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The Cardiovascular System: The Heart
• Heart pumps over
1 million gallons
per year
• Over 60,000 miles
of blood vessels
20-1
Heart Location
•
Heart is located in the
mediastinum
– area from the sternum to
the vertebral column and
between the lungs
•
•
•
•
•
•
Apex - directed anteriorly,
inferiorly and to the left
Base - directed posteriorly,
superiorly and to the right
Anterior surface - deep to the
sternum and ribs
Inferior surface - rests on the
diaphragm
Right border - faces right lung
Left border (pulmonary border)
- faces left lung
20-2
Pericardium
• Fibrous pericardium
– dense irregular CT
– protects and anchors the heart,
prevents overstretching
• Serous pericardium
– thin delicate membrane
– contains
• parietal layer-outer layer
• pericardial cavity with
pericardial fluid
• visceral layer (epicardium)
• Epicardium
– visceral layer of serous
pericardium
• Myocardium
– cardiac muscle layer is the
bulk of the heart
• Endocardium
– chamber lining & valves
20-3
Myocardium – cardiac muscle
• shares structural and functional characteristics with both skeletal
and smooth muscle
– skeletal & cardiac – striated
• thin filaments contain troponin and tropomyosin – regulates cross-bridge
formation
• possess a definitive tension-length relationship
• plentiful mitochondria and myoglobin
• well-developed T-tubule structure
– smooth & cardiac – calcium enters the cytosol of the muscle cell from the
SR and the ECF during excitation
• through voltage-gated calcium channels in the PM and the T-tubule membrane –
dihydropyridine receptors
• calcium entry from the ECF triggers its release from the SR
• displays pace-makes activity – initiates its own APs without external influence
• interconnected by gap junctions (intercalated discs) – enhance the spread of APs
• innervated by the ANS
• unique – 1. cardiac muscle fibers are joined in a branching
network
– 2. action potentials last longer than skeletal before repolarization
20-4
Heart Anatomy
20-5
Right Atrium
•
Receives blood from 3
sources
– superior vena cava, inferior
vena cava and coronary
sinus
•
•
•
Interatrial septum partitions
the atria
Fossa ovalis is a remnant of
the fetal foramen ovale
Tricuspid valve
– Blood flows through into
right ventricle
– has three cusps composed
of dense CT covered by
endocardium
Right Ventricle
•
•
•
•
•
Forms most of anterior surface of
heart
Papillary muscles are cone
shaped trabeculae carneae (raised
bundles of cardiac muscle)
Chordae tendineae: cords
between valve cusps and
papillary muscles
Interventricular septum:
partitions ventricles
Pulmonary semilunar valve:
blood flows into pulmonary trunk
20-6
Left Atrium
•
•
•
Forms most of the base of the heart
Receives blood from lungs - 4 pulmonary
veins (2 right + 2 left)
Bicuspid valve: blood passes through into
left ventricle
– has two cusps
– to remember names of this valve, try
the pneumonic LAMB
• Left Atrioventricular, Mitral, or
Bicuspid valve
Left Ventricle
•
•
Forms the apex of heart
Chordae tendineae anchor
bicuspid valve to papillary
muscles (also has trabeculae
carneae like right ventricle)
•
Aortic semilunar valve:
– blood passes through valve
into the ascending aorta
– just above valve are the
openings to the coronary
arteries
20-7
Atrioventricular Valves
• A-V valves open and allow blood
to flow from atria into ventricles
when ventricular pressure is lower
than atrial pressure
– occurs when ventricles are
relaxed, chordae tendineae are
slack and papillary muscles are
relaxed
• A-V valves close preventing backflow of
blood into atria
Semilunar
Valves
– occurs when ventricles contract, pushing
valve cusps closed, chordae tendinae are
pulled taut and papillary muscles contract
to pull cords and prevent cusps from
everting
• SL valves open with ventricular
contraction
– allow blood to flow into pulmonary
trunk and aorta
• SL valves close with ventricular
relaxation
– prevents blood from returning to
ventricles, blood fills valve cusps,
