NURS 330 MIDTERM EXAM – Questions With
Proper Solutions
Save
Terms in this set (180)
the volume of blood pumped out by a ventricle with
each heartbeat (normal is 70mLs) - how much enters
Stroke Volume minus how much is leftover = how much leaves.
Affected by AL, PL, contractility
CO = Heart Rate x Stroke Volume. amount of blood
Cardiac Output
pumped out each minute (4-8 L/min)
What is preload affected venous return, blood volume, heart rhythm (atrial kick),
by? heart rate
What is afterload affected Valves, Vessels (BP, plaque), Viscosity (hematocrit)
by?
Calcium, ability of myocytes, Starling's Law.
What is contractility
affected by? If we can improve contractility to the sweet spot, we
can increase CO
Fraction of diastolic volume pumped with each beat
Ejection Fraction
(normal is about 55-65%)
S1/lub sound closure of bicuspid and tricuspid valves
s2/dub sound closure of pulmonary and aortic valve
s3 tense chordinae during rapid filling
BP = CO x SVR
Blood Pressure
People with HTN have an increased CO, increased SVR
or both
, 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)
Hypertension Treatment
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 ACE-i, ARBs, Diuretics, B-1 blocker
Chronotropic effect change in heart rate
Inotropic effect change in the strength or contractility of the heart
Dromotropic effect change in the speed of conduction through AV junction
detect changes in blood pressure. stimulate SNS
(epinephrine) if low blood pressure and PNS
Baroreceptors (acetylcholine) if high blood pressure.
located in internal carotid arteries and aortic arch
Detect changes in pH, O2, and CO2 in blood. stimulate
SNS if oxygen is low, pH is low, CO2 is high
Chemoreceptors
located in internal carotid arteries and aortic arch
constrict peripheral vessels, increase HR (chronotropy),
SNS affects on heart
increase contraction force (inotropy)
alpha cell stimulation causes vasoconstriction;
beta-1 cell stimulation causes increased HR, increased
alpha and beta cells
force, increased conduction velocity;
beta-2 cells cause bronchodilation
chronic elevated BP w/ end organ damage.
Primary (Ideopathic) HTN
RAAS activation, vascular disease (stiffness), alpha
receptor stimulation (vasoconstriction)
1/3 of patients get HF from cardiomyopathy (disease of
heart muscle causing weakness)
Causes of HF
2/3 of patients get HF from coronary artery disease
, *Problem of FILLING
Usually from prolonged high afterload from chronic
HTN
Diastolic HF
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
*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
Systolic HF (dilated ventricles after contraction (decreased ejection
cardiomyopathy) fraction)
LV experiences congestion behind pump (lungs) -->
fluid in lungs
RV experiences congestion behind pump (body) -->
ascites, edema)
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
Right sided HF
can stress the right side of the heart and cause it to fail
causing backup of blood into the right atrium and
peripheral veins
Jugular venous distention
Ascites
Peripheral edema
, Left-sided HF (most common) from left ventricular
dysfunction preventing body from getting enough
oxygen rich blood
Left sided HF Excess blood accumulates in LV (volume overload) -->
backup of blood into the left atrium and pulmonary
veins
causing pulmonary congestion (SOB, cough), edema
reduce volume using diuretics
* look out for hypokalemia, hypovolemia
How to reduce preload in block aldosterone to prevent water/sodium retention
HF using ACE-i or ARBs
*look out for hypotension, renal dysfunction with ACE-i
*look out for hyperkalemia, muscle cramps,
rhabdomyolysis with ARBs
prevent angiotensin II vasoconstriction using ACE-i or
ARBs
How to reduce afterload in
HF *look out for hypotension, renal dysfunction with ACE-i
*look out for hyperkalemia, muscle cramps,
rhabdomyolysis with ARBs
Beta-blockers
How to slow SNS in HF
*look out for bradycardia, hypotension
Decreased blood flow in coronary arteries supplying
the heart
Main cause is coronary atherosclerosis which is an
Acute Coronary Syndrome
accumulation of lipid and fibrous tissue in the vessel
(ACS/Heart Attack/MI)
wall creating blockages or narrowing of the vessel that
reduces blood flow to myocardium
(thrombus can form)
Proper Solutions
Save
Terms in this set (180)
the volume of blood pumped out by a ventricle with
each heartbeat (normal is 70mLs) - how much enters
Stroke Volume minus how much is leftover = how much leaves.
