Biology 322 – Human Anatomy
Cardiac Anatomy
•Remember that the cardiovascular system refers to the (1) heart
and the (2) blood vessels
•CV system consists of two main divisions based on where the
blood is going after leaving the heart
1. Pulmonary circuit - carries blood that is O2-poor/CO2rich to the lungs so that O2 and CO2 can be exchanged,
returning O2-rich/CO2-poor blood back to the heart so
it can enter the systemic circuit
2. Systemic circuit – carries O2-rich/CO2-poor blood from
the heart out to all of the tissues of the body, THEN
carries the O2-poor/CO2-rich blood back to the heart so
that it can enter the pulmonary circuit
The right side of the heart pumps blood through the
pulmonary circuit….left side of the heart pumps blood
through the systemic circuit
•Heart is located roughly in the center of the
thoracic cavity (mediastinum) between the two
•The broad, superior portion is the BASE
•The narrower inferior portion is the APEX
•Heart is angled to the left so that about 2/3 of
the heart is to the left of the midsaggital plane
(despite what every cartoon would have you
•Several very large blood vessels are attached
at the base of the heart (GREAT VESSELS)
1. Aorta – carries oxygenated blood
from left ventricle out to systemic
2. Inferior and superior vena cava –
returns deoxygenated blood back to
the heart from the systemic circ.
•Heart is contained within a double-layered
sac known as the PERICARDIUM
•PARIETAL PERICARDIUM is the outer layer th
Consists of a outer fibrous layer and an
inner serous layer
•VISCERAL PERICARDIUM is the inner layer
closest to the heart (also known as the
Basically a continuation of the serous
layer of the parietal pericardium
•Between the two layers is the PERICARDIAL
Filled with PERICARDIAL FLUID that
allows the heart to operate in a low
friction environment
Heart Wall
•Three layers
1. Epicardium (visceral pericardium) – a
simple layer of squamous epithelia directly
on the surface of the heart
2. Myocardium – thickest layer composed of
the cardiac muscle cells that carry out
3. Endocardium – another simple layer of
squamous epithelial cells lining the interior
of the heart and valves
These three layers make up the wall of
each of the 4 chambers of the heart
 2 upper atria, 2 lower ventricles
 Thickness of the walls will vary
Chambers and valves of the heart
•Atria are chambers that receive blood from
lungs or rest of body
•Ventricles are chambers that expel blood
to the lungs or rest of body
•Atria and ventricles are separated by a
muscular wall called a septum
•Atrioventricular (AV) valves
prevent backflow of blood from
ventricle into atrium
Tendinous cords and
papillary muscles prevent
valve prolapse
•Pulmonary and aortic valves
(“semilunar valves”) and AV valves
ensure one-direction blood flow
•Faulty valves caused blood to flow back into atria (AV valves) or ventricles (semilunar valves)
•Increased pressures in these chambers force heart to contract more forcefully …more strain
on heart
•Faulty valves often are the cause of heart murmurs (abnormal heart sounds)
Flow of blood through the heart
1. Superior, inferior vena cava
2. Right atrium
3. Right AV valve
4. Right ventricle
5. Pulmonary valve
6. Pulmonary artery
8. Pulmonary vein
9. Left atrium
10. Left AV valve
11. Left ventricle
12. Aortic valve
13. Aorta
Coronary circulation
•Coronary arteries and cardiac veins supply
blood to the tissues of the heart
•Pattern is quite variable from person to person
•Most major vessels run along AV sulci and
interventricular sulci
•Most coronary venous blood drains into
CORONARY SINUS and then into Rt. Atrium
•Arterial blood comes from 2 coronary
arteries that branch directly off of aorta
and then give off multiple branches
•Clots in coronary blood vessels cause
myocardial infarction!!!
Nerve supply of the heart
•The heart is innervated by both divisions of the autonomic nervous system
•Allows us to regulate rate and force of heart contraction
1. Sympathetic division – generally increases force and rate of contraction, as well
as increasing blood flow through coronary blood vessels
• Important for “fight or flight” response
2. Parasympathetic division – generally reduces heart rate
• Main influence is through the VAGUS NERVE (CN X)
•Innervation by ANS is important for REGULATION of rate and force of contraction,
BUT heart will still beat even if all innervation is removed
Heart will naturally beat at about 100 beats/min without innervation
Regular, rhythmic beating of the heart is stimulated by SINOATRIAL NODE of
the right atrium
Signal conduction through the heart
•Sinoatrial node (SA node) is a patch of cells
in the right atrium known as the
“pacemaker” of the heart
•SA node cells depolarize much easier than
other muscle cells and will spontaneously
depolarize at regular intervals
•Depolarization of SA node triggers
depolarization of both atria
Cardiac cells possess GAP JUNCTIONS
that allow signals to rapidly pass from
one cell to another!!!
