THE CARDIOVASCULAR
SYSTEM: THE HEART
HEART LOCATION
• Size, Location, and
Orientation:
– The heart is the size of a
fist and weighs 250-300
grams
– The heart is found in
mediastinum and two-thirds
lies left of the midsternal
line
– The base is directed
toward the right shoulder
and the apex points toward
the left hip
HEART LOCATION
Coverings of the Heart
•
The heart is enclosed in a double-walled
sac called the pericardium:
–
The loosely fitting superficial part of this sac is
the fibrous pericardium (tough, dense
connective tissue)
•
•
•
•
Deep to fibrous pericardium is the
serous pericardium:
–
Thin, slippery, two-layer serous membrane
•
•
•
•
Protects the heart
Anchors it to surrounding structures
Prevents overfilling of the heart with blood
The parietal pericardium lines the internal
surface of the fibrous pericardium
Then parietal pericardium turns inferiorly and
continues over the external heart surface as the
visceral pericardium, or epicardium, which is
an integral part of the heart wall
Between the parietal and visceral layers
is the slitlike pericardial cavity, which
contains a film of serous fluid
The serous membranes, lubricated by the
fluid, glide smoothly past one another
during heart activity, allowing the mobile
heart to work in a relatively friction-free
environment
Coverings of the Heart
HOMEOSTATIC IMBALANCE
• Pericarditis: inflammation of the pericardium
– Hinders production of serous fluid and roughens the
serous membrane surface
– Heart rubs against its pericardial sac creating a
creaking noise (pericardial friction rub) that can be
heard with a stethoscope
– Deep pain to the sternum
– Pericardia stick together and impede heart activity
– Severe cases:
• Large amounts of inflammatory fluid seeps into the
pericardial cavity compressing the heart, limiting its ability to
pump blood (cardiac tamponade)
– Treated by inserting a syringe into the pericardial cavity and
draining off the excess fluid
Layers of the Heart
•
•
•
•
The heart wall is composed of three
layers, all richly supplied with blood
vessels
Superficial epicardium is the visceral layer
of the serous pericardium
– Often infiltrated with fat, especially in
older people
Middle layer, myocardium,is composed
mainly of cardiac muscle and forms the bulk
of the heart
– It is the layer that contracts
– Cardiac muscle cells are tethered to
one another by crisscrossing
connective tissue fibers and arranged
in spiral or circular bundles reinforcing
the myocardium internally and anchors
the cardiac muscle fibers
The third layer, the endocardium
(squamous epithelium), lines the chambers
of the heart and is continuous with the
endothelial linings of the blood vessels
leaving and entering the heart
HEART LAYERS
CARDIAC MUSCLE
CHAMBERS and ASSOCIATED GREAT VESSELS
• Heart has four chambers:
– Two superior atria
– Two inferior ventricles
• Internal partition that divides
the heart longitudinally is
called the interatrial septum
where it separates the atria,
and the interventricular septum
where it separates the
ventricles
• Right ventricle forms most of
the anterior surface of the
heart
• Left ventricle dominates the
infero-posterior aspect of the
heart and forms the heart apex
CHAMBERS and ASSOCIATED GREAT VESSELS
• Two grooves visible on
the heart surface indicate
the boundaries of its four
chambers and carry the
blood vessels supplying
the myocardium
• The atrioventricular
groove, or coronary
sulcus, encircles the
junction of the atria and
ventricles like a crown
CHAMBERS and ASSOCIATED GREAT VESSELS
• The anterior
interventricular sulcus,
cradling the anterior
interventricular artery,
marks the anterior
position of the septum
separating the right and
left ventricles
• It continues as the
posterior
interventricular sulcus,
which provides a similar
landmark on the heart’s
posteroinferior surface
CHAMBERS and ASSOCIATED GREAT VESSELS
CHAMBERS and ASSOCIATED GREAT VESSELS
HEART ANATOMY
Atria: The Receiving Chambers
• Small, wrinkled, protruding
appendages called auricles
increase the atrial volume
• Internally:
– Posterior portion smoothwalled
– Anterior portion the walls are
ridged with bundles of muscle
tissue (pectinate muscles)
– Anterior and posterior regions
are separated by a ridge
called the crista terminalis
– Interatrial septum bears a
shallow depression (fossa
ovalis), that marks the spot
where an opening, the
foramen ovale, existed in the
fetal heart
INTERNAL HEART ANATOMY
Atria: The Receiving Chambers
Atria: The Receiving Chambers
•
•
•
Receiving chambers for blood
returning to the heart from the
circulation
Small, thin-walled chambers which
contract only minimally to push blood
“next door” into the ventricles
Blood enters the right atrium via
three veins:
–
–
–
•
Superior vena cava returns blood from
body regions superior to the diaphragm
Inferior vena cava returns blood from
body areas below the diaphragm
Coronary sinus collects blood draining
from myocardium
Blood enters the left atrium via four
veins:
–
Pulmonary veins transport blood from
the lungs back to the heart
Atria: The Receiving Chambers
Ventricles: The Discharging Chambers
•
•
•
•
•
•
Together the ventricles make up
most of the volume of the heart
Marking the internal walls of the
ventricular chambers are irregular
ridges of muscle called trabeculae
carneae which add support and
strength
Papillary muscles play a role in valve
function
Discharging chambers
Pumps of the heart
When ventricles contract, blood is
propelled out of the heart into
circulation:
–
–
The right ventricle pumps blood into
the pulmonary trunk, which routes the
blood to the lungs where gas exchange
occurs
The left ventricle pumps blood into the
aorta, the largest artery in the body, to
the systemic trunk
Ventricles: The Discharging Chambers
INTERNAL HEART ANATOMY
Pathway of Blood Through the Heart
• The right side of the heart
pumps blood into the
pulmonary circuit:
– Blood returning from the body
is relatively oxygen-poor and
carbon dioxide-rich
– Blood enters the right atrium
and passes into the right
ventricle, which pumps it to
the lungs via the pulmonary
arteries (conduct blood away
from the heart)
– In the lungs, the blood unloads
carbon dioxide and picks up
oxygen (oxygenated)
• The left side of the heart
