THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
FUNCTIONAL ANATOMY
HEART
ANATOMY OF THE HEART
✓ Hollow, four-chambered muscular organ
approx. size of a fist
✓ Positioned obliquely in the middle
compartment of the mediastinum of the
chest, just behind the sternum
✓ Approx. two-thirds of the heart lies to the
left of the midline of sternum between the
2nd through the 6th rib
✓ Apex of the heart- formed by the tip of the
left ventricle and lies above the diaphragm
at the level of 5th intercostal space to the
left
✓ Base of the heart- formed by atria and
projects to the right lying just below the
second rib
✓ Heart rests on the bodies of 5th to 8th
thoracic vertebrae
✓ Sulci- surface grooved that mark the
boundaries of the heart chambers
✓ Atria- small, thin-walled chambers that
contribute little to the total pumping of
activity of heart
✓ Pericardium- sac where heart is enclosed
1. Fibrous pericardium- tough,
loose-fitting, and inelastic sac
surrounding the heart
2. Serous pericardium- has two
layers
a) Parietal layer: inner lining of
the fibrous pericardium
b) Visceral layer or epicardium-
covering the outer surface of
the heart and great vessels
✓ Pericardial fluid- thin layer of fluid that
separates the two layers of serous
pericardium
▪ Minimize friction
✓ Pericarditis- inflammation of the
pericardium
✓ Pericardial effusion- abnormal amount of
fluid that accumulate between the layers
▪ Large pericardial effusion – affect
the pumping action of the heart –
resulting in cardiac tamponade
✓ Cardiac tamponade- compress the heart
muscle → serious decrease of blood flow in
the body – may lead to shock and death
✓ Heart wall:
1. Outer epicardium
2. Middle myocardium- composes
bulk of the heart muscle and
consist of bands of involuntary
striated fibers – contraction of
these muscle fibers creates
pumplike action to move blood
3. Inner endocardium
✓ Support for the four interior chambers and
valves of the heart is provided by four
atrioventricular rings – forms fibrous
“skeleton”
▪ Annulus fibrosus cordis- dense
connective tissue that electrically
isolates the atria from ventricles
o where valves of the heart
(flaps of fibrous tissue)
firmly anchored
✓ Two atrial chambers – thin-walled cups of
myocardial tissue—separated by
interatrial septum
✓ Fossa ovalis cordis- oval depression at
right side of interatrial septum – remnant
of the fetal foramen ovale
✓ Appendage (or auricle)- unknown function
in atrium
▪ In cardiac dysrhythmias- blood
flow pool in appendages →
formation of thrombi
✓ Ventricles- lower heart chambers – make
up the bulk of the heart’s muscle mass and
do most of the pumping
✓ Mass of the left ventricle is approx. two-
thirds larger than the mass of the right
ventricle – spherical appearance
(anteriorly)
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
✓ Right ventricle- thin-walled – pocket like
attachment to left ventricle
✓ Left ventricular aid- explains why some
forms of right ventricular failure are less
harmful than might be expected
✓ Interventricular septum- separates the
ventricles
✓ Atrioventricular valves- valves located
between atria and ventricles
▪ Closes during systole (contraction
of the ventricles) – preventing
backflow of blood to the atria
▪ Free ends are anchored to
papillary muscles of endocardium
by chordae tendineae cordis
▪ During systole- papillary muscle
contraction prevents the av valves
from swinging upward to the atria
▪ Damage to either of two – impair
AV valves and cause leak in atria
✓ Tricuspid valve- right side valve
✓ Bicuspid / Mitral Valve- left side valve
✓ Regurgitation- backflow of blood through
an incompetent or a damaged valve
✓ Stenosis- pathologic narrowing or
constriction of a valve outlet, which causes
increased pressure in the proximal
chambers of the heart vessels
▪ Mitral Stenosis- high pressures in
the left atrium back up into the
pulmonary circulation → atrium or ventricle mixes with
pulmonary edema and diastolic
murmur
✓ Semilunar valves- separates ventricles
from arterial outflow tracts, the
pulmonary artery and aorta
▪ Three half-moon shaped cusps
attached to atrial wall
▪ Prevent backflow of blood into
