Heart Anatomy Approximately the size of your fist Location Download

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Heart Anatomy
Approximately the size of your fist
Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the
sternum
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Heart Anatomy
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Figure 18.1
Coverings of the Heart: Anatomy
Pericardium – a double-walled sac around the heart
composed of:
The visceral layer or epicardium lines the
surface of the heart
A superficial fibrous pericardium
A deep two-layer serous pericardium
The parietal layer lines the internal surface of
the fibrous pericardium
They are separated by the fluid-filled pericardial
cavity
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Coverings of the Heart: Physiology
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively frictionfree environment
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Pericardial Layers of the Heart
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Figure 18.2
Heart Wall
Epicardium – visceral layer of the serous pericardium
Myocardium – composed of aerobic muscle (contractile layer)
Composed of cardiac muscle bundles
Fibrous skeleton of the heart – crisscrossing, interlacing
layer of connective tissue
Endocardium – endothelial layer of the inner myocardial
surface
Lines the heart chamber and is continuous with the
endothelial linings of the blood vessels
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Brachiocephalic
trunk
Superior
vena cava
Left common
carotid artery
Left
subclavian artery
Aortic arch
Right
pulmonary artery
Ligamentum
arteriosum
Left pulmonary artery
Ascending
aorta
Pulmonary trunk
Right
pulmonary veins
Right atrium
Right coronary
artery (in coronary
sulcus)
Anterior
cardiac vein
Right ventricle
Marginal artery
Small cardiac vein
Inferior
vena cava
(b)
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Left pulmonary veins
Left atrium
Auricle
Circumflex
artery
Left coronary
artery (in coronary
sulcus)
Left ventricle
Great cardiac vein
Anterior
interventricular artery
(in anterior
interventricular sulcus)
Apex
Figure 18.4b
Aorta
Left
pulmonary artery
Left
pulmonary veins
Auricle
of left atrium
Left atrium
Superior
vena cava
Right
pulmonary artery
Right
pulmonary veins
Right atrium
Great cardiac vein
Inferior
vena cava
Posterior vein
of left ventricle
Right coronary
artery (in coronary
sulcus)
Coronary sinus
Apex
Posterior
interventricular artery
(in posterior
interventricular sulcus)
Middle cardiac vein
(d)
Right ventricle
Left ventricle
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Figure 18.4d
Aorta
Superior vena cava
Right
pulmonary artery
Pulmonary trunk
Right atrium
Right
pulmonary veins
Fossa
ovalis
Pectinate
muscles
Tricuspid
valve
Right ventricle
Chordae
tendineae
Trabeculae
carneae
Inferior
vena cava
(e)
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Left
pulmonary artery
Left atrium
Left
pulmonary veins
Mitral
(bicuspid) valve
Aortic
valve
Pulmonary
valve
Left ventricle
Papillary
muscle
Interventricular
septum
Myocardium
Visceral
pericardium
Endocardium
Figure 18.4e
Atria of the Heart
Atria are the receiving chambers of the heart
Each atrium has a protruding auricle
Atria are relatively small, thin walled chambers
Atria contribute little to the propulsive pumping of
the heart
Blood enters right atria from superior and inferior
venae cavae and coronary sinus
Blood enters left atria from pulmonary veins
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Ventricles of the Heart
Ventricles are the discharging chambers of the
heart
Make up most of the volume of the heart
Trabeculae carnae are irregular ridges of
myocardium
Papillary muscles are involved with valve function
Right ventricle pumps blood into the pulmonary
trunk
Left ventricle pumps blood into the aorta
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Pathway of Blood Through the Heart and
Lungs
Right atrium tricuspid valve right ventricle
Right ventricle pulmonary semilunar valve pulmonary arteries lungs
Lungs pulmonary veins left atrium
Left atrium bicuspid valve left ventricle
Left ventricle aortic semilunar valve aorta
Aorta systemic circulation
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Pathway of Blood Through the Heart
Pulmonary circuit is involved with gas
exchange
Systemic circuit pumps oxygenated
blood to the body
The two ventricles have unequal work
loads
Right ventricle: short, low-pressure
circulation
Left ventricle: long, high-pressure
circulation, 5x more resistance than
r. ventricle
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Coronary Circulation
Blood in the heart provides little nourishment to the heart
Coronary circulation is the shortest circulation in the body
Provided by the r. & l. coronary arteries arising from the base of
the aorta & encircling the heart in the coronary sulcus
These vessels lie in the epicardium and send branches inward
towards the myocardium
Venous blood is collected by the coronary veins following the
same path as the arteries leading to the coronary sinus and then
the r. atrium
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Coronary Circulation: Arterial Supply
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Figure 18.7a
Heart Valves
Heart valves ensure unidirectional blood flow through the
heart
Atrioventricular (AV) valves lie between the atria and the
ventricles & prevent backflow into the atria when
ventricles contract
R. AV: tricuspid valve (3 cusps)
L. AV: bicuspid valve (2 cusps aka mitral valve)
Chordae tendineae anchor AV valves (in the closed
position) to papillary muscles
Papillary muscles contract just prior to ventricular
contraction
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Heart Valves
Aortic & pulmonary semilunar (SL) valves prevent
backflow into the associated ventricles
Made of 3 cusps
Ventricular contraction forces valves open
Backflow fills the cusps thus moving (and closing them)
