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Cardiovascular system – the heart
Copyright © 2010 Pearson Education, Inc.
The cells of the heart
• Two types of cardiac muscle cells that are involved in
a normal heartbeat:
• Specialized muscle cells of the conducting system
• Contractile cells
• The heart is an autonomic system that can work
without neural stimuli – an intrinsic conduction
system.
• The autonomic function of the heart results from:
• The pacemaker function – Autorhythmic cells
• The conductive system that transfer those impulses
throughout the heart
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Properties of Cardiac Muscle
• Aerobic muscle
• No cell division after infancy - growth by hypertrophy
• 99% contractile cells (for pumping)
• 1% autorhythmic cells (set pace)
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Electrical Conduction in Myocardial Cells
Membrane potential
of autorhythmic cel
Membrane potential
of contractile cell
Cells of
SA node
Contractile cell
Intercalated disk
with gap junctions
Depolarizations of autorhythmic cells
rapidly spread to adjacent contractile
cells through gap junctions.
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Figure 14-17
Intrinsic cardiac conduction system – autorhythmic cells
• Have unstable resting potentials/ pacemaker potentials
• constantly depolarized slowly towards AP
• At threshold, Ca2+ channels open
• 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
Autorhythmic Cells
Location
Firing Rate at Rest
SA node
70–80 APs/min*
AV node
40–60 APs/min
Bundle of His
20–40 APs/min
Purkinje fibers
20–40 APs/min
• Cardiac cells are linked by gap junctions
• Fastest depolarizing cells control other cells
• Fastest cells = pacemaker = set rate for rest of heart
* action potentials per minute
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Autorythmic cells - ectopic pacemakers
• Autorythmic cells of the SA node (pacemaker) may be replaced
by ectopic pacemakers
• Ectopic pacemakers – other parts in the heart that can
induce beating
• The ectopic pacemakers may become dominant:
• If their rythmicity increased
• The pacemaker is inhibited/blocked
• The conduction system pathways are blocked
• First to take over will be the AV node
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Cardiac contractile cells
• Depolarization opens voltage-gated fast Na+ channels
in the sarcolemma
• Depolarization wave causes release Ca2+ that causes the
cell contraction
• Depolarization wave also opens slow Ca2+ channels in
the sarcolemma
• Ca2+ surge prolongs the depolarization phase (plateau)
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Electrical Activity: Contractile Cell
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Figure 13.13
Action Potentials
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Table 14-3
Heart Physiology: Sequence of Excitation
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Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5
Depolarization wave
spreads upward from
the apex.
AV node
AV bundle
4
Bundle
branches
Purkinje
fibers
5
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Figure 14-18, steps 1–5
Electrocardiography (ECG or EKG)
• Body fluids are good conductors which allows the
record of the myocardial action potential extracellularly
• EKG pairs of electrodes (leads) one serve as positive
side of the lead and one as the negative
• Potentials (voltage) are being measured between the 2
electrodes
• EKG is the summed electrical potentials generated by
all cells of the heart and gives electrical “view” of 3D
object (different from one action potential)
• EKG shows depolarization and repolarization
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Electrical Activity of Heart
• P wave: atrial depolarization
• QRS complex: ventricular
depolarization and atrial
repolarization
• T wave: ventricular
repolarization
• PQ segment: AV nodal delay
• QT segment: ventricular
systole
• QT interval: ventricular
diastole
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Electrical Activity of Heart – normal values
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Figure 13.16
Correlation between an ECG and electrical
events in the heart
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Electrical Activity
P wave: atrial
depolarization
START
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
QS
Atria contract
T wave:
ventricular
repolarization
R
Repolarization
T
P
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
QS
P
ST segment
R
Q wave
Q
R wave
R
P
QS
R
Ventricles contract
P
Q
P
S wave
QS
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Figure 14-21 (9 of 9)
Homeostatic Imbalances
•
Defects in the intrinsic conduction system may
result in
1. Arrhythmias: irregular heart rhythms
2. Uncoordinated atrial and ventricular contractions
(heart block)
3. Fibrillation: rapid, irregular contractions; useless
for pumping blood
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ECG Arrhythmias: Abnormal Rates
• Sinus rhythm = pace
generated by SA node
• Abnormal rates shown
• Tachycardia = fast
rhythm
• Bradycardia = slow
rhythm
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Figure 13.17 (1 of 4)
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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First and second degree Heart Block
• Slowed/diminished conduction through AV node occurs in
varying degrees
• First degree block
• Increases duration PQ segment
• Increases delay between atrial and ventricular contraction
• Second degree block
• Lose 1-to-1 relationship between P wave and QRS
complex
• Lose 1-to-1 relationship between atrial and ventricular
contraction
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Third Degree Heart Block
Third degree block
• Loss of conduction
through the AV node
• P wave becomes
independent of QRS
• Atrial and ventricular
contractions are
independent
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ECG Arrhythmias: Fibrillation
Ventricular Fibrillation
• Loss of coordination of
electrical activity of
heart
• Death can ensue within
minutes unless
corrected
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Figure 13.17 (4 of 4)
Cardiac Cycle
• Cardiac cycle - The period between the start of one heartbeat and the
beginning of the next.
