A&P II (The Cardiovascular System)
kmoore25
110LECTURECh17IIA.ppt*
The cardiac conduction system
Cardiovascular System: The Heart
Chapter 17(II)
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Cells of cardiac conduction system
Pacemaker cells – are concentrated in ►►
Sinoatrial (SA) node – in the wall of right atrium, below
opening of superior vena cava
SA cells generate action potentials at highest rate in the
heart – 60–80 per minute (our heart rate about 72-75/min)
serves as heart pacemaker that initiates heartbeats &
sets heart rate
Atrioventricular (AV) node – in the wall of right atrium,
at junction b/w atrium & ventricle, above tricuspid valve
AV cells generate action potentials at a rate of 40–60
per minute & serve as electrical gateway to ventricles
Conducting cells – pacemaker cells that make pathways
throughout myocardium & can generate action potentials at
lowest rate of about 20/min
Pacemaker cell from the dog heart
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By courtesy of Dr. Protas (Columbia University)
Pathways of cardiac conduction system
Conducting cells ▬►
Internodal pathways – conducting cells that propagate
action potentials to atrial muscle cells
Atrioventricular bundle (bundle of His) – conducting cells
between AV node & ventricular cells
branches of AV bundle – right & left divisions of AV bundle;
enter interventricular septum & spread in ventricular walls
Purkinje fibers – specific pacemaker cells make terminal
portions of AV bundle within walls of left & right ventricles
Purkinje fibers – thicker than other conducting cells & can
transmit action potentials faster than other cells
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There are no fibers in the conduction system
Pacemaker cells with low activity conduct action potentials
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Impulse propagation in conduction system
From SA node, action potentials travel through atria at 1 m/sec
AV node – slows speed of propagation to 0.05 m/sec ▬►
conducting cells here are thin & have few gap junctions
slower speed delays impulse propagation to ventricles for
130 msec ▬► delays the beginning of ventricular
contraction (systole)
this delay allows atria to complete contraction (systole) &
eject required amount of blood into ventricles ▬► entirely
fill ventricles with blood during their diastole
AV bundle & Purkinje fibers – speed up signal propagation
to ventricular cells to 4 m/sec
ventricular contraction (systole) begins at apex & moves up
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Pacemaker cells & sinus rhythm
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Action potentials in cardiac pacemaker cell (to remind)
repolarization
depolarization
level of the resting membrane potential
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Action potentials in contractile cardiac muscle cell
Contractile cardiac muscle cells – have stable resting
membrane potential of –80 mV
At threshold –75 mV, voltage-gated Na+ channels open
Na+ rushes into cell, causing rapid depolarization; action
potential peaks at +20 mV; Na+ channels close quickly ►►
However, depolarization continues for 200 msec longer,
making plateau, due to slow influx of Ca2+
Plateau extends ventricular contraction – so ventricles have
enough time to eject required amount of blood
Repolarization – Ca2+ channels close, K+ voltage-gated
channels open & K+ outflow returns membrane to resting level
Excitation-contraction coupling – action potentials spread to
sarcoplasmic reticulum, open Ca2+ channels there, Ca2+ enter
cytoplasm, cytoplasmic Ca2+ increases & contraction starts
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Action potentials of a cardiac ventricular cell
-100
-80
-40
-60
+20
0
-20
2
3
4
0
1
Membrane Potential
(mV)
seconds
phase 0 – fast voltage-gated Na+ channels open
phase 1 – Na+ channels close
phase 2 – slow voltage-gated Ca++ channels open
phase 3 – slow voltage-gated K+ channels open
phase 4 – return to the resting membrane potential
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Contractile cell action potential
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- Plateau in action potential of contractile cells lengthens
absolute refractory period of cardiac muscle to 200-250 ms
- during this time, cardiac muscle cells can not contract ►►
- Cardiac muscle has enough time to relax before next
contraction ▬► heart is protected against summation &
tetanus
Refractory period of cardiac muscle
10-15 msec
200-250 msec
What is highest
possible heart
rate?
