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3/1/2016
1
Part 2
The Cardiovascular System
• Cardiac muscle
–Striated
–Short
–Wide
–Branched
–Interconnected
• Skeletal muscle
–Striated
–Long
–Narrow
–Cylindrical
Properties of cardiac muscle
• Cells connected to each other by intercalated discs
– Passage of ions between cells
– Allows entire heart to work as a syncytium
• Numerous large mitochondria
–25–35% of cell volume
–Increases cell capacity to do what?
• Able to utilize many food molecules
–Example: lactic acid
–Most cells primarily use what?
Properties of Cardiac Muscle
Figure 18.11a
Nucleus
DesmosomesGap junctions
Intercalated discs Cardiac muscle cell
(a)
Figure 18.11b
Nucleus
Nucleus
I bandA band
Cardiac
muscle cell
Sarcolemma
Z disc
Mitochondrion
Mitochondrion
T tubule
Sarcoplasmic
reticulum
I band
Intercalated
disc
(b)
• Some cells are myogenic
– Contractile impulse originates in non-contractile pacemaker cells,
not in nerve cells
• Cardiac control center in medulla can increase or decrease rate
through ANS
• Primary innervation is inhibitory through vagus nerve
– Sympathetic or PNS?
–Because cells are joined by gap junctions, spontaneous
depolarization of pacemaker cells initiates depolarization of
contractile cells too
Properties of cardiac muscle
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2
• Heart contracts as a unit or not at all (video)
–Sodium channels leak slowly in specialized cells
• Spontaneous depolarization
• Leakage rate sets rhythm
–Compare to skeletal muscle
Properties of cardiac muscle
Figure 18.13
1 2 3Pacemaker potential
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.
Depolarization The
action potential begins when
the pacemaker potential
reaches threshold.
Depolarization is due to Ca2+
influx through Ca2+ channels.
Repolarization is due to
Ca2+ channels inactivating and
K+ channels opening. This
allows K+ efflux, which brings
the membrane potential back
to its most negative voltage.
Action
potential
Threshold
Pacemaker
potential
1 1
2 2
3
Action Potential in Myogenic Cells of the Heart
Figure 18.12
Absolute
refractory
period
Tension
development
(contraction)
Plateau
Action
potential
Time (ms)
1
2
3
Depolarization is
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.
Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
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.
1
2
3
Tensio
n (
g)
Me
mb
ra
ne
po
ten
tia
l (m
V)
Action Potential of Contractile Cardiac Muscle Cells
Allows sufficient refilling
of the heart before the next beat
• Terms
– Systole
• Contraction of ventricles
– Diastole
• Relaxation of ventricles
Conduction System of the Heart
• Specialized cardiac cells
– Initiate impulse
– Conduct impulse
Conduction System of the Heart
SA node (pacemaker)
Atrial depolarization and contraction
AV node
Bundle of His
Right and left bundle branches
Purkinje fibers
Myocardium
Contraction of ventricles
Conduction system of the heart
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1. Sinoatrial (SA) node (pacemaker)
– Generates impulses about 70-75 times/minute (sinus rhythm)
– Depolarizes faster than any other part of the myocardium
– Cut the vagus nerve = HR immediately increases by ~25bpm
2. Atrioventricular (AV) node
– Delays impulses approximately 0.1 second
– Depolarizes 50 times per minute in absence of SA node input
Conduction System of the Heart
3. Atrioventricular (AV) bundle (bundle of His)– Only electrical connection between the atria and
ventricles
4. Right and left bundle branches– Two pathways in the interventricular septum that
carry the impulses toward the apex of the heart
5. Purkinje fibers– Complete the pathway into the apex and ventricular
walls
Conduction system of the heart
Figure 18.14a
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
(Intrinsic Innervation)
Internodal pathway
Superior vena cava
Right atrium
Left atrium
Purkinje
fibers
Inter-
ventricular
septum
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
2 The impulses
pause (0.1 s) at the
atrioventricular
(AV) node.
The atrioventricular
(AV) bundle
connects the atria
to the ventricles.
4 The bundle branches
conduct the impulses
through the
interventricular septum.
3
The Purkinje fibers
depolarize the contractile
cells of both ventricles.
5
Conduction Pathway
• Intrinsic innervation
• External influences
• Normal:
– Average = 70 bpm
– Range = 60-100 bpm
Conduction System of the heart
Figure 18.15
Thoracic spinal cord
The vagus nerve (parasympathetic) decreases heart rate.
Cardioinhibitory center
Cardio-
acceleratory
center
Sympathetic cardiacnerves increase heart rateand force of contraction.