pumps blood into the
systemic circuit
Pathway of Blood Through the Heart
•
•
•
•
•
Freshly oxygenated blood from the
lungs is carried by the pulmonary
veins (toward the heart) back to the
left side of the heart
Left side of the heart is the
systemic circuit
Freshly oxygenated blood leaving the
lungs is returned to the left atrium and
passes into the left ventricle, which
pumps it into the aorta
The aorta transports blood via smaller
arteries to the body tissues, where
gases and nutrients are exchanged
across the capillary walls
Then the blood, once again loaded
with carbon dioxide and depleted of
oxygen, returns through the systemic
veins to the right atrium via the
superior vena cava and inferior vena
cava
Pathway of Blood Through the Heart
• Although equal volumes of
blood are pumped to the
pulmonary and systemic
circuits at any moment, the
two ventricles have unequal
work-loads:
– Pulmonary circuit, served by
the right ventricle, is a short,
low-pressure circulation
– Systemic circuit, associated
with the left ventricle, takes a
pathway through the entire
body and encounters about
five times as much friction, or
resistance to blood flow
Ventricles: The Discharging Chambers
SYSTEMIC AND PULMONARY
CIRCULATION
Pathway of Blood Through the Heart
•
•
•
•
Functional differences of the
two ventricles are revealed in
their anatomy
The walls of the left ventricle
are three-four times as thick as
those of the right ventricle, and
its cavity is nearly circular
The right ventricular cavity is
flattened into a crescent shape
that partially encloses the left
ventricle, much the way a hand
might loosely grasp a clenched fist
Consequently, the left ventricle
can generate much more
pressure than the right and is a
far more powerful pump
SYSTEMIC AND PULMONARY
CIRCULATION
Coronary Circulation
•
The heart receives no nourishment from the blood as it passes
through the chamber:
– The myocardium is too thick to make diffusion a practical means of nutrient
delivery
•
The coronary circulation provides the blood supply for the heart cells:
– The arterial supply of the coronary circulation is provided by the right and left
coronary arteries, both arising from the base of the aorta and encircling the heart
in the atrioventricular groove
Coronary Circulation
• The left coronary artery runs toward the left side of
the heart and then divides into its major branches:
– Anterior interventricular artery : follows the anterior
interventricular sulcus and supplies blood to the interventricular
septum and anterior walls of both ventricles
– Circumflex artery: supplies the left atrium and the posterior
walls of the left ventricle
Coronary Circulation
•
The right coronary artery: courses to the right side of the heart, where it also
divides into two branches
– Marginal artery: serves the myocardium of the lateral right side of the heart
– Posterior interventricular artery: runs to the heart apex and supplies the
posterior ventricular walls
• Near the apex of the heart, this artery merges (anastomoses) with the
anterior interventricular artery
• Together the branches of the right coronary artery supply the right
atrium and nearly all the right ventricle
CORONARY CIRCULATION
CORONARY CIRCULATION
• The arterial supply of the heart varies considerably
– Example:
• 15% of people, the left coronary artery gives rise to both the
anterior and posterior interventricular arteries
• 4% of people, a single coronary artery supplies the whole heart
– There may be both right and left marginal arteries
– There are many anastomoses among the coronary arterial
branches:
• These fusing networks provide additional (collateral) routes for
blood delivery to the heart
– Explains how the heart can receive adequate nutrition even when one
of its coronary arteries is almost entirely occluded
– Even so, complete blockage of a coronary artery leads to tissue death
and heart attack
CORONARY CIRCULATION
• After passing through then
capillary beds of the
myocardium, the venous blood
is collected by the cardiac
veins, whose paths roughly
follow those of the coronary
arteries
• These veins join together to
form an enlarged vessel called
the coronary sinus, which
empties the blood into the right
atrium
• Obvious on the posterior
aspect of the heart
CORONARY CIRCULATION
• The sinus has three large tributaries:
– Great cardiac vein: in the anterior interventricular sulcus
– Middle cardiac vein: in the posterior interventricular sulcus
– Small cardiac vein: running along the heart’s right inferior
margin
– Additionally, several anterior cardiac veins empty directly
into the right atrium anteriorly
HOMEOSTATIC IMBALANCE
• Blockage of the coronary arterial circulation can be serious and
sometimes fatal
• Angina pectoris:
– Thoracic pain caused by a fleeting deficiency in blood delivery to
the myocardium
• May result from stress-induced spasms of the coronary arteries or from
increased physical demands on the heart
• Myocardial cells are weakened by the temporary lack of oxygen but do not
die
• Myocardial infarction (MI):
– There is prolonged coronary blockage that leads to cell death
– Commonly called a heart attack or coronary
– Because adult cardiac muscle is essentially amitotic, most areas of cell
death are repaired with noncontractile scar tissue
• Whether or not a person survives a myocardial infraction depends on the
extent and location of the damage
• Damage to the left ventricle, which is the systemic pump, is most
serious
Heart Valves
• Blood flows through the heart in one direction: from
atria to ventricles and out the great arteries leaving the
superior aspect of the heart
• This one-way traffic is enforced by valves that open
and close in response to differences in blood pressure
on their two side
Heart Valves
Heart Valves
Heart Valves
• Two atrioventricular (AV)
valves, one located at each
atrial-ventricular junction (
tricuspid and bicuspid
valves) prevent backflow
into the atria when the
ventricles contract
– Right AV valve (tricuspid)
has three flexible cusps (flaps
of endocardium reinforced by
connective tissue cores)
– Left AV valve (bicuspid) has
two flexible cusps
• Commonly called the mitral
valve because of its
resemblance to the two-sided
bishop’s miter or hat
