08 Heart.ppt

 Students should not use this presentation for
study or any type of examination.
 Students should refer books prescribed in the
syllabus.

The Cardiovascular System:
The Heart

Anatomy of the Heart
 Located in the mediastinum – anatomical region
extending from the sternum to the vertebral column,
the first rib and between the lungs
 Apex at tip of left ventricle
 Base is posterior surface
 Anterior surface deep to sternum and ribs
 Inferior surface between apex and right border
 Right border faces right lung
 Left border (pulmonary border) faces left lung

Pericardium
 Membrane surrounding and protecting the heart
 Confines while still allowing free movement
 2 main parts
 Fibrous pericardium – tough, inelastic, dense irregular
connective tissue – prevents overstretching, protection,
anchorage
 Serous pericardium – thinner, more delicate membrane
– double layer (parietal layer fused to fibrous
pericardium, visceral layer also called epicardium)
 Pericardial fluid – secreted into pericardial cavity
Reduces friction during heart movement

Layers of the Heart Wall
Epicardium (external layer)
Visceral layer of serous pericardium
Smooth, slippery texture to outermost surface
Myocardium
95% of heart is cardiac muscle
Endocardium (inner layer)
Smooth lining for chambers of heart, valves and
continuous with lining of large blood vessels

Chambers of the Heart
 2 atria – receiving chambers
 Auricles increase capacity
 2 ventricles – pumping chambers
Sulci – grooves
 Contain coronary blood vessels
 Coronary sulcus
 Anterior interventricular sulcus
 Posterior interventricular sulcus

Right Atrium
 Receives blood from
 Superior vena cava
 Inferior vena cava
 Coronary sinus
 Interatrial septum has fossa ovalis
 Remnant of foramen ovale
 Blood passes through tricuspid valve (right
atrioventricular valve) into right ventricle

Right Ventricle
 Forms anterior surface of heart
 Trabeculae carneae – ridges formed by raised
bundles of cardiac muscle fiber
 Part of conduction system of the heart
 Tricuspid valve connected to chordae tendinae
connected to papillary muscles
 Interventricular septum
 Blood leaves through pulmonary valve (pulmonary
semilunar valve) into pulmonary trunk and then
right and left pulmonary arteries

Left Atrium
 About the same thickness as right atrium
 Receives blood from the lungs through pulmonary
veins
 Passes through bicuspid/ mitral/ left
atrioventricular valve into left ventricle

Left Ventricle
 Thickest chamber of the heart
 Forms apex
 Chordae tendinae attached to papillary muscles
 Blood passes through aortic valve (aortic
semilunar valve) into ascending aorta
 Some blood flows into coronary arteries,
remainder to body
 During fetal life ductus arteriosus shunts blood
from pulmonary trunk to aorta (lung bypass)
closes after birth with remnant called ligamentum
arteriosum

Myocardial thickness
 Thin-walled atria deliver blood under less
pressure to ventricles
 Right ventricle pumps blood to lungs
 Shorter distance, lower pressure, less resistance
 Left ventricle pumps blood to body
 Longer distance, higher pressure, more resistance
 Left ventricle works harder to maintain same rate
of blood flow as right ventricle

Fibrous skeleton
 Dense connective tissue that forms a structural foundation,
point of insertion for muscle bundles, and electrical
insulator between atria and ventricles

Heart Valves and Circulation of Blood
 Atrioventricular valves
 Tricuspid and bicuspid valves
 Atria contracts/ ventricle relaxed
 AV valve opens, cusps project into ventricle
 In ventricle, papillary muscles are relaxed and chordae
tendinae slack
 Atria relaxed/ ventricle contracts
 Pressure drives cusps upward until edges meet and
close opening
 Papillary muscles contract tightening chordae tendinae
 Prevents regurgitation