backward
Due to low back pressure, they are not reinforced with
cordae tendinae
Atrial contraction “pinches” off venae cavae and the
pulmonary veins preventing substantial backflow through
them
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Heart Valves
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Figure 18.8a, b
Heart Valves
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Figure 18.8c, d
Atrioventricular Valve Function
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Figure 18.9
Semilunar Valve Function
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Figure 18.10
Microscopic Anatomy of Heart Muscle
Cardiac muscle is striated, short, fat, branched, and interconnected
Contracts via the sliding filament mechanism
Connective tissue is found in the intercellular space
The connective tissue endomysium is connected to the fibrous skeleton
and acts as both tendon and insertion
The plasma membrane of adjacent muscle fibers interlock at intercalated
discs
The discs contain anchoring desmosomes & gap junctions
Cardiac cells are electrically coupled through these gap junctions
30% of the cell volume is mitochondria
70% of the cell is myofibrils containing typical sarcomeres
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Microscopic Anatomy of Cardiac Muscle
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Figure 18.11
Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and is self-excitable
(automaticity)
Contracts as a unit
Has a long (250 ms) absolute refractory period
(skeletal muscle = 1-2 ms)
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Cardiac Contraction
Cardiac muscle contraction is similar to skeletal muscle contraction:
Depolarization opens a few fast voltage-gated Na+ channels
Presence of T-tubules
Ca++, troponin binding, sliding myofilaments
Cardiac muscle contraction differs from skeletal muscle contraction by:
Sarcoplasmic reticulum Ca++ release:
20% Ca++ from extracellular space (slow Ca++ channels)
80% Ca++ from S.R.
K+ permeability decrease preventing rapid repolarization
As long as Ca++ is entering, contraction continues
After 200ms, Ca++ channels close and K+ channels open
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Heart Physiology: Intrinsic Conduction
System
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker
potentials
Use calcium influx (rather than sodium) for rising
phase of the action potential
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Energy & Electrical Requirements
The heart relies exclusively on aerobic respiration
Will use glucose and fatty acids, whichever is available
The heart does not rely on the nervous system to contract
However, autonomic nerve fibers can alter the basic
rhythem
Setting the basic rhythem: Intrinsic Conduction System:
Presence of gap junctions
“In house” conduction
Consists of non-contractile cardiac cells that
initiate and distribute impulses throughout the
heart
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Action potential Initiation by Autorhythmic Cells
Autorhythmic cells do not maintain a stable resting
membrane potential
Rather, they continuously depolarize drifting
towards threshold initiating the action potential
This is due to ion channels in the sarcolemma
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Action potential Initiation by Autorhythmic Cells
Hyperpolarization closes K+ channels and opens
slow Na+ channels
At 40 mV, Ca++ channels open producing the
rising phase of the action potential and reversal of
the membrane potential
Repolarization, as in skeletal muscle, reflects an
increase in K+ permeability and efflux from the
cell
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Pacemaker and Action Potentials of the Heart
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Figure 18.13
Cardiac Membrane Potential
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Figure 18.12
Heart Physiology: Sequence of Excitation
1) Sinoatrial (SA) node (located in the r. atrium)
generates impulses about 100 times/minute
Sets pace for the heart as a whole (pacemaker)
2) Atrioventricular (AV) node delays the impulse
approximately 0.1 second
3) Impulse passes from atria to ventricles via the
atrioventricular bundle
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Heart Physiology: Sequence of Excitation
4) AV bundle splits into two pathways in the
interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex of
the heart
5) Purkinje fibers carry the impulse to the heart apex,
ventricular walls, and papillary muscles
Ventriclular contraction begins at the apex and moves
superiorly
SA node: 100x/min (dominates)
AV node: 50x/min
AVbunde (Purkinje fibers): 30x/min
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Cardiac Intrinsic Conduction
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Figure 18.14a
Heart Excitation Related to ECG
SA node generates impulse;
atrial excitation begins
SA node
Impulse delayed
at AV node
AV node
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Impulse passes to
heart apex; ventricular
excitation begins
Bundle
branches
Ventricular excitation
complete
Purkinje
fibers
Figure 18.17
Extrinsic Innervation of the Heart
Heart is stimulated by
the sympathetic
cardioacceleratory
center
Heart is inhibited by
the parasympathetic
cardioinhibitory center
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Figure 18.15
Extrinsic Innervation of the Heart
Cardiac centers are located in the medulla
oblongata
Cardioacceleratory center projects to sympathetic
neurons in the T1-T5 level of the spinal cord
Cardioinhibitory center sends impulses to the
parasympathetic dorsal vagus nucleus in the
medulla
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Electrocardiography
Electrical activity is recorded by electrocardiogram (ECG)
Electrical currents generated in the heart spread throughout the body
3 waves (deflections)
P wave corresponds to depolarization of SA node thru the atria.
