Chapter 14 – The CV System: The Heart
14.1 Basic Design of the CV System
The CV system consists of the heart, blood vessels and blood
Pulmonary circulation: consists of blood vessels that carry blood from the right side of the heart, to the alveoli of the longs
and back to the left side of the heart (R-L)
Systemic circulation: consists of blood vessels that carry blood to the left side of the heart, to all organs and tissues (except
the alveoli) and back to the right side of the heart (L-R)
-In both circuits blood is carried away from the heart and then returned
-Blood is carried away by large vessels called arteries
-Arteries branch into smaller vessels called arterioles, which branch into even smaller vessels called capillaries
-From capillaries, blood enters larger vessels called venules, and venules give rise into even bigger vessels called veins which
carry blood back to the heart
Capillaries – smallest vessel of the body and where gas, nutrient and waste exchange occur between blood and surrounding
tissues
-Blood becomes oxygenated (picks up O2 drops off CO2) in pulmonary capillaries, and deoxygenated (picks up CO2 and
drops off O2) in systemic capillaries
Oxygenated blood: pulmonary veins, left side of the heart and systemic arteries
Deoxygenated blood: pulmonary arteries, right side of the heart and systemic veins
In systemic circulation parallel flow allows for each organ to receive its own fresh supply of oxygenated blood and allows
independent regulation of blood flow to different organs
Exceptions to parallel flow: hypothalamic-hypophyseal portal system, hepatic portal circulation and kidneys
Portal system: blood flows from one capillary network to a portal vein and then another capillary network before returning
to the heart
14.2 Organization of the Heart
-the heart has three layers and the pericardium protects and anchors the heart
Pericardium: a membranous sac that surrounds the heart made of two layers, the outer parietal layer and the inner visceral
layer (epicardium)
-the parietal layer made of tough, fibrous connective tissue anchors the heart by connecting it to nearby thoracic structures
while the visceral layer adheres to the surface of the heart
-in between these two layers is the pericardial cavity in which pericardial fluid resides to reduce internal friction
Three layers of the heart, epicardium, myocardium and endocardium
epicardium: epithelium and connective tissue
myocardium: the bulk of the heart wall, made of cardiac tissue and is why the heart pumps
endocardium: epithelium that lines the hearts chambers and covers the valves
Endothelium: endothelial cells that line the heart, blood vessels and lymphatic vessels
-the heart consists of 4 chambers, two upper atria and two lower ventricles
-right side of the heart serves as the pump for pulmonary circulation
-left side of the heart serves as pump for systemic circulation
-the heart is actually two separate pumps located within the same organ and is separated by a muscular partition called a
septum to prevent blood from mixing between the two sides of the heart
-the part of the septum between the atria is called the interatrial septum and the part of the septum between the ventricles
is called the interventricular septum
-the atria have thin walls because they deliver blood under less pressure into the ventricles
-the ventricles have thicker walls as they pump blood out of the heart under higher pressure and over greater distances,
more so the left ventricle, as structurally it is thicker than the right ventricle due to the fact that it does more work
-the right atrium receives deoxygenated blood from the superior (brings blood mainly from parts of the body above the
heart) and inferior (brings blood mainly from parts of the body below the heart) vena cava
-the right atrium then delivers blood to the right ventricle which pumps it into an artery called the pulmonary trunk, which
then divides into the pulmonary arteries, which carry deoxygenated blood into the lungs
-blood becomes oxygenated in the alveoli of the lungs (where O2 is picked up and CO2 is dropped off), then the oxygenated
blood is carried by the pulmonary veins to the left atrium of the heart, where it passes through the left ventricle which
pumps the blood into a large artery called the aorta
-the aorta branches off into many smaller arteries that carry oxygenated blood to all parts of the body except the alveoli