Semilunar valves
 Aortic and pulmonary valves
 Valves open when pressure in ventricle exceeds
pressure in arteries
 As ventricles relax, some backflow permitted but
blood fills valve cusps closing them tightly
 No valves guarding entrance to atria
 As atria contracts, compresses and closes
opening

Systemic and pulmonary circulation - 2 circuits in
series
 Systemic circuit
 Left side of heart
 Receives blood from lungs
 Ejects blood into aorta
 Systemic arteries, arterioles
 Gas and nutrient exchange in systemic capillaries
 Systemic venules and veins lead back to right atrium
 Pulmonary circuit
 Right side of heart
 Receives blood from systemic circulation
 Ejects blood into pulmonary trunk then pulmonary arteries
 Gas exchange in pulmonary capillaries
 Pulmonary veins takes blood to left atrium

Cardiac Muscle Tissue and the Cardiac
Conduction System
 Histology
 Shorter and less circular than skeletal muscle fibers
 Branching gives “stair-step” appearance
 Usually one centrally located nucleus
 Ends of fibers connected by intercalated discs
 Discs contain desmosomes (hold fibers together) and gap
junctions (allow action potential conduction from one fiber
to the next)
 Mitochondria are larger and more numerous than skeletal
muscle
 Same arrangement of actin and myosin

Autorhythmic Fibers
 Specialized cardiac muscle fibers
 Self-excitable
 Repeatedly generate action potentials that
trigger heart contractions
 2 important functions
1. Act as pacemaker
2. Form conduction system

Copyright 2009, John Wiley & Sons, Inc.
1)Cardiac excitation normally begins in the sinoatrial (SA) node,
located in the right atrial wall just inferior and lateral to the
opening of the superior vena cava. Each action potential from the
SA node propagates throughout both atria via gap junctions in the
intercalated discs of atrial muscle fibers.
2)By conducting along atrial muscle fibers, the action potential
reaches the atrioventricular (AV) node, located in the just
anterior to the opening of the coronary sinus
Conduction system

3)From the AV node, the action potential enters the atrioventricular
(AV) bundle (also known as the bundle of His). This bundle is the
only site where action potentials can conduct from the atria to the
ventricles
4) After propagating along the AV bundle, the action potential enters
both the right and left bundle branches.
5)Finally, the large-diameter Purkinje fibers rapidly conduct the
action potential beginning at the apex of the heart Then the ventricles
contract, pushing the blood upward toward the semilunar valves.

Conduction system
1. Begins in sinoatrial (SA) node in right atrial wall
 Propagates through atria via gap junctions
 Atria contact
2. Reaches atrioventricular (AV) node in interatrial septum
3. Enters atrioventricular (AV) bundle (Bundle of His)
 Only site where action potentials can conduct from atria to
ventricles due to fibrous skeleton
4. Enters right and left bundle branches which extends
through interventricular septum toward apex
5. Finally, large diameter Purkinje fibers conduct action
potential to remainder of ventricular myocardium
 Ventricles contract

Frontal plane
Right atrium
Right ventricle
Left atrium
Left ventricle
Anterior view of frontal section
Frontal plane
Left atrium
Left ventricle
SINOATRIAL (SA) NODE
1
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
ATRIOVENTRICULAR
(AV) NODE
1
2
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
ATRIOVENTRICULAR
(AV) NODE
ATRIOVENTRICULAR (AV)
BUNDLE (BUNDLE OF HIS)
1
2
3
Right atrium
Right ventricle
Frontal plane
Left atrium
Left ventricle
ATRIOVENTRICULAR
(AV) NODE
RIGHT AND LEFT
BUNDLE BRANCHES
1
2
3
4
Right atrium
Right ventricle
Frontal plane
ATRIOVENTRICULAR
(AV) NODE
Left atrium
Left ventricle
RIGHT AND LEFT
BUNDLE BRANCHES
PURKINJE FIBERS
1
2
3
4
5
Right atrium
Right ventricle