tightly closing the SL valves 20-8
Blood Circulation
•
Systemic circulation
– left side of heart pumps blood through body
– left ventricle pumps oxygenated blood into aorta
– aorta branches into many arteries that travel to organs
– arteries branch into many arterioles in tissue
– arterioles branch into thin-walled capillaries for exchange
of gases and nutrients
– deoxygenated blood begins its return in venules
– venules merge into veins and return to right atrium
•
Pulmonary circulation
– right side of heart pumps deoxygenated blood to lungs
– right ventricle pumps blood to pulmonary trunk
– pulmonary trunk branches into pulmonary arteries
– pulmonary arteries carry blood to lungs for exchange of gases
– oxygenated blood returns to heart in pulmonary veins
20-9
Passage of Blood through the Heart
Body
SVC/IVC
Right Atrium
(tricuspid valve)
Right Ventricle
(pulmonary semilunar valve)
Pulmonary Arteries
Lungs
Pulmonary Vein
Left Atrium
bicuspid (mitral) valve
Body
Aorta
(aortic semilunar valve)
Left Ventricle
20-10
Conduction System of Heart
• two types of cardiac muscle cells
– 1. contractile cells
• 99% of cardiac muscle cells
• Do mechanical work of pumping
• Normally do not initiate own action
potentials
– 2. autorhythmic cells
• Do not contract
• Specialized for initiating and
conducting action potentials
responsible for contraction of working
cells
20-11
• intercalated discs – join cardiac cells
– two types of membrane junctions
• a. desmosomes – abundant in tissues under considerable stress
– formation of a proteinaceous plaque on each PM surface (desmoglein,
desmocollin)
– plaques are joined to each other by adhesion proteins – cadherins
(require calcium for interaction)
– cadherins link to the underlying cytoskeleton (intermediate filaments)
• b. gap junctions – two PMs are connected by a “channel” made of
specific proteins = connexons
–
–
–
–
–
connexons are 6 protein subunits that form a hollow tube-like structure
two connexons join end to end to connect the cells
allow a free flow of materials from cell to cell
allow for the spread of electricity within each atrium and ventricle
no gap junctions connect the atrial and ventricular contractile cells –
block to electrical conduction from atria to ventricle!!!
– also a fibrous skeleton the supports the valves – nonconductive
– therefore a specialized conduction system must exist to allow the
spread of electricity from atria to ventricles
20-12
•
atrial conduction system/interatrial pathway – spread of electricity from right to left
atrium ending in the LA
– through gap junctions of the contractile cells
•
internodal pathway – spread of electricity to the AV node via autorhythmic cells
– SA to AV node – 30msec
– BUT spreads relatively slowly through the AV node
– this allows for complete filling of the ventricles before they are induced to contract = AV nodal
delay
•
ventricular conduction system (Purkinje system) – Bundles of His and Purkinje fibers
–
–
–
–
–
travel time = 30 msec
PFs conduct impulse 6 times faster than the ventricular muscle cells would on their own
the PFs do not connect with every ventricular contractile cell
so the impulse spreads via gap junctions through the ventricle muscle – similar to the atrial system
diffusion through the PFs allow for simultaneous contraction of all ventricular cells
20-13
Rhythm of Conduction System
• SA node fires spontaneously 90-100 times per minute
• AV node fires at 40-50 times per minute
• If both nodes are suppressed fibers in ventricles by themselves fire
only 20-40 times per minute
• Artificial pacemaker needed if pace is too slow
• Extra beats forming at other sites are called ectopic pacemakers
– caffeine & nicotine increase activity
20-14
Normal pacemaker activity
•
•
•
•
various autorhythmic cells
have different rates of
depolarization to threshold
– so the rate of generating
an AP differs
AP propagated through gap
junctions or through the
conduction system of the
heart
contraction rate is driven by
