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Physiology notes: 2nd half of Semester

1. Physiology of the cardiac muscle. Action Potentials.

Excitation contraction coupling. Control of heart activity
by autonomic nerves.

Physiology of the heart muscle:

- the heart is a pump, generating pressure by
contraction
• Arteries contain small percentage of blood &
are under high pressure, carrie blood from
heart to tissues (veins opposite)
- right side = blood to the lungs
- left side = systemic circulation
- Cardiac rhythmicity
- three major types of cardiac muscle:
• atrial muscle: & ventricular muscle:
- contract almost like skeletal muscle, but
duration is much longer
• specialised excitatory and conductive muscle
fibres:
- contract only feebly, because they contain
few contractile fibres
- exhibit either automatic rhythmical
electrical discharge (action
potentials) or conduction of action
potentials through the heart,
providing an extort system
controlling the rhythmical beating
of the heart
- Figure 9-2: muscle fiber arranged in
latticework, fibres dividing &
recombining
• myofibrils contain actin & myosin
filaments contracting like skeletal
muscle
• dark areas crossing muscle fibres

are called intercalated discs—> cell

membranes separating individual cells
connected in series and in parallel with one
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another, at each intercalated disc the cell membranes fuse with one another to form
permeable gap junctions allowing rapid diffusion ions
—> one cell becomes exited, action potential rapidly spreads to all of them
- two syncytium (artial & ventrical) —> separated by fibrous tissue surrounding the
atrioventricular openings, potentials aren't directly transmitted trough this tissue
(normally) —> specialised conductive system (AV bundle) bundle of conductive
fibres ==> atria contract ahead of ventricle

Action potential in Cardiac Muscle:

- very negative value (-85 millivolts) small
positive value (+20 millivolts) -> after initial
spike membrane stays depolarised for 0.2sec.
-> contraction lasts 15 times longer
than in skeletal muscles due to plateau
• abrupt repolarization
- cause of plateau:
• voltage activated sodium channels, fast
channels
• voltage activated calcium-sodium channels
L-type calcium channels
—> opening of fast channels causes the
spike portion of the action potential, whereas
the prolonged opening of the slow calcium ions
to enter the finer, which is largely responsible for
the plateau portion of the action potential
—> voltage gated potassium channels are slower to open than usual, often not
opening much until the end of plateau. This factor delays the return of membrane potential
toward its normal negative value of -80 to -90 millivolts. The plateau ends when the
calcium sodium channels close and permeability to potassium ions increases.

- Phases of cardiac muscle action potential:

• 0: depolarisation, fast sodium channels open
• 1: initial repolarisation, fast sodium channels close
• 2: Plateau, calcium channels close & fast potassium
channels close
• 3: rapid repolarisation, calcium channels close and slow
potassium channels open
• 4: resting membrane potential
Excitation Contraction Coupling
- Mechanism of action potential causing myofibrils of muscle
to contract
- action potential spreads along membranes of transverse
(T) tubules —> acting on membranes of longitudinal sarcoplasmic tubules, release of
calcium ions into muscle sarcoplasm from sarcoplasmic reticulum -> calcium ions diffuse
into myofibrils and catalyse the chemical reaction -> promoting sliding olfaction and
myosin filaments along one another => producing muscle contraction
- calcium ions ALSO diffuse into the sarcoplasmic from T tubules themselves -> opening
voltage-dependent calcium channels in membrane of T tubules -> calcium entering the
cell activates calcium release channels (ryanodine receptor channels) triggering release
of calcium into the sarcoplasm
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Control of heart activity autonomic nerves:

- strong sympathetic stimulation can increase heart rate from 70

to 180-200 even 250 beats/min
• also the amount and ejection pressure can be increased
• sympathy nerve fibers are constantly giving out stimulation
-> if they don't cardiac pumping would be 30% below normal
- parasympathetic (Vagal) stimulation can stop the heart for a
couple of seconds
• the strength of the heart muscle can be decreased by 30%
• vagal fibers mainly distributed to the atria
—> effecting more the rate than the strength of the
contraction
==> combination of vagal & synaptic stimuli can decrease
ventricular pumping by 50%
- changes in output caused by autonomic nervous system
stimulation result in changes in heart rate and contractile
strength of the heart
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2. Excitatory and Conductive System of the Heart. Velocity

of Conduction of the Impulse. Control of excitation and
conduction in the heart.

Excitatory and Conductive System of the Heart:

- controlling cardiac contractions

- rhythmical impulses are generated in S-A
(sinoatrial or sinus) node
- the internodal pathways that conduct impulses
from the sinus node to the A-V (atrioventricular)
node
- Purkinje fibers, which conduct the cardiac
impulses to all parts of the ventricles
- The Sinus Node : small flattened ellipsoid strip of
specialised cardiac muscle 3mm W. 15mm L. 1mm
thick, self-excitation -> gives rhythms of heart
• resting potential -55 to -60 millivolts (-85 to -90
millivolts for ventricular muscle fiber)
—> membranes of sinus finer are leaky to
Sodium & Calcium ions, and positive charges of
the entering sodium and calcium ions naturalise
some of the intercellular negativity
• Self-Excitation: leakiness of sinus node fibres to sodium and calcium ions causes self-
excitation
- high sodium ion concentration in extracellular fluid, moderate number of already
open sodium channels —> positive sodium
ions from outside the fibres tend to leak to
inside
- resting potential slowly rises ————>
- at -40 millivolts L-type calcium channels
become activated causing action potential
- constant depolarisation is prevented by
• L-type calcium channels become
inactivated 100-150 milliseconds after
opening and at the same time large
quantities of positive potassium ions
diffuse out of the fiber
• potassium channels remain remain open
for another tenths of a second —> moving
positive charges out of the cell
———> hyperpolarisation
- more potassium channels close progressively after action potential is over
- Ends of sinus nodal fibres connect directly with surrounding atrial muscle fibers to AV
Node (three bands anterior, lateral & posterior)
- the velocity of conduction in most atrial muscles is about 0.3 m/sec.
• in anterior intertribal band conducts more rapid 1m/sec.
- passing through the anterior walls of the atria to the left atrium
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- reaching AV Node 0.03sec. after origin in Sinus Node and 0.09sec. plus another
0.04 sec. in AV Bundel which is passing through the atrioventricular fibrous tissue
- Three main types of membrane ion channels:
- fast sodium channels
- L-type calcium channels (slow-calcium channels)
- potassium channels
• spike is caused by fast sodium channels
• “plateau” of ventricular action potential is caused by slower opening of the slow
sodium-calcium channels
• diffusion of large amounts of positive potassium in outward direction membrane
potential returns to resting level
——> different in sinus node:
- resting potential much less than -55 millivolts in nodal fiber (-90 millivolts in
ventricular muscle fiber)
- at -55 millivolts fast sodium channels are already inactivated
• only slow sodium-calcium channels can open, causing action potential
• —>return of the potential to its negative state occurs slowly as well
- A-V Node: impulses are delayed before passing to ventricles giving time for the atria to
empty the blood into the ventricles
• delay AV Node and Bundle = 0.13sec. (0.16sec.
from initiation to muscle of Ventricles)
• slow conduction due to diminished number of gap
junctions
• Special Purkinje fibers lead from AV Node through
AV Bundle into Ventricles
- very different to AV Nodal fibers
- transmitting velocity 1.5-4.0m/sec. (six times
higher than ventricular muscle and 150 times
higher than AV nodal fibers
- —>very high level of permeability of the gap
junctions
- —>also very little myofibrils —> little or no
contraction at all during impulse transmission
• AV is unable (Exception: abnormal condition) to
transmit action potential from ventricles to atria —>
preventing reentry of cardiac impulses
• AV Bundle is the only connection between Atria and
ventricle muscle
• cardiac arryhthmias can be triggered by abnormal
muscle bridge, cardiac impulses can reenter the
atria from ventricles
• The impulse is further transmitted by ventricular
muscle fibers with one sixth of the velocity of Purkinje fibers, after they end

