Transcript Ch 20 Student_Heart Revisedx

Chapter 20
The Heart
Circulatory System: The Heart
• cardiology – the scientific study of the heart and
the treatment of its disorders
• cardiovascular system
– heart and blood vessels
• circulatory system
– heart, blood vessels, and the blood
• major divisions of circulatory system
– pulmonary circuit - right side of heart
• carries blood to lungs for gas exchange and back to heart
– systemic circuit - left side of heart
• supplies oxygenated blood to all tissues of the body and
returns it to the heart
Position, Size, and Shape
Heart lies in mediastinum
(a central compartment of the
thoracic cavity made of loose
connective tissue) between
lungs; 2/3 of its mass is to
the left of the midline
• Size: equivalent to a
person’s closed fist.
• Shape: cone-shaped,
pointed apex inferior; flat
base is superior.
• Heart protected on the
anterior side by the
sternum; on the posterior
side by the vertebrae
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Aorta
Pulmonary
trunk
Base of
heart
Apex
of heart
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Diaphragm
(c)
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SULCI - GROOVES on surface of heart containing blood vessels and fat
1. coronary sulcus
o Separates the atria from the ventricles
2. anterior interventricular sulcus
o marks the boundary between ventricles anteriorly
3. posterior interventricular sulcus
o marks the boundary between ventricles posteriorly
Protective layers of the heart
Pericardium – 2 layered sac surrounds and protects the heart from
external jerk or shock.
• Fibrous pericardium dense irregular connective tissue, protects
and anchors the heart to diaphragm and mediastinum; prevents
overstretching
• Serous pericardium
• Parietal pericardium
• Visceral pericardium (epicardium) covers the heart surface
and becomes part of the heart wall
• Pericardial cavity lies between the parietal and visceral layers
of the serous pericardium; filled with pericardial fluid that
reduces friction between the two membranes.
pericarditis.inflammation
 pericarditis:
inflammation of the
ofpericardium
the pericardium
 cardiac
cardiactamponade:
tamponade
buildup
buildupofoffluid
fluidininthe
the
pericardial
pericardialcavitycavityresulting
in slow or rapid compression
of the heart.
Pericardium
Heart Wall
 Epicardium (visceral
pericardium)
– visceral serous
membrane covering
heart; adipose in thick
layer in some places
– Contain coronary blood
vessels
 Myocardium
– cardiac muscle layer
 Endocardium
– covers the valve
surfaces and
continuous with
endothelium of blood
vessels
Structure of CARDIAC MUSCLE
• Cardiocytes – small, striated, short, thick, branched cells, one
centrally located nucleus, involuntary control
• Abundant mitochondria, extensive blood supply
• intercalated discs - join cardiocytes end to end
– interdigitating folds –End of cells folded like the bottom of an egg
carton. Produces interlocking and increased surface contact area.
– mechanical junctions tightly join cardiocytes to prevent heart
cells from pulling apart during contraction
• fascia adherens –ribbon like structures that stabilizes nonepithelial tissue; actin of the thin myofilaments is anchored to
the plasma membrane
• desmosomes – prevents cardiocytes from being pulled apart
– gap junctions allow ions to flow between cells –produces
electrical stimulation to neighboring cells
• Propagate action potentials
– repair of damage of cardiac muscle is almost entirely by fibrosis
(scarring)
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4 CHAMBERS
2 upper atria
2 lower ventricles
Right and Left Atrium
1. Pectinate muscles internal ridges of
myocardium in right atrium and right
auricle. Increase force of contraction
w/o increasing heart mass
2. Interatrial septum separates right
and left atrium
3. Auricle flap like extension increases
surface area.
RIGHT ATRIUM
1.Receives blood from 3 veins: superior / inferior vena cava, coronary
sinus
2.Blood flows through the right atrioventricular valve (AV valve) or the
tricuspid valve) into the right ventricle.
• Each valve consists of 2-3 fibrous flaps of tissue called cusps.