Both divisions of the ANS send nerve fibers
to the SA node – control of rate and force
•Atrioventricular node (AV node) is another
patch of cells lying near the bottom of the
interatrial septum
Detects depolarization of atria and
sends signal that triggers depolarization
of ventricles
Signal conduction through the heart
•Fibers from the AV node travel down the
interventricular septum and split into right
and left bundle branches, then travel up
along the surface of both ventricles
•These branches give off modified nerves
called PURKINJE FIBERS that stimulate the
entire ventricle to contract
The depolarization (electrical activity) of different
parts of the heart are detected and reported on an
Cardiac muscle
•Although purkinje fibers carry the electrical signal, not
every cell is DIRECTLY stimulated by these fibers
•Cardiac muscle cells (cardiomyocytes) are linked to
•These connections are VERY strong and contain gap
junctions that allow signals to rapidly pass from one
cell to the next
•So…contraction of one cell can trigger contraction of
other cells nearby, and so on, and so on….
•Allows the heart to contract in coordinated fashion
Allows for efficient ejection of blood from one
chamber to the next
Cardiac muscle metabolism…..
•Cardiac muscle cells rely almost exclusively
needed for contraction
 Lots of myoglobin
 Lots of large mitochondria
 Lots of stored glycogen
• Makes heart very resistant to fatigue, BUT
very vulnerable when O2 is not available
(heart attack)
Cardiac rhythm and contraction
•Coordinated contraction and relaxation of atria and
ventricles are essential to efficient pumping of blood
through pulmonary and systemic circuits
Prevents overload of circuits – elevated
•SYSTOLE = contraction of chambers, ejects blood
•DIASTOLE = relaxation of chambers, allows filling of
chambers with blood
•All 4 chambers DO NOT contract at same time!!!
BOTH atria contract first, both ventricles
contract shortly after
Depolarization begins at SA node → causes atria to contract first
Signals travel to AV node and then on to the ventricles → delay causes ventricles
to contract shortly after atria ---- about 100 msec after atria contract
This delay is VERY important because it allows ventricles time to fill with blood
Cardiac rhythm and contraction
•Conduction of signal occurs very rapidly across
atria…allows atrial tissue to contract uniformly
•Ventricular cardiomyocytes receive signal to
contract in one of two ways
1. Signal is received via intercalated disks
from a nearby cell (slower)
2. Signal is receive directly from purkinje
fibers (faster)
•Ventricles are quite large and thick with many
more cells than in atria
Purkinje fibers allow signal to get to most of
the ventricle much faster than only by
diffusing through intercalated disks
Ventricular contraction
•In reality, the entire ventricular myocardium
doesn’t contract at EXACTLY the same time
•Path of signal along bundle branches and purkinje
fibers cause apex to contract first and the
contraction spreads upward (superiorly)
•This pattern of contraction helps “push” blood up
and out through pulmonary or aortic valves
Ventricles sort of wring themselves out to
ensure adequate ejection of blood
•In a normal heart rhythm, the contraction is
triggered by the SA node, spreads throughout
atria → AV node → bundle fibers, purkinje
fibers→ spreads throughout ventricle
•Damage to conduction system (SA node, AV
node, bundle branches, purkinje fibers) alters
heart rhythm and is known as HEART BLOCK
•Some electrolyte imbalances, drugs, or
damage to the SA node can cause part of
heart to depolarize BEFORE SA node fires
(either the atria or ventricles)
Often causes FIBRILLATION
•Any heart rhythm where depolarization
initiates away from the SA node is an
Atrial fibrillation
•Atrial fibrillation (A-fib) occurs when depolarizations occur at areas other than the AV node
•Causes atria to flutter or quiver
•Often goes undetected since adequate amounts of blood often still enter the ventricles
•Normally not life-threatening, episodes can come and go, but can be chronic
•Dramatically increases risk of stroke due to formation of blood clots
Clots could eventually get pumped out of the heart
Many people with diagnosed A-fib take anticoagulants each day (Coumadin is an
anticoagulant drug)
Ventricular fibrillation
•Signals are not carried through the conduction
system normally (AV node → bundle fibers,
purkinje fibers→ rest of ventricle)
•Instead, depolarizations o
•Causes ventricle to quiver or flutter
Blood is not pumped efficiently →no
systemic circulation→ no coronary
circulation (myocardium dies quickly)
•Abnormal rhythm can often be corrected in a
number of ways:
1. Antiarrhythmic drugs
2. Cardioversion – delivery of an electrical
shock at a very specific time of the
3. Defibrillation – normally only done in extreme circumstances. Large shock of electricity
depolarizes the ENTIRE HEART at the same time
• Hope is that normal sinus rhythm will resume – like a “reset” button
Pacemaker physiology
•Cells of the SA node will rhythmically fire action
potentials without any nerve stimulation and
allows heart to beat about every 0.8 sec……..But
•Remember depolarization requires flow of (+)
ions into the cell
Normally accomplished by opening of
ligand- or voltage-gated ion channels
•SA node cells contain 3 important ion channels : Na+ channel, Ca2+ channel, K+ channel
•Some Na+ channels are constantly open (Na+ is flowing into the cell) allowing cell to VERY
SLOWLY depolarize
•When the cell reaches an electrical threshold, LOTS AND LOTS of voltage-gated Ca2+
channels open and Ca2+ rushes in causing rapid depolarization of the cell
•Soon, K+ channels open and K+ quickly leaves the cell allowing it to become repolarized
•BUT!! Na+ channels are still open and slowly depolarizing the cell AGAIN!!!