the ventricles during diastole
(when chambers of the heart filled
with blood)
✓ Pulmonary valve- outflow tract of the right
ventricle
✓ Coronary circulation- heart’s own
circulatory system
✓ Heart has high metabolic rate which
requires more blood flow per gram of
tissue weight than any other organ except
kidneys – to meet needs – extensive
network of branches -- myocardial tissue
✓ Two main coronary arteries: left and right
▪ Underneath aortic semilunar
valves
▪ Get the maximal pulse of pressure
generated by contraction of the
left ventricle
▪ Blood flows through coronary
arteries ONLY during diastole
✓ Healthy heart muscle- requires
approximately 1/20 of the blood supply of
the body to function properly
✓ Angina pectoris- partial obstruction of the
coronary artery led to tissue ischemia
✓ Myocardial infarction- complete
obstruction that cause tissue death or
infarct
✓ Venous blood is collected by coronary
veins – these veins gather together into a
large vessel called coronary sinus – passes
left to right across the posterior surface of
the heart
✓ Coronary sinus- empties to right atrium
between the opening of the inferior vena
cava and tricuspid valve
✓ Thebesian veins- through this some
coronary venous blood flows back into the
heart – empty directly into all the heart
chambers
▪ Any blood coming from the
thebesian veins that enters the left
arterial blood coming from the
lungs
✓ Anatomic shunt- phenomenon when
thebesian veins bypass or shunt around
pulmonary circulation
▪ When combined with a similar
bypass in bronchial circulation
these normal anatomic shunt
account for approximately 2% to
3% of the total CO
PROPERTIES OF THE HEART MUSCLE
✓ Performance of the heart pump depends
on its ability to
1. Initiate and conduct electrical
impulses
2. Contract synchronously the
heart’s muscle fibers quickly and
efficiently
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
✓ These actions are possible only because
myocardial tissue possesses four key
properties:
1. Excitability – ability of cells to
respond to electrical, chemical, or
mechanical stimulation
2. Inherent rhythmicity automaticity-
unique ability of cardiac muscle to
initiate spontaneous electrical
impulse – highly developed in
specialized areas (heart pacemaker
or nodal tissues)
3. Conductivity- ability of myocardial
tissue to spread and conduct
electrical impulses
4. Contractility- in response to
electrical impulse – is the primary
function of myocardium
o Refractory period- period
during which the
myocardium cannot be
stimulated – lasts approx.
250 msec
MICROANATOMY OF THE HEART MUSCLE
✓ Cardiac cells- fat, branched, and
interconnected
✓ Sarcolemma- where individual cardiac
fibers are enclosed
✓ Intercalated discs- irregular transverse
thickening of the sarcolemma that
separates cardiac fibers
▪ Provide structural support and aid
in electrical conduction between
fibers
✓ Myofibrils- smaller unit in fibers – contain
repeated structures approximately 2μm
called sarcomeres –have contractile
protein filaments (responsible for
shortening myocardium during systole)
✓ 2 types of proteins:
▪ Thick filaments- composed mainly
of myosin
▪ Thin filaments- composed mostly
of actin
✓ Myocardial cells contract when actin and
myosin combine to form reversible
bridges between these thick and thin
filaments
✓ Frank-Starling law
▪ The more cardiac fiber is stretched
– the greater the tension it
generates when contracted
▪ Tension developed during the
myocardial contraction – directly
proportional to the number of
cross-bridges between the actin
and myosin filaments
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
VASCULAR SYSTEM
✓ Two major subdivisions:
1. Systemic circulation- begins with
aorta on the left ventricle and ends
in the right atrium
2. Pulmonary circulation- begins with
pulmonary artery out of the right
ventricle and ends in the left
atrium
✓ Superior vena cava (SVC)- venous, or
deoxygenated blood from the head and
upper extremities enters
✓ Inferior Vena Cava (IVC)- where blood
from the lower body enters
SYSTEMIC CIRCULATION
✓ 3 MAJOR COMPONENETS:
1. Arterial system
2. Capillary system
3. Venous system
✓ Regulate not only the amount of blood