LEFT ATRIUM
1. Forms MOST of the base (top) of the heart
2. Receives blood FROM LUNGS via 4 pulmonary veins (2 right / 2 left)
Remember blood always returns to the heart via veins
3. Blood flows through the left atrioventricular valve (AV valve) or the
bicuspid valve (has 2 cusps) into the left ventricle.
– This valve is also known as the mitral valve.
Right
auricle
Left
auricle
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Pectinate muscles
internal ridges of myocardium
in right atrium and both left
and right auricles. Increase
force of contraction w/o
increasing heart mass
Right and Left Ventricle
1. Inside ventricles are raised bundles of cardiac muscle called
trabeculae carneae
– cone shaped traberculae carnae are called papillary muscles.
2. Chordae tendineae cords connect cusps of the AV valves to the
papillary muscles
3. Interventricular septum: partitions the right and left ventricles
RIGHT VENTRICLE
Blood flows from the right ventricle into the pulmonary trunk
(pulmonary artery) through the pulmonary semilunar valve.
LEFT VENTRICLE
1. The aortic semilunar valve allows the passage of blood from
ventricle to the ascending aorta
– just above valve are openings to the coronary arteries
2. Myocardium much thicker in the left ventricle - produces greater
force for blood ejection to systemic tissues
NOTE: difference in
myocardium
thickness between left
and right ventricles
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Heart Valves
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Left AV
(bicuspid) valve
Right AV
(tricuspid) valve
Fibrous
skeleton
Openings to
coronary arteries
Aortic
valve
Pulmonary
valve
(a)
Fibrous cardiac
skeleton
collagenous and
elastic fiber provides
1. support structure
2. attachment for
cardiac muscle
3. anchor for valve
tissue
4. electrically
insulate
ventricular cells
from atrial cells
Valve Action
1. The heart valves open and close passively because of
pressure differences on either side of the valve. When
pressure is greater BEHIND the valve (Ex: as blood fills atria),
the cusps are blown open and the blood flows through the
valve; when pressure is greater in FRONT of the valve
(ventricles are full and press against the AV valves), the cusps
snap shut and blood flow is stopped (from atria). The motion
of a heart valve is analogous to the motion of the front door of
your house. The door, which only opens in one direction, opens
and closes due to pressure on the door.
2. Ventricle value action: Electrical stimulation signal from SA
node in right atrium reaches papillary muscles on the floor of
the ventricles before the myocardium muscle fibers.
3. Causes tension that pulls the chordae tendinae and they tighten
pulling the AV valves shut as blood in ventricles surges
against valves closing them.
Atrioventricular and Semilunar Valves
Values ensure a one-way flow of blood thru the heart; open and close
in response to pressure changes as the heart contracts and relaxes.
AV Valves
• When atria contract, the ventricular pressure is lower than atrial
pressure
–cusps OPEN chordae tendineae slack; papillary muscles relaxed
• When ventricles initiate contraction:
–AV cusps CLOSED, chordae tendinae are pulled taut and
papillary muscles contract to pull cords and prevent cusps from
slipping inside out
• AV valves close preventing backflow of blood into atria
Semilunar Valves
• SL valves open with ventricular contraction allow blood to flow
into pulmonary trunk and aorta. Pressure inside ventricles
overpowers the pressure inside the aorta and pulmonary trunk.
• SL valves close with ventricular relaxation prevents blood from
returning to ventricles. Pressure inside aorta and pulmonary trunk
higher, closing the values.
AV and SL
Values
Valve Disorders
1. Stenosis - narrowing of a heart valve
which restricts blood flow.
2. Rheumatic Fever- inflammatory disease
that occurs following a Streptococcus
pyogenes infection (usually in the throat).
• The immune system stimulates
antibodies to attack the infection.
Inadvertently, the antibodies also
attack the heart tissue damaging the
heart valves. The damaged valves can
lead to heart failure.
3. Mitral valve prolapse- bulge too far into
the left atrium during contraction
4. A heart murmur is an abnormal sound
that consists of a flow noise that is heard before, between, or after
the lubb-dupp or that may mask the normal sounds entirely.
