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PowerPoint® Lecture Slides
prepared by
Janice Meeking,
Mount Royal College
CHAPTER
18
The
Cardiovascular
System: The
Heart: Part B
Copyright © 2010 Pearson Education, Inc.
Cardiac Muscle Contraction
• Depolarization of the heart is rhythmic and
spontaneous
• About 1% of cardiac cells have automaticity—
(are self-excitable)
• Gap junctions ensure the heart contracts as a
unit
• Long absolute refractory period (250 ms)
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Cardiac Muscle Contraction
• Depolarization opens voltage-gated fast Na+
channels in the sarcolemma
• Reversal of membrane potential from –90 mV to
+30 mV
• Depolarization wave in T tubules causes the SR
to release Ca2+
• Depolarization wave also opens slow Ca2+
channels in the sarcolemma
• Ca2+ surge prolongs the depolarization phase
(plateau)
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1 Depolarization is
2
Tension
development
(contraction)
3
1
Absolute
refractory
period
Time (ms)
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Tension (g)
Membrane potential (mV)
Action
potential
Plateau
due to Na+ influx through
fast voltage-gated Na+
channels. A positive
feedback cycle rapidly
opens many Na+
channels, reversing the
membrane potential.
Channel inactivation ends
this phase.
2 Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
3 Repolarization is
due to Ca2+ channels
inactivating and K+
channels opening. This
allows K+ efflux, which
brings the membrane
potential back to its
resting voltage.
Figure 18.12
Cardiac Muscle Contraction
• Ca2+ influx triggers opening of Ca2+-sensitive
channels in the SR, which liberates bursts of Ca2+
• E-C coupling occurs as Ca2+ binds to troponin and
sliding of the filaments begins
• Duration of the AP and the contractile phase is much
greater in cardiac muscle than in skeletal muscle
• Repolarization results from inactivation of Ca2+
channels and opening of voltage-gated K+ channels
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Heart Physiology: Electrical Events
• Intrinsic cardiac conduction system
• A network of noncontractile (autorhythmic)
cells that initiate and distribute impulses to
coordinate the depolarization and contraction
of the heart
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Autorhythmic Cells
• Have unstable resting potentials (pacemaker
potentials or prepotentials) due to open slow
Na+ channels
• At threshold, Ca2+ channels open
• Explosive Ca2+ influx produces the rising
phase of the action potential
• Repolarization results from inactivation of
Ca2+ channels and opening of voltage-gated
K+ channels
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Threshold
Action
potential
2
2
3
1
1
Pacemaker
potential
1 Pacemaker potential
2 Depolarization The
3 Repolarization is due to
This slow depolarization is
due to both opening of Na+
channels and closing of K+
channels. Notice that the
membrane potential is
never a flat line.
action potential begins when
the pacemaker potential
reaches threshold.
Depolarization is due to Ca2+
influx through Ca2+ channels.
Ca2+ channels inactivating and
K+ channels opening. This
allows K+ efflux, which brings
the membrane potential back
to its most negative voltage.
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Figure 18.13
Heart Physiology: Sequence of Excitation
1. Sinoatrial (SA) node (pacemaker)
• Generates impulses about 75 times/minute
(sinus rhythm)
• Depolarizes faster than any other part of the
myocardium
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Heart Physiology: Sequence of Excitation
2. Atrioventricular (AV) node
•
Smaller diameter fibers; fewer gap junctions
•
Delays impulses approximately 0.1 second
•
Depolarizes 50 times per minute in absence
of SA node input
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Heart Physiology: Sequence of Excitation
3. Atrioventricular (AV) bundle (bundle of His)
• Only electrical connection between the atria
and ventricles
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Heart Physiology: Sequence of Excitation
4. Right and left bundle branches
•
Two pathways in the interventricular septum
that carry the impulses toward the apex of
the heart
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Heart Physiology: Sequence of Excitation
5. Purkinje fibers
•
Complete the pathway into the apex and
ventricular walls
•
AV bundle and Purkinje fibers depolarize
only 30 times per minute in absence of AV
node input
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Superior vena cava
Right atrium
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
Internodal pathway
2 The impulses
pause (0.1 s) at the
atrioventricular
(AV) node.
3 The atrioventricular
(AV) bundle
connects the atria
to the ventricles.
4 The bundle branches
conduct the impulses
through the
interventricular septum.
