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Heart 2
THE CARDIOVASCULAR SYSTEM
Cardiac muscle
Striated
Short
Wide
Branched
Interconnected
Skeletal muscle
Striated
Long
Narrow
Cylindrical
PROPERTIES OF CARDIAC MUSCLE
Intercalated discs passage of ions
Numerous large mitochondria
25–35% of cell volume
Able to utilize many food molecules
Example: lactic acid
PROPERTIES OF CARDIAC MUSCLE
Figure 18.11a
Nucleus
Desmosomes Gap junctions
Intercalated discs Cardiac muscle cell
(a)
Figure 18.11b
Nucleus
Nucleus
I band A band
Cardiac
muscle cell
Sarcolemma
Z disc
Mitochondrion
Mitochondrion
T tubule
Sarcoplasmic
reticulum
I band
Intercalated
disc
(b)
Some cells are myogenic
Heart contracts as a unit or not at all
Sodium channels leak slowly in specialized cells
Spontaneous deoplarization
Compare to skeletal muscle
PROPERTIES OF CARDIAC MUSCLE
Figure 18.13
1 2 3 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.
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
Te
nsio
n (g
)
Me
mb
ra
ne
p
ote
ntia
l (m
V)
Action Potential of Contractile Cardiac Muscle Cells
Terms
Systole versus diastole
Specialized cardiac cells
Initiate impulse
Conduct impulse
CONDUCTION SYSTEM OF THE HEART
Conduction pathway
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
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
1. Sinoatrial (SA) node (pacemaker)
Generates impulses about 70-75 times/minute (sinus rhythm)
Depolarizes faster than any other part of the myocardium
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
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 cardiac
nerves increase heart rate and force of contraction.
Medulla oblongata
Sympathetic trunk ganglion
Dorsal motor nucleus of vagus
Sympathetic trunk
AV node
SA node Parasympathetic fibers
Sympathetic fibers
Interneurons
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, initiated by the SA node, causes the P wave.
P
R
T
Q S
SA node
AV node
With atrial depolarization complete, the impulse is delayed at the AV node.
Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs.
P
R
T
Q S
P
R
T
Q S
Ventricular depolarization is complete.
Ventricular repolarization begins at apex, causing the T wave.
Ventricular repolarization is complete.
P
R
T
Q S
P
R
T
Q S
P
R
T
Q S
Depolarization Repolarization
1
2
3
4
5
6
Figure 18.18
(a) Normal sinus rhythm.
(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.
(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.
All events associated with blood flow through the
heart during one complete heartbeat
Systole—contraction (ejection of blood)
Diastole—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 > aortic 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 Open Closed
Closed Closed Open
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
1 1 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
Ve
ntric
ula
r
vo
lu
me
(m
l)
Pre
ssu
re
(m
m H
g)
EKG
Pressure
changes
Changes in
volume
Contraction
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 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
Figure 18.20
1 2a 2b 3
Atrioventricular valves
Aortic and pulmonary valves
Open Open Closed
Closed Closed Open
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
1 1 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
Ve
ntric
ula
r
vo
lu
me
(m
l)
Pre
ssu
re
(m
m H
g)
Pressure
changes
Changes in
volume
Mitral Stenosis
HEART SOUNDS
Valvular insufficiency (regurgitation)
HEART SOUNDS
Definition: volume of blood pumped by each ventricle
in one minute
Minute volume
2 major factors
Stroke volume
Heart rate
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
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 Open Closed
Closed Closed Open
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
1 1 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
Ve
ntric
ula
r
vo
lu
me
(m
l)
Pre
ssu
re
(m
m H
g)
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)
If you increase stroke volume what would happen to
cardiac output?
Remember: CO = HR x SV
THOUGHT QUESTION
Stroke Volume
Three main factors affect SV
Preload
Contractility
Afterload
REGULATION OF STROKE VOLUME
Preload
Frank-Starling law of the heart
Degree of stretch of cardiac muscle cells before they
contract
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
REGULATION OF STROKE VOLUME
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 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
Parasympathetic nervous system
Vagus nerve
Decreases HR
Who dominates at rest?
CONTROL OF HEART RATE
Figure 18.22
Venous return
Contractility Sympathetic
activity Parasympathetic
activity
EDV (preload)
Stroke volume
Heart rate
Cardiac output
ESV
Exercise (by skeletal muscle and respiratory pumps;
see Chapter 19)
Heart rate (allows more
time for ventricular
filling)
Bloodborne epinephrine,
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 cardiac
nerves increase heart rate and force of contraction.
Medulla oblongata
Sympathetic trunk ganglion
Dorsal motor nucleus of vagus
Sympathetic trunk
AV node
SA node Parasympathetic fibers
Sympathetic fibers
Interneurons
Other factors…
CONTROL OF HEART RATE
QUESTIONS?