NURS 5334 MODULE 5 STUDY QUESTIONS & ANSWERS EXAM
CV
▪ What is cardiac output?
o cardiac output is about 5 L/ minute.
o Hence, every minute, the heart pumps the equivalent of all the blood in the
body.
o CO = HR x SV
o an increase in HR or SV will increase CO,
o whereas a decrease in HR or SV will decrease CO.
▪ Stroke volume?
o Stroke volume is determined largely by three factors:
▪ (1) myocardial contractility,
▪ (2) cardiac afterload, and
▪ (3) cardiac preload.
o Myocardial contractility is defined as the force with which the ventricles
contract.
o Contractility is determined primarily by the degree of cardiac dilation, which in
turn is determined by the amount of venous return.
o In addition to regulation by venous return, contractility can be increased by
the sympathetic nervous system,
▪ acting through beta1-adrenergic receptors in the myocardium.
▪ Preload?
o Preload is formally defined as the amount of tension (stretch) applied to a
muscle before contraction.
o In the heart, stretch is determined by ventricular filling pressure, that is, the
force of venous return:
▪ the greater filling pressure is, the more the ventricles will stretch.
o Cardiac preload can be expressed as either end-diastolic volume or end-
diastolic pressure.
o As discussed later, an increase in preload will increase SV,
o whereas a decrease in preload will reduce SV.
o Frequently, the terms preload and force of venous return are used
interchangeably— although they are not truly equivalent.
▪ Afterload?
o Afterload is formally defined as the load against which a muscle exerts its
force (i.e., the load a muscle must overcome in order to contract).
o For the heart, afterload is the arterial pressure that the left ventricle must
overcome to eject blood.
o Common sense tells us that, if afterload increases, SV will decrease.
o Conversely, if afterload falls, SV will rise.
o Cardiac afterload is determined primarily by the degree of peripheral
resistance,
▪ which in turn is determined by constriction and dilation of arterioles.
1
,NURS 5334 MODULE 5 STUDY QUESTIONS & ANSWERS EXAM
▪ That is, when arterioles constrict, peripheral resistance rises, causing
AP (afterload) to rise as well.
▪ Conversely, when arterioles dilate, peripheral resistance falls, causing
AP to decline.
▪ What is Starling’s Law? - venous return is the primary determinant of SV
o Starling's law states that the force of ventricular contraction is proportional to
muscle fiber length (up to a point).
o Accordingly, as fiber length (ventricular diameter) increases, there is a
corresponding increase in contractile force (Fig. 34.5).
o Because of this built-in mechanism, when more blood enters the heart, more
is pumped out.
o As a result, the healthy heart is able to precisely match its output with the
volume of blood delivered by veins.
o That is, when venous return increases, CO increases correspondingly.
o Conversely, when venous return declines, CO declines to precisely the same
extent.
o Hence, under normal, nonstressed conditions, SV is determined by factors
that regulate venous return.
▪ What regulates artial pressure?
o Arterial pressure is the driving force that moves blood through the arterial side
of the systemic circulation.
o The general formula for AP is: AP = PR × CO
▪ where AP is arterial pressure,
▪ PR is peripheral resistance, and
▪ CO is cardiac output.
o Accordingly, an increase in PR or CO will increase AP,
o whereas a decrease in PR or CO will decrease AP.
o Peripheral resistance is regulated primarily through constriction and dilation of
arterioles.
o Cardiac output is regulated by the mechanisms discussed previously.
▪ AP is regulated primarily by three systems:
o the ANS,
o the renin-angiotensin-aldosterone system (RAAS),
o kidneys.
o These systems differ greatly with regard to timeframe of response.
o The ANS acts in two ways:
▪ (1) it responds rapidly (in seconds or minutes) to acute changes in
blood pressure and
▪ (2) it provides steady-state control.
o The RAAS responds more slowly, taking hours or days to influence AP.
o The kidneys are responsible for long-term control and hence may take days
or weeks to adjust AP.
2
, NURS 5334 MODULE 5 STUDY QUESTIONS & ANSWERS EXAM
o Arterial pressure is also regulated by a fourth system: a family of natriuretic
peptides.