5 The Purkinje fibers
Left atrium
Purkinje
fibers
Interventricular
septum
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
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Figure 18.14a
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Homeostatic Imbalances
•
Defects in the intrinsic conduction system
may result in
1. Arrhythmias: irregular heart rhythms
2. Uncoordinated atrial and ventricular
contractions
3. Fibrillation: rapid, irregular contractions;
useless for pumping blood
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Homeostatic Imbalances
• Defective SA node may result in
• Ectopic focus: abnormal pacemaker takes over
• If AV node takes over, there will be a junctional
rhythm (40–60 bpm)
• Defective AV node may result in
• Partial or total heart block
• Few or no impulses from SA node reach the
ventricles
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Extrinsic Innervation of the Heart
• Heartbeat is modified by the ANS
• Cardiac centers are located in the medulla
oblongata
• Cardioacceleratory center innervates SA and
AV nodes, heart muscle, and coronary arteries
through sympathetic neurons
• Cardioinhibitory center inhibits SA and AV
nodes through parasympathetic fibers in the
vagus nerves
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Neuroanatomy terms
• Nucleus – cluster of neuron cell bodies in the
CNS – performs a certain function – like
temperature center, cardiac center, etc.
• Tract – group of neuron cell fibers (axons &
dendrites) in the CNS – some tracts are
descending (motor) tracts and some are
ascending (sensory)
• Ganglion – a cluster of neuron cell bodies in
the PNS – like the dorsal root ganglion or the
ganglia of the ANS
• Nerve – group on neuron cell fibers in PNS
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Autonomic Motor Summary
• The autonomic motor is a two neuron pathway- pathway
one from comes from the CNS to the ganglion – thus
termed pre-ganglionic fibers. These fibers synapse on
neuron cell bodies in the ganglion. The fibers from the
ganglion cell bodies going to the organ (effector) are
termed post ganglionic fibers.
• The original neuron cell bodies for the parasympathetic
nervous system are in the brain and sacral area of
spinal cord – thus a cranio-sacral origin – those for the
sympathetic are in the Thoracic and Lumbar area of the
spinal cord – thus Thoraco-lumbar origin.
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• The preganglionic fibers synapse on the ganglion
cell bodies – the neurotransmitter is acetylcholine
for both the sympathetic and parasympathetic.
The type of receptor is nicotinic
• The postganglionic fibers for the parasympathetic
synapse on the organ it innervates – the
neurotransmitter is acetylcholine – generally
going to a muscarinic receptor
• The postganglionic fibers for the sympathetic
synapse on the organ – the neurotransmitter is
generally norepinephrine on alpha or beta
receptors depending on the organ
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Sympathetic
Parasympathetic
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Table 14.1
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Table 14.3
FFF
RR
FFF – Fear, Fight & Flight
RR – Rest and Recluse
Receptors for NE are alpha and beta with subtypes. The receptors for
Acetylcholine are nicotinic and muscarinic. On the heart there are
Beta 1 receptors for NE and muscarinic for acetylcholine.
Copyright © 2010 Pearson Education, Inc.
Extracellular fluid
Norepinephrine
Adenylate cyclase
Ca2+
b1-Adrenergic
receptor
G protein (Gs)
Ca2+
channel
ATP is converted
Cytoplasm
to cAMP
a
GDP
Inactive protein
kinase A
Enhanced
actin-myosin
interaction
Troponin
Cardiac muscle
force and velocity
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Phosphorylates SR Ca2+ channels,
increasing intracellular Ca2+
b
release
binds Ca2+
to
Active
Phosphorylates
plasma membrane
Ca2+ channels,
increasing extracellular Ca2+ entry
protein
kinase A
Phosphorylates SR Ca2+
pumps, speeding Ca2+
c
removal and relaxation
Ca2+
Ca2+ uptake
pump
SR Ca2+
channel
Sarcoplasmic
reticulum (SR)
Figure 18.21
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Medulla oblongata
Cardioacceleratory
center
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
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Figure 18.15
Cardiovascular center
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Electrocardiography
•
Electrocardiogram (ECG or EKG): a
composite of all the action potentials
generated by nodal and contractile cells at a
given time
•
Three waves
1. P wave: depolarization of SA node
2. QRS complex: ventricular depolarization
3. T wave: ventricular repolarization
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QRS complex
Sinoatrial
node
Atrial
depolarization
Ventricular
depolarization
Ventricular
repolarization
Atrioventricular
node
P-Q
Interval
S-T
Segment
Q-T
Interval
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Figure 18.16
SA node
Depolarization
R
Repolarization
R
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
R
AV node
T
P
Q
Q
S
4 Ventricular depolarization
is complete.