•This cycle allows SA node cells to depolarize routinely without stimulation
The Electrocardiogram (EKG or ECG)
•Depolarizations and repolarizations are really
changes in the electrical activity of the heart
•An EKG measures electrical activity throughout
the cardiac cycle
•Electrodes positioned on the wrists, ankles, and
chest send info on electrical activity to an
•Each peak on an EKG represents the
depolarization or repolarization of a certain
portion of the heart
1. P-wave – represents the depolarization of the SA node and
subsequent depolarization of the atria
2. QRS complex – represents the depolarization of the AV node and
then the ventricles
3. T-wave – represents the repolarization of the ventricles
• NOTE – the repolarization of the atria is not seen on an EKG
since the larger QRS complex masks it…
One complete
heartbeat or
cardiac cycle
Principles of pressure, blood flow, and the cardiac cycle
A little bit of fluid dynamics……
•A given amount of fluid will occupy a certain volume at a particular pressure
Assuming there is no outlet to relieve the pressure
•As the volume of a space increases, the pressure decreases
Explains why blood is drawn into ventricle when it expands (during relaxation/diastole)
•As the volume of a space decreases, the pressure increases
Blood is ejected from ventricles when they contract (i.e., during systole)
•PRESSURE GRADIENTS (the difference in fluid pressure between two areas) dictate when and under
what pressure a fluid will move between two places
These principles govern how blood moves between chambers and vessels
Ex. #1 As the pressure inside the right ventricle increases (contraction) blood is forced into the
lower pressure area of the pulmonary trunk
Ex. #2 As the pressure inside the right ventricle decreases (relaxation) blood flows from the
area of higher pressure (atrium) into the area of lower pressure (ventricle)
•Generally, pressure gradients cause fluids to flow
Blood from pulmonary or systemic circuits → atria, or atria→ ventricles, or ventricles
→ great vessels
•However, AV and semilunar valves prevent this flow even though there is a gradient!!!
Positive pressure in RV and LV force the AV valves to close (no flow back into atria)
Positive pressure in pulmonary trunk and aorta force semilunar valves closed (no back
flow into ventricles)
Heart Sounds
•Listening to the sounds of the body (heart, lungs, etc…) is known as AUSCULTATION
•Important part of a physical exam
•Normal adult heartbeat has two sounds ”LUBB….DUBB”
•First sound is caused by closing of AV valves during ventricular systole (lubb)
•Second sound is caused by closing of semilunar valves during diastole (dubb)
Abnormal heart sounds often indicate damaged or impaired AV or semilunar valves
Cardiac output
Defined as the amount of blood ejected from the heart each minute
Stroke volume (SV) X Heart rate (HR) in beats per minute = Cardiac output (CO)
So, for a normal resting person…..
70 mL X 75 beats per minute = 5,250 mL/min
•Since most people have about 5L of blood, all of the blood in the body passes through the
ENTIRE pulmonary and systemic circuits every single minute!
•CO will vary slightly from person to person (variations in stroke volume, resting heart rate)
•CO is affected by exercise and condition of individual
Exercise elevates HR → increased CO (most people can increase CO by
Well trained athletes often have increased SV
Balanced ventricular output
•Imbalances in ventricular output lead to abnormal
blood pressures in the pulmonary and systemic
•If RV output exceeds LV output (i.e, more blood is
sent to the lungs than returns to the heart), blood
backs up in the lungs → pulmonary edema
Under high pressures fluid escapes from blood
vessels and accumulates in tissues
•So, if the RV ejects 60 mL of blood into the lungs, the
LV needs to be able to accept 60 mL of blood from
the left atrium (which is receiving blood from the
•Pulmonary edema is a serious complication of cardiovascular disease
•Often the result of LV failure (less ejection means less filling!)