flow per minute (CO) but also the
distribution of blood to organs and tissues
(perfusion)
✓ Arterial system- consist of large, highly
elastic, low resistance arteries and small,
muscular arterioles of varying resistance
✓ Conductance vessels- help transmit and
maintain head of pressure generated by
the heart
✓ Resistance vessels-referred to when
arterioles play a major role in the
distribution and regulation of blood
pressure
▪ Smaller arterioles control blood
flow to capillaries
▪ Arterioles provide this by varying
flow resistance
✓ Capillary System (microcirculation)-
maintains a constant exchange of nutrients
and waste products for the cells and
tissues of the body
✓ Capillary are commonly referred to as
Exchange vessels
✓ Arteriovenous anastomosis- direct
communication between vessels
▪ Blood flows from network by an
arteriole and out through venule
▪ When open, this anastomosis
allows arterial blood to shunt
around the capillary bed and flow
directly into the venules
✓ Precapillary sphincters- smooth muscle
ting at proximal ends of capillaries
▪ Contraction- decreases blood flow
locally
▪ Relaxation- increases perfusion
✓ Venous system- consist of small,
expandable venules and veins and larger,
more elastic veins
▪ Conducting blood back to the
heart
▪ Act as reservoir for circulatory
system
▪ The veins and venules hold
approximately three quarters of
the body’s total blood volume
▪ Capacitance vessels- components
of venous system especially the
small, expandable venules and
veins
▪ Must overcome gravity to return
blood to the heart
▪ Four mechanisms combine to aid
in venous return to the heart
1. Sympathetic venous tone
2. Skeletal muscle pumping
or “milking”
3. Cardiac suction
4. Thoracic pressure
differences caused by
respiratory efforts
✓ Thoracic pump- Important to RTs because
artificial ventilation with positive pressure
reverses normal thoracic pressure
gradients
▪ Positive pressure ventilation-
impedes venous return
▪ Hypovolemic or cardiac failure –
reduction in CO when PPV is
applies
✓ Two separate heart pumps
1. Right side of the heart – generates
a pressure of approximately
25mmHg (low resistance, low
pressure) pulmonary circulation
2. Left side- generates pressures of
approx. 120mmHg (high pressure,
high resistance) systemic
circulation
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
VASCULAR RESISTANCE
✓ Systemic Vascular Resistance (SVR)- sum
of all frictional forces opposing blood flow
through
▪ Must equal the difference in
pressure between the beginning
and end of circuit, divided by flow
✓ NORMAL SVR:
▪ Normal mean aortic pressure =
90mmHg
▪ mean right atrial pressure of
approximately 4 mm Hg
▪ normal CO of 5 L/min
✓ Central venous pressure (CVP)- The
beginning pressure for the systemic
circulation is the mean aortic pressure;
ending pressure equals right atrial
pressure or central venous pressure
✓ Beginning pressure for the pulmonary
circulation is the mean pulmonary artery
pressure; ending pressure equals left atrial
pressure. Pulmonary vascular Resistance
formula:
✓ NORMAL PVR:
▪ Normal mean pulmonary pressure
= 16mmHg
▪ mean left atrial pressure of
approximately 8 mm Hg
▪ normal CO of 5 L/min
✓ Resistance to blood flow in the pulmonary
circulation is approx. one-tenth (1/10) of
the systemic circulation
DETERMINANTS OF BLOOD PRESSURE
✓ If the equation for computing SVR is
rearranged by deleting the normally low
atrial pressure, the average blood pressure
in the circulation is directly related to both
CO and flow resistance, as follows:
✓ MAP is directly related to the volume of
blood in the vascular system and inversely
related to its capacity
✓ MAP is regulated by changing the volume
of circulating blood, changing the capacity
of the vascular system, or changing both
✓ Vascular space decreases when
vasoconstriction (constriction of the
smooth muscles in the peripheral blood
vessels) occurs;
▪ causes blood pressure to increase
even though blood volume is the
same
✓ Vascular space increases when
vasodilation (relaxation of the smooth
muscles in the arterioles) occurs;
▪ blood pressure to decrease even
though blood volume has not
changed.