R
T
P
T
P
Q
S
2 With atrial depolarization
complete, the impulse is
delayed at the AV node.
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
T
P
T
P
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
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Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
R
SA node
Depolarization
Repolarization
T
P
1
Q
S
Atrial depolarization, initiated by
the SA node, causes the P wave.
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Figure 18.17, step 1
R
SA node
Depolarization
Repolarization
T
P
Q
S
1
Atrial depolarization, initiated by
the SA node, causes the P wave.
R
AV node
T
P
Q
2
S
With atrial depolarization complete,
the impulse is delayed at the AV node.
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Figure 18.17, step 2
R
SA node
Depolarization
Repolarization
T
P
Q
S
1
Atrial depolarization, initiated by
the SA node, causes the P wave.
R
AV node
T
P
Q
2
S
With atrial depolarization complete,
the impulse is delayed at the AV node.
R
T
P
Q
S
3 Ventricular depolarization begins
at apex, causing the QRS complex.
Atrial repolarization occurs.
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Figure 18.17, step 3
Depolarization
Repolarization
R
T
P
Q
4
S
Ventricular depolarization is
complete.
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Figure 18.17, step 4
Depolarization
Repolarization
R
T
P
Q
4
S
Ventricular depolarization is
complete.
R
T
P
Q
5
S
Ventricular repolarization begins
at apex, causing the T wave.
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Figure 18.17, step 5
Depolarization
Repolarization
R
T
P
Q
4
S
Ventricular depolarization is
complete.
R
T
P
Q
5
S
Ventricular repolarization begins
at apex, causing the T wave.
R
T
P
Q
6
S
Ventricular repolarization is
complete.
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Figure 18.17, step 6
SA node
Depolarization
R
Repolarization
R
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
R
AV node
T
P
Q
Q
S
4 Ventricular depolarization
is complete.
R
T
P
T
P
Q
S
2 With atrial depolarization
complete, the impulse is
delayed at the AV node.
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
T
P
T
P
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
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Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
(a) Normal sinus rhythm.
(b) Junctional rhythm. The SA
node is nonfunctional, P waves
are absent, and heart is paced by
the AV node at 40 - 60 beats/min.
(c) Second-degree heart block. (d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
Some P waves are not conducted
deflections are seen in acute
through the AV node; hence more
heart attack and electrical shock.
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
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Figure 18.18
Heart Sounds
• Two sounds (lub-dup) associated with closing
of heart valves
• First sound (S1) occurs as AV valves close
and signifies beginning of systole
• Second sound (S2) occurs when SL valves
close at the beginning of ventricular diastole
• Heart murmurs: abnormal heart sounds most
often indicative of valve problems
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Normal Human Heart Sounds
S1 – (M1 then T1) - closure of mitral valve first – then closure of
tricuspid valve
S2 – (A2 then P2) – closure of the aortic valve first then the
pulmonic
The time (milliseconds) difference between A2 and P2 is generally
great enough to be heard (resolved) by the human ear –
particularly during inspiration. This is termed the physiologic
splitting of the second heart sound
The rate of closure of a valve depends on the pressure
differences in the two communicating chambers – since the
pressure differentials on the left side of the heart are normally
higher than those on the right the -left heart valves close prior to
the right heart valves.
