Download Properties of cardiac muscle Properties of Cardiac Muscle

3/1/2016
Properties of cardiac muscle
• Cardiac muscle
–Striated
–Short
–Wide
–Branched
–Interconnected
The Cardiovascular System
Part 2
Nucleus
Properties of Cardiac Muscle
• Skeletal muscle
–Striated
–Long
–Narrow
–Cylindrical
Intercalated discs
Cardiac muscle cell
• Cells connected to each other by intercalated discs
– Passage of ions between cells
– Allows entire heart to work as a syncytium
• Numerous large mitochondria
Gap junctions
–25–35% of cell volume
–Increases cell capacity to do what?
Desmosomes
• Able to utilize many food molecules
–Example: lactic acid
–Most cells primarily use what?
(a)
Figure 18.11a
Properties of cardiac muscle
Cardiac
muscle cell
Mitochondrion
Intercalated
disc
Nucleus
• 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
T tubule
Mitochondrion
Sarcoplasmic
reticulum
Z disc
Nucleus
Sarcolemma
(b)
I band
A band
– Sympathetic or PNS?
– Because cells are joined by gap junctions, spontaneous
depolarization of pacemaker cells initiates depolarization of
contractile cells too
I band
Figure 18.11b
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Action Potential in Myogenic Cells of the Heart
Properties of cardiac muscle
Threshold
Action
potential
2
• Heart contracts as a unit or not at all (video)
2
3
– Sodium channels leak slowly in specialized cells
• Spontaneous depolarization
• Leakage rate sets rhythm
1
– Compare to skeletal muscle
1 Pacemaker 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.
Pacemaker
potential
2 Depolarization The
action potential begins when
the pacemaker potential
reaches threshold.
Depolarization is due to Ca2+
influx through Ca2+ channels.
1
3 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.
Figure 18.13
Action Potential of Contractile Cardiac Muscle Cells
2
Tension
development
(contraction)
3
1
Absolute
refractory
period
Time (ms)
Allows sufficient refilling
of the heart before the next beat
Tension (g)
Membrane potential (mV)
Action
potential
Plateau
1 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.
2 Plateau phase is
due to Ca2+ influx through
slow Ca2+ channels. This
keeps the cell depolarized
because few K+ channels
are open.
Conduction System of the Heart
• Terms
– Systole
• Contraction of ventricles
– Diastole
• Relaxation of ventricles
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
Conduction System of the Heart
Conduction system of the heart
• Specialized cardiac cells
SA node (pacemaker)
– Initiate impulse
– Conduct impulse
Atrial depolarization and contraction
AV node
Bundle of His
Right and left bundle branches
Purkinje fibers
Myocardium
Contraction of ventricles
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Conduction System of the Heart
Conduction system of the heart
3. Atrioventricular (AV) bundle (bundle of His)
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
– 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
2. Atrioventricular (AV) node
–
–
5. Purkinje fibers
Delays impulses approximately 0.1 second
Depolarizes 50 times per minute in absence of SA node
input
–
Superior vena cava
Conduction Pathway
Complete the pathway into the apex and ventricular
walls
Conduction System of the heart
Right atrium
1 The sinoatrial (SA)
node (pacemaker)
generates impulses.
• Intrinsic innervation
• External influences
Internodal pathway
Left atrium
2 The impulses
• Normal:
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.
– Average = 70 bpm
– Range = 60-100 bpm
Purkinje
fibers
Interventricular
septum
5 The Purkinje fibers
depolarize the contractile
cells of both ventricles.
(a) Anatomy of the intrinsic conduction system showing the
sequence of electrical excitation
(Intrinsic Innervation)
Figure 18.14a
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Conduction System of the heart
Medulla oblongata
Cardioacceleratory
center
• Sympathetic stimulation
– Enhances Ca2+ movement in contractile cells
– Increases HR, contractility
Sympathetic trunk ganglion
Thoracic spinal cord
Sympathetic trunk
Sympathetic cardiac
nerves increase heart rate
and force of contraction.
• Stroke volume decreases due to less ventricular filling time
– Speeds relaxation
AV node
SA node
Parasympathetic fibers
Sympathetic fibers
Interneurons
Figure 18.15
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Conduction System of the heart
Conduction System of the heart
• 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
• 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
Homeostatic Imbalances
Electrocardiography
• A composite of all the action potentials generated by nodal
and contractile cells at a given time
Defects in the intrinsic conduction system may
result in
1.
2.
3.
4.
– Represents movement of ions = bioelectricity
– Three waves
Arrhythmias: irregular heart rhythms
Bradycardia < 60 bpm
Tachycardia >100 bpm
Maximum is about 300 bpm
1.
2.
3.
P wave: electrical depolarization of atria
QRS complex: ventricular depolarization
T wave: ventricular repolarization
SA node
Depolarization
R
QRS complex
Sinoatrial
node
T
P
S
1 Atrial depolarization, initiated
by the SA node, causes the
P wave.
Ventricular
depolarization
Ventricular
repolarization
R
AV node
T
P
Q
Atrial
depolarization
Repolarization
R
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.
Atrioventricular
node
R
Q
S
5 Ventricular repolarization
begins at apex, causing the
T wave.
R
P-Q
Interval
S-T
Segment
T
P
T
P
Q-T
Interval
Q
S
3 Ventricular depolarization
begins at apex, causing the
QRS complex. Atrial
repolarization occurs.