Heart Valves
Heart Valves
INTERNAL HEART ANATOMY
Heart Valves
• Attached to each AV
valve flap are tiny
white collagen
cords called
chordae tendineae
(heart strings):
– Anchor the cusps to
the papillary muscles
protruding from the
ventricular walls
HEART VALVES
Heart Valves
•
Blood returning to the heart fills
atria, putting pressure against
AV valve
– AV valve opens
•
•
When the heart is relaxed, the AV
valves are open hanging limply
into the ventricular chambers
below and blood flows into the
atria and then through the open
AV valves into the ventricles
When ventricles contracts,
compressing the blood in their
chambers, the intraventricular
pressure rises, forcing the
blood superiorly against the
valve flaps
– As a result, the flaps edges
meet, closing the AV valve
Heart Valves
• The chordae tendineae
and the papillary
muscles serve as guywires to anchor the
valve flaps in their
closed position
– If the cusps were not
anchored in this manner,
they would be blown
upward into the atria, in the
same way an umbrella is
blown inside out by a gusty
wind
Heart Valves
Heart Valves
•
•
•
The aortic and pulmonary semilunar
valves are found in the major
arteries leaving the heart (aorta and
pulmonary trunk)
– They prevent backflow of blood
into the ventricles
Each SL valve is fashioned from three
pocketlike cusps, each shaped like a
crescent moon (half-moon)
Mechanism of action differs from that
of the AV valves
– When the ventricles contracts and
intraventricular pressure rises
above the pressure in the aorta
and pulmonary trunk, the SL
valves are forced open and their
cusps flatten against the arterial
walls as blood rushes past them
the semilunar valves are open
HEART VALVE OPERATION
Heart Valves
• When the ventricles
relax, and the blood
(no longer propelled
forward by the
pressure of
ventricular
contraction) flows
backward toward
the heart, it fills the
cusps and closes
the valves
HEART VALVE OPERATION
Heart Valves
• There are no valves guarding the entrances
of the venae cavae and pulmonary veins into
the right and left atria, respectively
• Small amounts of blood do spurt back into these
vessels during atrial contraction, but backflow is
minimal because as it contracts, the atrial
myocardium compresses ( and collapses)
these venous entry points
HOMEOSTATIC IMBALANCE
•
•
Heart valves are simply devices, and the heart—like any mechanical
pump—can function with “leaky” valves as long as the impairment is
not too great
Severe valve deformities can seriously hamper cardiac function
– Incompetent valve:
• Forces the heart to repump the same blood over and over because the valve does not
close properly and blood backflows
– Valvular stenosis (narrowing):
• The valve flaps become stiff (typically because of scar tissue formation following
endocarditis or calcium salt deposit) and constrict then opening
• This stiffness compels the heart to contract more forcibly than normal
• Heart’s work load increases
• Heart may be severely weakened
•
Valve replacement:
– Synthetic valve
• Pig heart valve chemically treated to prevent rejection
• Cryopreserved valves from human cadavers
• Tissue-engineered polymer valves
CARDIAC MUSCLE CELLS
• Cardiac muscle (like skeletal
muscle) is striated and
contraction occurs via the
sliding filament mechanism
• In contrast to skeletal muscle,
cardiac muscle is short, fat,
branched
• Intercellular spaces are filled
with a loose connective tissue
matrix containing numerous
capillaries
CARDIAC MUSCLE CELLS
•
Plasma membranes of adjacent
cardiac cells interlock like the
ribs of two sheets of corrugated
cardboard (intercalated discs)
– Disc contain anchoring
desmosomes and gap
junctions:
• Desmosomes prevent adjacent
cells from separating during
contraction
• Gap junctions allow ions to pass
from cell to cell
•
Large mitochondria account for
about 25% of the volume of the
cardiac cell (compared with
only about 2% in skeletal
muscle)
– Gives cardiac cells a high
resistance to fatigue
Mechanism and Events of Contraction
• 1. Means of stimulation:
• Some cardiac muscle cells are self-excitable and can initiate
their own depolarization in a spontaneous and rhythmic way
• 2. Organ versus motor unit contraction
– Skeletal muscle:
• All cells of a given motor unit (but not the entire muscle) are
stimulated and contract at the same time
• Impulses do not spread from cell to cell
– Cardiac muscle:
• The heart contracts as unit or not at all
• Transmission of the depolarization wave across the heart from cell
to cell via ion passage through gap junctions, which tie all cardiac
muscle cells together into a single contractile unit
Mechanism and Events of Contraction
• 3. Length of absolute refractory period:
– Refractory period: repolarization period in which the cell cannot
be stimulated again until repolarization is complete
• Repolarization: movement of the membrane potential to the initial
resting (polarized) state
– The heart’s absolute refractory period (the inexcitable period
when Na+ channels are still open or are closed or inactivated) is
longer than a skeletal muscle’s preventing tetanic contractions
(smooth, continues contraction without any evidence of
relaxation)
• Long cardiac refractory period normally prevents tetanic
contractions, which would stop the heart’s pumping action
– 250ms in cardiac muscle (nearly as long as the contraction)
– 1-2 ms in skeletal muscle (contraction last 20 to 100ms)
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
• (a) relationship between the action potential,
period of contraction, and absolute refractory
period in a single ventricular cell
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
• (b) Membrane permeability changes during the
action potential (The Na+ permeability rises to a
point off the scale during the action potential)
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
• Influx of Na+ from the extracellular fluid into cardiac cells initiates a
positive feedback cycle that causes the rising phase of the action
potential (-90 mV to nearly + 30 mV) by opening voltage-regulated
fast Na+ channels
• Period of increased Na+ permeability is very brief, because the
sodium gates are quickly inactivated and the Na+ channels close
