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NURS 5315 Module 5 (2025) Newest Questions and
Answers (Verified Answers)
Cardia structure/blood flow - (answers)The right atrium receives deoxygenated
blood from the body. The blood travels from the right atrium, through the
tricuspid valve to the right ventricle. From the right ventricle the blood travels
through the pulmonic valve, into the pulmonary artery (this is the only artery in
the body which carries deoxygenated blood), into the lungs, where it goes to the
alveoli and gas exchange occurs. The oxygenated blood then enters the
pulmonary vein and is delivered to the left atrium. From the left atrium it travels
through the mitral valve into the left ventricle. From the left ventricle the blood
travels through the aortic valve into the aorta
Fetal circulation - (answers)The umbilical vein receives oxygenated blood from
the placenta. The umbilical vein connects to the hepatic circulation but also
connects to the inferior vena cava by the ductus venosus. The ductus venosus
allows the oxygen-rich blood to enter the inferior vena cava and some blood does
enter the hepatic circulation. From the inferior vena cava, the blood is emptied
into the right atrium. The most oxygenated blood in the right atrium is shunted
through the foramen ovale (this is an opening between the right and left atria)
into the left atrium. The blood then enters the left ventricle and is pumped out to
the head and the rest of the body. The deoxygenated blood also enters the right
atrium just as the oxygenated blood does. There are two streams that help to
keep the blood separate. Sixty percent of the blood in the right atrium (which is
oxygenated blood) will be moved forward as described above. The remaining 40%
of the blood is mixed blood (oxygenated and deoxygenated) and will move from
the right atrium, to the right ventricle, and into the pulmonary artery. From the
pulmonary artery it will pass through the patent ductus arteriosus (which is a
connection between the pulmonary artery and the aorta) into the aorta. The
aorta will connect with the umbilical artery, where the blood will go back to the
placenta to exchange gas, get rid of waste products and pick up nutrients. The
right side of the heart has the higher pressure prior to birth. After birth, this
, 2
changes with the neonate's first breath and the left side of the heart becomes the
one with the higher pressure.
Factors which increase contraction - (answers)**Catecholamines-increase activity
of the calcium pump in the sarcoplasmic reticulum; therefore it increases the
release of calcium from the SR**Increases in intracellular calcium**Decreased
extracellular sodium-decreases the activity of the Na/Ca exchanger**Digitalis-
blocks the Na/K pump which increases intracellular Na, decreases the activity of
the NA/Ca exchanger, and increases intracellular Ca
Factors which decrease contraction - (answers)**Beta blockers-block the effects
of the catecholamines**heart failure with systolic
dysfunction**acidosis**hypoxia/hypercapnia **nondihydropyridine calcium
channel blockers
Cardiac output (CO) - (answers)Amount of blood pushed from the left ventricle in
1 minutes. HR X STROKE VOLUME = CO. Normal output is 5L/minute
Stroke Volume - (answers)Amount of blood ejected by the ventricle for each
cardiac cycle. Highly dependent on the force of contraction. Contraction is
dependent upon amount of preload, stimulation by endogenous positive
inotropic agents such as epi and norepi, presence of negative inotropic agents and
adequacy of myocardial oxygenation
Ejection fraction (EF) - (answers)Percentage of blood which is ejected from the
ventricle with each contraction. Calculated by dividing the stroke volume by the
end diastolic volume. Normal EF is 55-65%. EF decreases with systolic heart failure
but not in diastolic heart failure
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Preload - (answers)Made up of end diastolic volume and end diastolic pressure.
Dependent upon the amount of venous return to the heart and the amount of
blood left in the left ventricle at the end of systole. Increased preload can cause
heart failure from a decline in stroke volume and a back up into pulmonary
circulation
Afterload - (answers)Resistance that the ventricle pushes against to contract. This
includes aortic pressure and systemic vascular resistance. High afterload increases
the work of the ventricle and results in hypertrophy. A low afterload enables the
heart to contract faster
Diltiazem and verapamil - (answers)non-dihydropyridine calcium channel
blockers. They inhibit the influx of calcium into the myocardium. This decreases
intracellular calcium concentration which in turn decreases myocardial tension
and contractility. They have negative inotropic effects. As such these medications
should be avoided in persons with systolic heart failure.