-the valves of the heart prevent backflow, they are made of connective tissue and covered by endocardium and open and
close in response to pressure changes as the heart contracts and relaxes
-each of the for valves ensure one-way blood flow by opening to let blood through and then closing to prevent its backflow
-there are two atrioventricular (AV) valves and two semilunar valves
-the AV valves lie between the atria and ventricles (right AV valve between right atria and right ventricle, left AV valve
between left atria and ventricle)
-the right AV valve is also known as the tricuspid valve as it has 3 cusps
-the left AV valve is also known as the bicuspid valve as it has 2 cusps, or the mitral valve
-the cusps of the AV valves are connected to tendon like cords called chordae tendineae which are in turn connected to
papillary muscles
-the chordae tendineae prevent the valve cusps from everting (opening into the atria) when the ventricles contract and are
aligned to allow the valve cusps to tightly close the valve
-the AV valves open when pressure in the atria > pressure in the ventricles, when ventricles contract, the pressure of the
blood drives the cusps upwards causing them to close
-the two semilunar (SL) valves include the pulmonary valve (located between the right ventricle and the pulmonary trunk)
and the aortic valve (located between the left ventricle and the aorta)
-they are both made up of 3 half-moon shaped cusps, the cusps are attached to the walls of the pulmonary trunk and the
aorta and project into the lumen of each of these arteries
-SL valves allow ejection of blood from the heart into the arteries but prevent backflow of blood into ventricles
-SL valves open when pressure in the ventricles > arteries, allowing blood to be ejected into the pulmonary trunk and aorta,
when the ventricles relax, blood starts to flow back into the heart, filling the valve cusps and causing the semilunar valves to
close tightly
-the heart wall contains connective tissue that forms the fibrous skeleton of the heart, which consists of four dense
connective tissue rings that surround the valves of the heart, fuse with one another and verge with the interventricular
septum
-the fibrous skeleton of the heart provides a structural foundation for the heart valves, prevents overstretching of the
valves, and serves as an attachment for bundles of cardiac muscle fibers and an electrical insulator between the atria and
ventricles
-the heart wall has its own network of blood vessels known as the coronary or cardiac circulation
-the coronary arteries branch from the aorta and encircle the heart
-when the heart is relaxed the high pressure of blood in the aorta propels blood through the coronary arteries, into
capillaries and then into coronary veins
-the blood from coronary veins drains into a large vein called the coronary sinus, which empties into the right atrium
14.3 Cardiac Muscle and the Conduction System
The following components of the heart contain autorhythmic fibres: SA node, AV node, AV bundle, right and left bundle
branches, Purkinje fibers
-unlike skeletal muscle ends of cardiac muscle fibers are connected via intercalated discs, which contain two types of cell
junctions:
1) desmosomes: mechanically bind cardiac muscle fibers together and are resistant to mechanical stress
2) gap junctions: electrically couple cardiac muscle fibers to each other and allow APs to conduct from one cardiac muscle
fiber to its neighbors
-a mass of interconnected muscle fibers that act as a single, coordinated unit are called a functional syncytium
-atria and ventricles have two separate functional syncytiums and thus contract separately
Cardiac APs:
-cardiac excitation begins in the SA node where cells spontaneously depolarize to threshold by producing a pacemaker
potential
-once threshold is reached an AP is generated and propagates throughout both atria, causing them to contract
-AP propagates from the atria to the AV node, then AV bundle, then both the right and left bundle branches, then to the
Purkinje fibres which conduct an AP at the apex of the heart to the remainder of the ventricular myocardium, then the
ventricles contract, pushing blood upwards towards the semilunar valves
-autorhythmic fibers can generate their own APs because they have unstable resting membrane potentials, they start
