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Transcript
Objective 15
Cardiac Output
Cardiac Output: The volume of blood ejected by each ventricle per minute
at rest, averages 5 L/minute
What is the term for the volume of blood ejected by each ventricle per beat?
How do you calculate it?
Stroke Volume:
The volume of blood ejected by each
ventricle per beat, at rest, averages 70
ml/beat
Recall SV = EDV - ESV
Heart Rate:
the number of times that the heart
beats per minute (the number of
cardiac cycles per minute) at rest,
averages 75/minute
Cardiac Output (ml/min) = Stroke Volume (SV) X Heart Rate (HR)
(ml/beat)
(beats/minute)
Cardiac
Reserve
:
the difference between resting and
maximal cardiac output
CO (ml/min) = SV (mls) X HR (b/min)
So , let’s think:
• What happens to cardiac output if stroke volume increases?
• What happens to cardiac output if stroke volume decreases?
• What happens to cardiac out put if heart rate increases?
• What happens to cardiac out put if heart rate decreases?
B. Stroke Volume (SV):

is the difference between end diastolic volume (EDV) and end
systolic volume (ESV)
end diastolic volume: the volume of blood that fills a ventricle during
diastole; averages 120 ml
end systolic volume: the volume of blood remaining in a ventricle after
systole; averages 50 ml
SV
70 ml =
=
EDV – ESV
120 ml – 50 ml
Ejection Fraction =
SV/EDV

An ejection fraction of less than 50% is considered to be
abnormal, a condition that may occur in cardiac failure.

During exercise in highly conditioned individuals, the
increased stroke volume can result in the EF exceeding
90%.
B. Factors that Affect Stroke Volume:
Preload
:
the degree to which cardiac muscle fibers are
stretched prior to contraction
Frank Starling Law of the Heart
If cardiac muscle sarcomeres are
stretched, within limits, they contract
more forcibly
As sarcomeres are stretched,
there are more sites available
for cross bridge interaction
Question: what happens if
sarcomeres are stretched too
much ????????
No contraction is possible
Factors which increase preload:
1.
Increased venous return
venous return (VR) is the volume of blood
delivered to the ventricles during the
cardiac cycle by the veins
VR is increased by

increases in blood volume

increased skeletal muscle activity

inspiration

venoconstriction
2. Increased time for ventricular filling (length of
diastole)
reduction in heart rate or arrhythmias that lower the
ventricular rate
Contracility
any change in muscle contractile strength that is
independent of EDV and sarcomere length (think EF)
Inotropic
Positive
Inotropic
Effect
Negative
Effect
ANS
sympathetic nervous system
parasympathetic nervous system
Chemicals
epinephrine
norepinephrine
excess Ca2+
glucagon
thyroxine
digitalis
acetylcholine
excess H+
excess K+
calcium channel blockers
Afterload

the pressure that the ventricles must overcome to
eject blood into the arteries
higher arterial pressure makes it difficult for the
ventricles to eject blood and leads to reduced stroke
volumes
Summary of factors:
Preload
Contractility
1.Venous
return
1. Positive
inotropic
effect
2.
HR
2. Negative
inotropic
effect
Afterload
D. Regulation of Heart Rate
Positive
Chronotropic
Effect Negative
Chronotropic
Effect
ANS
sympathetic nervous system
parasympathetic nervous system
Chemicals
norepinephrine
epinephrine
thyroid hormone
excess Ca2+
aceylcholine
excess Na+
excess K+
Other
young age
increased body temperature
female gender
older age
decreased body temperature
male gender
Pathway
Sensory input (cerebral cortex, limbic system, hypothalamus,
baroreceptors, chemoreceptors)
Afferent pathways – CN IX, CN X (and others, see above)
Control centers – medulla cardiac acceleratory center (CAC)
and cardiac inhibitory center (CIC)
Efferent pathway – sympathetic nerves, parasympathetic nerves
Effectors – nodal cells (heart rate, chronotropic effect) and
cardiac myocytes (contractility, inotropic effect)
Neural Control of Heart Rate
Medulla Oblongata
CAC
CIC
Glossopharyngeal (IX)
Vagus(X)
PNS - Vagus
SNS - Cardiac Nerves
Note – when HR is increased the CAC is activated and CIC is inhibited,
when HR is decreased the CIC is activated and CAC is inhibited
Control of heart rate – if BP is elevated
Sensory input – baroreceptors activated
Afferent pathways – CN IX, CN X
Control center – CAC is inhibited, CIC activated
Efferent pathway – CN X (Vagus nerve)
Effectors – nodal cells decrease heart rate, negative
chronotropic effect
Control of heart rate – if BP is too low
Sensory input – baroreceptors decrease firing
Afferent pathways – CN IX, CN X
Control center – CAC is activated, CIC inhibited
Efferent pathway – Sympathetic cardiac nerves
Effectors – nodal cells increase heart rate, positive
chronotropic effect
Right Atrial (Bainbridge) Reflex
Stimulation of pressoreceptors in right atrial
wall (increased VR)
Increased stretch of myocardium
SA Node and pressoreceptors stretch
HR Elevated
Preload
Contractility
1.Venous
return
1. Positive
inotropic
effect
2.
HR
2. Negative
inotropic
effect
Afterload
Positive
chronotropic
Negative
chronotropic
Atrial
reflex
So, let’s think:
If preload increases what happens to CO?
If contractility increases what happens to CO?
If afterload increases what happens to CO
If there is an increase in HR what happens to
CO?
Cardiac =
Output
Stroke Volume
X Heart Rate
Preload
Contractility
1.Venous
return
1. Positive
inotropic
effect
2.
HR
2. Negative
inotropic
effect
Afterload
Positive
chronotropic
Negative
chronotropic
Atrial
reflex
So, let’s think:
If preload increases what happens to CO?
If contractility increases what happens to CO?
If afterload increases what happens to CO?
If there is an increase in HR what happens to
CO?
Congestive Heart Failure