▪ These peptides come into play primarily under conditions of volume
overload.
▪ What are baroreceptors?
o The baroreceptor reflex serves to maintain AP at a predetermined level.
When AP changes, the reflex immediately attempts to restore AP to the preset
value.
o Baroreceptors (pressure sensors) in the aortic arch and carotid sinus sense
AP and relay this information to the vasoconstrictor center of the medulla.
o When AP changes, the vasoconstrictor center compensates by sending
appropriate instructions to arterioles, veins, and the heart.
o For example, when AP drops, the vasoconstrictor center causes
▪ (1) constriction of nearly all arterioles, thereby increasing PR;
▪ (2) constriction of veins, thereby increasing venous return; and
▪ (3) acceleration of HR (by increasing sympathetic impulses to the heart
and decreasing parasympathetic impulses).
o The combined effect of these responses is to restore AP to the preset level.
o When AP rises too high, opposite responses occur: the reflex dilates
arterioles and veins and slows the heart.
▪ What is the role of the natriuretic peptides?
o Natriuretic peptides serve to protect the cardiovascular system in the event of
volume overload,
▪ a condition that increases preload, and thereby increases CO and AP.
o Volume overload is caused by excessive retention of sodium and water.
o Natriuretic peptides work primarily by
▪ (1) reducing blood volume and
▪ (2) promoting dilation of arterioles and veins.
o Both actions lower AP.
o The family of natriuretic peptides has three principal members:
▪ atrial natriuretic peptide (ANP),
▪ B- or brain natriuretic peptide (BNP), and
▪ C-natriuretic peptide (CNP).
o ANP is produced by myocytes of the atria;
o BNP is produced by myocytes of the ventricles (and to a lesser extent by cells
in the brain, where BNP was discovered); and
o CNP is produced by cells of the vascular endothelium.
o When blood volume is excessive, all three peptides are released.
▪ (Release of ANP and BNP is triggered by stretching of the atria and
ventricles, which occurs because of increased preload.)
▪ ANP and BNP have similar actions.
• Both peptides reduce blood volume and increase venous
capacitance and thereby reduce cardiac preload.
3
CV
▪ What is cardiac output?
o cardiac output is about 5 L/ minute.
o Hence, every minute, the heart pumps the equivalent of all the blood in the
body.
o CO = HR x SV
o an increase in HR or SV will increase CO,
o whereas a decrease in HR or SV will decrease CO.
▪ Stroke volume?
o Stroke volume is determined largely by three factors:
▪ (1) myocardial contractility,
▪ (2) cardiac afterload, and
▪ (3) cardiac preload.
o Myocardial contractility is defined as the force with which the ventricles
contract.
o Contractility is determined primarily by the degree of cardiac dilation, which in
turn is determined by the amount of venous return.
o In addition to regulation by venous return, contractility can be increased by
the sympathetic nervous system,
▪ acting through beta1-adrenergic receptors in the myocardium.
▪ Preload?
o Preload is formally defined as the amount of tension (stretch) applied to a
muscle before contraction.
o In the heart, stretch is determined by ventricular filling pressure, that is, the
force of venous return:
▪ the greater filling pressure is, the more the ventricles will stretch.
o Cardiac preload can be expressed as either end-diastolic volume or end-
diastolic pressure.
o As discussed later, an increase in preload will increase SV,
o whereas a decrease in preload will reduce SV.
o Frequently, the terms preload and force of venous return are used
interchangeably— although they are not truly equivalent.
▪ Afterload?
o Afterload is formally defined as the load against which a muscle exerts its
force (i.e., the load a muscle must overcome in order to contract).
o For the heart, afterload is the arterial pressure that the left ventricle must
overcome to eject blood.
o Common sense tells us that, if afterload increases, SV will decrease.
o Conversely, if afterload falls, SV will rise.
o Cardiac afterload is determined primarily by the degree of peripheral
resistance,
▪ which in turn is determined by constriction and dilation of arterioles.
1
,NURS 5334 MODULE 5 STUDY QUESTIONS & ANSWERS EXAM
▪ That is, when arterioles constrict, peripheral resistance rises, causing
AP (afterload) to rise as well.