Heart Sounds
 Auscultation
 Sound of heartbeat comes
primarily from blood
turbulence caused by
closing of heart valves
 4 heart sounds in each
cardiac cycle – only 2 loud
enough to be heard
 Lubb – AV valves close
 Dupp – SL valves close

Cardiac Output
 CO = volume of blood ejected from left (or right)
ventricle into aorta (or pulmonary trunk) each minute
 CO = stroke volume (SV) x heart rate (HR)
 In typical resting male
 5.25L/min = 70mL/beat x 75 beats/min
 Entire blood volume flows through pulmonary and
systemic circuits each minute
 Cardiac reserve – difference between maximum CO
and CO at rest
 Average cardiac reserve 4-5 times resting value

A healthy heart will pump out the blood that entered its chambers during the
previous diastole. In other words, if more blood returns to the heart during
diastole, then more blood is ejected during the next systole
Three factors regulate stroke volume and ensure that the left and
right ventricles pump equal volumes of blood: (1) preload, the
degree of stretch on the heart before it contracts; ( amount of blood in
ventricle before contraction) end diastolic volume (2) contractility,
the forcefulness of contraction of individual ventricular muscle
fibers; and (3) afterload, volume of blood in the ventricle after
contraction, end systolic volume
Regulation of stroke volume

Regulation of stroke volume
 3 factors ensure left and right ventricles pump
equal volumes of blood
1. Preload
2. Contractility
3. Afterload

Preload
 Degree of stretch on the heart before it contracts
 Greater preload increases the force of
contraction
 Frank-Starling law of the heart – the more the
heart fills with blood during diastole, the greater
the force of contraction during systole
 Preload proportional to end-diastolic volume (EDV)
 2 factors determine EDV
1. Duration of ventricular diastole
2. Venous return – volume of blood returning to right
ventricle

When heart rate increases, the duration of diastole is shorter. Less filling
time means a smaller EDV, and the ventricles may contract before they
are adequately filled. By contrast, when venous return increases, a
greater volume of blood flows into the ventricles, and the EDV is
increased. When heart rate exceeds about 160 beats/min, stroke volume
usually declines due to the short filling time. At such rapid heartrates,
EDV is less, and the preload is lower.

Contractility
The second factor that influences stroke volume is myocardial contractility, the
strength of contraction at any given preload. Substances that increase contractility
are positive inotropic agents; those that decrease contractility are negative i.a.
 Strength of contraction at any given preload
 Positive inotropic agents increase contractility
 Often promote Ca2+ inflow during cardiac action potential
 Increases stroke volume
 Epinephrine, norepinephrine, digitalis
 Negative inotropic agents decrease contractility
 Anoxia, acidosis, some anesthetics, and increased K+ in interstitial
fluid

Ejection of blood from the heart begins when pressure in the right
ventricle exceeds the pressure in the pulmonary trunk (about 20
mmHg), and when the pressure in the left ventricle exceeds the
pressure in the aorta (about 80 mmHg). At that point, the higher
pressure in the ventricles causes blood to push the semilunar valves
open. The pressure that must be overcome before a semilunar valve can
open is termed the afterload. An increase in afterload causes stroke
volume to decrease, so that more blood remains in the ventricles at the
end of systole.
Afterload

Afterload
 Pressure that must be overcome before a
semilunar valve can open
 Increase in afterload causes stroke volume to
decrease
 Blood remains in ventricle at the end of systole
 Hypertension and atherosclerosis increase
afterload

Action Potentials and Contraction
 Action potential initiated by SA node spreads out
to excite “working” fibers called contractile fibers
1. Depolarization
2. Plateau
3. Repolarization

1. Depolarization – contractile fibers have stable
resting membrane potential
 Voltage-gated fast Na+ channels open – Na+ flows in
 Then deactivate and Na+ inflow decreases
2. Plateau – period of maintained depolarization
 Due in part to opening of voltage-gated slow Ca2+
channels – Ca2+ moves from interstitial fluid into cytosol
 Ultimately triggers contraction
 Depolarization sustained due to voltage-gated K+
channels balancing Ca2+ inflow with K+ outflow