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
• Transmission of the depolarization causes
causes the sarcoplasmic reticulum to release
Ca2+ into the sarcoplasm (cytoplasm)
• Ca2+ provides the signal for cross bridge
activation
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
•
•
•
•
Although Na+ permeability has plummeted to its resting levels and
repolarization has begun by this point, the calcium surge across the
membrane prolongs the depolarization potential tracing (a)
At the same time, K+ permeability decreases, which also prolongs the
plateau and prevents rapid repolarization
As long as Ca2+ is entering, the cells continue to contract
Notice in (a) that muscle tension develops during the plateau, and peaks
just after the plateau ends
Membrane Potential and Membrane Permeability
during Action Potentials of Contractile Cardiac
Muscle Cells
•
•
•
After about 200ms, the slope of the action potential tracing falls rapidly
This results from closure of Ca2+ channels, Ca2+ transport from the cytosol
into the extracellular space or SR (or mitochondria), and opening of voltageregulated K+ channels, which allows a rapid loss of potassium from the cell
that restores the resting membrane potential
During repolarization, Ca2+ is pumped back into the SR and the extracellular
space
Energy Requirements
• Cardiac muscle has more mitochondria than skeletal
muscle does, reflecting its greater dependence on
oxygen for its energy metabolism
– The heart relies exclusively on aerobic respiration for its energy
demands (skeletal muscle during oxygen deficits can carry out
anaerobic respiration)
– Cardiac muscle cannot incur much of an oxygen debt and still
operate effectively
• Cardiac muscle is capable of switching nutrient
pathways to use whatever nutrient supply is
available
– Thus, the real danger of an inadequate blood supply to the
myocardium is lack of oxygen, not of nutrient fuels
HOMEOSTATIC IMBALANCE
• When a region of heart muscle is deprived of blood
(is Ischemic), the oxygen-starved cells begin to
metabolize anaerobically, producing lactic acid
• The rising H+ level that results hinders the cardiac cells’
ability to produce the ATP they need to pump Ca2+ into
the extracellular fluid
• The resulting increase in intracellular H+ and Ca2+ levels
causes the gap junctions (which are usually open) to
close, electrically isolating the damaged cells and forcing
generated action potentials to find alternate routes to the
cardiac cells beyond them
• If the ischemic area is large, the pumping activity of
the heart as a whole may be severely impaired,
leading to a heart attack
HEART PHYSIOLOGY
• Electrical Events:
– Intrinsic conduction system is made up of
specialized cardiac cells that initiate and
distribute impulses, ensuring that the
heart depolarizes in an orderly fashion
• Even if all nerve connections to the heart are
severed, the heart continues to best
HEART PHYSIOLOGY
•
•
•
The autorhythmic cells have an
unstable resting potential, called
pacemaker potentials, that
continuously depolarizes
The mechanism of the pacemaker
potential is believed to result from
gradually reduced membrane
permeability to K+
Then, because Na+ permeability is
unchanged and Na+ continues to
diffuse into the cell at a slow rate,
the balance between K+ loss and
Na+ entry is upset and the
membrane interior becomes less
and less negative (more positive)
HEART PHYSIOLOGY
•
•
•
Ultimately, at threshold
(approximately -40 mV), fast Ca2+
channels open, allowing explosive
entry of Ca2+ (as well as some
Na+) from the extracellular space
Thus, in autorhythmic cells, it is
the influx of Ca2+ (rather than Na+)
that produces the rising phase of
the action potential and reverses
the membrane potential
Once repolarization is complete,
K+ channels are inactivated, K+
permeability declines, and the
slow depolarization to threshold
begins again
Pacemaker and Action Potentials of
Autorhythmic Cells of the Heart
HEART PHYSIOLOGY
• Autorhythmic
cardiac cells are
found in the
following areas:
–
–
–
–
Sinoatrial node
Atrioventricular node
Atrioventricular bundle
Right and left bundle
branches
– Ventricular walls
(Purkinje fibers)
HEART PHYSIOLOGY
• Impulses pass
across the heart in
the same order:
sinoatrial node,
atrioventricular
node,
atrioventricular
bundle, right and
left bundle
branches, and
Purkinjie fibers
The intrinsic conduction system of the heart and
succession of the action potential through selected
areas of the heart during one heartbeat
Sequence of Excitation
• Sinoatrial node (SA):
Pacemaker:
– Located in the right atrium
wall, just inferior to the
entrance of the superior vena
cava
– Typically generates impulses
about 75 times every minute
• Its inherent rate in the
absence of extrinsic neural
and hormonal factors is closer
to 100 times per minute
• Sets the pace for the heart
• Its characteristic rhythm
(sinus rhythm) determines
heart rate
Sequence of Excitation
• Atrioventricular node:
– From the SA node, the
depolarization wave
spreads via gap junctions
throughout the atria and via
the internodal pathway to
the atrioventricular (AV)
node, located in the inferior
portion of the interatrial
septum immediately above
the tricuspid valve
Sequence of Excitation
• Atrioventricular bundle:
– From the AV node, the
impulse sweeps to the
atrioventricular bundle (bundle
of His) in the superior oart of
the interventricular septum
– Although the atria and
ventricles abut each other,
they are not connected by gap
junctions
– The AV bundle is the only
electrical connection between
them
– The balance of the AV junction
is insulated by the
nonconducting fibrous
skeleton of the heart
Sequence of Excitation
• Right and Left Bundle
Branches:
• The AV bundle persists
only briefly before
splitting into two
pathways—the right and
left bundle branches
which course along the
interventricular septum
toward the heart apex
Sequence of Excitation
•
Purkinje Fibers:
– Long strands of barrel-shaped
cells with few myofibrils
– Complete the pathway through the
interventricular septum, penetrate
into the apex, and then turn
superiorly into the ventricular walls
– Bulk of ventricular depolarization
depends on these fibers and,
ultimately, on cell-to-cell
transmission of the impulses via