✓ In a normal adult, MAP ranges from 80 to
100 mm Hg
▪ MAP decreases below 60 mm Hg,
perfusion to the brain and the
kidneys is severely compromised
and organ failure may occur in
minutes.
CONTROL OF THE CARDIOVASCULAR
SYSTEM
✓ Coordination is achieved by integrating
the functions of the heart and vascular
system. The goal is to maintain adequate
perfusion to all tissues according to their
needs
✓ The heart plays only a secondary role in
regulating blood flow. In essence, the
vascular system tells the heart how much
blood it needs
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
✓ LOCAL OR INTRINSIC – without central
nervous system control – independent –
alters perfusion under normal conditions
to meet metabolic needs
▪ heart’s ability to change SV solely
according to the EDV
✓ CENTRAL OR EXTRINSIC – involves both
CNS and circulation humoral agents –
maintain normal level of vascular tone
REGULATION OF PERIPHERAL
VASCULATURE
LOCAL CONTROL
✓ Myogenic control- involves the
relationship between vascular smooth
muscle tone and perfusion pressure.
▪ ensures relatively constant flows
to the capillary beds despite
changes in perfusion pressures.
✓ Metabolic control- involves the
relationship between vascular smooth
muscle tone and the level of local cellular
metabolites
CENTRAL CONTROL
✓ Central control of blood flow is achieved
primarily by the sympathetic division of
the autonomic nervous system
✓ Smooth muscle contraction and increased
flow resistance are mostly caused by
adrenergic stimulation and the release of
norepinephrine
✓ Smooth muscle relaxation and vessel
dilation occur as a result of stimulation of
either cholinergic or specialized beta-
adrenergic receptors.
✓ blood flow through the large veins can also
be affected by abdominal and
intrathoracic pressure changes.
REGULATION OF CARDIAC
OUTPUT
✓ Cardiac Output (CO)- total amount of
blood pumped by the heart per minute
▪ simply the product of the HR and
the volume ejected by the left
ventricle on each contraction, or
stroke volume
✓ NORMAL CO: 5 L/min
▪ Normal Heart Rate = 70
contraction/min
▪ Normal stroke volume = 75ml or
0.075L / contraction
✓ SV is affected primarily by intrinsic control
of three factors:
1. Preload
2. Afterload
3. Contractility
✓ HR is affected primarily by extrinsic or
central control mechanisms.
CHANGES IN STROKE VOLUME
✓ End-systolic volume (ESV)- blood remains
in the ventricle after a systole
✓ Diastole (resting phase)- ventricles fill
✓ End-systolic volume (EDV)- volume filling
of ventricles during diastole
✓ SV equals the difference between the EDV
and the ESV
✓ Healthy man – normal SV = 70ml
▪ EDV = 110 to 120 ml
✓ Ejection fraction = 64% -- proportion of the
EDV ejected on each stroke
✓ Each Contraction - healthy heart ejects
approximately two-thirds of its stored
volume
✓ Decrease in EF – weakened myocardium
(heart failure), decreased contractility or
both
✓ EF below 30% - exercise tolerance is
severely limited
✓ force of the ventricle can generate results
from the length of the myocardial fibers
just before contraction
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
INCREASED SV DEACREASED SV
↑EDV ↓ESV ↓EDV ↑ESV
✓ relationship between cardiac muscle
length and tension ► Ventricles filled with
blood → myocardial fibers stretch →
stretch increases → tension in walls of the
heart increases –Frank-Starling law of the
heart
✓ PRELOAD (EDV)- the combined force of all
the factors that contribute to ventricular
wall stretch at the end of diastole
✓ AFTERLOAD- the combined force of all the
factors that the left ventricle encounters
and must overcome when stimulated to
contract and achieve the end of systole
▪ factors determine afterload- most
notably peripheral vascular
resistance and the physical
characteristics of arterial blood
✓ The greater the afterload on the
ventricles, the harder it is for the ventricles
to eject their volume
✓ Healthy heart muscle responds to increase
afterload by altering its contractility
✓ Contractility represents the amount of
systolic force exerted by the heart muscle
at any given preload
✓ At a given preload (or EDV), an increase in
contractility = increased EF, a decreased
ESV, and an increased SV.