the SA node – fastest
autorhythmic tissue
in some cases – the
normally slowest Purkinje
fibers can become
overexcited = ectopic focus
failure of SA node
blockage of transmission from SA through the AV node
– premature APs
– premature ventricular
contraction (PVC)
– occurs upon excess
caffeine, alcohol, lack of
sleep, anxiety and stress
– some organic conditions
can also lead to this
20-15
Cardiac excitation
• efficient cardiac function requires three criteria
• 1. atrial excitation and contraction should be complete before
ventricular excitation and contraction
– opening and closing of valves within the heart depend upon pressure –
which is generated by muscle contraction
– so simultaneous contractions of atria and ventricles would lead to
permanent closure of the AV valves – myocardium of the ventricles is
larger and stronger
– normally – atrial excitation and contraction occurs about 160 msec before
ventricular
• 2. cardiac fiber excitation should be coordinated to ensure each
chamber contracts as a unit
– muscle fibers cannot become excited randomly
– role of the gap junctions
• 3. atria and ventricles should be functionally coordinated
– atria contract together, ventricles contract together
– permits efficient pumping of blood into the pulmonary and systemic
circuits
– uncontrolled excitation and contraction of ventricular cells – fibrillation
– correction by:
• 1. electrical defibrillation
• 2. mechanical defibrillation
20-16
Cardiac muscle
action potentials
• pacemaker potential of the autorhythmic cells
• provided by the SA node
– interactions by several different ionic mechanisms
– cells do NOT have voltage- gated Na+ channels
– 1. decreased outward K+ current
• “Normal” leak of Na in coupled to a decreased leak in K+ out
• so the Na+ inflow doesn’t change but the K+ flow decreases – membrane
constantly drifts toward threshold
– 2. increased inward Ca+ current
• T-type Ca+ channels (voltage-gated) open as the membrane drifts toward threshold
– open before threshold is reached
• brief and extra influx of Ca increases the depolarization to threshold
• at threshold – L-type Ca channels open – longer lasting voltage-gated channel
• greater influx of calcium – so the influx of calcium (rather than Na) is what drives
the depolarization phase of the action potential
• repolarization through the closing of these Ca channels and the opening of voltagegated K+ channels
20-17
Cardiac muscle
action potentials
• AP in the contractile cells of the myocardium are
initiated by the autorhythmic cells and spread via gap
junctions
• but the mechanism differs from that of the
autorhythmic cells
– 1. AP from autorhythmic cells activates “fast” voltagegated Na+ channels (similar to neurons) = Na+ entry
– 2. Na+ permeability will then plummet to its resting level
due to the action of Na+ pumps
– 3. BUT the MP potential is held a positive for an
extended period of time due to the opening of L-type
voltage-gated Ca+ channels PLUS the delay in the
opening of voltage-gated K+ channels for repolarization
• prolongs the positivity inside the cell
• Produces a plateau phase
– 4. inactivation of these Ca+ channels and delayed
opening of voltage-gated K+ channels
• results in a sudden opening of K+ channels and a rapid
repolarization
20-18
AP and
contraction
• the “slow” L-type Ca+ channels are
found within the T-tubules
• triggers the opening of Ca+ channels
within the adjacent lateral sacs of the
SR (foot proteins) –
• this “Ca-induced Ca release” triggers
a very large release of Ca+ from the SR
• burst of Ca+ = Ca+ sparks
• SR supplies 90% of the Ca+ required
for contraction
• together with the slow removal of Ca+ results in a long sustained contraction of
heart muscle
20-19
AP and contraction
• Ca+ triggers the same series of events as seen in
skeletal muscle
– BUT – the amount of Ca+ release can directly affect
the number of cross-brides formed in cardiac muscle
and can directly affect the strength of the
contraction!