Medulla oblongata
Sympathetic trunk ganglion
Dorsal motor nucleus of vagus
Sympathetic trunk
AV node
SA nodeParasympathetic fibers
Sympathetic fibers
Interneurons
• Sympathetic stimulation
– Enhances Ca2+ movement in contractile cells
– Increases HR, contractility
• Stroke volume decreases due to less ventricular filling time
– Speeds relaxation
Conduction System of the heart
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4
• Parasympathetic stimulation
– Dominant signal under resting conditions
– Cardiac response mediated by acetylcholine
– Opens K+ channels, hyperpolarizes cells
– Decreases HR
– Innervation of ventricles is sparse = little effect on contractility
Conduction System of the heart
• Other influences
– Blood pressure
– Atrial reflex
• Increased rate of blood returning to heart -> atrial stretching ->
increased HR
– Hormonal
• Epinephrine, thyroxine = increase HR
– Ion balance
– Exercise
– Temperature
– Exercise
– Age
Conduction System of the heart
Defects in the intrinsic conduction system may
result in
1. Arrhythmias: irregular heart rhythms
2. Bradycardia < 60 bpm
3. Tachycardia >100 bpm
4. Maximum is about 300 bpm
Homeostatic Imbalances
• A composite of all the action potentials generated by nodal
and contractile cells at a given time
– Represents movement of ions = bioelectricity
– Three waves
1. P wave: electrical depolarization of atria
2. QRS complex: ventricular depolarization
3. T wave: ventricular repolarization
Electrocardiography
Figure 18.16
Sinoatrial
node
Atrioventricular
node
Atrial
depolarization
QRS complex
Ventricular
depolarization
Ventricular
repolarization
P-Q
Interval
S-T
Segment
Q-T
Interval
Figure 18.17
Atrial depolarization, initiatedby the SA node, causes theP wave.
P
R
T
QS
SA node
AV node
With atrial depolarizationcomplete, the impulse isdelayed at the AV node.
Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.
P
R
T
QS
P
R
T
QS
Ventricular depolarizationis complete.
Ventricular repolarizationbegins at apex, causing theT wave.
Ventricular repolarizationis complete.
P
R
T
QS
P
R
T
QS
P
R
T
QS
Depolarization Repolarization
1
2
3
4
5
6
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Figure 18.18
(a) Normal sinus rhythm.
NORMAL HEART RHYTHM
Figure 18.18
(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.
ARRHYTHMIAS
Figure 18.18
(c) Second-degree heart block.
Some P waves are not conducted
through the AV node; hence more
P than QRS waves are seen. In
this tracing, the ratio of P waves
to QRS waves is mostly 2:1.
ARRHYTHMIAS
Figure 18.18
(d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
deflections are seen in acute
heart attack and electrical shock.
ARRHYTHMIAS
Video
Atrial fibrillation . Rapid, irregular heartbeat. Note the
absence of P waves (which represent depolarization of
the top of the heart)
ARRHYTHMIAS
Atrial
fibrillation
Normal
Normal Atrial fibrillation
ARRHYTHMIAS
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6
• All events associated with blood flow through the heart
during one complete heartbeat
–Systole— ventricular contraction (ejection of blood)
–Diastole— ventricular relaxation (receiving of
blood)
The Cardiac Cycle
• Three events
1) Recordable bioelectrical disturbances (EKG)
2) Contraction of cardiac muscle
3) Generation of pressure and volume changes
• Blood flows from areas of higher pressure to areas of lower
pressure
– Valves prevent backflow
The Cardiac Cycle
• Ventricular filling → ventricular systole
– Backpressure closes AV valves = isovolumetric
contraction
– Ventricular pressure becomes greater than aorta &
pulmonary artery pressure = semilunar valves open
• Portion of ventricular contents ejected
The cardiac cycle
Figure 18.20
1 2a 2b 3
Atrioventricular valves
Aortic and pulmonary valves
Open OpenClosed
Closed ClosedOpen
Phase
ESV
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Ventricular filling
(mid-to-late diastole)
Ventricular systole
(atria in diastole)
Isovolumetric
contraction phase
Ventricular
ejection phase
Early diastole
Isovolumetric
relaxation
Ventricular
filling
11 2a 2b 3
Electrocardiogram
Left heart
P
1st 2nd
QRS
P
Heart sounds
Atrial systole
Dicrotic notch
Left ventricle
Left atrium
EDV
SV
Aorta
T
Ventric
ula
r
volu
me (
ml)
Pressure (
mm
Hg)
EKG
Pressure
changes
Changes in
volume
Contraction
Control of blood flow
• Two sounds associated with closing of heart valves
–First sound occurs as AV valves close and signifies
beginning of systole = Lub
–Second sound occurs when SL valves close at the
beginning of ventricular diastole = Dub
• Heart murmurs = abnormal heart sounds
– Most often indicative of valve problems
Heart Sounds
Figure 18.19
Tricuspid valve sounds typically heard in right sternal margin of 5th intercostal space