• Not all murmurs are abnormal or symptomatic, but most
indicate a valve disorder. Sounds are thought to be produced
by regurgitation through valves
• The sound of a heartbeat comes
primarily from the turbulence in
blood flow caused by the
closure of the valves.
• Listening to sounds within the
body is called auscultation,
usually done with a stethoscope.
• First heart sound S1 (lubb)
created by blood turbulence
associated with the closing of
the ATRIOVENTRICULAR
valves
• The second heart sound S2
(dupp) represents the closing
of the SEMILUNAR valves
close to the end of the
ventricular systole.
Heart Sounds
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Blood Circulation
Two closed circuits
• Systemic circulation
– left side of heart pumps blood through
body
– Receives oxygenated blood FROM
the lungs and distributes it to body
cells
– left ventricle  aorta  arteries 
arterioles  capillaries  gas and
nutrient exchange  venules  veins
 right atrium
• Pulmonary circulation
– right side of heart pumps
deoxygenated blood TO LUNGS for
oxygenation.
– right ventricle  pulmonary trunk 
pulmonary arteries  lungs 
exchange of gases  pulmonary veins
 left atrium
Blood Circulation
Coronary Circulation
Blood Circulation
• delivers oxygenated blood and
nutrients to the heart and removes
carbon dioxide and wastes from the
myocardium.
• Left Coronary Artery blood to: left
ventricle; left atrium; interventricular
septum. Located above SL valve.
• Right Coronary Artery blood to: right
atrium; portions of both ventricles;
cells of sinoatrial (SA) and AV nodes.
Located above SL value
• Route:
– Left Ventricle  Aorta  left and right coronary arteries 
supply blood to the atrium and the ventricles  large coronary
sinus  right atrium.
• Sinus - large vein without smooth muscle layer
• Anastomoses provides alternate backup routes for blood to flow
if one vessel is blocked or compromised.
Right atrium pumps deoxygenated blood
Blood Flow
 Thru AV (tricuspid) Valve
 To right ventricle which pumps blood
 Thru pulmonary semilunar valve
 Into the pulmonary trunk
 Which divides into a right and left pulmonary artery
 Which carry deoxygenated blood to the lungs
 Gas exchange occurs
 Oxygenated blood returns via pulmonary veins (2 from left/2 from right
 Into the left atrium
 Thru the AV (bicuspid) valve
 Into the left ventricle pumps blood
 Thru the aortic semilunar valve
 Into the aorta
 In the ascending aorta which branches into 2 coronary arteries to heart
 Then the aorta arch with 3 branches to upper regions of the body
 Then to descending aorta with branches to lower regions of the body
 Where blood drops off oxygen and picks up carbon dioxide
 Returning the deoxygenated blood back to the atrium via
Superior vena cava –upper body; inferior vena cava-lower; coronary sinusheart = TAKES APPROXIMATELY ONE MINUTE!!!!
Specialized Anatomy of
Fetal Heart Circulation
• Foramen ovale
– an opening through interatrial
septum in the right atrium
– Connects the two atria
– Seals off at birth, forming
fossa ovalis
Fossa ovalis
• Ductus arteriosus – is a blood
vessel CONNECTING the
pulmonary artery (pulmonary trunk)
to the proximal descending aorta. It
allows most of the blood from the
right ventricle to bypass the fetus's
fluid-filled non-functioning lungs.
O2 for the fetus is provided by
the placenta. Closes at birth and
becomes the nonfunctional
ligamentum arteriosum.
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Clinical Problems
CONGESTIVE HEART FAILURE (CHF)
• results from the FAILURE of EITHER ventricle to eject
blood effectively
 usually due to a heart weakened by myocardial infarction,
chronic hypertension, valve insufficiency, or congenital
defects in heart structure.