Control of excitation and conduction in the heart:

- The impulse normally arrises in the sinus node but in abnormal conditions other parts of
the heart exhibit intrinsic rhythmical excitation (especially AV nodal and Purkinje fibers)
• AV Node 40-60 times per min.
• Purkinje fibers 15-40 times per min. (Sinus Node 70-80)
- normally the Sinus node discharges again before AV node or Purkinje fibers can reach
their own threshold value for self-excitation => that is why the sinus node controls the
heart beat
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- abnormal “Ectopic” Pacemaker
• AV Node & Purkinje Fibers can become pacemaker or even atrial or ventricular
muscle develop excessive excitability (new pacemaker)
• can also occur when the transmission of sinus is blocked
• or AV block (no transmission from atria to Ventricles)
- in the case of a sudden AV Block Purkinje fibers do not emit intrinsic rhythmical
impulses until 5-20sec. after block —> “Stokes Adam Syndrome” can lead to death
• causes significant debility of heart pumping
- both Ventricles contract at almost the same time (0.03-0.06s difference from 1st to last
ventricular muscle contracting), continue contracting for 0.03s
• effectiveness of pumping can be decreased by 20-30% by uneven contraction
- Parasympathetic (Vagal) stimulation slows the cardiac rhythm and contraction
• decreases the rate of rhythm of the sinus node
• decreases excitability of the AV junctional fibers between the atrial musculature and
the AV node, slowing the transmission of the cardiac impulse to the ventricles
• stimulation of the vagi to the heart causes release of acetylcholine to be released into
vagal endings
- > increasing the permeability of the fiber membranes to potassium ion, allowing
rapid leakage of potassium out of the conductive fiber
- >>increases negativity of inside the fibers “hyperpolarisation” -> less excitable
- >>> resting potential in sinus now: -65 to -75 millivolts
- —> inward sodium & calcium leakage takes more time to reach threshold potential
- if stimulation is strong enough it can stop the self-excitation of the node
• a small area usually in the ventricular septal portion of AV Bundle causes
contraction of ventricles called “Ventricular escape”
- Sympathetic stimulation increases cardiac rhythm and conduction
• increases rate of sinus nodal discharge
• increases rate of conduction, level of excitability in all parts
• increases greatly the force of contraction of all the cardiac musculature, atrial and
ventricular
• maximal stimulation can almost triple the heartbeat frequency and double contraction
strength
- Norepinephrine is released into sympathetic nerve endings
- > stimulating beta-1 adrenergic receptors mediating the effects on the heart rate
- >> increased permeability to of the finer membrane to sodium and calcium ions ->
more positive resting potential, accelerating self-excitation
- in AV node and bundle increased sodium-calcium permeability makes it easier for
action potential to excite decreasing conduction time from atria to ventricle
- increase of permeability to calcium ions also partially increases contractile strength
—> calcium ions play a powerful role in exciting the contractile process of myofibrils

3.The Electrocardiogram (ECG). Characteristics of the

normal ECG. ECG leads. Mean electrical axis. Cardiac
arrhythmias.

The Electrocardiogram (ECG):

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- when cardiac impulses pass through the heart and a small portion of that current
spreads to the surface
- electrodes are placed on the skin on the opposite side of the heart —> electric potentials
generated by the current can be recorded “Electrocardiogramm (ECG)”

Characteristics of a normal ECG:

- P wave is caused by electrical potentials generated when the atria depolarise before
atrial contraction begins
- QRS complex potentials generated when
as the ventricles depolarise before
contraction, that is, as the depolarisation
wave spreads through the ventricles
• >Bothe are depolarisation waves
- T wave potential generated as the
ventricles from depolarisation

- >Figure 11-2A:
• depolarisation reached halfway mark,
maximum positive value
- >Figure 11-2B:
• depolarisation over entire muscle fiber
• recording returned to zero baseline,
because both electrodes are now in
areas of equal negativity ->
depolarisation wave
- >Figure 11-2C:
• halfway depolarisation, positivity
returning to the other side of the fiber
- >Figure 11-2D
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• potential returns to Zero again completed repolarization wave
- Before contraction can occur depolarisation must spread through the muscle to initiate
the chemical process of contraction
- The ventricles remain contracted until after repolarisation (after end of T wave)
- atria repolarise about 0.15-0.20sec. after termination of P wave (when QRS complex is
recorded)
• >the “atrial T wave” (atrial repolarisation wave) is usually obscured by the much larger
QRS complex, so not often observed
- the ventricular repolarization is the T wave on the ECG
• this T wave is a prolonged wave, because ventricular depolarisation extends over a
long time
• —>this is partly the reason why the voltage of the T
wave is much less than the voltage of the QRS
complex
- the rate of heartbeat is the reciprocal of the time
interval between two successive heartbeats (two
successive QRS complexes)