Aortic valve sounds heard in 2nd intercostal space atright sternal margin
Pulmonary valvesounds heard in 2ndintercostal space at leftsternal margin
Mitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle
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Figure 18.20
1 2a 2b 3
Atrioventricular valves
Aortic and pulmonary valves
Open OpenClosed
Closed ClosedOpen
Phase
ESV
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Ventricular filling
(mid-to-late diastole)
Ventricular systole
(atria in diastole)
Isovolumetric
contraction phase
Ventricular
ejection phase
Early diastole
Isovolumetric
relaxation
Ventricular
filling
11 2a 2b 3
Electrocardiogram
Left heart
P
1st 2nd
QRS
P
Heart sounds
Atrial systole
Dicrotic notch
Left ventricle
Left atrium
EDV
SV
Aorta
T
Ventric
ula
r
volu
me (
ml)
Pressure (
mm
Hg)
Pressure
changes
Changes in
volume
• Mitral stenosis
Heart Sounds
• Valvular insufficiency (regurgitation)
Heart sounds
• Example: mitral valve prolapse
Heart Sounds
• Definition: volume of blood pumped by each ventricle in one
minute
– AKA: Minute volume
• 2 major factors
– Stroke volume (SV)
– Heart rate (HR)
Cardiac Output (CO)
• CO (ml/min) = 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 (ml/min)
Cardiac output
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8
• Stroke volume
– Difference between EDV and ESV
• EDV-ESV=SV
– Average is about 75 ml
Cardiac output
Figure 18.20
1 2a 2b 3
Atrioventricular valves
Aortic and pulmonary valves
Open OpenClosed
Closed ClosedOpen
Phase
ESV
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
Ventricular filling
(mid-to-late diastole)
Ventricular systole
(atria in diastole)
Isovolumetric
contraction phase
Ventricular
ejection phase
Early diastole
Isovolumetric
relaxation
Ventricular
filling
11 2a 2b 3
Electrocardiogram
Left heart
P
1st 2nd
QRS
P
Heart sounds
Atrial systole
Dicrotic notch
Left ventricle
Left atrium
EDV
SV
Aorta
T
Ventric
ula
r
volu
me (
ml)
Pressure (
mm
Hg)
EKG
Pressure
changes
Changes in
volume
• 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
– CO may reach 30 L/min in trained athletes
– Cardiac reserve
• Difference between resting and maximal CO
Cardiac Output (CO)
• Stroke volume
– Three main factors affect SV
• Preload
• Contractility
• Afterload
Regulation of stroke volume
• Preload
– Frank-Starling law of the heart: the heart can change its CO
according to the incoming volume of blood
• At rest, cardiac muscle cells are shorter than optimal length
• Must be a degree of stretch of cardiac muscle cells before they contract
–Slow heartbeat and exercise increase venous return
–Increased venous return distends (stretches) the ventricles
and increases contraction force
Regulation of Stroke Volume Regulation of Stroke Volume
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• Contractility
– Contractile strength at a given muscle length, independent of muscle stretch and EDV
• Agents increasing contractility
– Increased Ca2+ influx
» Sympathetic stimulation
– Hormones
» Thyroxin, glucagon, and epinephrine
• Agents decreasing contractility
– Calcium channel blockers
Regulation of Stroke Volume
Increase SV
Decrease ESV
• Afterload
– Pressure (resistance) that must be overcome for ventricles to eject
blood
• Hypertension increases afterload
– Results in increased ESV and reduced SV
Regulation of Stroke Volume
• Sympathetic nervous system
–Norepinephrine
• Increased SA node firing rate
• Faster conduction through AV node
• Increases excitability of heart by increasing Ca2+ availability
• Parasympathetic nervous system
– Vagus nerve
• Decreases HR
Who dominates at rest?
Control of Heart rate
Figure 18.22
Venousreturn
ContractilitySympathetic
activityParasympathetic
activity
EDV(preload)
Strokevolume
Heartrate
Cardiacoutput
ESV
Exercise (byskeletal muscle andrespiratory pumps;
see Chapter 19)
Heart rate(allows more
time forventricular
filling)
Bloodborneepinephrine,
thyroxine,excess Ca2+
Exercise,fright, anxiety
Initial stimulus
Result
Physiological response
Figure 18.15
Thoracic spinal cord
The vagus nerve (parasympathetic) decreases heart rate.
Cardioinhibitory center
Cardio-
acceleratory
center
Sympathetic cardiacnerves increase heart rateand force of contraction.
Medulla oblongata
Sympathetic trunk ganglion
Dorsal motor nucleus of vagus
Sympathetic trunk
AV node
SA nodeParasympathetic fibers
Sympathetic fibers
Interneurons
• Other factors…
Control of heart rate
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10
Cardiac Output
Cardiac output
Stroke volumeHeart rate
Usually set by SA
node
Preload Contractility Afterload
Rate of venous
return
Ca2+, hormones Blood pressureAutonomic
nervous system
(among other things)