240-300/min
mV
SKELETAL
MUSCLE
CARDIAC
MUSCLE
Action potential
mV
Contraction
Tension
Time (msec)
Time (msec)
Contraction
Tension
Action
potential
Absolute refractory
period
Relative refractory
period
Action potential, contraction
& refractory period in skeletal & cardiac muscle cells
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duration of action potential ~300 ms; duration of contraction ~170 ms
duration of action potential ~15 ms; duration of contraction ~25 ms
Complete tetanus
Stimulus frequency is so high that
relaxation phase is eliminated &
tension plateaus at maximal levels.
Incomplete tetanus
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Your take-home (“prerequisite”) test is on “Canvas”, in the folder
“Quizzes”
You may take the test between 12:00 PM (noon) Sunday, January
26, and 11:59 PM Tuesday, January 28 ONLY
Make sure your computer and Internet work properly
There are 35 questions on material of Chapters 10, 11, 14 in the
test (see p. 4 in my syllabus)
After you open the test, you have one attempt ONLY to complete
and submit it
You can see one question at a time
You cannot go back to a previous question and change your
answer
You have 40 min to answer all questions and submit the test
Don't forget to click the "Submit" button after the test is
completed
You can see your result and correct answers between 8:00 AM
and 11:59 PM Wednesday, January 29
Take-home Test
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Recording electrocardiogram
ECG – summation of
all action potentials of
nodal & myocardial cells
recorded by electrodes
on arms, legs & chest
Electrical changes are
seen as ECG waves
ECG is recorded with
electrocardiograph
Most obvious
changes in heart seen
in ECG is disturbances
in electrical rhythm –
arrhythmia
Electrocardiogram (ECG, EKG) – graphic representation of
changes in electrical activity in the whole cardiac muscle
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ECG waves, intervals, segments
- Waves – P wave, QRS complex, T wave
- periods between waves – represent action potential
phases & spread of electrical activity through heart
Intervals – include a
component of at least
one wave: R-R interval,
P-R interval, Q-T
interval
Segments – do not
include any wave
components: ST
segment
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P wave – depolarization of
atrial cells, except SA node
QRS complex –cells in
ventricles depolarize
T wave – ventricular
repolarization
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onset of pain; beginning of MI
1 hr later; onset of necrosis
inverted T; sign of reperfusion
24 hrs later; ST returned to iso-electric line; T stays inverted
EKG looks normal; deep Q indicates dead myocardium; will remain in EKG
recent myocardial wall infarction
scar formation in the infarction place
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P-R interval – period from
beginning of P wave to
beginning of R wave; time
required for spread of
depolarization from SA node
through atria to ventricles;
includes AV node delay
Q-T interval – time from
beginning of QRS complex
to end of T wave; action
potentials spread through
ventricular cells
ECG intervals
R-R interval – time between two successive R waves shows
duration of generation & spread of action potential through
the heart; can be measured to determine heart rate
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- Disturbances in heart rate
- Bradycardia – heart rate
under 60 beats/minute
- Tachycardia – heart rate
over 100 beats/minute
- sinus tachycardia –
regular fast rhythm
Cardiac arrhythmias
- Disturbances in conduction –
blockage along conduction
system ► heart block
- Partial blockage at AV node
- P-R interval is longer, due to
increased time for spread to ventricles through AV node
- extra P waves – some SA node action potentials are not
conducted through AV node
- Ectopic (abnormal) location of pacemaker cells – results in
arrhythmias
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Complete AV heart block with atrial tachycardia
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rate of atria ~120/min rate of ventricles ~33/min
1 sec – 25 mm
R
P+T
P
P
P
P
P
R
R
R
R
P+T
P+T
P+QRS
four P for one R
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- Atrial fibrillation – not life threatening because atrial
contraction is not necessary for ventricular filling
- ECG recording lacks many P waves
Cardiac arrhythmias: fibrillation
Ventricular fibrillation – immediately life-threatening !!