•Patients have extreme difficulty in breathing and cough up blood
Balanced ventricular output
•Similar situation develops if LV output exceeds RV
•LV is ejecting more blood into the systemic circuit
than the RV is sending to the lungs
•Pressure builds up in systemic circuit → systemic
Swelling of legs, feet, and hands can be
indicative of heart failure
•Both situations can be caused by damage to the ventricles after a
heart attack
A damaged ventricle cannot pump as much blood
If one ventricle fails, eventually the other fails too
Heart Rate Regulation
•Easily measured by counting pulsations in a superficial artery (pulse)
•“Normal” resting heart rate is around 75 beats/min
•Tachycardia – resting heart rate about 100 beats/min
Can be result of stress, drugs, heart disease, etc…
Can also compensate for low SV
•Bradycardia – resting heart rate below 60 beats/min
Common during sleep, and in very well trained athletes
Can also be caused by some medications (depressants)
•Factors (hormones, drugs, etc..) that change the HR are known as CHRONOTROPIC AGENTS
Positive chronotropic agents INCREASE rate
Negative chronotropic agents DECREASE rate
Influence of ANS on heart rate
Heart Rate Acceleration –
Sympathetic nerve fibers travel from medulla oblongata to SA node, AV node,
and myocardium
Nerve fibers release norepinephrine that binds to β-adrenergic receptors
Norepinephrine increases HR
“Beta-blockers” are often prescribed to treat hypertension – reduces heart
rate and therefore CO and therefore BP
Heart Rate Inhibition –
• Parasympathetic nerve fibers (via VAGUS nerve) travel to SA and AV nodes
•Nerve fibers release acetylcholine(ACh)
ACh binds to ligand-gated K+ channels causing K+ to flow OUT of S.A. node cells
making them HYPERPOLRIZED and very difficult to depolarize
Slows down depolarization of node cells → slows HR
•Vagus nerve is always affecting HR
Called VAGAL TONE – reduces HR to normal 75 beats/min (SA node normally
fires at rate of about 100 beats/min)
VASOVAGAL SYNCOPE – fainting due to overactivation of vagus nerve
Autonomic control of heart rate
Cardiovascular control centers in the brainstem receive info from various parts of the body
and direct appropriate changes in HR
Excellent example of a FEEDBACK LOOP
Proprioceptors – mechanical sensors in joints and muscles tell cardiac center to increase HR (via
sympathetic division of ANS) – these sensors detect movement of limbs
Baroreceptors – pressure receptors located in various parts of the body that send info to
cardiovascular centers
•Elevation in blood pressure causes decrease in HR
•Decrease in blood pressure causes increase in HR
Chemoreceptors – receptors that sense levels of CO2, 02, and pH
•CO2 in blood gets converted to carbonic acid (lowers blood pH) – need to get rid of CO2
through the lungs → increase in HR
•Low O2 levels also increase HR…..need to pump more blood to satisfy tissue needs for O2
Control of stroke volume
Other way to regulate cardiac output is by changing stroke volume
Stroke volume is influenced by three factors:
1. Preload – amount of blood in ventricles (EDV) dictates stroke volume
• Remember ventricle needs to eject as much blood as it receives
• STARLING LAW OF THE HEART basically says that the more you stretch the
heart (larger EDV), the more forcefully it will contract (TO A CERTAIN LIMIT!!!!)
• Unlike skeletal muscle, resting cardiac muscle is not naturally at optimal
resting length…..so some stretching is good for contraction
2. Contractility – describes the force with which the heart contracts for a given
• Positive and negative INOTROPIC agents increase or decrease contractility of
• Ca2+ and agents that increase Ca2+ levels make the heart muscle cells contract
more forcefully (more myosin heads binding to active sites on actin)
•Elevation in Ca2+ also lengthens the plateau phase of
cardiac muscle cell depolarization (longer contraction)
3. Afterload – describes the pressure of blood “after” the
heart beats
• Basically the amount of blood pressure in the
pulmonary trunk or aorta
• A very large afterload limits how much blood the
ventricles will be able to eject into the circulation
• Afterload is very high in pulmonary and systemic
 Eventually, ventricles have to beat so hard to
overcome afterload, that they fail