gap junctions between the
ventricular muscle cells
– Because the left ventricle is much
larger than the right, the fibers are
more elaborate in the left ventricle
– Directly supply the papillary
muscles which are excited to
contract before the rest of the
ventricular muscles
Sequence of Excitation
• The total time between
initiation of an impulse by the
SA node and depolarization of
the last of the ventricular
muscle cells is approximately
0.22 s (220 ms) in a healthy
human heart
• A wringing contraction begins
at the heart apex and moves
toward the atria, following the
direction of the excitation wave
through the ventricle walls
• This ejects some of the
contained blood superiorly into
the large arteries leaving the
ventricles
HOMEOSTATIC IMBALANCE
• Arrhythmias:
– Uncoordinated atria and ventricular contractions
• Fibrillation:
– Condition of rapid and irregular or out-of-phase contractions in
which control of heart rhythm is taken away from the SA node by
rapid activity in other heart regions
• Compared to a squirming bag of worms
• Fibrillating ventricles are useless as pumps
• Unless defibrillated, circulation stops and brain death occurs
– Accomplished by electrically shocking the heart
» Depolarizes the entire myocardium (hope is: the slate is wiped
clean)
» SA node will begin to function normally and sinus rhythm
reestablished
– Implantable cardioverter defibrillators (ICDs)
» Slows an abnormally fast heart or emits an electrical shock if the
heart begins to fibrillate
Defibrillator
Defibrillator
Defibrillator
Defibrillator
HOMEOSTATIC IMBALANCE
• A small region of the heart becomes hyperexcitable, sometimes as a
result of too much caffeine or nicotine, and generates impulses more
quickly than the SA node
– Leads to premature contractions (extrasystole)
• Heart Block:
– A blockage that interferes with the impulse transmission route from atria
to ventricle
– Interferes with the ability of the ventricles to receive pacing impulses
– In total heart block no impulses get through and the ventricles beat at
their intrinsic rate, which is too slow to maintain adequate circulation
– A fixed-rate artificial pacemaker, set to deliver impulses at a constant
rate, is usually implanted
– Those suffering from partial block, in which some of the atrial impulses
reach the ventricles, commonly receive demand-type pacemakers,
which deliver impulses only when the heart is not transmitting on its own
PACEMAKERS
PACEMAKERS
PACEMAKER
PACEMAKER
Extrinsic Innervation of the Heart
• Although the basic heart rate is set by the
intrinsic conduction system, fibers of the
autonomic nervous system modify the beat
and introduce a subtle variability from one
beat to the next
• The autonomic nervous system modifies the
heartbeat:
– Sympathetic center increases rate and depth of
the heartbeat
– Parasympathetic center slows the heartbeat
Extrinsic Innervation of the Heart
•
•
•
Cardiac centers are located in
the medulla oblongata
Sympathetic
(Cardioacceleratory Center)
projects to motor neurons in the
T1-T5 level of the spinal cord
– Innervate with the SA and AV
nodes, heart muscle, and the
coronary arteries
– Stimulates heart rate
Parasympathetic
(Cardioinhibitory Center) sends
impulses to the dorsal vagus
nucleus in the medulla, which in
turn sends inhibitory impulses to
the heart via branches of the
vagus nerves
– Project most heavily to the SA
and AV nodes
– Slows heart rate
Autonomic innervation of the Heart
Electrocardiography
• The electrical currents generated in and transmitted
through the heart spread throughout the body and
can be amplified with an electrocardiograph
– Graphic recording of heart activity obtained is called an
electrocardiogram (ECG or EKG)
• An ECG is a composite of all of the APs (action potentials)
generated by nodal and contractile cells at a given time and not, as
sometimes assumed, a tracing of a single AP
• Typically 12 leads used (positioned at various sites on the body
surface)
• 3 are bipolar (two poles: AC current ?) leads that measure the
voltage difference either between the arms or between an arm and
a leg
• 9 are unipolar (one pole) leads
• Together the 12 leads provide a fairly comprehensive picture of the
heart’s electrical activity
Electrocardiography
Electrocardiography
• A typical ECG has three
distinguishable waves
called deflection waves
– Small P wave:
• Lasts about 0.08 s
• Results from movement of
the depolarization wave
from the SA node
through the atria
• Approximately 0.1 s after
the P wave begins, the
atria contract
The sequence of excitation of the heart related to
the deflection waves of an ECG tracing
Electrocardiography
• P-Q interval:
– The time from the beginning of
atrial excitation to the
beginning of ventricular
excitation
– About 0.16 s
– Sometimes called the P-R
interval because the Q wave
tends to be very small
– It includes atrial
depolarization (and
contraction) as well as the
passage of the
depolarization wave through
the rest of the conduction
system
The sequence of excitation of the heart related to
the deflection waves of an ECG tracing
Electrocardiography
• The large QRS complex:
– Results from ventricular
depolarization and
precedes ventricular
contraction
– It has a complicated shape
because the paths of the
depolarization waves
through the ventricular
walls change continuously,
producing corresponding
changes in current
direction
– Average duration is 0.08 s
The sequence of excitation of the heart related to
the deflection waves of an ECG tracing
Electrocardiography
• S-T segment:
– Action potential is in its
plateau phase
– Entire ventricular
myocardium is
depolarized
Electrocardiography
• The T wave:
– Caused by ventricular
repolarization
– Typically lasts about 0.16 s
– Repolarization is slower than
depolarization
• T wave is more spread out
and has a lower amplitude
(height) than the QRS wave
– Because atrial repolarization
takes place during the period
of ventricular excitation, the
wave representing atrial
repolarization is normally
obscured by the large QRS
complex being recorded at the
same time
Electrocardiography
• Q-T interval:
– Lasting about 0.8 s
– Period from the
beginning of
ventricular
depolarization
through ventricular
repolarization
Electrocardiography