• refers to all events associated with blood flow through the heart
• During the cycle, each of the four chambers goes through
• Systole – contraction of heart muscle
• Diastole – relaxation of heart muscle
• An average heart beat (HR)/cardiac cycle is 75 bpm. That means that
a cardiac cycle length is about 0.8 second.
• Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation
and ventricular contraction.
• The remaining 0.4 seconds are called the quiescent period which
represent the ventricular relaxation
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Phases of the Cardiac Cycle
1. Ventricular filling — takes place in mid-to-late
diastole
•
AV valves are open
•
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
2. 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
3. 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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Phases of the Cardiac Cycle
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Figure 20.16
Cardiodynamics
• Movements and forces generated during cardiac contractions
• End-diastolic volume (EDV) – the amount of blood in each
ventricle at the end of ventricular diastole (before contraction
begins)
• End-systolic volume (ESV) - the amount of blood remains in
each ventricle at the end of ventricular systole
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Cardiodynamics
• Stroke volume (SV) – The amount of blood that leaves the
heart with each beat or ventricular contraction; EDVESV=SV
• Not all blood ejected
• Normal Adult 70 ml / beat
• Ejection fraction – The percentage of end-diastole blood
actually ejected with each beat or ventricular contraction.
• Normal adult 55-70% (healthy heart)
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Stroke Volume and Cardiac Output
• Cardiac output (CO) – the amount of blood pumped by
each ventricle in one minute.
• Physiologically, CO is an indication of blood flow through
peripheral tissues
• Cardiac output equals heart rate times stroke volume;
Normal CO: Approximately 4-8 liters/minute
CO
Cardiac output
(ml/min)
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SV
HR
=
Heart rate
(beats/min)
X
Stroke
volume
(ml/beat)
Factors Affecting Cardiac Output
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Figure 20.20
Stroke Volume and Heart Rate Determine Cardiac Output
CARDIAC OUTPUT
is a function of
Heart rate
Stroke volume
determined by
determined by
Rate of depolarization
in autorhythmic cells
Force of contraction in
ventricular myocardium
is influenced by
Decreases
Due to
parasympathetic
innervation
Increases
increases
Contractility
Sympathetic
innervation and
epinephrine
increases
End-diastolic
volume
which varies with
Venous constriction
Venous return
aided by
Skeletal muscle
pump
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Respiratory
pump
Figure 14-31
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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• Effect inotropy – (from Greek, meaning fiber) effect
on contractility of the heart
• Effect chronotropy – effect on HR
• Effect dromotropy – Derives from the Greek word
"Dromos", meaning running.
• A dromotropic agent is one which affects the
conduction speed in the AV node
• Sympathetic stimuli has a positive effect (increase) all
• Parasympathetic
(decrease) all
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stimuli
has
a
negative
effect
Heart Rate — Determined by SA Node Firing Rate
• SA node intrinsic firing rate = 100/min
• No extrinsic control on heart, HR = 100
• SA node under control of ANS and hormones
• Rest: parasympathetic dominates, HR = 75
• Excitement: sympathetic takes over, HR increases
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Autonomic Nervous System Regulation
• In healthy conditions, parasympathetic effects dominate and slows
the rate of the pacemaker from 80-100 bpm to a 70-80 bpm.