– so cardiac muscle must ensure adequate release of
Ca+
– elevated ECF Ca+ can increase the strength of
contraction
• e.g. digitalis – alters the activity of the Na/K
transporter = increases Ca transport into the cell
– elevates intracellular contraction, increases the plateau
phase which increases the strength of contraction and
the duration of the contraction
• e.g. verapamil – Ca+ channel blocker – blocks inflow
of Ca from the ECF – decreases contraction
• refractory period of cardiac muscle is longer than
skeletal muscle (250msec)
– cannot be restimulated until the contraction is almost
over
– prevents the development of tetanus
– allows for the emptying of the chambers
20-20
Electrocardiogram---ECG or
EKG
• electrical currents generated by the heart are
•
•
•
•
•
also transmitted through the body fluids
can be measured on the surface of the chest
therefore it is not a direct measurement of the
actual electrical conductivity of the heart itself
represents the overall spread of activity through
the heart during depolarization – sum of all
electrical activity
measured through the placement of 6 leads on
the chest wall (V1 – V6) PLUS 6 limb leads (I,
II, III, aVR, aVL and aVF)
it's usual to group the leads according to which
part of the left ventricle (LV) they look at.
–
–
•
•
AVL and I, as well as V5 and V6 are lateral,
while II, III and AVF are inferior.
V1 through V4 tend to look at the anterior
aspect of the LV
see EKG lab handouts
ECG paper is traditionally divided into 1mm
squares. Vertically, ten blocks usually
correspond to 1 mV, and on the horizontal axis,
the paper speed is usually 25mm/s, so one
block is 0.04s (or 40ms).
–
Note that we also have "big blocks" which are
5mm on their side.
20-21
Electrocardiogram---ECG or EKG
•
P wave
–
–
–
–
•
PR segment/PQ interval – AV nodal delay
–
–
–
–
•
ventricles are completely depolarized and the cells are in their
plateau phase
T wave
–
•
ventricular depolarization
will be affected by the appearance of an ectopic focus (region
of hyperactive ventricular contraction)
ST segment – time during which ventricles are
contracting and emptying
–
•
P to Q interval
conduction time from atrial to ventricular excitation
no net current flow within the heart musculature & the flow
through the AV node is too small to measure– baseline
if activity in the AV node is abnormal – this interval ill be
affected
QRS complex
–
–
•
atrial depolarization
SA depolarization is too weak to measure
smaller than the QRS complex due to the smaller size of the
atrial muscle mass
will be affected by abnormalities in the pacemaker activity of
the SA node
ventricular repolarization
TP interval
–
time during which ventricles are relaxing and filling
http://www.ecglibrary.com/ecghist.html
http://www.anaesthetist.com/icu/organs/heart/ecg/Findex.htm
20-22
The
Heartbeat
-contraction of
atria
-AV valves open
-filling of
ventricles =
“Ventricular
Filling stage”
each heartbeat = cardiac cycle
-SL valves close
“dup”
-AV valves open
-filling of atria &
ventricles begins
-contraction of ventricles
-AV valves close “lub”
-SL valves open
-blood to lungs and body
**Heart Murmur**
20-23
Cardiac cycle
• A. Midventricular diastole
– during most of the ventricular
diastole, the atrium is also in
diastole = TP interval on the
EKG
– as the atrium fills during its
diastole, atrial pressure rises
and exceeds ventricular
pressure (1)
– the AV valve opens in
response to this difference and
blood flows into the right
ventricle
– the increase in ventricular
volume rises even before the
onset of atrial contraction (2)
20-24
Cardiac cycle
•
B. Late ventricular diastole
– SA node reaches threshold and fires its
impulse to the AV node = P wave (3)
– atrial depolarization results in contraction –
increases the atrial pressure curve (4 – green
line)
– corresponding rise in ventricular pressure (5
– red line) occurs as the ventricle fills &
ventricular volume increases (6)