Electrocardiography
• In a healthy heart, the size, duration,
and timing of the deflection waves tend
to be consistent
• Changes in the pattern or timing of the
ECG may reveal a diseased or damaged
heart or problems with the heart’s
conduction system
Electrocardiography
• An enlarged R wave:
hints of enlarged
ventricles
• Flattened T wave:
indicates cardiac
ischemia (deficient
blood flow)
• Prolonged Q-T interval:
reveals are polarization
abnormality that
increases the risk of
ventricular arrhythmias
ELECTROCARDIOGRAM
Normal and Abnormal
ECG Tracings
• a: Normal sinus
rhythm
• b: Junctional
rhythm:
– SA node nonfunctional
– P waves absent
– Heart rate paced by
AV node at 40-60
beats/min
Normal and Abnormal
ECG Tracings
• c: Second degree heart
block:
– Some P waves not
conducted through AV
node
– More P than QRS waves
• Where P waves are
conducted normally, the
P:QRS ratio is 1:1
• In total heart block, there
is no whole number ratio
between P and QRS
waves, and the ventricles
are no longer paced by
the SA node
Normal and Abnormal
ECG Tracings
• d: Ventricular
fibrillation:
– Chaotic, grossly
irregular, bizarre ECG
deflections
– Acute heart attack and
electric shock
HEART SOUNDS
• Normal: two sounds (lub-dub)
– The basic rhythm of the heart sounds is lub-dup,
pause, lub-dup, pause, and so on, with the pause
indicating the quiescent period
• The first heart sound, lub, corresponds to closure of the
AV valves
– Signifies the beginning of systole when ventricular pressure
rises above atrial pressure
– Tends to be louder, longer, and more resonant than the second
• The second heart sound, dup, corresponds to the
closure of the semilunar valves
– Short, sharp sound
– Beginning of ventricular diastole
Summary of events occurring in the
Heart during the Cardiac Cycle
HEART SOUNDS
•
Because the mitral valve closes
slightly before the tricuspid
valve does, and the aortic SL
valve generally snaps shut just
before the pulmonary valve, it is
possible to distinguish the
individual valve sounds by
auscultating (listening for
sounds within the body) four
specific regions of the thorax
– Notice that these four points,
while not directly superficial to
the valves (because the sounds
take oblique paths to reach the
chest wall), do define the four
corners of the normal heart
– Knowing normal heart size and
location is essential for
recognizing an enlarged (and
often diseased) heart
HEART SOUNDS
HOMEOSTATIC IMBALANCE
•
Abnormal Heart Sounds: blood flows silently as long as the flow is smooth
and uninterrupted
– If it strikes obstructions, its flow becomes turbulent
•
Heart murmurs are extraneous heart sounds due to turbulent backflow of
blood through a valve that does not close tightly
– Fairly common in young children and some elderly people with perfectly healthy
hearts
• Probably because their heart walls are relatively thin and vibrate with rushing blood
•
Most often, murmurs indicate valve problems
– Incompetent valve:
• Swishing sound is heard as the blood backflows or regurgitates through the partially
open valve, after the valve has (supposedly) closed
– Stenotic valve:
• Valve opening is narrowed
• Restricts blood flow through the valve
• High pitched sound or click can be detected when the valve should be wide open during
systole, but is not
Mechanical Events: The Cardiac Cycle
• Cardiac Cycle:
– Includes all events associated with the blood flow
through the heart during one complete heartbeat, that
is, atrial systole and diastole followed by ventricular
systole and diastole
• Systole is the contractile phase of the cardiac cycle
• Diastole is the relaxation phase of the cardiac cycle
– Marked by a succession of pressure and blood
volume changes in the heart
• Cardiac Cycle:
• Ventricular Filling: Mid-to-Late Diastole
• Ventricular Systole
• Isovolumetric Relaxation: Early Diastole
(1) Ventricular Filling
•
•
•
•
•
Mid-to-late diastole
Pressure in the heart is low
Blood returning from the circulation is
flowing passively through the atria and the
open AV valves into the ventricles
Aortic and pulmonary semilunar valves are
closed
70% of ventricular filling occurs during this
period
–
•
•
•
The remaining 30% is delivered to the
ventricles when the atria contract toward the
end of this phase
AV valve flaps begin toward the closed
position
NOW the stage is set for atrial systole
Following depolarization (P wave of ECG)
–
The atria contract, compressing the blood in
their chambers
•
•
•
Causes a rise in atria pressure, which propels
residual blood out of the atria into the ventricles
At this point the ventricles are in the last part of
their diastole and have the maximum volume of
blood
Then the atria relax and the ventricles
depolarize (QRS complex)
Summary of events occurring in the
Heart during the Cardiac Cycle
(2a) Ventricular Systole
• As the atria relax, the
ventricles begin
contracting
• Ventricular pressure
rises, closing the AV
valves
• Isovolumetric
contraction phase: for a
split second, the
ventricles are completely
closed chambers and
blood volume in the
chambers remains
constant
Summary of events occurring in the
Heart during the Cardiac Cycle
(2b) Ventricular Systole
• Ventricular pressure continues
to rise and when it finally
exceeds the pressure in the
large arteries issuing from the
ventricles, the isovolumetric
stage ends as the SL valves
are forced open and blood is
expelled from the ventricles
into the aorta and pulmonary
trunk (ventricular ejection
phase)
– Pressure in the aorta normally
reaches about 120 mm Hg
Summary of events occurring in the
Heart during the Cardiac Cycle
(3) Isovolumetric Relaxation
•
•
•
•
•
•
Early diastole
Brief phase following the T wave
Ventricles relax
Blood remaining in their chambers
is no longer compressed
Ventricle pressure drops
Blood in the aorta and pulmonary
trunk backflows toward the heart,
closing the SL valves
– Closure of the Aortic SL valve
causes a brief rise in aortic
pressure as backflowing blood
rebounds off the closed valve
cusps (dicrotic notch)
– Ventricles are totally closed
Summary of events occurring in the
Heart during the Cardiac Cycle
(a) An ECG tracing correlated with graphs of pressure and volume
changes. Time occurrence of heart sounds is also indicated.