around -60 mV and depolarize to -40mV in which threshold is met to generate an AP, this spontaneous depolarization that
occurs in autorhythmic fibers in cardiac muscle is known as pacemaker potential
-SA node acts as the natural pacemaker of the heart
-autorhythmic fibers in the SA node are faster than other autorhythmic fibers in the heart and can initiate an AP every 0.6
seconds, or 100 times per minute
-APs from the ANS and blood-borne hormones such as epinephrine modify the timing and strength of a heartbeat but they
do not establish the fundamental rhythm
-e.g. at rest, ACh released by the PNS reduces the SA node AP speed to 0.8 seconds, therefore resting heart rate is 75 bpm
-if SA node is damaged, AV node can act as a pacemaker, however heart rate is slower and about 40-60 bpm with AV node
as pacemaker
-if both SA node and AV node are damaged heart, AV bundle or Purkinje fibers can act as pacemaker but at an extremely
slow rate of 20-35 bpm, and at such a low heart rate blood flow to the brain is inadequate
-contractile fibers produce APs in response to autorhythmic fibers
-contractile fibers have a stable resting membrane potential of about -90mV due to the fact that they are very permeable to
potassium ions and not very permeable to other ions, so the membrane resting potential stabilizes around the potassium
equilibrium potential of -90mV
-contractile fibers are depolarized to threshold by APs initiated by autorhythmic fibers, and produce their own AP
Contractile APs consist of 4 phases
1) Depolarizing Phase – fast voltage gated sodium channels open in response to a threshold-level depolarization,
sodium flows into the cell and increases the membrane potential to about +20mV
2) Initial Repolarizing Phase – within a few milliseconds, fast sodium channel inactivate, preventing sodium inflow, and
fast potassium channels open, allowing potassium ions to leave the cell and the membrane potential begins to
decrease
3) Plateau Phase – fast potassium channels close, L-type calcium channels open and allow calcium into the cell, slow
potassium channels partially open and potassium slowly exits the cell, the efflux just enough to balance the calcium
influx and causing the action potential curve to plateau
4) Final Repolarizing Phase – slow potassium channels fully open to allow potassium out and calcium channels close, to
end calcium inflow, once membrane potential reaches around -90mV, slow potassium channels close
Membrane channels involved
Initial repolarizing
phase
Depolarizing phase: Fast voltage-gated Na+ channels open
Plateau phase
Initial repolarizing phase: Fast voltage-gated Na+ channels close
and fast voltage-gated K+ channels open
Depolarizing Final
Plateau phase: L-type voltage-gated Ca2+ channels
phase repolarizing
open, fast voltage-gated K+ channels
close, and slow voltage-gated K+ phase
channels partially open
Final repolarizing phase: L-type voltage-gated Ca2+ channels close
and slow voltage-gated K+ channels fully
open
-once an AP is generated in cardiac contractile fiber, it ultimately causes the muscle fiber to contract by increasing calcium
concentration in the sarcoplasm, the muscle AP and contraction are connected by a sequence of events called the
excitation-contraction (EC) coupling
-this coupling involves L-type calcium channels in the membrane of transverse (T) tubules and nearby calcium release
channels in the terminal cisternal membrane of the sarcoplasmic reticulum (SR)
-calcium that enters via the open L-channel act as trigger calcium which then bind to and open calcium release channels in
the SR which allow even more calcium into the sarcoplasm, this process is known as calcium induced calcium release (CICR)
and about 90% of calcium needed for a cardiac contraction comes from the SR via CICR, while the other 10% comes from
extracellular fluid
-cardiac muscle fibers are capable of producing a graded potential and because the muscle is a part of a functional
syncytium, all the muscle fibers contract at the same time, the graded potential is produced by increasing the strength of
contraction of the existing muscle fibers in the syncytium by adding more calcium to the sarcoplasm, which increases
crossbridge formation
-relaxation of cardiac muscle fibers involve decreasing calcium levels in the sarcoplasm to resting levels
-cardiac muscle fibers have a long refractory period, this occurs because the sodium channels that were initially activated