• The binding of Ach to muscarinic receptors (M2) inhibit NE
release (mechanism by which vagal stimulation override
sympathetic stimulation)
• 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)
• 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 Neurotransmitters Alter Heart Rate
KEY
Integrating center
Cardiovascular
control
center in medulla
oblongata
Efferent path
Effector
Tissue response
Sympathetic neurons
(NE)
Parasympathetic
neurons (Ach)
 1-receptors of
autorhythmic cells
Muscarinic receptors
of autorhythmic cells
Na+ and Ca2+ influx
K+ efflux; Ca2+ influx
Rate of depolarization
Hyperpolarizes cell and
rate of depolarization
Heart rate
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Heart rate
Figure 14-27
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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Pacemaker Function
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Figure 20.22
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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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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Factors Affecting Stroke Volume
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Figure 20.23
Regulation of Stroke Volume
• SV = EDV – ESV
• Three main factors affect SV
• Preload
• Contractility
• Afterload
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Regulation of Stroke Volume
• Preload
• The amount of tension on a muscle before it begins to
contract. The preload of the heart is determined by
the EDV.
• In general, the greater the EDV the larger is the
stroke volume : EDV-ESV=SV
• These relationships is known as the FrankStarling principle/Sterling’s law of the heart :
• The force of cardiac muscle contraction is
proportional to its initial length
• The greater the EDV the larger the preload
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Preload and Stroke Volume
• Frank-Starling law states
• Stroke volume increase as EDV increases
• EDV is affected by venous return
• Venous return is affected by
• Skeletal muscle pump
• Respiratory pump
• Sympathetic innervation
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Factors Affecting stroke volume - Preload/EDV
• Stroke volume is the difference between the EDV and ESV.
Changes in either one can change the stroke volume and
cardiac output:
• The EDV volume is affected by 2 factors:
• The filling time – duration of ventricular diastole;
depends on HR – the faster the HR the shorter is the
available filing time
• The venous return – changes in response to several
changes: cardiac output, blood volume, peripheral
circulation.
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Reminder - Length-tension relationship
• The force of muscle contraction depends on the length
of the sarcomeres before the contraction begins
• On the molecular level, the length reflects the
overlapping between thin and thick filaments
• The tension a muscle fiber can generate is directly
proportional to the number of crossbridges formed
between the filament
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Stroke Volume
• Length-force relationships in intact heart: a Starling
curve
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Figure 14-28
Diastolic filling increased
EDV increase (preload increased)
Cardiac muscle stretch increased
Force of contraction increased
Ejection volume increased
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Regulation of Stroke Volume - Contractility
• Force of ventricular contraction (systole) regardless of
EDV
• Positive inotropic agents increase contractility
• Increased Ca2+ influx due to sympathetic
stimulation
• Hormones (thyroxine and epinephrine)
• Negative inotropic agents decrease contractility
• Increased extracellular K+ (hyperpolarization)
• Calcium channel blockers (decrease calcium
influx)
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Regulation of Stroke Volume - Afterload
• The amount of resistance the ventricular wall must
overcome to eject blood during systole (influenced by
arterial pressure).
• The greater is the afterload, the longer is the period of
isovolumetric contraction (ventricles are contracting
but there is no blood flow), the shorter the duration of
ventricular ejection and the larger the ESV – afterload
increase – stroke volume decrease
• Hypertension increases afterload,
increased ESV and reduced SV
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resulting
in
Factors Influencing Stroke Volume
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Regulation of Cardiac Output
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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 (decreased blood supply
and myocardial cell death)
• Dilated cardiomyopathy (DCM) – heart wall weakens
and can not contract efficiently. Causes are unknown but
sometimes associated with toxins (ex. Chemotherapy),
viral infections, tachycardia and more
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