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Aortic valve sounds heard
in 2nd intercostal space at
right sternal margin
Pulmonary valve
sounds heard in 2nd
intercostal space at left
sternal margin
Mitral valve sounds
heard over heart apex
(in 5th intercostal space)
in line with middle of
clavicle
Tricuspid valve sounds typically
heard in right sternal margin of
5th intercostal space
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Figure 18.19
Abnormal Heart Sounds
S3 - occurs at the beginning of diastole after S2 and is lower in pitch
than S1 or S2 as it is not of valvular origin. S3 is thought to be caused by
the oscillation of blood back and forth between the walls of the
ventricles initiated by in rushing blood from the atria. The reason the
third heart sound does not occur until the middle third of diastole is
probably because during the early part of diastole, the ventricles are not
filled sufficiently to create enough tension for reverberation. It may also
be a result of tensing of the chordae tendineae during rapid filling and
expansion of the ventricle. It can be normal in youth, some trained
athletes, and sometimes in pregnancy
S4 – This sound is produced by the blood being forced into a
stiff/hypertrophic ventricle. It is a sign of a pathologic state, usually a
failing left ventricle, but can also be heard in other conditions such as
restrictive cardiomyopathy. The sound occurs just after atrial contraction
("atrial kick") at the end of diastole and immediately before S1
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Abnormal Heart Sounds
• Murmurs are produced as a result of turbulent flow of blood,
turbulence sufficient to produce audible noise. They are usually
heard as a whooshing sound (Regurgitation, Stenosis, Septal
Defects)
Murmur Grading Scale
Grade I – very faint- heard only with listener really tuned in
Grade II – Quiet – but heard immediately after placing stethoscope on the chest
Grade III – Moderately loud
Grade IV – Loud with palpable thrill (chest vibration)
Grade V – Very loud, with thrill. May be heard with stethoscope partially off the
chest
Grade VI – Very loud, with thrill. May be heard with stethoscope entirely off the
chest
Note: Turbulent Flow is presented in Blood Vessels (the study of)
PowerPoint
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Mechanical Events: The Cardiac Cycle
• Cardiac cycle: all events associated with
blood flow through the heart during one
complete heartbeat
• Systole—contraction
• Diastole—relaxation
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Cardiac Cycle – what happens during a heart beat
• Step One – Atrial Filling – totally passive – no
contraction of muscle
• Step Two – Atrial emptying which is the same as
Ventricular Filling
- Rapid Ventricular Filling
- Diastasis Filling
- Slow Ventricular Filling
Step Three – Ventricular Emptying
- Isovolumetric Contraction
- Ejection Contraction
- Contraction- Relaxation
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Phases of the Cardiac Cycle
2. Ventricular filling—takes place in mid-to-late
diastole
•
AV valves are open – blood waiting in the atria
rushes into ventricles from atria (Rapid
Ventricular Filling) - Passive
•
Diastasis Filling – new blood coming into atria
goes directly into ventricles – since valves are
already open - Passive
•
80% of blood passively flows into ventricles
•
Atrial systole occurs, delivering the remaining
20%
•
End diastolic volume (EDV): volume of blood in
each ventricle at the end of ventricular diastole
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Phases of the Cardiac Cycle
3. Ventricular Emptying (Ventricular systole)
•
Atria relax and ventricles begin to contract
•
Rising ventricular pressure results in closing of AV
valves
•
Isovolumetric contraction phase (all valves are
closed)
•
In ejection phase, ventricular pressure exceeds
pressure in the large arteries, forcing the SL valves
open
•
End systolic volume (ESV): volume of blood
remaining in each ventricle
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Phases of the Cardiac Cycle
4. Isovolumetric relaxation occurs in early
diastole
•
Ventricles relax
•
Backflow of blood in aorta and pulmonary
trunk closes SL valves and causes dicrotic
notch (brief rise in aortic pressure)
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Left heart
QRS
P
Electrocardiogram
T
1st
Heart sounds
P
2nd
Pressure (mm Hg)
Dicrotic notch
Aorta
Left ventricle
Ventricular
volume (ml)
Atrial systole
Left atrium
EDV
SV
ESV
Atrioventricular valves
Aortic and pulmonary valves
Phase
Open
Closed
Open
Closed
Open
Closed
1
2a
2b
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
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Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
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Aorta S – 100 – 140
D – 60 - 80
Left atrium 4 - 12
S 20 – 30
D 6 -10
O – 7 mmHg
S – systolic
D- diastolic
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S 100 – 140 D 4 - 12
S 20 – 30
D 0-7
Numbers in mm mercury pressure
Measuring Left Sided Heart Pressures
To measure left sided
Heart pressures – insert
catheter into femoral
artery (leg) or brachial artery
(arm) then advance it into
the Aorta – then into left
ventricle and then into
left atrium -if advance
further into pulmonary
veins can obtain
Pulmonary venous pressure.
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Right Heart
Catheterization
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Catheter is inserted into a main
Vein going into right atrium
Measuring Heart Pressures (Right Sided)
• Central Venous Pressure (CVP) – a measurement of right
sided heart pressures - a catheter placed into a large vein in
the neck (internal jugular vein), chest (subclavian vein) or
groin (femoral vein). It is used to administer medication or
fluids, obtain blood tests, and directly obtain cardiovascular
measurements such as the central venous pressure. Certain
medications, such as inotropes and amiodarone, are
preferably given through a central line
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Measuring Pulmonary Artery Pressure
Pulmonary Wedge Pressure is the pressure measured
in a pulmonary artery distal to an occlusion (wedge) of that
artery.