✓ decrease in contractility = decreased EF,
an increased ESV, and a decreased SV
✓ Positive inotropism- higher SV for a given
preload (increased slope) indicates a state
of increased contractility
▪ Positive inotropes- Drugs that
increase contractility of the heart
muscle
✓ Negative inotropism- A lower SV for a
given preload indicates decreased
contractility
▪ Negative inotropes- drugs that
decrease contractility
✓ Neural or drug-mediated sympathetic
stimulation has a positive inotropic effect.
Conversely, parasympathetic stimulation
exerts a negative inotropic effect
✓ Profound hypoxia and acidosis impair
myocardial function and decrease cardiac
contractility and CO
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
CHANGES IN HEART RATE
✓ factors affecting HR are mainly of central
origin (i.e., neural or hormonal)
✓ positive chronotropic factors- Factors that
increase HR
✓ negative chronotropic factors- Factors
that decrease HR
✓ Hyperdynamic heart- decreased afterload,
increased contractility (decreased ESV),
and increased HR.
✓ Hypodynamic heart- include increased
afterload, decreased contractility
(increased ESV), and decreased HR.
✓ Congestive Heart Failure- the pumping
efficiency of the heart is so low that CO is
inadequate to meet tissues needs
CARDIOVASCULAR CONTROL
MECHANISMS
CARDIOVASCULAR CONTROL CENTERS
✓ Closely associated to vasoconstrictor
center is a cardioaccelerator area.
▪ Stimulation of this center
increases HR by increasing
sympathetic discharge to the SA
and AV nodes of the heart
✓ cardioinhibitory area- opposite to
cardioaccelerator
▪ Stimulation of this center
decreases HR by increasing vagal
(parasympathetic) stimulation to
the heart.
MINI CLINI: Heart Rate and the Administration of
Bronchodilator Drugs
PROBLEM: You are giving a bronchodilator
aerosolized drug to a patient, and you notice a
significant increase in the patient’s HR. Would you
expect increased HR to be a common side effect of
drugs that cause bronchodilation?
DISCUSSION: The discharge rate of the sinus node
and the HR are increased by sympathetic nervous
stimulation and decreased by parasympathetic
nervous stimulation. The airways of the lung are
dilated by sympathetic nervous stimulation and
constricted by parasympathetic stimulation. Drugs
that cause bronchodilation either mimic
sympathetic stimulation (sympathomimetic) or
block parasympathetic stimulation
(parasympatholytic). Both of these drug actions
also cause the HR to increase. Parasympatholytic
drugs bring about effects similar to those of
sympathetic stimulation; by inhibiting
parasympathetic activity, they allow sympathetic
impulses to predominate
✓ Signals coming from the cerebral cortex in
response to exercise, pain, or anxiety pass
directly through the cholinergic fibers to
the vascular smooth muscle, causing
vasodilation
✓ Decreased levels of CO2 tend to inhibit the
medullary centers.
▪ inhibition of these centers causes
a decrease in vascular tone and a
decrease in blood pressure
✓ Decrease in O2 tension has the opposite
effect
▪ Mild hypoxia in this area increases
sympathetic discharge rates; this
tends to elevate both HR and
blood pressure. Severe hypoxia
has a depressant effect.