▪ Conversely, when arterioles dilate, peripheral resistance falls, causing
AP to decline.
▪ What is Starling’s Law? - venous return is the primary determinant of SV
o Starling's law states that the force of ventricular contraction is proportional to
muscle fiber length (up to a point).
o Accordingly, as fiber length (ventricular diameter) increases, there is a
corresponding increase in contractile force (Fig. 34.5).
o Because of this built-in mechanism, when more blood enters the heart, more
is pumped out.
o As a result, the healthy heart is able to precisely match its output with the
volume of blood delivered by veins.
o That is, when venous return increases, CO increases correspondingly.
o Conversely, when venous return declines, CO declines to precisely the same
extent.
o Hence, under normal, nonstressed conditions, SV is determined by factors
that regulate venous return.
▪ What regulates artial pressure?
o Arterial pressure is the driving force that moves blood through the arterial side
of the systemic circulation.
o The general formula for AP is: AP = PR × CO
▪ where AP is arterial pressure,
▪ PR is peripheral resistance, and
▪ CO is cardiac output.
o Accordingly, an increase in PR or CO will increase AP,
o whereas a decrease in PR or CO will decrease AP.
o Peripheral resistance is regulated primarily through constriction and dilation of
arterioles.
o Cardiac output is regulated by the mechanisms discussed previously.
▪ AP is regulated primarily by three systems:
o the ANS,
o the renin-angiotensin-aldosterone system (RAAS),
o kidneys.
o These systems differ greatly with regard to timeframe of response.
o The ANS acts in two ways:
▪ (1) it responds rapidly (in seconds or minutes) to acute changes in
blood pressure and
▪ (2) it provides steady-state control.
o The RAAS responds more slowly, taking hours or days to influence AP.
o The kidneys are responsible for long-term control and hence may take days
or weeks to adjust AP.
2
, NURS 5334 MODULE 5 STUDY QUESTIONS & ANSWERS EXAM
o Arterial pressure is also regulated by a fourth system: a family of natriuretic
peptides.
▪ These peptides come into play primarily under conditions of volume
overload.
▪ What are baroreceptors?
o The baroreceptor reflex serves to maintain AP at a predetermined level.
When AP changes, the reflex immediately attempts to restore AP to the preset
value.
o Baroreceptors (pressure sensors) in the aortic arch and carotid sinus sense
AP and relay this information to the vasoconstrictor center of the medulla.
o When AP changes, the vasoconstrictor center compensates by sending
appropriate instructions to arterioles, veins, and the heart.
o For example, when AP drops, the vasoconstrictor center causes
▪ (1) constriction of nearly all arterioles, thereby increasing PR;
▪ (2) constriction of veins, thereby increasing venous return; and
▪ (3) acceleration of HR (by increasing sympathetic impulses to the heart
and decreasing parasympathetic impulses).
o The combined effect of these responses is to restore AP to the preset level.
o When AP rises too high, opposite responses occur: the reflex dilates
arterioles and veins and slows the heart.
▪ What is the role of the natriuretic peptides?
o Natriuretic peptides serve to protect the cardiovascular system in the event of
volume overload,
▪ a condition that increases preload, and thereby increases CO and AP.
o Volume overload is caused by excessive retention of sodium and water.
o Natriuretic peptides work primarily by
▪ (1) reducing blood volume and
▪ (2) promoting dilation of arterioles and veins.
o Both actions lower AP.
o The family of natriuretic peptides has three principal members:
▪ atrial natriuretic peptide (ANP),
▪ B- or brain natriuretic peptide (BNP), and
▪ C-natriuretic peptide (CNP).
o ANP is produced by myocytes of the atria;
o BNP is produced by myocytes of the ventricles (and to a lesser extent by cells
in the brain, where BNP was discovered); and
o CNP is produced by cells of the vascular endothelium.
o When blood volume is excessive, all three peptides are released.
▪ (Release of ANP and BNP is triggered by stretching of the atria and
ventricles, which occurs because of increased preload.)
▪ ANP and BNP have similar actions.
• Both peptides reduce blood volume and increase venous
capacitance and thereby reduce cardiac preload.
3