ECG Leads:
- three bipolar limb leads:
• bipolar means that the electrocardiogram is
recorded from two electrodes located on different
sides of the heart (in this case limbs)
• Lead I —>connected to right arm & positive terminal
connected to the left arm
• positive voltage is recorded at connection of
arm and chest
• Lead II —>Negative terminal is connected to the
right arm and positive terminal to the left leg
• ECG records positively
• Lead III —>negative terminal is connected to left leg
and positive terminal to left leg
• ECG records positively
- Eidenhoven’s Triangle
• around the are of the heart
• illustrating that two arms and one leg from a triangle
surrounding the heart
• the two upper corners represent the points at which
the arms connect electrically
• the lower corner is the point at which the left leg
connects with the fluids
- Eidenhoven’s law
• Lead I potential + Lead III potential = Lead II potential
- Chest Leads
• As illustrated in the picture electrodes are placed on
the heart V1-V6 ———————————————>
• cardiac potential is immediately beneath the electrode
• V1,V2: QRS recordings are mainly negative, because
closer to the base of the heart than to the apex
• V4-6 mainly positive near to the heart apex
Mean electrical axis:
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-Axis for
each
standard
bipolar
lead and
each
unipolar
limb
lead:
•Lead I is 0°
• Lead II is +60°
• Lead III is +120°
• Lead aVR +210°
• Lead aVF +90°
• Lead aVL -30°
- Vectorial analysis of potentials recorded in different Leads:
• A is +55° and voltage represented by its length is 2
millivolts
• >Lead I is 0°, a line perpendicular to I is drawn to
the tip of Vector A to determine the voltage of A
recorded in Lead I (Vector B)
• >> B points to positive end (recording positive),
voltage is equal to length of B divided by length of
A times two millivolts, or about one Millivolt
• Figure 12-5 another example
• Figure 12-6:
- Vector A depicts the instantaneous electrical
potential a partially depolarised heart
- B depicts the potential recorded in Lead I
- C potential in Lead II and
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- D potential in Lead III
- changes in the position of the heart can shift the axis of the heart
• end of deep inspiration
• lying down
• person is obese
- Hypertrophy of a Ventricle shifts to the side of the hypertrophy (also the voltage
increases)
- more time is required for repolarisation
- greater quantity of muscle exits
- bundel branch block
• normally Purkinje system transmits the impulse in almost the same instant
- the ventricle with the blocked bundle is receives the impulse later
- decreased voltage is a sign of
• Myopathy
• fluid in the pericardium
• Pulmonary emphysema
Cardiac Arrhythmias:

- Tachycardia
• faster than 100 beats/min in adult
• Causes:
- increase of temperature (normally 10 beats/min per degree celsius)
- severe blood lost
- weakening of the myocardium
- Bradycardia
• slower than 60 beats/min
• can be seen in well trained athletes
• stimulation of the vagus nerve causing acetylcholine release at the vagal ending in the
heart —> parasympathetic effect —>occurring in patients with carotid sinus syndrome
- pressure receptors (baroreceptors) in the carotid sinus region of the arteria carotis
are excessively sensitive
- can be powerful enough to stop the heart for 5 to 10 seconds
- incomplete intraventricular block
• condition know as electrical
alternans
- resulting from partial
intraventricular block every
other heartbeat
- conditions depressing the
heart (ischemia,
myocarditis, digitalis toxin)
can cause incomplete
intraventricular block
- Premature contraction = a contraction before the normal contraction would have been
expected “extrasystole, premature beat, ectopic beat”
• Causes:
- sending abnormal impulses at odd times during cardiac rhythm (ectopic foci)
• local areas of ischemia
• small calcified plaques at different points in the heart, which press against the
adjacent cardiac muscle so that some of the fibres are irritated
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• toxic irritation of the AV node, Purkinje system, or myocardium caused by
infection, drugs nicotine or coffee
- mechanical initiation of premature contraction is frequent during cardiac
catheterization —> when catheter enters right ventricle, pressing against the
endocardium
• premature atrial contraction:
-P wave of this beat occurred
too soon in the heart cycle
-P-R interval is shortened —>
indicating origin in atria near
AV node
-interval between premature
and succeeding contraction is
prolonged “compensatory
pause”
- occur also in “healthy” people
or athletes
- factors to initiate contractions: lack of sleep, smoking, alcoholism, various drugs
- >> Pulse deficit: when the heart contracts ahead of schedule it could not fully fill
with blood so the pulse wave might not be felt
• AV Nodal or AV Bundle Premature Contraction:
-P wave is missing of
premature contraction
-P wave is superimposed onto
the QRS-T complex, because
the impulse traveled backward
into the atria while it traveled
forward into the the ventricles
-same significance and causes
as atrial contractions
• Premature ventricular contractions
-
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4. Cardiac cycle. Function of atria and ventricles as

pumps.Pressure and volume changes in the heart
chambers. Cardiac volumes.

Cardiac cycle:

- each cycle is generated by generation of action potential in the sinus node

• delay of 0.1 sec. in transition from atria to ventricles (AV bundle)
- the cycle consist of diastole and systole
• diastole: heart fills with blood
• systole: period of contraction
- duration of the cardiac cycle is (e.g.: 72 beats/min = 1/72 min -> 0.0139min (0.833esc.)
per beat