during depolarization, quickly inactivate and need to wait for the membrane to repolarize and reach resting state before
they can be activate again
-refractory period in cardiac muscles is about 250 ms due to the prolonged plateau phase of the AP, the duration of the
contraction is about 300 ms so the refractory period lasts for almost the entire time
-summation of contractions and tetanus do not occur in cardiac muscle fibers
-contraction: heart ejects blood, relaxation: heart fills with blood; in a situation like tetanus, the heart would no longer be
able to function like a pump as it would not be able to relax and refill with blood, which would be fatal
-cardiac muscle almost exclusively relies on aerobic respiration in its multiple mitochondria
-oxygen needed for aerobic respiration is diffused from blood in the coronary circulation and released from myoglobin inside
cardiac muscle fibers
-at rest, cardiac muscle’s ATP comes mainly from fatty acid catabolism (60%) and glucose (35%) and smaller contributions
from lactic acids, amino acids and ketone bodies
-during exercise cardiac muscle’s use of lactic acid (being released by skeletal muscles) increases
-cardiac muscle can also create muscle from creatine phosphate, a sign of a myocardial infarction (heart attack) is an
increase in creatine kinase (CK) levels in the blood, injured or dying cardiac and skeletal muscles release CK, CK catalyzes the
transfer of a phosphate from creatine phosphate to ADP to make ATP
-an electrocardiogram (ECG) is a recording of electrical signals through the heart, a composite record of action potentials
produced by all of the heart muscle fibers during each heartbeat
-in a typical ECG, there are three clearly recognizable waves that appear, the P wave, the QRS complex and the T wave
-the P wave represents atrial depolarization, which spreads from the SA node through contractile fibers in both atria
-the QRS complex represents ventricular depolarization as the AP spreads though ventricular contractile fibers
-the T wave represents ventricular repolarization and occurs when the ventricles are starting to relax
ECG abnormalities
-large P wave can indicate enlargement of an atrium
-large Q wave may indicate a myocardial infarction
-large R wave indicates enlarged ventricles
-flatter than usual T wave could mean heart muscle is receiving inadequate oxygen, this can be seen in coronary artery
disease
-elevated T wave could indicate hyperkalemia (high potassium levels)
ECG analysis involves measuring the time spans between waves which are called intervals or segments:
1) P-Q interval (or P-R) – time from the beginning of the P wave to the begging of the QRS complex, conduction time
from the beginning of atrial excitation to the beginning of ventricular excitation, time required for AP to travel
through atria, AV node and the remaining fibers of the conduction system
-when the AP has to detour around scar tissue caused by disorders, the P-Q interval lengthens
2) The S-T segment – beginning of the S wave to the beginning of the T wave, represents the time ventricular
contractile fibers are depolarized during the plateau phase of the action potential
-S-T segment is elevated in acute myocardial infarction and depressed when the heart muscle receives insufficient
oxygen
3) The Q-T interval – start of the QRS complex to the end of the T wave, the time from the beginning of ventricular
depolarization to the end of ventricular repolarization
-interval could be lengthened by myocardial damage, myocardial ischemia or conduction abnormalities
systole: contraction phase
diastole: relaxation phase
-ECG waves can predict the timing of atrial and ventricular systole and diastole
1 Depolarization of atrial
contractile fibers
produces P wave
6 Ventricular diastole
(relaxation)
P
Action potential
in SA node
0 0.2
2 Atrial systole
Seconds (contraction)
P
0 0.2 0.4
0.6 0.8
Second
s
5 Repolarization of 0 0.2
ventricular contractile
fibers produces T Seconds
wave
3 Depolarization of
ventricular contractile
fibers produces QRS
complex
T
P R
P
0 0.2 0.4 0.6 4 Ventricular systole
Seconds (contraction) Q
S
0 0.2 0.4
Seconds
P
14.4 The Cardiac Cycle
-a single cardiac cycle includes all the events associated with one heartbeat, thus a cardiac cycle
consists of the diastole(relaxation) and systole (contraction) of the atria plus diastole and
systole of the ventricles