– left ventricular failure – blood backs up into the
LUNGS causing pulmonary edema
• shortness of breath or sense of suffocation
– right ventricular failure – blood backs up in the VENA
CAVA causing SYSTEMIC or generalized edema
• enlargement of the liver, ascites (pooling of fluid in
abdominal cavity), distension of jugular veins, swelling
of the fingers, ankles, and feet
– eventually leads to total heart failure
Figure 19.21
Clinical Problems
Coronary Artery Disease (CAD) - partial or complete blockage of
coronary circulation
Atherosclerosis -artery wall thickens as a result of the accumulation of
fatty materials (plaque) producing a narrowing of vessels---results in
artery spasm or clot
– first symptoms of CAD is commonly angina pectoris (chest pain due
to obstruction or spasm of the coronary arteries)
– Angina pectoris – temporary ischemia (slow blood flow)
• obstructing 75% or more of the blood flow to cardiac
muscle- produces lack of blood and oxygen
• When partially or fully blocked coronary artery constricts
produces heaviness and pain. O2 deprived tissue shifts to
anaerobic respiration resulting in lactic acid synthesis which
stimulates pain receptors. The intermittent chest pain may
radiate from the sternal area to the arms, back, and neck.
– Arteriosclerosis hardening/loss
of elasticity of medium or large
arteries
– Arteriolosclerosis
hardening/loss
of elasticity of arterioles
Clinical Problems
Myocardial infarction (MI) (heart attack)
• sudden death of a area of myocardium due to long-term
obstruction of coronary circulation
• interruption of blood supply due to a blood clot or fatty deposit- can
result in death of cardiac cells within minutes
• protection from MI is provided by arterial anastomoses alternative
route of blood flow (collateral circulation) within the myocardium
• MI responsible for about ½ of all deaths in the US
– 25% of MI patients die before obtaining medical assistance
– 65% of MI deaths under age 50 occur within an hour of infarction
Diagnosis:
– 1) ECG (EKG)
– 2) damaged
myocardial cells release
ENZYMES measured by
blood tests.
Prevention
and
Treatment
> Medication –know for exam
• beta blockers [blocks sympathetic response that
increases heart rate- Ex: inhibit receptors for
norepinephrine and epinephrine; used for secondary
heart attack, stroke and hypertension]
• ACE inhibitors [decrease BP; inhibit RAAS]
• Aspirin -thins blood – prevents platelet aggregation
• Heparin/Warfarin (Coumadin) blood thinners that
interfere with chemical formation of clot
• Nitroglycerin [nitric oxide- dilates arteries offsets
angina increasing blood flow]
• Calcium channel blockers [slows heart lowers
electrical impulses, lowers BP]
> Coronary Artery Bypass Graft (CABG)
– section of artery or vein (ex; great saphenous vein)
used to create a detour around the obstructed portion
of a coronary artery
– procedures named by number of vessels repairedsingle, double, triple, or quadruple coronary bypasses
> balloon angioplasty
> laser angioplasty
– similar to balloon angioplasty uses laser tipped
catheter instead of a balloon
Electrical Conduction System of the Heart.
• NODE special tissue acts like muscle and nervous tissue.
• A system of SPECIALIZED CARDIAC MUSCLE CELLS initiates and
distributes electrical impulses that stimulate contraction.
• Automaticity - heart cells act as both nervous and muscle tissue.
Cardiac muscle contracts automatically and generate spontaneous action
potential that goes through ENTIRE heart muscle.
The Beginning
 The human heart begins to beat and pump blood through the embryo
around day 22 of gestation.
 The electric stimulus that triggers contractions in the myocardium arise
spontaneously within the myocardium itself, and propagate from cell to
cell. Input from the central nervous system can modify the heart rate (the
frequency of heart beats), but it does not initiate beats.
 The ability of cardiac myocytes to beat is an intrinsic property of these
cells. It has been found that myocytes removed from the early heart and
grown in culture will beat sporadically, and if they become connected to
each other, will then begin to beat rhythmically, in unison.
 As a functional organ, the heart begins to beat very early,
even before it has assumed its final form.
 Interestingly, the heart begins to beat even before structures
such as valves and septa (singular: septum; the muscular walls
that divide the chambers) have formed! The initial contractions are
peristaltic--that is, they proceed in a wave-like fashion along the
length of the heart.
Electrical Conduction System of Heart
• SA (sinoatrial) node- pacemaker - cluster of cells in right atria wall
– When nodal tissue contracts it generates nervous impulses that
travels to BOTH atria simultaneously, then to the AV node.