- phonocardiogram records the sounds produced by the heart (mainly heart valves)
- heart rate increases, duration of cardiac cycle decreases
• the systole deceases not as much as does the diastole
- a heart beating at beating at a very fast pace does not remain relaxed long enough
to completely fill the chambers before next contraction
- Relation to electrocardiogram:
• P wave causes (is followed by) a slight change inertial pressure
• QRS complex initiates rising of ventricle pressure (complex begins slightly before
QRS complex)
• T wave occurs slightly before end of ventricular contraction
- Atria function as primer pumps for the ventricles
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• blood flows continuously from the great vessels into the atria
• 80% of the blood flows from the atria directly in the ventricles and another 20% is
added by the atrial contraction
- the heart can operate under most condition without the 20%
• not notice until exercising => shortness of breath, acute signs of heart failure
occasionally develop
- Ventricles function as pumps
• filling with blood during diastole (during ventricular systole atria fill with blood)
- rise of ventricular volume curve “period of rapid filling of the ventricles”
- very rapid only for first 1/3 of diastole
- during second third only a small amount enters
- last third of diastole atrial contraction forces blood into the ventricles additionally
• Outflow of blood from the ventricles during systole
- period of isovolumic (isometric) contraction
• immediately after ventricular contraction begins, ventricular pressure rises
abruptly —> AV valves close
• 0.02-0.03sec. delay to build up pressure to push semilunar valves open
• isovolumic (isometric) contraction because cardiac muscle tension is increasing
but little or no shortening of muscle fibres occurs
- Period of ejection
• left ventricular pressure rises slightly above 80mmHg (right ventricular pressure
rises slightly above 8mmHg
• semilunar valves open—> blood pushes out (ca. 60% of blood is ejected during
systole) —> 70% flows out during the first third of the systole, the last 30% in the
other 2/3
- first third is called “period of rapid ejection”, rest “period of slow ejection”
- Period of isovolumic (Isometric) relaxation
• ventricular relaxation begins suddenly, pressure in arteries and the rapidly
decreasing pressure in the ventricles push blood back, closing the valves
• 0.03-0.06sec. ventricular muscle continues to relax but ventricular volume does
not change “isovolumic (isometric) relaxation”
• intravertricular pressures rapidly decrease to their low diastolic levels
• AV valves open to begin a new cycle of ventricular pumping
- End diastolic volume, end systolic volume, and stroke volume output
• during diastole normal filling of ventricles —> 110-120 millilitres
• ventricles empty during systole volume decreases by 70 millilitres
- remaining 40-50 millilitres called end systolic volume
- the fraction of the end diastolic volume that is ejected is called the end systolic
volume
- the fraction of the end diastolic volume that is ejected is called “ejection fraction”
- at strong contractions the volume can decrease to 10-20 Millilitre
- the ventricular end diastolic volumes can become 150-180 millilitre in a healthy
heart
- > by increasing end diastolic volume and decreasing end systolic volume, the
stroke volume output can be increased to more than double that which is normal
- Pressure changes in Atria - a,c, and v Waves
• three minor pressure waves a, and v atrial pressure waves
- a wave caused by atrial contraction, pressure increases by 4-6 mmHg (right
atrium) / 7-8 mmHg (left atrium)
- c waves occur when ventricles contract
• partly caused by a slight back flow into atria
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• manly by bulging of AV valves backward toward the atria because of increasing
pressure in ventricles
- v waves caused by blood flow into the atria while AV valves are closed during
ventricular contraction, when contraction is over AV values open —> v wave is over
- Atrioventricular vales (AV valves) (tricuspid and mitral valves)
• prevent back flow of blood from ventricles during systole
• close and open passively (pressure gradient)
• papillary muscles (attached by chordae tendineae) contract with the ventricles
- preventing valves to bulge into the atria to far during contraction
- if they are paralysed or ruptured ventricles may leak into atria—> sever or lethal
cardiac incapacity
- Aortic and Pulmonary Artery valves
• higher pressure in the arteries closes valves at the end of the systole
• they are smaller so velocity of blood flow is greater than in AV valves
• snap close, AV valves close more soft
• semilunar valves have no tendineae
• especially strong, yet pliable tissue
- The aortic pressure curve:
• left ventricle contracts, ventricular pressure increases until aortic valves open, after
valves open ventricle pressure rises less rapid, blood is released into systemic
circulation, blood entering arteries during systole increasing pressure to 120mmHg,
elastic valves remain under high pressure in the arteries even in diastole
• incisura occurs in curve when aortic valves close, short period of backward flow,after
closure the pressure in aorta decreases slowly during diastole before the ventricles
contract again pressure has usually fallen to 80mmHg
• pressure curves of pulmonary arteries and the right ventricle are are similar to the
aortic pressure curve
- Relationship of heart sounds to pumping
• first sound is caused by the AV valves closing
• second is the closure of the pulmonary and aortic valve
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5. Heart valves. Heart Sounds. Relationship of the heart

sounds to heart pumping. Heart murmurs caused by
valvular lesions.

Heart valves:
- AV valves prevent backflow of blood from ventricles to atria during systole
• AV valves are thin and light, hence almost no
backflow before they close softly
• Papillary muscles attaching to the vanes of the A-V
valves by the chordea tendinea
- papillary muscles contract when the ventricular
valves contract
- >preventing the valves to bulge too far backward
into the atria
- semilunar valves prevent back flow from aorta and
pulmonary arteries to ventricles during diastole
• Semilunar valves are much heavier, requiring rather
rapid backflow for a few milliseconds before they
snap close
• especially strong yet very pliable fibrous tissue to
withstand the greater physical stress

Heat Sounds:
- opening of the valves is inaudible (relatively slow
process)
- BUT when the ventricles contract the sound the
first sound comes from the AV valves (first heart
sound), when the aortic and pulmonary valves close
at the end of the systole a rapid snap is audible
(second heart sound)
• first heart sound
- vibration system: ventricular chambers
- 0.14 seconds audible
• second heart sound
- vibrating system: arterial valves
- 0.11 seconds audible
- higher frequency than the first
• >much higher tautness of semilunar valves as AV
valves
• >greater elastic coefficient of the taut arterial walls
• lowest frequency the ear can detect 40 cycles/sec,
highest frequency 500 cycles/sec
- occasionally a weak, rumbling third sound is heard during
the diastole
• usually the frequency is too low to hear it
• generally indicates systolic heart failure in older adults
- sometimes a fourth sound can be recorded on a
phonocardiogram
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Relationship of heart sounds to heart pumping:

Heart murmurs caused by valvular lesions:

- greatest number of vulvar lesions results from
rheumatic fever
• an autoimmune disease where heart vales are damaged or destroyed
• initiated by streptococcal toxin (streptococcal infection by bacterium group A
haemolytic streptococci -> symptoms are sore throat, scarlet fever or middle ear
infection
• lesions of acute rheumatic fever frequently occur on adjacent valve leaflets
simultaneously, so the edges of the leaflets become stuck together
- lesions become scare tissue after a long time
- >stenosed
- Systolic murmur of Aortic Stenosis
• blood is ejected through only a small fibrous opening of the aortic valve
• blood pressure rises up to 300mm Hg in the left ventricle but the pressure in the aorta
is still normal
- >severe turbulence in the root of the aorta
- Diastolic murmur of aortic regurgitation
• abnormal sound during diastole audible caused by blood flowing back from aorta into
the left ventricle
- Systolic murmur of mitral regurgitation
• blood flows backwards through the mitral valve into the left atrium during systole
- sound is manly transmitted left ventricle to the apex of the heart
- Diastolic murmur of mitral stenosis
• blood passed with difficulty through the stenosed mitral valve from the left atrium to
the left ventricle
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6. Basic principles of circulatory function. Interrelationships

of pressure, flow and resistance. Laminar and turbulent
blood flow.