chaotic activity on ECG;
SA node may resume
pacing heart after shock
by electrical defibrillation
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Relationships between pressure, valve position & blood flow (left ventricle)
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Cardiac cycle – sequence of events in heart during time
between start of one heartbeat and beginning of the next
Each cardiac cycle – consists of relaxation period –
diastole & contraction period – systole, for each chamber
Atrial & ventricular diastoles & systoles – occur at
different times as result of AV node delay
Left & right heart ventricles – pump blood into
corresponding circuits simultaneously
Cycle is divided into four main phases – defined by
actions of ventricles & positions of valves: filling,
contraction, ejection & relaxation
Cardiac cycle and its phases
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Ventricular filling phase
- Ventricular filling – blood drains from atria into ventricles,
ventricular pressures – lower than in atria, p. trunk, aorta
- Pressure in pulmonary trunk & aorta increases ► semilunar
valves closes; no blood flow from the vessels into ventricles
AV valves open due to
higher atrial pressure ►
blood flows passively from
atria into ventricles – 70-80%
of volume ► passive filling
Atrial systole – contracting
atria eject remaining 20-30%
At end of atrial systole and
ventricular diastole –
ventricles contain ~120 ml
of blood ► end-diastolic
volume (EDV)
0.1 sec
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Starts with short isovolumetric contraction in the beginning
of ventricular systole
Ventricular contraction phase
(systole)
Pressure in ventricles – rises
rapidly ▬► high pressure closes
AV valves & causes S1 heart
sound
Ventricular pressure – not high
enough to open semilunar valves
both semilunar valves are still
closed – ventricular volume
does not change (isovolumetric =
same volume)
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Systole of ventricles continues ►
ventricular ejection phase starts –
pressure in ventricles rises higher
than in pulmonary trunk & aorta
semilunar valves open – rapid
outflow of blood from ventricles
Ejection continues ► pressure in
pulmonary trunk & aorta approaches
that in ventricles
ejection of blood into vessels
decreases considerably
About 70 ml of blood pumped from
each ventricle in ejection phase ►
stroke volume (SV)
50 ml remains in each ventricle after
ejection ► end-systolic volume (ESV)
Ventricular
ejection phase
0.3 sec
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When ventricular diastole
begins, brief isovolumetric
relaxation occurs ► blood
pressure in ventricles declines
Semilunar valves – shut,
S2 heart sound is heard
Pressure in ventricles – still
higher than in atria & AV
valves remain closed
No blood ejected from
ventricles or enters ventricles
– ventricular blood volume
briefly remains constant
Ventricular relaxation phase
(diastole)
0.4 sec
One cardiac
cycle total
time 0.8 sec
When heart rate increases – all phases
of cardiac cycle shorten, particularly
diastole !!!
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Normal blood flow through open AV & semilunar valves –
does not produce sounds
Sounds – generated only when valves closing & result from
vibrations of ventricular & blood vessel walls
Two heart sounds: S1 – “lub” ► when AV valves close & S2
“dub” ► when semilunar valves close; S1 is typically longer
louder than S2
Heart murmur – when blood flow through heart is turbulent;
heart murmurs are generally caused by defective valves
Children often have heart murmurs – do not represent defects
Stethoscope – clinical device used to listen to (auscultate)
rhythmic heart sounds, to measure blood pressure; to listen
to sounds produced by (i) breathing, (ii) gastrointestinal
tract, (iii) developing fetus in the uterus
Heart sounds
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Auscultation of heart sounds
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Blood volume in ventricles
End-systolic volume ESV 50 ml
Passively added to ventricle
before atrial systole 50 ml
Added by atrial systole 20 ml
End-diastolic volume EDV 120 ml
Stroke volume SV – blood ejected
by one ventricular systole 70 ml
End-systolic volume ESV 50 ml
- Both ventricles eject same amount of blood
- When heart rate increases – all phases of cardiac cycle
shorten, particularly diastole
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Characteristic ventricular volumes
End-diastolic volume EDV 120 ml
End-systolic volume ESV 50 ml
Stroke volume SV SV = EDV – ESV
120 ml – 50 ml = 70 ml per one heart beat
Ejection fraction – percentage of EDV represented by SV
(SV x 100) / EDV (70 x 100) /120 ~ 58% normal 50-65%
Cardiac output CO – volume pumped by each ventricle into
systemic or pulmonary circuit in one minute
CO = SV x HR 70 ml x 72/min = 5040 ml/min