– Sets heart rhythm.
– Right atria contracts slightly before left as it receives signal from
the SA node first.
• AV (atrioventricular) node- in atrial septum (alternative
pacemaker)
– Slows the transmission of the action potential; transmits
signal to bundle of His
– Fibrous skeleton helps to insulate and prevent currents from
getting to the ventricles from other routes
• Bundle of His (AV Bundle) -connection between atria and
ventricles; continues to slow the action potential allowing more
time for ventricles to fill with blood for ejection.
• Right and Left Bundle Branches extend from the Bundle of His
or AV bundle, and action potentials descend to the apex of the heart.
• Purkinje fibers in right and left ventricles carry action potentials
from the bundle branches to trigger muscle fibers in ventricles to
contract.
Fibrous skeleton
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Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje fibers
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
GOOD ANIMATION
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nimation__conducting_system_of_the_heart.html
Begins atrial activation
Receives impulse from
SA Node
Delays impulse
Conduction System of Heart
• Heart contractions do not require nervous system intervention.
Signals from the autonomic nervous system and hormones, such as
epinephrine, MODIFY the heartbeat (rate and strength of contraction),
but they do not ESTABLISH the fundamental rhythm.
Cycle of events in heart
 SYSTOLE – “START” of atrial or ventricular CONTRACTION
DIASTOLE – “DONE” with contraction atrial or ventricular = relaxation
Sinus rhythm - normal heartbeat; SA node triggers; 60 – 100 bpm
 adult at rest is 70 to 80 bpm (vagal tone)
 Parasympathetic stimulation slows heart rate
Ectopic focus – another area of heart fires BEFORE SA node
 Premature ventricular contraction (PVC) initiated by the Purkinje
fibers–extra heartbeat can be caused by hypoxia (low oxygen),
electrolyte imbalance, or caffeine, nicotine, and other drugs. Produces
insufficient blood ejection from ventricles; may be perceived as a
"skipped beat" or felt as palpitations in the chest.
 Nodal rhythm – if SA node is damaged, heart rate is set by AV
node, 40 to 60 bpm (action potentials per minute)
 Intrinsic ventricular rhythm – if BOTH SA and AV nodes are not
functioning, rate set at 20 to 40 bpm
 If occurs would require artificial pacemaker to sustain brain function
REVIEW Muscle Physiology - Membrane Potential
• Membrane potentials result
from a separation of positive
(+) and negative (-) charges
(ions) across the membrane
• Voltage is a difference in
electrical potential between
the opposite sides of a
plasma membrane. Voltage
drives an electric current
(the flow of electrons or
electrical charge).
• Action potentials are
generated by the movement
of ions through membrane
ion channels in muscle cells.
This shift from a negative to a
positive internal cellular
environment allows for the
transmission of electrical
impulses
REVIEW Muscle Physiology - Membrane Potential
 When the muscle cell is not in a state of contracting it is said to be in
a resting state, the INSIDE of the cell is more NEGATIVE than the
OUTSIDE. Membrane is polarized. Each cell has an “at rest”
potential to transmit an electrical current. This potential varies in
different types of muscle cells.
 For a muscle cell to contract, the negative (-) value inside the cell
must become more positive (+). This is called depolarization.
1. Ion channels in the membrane open and positively charged ions
move from the extracellular fluid into the interior of the cell
2. Positively charge channels close to prevent release of positive ions.
3. The change in electrical voltage generates electrical impulses that
move along the surface of the membrane, alerting mechanisms inside
the cell to produce a contraction.
 Following the contraction, the ion channels that opened or closed to
increase the positive value inside the cell CLOSE and the cell begins to
resume a more negative value. This is a state of repolarization or
relaxing.
The electrical current released during an action potential
opens calcium channels that enable the binding of contractile
proteins to produce contractions
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Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje fibers
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
Pacemaker Physiology – Atria Action Potential
The resting membrane potential of a SA node cardiac muscle
CELL, is less constant than a skeletal muscle cell, due primarily to
the increased permeability ("leakiness") of its cell membrane to
Na+ and K+ ions; as a result:
• SA node cardiac muscle cells depolarize more easily.