– the impulse travels through the AV node
– the atria continue to contract filling the
ventricles
•
C. End of ventricular diastole
– once filled the ventricle will start to contract
and enter its systole phase
– ventricular diastole ends at the onset of
ventricular contraction
– atrial contraction has also ended
– ventricular filling has completed
– ventricle is at its maximum volume (7) =
end-diastolic volume (EDV), 135ml
20-25
Cardiac cycle
• D. Start of ventricular systole
– at the end of this contraction is
the onset of ventricular
excitation (8) = QRS complex
– the electrical impulse has left the
AV node and enters the
ventricular musculature
– this induces ventricular
contraction
– ventricular pressure will begin to
rise rapidly after the QRS
complex (red line)
– this increase signals the onset of
ventricular systole (9)
– atrial pressure is at its lowest
point as its contraction has
ended and the chamber is empty
(green line)
– the ventricular pressure now
exceeds atrial – AV valve closes
20-26
Cardiac cycle
•
E. isovolumetric ventricular contraction
–
–
–
•
F. Ventricular ejection
–
–
–
–
–
•
ventricular pressure will now exceed aortic pressure as the
ventricle continues is contraction (12)
aortic SL is forced open and the ventricle empties
this volume of blood – stroke volume (SV)
the ejection of blood into the aorta increases its pressure (aortic
pressure) and the aortic pressure curve rises (13 – purple line)
ventricular volume now decreases (14 – blue line)
F. End of ventricular systole
–
–
–
–
•
ventricular pressure also opens the semilunar valves
however, just after the closing of the AV and opening of the SL
is a brief moment where the ventricle is a closed chamber (10) =
isovolumetric contraction
ventricular pressure continues to rise (red line) but the volume
within the ventricle does not change (11)
as the ventricular volume drops
BUT ventricular pressure continues to rise as the contraction
increases its force (red line) – then starts to decrease as blood
begins to be ejected
at the end of the systole there is a small volume of blood that
remains in the ventricle – end-systole volume (ESV), 65ml (15)
EDV-ESV = SV (point 7 – point 15)
G. Ventricular repolarization
–
–
–
T wave – point 16
as the ventricle relaxes – ventricular pressure falls below aortic
and the aortic SL closes (17)
this closure produces a small disturbance in the aortic pressure
curve – dicrotic notch (18)
20-27
Cardiac cycle
•
H. Isovolumetric ventricular relaxation
– Start of Ventricular Diastole
–
–
•
all valves are closed because ventricular
pressure still exceeds atrial pressure –
isovolumetric relaxation (19)
chamber volume remains constant (20)
I. Ventricular filling/MidVentricular
Diastole
–
–
–
–
–
–
as VP falls below AP – the AV valve
opens again (21) and ventricular filling
starts again increasing ventricular volume
(blue line)
as the atria fills from blood from the
pulmonary veins (lungs) it increases AP
with the AV valve open this blood fills the
ventricle rapidly (23)
then slows down (24) as the blood drains
the atrium
during this period of reduced filling, blood
continues to come in from the pulmonary
veins – goes directly into the ventricle
cycle starts again with a new SA
depolarization
20-28
• Heart sounds
Auscultation
• Stethoscope
• Sounds of heartbeat
are from turbulence in
blood flow caused by
valve closure
– first heart sound (lubb)
is created with the
closing of the
atrioventricular valves
– second heart sound
(dupp) is created with
the closing of semilunar
valves
20-29
20-30
Cardiac Output
• Amount of blood pushed into aorta or pulmonary
trunk by a ventricle
• Determined by stroke volume and heart rate
• CO = SV x HR
– at 70ml stroke volume & 75 beat/min----5 and 1/4
liters/min
– entire blood supply passes through circulatory system
every minute – each half of the heart pumps half the total
volume of blood
– at rest the heart pumps 2.5 million liters of blood per year!