-pressure on the left side of the heart is significantly higher than pressure on the right side of
the heart
The Cardiac Cycle has 5 Phases:
1) Passive ventricular filling – both atria and ventricles are in diastole, atrial pressure >
ventricular pressure because blood returning to the heart by veins is filling the atria, the
pressure difference causes the AV valves to open and blood flows from the atria to the
ventricles, it’s passive because no muscle contractions are involved and about 80% of
ventricular filling occurs in this phase, while the remaining 20% occurs in atrial
contraction, at the end of atrial diastole and AP arises in the SA node and causes the
atria to depolarize, this is indicated by the P wave
2) atrial contraction – atrial depolarization causes atrial systole, while atria are in systole,
ventricles remain in diastole, as atria contract atrial pressure increases and more blood
is forced through AV valves, atrial contraction contributes a final 25 mL of blood into the
ventricles, which already had 105 mL, so each ventricle contains 130 mL of blood at the
end of diastole (end-diastolic volume), end of atrial systole and onset of ventricular
depolarization indicated by QRS complex
3) isovolumetric ventricular contraction – ventricular depolarization causes ventricular
systole, while ventricles are in systole, atria are in diastole, all four valves remain shut
during this time, muscles are contracting but not shortening so staying the same length,
and no volume is lost so isovolumetric
4) ventricular ejection – when pressure in left ventricle surpasses aortic pressure at about
80 mmHg and right ventricular pressure surpasses pulmonary trunk pressure (around 20
mmHg) both SL valves open and blood is pumped out of the heart, left ventricle ejects
about 70mL of blood into the aorta and right ventricle ejects the same amount into the
pulmonary trunk, leaving about 60 mL left in each ventricle (end-systolic volume) ESV, T
wave appears near the end of ventricular systole and before the onset of ventricular
repolarization
5) isovolumetric ventricular relaxation – ventricular repolarization causes ventricular
diastole, ventricles relax, pressure in the chambers fall and blood in the aorta and
pulmonary trunk begin to flow backwards, catching in the valve cusps and closing the SL
valves, blood volume remains unchanged because all 4 valves are closed, thus
isovolumetric ventricular relaxation, as pressure continues to fall and ventricular
pressure < atrial pressure, the AV valves open and another cardiac cycle repeats itself as
passive ventricular filling begins
dicrotic wave or aortic pressure curve caused by rebound of blood off the closed cusps of the
aortic valve
stroke volume = EDV – ESV, at rest the SV is 70 mL SV = EDV – ESV SV = 130 mL – 60 mL
SV = 70 mL
ejection fraction is the percent of end diastolic volume that is ejected
EF = SV/EDV x 100
under normal conditions the EF is around 54%
-at rest a cardiac cycle lasts about 0.8 seconds, atria are in diastole for about 0.7 seconds and in
systole for about 0.1 seconds, ventricles are in diastole for 0.5 seconds and systole for 0.3
seconds, and when heart rate increases due to exercise, the amount of time in diastole and
systole decreases for both atria and ventricles, with the duration of diastole decreasing the
most
two sounds can be heard during each cardiac cycle:
S1, the lubb, is louder and longer and caused by the vibrations associated with the
closure of the AV valves when ventricular systole begins
S2, the dupp, is shorter and quieter and cause by the vibrations associated with the
closure of the SL valves at the beginning of ventricular diastole
14.5 Cardiac Output
cardiac output (CO) is the volume of blood ejected from each ventricle of the heart per minute
and it equals the stroke volume (SV) multiplied by the heart rate
-in a typical adult male at rest it is about 5.25 L/min
cardiac reserve is the difference between a person’s maximum cardiac output and cardiac
output at rest, the average person has a cardiac reserve of 4-5 times their resting value, while a
top endurance athlete might have a cardiac reserve of 7-8 times their resting CO
-people with heart disease have very little cardiac reserve which greatly limits their ability to
perform day to day living tasks
SV is regulated by preload, contractility and afterload
-preload: degree of stretch on the heart before it contracts