1) SA node CELLS’ resting potential start at -60 mV and drifts
upward (to a more positive value) from a SLOW inflow of Na+ and
no compensating outflow of K+ (K+ channels are closed)
– This gradual depolarization is called pacemaker potential
2) When potential reaches threshold of -40 mV, voltage-gated
FAST Ca2+ and Na+ channels open; Ca2+ and Na+ flow in rapidly
– depolarization occurs - peaking (maximum + value) at 0 mV
3) At 0 mV “K+” channels open and K+ exits the cell triggering
repolarization
• Each depolarization of the SA node produces one heartbeat
–at rest, fires every 0.8 seconds or 75 bpm
–Signal travels 1 m/sec thru atrial myocardium reaches AV node
in approximately 50m/sec
Graph Depiction of Atria Potentials
Animation: Atria
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nimation__conducting_system_of_the_heart.html
Ventricular Filling from Atria
• The ventricles RECEIVE blood from the atrium both
PASSIVELY and as a result of ATRIAL CONTRACTIONS.
1. The first one third (1/3) occurs quite rapidly (passive)
2. The second one third (1/3) is somewhat slower
(passive)
3. The final third (1/3) completes the filling process and is
the RESULT of atrial systole (contraction)
Animation:
http://highered.mcgrawhill.com/sites/0072495855/student_view0/chapter22/animation__th
e_cardiac_cycle__quiz_1_.html
Myocardium Conduction-AV Node
• An impulse in a ventricular contractile muscle fiber is
characterized by RAPID depolarization, plateau, and
repolarization.
• AV node delays cardiac impulses from SA node to allow atria to
contract and EMPTY
• Signal slows at AV node DUE to
– 1) less numbers of cardiocytes
– 2) less gap junctions
– 3) cardiocytes have a stable resting membrane potential
– 4) depolarize only when stimulated
• Depolarization
– Ventricular cardiac cell resting membrane potential is - 90mv
– Na+ channels open and depolarize the membrane.
• This triggers a positive feedback that initiates the opening of
more Na+ channels resulting in a RAPID ALMOST
VERTICAL RISING membrane voltage. Peaks at 30+ mV.
Na+ channels then close.
Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
1 SA node fires.
Right atrium
2 Excitation spreads through
atrial myocardium.
2
1
Sinoatrial node
(pacemaker)
Left
atrium
2
Atrioventricular
node
Atrioventricular
bundle
Purkinje fibers
Purkinje
fibers
3
Bundle
branches
4
5
3 AV node fires.
4 Excitation spreads down AV
bundle.
5 Purkinje fibers distribute
excitation through
ventricular myocardium.
Graph Depiction of Ventricular Action Potential
Na+ channels close
Ca2+ channels open
Myocardium Conduction-AV Node
Plateau phase – result of Ca2+ inflow
• Period of prolonged, sustained depolarization (200-250 msec)
allows for the greater ejection of blood from the ventricles
• Na+ channels close but slow Ca2+ channels open, Ca2+ enter from
OUTSIDE the cell and binds to Ca2+ channels on sarcoplasmic
reticulum releasing more Ca2+ ; cardiac muscle tissue very sensitive
to extracellular calcium concentrations
– Ca2+ binds to troponin to allow for actin-myosin crossbridge formation & muscle contraction.
• The plateau declines slightly due to leaky potassium (K+) channels
but most K+ channels remain closed sustaining the depolarization.
Repolarization
• Ca+2 channels CLOSE and K+ channels OPEN allowing K+ to
rapidly LEAVE the cell restoring resting membrane potential -90mv.
Refractory period
• the time interval when a second contraction cannot be triggered
• Prevents wave summation and tetanus which would stop the
pumping actions of the heart and decrease amount of blood ejected
from ventricles.