PWP is measured by inserting a balloon-tipped, multi-lumen
catheter (Swan-Ganz catheter) into a peripheral vein, then
advancing the catheter into the right atrium, right ventricle,
pulmonary artery, and then into a branch of the pulmonary
artery.
The catheter has one opening (port) at the tip (distal to the
balloon) and a second port several centimeters proximal to the
balloon.
When properly positioned in a branch of the pulmonary artery,
the distal port measures pulmonary artery pressure (~ 25/10
mmHg) and the proximal port measures right atrial pressure (~
0-3 mmHg).
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Swan Ganz line in Pulmonary
capillary wedge pressure
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Cardiac Output (CO)
• Volume of blood pumped by each ventricle in
one minute
• CO = heart rate (HR) x stroke volume (SV)
• HR = number of beats per minute
• SV = volume of blood pumped out by a
ventricle with each beat
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Cardiac Output (CO)
• At rest
• CO (ml/min) = HR (75 beats/min)  SV (70 ml/beat)
= 5.25 L/min
• Maximal CO is 4–5 times resting CO in nonathletic
people
• Maximal CO may reach 35 L/min in trained athletes
• Cardiac reserve: difference between resting and
maximal CO
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Regulation of Stroke Volume
• SV = EDV – ESV
• Three main factors affect SV
• Preload - the muscle length prior to contractility, and it is
dependent of ventricular filling (or end diastolic volume.)
• Afterload - is the tension (or the arterial pressure) against
which the ventricle must contract. Afterload for the left
ventricle is determined by aortic pressure, afterload for the
right ventricle is determined by pulmonary artery
pressure.
• Contractility- the intrinsic ability of cardiac muscle to
develop force for a given muscle length. It is also referred to
as the inotropic effect.
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Figure 18.21
Sarcomeres
greatly
shortened
Sarcomeres at
resting length
Sarcomeres excessively
stretched
75%
100%
170%
Optimal sarcomere
operating length
(80%–120% of
resting length)
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Figure 9.22
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Figure 9.6
Regulation of Stroke Volume
• Preload: degree of stretch of cardiac muscle cells
before they contract (Frank-Starling law of the heart)
• Cardiac muscle exhibits a length-tension relationship
• At rest, cardiac muscle cells are shorter than optimal
length
• Slow heartbeat and exercise increase venous return
• Increased venous return distends (stretches) the
ventricles and increases contraction force
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Regulation of Stroke Volume
• Afterload: pressure that must be overcome
for ventricles to eject blood
• Hypertension increases afterload, resulting in
increased ESV and reduced SV
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Regulation of Stroke Volume
• Contractility: contractile strength at a given muscle
length, independent of muscle stretch and EDV
• Positive inotropic agents increase contractility
• Increased Ca2+ influx due to sympathetic stimulation
• Hormones (thyroxine, glucagon, and epinephrine)
• Negative inotropic agents decrease contractility
• Acidosis
• Increased extracellular K+
• Calcium channel blockers
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Extracellular fluid
Norepinephrine
Adenylate cyclase
Ca2+
b1-Adrenergic
receptor
G protein (Gs)
Ca2+
channel
ATP is converted
Cytoplasm
to cAMP
a
GDP
Inactive protein
kinase A
Enhanced
actin-myosin
interaction
Troponin
Cardiac muscle
force and velocity
Copyright © 2010 Pearson Education, Inc.