3. Repolarization – recovery of resting membrane potential
 Resembles that in other excitable cells
 Additional voltage-gated K+ channels open
 Outflow K+ of restores negative resting membrane potential
 Calcium channels closing
 Refractory period – time interval during which
second contraction cannot be triggered
 Lasts longer than contraction itself
 Blood flow would cease

Depolarization Repolarization
Refractory period
Contraction
Membrane
potential (mV) Rapid depolarization due to
Na+ inflow when voltage-gated
fast Na+ channels open
0.3 sec
+ 20
0
–20
–40
– 60
– 80
–100
1
1
Refractory period
Contraction
Membrane
potential (mV) Rapid depolarization due to
Plateau (maintained depolarization) due to Ca2+ inflow
when voltage-gated slow Ca2+ channels open and
K+ outflow when some K+ channels open
0.3 sec
+ 20
0
–20
–40
– 60
– 80
–100
2
1
1
2
Refractory period
Contraction
Membrane
potential (mV)
Repolarization due to closure
of Ca2+ channels and K+ outflow
when additional voltage-gated
K+ channels open
Rapid depolarization due to
Plateau (maintained depolarization) due to Ca2+ inflow
when voltage-gated slow Ca2+ channels open and
K+ outflow when some K+ channels open
0.3 sec
+ 20
0
–20
–40
– 60
– 80
–100
2
1
3
1
2
3

Electrocardiogram
 ECG or EKG
 Composite record of
action potentials
produced by all the
heart muscle fibers
 Compare tracings
from different leads
with one another and
with normal records
 3 recognizable
waves
 P, QRS, and T

Correlation of ECG Waves and Systole
 Systole – contraction/ diastole – relaxation
1. Cardiac action potential arises in SA node
 P wave appears
2. Atrial contraction/ atrial systole
3. Action potential enters AV bundle and out over ventricles
 QRS complex
 Masks atrial repolarization
4. Contraction of ventricles/ ventricular systole
 Begins shortly after QRS complex appears and continues
during S-T segment
5. Repolarization of ventricular fibers
 T wave
6. Ventricular relaxation/ diastole

1 Depolarization of atrial
contractile fibers
produces P wave
0.2
0
Seconds
Action potential
in SA node
P
1
Atrial systole
(contraction)
Depolarization of atrial
contractile fibers
produces P wave
0.2
0
Seconds
0.2
0
Seconds
Action potential
in SA node
P
P
2
1
Depolarization of
ventricular contractile
fibers produces QRS
complex
Atrial systole
(contraction)
contractile fibers
produces P wave
0.2 0.4
0
Seconds
0.2
0
Seconds
0.2
0
Seconds
Action potential
in SA node
R
S
Q
P
P
2
3
P
1
Ventricular
systole
(contraction)
Depolarization of
fibers produces QRS
complex
Atrial systole
(contraction)
contractile fibers
produces P wave
0.2 0.4
0
Seconds
0.2 0.4
0
Seconds
0.2
0
Seconds
0.2
0
Seconds
Action potential
in SA node
R
S
Q
P
P
P
2
3
4
P
1
5
Repolarization of
fibers produces T
wave
Ventricular
systole
(contraction)
Depolarization of
fibers produces QRS
complex
Atrial systole
(contraction)
contractile fibers
produces P wave
0.6
0.2 0.4
0
Seconds
0.2 0.4
0
Seconds
0.2 0.4
0
Seconds
0.2
0
Seconds
0.2
0
Seconds
Action potential
in SA node
R
S
Q
P
P
P
P
T
2
3
4
5
P
1
6
Ventricular diastole
(relaxation)
5
Repolarization of
fibers produces T
wave
Ventricular
systole
(contraction)
Depolarization of
fibers produces QRS
complex
Atrial systole
(contraction)
contractile fibers
produces P wave
0.6
0.2 0.4
0 0.8
Seconds
0.6
0.2 0.4
0
Seconds
0.2 0.4
0
Seconds
0.2 0.4
0
Seconds
0.2
0
Seconds
0.2
0
Seconds
Action potential
in SA node
R
S
Q
P
P
P
P
T
P
2
3
4
5
6
P