Each ventricle pumps into its circuit ~5 liters per minute
Adult blood volume ~5 liters ► entire stock of blood passes
through heart every minute
Factors that influence cardiac output
Cardiac output (CO = SV x HR) – affected by changes in
both heart rate & stroke volume
Stroke volume (SV = EDV – ESV) – affected by changing
EDV or ESV
Heart rate – regulated by autonomic nervous system,
circulating hormones, venous return & stretch receptors
although heart is autorhythmic, it still requires regulation to
ensure that cardiac output meets body needs at all times
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A. Factors affecting heart rate
Agents that influence rate of SA node pacemaker cells –
chronotropic agents
Increase rate – positive chronotropic agents ► sympathetic
nervous system, certain hormones, elevated body T0
Decrease rate – negative chronotropic agents ► para-
sympathetic nervous system & decreased body T0
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Autonomic heart
regulation
Sympathetic system –
increases cardiac output
with positive (A) chronotropic
and (B) inotropic effects
A. heart rate increases due to
accelerated SA pacemaker
cells (up to 180–200 per min)
B. stroke volume increases
due to increased cardiac
muscle cell contractility
Parasympathetic system –
decreases cardiac output
with negative (A) chronotropic
and (B) inotropic effects
A. heart rate decreases due to
suppressed SA cells
B. stroke volume decreases
due to decreased cardiac cell
contractility
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Sympathetic effects on the heart (1)
Cardioacceleratory center in
medulla oblongata activates
sympathetic spinal neurons &
sympathetic cardiac nerves
that terminate on SA node cells
& on some cardiac muscle cells
in ventricles
Nerves release norepinephrine
(NE) that binds to & activates
-1 adrenoreceptors in SA
pacemaker cells & cardiac
muscle cells
Activated receptors open Na+ &
Ca2+ channels & cause depo-
larization of pacemaker &
contractile cells
Cardioacceleratory
center
Cardioinhibitory
center
Sympathetic effects on the heart (2)
Under sympathetic stimulation ►►
A. the rate of action potentials in SA cell increases –
positive chronotropic effect
B. the strength of cardiac muscle contractions increases –
positive inotropic effect
Hormones epinephrine, norepinephrine, thyroid hormone &
certain drugs also have positive chronotropic effect
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No stimulation
Heart rate 75 bpm
threshold
Resting potential
Sympathetic stimulation
Heart rate 120 bpm
Resting potential
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Parasympathetic effects on the heart
Cardioinhibitory center in medulla oblongata activates
vagus nerve & postganglionic parasympathetic fibers that
terminate on SA node pacemaker cells & on some cardiac
muscle cells in ventricles
The terminals release acetylcholine (ACh) that binds to &
activates muscarinic receptors in pacemaker cells &
cardiac muscle cells
Activated receptors open K+ channels & cause hyper-
polarization of pacemaker & contractile cells
A. the rate of pacemaker cell action potentials decreases
– negative chronotropic effect
B. the strength of cardiac muscle contractions decreases
– negative inotropic effect
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Parasympathetic effect on heart rate
No stimulation
Heart rate 75 bpm
Resting potential
Resting potential
Parasympathetic stimulation
Heart rate 40 bpm
Autonomic tone Sinus rhythm
Sympathetic & parasympathetic fibers – have tonic activity
at rest ►► autonomic tone
Parasympathetic influence, called vagal tone, is stronger
If vagus nerve is separated from the heart – rate of SA pace-
makers increases from ~75 to ~95 beats per minute (bpm)
Vagal tone causes slight hyperpolarization of SA cells &
holds them at a lower rate of 70–80 bpm ► sinus rhythm
Strong vagal stimulation – decreases heart rate to 20 bpm
Maximum vagal stimulation – can stop heart for a few
seconds; then, heart “escapes” & starts beating at initial
rate of 20-40 bpm
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25
20
15
10
5
0
-4
0
+4
+8
Cardiac Output (L/min)
Right atrial pressure (mm Hg)
Parasympathetic
stimulation
Zero
sympathetic stimulation
Intermediate
sympathetic stimulation
Maximum
sympathetic stimulation
Effect of sympathetic & parasympathetic stimulation on cardiac output (via heart rate)
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Receptors, cardiac centers, heart rate
Interoreceptors signal about changes in interior activity to
cardiac centers in medulla oblingata ► heart rate (HR)
changes to meet metabolic demands
Higher centers – cerebral cortex, hypothalamus, limbic
structures – influenced by sensory & emotional stimuli, adjust
heart rate by effects on medulla oblongata
Baroreceptors, located in aorta & internal carotid artery,