Basic principles of circulatory function:

- 1) Blood flow to most tissues is controlled according
to the tissue need
• an increase of blood flow is not only controlled by
the heart, micro-vessels monitor the tissue needs
and constrict/dilate accordingly (the kidneys also
play a important role in pressure control)
- 2) cardiac output is the sum of all the local tissue
flows
- 3) arterial pressure regulation is generally
independent of either local blood flow control or
cardiac output control

Interrelationships of pressure, flow and resistance:

- Blood flow through a blood vessel is determined by
two factors:
• pressure difference “pressure gradient” between
the two ends of the vessel ( P1 & P2)
• vascular resistance - the impediment to blood flow
through the vessel
- resistance occurs as the result of friction between
the flowing blood and the intravascular endothelium
all along the side of the inside of the vessel ======> Ohm’s law
• >R=resistance ; delta-P = the difference in pressure (P1-P2)
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Laminar and turbulent blood flow:

- (Laminar) when blood flows at a steady rate
through a long, smooth blood vessel, flowing
in streamlines, each layer of blood remaining
at the same distance from the vessel wall
• velocity in the centre is greater in the
centre than towards the outer edges
• “parabolic profile for velocity of blood”
- molecules closer to the wall move slower
due to adherence
- (Turbulent) when passing an obstruction,
making a sharp turn, passing over a rough surface the flow becomes turbulent
• flowing crosswise in and along the vessel
• whorls in the blood form eddy currents, if present overall friction
increases
- Re=reynolds’ number, a measure of the turbulences to occur
- d=vessel diameter (in cm) ; ro is density ; eta is viscosity (in poise)

7. Functional parts of the circulation. Volumes of blood and

pressures in the different parts of the circulation. Cross
sectional areas and velocities of blood flow.

Functional parts of the circulation:

- Systemic and Pulmonary circulation
- Arteries transport blood under high pressure to the tissues
• strong vascular walls, blood flows at a high velocity
- arterioles are the last small branches of the arterial system
• act as control conduits through which blood is realised into capillaries
• strong muscular walls that can close the arterioles completely or can, by relaxing
dilate vessels severalfold
- in Capillaries fluids, nutrients, electrolytes, hormones, etc. are exchanged between
blood and intestinal fluid
• walls are thin and have numerous minute capillary pores
- Venules collect blood from the capillaries s and gradually coalesce into progressively
larger veins
- Veins function as conduits for transport of blood from venules back to the heart
• also so serve as major reservoir of extra blood, pressure in the venous system is very
low and the venous walls are thin
- but muscular enough to contract or expand
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Volumes of blood and pressures in the different
parts of the circulation:
- the pressure in the aorta is high, on average
100mm Hg
- heart pumping is pulsatile, so the arterial
pressure varies between a systolic pressure level
of 120mm Hg and a diastolic pressure level of
80mm Hg
- the pressure falls progressively during circulation
- >to about 0mm Hg at venae cava superior/
inferior
- the pressure in the systemic capillaries varies
from as high 35 mm Hg near arteriolar ends to
10mm Hg near the venous ends
• average functional pressure in most vascular
beds is 17mm Hg, low enough so only little
plasma leaks through the pores

Cross sectional areas and velocities of blood

flow:

Because the same volume of blood ow (F)

must pass through each segment of the
circulation each minute, the velocity of blood
ow (v) is inversely proportional to vas- cular
cross-sectional area (A):

-average velocity of
blood in the aorta is
33cm/sec.

-about 0.3mm/sec. in capillaries (length

0.3-1mm), only 1-3sec. in the capillaries
 Page 20 of 37

8. Arterial pressure. Aortic pressure curve. Arterial pulse.

Transmission of pulse wave.
Arterial pressure:
- the influence of arterial pressure on blood flow is small

- the arterial system of an adult person is filled with

about 700 millilitres of blood
- mean arterial pressure is 100mm Hg
- >BUT when it is filled with only 400 millilitres it
falls to 0
- at entry of blood in the arteries the arterial walls
stretch and pressure rises to 120mm Hg during
systole
- incisura occurs when aortic valve closes
- after aortic valve closed the pressure decreases
slowly to around 80mm Hg

Aortic pressure curve:

 Page 21 of 37

Arterial pulse:
- units of vascular distensibility
• is normally expressed as the fractional
increase of mercury rise in pressure

-compliance or capacity is the total

amount of blood that can be stored in
a given portion of the circulation for
each mm Hg pressure rise
- compliance is equal to distensibility times volume



Transmission pulse wave:
 Page 22 of 37

9. Veins and their functions.

Venous pressures. Effect of gravity
on venous pressure. Specific blood
reservoirs.

Veins and their functions:

- the entire venous blood system contains
2000-3500 millilitres of blood (around 60%)
- blood flow to the heart
- capable of constricting and enlarging
- storing blood
- “venous pumping”
- even help to regulate cardiac output

Venous pressures:
- a change of several hundred millilitres of the entire
venous blood volume is required to change the
venous pressure from only 3 to 5mm Hg

- pressure in the right atrium is called

“central venous pressure”
•regulated by 1) the ability of the heart
to pump blood from the right atrium
and ventricle to the lungs; 2) the
tendency for blood to flow from the
peripheral veins into the right atrium
•if the heart pumps strongly pressure
in the atrium decreases / weakness of
the heart increases atrial pressure
-increase of venous return
•increased blood volume
•increased large vessel tone
throughout the body with resultant
increased peripheral venous pressure
•dilation of arterioles, decreasing the
peripheral resistance and allows rapid
flow of blood from arteries to veins
•increased venous return increases
atrial pressure
•normal right atrial pressure lyes at
0mm Hg
->can increase to 20-30mm Hg
 Page 23 of 37
- >> conditions like serious heart failure or
massive transfusion of blood
- lower limit is -3 to -5mm Hg below atmospheric
pressure
• severe hemorrhage or exceptional vigor
heart pumping
- large veins have almost no resistance but veins are
easily compressed in may points of the thorax
• if the atrial pressure is high “back up” in large vein
enlarges
• the pressure in the abdominal cavity is around
6mm Hg
- can rise to 15-30 incase of pregnancy, large
tumors, abdominal obesity or excessive fluid in
the cavity

Effect of gravity on venous pressure: see Figure 15-10

- compression of the subclavian vein by the first rib adds another 6mm Hg of pressure to
the value of the arm
- the venous pressure in the sagittal sinus at the top of the brain is about -10mm Hg
• if the sagittal sinus is opened during surgery air can be sucked in, air embolism in the
heart and death can occur
- the venous pump see picture ——————>
- > every time muscles are tensed or legs are
moved the blood is pumped up
- >> so if an adult is walking the pressure is
around 20mm Hg in the feet
• if a solider is forced to stand in rigid
“attention” he might faint because 10-20% of
the blood can be lost in the circulatory
system, also the pressure in the legs and
feet capillaries is increased so liquid is
leaking and causing the tissues to swell

Specific blood reservoirs:

- spleen, can decrease in size so up to 100 ml of blood are released
• two areas
- the venous sinuses, storing whole blood by swelling
- splenic pulp, the red pulp contains large quantities of concentrated red blood cells
• 50ml of concentrated RBC can be released, raising the hematocrit 1 to 2
- liver, the sinuses of which can release several hundred ml of blood
- large abdominal veins can release 300 ml
- venous plexus can release several hundred ml
- heart can shrink and contribute 50-100ml
- the lungs can contribute another 100-200ml when pulmonary pressure deceases to very
low values
 Page 24 of 37

10. Cardiac output (CO). Control of CO by venous return.

Frank-Starling mechanism. Factors affecting venous return.