Affected by AL, PL, contractility
CO = Heart Rate x Stroke Volume. amount of blood
Cardiac Output
pumped out each minute (4-8 L/min)
What is preload affected venous return, blood volume, heart rhythm (atrial kick),
by? heart rate
What is afterload affected Valves, Vessels (BP, plaque), Viscosity (hematocrit)
by?
Calcium, ability of myocytes, Starling's Law.
What is contractility
affected by? If we can improve contractility to the sweet spot, we
can increase CO
Fraction of diastolic volume pumped with each beat
Ejection Fraction
(normal is about 55-65%)
S1/lub sound closure of bicuspid and tricuspid valves
s2/dub sound closure of pulmonary and aortic valve
s3 tense chordinae during rapid filling
BP = CO x SVR
Blood Pressure
People with HTN have an increased CO, increased SVR
or both
, 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)
Hypertension Treatment
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 ACE-i, ARBs, Diuretics, B-1 blocker
Chronotropic effect change in heart rate
Inotropic effect change in the strength or contractility of the heart
Dromotropic effect change in the speed of conduction through AV junction
detect changes in blood pressure. stimulate SNS
(epinephrine) if low blood pressure and PNS
Baroreceptors (acetylcholine) if high blood pressure.
located in internal carotid arteries and aortic arch
Detect changes in pH, O2, and CO2 in blood. stimulate
SNS if oxygen is low, pH is low, CO2 is high
Chemoreceptors
located in internal carotid arteries and aortic arch
constrict peripheral vessels, increase HR (chronotropy),
SNS affects on heart
increase contraction force (inotropy)
alpha cell stimulation causes vasoconstriction;
beta-1 cell stimulation causes increased HR, increased
alpha and beta cells
force, increased conduction velocity;
beta-2 cells cause bronchodilation
chronic elevated BP w/ end organ damage.
Primary (Ideopathic) HTN
RAAS activation, vascular disease (stiffness), alpha
receptor stimulation (vasoconstriction)
1/3 of patients get HF from cardiomyopathy (disease of
heart muscle causing weakness)
Causes of HF
2/3 of patients get HF from coronary artery disease
, *Problem of FILLING
Usually from prolonged high afterload from chronic
HTN
Diastolic HF
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
*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
Systolic HF (dilated ventricles after contraction (decreased ejection
cardiomyopathy) fraction)
LV experiences congestion behind pump (lungs) -->
fluid in lungs
RV experiences congestion behind pump (body) -->
ascites, edema)
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
Right sided HF
can stress the right side of the heart and cause it to fail
causing backup of blood into the right atrium and
peripheral veins
Jugular venous distention
Ascites
Peripheral edema
, Left-sided HF (most common) from left ventricular
dysfunction preventing body from getting enough
oxygen rich blood
Left sided HF Excess blood accumulates in LV (volume overload) -->
backup of blood into the left atrium and pulmonary
veins
causing pulmonary congestion (SOB, cough), edema
reduce volume using diuretics
* look out for hypokalemia, hypovolemia
How to reduce preload in block aldosterone to prevent water/sodium retention
HF using ACE-i or ARBs
*look out for hypotension, renal dysfunction with ACE-i
*look out for hyperkalemia, muscle cramps,
rhabdomyolysis with ARBs
prevent angiotensin II vasoconstriction using ACE-i or
ARBs
How to reduce afterload in
HF *look out for hypotension, renal dysfunction with ACE-i
*look out for hyperkalemia, muscle cramps,
rhabdomyolysis with ARBs
Beta-blockers
How to slow SNS in HF
*look out for bradycardia, hypotension
Decreased blood flow in coronary arteries supplying
the heart
Main cause is coronary atherosclerosis which is an
Acute Coronary Syndrome
accumulation of lipid and fibrous tissue in the vessel
(ACS/Heart Attack/MI)
wall creating blockages or narrowing of the vessel that
reduces blood flow to myocardium
(thrombus can form)