Physiology of Contraction
1) Na+ gates open
2) Rapid
depolarization
3) Na+ gates close-cell
depolarizes
4) Slow Ca2+ channels
open prolonging
depolarization
creates plateau
5) Ca2+ channels
close, K+ channels
open (repolarization)
Plateau is the ST segment
of the ECG –ventricle
contraction and blood ejection.
Electrocardiogram---ECG or EKG
• A recording of the
electrical changes
(“ACTION POTENTIAL”)
that accompany each
cardiac cycle (heartbeat)
– Equipment detects
and amplifies
electrical changes on
the skin when the
heart muscle impulse
is generated
• ECG helps to determine
abnormal conduction
pathway; if the heart is
enlarged or has damaged
regions
Electrocardiogram---ECG or EKG
• P wave
– atrial depolarization
• systole
• P to Q interval
– conduction time from SA
node to AV node
• QRS complex
– Atrial repolarization
• diastole
– Ventricular depolarization
• systole
• ST
– plateau period of
sustained contraction
• T wave
ECG/EKG Good Animation
– ventricular repolarization
http://www.youtube.com/watch?v=v3b• diastole
YhZmQu8&feature=endscreen (3.34 min)
Normal Electrocardiogram (ECG)
Atria contract
Ventricles contract
http://www.merckmanuals.com/media/home/figures/MMHE_03_021_01_eps.gif
Fibrillation
Cardiac
Cycle
• A cardiac cycle includes all the events occurring in a SINGLE
heart beat (0.8 sec)
• It consists of repetitive contraction (systole) and relaxation
(diastole) of heart chambers
• In a cardiac cycle the atria then the ventricles contract and relax
forcing blood from areas of high pressure to areas of lower
pressure
1) atrial depolarization
begins
2) atrial depolarization
complete (atria
contracted)
3) ventricles begin to
depolarize at apex; atria
repolarize (atria relaxed)
4) ventricular depolarization
complete (ventricles
contracted)
5) ventricles begin to
repolarize at apex
6) ventricular repolarization
complete (ventricles
relaxed)
Phases of Cardiac Cycle
1. Isovolumetric contraction
• Blood enters atria flows to the ventricles via the opened tricuspid
and mitral valves. Atrial contraction follows
• As atria diastole ends, the ventricles BEGIN depolarizing- start
contracting, the AV valves close, to prevent back flow to the atria;
corresponds to the R peak or the QRS complex seen on an ECG
• Aortic and pulmonary valves are also closed; no overall change in
volume as all four valves are closed. The isovolumetric
contraction lasts about 0.03 sec, enough time to build sufficiently
high pressure to overcome aortic and the pulmonary trunk
semilunar valves (blood in ventricles)
2. Relaxation period: isovolumetric relaxation Both atria and
ventricles are relaxed. Pressure in the ventricles fall and the SL
valves close. All four valves are closed (blood begins flowing
into the atria). Pressure in the ventricles continues to fall, the AV
valves open, and ventricular filling begins. It can be used as an
indicator of diastolic dysfunction.
Phases of Cardiac Cycle
•
•
•
•
•
Ventricular Filling and Ejection
Pressure continues to rise as ventricle muscles decrease chamber
volume size opening SL valves leading to ventricular ejection.
In cardiovascular physiology, end-diastolic volume (EDV) is the
volume of blood in the right and/or left ventricle at end load or filling in
(atrial diastole) or the amount of blood in the ventricles just before
systole.
The amount of blood REMAINING in a ventricle AFTER it has
contracted is End Systolic Volume (ESV)
Stroke volume (SV) is the volume of blood ejected by a ventricle with
each heart beat. SV = EDV minus ESV
Ejection fraction - % of blood at EDV ejected during SV (SV/EDV)
– A normal heart's ejection fraction may be between 55 and 70
– Between 40 and 55 indicates damage, perhaps from a previous
heart attack, but it may not indicate heart failure.
– Under 40 may be evidence of heart failure or cardiomyopathy.
Examples:
EDV = amount of blood available prior to ejection = 150
ESV = amount of blood left in ventricle following contraction = 50
Amount of blood ejected (SV) = 100ml (150-50)
Ejection Factor: Divide SV by EDV EF= 100ml/150 ml= 67%
CARDIAC OUTPUT
Cardiac output (CO) is the volume of blood ejected from the
ventricles into the aorta or pulmonary trunk in ONE MINUTE.
