during rapid filling
Blood Pressure - answer BP = CO x SVR
People with HTN have an increased CO, increased SVR or both
Hypertension Treatment - answer Treat HTN if SBP > 160 OR >140
with end organ damage. Goal of treatment is to reduce risk of CVA,
HF, CAD.
Thiazide diuretics is best evidence (Grade A)
Grade B = beta-blockers (if younger than 60), ACE-i (angiotensin
converting enzyme inhibitor), long-acting CCB, ARB (angiotensin-II
receptor blockers)
Heart Failure Meds - answer ACE-i, ARBs, Diuretics, B-1 blocker
Chronotropic effect - answer change in heart rate
Inotropic effect - answer change in the strength or contractility of
the heart
Dromotropic effect - answer change in the speed of conduction
through AV junction
,Baroreceptors - answer detect changes in blood pressure. stimulate
SNS (epinephrine) if low blood pressure and PNS (acetylcholine) if
high blood pressure.
located in internal carotid arteries and aortic arch
Chemoreceptors - answer Detect changes in pH, O2, and CO2 in
blood. stimulate SNS if oxygen is low, pH is low, CO2 is high
located in internal carotid arteries and aortic arch
SNS affects on heart - answer constrict peripheral vessels, increase
HR (chronotropy), increase contraction force (inotropy)
alpha and beta cells - answer alpha cell stimulation causes
vasoconstriction;
beta-1 cell stimulation causes increased HR, increased force,
increased conduction velocity;
beta-2 cells cause bronchodilation
Primary (Ideopathic) HTN - answer chronic elevated BP w/ end organ
damage.
RAAS activation, vascular disease (stiffness), alpha receptor
stimulation (vasoconstriction)
Causes of HF - answer 1/3 of patients get HF from cardiomyopathy
(disease of heart muscle causing weakness)
, 2/3 of patients get HF from coronary artery disease
Diastolic HF - answer *Problem of FILLING
Usually from prolonged high afterload from chronic HTN
LV becomes hypertrophic and cannot fill properly because it is stiff
and smaller size from increased muscle = lower stroke volume
Blood backs up into lungs
Systolic HF (dilated cardiomyopathy) - answer *Problem of ejecting
blood
Usually due to damage to walls of ventricles due to CAD making
them weak
Ventricles lose ability to eject blood so it remains in ventricles after
contraction (decreased ejection fraction)
LV experiences congestion behind pump (lungs) --> fluid in lungs
RV experiences congestion behind pump (body) --> ascites, edema)
Right sided HF - answer usually triggered by left-sided heart failure
--> accumulation of blood in the lungs caused by left-sided heart
failure makes the right ventricle work harder. could also be caused
by CF or PE because this increases pressure in lungs and heart has
to work harder
solved & updated 2025-
2026(100% verified for
accuracy)
Stroke Volume - answer the volume of blood pumped out by a
ventricle with each heartbeat (normal is 70mLs) - how much enters
minus how much is leftover = how much leaves.
Affected by AL, PL, contractility
Cardiac Output - answer CO = Heart Rate x Stroke Volume. amount
of blood pumped out each minute (4-8 L/min)
What is preload affected by? - answer venous return, blood volume,
heart rhythm (atrial kick), heart rate
What is afterload affected by? - answer Valves, Vessels (BP, plaque),
Viscosity (hematocrit)
What is contractility affected by? - answer Calcium, ability of
myocytes, Starling's Law.
If we can improve contractility to the sweet spot, we can increase
CO
Ejection Fraction - answer Fraction of diastolic volume pumped with
each beat (normal is about 55-65%)
,S1/lub sound - answer closure of bicuspid and tricuspid valves
s2/dub sound - answer closure of pulmonary and aortic valve
s3 - answer tense chordinae during rapid filling
Blood Pressure - answer BP = CO x SVR
People with HTN have an increased CO, increased SVR or both
Hypertension Treatment - answer Treat HTN if SBP > 160 OR >140
with end organ damage. Goal of treatment is to reduce risk of CVA,
HF, CAD.
Thiazide diuretics is best evidence (Grade A)
Grade B = beta-blockers (if younger than 60), ACE-i (angiotensin
converting enzyme inhibitor), long-acting CCB, ARB (angiotensin-II
receptor blockers)
Heart Failure Meds - answer ACE-i, ARBs, Diuretics, B-1 blocker
Chronotropic effect - answer change in heart rate
Inotropic effect - answer change in the strength or contractility of
the heart
Dromotropic effect - answer change in the speed of conduction
through AV junction
,Baroreceptors - answer detect changes in blood pressure. stimulate
SNS (epinephrine) if low blood pressure and PNS (acetylcholine) if
high blood pressure.
located in internal carotid arteries and aortic arch
Chemoreceptors - answer Detect changes in pH, O2, and CO2 in
blood. stimulate SNS if oxygen is low, pH is low, CO2 is high
located in internal carotid arteries and aortic arch
SNS affects on heart - answer constrict peripheral vessels, increase
HR (chronotropy), increase contraction force (inotropy)
alpha and beta cells - answer alpha cell stimulation causes
vasoconstriction;
beta-1 cell stimulation causes increased HR, increased force,
increased conduction velocity;
beta-2 cells cause bronchodilation
Primary (Ideopathic) HTN - answer chronic elevated BP w/ end organ
damage.
RAAS activation, vascular disease (stiffness), alpha receptor
stimulation (vasoconstriction)
Causes of HF - answer 1/3 of patients get HF from cardiomyopathy
(disease of heart muscle causing weakness)
, 2/3 of patients get HF from coronary artery disease
Diastolic HF - answer *Problem of FILLING
Usually from prolonged high afterload from chronic HTN
LV becomes hypertrophic and cannot fill properly because it is stiff
and smaller size from increased muscle = lower stroke volume
Blood backs up into lungs
Systolic HF (dilated cardiomyopathy) - answer *Problem of ejecting
blood
Usually due to damage to walls of ventricles due to CAD making
them weak
Ventricles lose ability to eject blood so it remains in ventricles after
contraction (decreased ejection fraction)
LV experiences congestion behind pump (lungs) --> fluid in lungs
RV experiences congestion behind pump (body) --> ascites, edema)
Right sided HF - answer usually triggered by left-sided heart failure
--> accumulation of blood in the lungs caused by left-sided heart
failure makes the right ventricle work harder. could also be caused
by CF or PE because this increases pressure in lungs and heart has
to work harder