In reading an ECG, the size of the waves can provide clues to
abnormalities. Larger P waves indicate enlargement of an atrium;
an enlarged Q wave may indicate a myocardial infarction;
and an enlarged R wave generally indicates enlarged ventricles.
The T wave is flatter than normal when the heart muscle is receiving
insufficient oxygen—as, for example, in coronary artery disease. The T
wave may be elevated in hyperkalemia(high blood K level).

Cardiac Cycle
 All events associated with one heartbeat
 Systole and diastole of atria and ventricles
 In each cycle, atria and ventricles alternately
contract and relax
 During atrial systole, ventricles are relaxed
 During ventricle systole, atria are relaxed
 Forces blood from higher pressure to lower pressure
 During relaxation period, both atria and ventricles
are relaxed
 The faster the heart beats, the shorter the relaxation period
 Systole and diastole lengths shorten slightly

1
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
1 Atrial depolarization
1
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
2
1
2
Atrial depolarization
Begin atrial systole
1
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
End (ventricular) diastolic volume
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
2
3
1
2
3
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
4
1
2
3
4
Ventricular depolarization
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
4
5
1
2
3
4
5
Isovolumetric contraction
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
4
6
1
2
3
4
5
6
Begin ventricular ejection
5
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
4
7
1
2
3
4
5
6
7
End (ventricular) systolic volume
6
5
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
8 1
2
3
4
5
6
7
8
Begin ventricular repolarization
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
8
9
1
2
3
4
5
6
7
8
9
Isovolumetric relaxation
0
20
40
60
80
100
120
(d) Volume in
ventricle (mL)
(c) Heart sounds
(b) Pressure
(mmHg)
(a) ECG P
R
Q
S
Dicrotic wave
Left atrial
pressure
Aortic
pressure
Left
ventricular
pressure
T
130
60
0
Atrial
contraction
Atrial
contraction
Isovolumetric
contraction
Isovolumetric
relaxation
Ventricular
ejection
Ventricular
filling
(e) Phases of the
cardiac cycle
Stroke
volume
0.3 sec
0.1
sec 0.4 sec
Ventricular
systole
Relaxation
period
Atrial
systole
S1 S2 S3 S4
10
1
2
3
4
5
6
7
8
9
10
Isovolumetric relaxation
Ventricular filling
8
9

Regulation of Heart Beat
 Cardiac output depends on heart rate and stroke
volume
 Adjustments in heart rate important in short-term
control of cardiac output and blood pressure
 Autonomic nervous system and epinephrine/
norepinephrine most important

Autonomic regulation
 Originates in cardiovascular center of medulla oblongata
 Increases or decreases frequency of nerve impulses in
both sympathetic and parasympathetic branches of ANS
 Noreprinephrine has 2 separate effects
 In SA and AV node speeds rate of spontaneous depolarization
 In contractile fibers enhances Ca2+ entry increasing
contractility
 Parasympathetic nerves release acetylcholine which
decreases heart rate by slowing rate of spontaneous
depolarization

Nervous System Control of the Heart

Chemical regulation of heart rate
 Hormones
 Epinephrine and norepinephrine increase heart rate and
contractility
 Thyroid hormones also increase heart rate and
contractility
 Cations
 Ionic imbalance can compromise pumping effectiveness
 Relative concentration of K+, Ca2+ and Na+ important

08 Heart.ppt

Recommended

Recommended

More Related Content

Similar to 08 Heart.ppt

Similar to 08 Heart.ppt (20)

Recently uploaded

Recently uploaded (20)

08 Heart.ppt