• Cardiac output equals the stroke volume (the volume of blood
ejected by the ventricles with each contraction) multiplied by the
heart rate (the number of beats per minute).
– CO = SV x HR
• 70 ml blood x 75 beats/min = 5250 ml divided by 1000 =
5.25 L/min
• Entire blood supply of the body passes through the
circulatory system every minute.
• Cardiac reserve is the ratio between the maximum cardiac
output a person can achieve and the cardiac output at rest.
– Average is 4-5 times the normal output (5.25 L/min x 4 = 21
L/min)
– Trained athlete’s cardiac reserve can be as much as 7-8
times the normal amount of blood sent through the
circulatory system during intense exercise
SV= 70ml
EDV= amount available that
can be ejected
150
-
ESV = amount remaining
after contraction
80
Influences on Stroke Volume
• the more EACH muscle fiber sarcomere is stretched, greater the
contraction force; STRETCH RESULT OF GREATER BLOOD VOLUME
–Ex: stretching a rubber band produces more tension
• Preload is affected by venous blood pressure and the rate of
venous return to the heart. More blood volume in ventricles - greater
tension; greater force of contraction -more blood ejected
• Higher volume = higher preload
• Frank Starling Law - stroke volume (SV) proportional to EDV
– Amount of blood ejected dependent on available blood in ventricles.
• The more responsive cardiocytes are to stimulation the more
force they can create; stimulation dependent on binding capacity of
actin and myosin contractile proteins which is regulated by Ca2+ .
Are all the fibers contracting together?
• Affected by: autonomic nerves (sympathetic, parasympathetic),
hormones, pharmaceutical drugs, Ca2+ or K+ levels
– Positive inotropic agents increase force of contraction
Ca2+ prolongs plateau increases actin/myosin coupling
– Negative inotropic agents decrease force of contraction
Ca2+ reduces strength of myocardium action potential
Influences on Stroke Volume
If pressure increases, afterload also increases.
– It is the result of the pressure exerted
in the aorta and pulmonary trunk.
– The pressure in the ventricles must be greater
than the aortic and pulmonary pressure to
open the aortic and pulmonic SL valves. As
afterload increases, cardiac output
DECREASES.
• The longer time it takes to open the
valves the less time available for blood
ejection during plateau; reducing blood
output.
– Limits stroke volume (SV) [ventricle output]
– high BP creates high afterload decreasing
ventricular ejection
Regulation of Heart Rate
1. Intrinsic regulation: normal natural characteristics inside the
heart - Gap junctions, SA rhythmic cells
2. Chemoreceptors, proprioceptors, baroreceptors; Bainbridge
reflex (causes increase in heart rate)
3. Cations (Na+, K+, Ca+2)
4. Cardiac centers of medulla oblongata control
– Parasympathetic stimulation (slow as 20-30 bpm)
• Supplied by vagus nerve, DECREASES HEART RATE,
acetylcholine is secreted and hyperpolarizes the heart
– Sympathetic stimulation (high as 250-300 bpm)
• Cardiac nerves innervate the SA and AV nodes, coronary
vessels and the atrial and ventricular myocardium.
INCREASES HEART RATE and force of contraction.
Epinephrine and norepinephrine released
5. Nicotine, caffeine, medications, stress, emotional excitement
6. Age, gender, physical fitness, temperature,
Clinical Problems
Congenital Heart Defect an abnormality or defect that
exists AT or BEFORE birth.
Arrhythmia (dysrhythmia) is an irregularity in heart
rhythm resulting from a defect in the conduction system
of the heart.
• Bradycardia- slow rate below 60 bpm
– resting-sleep, well-conditioned hearts
• Tachycardia – fast rate above 100 bpm
– stress, anxiety, drugs, heart disease
• Fibrillation – asynchronous contraction that can kill very
easily- heart loses its rhythm- some parts of the atria and
ventricle contract while others remain un-stimulated