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex
P-Q interval is the time from the beginning of atrial excitation to the
beginning of ventricular excitation
S-T segment is the time when the ventricle is depolarized
Q-T interval is the beginning of ventricular depolarization thru ventricular
repolarization
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Electrocardiography
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Figure 18.16
Cardiac Cycle
Cardiac cycle refers to all events associated with
blood flow through the heart
Systole – contraction of heart muscle
Diastole – relaxation of heart muscle
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Heart Sounds
Two sounds can be distinguished when the thorax
is ausculated (listened to) w/ stethescope
They are associated w/ the closing of heart valves
First sound occurs as AV valves close and signifies
beginning of systole
Second sound occurs when SL valves close at the
beginning of ventricular diastole
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Heart Sounds
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Figure 18.19
Phases of the Cardiac Cycle
Ventricular filling – mid-to-late diastole
Heart blood pressure is low as blood
enters atria and flows into ventricles
AV valves are open but drift to closed
position as blood fills ventricle (80%)
Atrial systole fills remaining 20% of
ventricle
Atrial systole: depolarization (Pwave)
Atria contract, rise in atrial
pressure
Ventricle in final part of diastole
phase
Atrial diastole
Ventricles depolarize (QRS complex)
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Phases of the Cardiac Cycle
Ventricular systole
Atria are in diastole
Ventricles begin
contracting
Rising ventricular pressure
results in closing of AV
valves
Ventricular ejection phase
opens semilunar valves
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Phases of the Cardiac Cycle
Early diastole (following T wave)
Ventricles relax
SL valves close w/ backflow from
aorta and pulmonary arteries
When blood pressure on the atrial
side excedes that in the ventricles,
the AV valves open and
ventricular filling begins again
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Phases of the Cardiac Cycle
Notes:
Blood flow thru the heart is controlled totally by
pressure changes
Blood flows down pressure gradients toward the
lower pressure
Right side is low pressure
Left side is high pressure
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Cardiac Output (CO) and Reserve
CO is the amount of blood pumped by each
ventricle in one minute
CO is the product of heart rate (HR) and stroke
volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a
ventricle with each beat
Cardiac reserve is the difference between resting
and maximal CO
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Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70
ml/beat)
CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke Volume
SV = end diastolic volume (EDV; fill) minus end
systolic volume (ESV; contraction)
EDV = End Diastolic Volume. Amount of blood
collected in a ventricle during diastole
ESV = End Systolic Volume. Amount of blood
remaining in a ventricle after contraction
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Factors Affecting Stroke Volume
Most important factors are:
Preload – amount ventricles are stretched by
contained blood (affects EDV)
Contractility – cardiac cell contractile force due to
factors other than EDV (affects ESV)
Afterload – back pressure exerted by blood in the
large arteries leaving the heart (affects ESV)
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Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle
cells before they contract is the critical factor
controlling stroke volume
Slow heartbeat and exercise increase venous return
to the heart, increasing SV by allowing more time
to fill
Blood loss and extremely rapid heartbeat decrease
SV
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Preload and Afterload
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Figure 18.21
Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength,
independent of stretch and EDV
Enhanced contractility results in increased ejection
from the heart (SV)
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs
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Extrinsic Factors Influencing Stroke Volume
Afterload: back pressure exerted by arterial blood
The pressure that must be overcome for ventricles
to eject blood
Hypertension (high blood pressure) reduces the
ability of ventricles to eject blood
More blood remains in the heart after systole
which increases ESV and decreases SV
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Regulation of Heart Rate
Autonomic Nervous System is the most important
controller
NE binds to B-adrenergic receptors (GPCRs) in the
heart causing threshold to be reached more quickly
accelerating relaxation phase
Pacemaker fires more rapidly, heart rate increases
Also enhances Ca++ entry into contractile cells
ESV & EDV fall (less time to fill)
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Heart Contractility
and Norepinephrine
Sympathetic
stimulation releases
norepinephrine and
initiates a cyclic AMP
second-messenger
system
Extracellular fluid
Norepinephrine
β1-Adrenergic
receptor
Adenylate cyclase Ca2+
Ca2+
channel
Cytoplasm
GTP
GTP
1
GDP
ATP
cAMP
Active
protein
kinase A
Ca2+
Inactive
protein
kinase A
3
Ca2+
2
Enhanced
actin-myosin
interaction
Troponin
uptake
pump
binds
to
Ca2+
SR Ca2+
channel
Cardiac muscle
force and
velocity
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Sarcoplasmic
reticulum (SR)
Figure 18.22
Regulation of Heart Rate: Autonomic Nervous
System
Sympathetic nervous system (SNS) stimulation is activated
by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is
mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart
rate and causing vagal tone
E.g. cutting the vagus nerve results in increased heart
rate equal to that of the pacemaker (100 beats/min)
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Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex
Increased atrial filling leads to increased heart rate
by stimulating both the SA node and atrial stretch
receptors
This leads to reflex adjustments causing increased
stimulation of the heart
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Chemical Regulation of the Heart
The hormones epinephrine and thyroxine increase
heart rate
Intra- and extracellular ion concentrations must be
maintained for normal heart function
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Here endth the lesson
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