NR 5344: STUDY QUESTIONS MODULE 5
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▪ 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.
, ▪ 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.
100% CORRECT DOWNLOAD TO SCORE
A RATED A+
▪ 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.
, ▪ 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.