-contractility: the forcefulness of contraction of individual ventricular muscle fibers
-afterload: the pressure that must be exceeded before ejection of blood from the ventricles can
occur
-larger preload = larger force of contraction
Frank-Starling law – the more the heart fills with blood during diastole, the larger the force of
contraction during systole
-preload is proportional to the EDV, the greater the EDV, the more forceful the next contraction
-two key factors determine EDV: filling time (duration of ventricular diastole) and venous return
(the volume of blood returning to the right ventricle)
-when heart rate increases, filling time is shorter, which means a smaller EDV
-when venous return increases, EDV increases as a greater volume of blood flows into the
ventricles
-the Frank-Starling law of the heart equalizes the output of the right and left ventricles and
keeps the same volume flowing to both the pulmonary and systemic circulations
-myocardial contractility is the strength of contraction at any given preloads
-agents that alter contractility are said to have an inotropic effect, those that increase
contractility have a positive inotropic effect while those that decrease contractility have a
negative inotropic effect
-stimulation of the SNS, hormones such as epinephrine and NE, increased extracellular calcium
and the drug digitalis all have positive inotropic effects
-positive inotropic agents enhance contractility by increasing the amount of calcium available in
the sarcoplasm during cardiac action potentials while negative inotropic agents decrease
contractility by reducing the amount of calcium available
-drugs known as calcium channel blockers have negative inotropic effects
-ejection of blood from the heart occurs when the pressure in the right ventricle exceeds the
pressure in the pulmonary trunk (about 20 mmHg) and when the pressure in the left ventricle
exceeds the pressure in the aorta (about 80 mmHg)
-the higher pressure causes blood to push the semilunar valves open
-the pressure that must be overcome before a semilunar valve can open is termed the afterload
-an increase in afterload causes stroke volume to decrease
-conditions that increase afterload include hypertension (high blood pressure) and narrowing of
arteries by atherosclerosis
-heart rate is regulated mainly by the ANS and certain chemicals
-the SA node initiates contraction and if left to itself would set a constant rate of about 100
bpm
-other factors that contribute to regulation of heart rate include age, gender, physical fitness
and body temperature
-agents that alter the heart rate re said to have a chronotropic effect, those that increase heart
rate have a positive chronotropic effect while those that decrease heart rate have a negative
chronotropic effect
-the heart receives innervation from both the SNS and PNS divisions of the ANS
-axons of the sympathetic postganglionic neurons in turn form sympathetic nerves known as
cardiac accelerator nerves that extend to the SA node, AV node and ventricular myocardium
sympathetic regulation has 3 main effects on the heart
1) increases heart rate – via sympathetic stimulation of the SA node, rate of spontaneous
depolarization of SA node is increased
2) increase in rate of APs from the atria to the ventricles – via sympathetic stimulation of
AV node, speed of conduction velocity through the AV node increases
3) increase in contractility – via sympathetic stimulation of the ventricular myocardium
parasympathetic regulation has two main effects on the heart
1) decrease in heart rate – via decrease in spontaneous depolarization of the SA node
2) decrease in action potential conduction from atria to ventricles
-a continual shifting balance exists between the sympathetic and parasympathetic stimulation
of the heart
the heart is chemically regulated by hormones, norepinephrine and epinephrine enhance the
heart’s pumping effectiveness by binding to beta receptors in cardiac cells, thyroid hormones
enhance cardiac contractility
ions such as potassium, sodium and calcium have a big effect on cardiac function
high K+ or Na+ = decreased heart rate and contractility
high Na+ = blocked Ca2+ inflow during cardiac APs, therefore decreasing the force of
contraction
high K+ = blocks generation of APs
high Ca2+ = increased heart rate and stronger heartbeat
-age, gender, physical fitness and body temperature also influence resting heart rate