Mechanical Events: The Cardiac Cycle
• All during ventricular systole,
the atria have been in diastole;
they have been filling with
blood and the intra-atrial
pressure has been rising
• When blood pressure on the
atrial side of the AV valves
exceeds that in the ventricles,
the AV valves are forced open
and ventricular filling, phase 1,
begins again
• Atrial pressure drops to its
lowest point and ventricular
pressure begins to rise,
completing the cycle
Summary of events occurring in the
Heart during the Cardiac Cycle
Mechanical Events: The Cardiac Cycle
• Average heart beats:
– 75 beats / minute
– 4500 beats / hour
– 108,000 beats / day
– 39,420,000 beats / year
– 709,560,000 beats / 18 years
– 2,759,400,000 beats / 70 years
Mechanical Events: The Cardiac Cycle
• Two important points:
– 1. Blood flow through the heart is controlled entirely by pressure
changes
– 2. Blood flows down a pressure gradient through any available opening
• The pressure changes, in turn, reflect the alternating
contraction and relaxation of the myocardium and cause the
heart valves to open, which keeps blood flowing in the forward
direction
• The pulmonary circulation is a low-pressure circulation as
evidenced by the much thinner myocardium of its right
ventricle
– Systemic aortic pressure: 120 mm Hg (systolic) and 80 mm Hg
(diastolic)
– Pulmonary artery pressure: 24 mm Hg (systolic) and 8 mm Hg
(diastolic)
CARDIAC OUTPUT (CO)
– The amount of blood pumped out by each
ventricle in 1 minute
– Stroke Volume is defined as the volume of blood
pumped out of a ventricle per beat
– Calculated as the product of stroke volume
(SV) and heart rate (HR)
• CO = HR x SV
• CO = 75 beats / min x 70 ml / beat
• CO = 5250 ml / min (5.25 L / min)
– The normal adult blood volume is about 5 L (1.32
gallons)
• Thus, the entire blood supply passes through each side
of the heart once each minute
Regulation of Stroke Volume
Preload
• The Frank-Starling law of the
heart states that the critical
factor controlling stroke
volume is the degree of
stretch of cardiac muscle
cells immediately before
they contract
• Stretching cardiac cells can
produce dramatic increases in
contractile force
• The most important factor
stretching cardiac muscle is
the amount of blood
returning to the heart and
distending its ventricles
(a) Preload is related to the amount of blood
stretching the ventricular fibers just before systole
CARDIAC OUTPUT
Regulation of Stroke Volume
Contractility
•
•
•
Defined as an increase in
contractile strength that is
independent of muscle stretch end
systolic volume
The more vigorous contractions
are a direct consequence of
Ca2+ influx into the cytoplasm
from extracellular fluid and the
SR (sarcoplasmic reticulum)
Enhanced contractility results
in ejection of more blood from
the heart:
– Result of increased
sympathetic stimulation of the
heart
– Increased Ca2+ promotes more
cross bridge binding (actin and
myosin) and enhances
ventricular contractility
Regulation of Stroke Volume
Contractility
• Factors that
increase
contractility:
positive inotropic:
– Calcium
– Hormones:
• Glucagon
• Thyroxine
• Epinephrine
– Drug:
• digitalis
Regulation of Stroke Volume
Contractility
• Factors that impair
or decrease
contractility:
negative inotropic:
– Acidosis: excess H+
– Rising extracellular K+
– Drugs:
• Calcium channel
blockers
CARDIAC OUTPUT
Regulation of Stroke Volume
Afterload
•
•
Ventricular pressure that must
be overcome before blood can
be ejected from the heart
It is essentially the back
pressure exerted on the aortic
and pulmonary valves by
arterial blood
– 80mm Hg in the aorta
– 8 mm Hg in the pulmonary artery
•
•
Normal individual: not a major
concern
Individual with hypertension: it
reduces the ability of the
ventricles to eject blood:
– More blood remains in the heart
after systole, resulting in
increased end systolic volume
(ESV) and reduced stroke volume
(b) Afterload is the pressure that the ventricles
must overcome to force open the aortic and
pulmonary valves
Preload and Afterload influence
Stroke Volume
CARDIAC OUTPUT
Regulation of Heart Rate
• A healthy cardiovascular system, SV tends to be
relatively constant
• When blood volume drops or heart is weakened:
– SV declines and CO is maintained by increasing HR
and contractility
• Sympathetic stimulation of pacemaker cells
increases heart rate and contractility, while
parasympathetic inhibition of cardiac pacemaker
cells decreases heart rate
• Epinephrine, thyroxine, and calcium influence
heart rate
Autonomic Nervous System Regulation
• Extrinsic controls affecting
heart rate
• When sympathetic nervous
system is activated by
emotional or physical
stressors, such as fright,
anxiety, or exercise:
– Sympathetic nerve fibers
release norepinephrine at their
cardiac synapses
• Binds to beta adrenergic
receptors in the heart
• Pacemaker fires more rapidly
• Heart responds by beating
faster
CARDIAC OUTPUT
Autonomic Nervous System Regulation
• Sympathetic
stimulation also
enhances
contractility by
enhancing Ca2+
entry into
contractile cells
Mechanism by which Norepinephrine influences
Heart contractility
Autonomic Nervous System Regulation
• The parasympathetic division opposes
sympathetic effects and effectively
reduces heart rate when a stressful
situation has passed
– May be persistently activated in certain
emotional conditions, such as grief and
severe depression
– Responses are mediated by acetylcholine,
which hyperpolarizes the membranes of its
effector cells by opening K+ channels
Autonomic Nervous System Regulation
• Under resting conditions, both autonomic
divisions continuously send impulses to
the SA node of the heart, but the dominant
influence is inhibitory
– Exhibits vagal tone
• Heart rate is generally slower than it would be if
the vagal nerves were not innervating it
– Cutting the vagal nerves results in an almost immediate
increase in heart rate of about 25 beats / min
Chemical Regulation
• Hormones:
– Epinephrine: liberated by the
adrenal medulla during
sympathetic nervous system
activation
• Produces the same effect as
does norepinephrine released
by the sympathetic nerves
• Enhances heart rate and
contractility