signal medulla oblongata centers about blood pressure (BP)
if BP decreases ► impulse rate from receptors drops &
cardiac center activates sympathetic system
if BP increases ► impulse rate from receptors rises &
cardiac center activates parasympathetic system
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Location of
arterial baro-
and chemo-
receptors
- Chemoreceptors sensitive to blood
pH, CO2, O2 – located in aortic arch
& external carotid artery – signal
medulla oblongata
- if blood CO2 increases ► impulse
rate from receptors rises & cardiac
center activates sympathetic
system
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Autonomic reflex arc
in regulation of blood
pressure
Increasing BP was detected by
arterial baroreceptors (1)
Afferent nerve carries receptor
signal to medulla oblongata (2)
Efferent signals from medulla
oblongata travel in vagus
nerve to heart (3)
Heart rate decreases, reducing
blood pressure (4)
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Venous return, atrial (Bainbridge) reflex & heart rate
Venous return – amount of blood returning by veins to the
right atrium every minute
If right atrium receives larger blood volume ► its walls & SA
pacemaker cells inside them stretch ► SA cells stimulated
► rate of SA cell action potentials & then heart rate increase
direct effect on heart rate
Bainbridge reflex adjusts heart rate in response to venous
return ▬► if right atrium receives larger blood volume ►
stretch receptors in its wall are stimulated ► they activate
neurons in medulla oblongata ► the neurons activate cells
of sympathetic system ► heart rate & cardiac output increase
indirect effect on heart rate
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B. Factors affecting stroke volume:
Preload
- Three factors influence stroke volume – preload, heart
contractility & afterload
- Preload – degree of stretching of ventricular muscle cells
during diastole; directly proportional to EDV
- in turn, EDV depends on filling time & venous return
- Preload – ability of muscle cells to produce tension
- Frank-Starling law – about relationship between preload &
stroke volume ►► “the more ventricular muscle cells
stretch, the more forcefully they contract”
(principle ▬► more IN – more OUT)
- stretching causes more optimal overlap of actin & myosin filaments
& enables stronger contraction & higher stroke volume (p. 365)
- Hormonal regulation may occur through changing blood volume ►
atrial natriuretic peptide ANP increases loss of fluid in urine, thus
decreasing blood volume and, in turn, stroke volume
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Factors affecting stroke volume:
Contractility & afterload
- Contractility – heart intrinsic ability to generate tension
- contractility increases ► stroke volume increases & ESV
decreases; contractility decreases ► opposite effects
- Agents that affect contractility – inotropic agents
- positive inotropic agents – sympathetic activation; hormones
NE, epinephrine, thyroid hormone, dopamine
- negative inotropic agents – -blockers, Ca channel blockers
- Afterload – force that ventricles must overcome to eject blood
into aorta & pulmonary trunk
- Mostly determined by blood pressure in arteries
- Afterload increases – ventricular pressure must be greater to
open semilunar valves; stroke volume drops & ESV increases
- Afterload decreases – stroke volume rises & ESV decreases
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Ventricular hypertrophy
- Long increase in preload & afterload – results in enlargement
of ventricles ► ventricular hypertrophy
- Cardiac muscle cells generate higher tension to continue
pumping against higher afterload
- muscle fibers make more myofibrils & organelles & get bigger
- Right ventricular hypertrophy – results from respiratory
disease or high blood pressure in pulmonary circuit
- Left ventricular hypertrophy – results from high blood
pressure in systemic circuit
- Ventricular hypertrophy – can increase heart pumping up to
certain point; however, heart lumen & filling space decreases
- Risk for heart failure increases
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Heart failure – reduced heart ability to pump effectively
Causes – (i) reduced contractility (myocardial ischemia,
infarction), (ii) any valvular heart disease, (iii) disease of
heart muscle (cardiomyopathy) & electrolyte imbalances
Heart pathology results in – decreased stroke volume, which
reduces cardiac output
Left ventricular failure – blood backs up within pulmonary
circuit – pulmonary congestion
this increases pressure in pulmonary vessels, driving fluid
out of capillaries into lungs – pulmonary edema
Right & left ventricular failure – may produce peripheral
edema, in which blood backs up in systemic capillaries –
systemic congestion
Treatment – increasing cardiac output
Heart failure
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