Cardiac output (CO):

The overall blood flow in the total circulation of an adult person at rest is about 5000 ml/
min. it is called the cardiac output because it is the amount of blood pumped into the aorta
by the heart each minute.
 Page 25 of 37
Control of CO by venous return:
- increase of venous return
• increased blood volume
• increased large vessel tone throughout the body with resultant increased peripheral
venous pressure
• dilation of arterioles, decreasing the peripheral resistance and allows rapid flow of
blood from arteries to veins
• increased venous return increases atrial pressure
- as long as the arterial pressure doesn’t raise over 160mm Hg the cardiac output
almost entirely depends on the venous return

Frank-Starling mechanism:
- whatever amount of blood enters the right atrium from
the veins can be pumped out automatically
• means that the greater the heart muscle is
stretched during filling, the greater is the quantity of
blood pumped into the aorta
• Or “Within physiological limits, the heart pumps all
the blood that returns to it by way of the veins
- for an extra amount of blood the cardiac muscle is
stretched further
• muscle contracts with increased force because the
actin and myosin filaments are brought to more
nearly optimal degree of overlap for force
generation
• >extra blood into arteries
- also: stretch of the atrial wall increases heart rate by
10-20%

Factors affecting venous return:

- increase of venous return
• increased blood volume
• increased large vessel tone throughout the body with resultant increased peripheral
venous pressure
• dilation of arterioles, decreasing the peripheral resistance and allows rapid flow of
blood from arteries to veins
• increased venous return increases atrial pressure
- as long as the arterial pressure doesn’t raise over 160mm Hg the cardiac output
almost entirely depends on the venous return
 Page 26 of 37

11. Preload, afterload, contractility. Cellular mechanisms

involved in regulation of myocardial contractility. Inotropic
agents.

Preload, afterload, contractility:

- when the muscle begins to contract it is called
“Preload”
• the degree of tension is determined
• for the cardiac contraction preload is usual
considered to be the end-diastolic pressure,
when the ventricle has become filled
- “Afterload” of the ventricle is the pressure in
the aorta leading from the ventricle
• corresponding to the systolic pressure in
Phase III
- The importance of the concepts of preload and
after- load is that in many abnormal functional
states of the heart or circulation, the pressure
during filling of the ventricle (the preload), the
arterial pressure against which the ventricle
must contract (the afterload), or both are altered from normal to a severe degree

- Contractility or inotropism is the intrinsic ability of myocardial cells develop force at a

given muscle cell length

Cellular mechanisms involved in regulation of myocardial contractility:

- Effect of potassium Ions
• excess of potassium in the extracellular fluids, causes the heart to become diluted and
flaccid, it also slows the heart rate
• already two to three times the normal value can cause severe weakness of the heart,
abnormal rhythm, and death
• potassium decreases the resting membrane potential, membrane potential is less
negative
- Effect of calcium Ions
• almost exactly opposite to potassium ions
• heart moves toward spastic contraction
• calcium ions initiate the contractile process
•
Inotropic agents:
- agents that have that produce an increase in contractility are said to have positive
inotropic effects
• increasing both the rate of tension development and the peak tension
- agents that produce a decrease in contractility are said to have negative inotropic effects
• decreasing both the rate of tension development and the peak tension
 Page 27 of 37

12. Effects of total peripheral resistance, blood volume and

nervous stimulation on the CO. Cardiac and non-cardiac
factors affecting CO.

Effects of total peripheral resistance, blood volume and nervous stimulation on the
CO:
- an increase in blood volume (by transfusion for
example) increases the mean systemic pressure
• right atrial pressure is increased and cardiac output is
increased
- a decrease in blood volume ( hemorrhage for example)
• mean systolic pressure is reduced
• right atrial pressure is decreased cardiac output is
decreased
- changes in venous compliance produce effects similar to
those caused by blood volume changes
• decreased venous compliance cause a shift out of the
unstressed volume into the stressed volume
- changes are similar to increase in blood volume
• increased venous compliance cause a shift into
unstressed volume out of the stressed volume
- changes are similar to decrease in blood volume

Cardiac and non-cardiac factors affecting CO:

- changes in total peripheral resistance (TPR)
• blood is “held”on the arterial side of the circulation,
hence an increase in arterial pressure and a decrease
in venous return
- restricting flow of blood out of the arteries by an increase in TPR

13. Structure of the microcirculation. Types of capillaries.

Exchange of water and substances through the capillary
membrane. Role of pressures and
filtration coefficient in fluid filtration.

Structure of microcirculation:
- nutrient artery entering an organ branches six - eight
times until it is small enough to be called an arteriole
(diameter 10-15 micrometers)
- arterioles themselves branch two - five times reaching a
diameter of five - nine micrometers at their ends where
they supply blood to the capillaries
- arterioles are highly muscular, can change diameter
- metarterioles (the terminal arterioles) do not have a
muscular coat but smooth muscle fibres encircle the
vessel at intermediate points
 Page 28 of 37
- at the point where each true capillary originates from a metarteriole a smooth muscle
finer encircles the capillary “precapillary sphincter”

Types of capillaries:

Exchange of water and substances through the capillary membrane:

- occurs by simple diffusion
• some solutes can diffuse through endothelial
cells, others must diffuse between the cells
• the route of diffusion depends on whether the
solute or gas is lipid soluble
- gases are highly lipid soluble, crossing the
capillary wall by diffusing through the
endothelial cells, the driving force is partial
pressure difference for the gas
- water-soluble substances such as water, ions,
glucose, amino acids can’t cross endothelial
membrane
• diffusion is limited to the aqueous clefts
• only 1/1000 of the capillary surface area
• the velocity of the thermal molecular motion
in clefts is so great that even the small area
is sufficient to allow tremendous diffusion
- fluids are transferred by osmosis, and driven by osmotic and hydrostatic pressure

Role of pressures and filtration coefficient fluid filtration:

Fluid movement across a capillary wall is driven by the
Starling pressures across the wall and is described by the
Starling equation as follows:

- Ki hydraulic conductance, is the water permeability of

the capillary wall
- Pc capillary hydrostatic pressure, is the force favouring
 Page 29 of 37
filtration
- Pi interstitial hydrostatic pressure, is the force opposing filtration
- Pie c capillary oncotic pressure, is a force opposing filtration
- Pie i interstitial oncotic pressure, is a force favouring filtration

14. Lymphatic system – structure, function. Formation of

lymph. Mechanism of lymph flow. Functions of the spleen.