– Thyroxine: thyroid gland
hormone that increases
metabolic rate and body heat
production
• Causes a slower but more
sustained increase in heart
rate than that caused by
epinephrine
Chemical Regulation
• Ions:
– Physiological relationships between
intracellular and extracellular ions must be
maintained for normal heart function
– Plasma electrolyte imbalance pose real
dangers to the heart
HOMEOSTATIC IMBALANCE
• Hypocalcemia: reduced Ca2+ blood levels
– Depress the heart
• Hypercalcemia: above-normal levels of Ca2+
– Prolong the plateau phase of action potential
– Dramatically increase heart irritability
– Lead to spastic (abnormal muscle contraction) heart contractions that
permit little rest
• Excess Na+ and K+ are equally dangerous
– Hypernatremia : excessive Na+
• Inhibits transport of Ca2+ into the cardiac cells, thus blocking heart
contraction
– Hyperkalalemia: excessive K+
• Interferes with depolarization by lowering the resting potential, and may lead
to heart block and cardiac arrest
– Hypokalemia: low K+
• Is also life threatening, in that the heart beats feebly and arrhythmically
HOMEOSTATIC IMBALANCE
• Age:
– Fetus: 140-160 beats/min
– Gradually declines throughout life
• Gender:
– Females: 72-80 beats/min
– Male: 64-72 beats/min
• Exercise:
– Raises HR by acting through the sympathetic nervous system
– Increases systemic blood pressure and routes more blood to the
working muscles
– Trained athletes HR may be as slow as 40 beats/min
• Body Temperature:
– Increases HR by enhancing the metabolic rate of cardiac muscle
– Exercising muscle generate heat: increase HR
– Cold: decreases HR
HOMEOSTATIC IMBALANCE
• Tachycardia: abnormally fast heart rate (more
than 100 beats/min)
– Occasionally promotes fibrillation (irregular electrical
activity in the heart)
– Considered pathological (due to a disease)
• Bradycardia: heart rate slower than 60
beats/min
– Desirable, consequence of endurance training
– BUT, persistent in poorly conditioned people may
result in grossly inadequate blood circulation to body
tissues
• Frequent warning of brain edema (excessive amount of fluid)
after head trauma
Homeostatic Imbalance of Cardiac Output
• The heart’s pumping action ordinarily
maintains a balance between cardiac output
and venous return
• Cogestive Heart Failure:
– Occurs when the pumping efficiency of the heart
is so low that blood circulation cannot meet
tissue needs
– Reflects weakening of the myocardium by various
conditions which damage it in different ways:
•
•
•
•
1. Coronary Atherosclerosis
2. Persistent High Blood Pressure
3. Multiple Myocardial Infarcts
4. Dilated Cardiomyopathy (DCM)
(1) Coronary Atherosclerosis
• Clogging of the coronary vessels with fatty
buildup
• Heart becomes increasingly hypoxic
(inadequate oxygen) and begins to
contract ineffectively
(2) Persistent High Blood
Pressure
• Aortic pressure is normally 80mm Hg during
diastole
• When aortic diastolic blood pressure rises to 90
mm Hg or more, the myocardium must exert
more force to open the aortic valve and pump
out the same amount of blood
• Myocardium hypertrophies (increased size of
tissue / organ)
• Stress takes its toll and the myocardium
becomes progressively weaker
(3) Multiple Myocardial Infarcts
• Infarct: region of dead, deteriorating
tissue resulting from a lack of blood supply
• Succession of MIs depress pumping
efficiency because the dead heart cells
are replaced by noncontractile fibrous
(scar) tissue
(4) Dilated Cardiomyopathy
(DCM)
• Ventricles stretch and become flabby and the
myocardium deteriorates
• Cause often unknown
• Drug toxicity (alcohol, cocaine, excess catecholamines,
chemotherapeutic agents), hypothyroidism, and
inflammation of the heart are implicated in some cases,
as is congestive heart failure
• The heart’s attempts to work harder result in increasing
levels of Ca2+ in the cardiac cells which activates a
calcium-sensitive enzyme that initiates a cascade which
switches on genes that cause heart enlargement
• Because ventricular contractility is impaired, CO is poor
and the condition progressively worsens
Pulmonary Congestion
• Pulmonary congestion occurs when the left
side of the heart fails, resulting in pulmonary
edema:
– Right side of the heart continues to pump blood to the
lungs
– Left side does not adequately eject the returning
blood into the systemic circulation
– Blood vessels in the lungs become engorged with
blood, pressure in them increases, and fluid leaks
from the circulation into the lung tissue, causing
pulmonary edema
Peripheral Congestion
• If the right side of the heart fails,
peripheral congestion occurs
• Blood stagnates in body organs, and
pooled fluids in the tissue spaces impair
the ability of body cells to obtain adequate
amounts of nutrients and oxygen and to rid
themselves of wastes
• Resulting edema is most noticeable in the
extremities (feet, ankles, and fingers)
DEVELOPMENTAL ASPECTS
OF
THE HEART
•
Embryological Development:
– The heart begins as a pair of
endothelial tubes that fuse to
make a single heart tube with four
bulges representing the four
chambers
– The foramen ovale is an opening
in the interatrial septum that
allows blood returning to the
pulmonary circuit to be directed
into the atrium of the systemic
circuit (bypass the pulmonary
circuit and the collapsed,
nonfunctional fetal lungs)
– The ductus arteriosus is a vessel
extending between the pulmonary
trunk to the aortic arch that allows
blood in the pulmonary trunk to be
shunted to the aorta (bypass the
lungs)
EMBRYONIC DEVELOPMENT
EXAMPLES of CONGENITAL HEART DEFECTS
Purple indicates heart areas where the defects are present
HEART DEVICES
DEVELOPMENTAL ASPECTS
OF
THE HEART
• Aging Aspects of the Heart
– Sclerosis and thickening of the valve flaps occurs
over time, in response to constant pressure of the
blood against the valve flaps
– Decline in cardiac reserve occurs due to a decline in
efficiency of sympathetic stimulation
– Fibrosis of cardiac muscle may occur in the nodes of
the intrinsic conduction system, resulting in
arrhythmias
– Atherosclerosis is the gradual deposit of fatty plaques
in the walls of the systemic vessels