Figure 18.16
Q
S
6 Ventricular repolarization
is complete.
Figure 18.17
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NORMAL HEART RHYTHM
ARRHYTHMIAS
(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.
(a) Normal sinus rhythm.
Figure 18.18
Figure 18.18
ARRHYTHMIAS
ARRHYTHMIAS
(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.
(d) Ventricular fibrillation. These
chaotic, grossly irregular ECG
deflections are seen in acute
heart attack and electrical shock.
Video
Figure 18.18
Figure 18.18
ARRHYTHMIAS
ARRHYTHMIAS
Atrial
fibrillation
Normal
Atrial fibrillation . Rapid, irregular heartbeat. Note the
absence of P waves (which represent depolarization of
the top of the heart)
Normal
Atrial fibrillation
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The Cardiac Cycle
• 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
Left heart
The cardiac cycle
QRS
P
Electrocardiogram
EKG
T
1st
Heart sounds
P
2nd
– Backpressure closes AV valves = isovolumetric
contraction
– Ventricular pressure becomes greater than aorta &
pulmonary artery pressure = semilunar valves open
Pressure
changes
Aorta
Left ventricle
Atrial systole
Left atrium
Control of blood flow
Ventricular
volume (ml)
• Ventricular filling → ventricular systole
Pressure (mm Hg)
Dicrotic notch
Changes in
volume
EDV
SV
ESV
• Portion of ventricular contents ejected
Atrioventricular valves
Open
Aortic and pulmonary valves
Closed
Phase
Contraction
1
Closed
Open
Open
2a
2b
Closed
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
Heart Sounds
• 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
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
Figure 18.19
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Left heart
Heart sounds
Heart Sounds
QRS
P
Electrocardiogram
P
T
1st
2nd
Pressure (mm Hg)
Dicrotic notch
Changes in
volume
• Mitral stenosis
Aorta
Left ventricle
Atrial systole
Ventricular
volume (ml)
Pressure
changes
Left atrium
EDV
SV
ESV
Atrioventricular valves
Open
Aortic and pulmonary valves
Closed
Phase
1
Closed
Open
Open
2a
2b
Closed
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
Heart sounds
• Valvular insufficiency (regurgitation)
Cardiac Output (CO)
• Definition: volume of blood pumped by each ventricle in one
minute
– AKA: Minute volume
• 2 major factors
– Stroke volume (SV)
– Heart rate (HR)
Heart Sounds
• Example: mitral valve prolapse
Cardiac output
• 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)
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Left heart
Cardiac output
QRS
P
Electrocardiogram
EKG
T
1st
Heart sounds
P
2nd
• Stroke volume
– Difference between EDV and ESV
Pressure (mm Hg)
Dicrotic notch
Pressure
changes
Aorta
Left ventricle
Atrial systole
Left atrium
• EDV-ESV=SV
Ventricular
volume (ml)
– Average is about 75 ml
Changes in
volume
EDV
SV
ESV
Atrioventricular valves
Open
Aortic and pulmonary valves
Closed
Phase
1
Closed
Open
Open
2a
2b
Closed
3
1
Left atrium
Right atrium
Left ventricle
Right ventricle
Ventricular
filling
Atrial
contraction
1
Ventricular filling
(mid-to-late diastole)
Isovolumetric
contraction phase
2a
Ventricular
ejection phase
2b
Ventricular systole
(atria in diastole)
Isovolumetric
relaxation
3
Ventricular
filling
Early diastole
Figure 18.20
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
– CO may reach 30 L/min in trained athletes
– Cardiac reserve
Regulation of stroke volume
• Stroke volume
– Three main factors affect SV
• Preload
• Contractility
• Afterload
• Difference between resting and maximal CO
Regulation of Stroke Volume
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
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Regulation of Stroke Volume
Regulation of Stroke Volume
• Contractility
• Afterload
– Contractile strength at a given muscle length, independent of
muscle stretch and EDV
– Pressure (resistance) that must be overcome for ventricles to eject
blood
• Agents increasing contractility
• Hypertension increases afterload
– Increased Ca2+ influx
» Sympathetic stimulation
– Results in increased ESV and reduced SV
Increase SV
Decrease ESV
– Hormones
» Thyroxin, glucagon, and epinephrine
• Agents decreasing contractility
– Calcium channel blockers
Control of Heart rate
Exercise (by
skeletal muscle and
respiratory pumps;
see Chapter 19)
• Sympathetic nervous system
– Norepinephrine
• Increased SA node firing rate
• Faster conduction through AV node
• Increases excitability of heart by increasing Ca2+ availability
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
• Parasympathetic nervous system
– Vagus nerve
Heart
rate
Stroke
volume
• Decreases HR
Cardiac
output
Who dominates at rest?
Initial stimulus
Physiological response
Result
Figure 18.22
The vagus nerve
(parasympathetic)
decreases heart rate.
Dorsal motor nucleus of vagus
Cardioinhibitory center
Control of heart rate
Medulla oblongata
Cardioacceleratory
center
• Other factors…
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
Figure 18.15
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Cardiac Output
Cardiac output
Heart rate
Stroke volume
Usually set by SA
node
Preload
Contractility
Afterload
Autonomic
nervous system
(among other things)
Rate of venous
return
Ca2+, hormones
Blood pressure
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