Phosphorylates SR Ca2+ channels,
increasing intracellular Ca2+
b
release
binds Ca2+
to
Active
Phosphorylates
plasma membrane
Ca2+ channels,
increasing extracellular Ca2+ entry
protein
kinase A
Phosphorylates SR Ca2+
pumps, speeding Ca2+
c
removal and relaxation
Ca2+
Ca2+ uptake
pump
SR Ca2+
channel
Sarcoplasmic
reticulum (SR)
Figure 18.21
Aorta S – 100 – 140
D – 60 - 80
Left atrium 4 - 12
S 20 – 30
D 6 -10
O – 7 mmHg
S – systolic
D- diastolic
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S 100 – 140 D 4 - 12
S 20 – 30
D 0-7
Numbers in mm mercury pressure
Regulation of Heart Rate
• Positive chronotropic factors increase heart
rate
• Negative chronotropic factors decrease heart
rate
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Autonomic Nervous System Regulation
• Sympathetic nervous system is activated by
emotional or physical stressors
• Norepinephrine causes the pacemaker to fire
more rapidly (and at the same time increases
contractility)
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Autonomic Nervous System Regulation
• Parasympathetic nervous system opposes
sympathetic effects
• Acetylcholine hyperpolarizes pacemaker cells
by opening K+ channels
• The heart at rest exhibits vagal tone
(parasympathetic)
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Autonomic Nervous System Regulation
• Atrial (Bainbridge) reflex: a sympathetic reflex
initiated by increased venous return
• Stretch of the atrial walls stimulates the
SA node
• Also stimulates atrial stretch receptors
activating sympathetic reflexes
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Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
Heart rate
(allows more
time for
ventricular
filling)
Bloodborne
epinephrine,
thyroxine,
excess Ca2+
Venous
return
Contractility
EDV
(preload)
ESV
Exercise,
fright, anxiety
Sympathetic
activity
Parasympathetic
activity
Heart
rate
Stroke
volume
Cardiac
output
Initial stimulus
Physiological response
Result
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Figure 18.22
Chemical Regulation of Heart Rate
1. Hormones
•
Epinephrine from adrenal medulla enhances
heart rate and contractility
•
Thyroxine increases heart rate and enhances
the effects of norepinephrine and
epinephrine
2. Intra- and extracellular ion concentrations
(e.g., Ca2+ and K+) must be maintained for
normal heart function
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Other Factors that Influence Heart Rate
• Age
• Gender
• Exercise
• Body temperature
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Homeostatic Imbalances
• Tachycardia: abnormally fast heart rate
(>100 bpm)
• If persistent, may lead to fibrillation
• Bradycardia: heart rate slower than 60 bpm
• May result in grossly inadequate blood
circulation
• May be desirable result of endurance training
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Congestive Heart Failure (CHF)
• Progressive condition where the CO is so low
that blood circulation is inadequate to meet
tissue needs
• Caused by
• Coronary atherosclerosis
• Persistent high blood pressure
• Multiple myocardial infarcts
• Dilated cardiomyopathy (DCM)
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Developmental Aspects of the Heart
• Embryonic heart chambers
• Sinus venous
• Atrium
• Ventricle
• Bulbus cordis
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Arterial end
4a
4
3
2
1
Tubular
heart
Arterial end
Ventricle
Atrium
Ventricle
Venous end
(a) Day 20:
(b) Day 22: (c) Day 24: Heart
Endothelial
Heart
continues to
tubes begin
starts
elongate and
to fuse.
pumping.
starts to bend.
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Aorta
Superior
vena
cava
Venous end
Inferior
vena cava
(d) Day 28: Bending
continues as ventricle
moves caudally and
atrium moves cranially.
Ductus
arteriosus
Pulmonary
trunk
Foramen
ovale
Ventricle
(e) Day 35: Bending
is complete.
Figure 18.23
Developmental Aspects of the Heart
• Fetal heart structures that bypass pulmonary
circulation
• Foramen ovale connects the two atria
• Ductus arteriosus connects the pulmonary
trunk and the aorta
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Developmental Aspects of the Heart
• Congenital heart defects
• Lead to mixing of systemic and pulmonary
blood
• Involve narrowed valves or vessels that
increase the workload on the heart
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Narrowed
aorta
Occurs in
about 1 in
every
500 births
(a) Ventricular septal defect.
The superior part of the interventricular septum fails to
form; thus, blood mixes
between the two ventricles.
More blood is shunted from
left to right because the left
ventricle is stronger.
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Occurs in
about 1 in
every 1500
births
(b) Coarctation of the
aorta. A part of the
aorta is narrowed,
increasing the workload
of the left ventricle.
Occurs in
about 1 in
every 2000
births
(c) Tetralogy of Fallot.
Multiple defects (tetra =
four): (1) Pulmonary trunk
too narrow and pulmonary
valve stenosed, resulting
in (2) hypertrophied right
ventricle; (3) ventricular
septal defect; (4) aorta
opens from both ventricles.
Figure 18.24
Age-Related Changes Affecting the Heart
• Sclerosis and thickening of valve flaps
• Decline in cardiac reserve
• Fibrosis of cardiac muscle
• Atherosclerosis
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