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
PERIPHERAL RECEPTORS
✓ TWO (2) TYPES OF PERIPHERAL
CARDIOVASCULAR RECEPTORS:
▪ Baroreceptors (stretch receptors)
o respond to pressure
changes
o Baroreceptor output is
directly proportional to
the stretch on the vessel
wall
o Greater the blood
pressure, the greater is
the stretch and the higher
the rate of neural
discharge to the medulla
▪ Chemoreceptors
o respond to changes in
blood chemistry
✓ 2 different SETS of BARORECEPTORS:
▪ FIRST SET: Located in the aortic
arch and carotid sinuses
o monitor arterial pressures
generated by the left
ventricle
▪ SECOND SET: Located in the walls
of the atria and the large thoracic
and pulmonary veins
o Low-pressure sensors
respond mainly to
changes in vascular
volumes
✓ NEGATIVE FEEDBACK LOOP- stimulation of
a receptor causes an opposite response by
the effector
▪ In arterial receptor-- ↑ in BP → ↑
aortic and carotid receptor stretch
and their neuronal discharge rates
▪ ↓ in BP (decreased baroreceptor
output) has the opposite effect, ✓ CHEMORECEPTORS- small and highly
causing peripheral vessel vascularized tissues located near the high-
constriction and increased HR and pressure sensors in the aortic arch and
contractility. This mechanism carotid sinus that are sensitive to changes
usually restores blood pressure to in blood chemistry
normal ▪ strongly stimulated by decreased
✓ high-pressure arterial receptors- O2 tensions, although low pH or
constantly control blood pressure high levels of CO2 also can
✓ low-pressure sensors- responsible for increase their discharge rate
long-term regulation of plasma volume. ▪ major cardiovascular effects of
✓ Combined with a central nervous system– chemoreceptor stimulation are
mediated increase in renal filtration, these vasoconstriction and increased
humoral mechanisms decrease the overall HR
plasma volume (FIG 10-12)
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S
RESPONSE TO CHANGES IN OVERALL
VOLUME
✓ With 10% blood loss, the immediate
decline in the CVP causes a 50% decrease
in the discharge rate of the low-pressure
(atrial) baroreceptors.
▪ plasma levels of antidiuretic
hormone (vasopressin) begin to
increase, thus maintaining normal
arterial blood pressure
✓ As the blood loss becomes more severe
(20%),
▪ atrial receptor activity decreases
further; this increases the intensity
of sympathetic discharge from the
cardiovascular centers. Plasma
antidiuretic hormone and HR
continue to increase, as does
peripheral vasculature tone. An
increase in vascular tone occurs
through constriction of the
capacitance vessels in the venous
system, slowing the decrease in
CVP
✓ The arterial pressure does not start to
decrease until blood loss approaches 30%-
- At this point, arterial receptor activity
begins to decrease, resulting in a marked
increase in systemic vascular tone. Despite
the magnitude of blood loss, CVP levels off.
As long as no further hemorrhage occurs,
blood pressure and tissue perfusion can be
maintained at adequate levels
✓ If blood loss continues, central control
mechanisms begin to take over.
EVENTS OF CARDIAC CYCLE
▪ Massive vasoconstriction occurs in
the resistance vessels, shunting P wave (Atrial depolarization)
blood away from skeletal muscle • Within 0.1 second, the atria contract,
to maintain blood flow to the brain causing a slight increase in both atrial and
and heart. Increasing levels of local ventricular pressures (a wavs)
metabolites in these areas, o helps preload the ventricles,
especially CO2 and other acids, increasing their volume by 25%
override central control and cause o ATRIAL KICK – help from atria to
further vessel dilation and ventricular filling
increased blood flow. As these QRS Complex (ventricular depolarization)
metabolites build up and as the • As soon as ventricular pressures exceed
tissues become hypoxic, cardiac pressures in the atria, the AV valves close.
function becomes impaired and • Closure of the mitral valve (first), closure
vasodilation occurs throughout of the tricuspid valve (second). – Closure
the body. This vasodilation signals of Atrioventricular valves (AV Valves)
the onset of irreversible shock,
after which death ensues
THE CARDIOVASCULAR SYSTEM
CHAPTER 10: EGAN’S

• This closure marks the end of

ventricular diastole, first heart
sound on the phonocardiogram.
• When arterial pressures exceed
pressures in the relaxing ventricles,
the semilunar valves shut. Closure
of the semilunar valves generates
the second heart sound.
• Dicrotic notch -- caused by the
elastic recoil of the arteries. This
recoil provides the extra “push”
that helps maintain the pressure
created by the ventricle
• V wave – rapid decrease in atrial
pressures