– during exercise – rise to 20 to 25 liters per minute
• Cardiac reserve is the ratio of the maximum output
to normal cardiac output at rest
– average is 4-5 while athlete is 7-8
20-31
Stroke volume
•
•
end-diastolic volume (amount of blood in a ventricle after filling) - end-systolic volume
(amount of blood left in a ventricle after systole)
SV = EDV- ESV
– ESV – measured by EKG – end of the T wave
– EDV – measured using MRI, CT scan or a ventriculography (catheter in the ventricle and injection
of an X-ray visible dye)
•
•
two components influence SV
1. intrinsic control
–
–
–
–
–
–
heart’s inherent ability to vary SV
depends on the direct correlation between end-diastolic volume (EDV) and stroke volume
as more blood returns to the heart, the heart pumps out more blood
BUT the heart does not eject all the blood it contains
this control depends on the length-tension relationship of cardiac muscle – similar to skeletal muscle
for cardiac muscle – resting cardiac muscle length is less than lo
• muscle length is determined by the extent of ventricular filling – increased EDV, increased ventricular
volume
• filling the ventricle with more blood stretches the cardiac muscle
• as the cardiac cell is stretched – the spacing between thick and thin microfilaments is reduced
• the myofilaments are pulled closer together
• allows more cross-bridge formation
•
2. extrinsic control
– sympathetic and parasympathetic control
20-32
20-33
Regulation of Heart Rate
•
Nervous control from the cardiovascular center in the medulla
– OUTPUT: 1. Sympathetic impulses increase heart rate and force of contraction
–
2. Parasympathetic impulses decrease heart rate through the vagus
– INPUT : 1. Chemoreceptors detect changes in blood chemistry
–
2. Proprioceptors monitor changes in body activity
–
3. Baroreceptors (pressure receptors) detect changes in BP
– Heart rate is also affected by hormones and ions
– epinephrine & norepinephrine from adrenal medulla, thyroid hormones
– ions (Na+, K+, Ca2+)
– age, gender, physical fitness, and temperature
20-34
Regulation of Heart Rate
– Sympathetic impulses increase heart rate and force of contraction
• supplies the atrial and ventricular musculature (including the SA and AV
nodes)
• speeds up contraction rate by speeding up the rate of depolarization of
the autorhythmic cells of the SA node
– decreases K+ permeability by inactivating K+ channels
– with fewer K+ ions leaving the cell – the inside becomes less negative –
depolarizing effect
– swifter drift towards threshold
• also reduces the AV delay by enhancing the L-type Ca+ channels
• speeds the rate of conduction through the Bundles and Purkinje fibers
– parasympathetic impulses decrease heart rate through the vagus
nerve
• primarily supplies the SA and AV nodes
• little effect on ventricular conduction system or ventricular contractile cells
• decreases the excitability of the AV node – increases AV delay
(hyperpolarizes the AV node)
• in contractile cells of the atria – shortens the AP and reduces the inward
Ca+ flow shortening the plateau phase – weakened atrial contraction
20-35
20-36
20-37
20-38
Risk Factors for Heart
Disease
• Risk factors in heart disease:
– high blood cholesterol level
– high blood pressure
– cigarette smoking
– obesity & lack of regular exercise.
• Other factors include:
–
–
–
–
–
diabetes mellitus
genetic predisposition
male gender
high blood levels of fibrinogen
left ventricular hypertrophy
20-39
Plasma Lipids and Heart Disease
• Risk factor for developing heart disease is high blood cholesterol level.
– promotes growth of fatty plaques
– Most lipids/cholesterol are transported as lipoproteins
– cholesterol is unable to travel freely in the blood – combined with a
protein (apolipoproteins) made in the liver = lipoprotein
• low-density lipoproteins (LDLs)
• high-density lipoproteins (HDLs)
• very low-density lipoproteins (VLDLs)
– HDLs remove excess cholesterol from circulation – travels to the liver
where it is degraded
– LDLs are associated with the formation of fatty plaques – LDLs are
oxidized by the liver
• oxidized LDL can damage endothelial linings – inflammatory response
• inflammatory response leads to the accumulation of a fatty plaque at the
area of damage
• this plaque becomes covered with smooth muscle cells and fibroblasts
• the fibroblasts can become calcified into a bone-like material
– VLDLs contribute to increased fatty plaque formation
– mutations in apolipoprotein genes may contribute to plaque formation
also
• There are two sources of cholesterol in the body:
– in foods we ingest & formed by liver
20-40