Lymphatic system - structure, function:

- represents an accessory route through which fluid can flow from the intestinal spaces
into the blood
- lymphatics can carry proteins and large particulate matter away from the tissue spaces,
neither can be absorbed directly into the blood capillaries
- without lymph system we would die in 24h
- special lymph channels that drain excess fluid directly from the interstitial spaces
- even large particles like bacteria push through between endothelial cells of lymph
capillaries, as lymph passes through lymph nodes these particles are picked and
destroyed

Formation of lymph:
- Lymph is derived from interstitial fluid that flows through the lymphatics
- the protein concentration in the interstitial fluid of most issues is 2g/dl
• lymph formed in the liver has a protein concentration as high as 6g/dl
• formed in intestines 3-4g/dl
 Page 30 of 37

Mechanism of lymph flow:

- about 100ml per hour of lymph flows through the thoracic duct of a resting human and
20ml flows into circulation each hour through the channels

Function of the spleen:

- spleen, can decrease in size so up to 100 ml of blood are released
• two areas
- the venous sinuses, storing whole blood by swelling
- splenic pulp, the red pulp contains large quantities of concentrated red blood cells
• 50ml of concentrated RBC can be released, raising the hematocrit 1 to 2

15. Local control of blood flow. Control of blood flow by

endothelial factors.

Local control of blood flow:

- most tissues have the ability to control their own local blood flow for their needs:
• delivery of other nutrients
• delivery of oxygen to the tissues
• removal of carbon dioxide from the tissues
• removal of hydrogen ions from the tissues
• maintenance of proper concentration of ions in the tissues
• transport of various hormones and other substances to the different tissues
- controlling heat loss e.g.
- acute control is achieved by rapid changes in vasodilation or vasoconstriction of
arterioles, metarterioles, and precapillary sphincter, occurring within seconds or minutes
• reduced oxygen availability increases tissue blood flow
- high altitude, ppneumonia, carbon monoxide poisoning, cyanid poisoning
• tissue dilators adenosine, carbon dioxide, adenosine phosphate compounds,
histamine, potassium ions, and hydrogen ions
• decreased oxygen availability releases lactic acid and adenosine
- long term control means slow, controlled changes in flow over a period of days, weeks
or even months, providing a better control

Control of blood flow by endothelial factors:

- endothelial cells lining the blood vessel synthesise several substances that, when
released can affect the degree of relaxation or contraction of the arterial wall
• nitric oxide (NO), a lipophilic gas is one relaxing factor released from endothelial cells
• endothelin a large 27-amino acid peptide, is a powerful vasoconstrictor
 Page 31 of 37

16. Humoral control of the circulation.

Humoral control of the circulation:

- control by substances secreted or absorbed into the body fluids, such as hormones and
locally produced factors
- Vasoconstrictor agents
• Norepinephrine and Epinephrine
- norepinephrine is a stronger vasoconstrictor than Epinephrine, epinephrine might
even cause slight vasodilation in some tissues (coronary artery)
- dual system:
• 1. direct nerve stimulation
• 2. indirect effects of norepinephrine and/or epinephrine in circulating blood
• Angiotensin II
- one millionth of a gram can increase the arterial pressure of a human being 50mm
Hg or more
- constricting the small arterioles
• increasing total peripheral resistance and decreases sodium and water secretion
- >increasing arterial pressure
• Vasopressin “the antidiuretic harmon”
- more powerful constrictor the Angiotensin II
- formed in the nerve cells of the hypothalamus in the brain
- transported downward by the axon to the pituitary gland, where it is finally secreted
into the blood
- rising arterial blood pressure by 60mm Hg after severe hemorrhage
- Vasodilator agents
• Bradykinin
- many substances with -kinin cause vasodilation
- causes powerful arteriolar dilation and increased capillary permeability
• Histamine
- released in essentially every tissue if inflamed or damaged, or allergic reaction
- derived mostly from mast cells in damaged tissues and from basophils in blood
- powerful vasodilator effect on the arterioles and like bradykinin has the ability to
increase capillary porosity, allowing both fluid and plasma protein into the tissues
- Vascular control by ions and other chemical factors
1. an increase in calcium ion concentration causes vasodilation, because of the
general effect of calcium to stimulate smooth muscle contraction
2. an increase in potassium ion concentration, within the physiological range , causes
vasodilation. this effect results from the ability of potassium ions to inhibit smooth
muscle contraction
3. an increase in magnesium ion concentration causes powerful vasodilation because
magnesium ions inhibit smooth muscle contraction
4. an increase in hydrogen ions concentration (decrease in pH) causes dilation of
arterioles. Conversely, a slight decrease in hydrogen ion concentration causes
arteriolar constriction
5. Anions that have significant effects on blood vessels are acetate and citrate, both
which cause mild degrees of vasodilation
6. an increase in carbon dioxide conc. causes moderate vasodilation in most tissues
but marked vasodilation in the brain; also CO2 in blood, acting on the brain
vasomotor centre has an extremely powerful indirect effect, transmitted through the
sympathetic nervous vasoconstriction throughout the body
 Page 32 of 37

17. Nervous regulation of the

circulation. Vasomotor center.

Nervous regulation of the circulation:

- the autonomic nervous system controls almost the
entire circulation
• the parasympathetic system only contributes to
the regulation of the heart function
• sympathetic nervous system
- sympathetic vasomotor nerve fibres leave the
spinal cord through all the thoracic spinal
nerves, passing immediately into the
circulation, lying on each side of vertebral
column
• passing two routes to the circulation
- 1. through specific nerves that innervate
mainly the vasculature of the internal
viscera and the heart
- 2. almost immediately into peripheral
portions of the spinal nerves distributed to
the vasculature of the peripheral areas

• all vessels except capillaries are capillaries are innervated

- innervation of the small arteries and arterioles allow sympathetic stimulation to
increase resistance to blood flow lowering the rate of blood flow through tissue
- innervation of large vessels (particular veins) by sympathetic stimulation
decrease the volume of the vessel, pushing more blood to the heart
- sympathetic stimulation also increase the activity of the heart, enhancing its
strength and volume of pumping
• Parasympathetic stimulation decreases heart rate and contractility
- the parasympathetic exceedingly important for many other autonomic functions of
the body it has a minor role in regulating vascular function
- parasympathetic nerve fibres go to the heart in the vagus nerve
 Page 33 of 37
Vasomotor center:
- located bilaterally mainly in the reticular substance of
the medulla and of the lower third of the pons
- transmitting parasympathetic impulses
- important areas:
1. vasoconstrictor area located bilaterally in the
anterolateral portion of the upper medulla
1. exiting preganglionic vasoconstrictor
neurons of the sympathetic nervous system
2. vasodilator area located bilaterally in the
anterolateral portions of the lower half of the
medulla
1. they inhibit vasoconstriction, permitting
vasodilation
3. sensory area located bilaterally in the nucleus
tractus solitarius in the posterolateral portions of
the medulla and lower pons
1. receiving sensory signal from circulatory
system, through the vagus and the glossopharyngeal nerve
2. output signals help to control activities of both vasoconstrictor and vasodilator
areas of the vasomotor centre
3. >providing reflex control

18. Rapid control of arterial pressure. Reflex mechanisms.

CNS ischemic response.