Dobuamine - (answers)Stimulates the beta 1 receptors in the myocardium and
improves contractility and increases heart rate
Epinephrine - (answers)Primarily stimulates beta 1 receptors of the heart which
results in an increase in myocardial contractility and heart rate. Also effects beta 2
and alpha 1 receptors which cancel each other out and does not change vascular
tone. In high doses alpha 1 overrides beta 2 which causes vasocontriction and
increased systemic vascular resistance while still enhancing contractility and
cardiac output
NURS 5315 Module 5 (2025) Newest Questions and
Answers (Verified Answers)
Cardia structure/blood flow - (answers)The right atrium receives deoxygenated
blood from the body. The blood travels from the right atrium, through the
tricuspid valve to the right ventricle. From the right ventricle the blood travels
through the pulmonic valve, into the pulmonary artery (this is the only artery in
the body which carries deoxygenated blood), into the lungs, where it goes to the
alveoli and gas exchange occurs. The oxygenated blood then enters the
pulmonary vein and is delivered to the left atrium. From the left atrium it travels
through the mitral valve into the left ventricle. From the left ventricle the blood
travels through the aortic valve into the aorta
Fetal circulation - (answers)The umbilical vein receives oxygenated blood from
the placenta. The umbilical vein connects to the hepatic circulation but also
connects to the inferior vena cava by the ductus venosus. The ductus venosus
allows the oxygen-rich blood to enter the inferior vena cava and some blood does
enter the hepatic circulation. From the inferior vena cava, the blood is emptied
into the right atrium. The most oxygenated blood in the right atrium is shunted
through the foramen ovale (this is an opening between the right and left atria)
into the left atrium. The blood then enters the left ventricle and is pumped out to
the head and the rest of the body. The deoxygenated blood also enters the right
atrium just as the oxygenated blood does. There are two streams that help to
keep the blood separate. Sixty percent of the blood in the right atrium (which is
oxygenated blood) will be moved forward as described above. The remaining 40%
of the blood is mixed blood (oxygenated and deoxygenated) and will move from
the right atrium, to the right ventricle, and into the pulmonary artery. From the
pulmonary artery it will pass through the patent ductus arteriosus (which is a
connection between the pulmonary artery and the aorta) into the aorta. The
aorta will connect with the umbilical artery, where the blood will go back to the
placenta to exchange gas, get rid of waste products and pick up nutrients. The
right side of the heart has the higher pressure prior to birth. After birth, this
, 2
changes with the neonate's first breath and the left side of the heart becomes the
one with the higher pressure.
Factors which increase contraction - (answers)**Catecholamines-increase activity
of the calcium pump in the sarcoplasmic reticulum; therefore it increases the
release of calcium from the SR**Increases in intracellular calcium**Decreased
extracellular sodium-decreases the activity of the Na/Ca exchanger**Digitalis-
blocks the Na/K pump which increases intracellular Na, decreases the activity of
the NA/Ca exchanger, and increases intracellular Ca
Factors which decrease contraction - (answers)**Beta blockers-block the effects
of the catecholamines**heart failure with systolic
dysfunction**acidosis**hypoxia/hypercapnia **nondihydropyridine calcium
channel blockers
Cardiac output (CO) - (answers)Amount of blood pushed from the left ventricle in
1 minutes. HR X STROKE VOLUME = CO. Normal output is 5L/minute
Stroke Volume - (answers)Amount of blood ejected by the ventricle for each
cardiac cycle. Highly dependent on the force of contraction. Contraction is
dependent upon amount of preload, stimulation by endogenous positive
inotropic agents such as epi and norepi, presence of negative inotropic agents and
adequacy of myocardial oxygenation
Ejection fraction (EF) - (answers)Percentage of blood which is ejected from the
ventricle with each contraction. Calculated by dividing the stroke volume by the
end diastolic volume. Normal EF is 55-65%. EF decreases with systolic heart failure
but not in diastolic heart failure
, 3
Preload - (answers)Made up of end diastolic volume and end diastolic pressure.
Dependent upon the amount of venous return to the heart and the amount of
blood left in the left ventricle at the end of systole. Increased preload can cause
heart failure from a decline in stroke volume and a back up into pulmonary
circulation
Afterload - (answers)Resistance that the ventricle pushes against to contract. This
includes aortic pressure and systemic vascular resistance. High afterload increases
the work of the ventricle and results in hypertrophy. A low afterload enables the
heart to contract faster
Diltiazem and verapamil - (answers)non-dihydropyridine calcium channel
blockers. They inhibit the influx of calcium into the myocardium. This decreases
intracellular calcium concentration which in turn decreases myocardial tension
and contractility. They have negative inotropic effects. As such these medications
should be avoided in persons with systolic heart failure.
Dobuamine - (answers)Stimulates the beta 1 receptors in the myocardium and
improves contractility and increases heart rate
Epinephrine - (answers)Primarily stimulates beta 1 receptors of the heart which
results in an increase in myocardial contractility and heart rate. Also effects beta 2
and alpha 1 receptors which cancel each other out and does not change vascular
tone. In high doses alpha 1 overrides beta 2 which causes vasocontriction and
increased systemic vascular resistance while still enhancing contractility and
cardiac output