Rapid control of arterial pressure:

- the entire vasoconstrictor and cardioaccelerator functions of the circulatory system are
stimulated together to cause a rapid increase in arterial pressure
• Most arterioles of the systemic circulation are constricted (increasing TPR)
• The veins especially (but the other large vessels of the circulation as well) are
constricted, blood “stored” in big veins is displaced towards the heart
• the heart is directly stimulated by the autonomic nervous system further enhancing
cardiac pumping
- pressure can be increased to two times its normal value in 5-10sec.
- sudden inhibition of nervous cardiovascular stimulation can decrease the arterial
pressure to as little as one half normal within 10-40sec.

Reflex mechanisms:
- special nervous control mechanisms operate all the time to maintain arterial pressure at
or near normal, almost all of these are negative feedback reflex mechanisms
• best known is the baroreceptor reflex
- initiated by stretch receptors “baroreceptors” or “pressoreceptors”, located in
specific points in the walls of many large systemic arteries
- signals are transmitted to CNS when a rise in arterial pressure causes the arterial
walls to stretch
- >feedback is sent back through the autonomic nervous system, to reduce arterial
pressure
 Page 34 of 37
- receptors are extremely abundant, in 1. the wall of each internal carotid artery
slightly above the carotid bifurcation, an area known as the carotid sinus and 2. the
wall of the aortic arch
- carotid sinus baroreceptors are not stimulated at all by pressures between 0 and
50-60 mm Hg, above these levels they respond progressively more rapidly

- falling pressure on standing up initiates an immediate reflex, resulting in strong

sympathetic discharge throughout the body t minimise the decline in pressure

CNS ischemic response:

- when blood flow to the vasomotor centre in the lower brain stem becomes decreased
severely enough to cause a nutritional deficiency - that is, to cause cerebral ischemia -
the vasoconstrictor and the cardioaccelerator become strongly exited
- >systemic arterial pressure is risen to a level as high as the heart could possibly pump
 Page 35 of 37

19. Role of the kidneys in long-term

regulation of arterial pressure.
Renin-angiotensin system.

Role of the kidneys in long-term regulation of

arterial pressure:
- the kidney can excrete the excess volume into the
urine if the pressure is to high
- at a pressure of 50mm Hg the urinary output is
essentially zero
- at 100mm Hg it is normal
- at 200mm Hg it is about six times than normal
-

Renin-angiotensin system:
- Renin is a protein enzyme released into kidneys
when the arterial pressure falls too low
- Renin is synthesised and stored in an inactive
form called prorenin in the juxtaglomerular cells
(JG-cells)
• JG-cells are manly located in the walls of the
afferent arterioles immediately proximal to the
glomeruli
• when pressure falls kidneys cause prorenin
molecules in the JG cells to split and release
renin
- most renin molecules go into circulation, a
few remain in kidneys to initiate internal
functions
• Renin is not a vasoactive substance, it acts
enzymatically on another plasma protein
- angiotensinogen
- >releasing angiotensin I (has no great
vasoconstrictor properties)
- >> angiotensinconverting enzyme in the
endothelium of the lung vessels
- >>> angiotensin I is converted to
angiotensin II
 Page 36 of 37

20. Coronary circulation. Phasic changes

in coronary blood flow during cardiac
cycle. Control of coronary blood flow.
Ischemic heart disease.

Coronary circulation:
- only the inner 1/10mm of the endocardial surface can
obtain significant nutrition from blood inside cardiac
chambers
- the rest has to be supplied by the arteries on the hearts
surface
- the left coronary artery supplies mainly the anterior and
left lateral portions of the left ventricle, whereas the
right coronary artery supplies most of the left ventricle
in 80-90% of people
- most of the coronary venous blood flow from the left ventricular muscle returns to the
right atrium of the heart by way of the coronary sinus, which is about 75% of coronary
blood flow, but most of the venous blood from the right ventricular muscle returns
through small anterior cardiac veins that flow directly into the right atrium
- a very small amount of coronary venous blood also flows back into the heart through
very minute thebesian veins, which empty directly into the chamber
- coronary blood flow in a human being averages 70ml/min/100g heart weight, or about
225ml/min (4-5% of cardiac output)

Phasic changes in coronary blood flow:

- Note from this diagram that the coronary capillary blood
flow in the left ventricle muscle falls to a low value
during systole, which is opposite to flow in vascular
beds elsewhere in the body

Control of coronary blood flow:

- Primary control is local metabolism
• regulated by local arterial vasodilation in response to the nutritional needs
• decreased heart activity is accompanied by decreased coronary flow
• normally 70% of the oxygen is removed from blood in coronary circulation
• coronary heart flow increases almost in direct proportion to any additional metabolic
consumption
- effect from nerves:
• direct effects result from action of the vagus transmitter substances acetylcholine from
the vagus nerves and norepinephrine from the sympathetic nerves on the coronary
vessel
• indirect effects result from secondary changes in coronary blood flow caused by
increased or decreased activity of the heart
• indirect effects are mostly opposite to direct effects
• indirect effects play afar more important role in normal coronary flow control
 Page 37 of 37
Ischemic heart disease:
- results from insufficient coronary blood flow
- some deaths are sudden due to acute coronary occlusion or fibrillation of the heart
- some are slow and over a long period of time due to progressive weakening of heart
pumping
- in people who have a genetic predisposition to atherosclerosis, who are overweight or
obese and have a sedentary lifestyle, or who have high blood pressure and damage to
the endothelial cells of the coronary blood vessels of the coronary blood vessels, large
quantities of cholesterol gradually become deposited beneath the endothelium at many
points in the arteries throughout the body —> gradually these areas are invaded by
fibrous tissue and frequently become calcified
- atherosclerotic plaque can cause a local blood clot called thrombus