Transcript No Slide Title

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
•
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 skeletal and
muscle
• 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
20-4
Myocardium – cardiac muscle
• shares structural and functional characteristics with
smooth muscle
• calcium entry from the ECF triggers its release from the SR
• displays pace-maker activity – initiates its own APs without external
influence
• interconnected by gap junctions (intercalated discs) – enhance the
spread of APs
• innervated by the ANS
• unique – cardiac muscle fibers are joined in a branching
network
– action potentials last longer than skeletal before repolarization
20-5
Heart Anatomy Review
20-6
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
– separates right atrium from right
ventricle
– has three cusps
Right Ventricle
•
•
•
•
•
Forms most of anterior surface of heart
Papillary muscles are cone shaped &
raised bundles of cardiac muscle
Chordae tendineae: cords linking
valve cusps to papillary muscles
Interventricular septum: partitions
ventricles
Pulmonary semilunar valve: blood
flows through this valve into
pulmonary trunk
20-7
Left Atrium
•
•
•
Forms most of the base of the heart
Receives blood from lungs - 4 pulmonary
veins (2 right + 2 left)
Bicuspid valve: separates left atrium from
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
Aortic semilunar valve:
– blood passes through this valve into
the ascending aorta
– just above valve are the openings to
the coronary arteries
20-8
Atrioventricular Valves
• A-V valves open and allow blood
to flow from atria into ventricles
when ventricular blood pressure
is lower than atrial pressure
– occurs when ventricles are
relaxed, chordae tendineae
are slack and papillary
muscles are relaxed
• A-V valves close when ventricular blood pressure is higher than
atrial pressure
• chordae tendinae of the AV valves prevent backflow of blood
into atria
• ventricles contract, pushing valve cusps closed, chordae
tendinae are pulled taut and papillary muscles contract to pull
cords and prevent cusps from everting
20-9
Semilunar Valves
• SL valves open with ventricular
contraction/increased ventricular
blood pressure
– allow blood to flow into pulmonary
trunk and aorta
• SL valves close with ventricular
relaxation
– prevents blood from returning to
ventricles
20-10
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 found 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 via the
two vena cava
•
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
20-11
Passage of Blood through the Heart
Body
SVC/IVC
Right Atrium
(tricuspid valve)
Right Ventricle
(pulmonary semilunar valve)
Pulmonary Artery
Lungs
Pulmonary Vein
Left Atrium
bicuspid (mitral) valve
Body
Aorta
(aortic semilunar valve)
Left Ventricle
20-12
Conduction System of Heart
• two types of cardiac muscle cells
– 1. contractile cells
• 99% of cardiac muscle cells
• Do mechanical work of pumping by contracting
• 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
20-13
• intercalated discs – region that
joins two cardiac cells
– site of intermembrane junctions
– two types of membrane junctions:
• a. desmosomes – abundant in tissues
under considerable stress
– formation of a protein-rich plaque on the
PM surface of each cardiomyocyte
– plaques link to the underlying
cytoskeleton
– plaques are joined to each other by
adhesion proteins – cadherins (require
calcium for interaction)
20-14
– two types of membrane junctions:
• b. gap junctions – two PMs are
connected by a “channel” made of specific
proteins = connexons
– 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
20-15
Conduction System of Heart
• SA node = 1.
– cluster of cells in wall of Rt.
Atria
– begins heart activity that spreads
to both atria
– excitation spreads to AV node
• AV node = 2.
– in atrial septum, transmits signal
to bundle of His
• AV bundle (bundle of His) =
3.
– the connection between atria and
ventricles
• Bundle branches = 4.
– for conduction of action potential
through the interventricular
septum
• Purkinje fibers = 5.
– large diameter fibers that conduct
signals quickly
20-16
Conduction Pathways
• 1. atrial conduction system/interatrial pathway – spread of electricity from right
to left atrium ending in the LA
– through gap junctions of the contractile cells
• 2. internodal pathway – spread of electricity to the AV node via autorhythmic cells
– slow spread through the AV node allows for complete filling of the ventricles before they
are induced to contract = AV nodal delay
• 3. ventricular conduction system (Purkinje system) – Bundles, Purkinje fibers,
ventricular muscle
– simultaneous contraction of all ventricular cells
– BUT the PFs do not connect with every ventricular contractile cell
– so the impulse spreads via gap junctions through the ventricle muscle
20-17
Rhythm of Conduction System
• various autorhythmic cells have different rates of depolarization to
threshold – so the rate of generating an AP differs
– SA node fires spontaneously 70-100 times per minute
– AV node fires at 40-50 times per minute
– If both nodes are suppressed fibers in ventricles by themselves fire only 2040 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
20-18
failure of SA node
blockage of transmission from SA through the AV node
•
•
•
contraction rate is driven by the SA node – fastest autorhythmic tissue
AV node is necessary to link the atrial rate to ventricular rate
in some cases – the normally slowest Purkinje fibers can become overexcited = ectopic
focus
– premature ventricular contraction (PVC)
– occurs upon excess caffeine, alcohol, lack of sleep, anxiety and stress, some organic conditions
Cardiac excitation
• efficient cardiac function requires three criteria:
• 1. atrial excitation and contraction should be
complete before ventricular excitation and
contraction
• 2. cardiac fiber excitation should be coordinated to
ensure each chamber contracts as a unit
• 3. atria and ventricles should be functionally
coordinated (atria contract together, ventricles contract
together)
20-20
Cardiac muscle
action potentials
• pacemaker potential of the autorhythmic cells
• provided by the SA node
– Autorhythmic cells do NOT have voltage- gated Na+ channels !!!!!
– two important events:
– 1. decreased outward K+ current
• coupled to constant inward leak inward of Na+ is a decreased leak of K+ outward
• as the K+ outflow decreases – membrane constantly drifts toward threshold (doesn’t
balance out the Na+ inward flow)
20-21
Cardiac muscle
action potentials
– 2. increased inward Ca+ current
• T-type Ca+ channels (voltage-gated) open as the membrane drifts toward
threshold
• brief influx of Ca increases the depolarization – reach threshold
• at threshold – L-type Ca channels open – longer lasting voltage-gated
channels
• big influx of calcium – so the influx of calcium (rather than Na) is what
drives the membrane potential of a cardiac cell toward positive
• resets through the closing of these Ca channels and the opening of voltagegated K+ channels
20-22
Cardiac muscle
action potentials
• action potentials in the contractile cells of the myocardium
are initiated by the SA node and spread via gap junctions –
induces an AP in the contractile cells
• AP mechanism:
•
•
•
1. almost “instantaneous” rising phase of depolarization –
activation of Na+ entry through voltage-gated channels (similar to
neurons) = “fast” Na+ channels
2. Na+ permeability then rapidly plummets to its resting level –
this could cause repolarization
3. BUT the membrane potential instead of rapidly returning
to negative is held a positive for an extended period of time =
plateau phase
•
•
•
•
result of “slow” L-type voltage-gated Ca+ channels
plus a delay in the outflow of K+ ions
delay in repolarization
prolongs the positivity inside the cell
4. rapid falling phase results – inactivation of Ca+ channels and
eventual opening of voltage-gated K+ channels
20-23
The 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
• together with the slow removal of Ca+ - results in a
long sustained contraction of heart muscle
20-24
AP and contraction
• Ca+ triggers the same series of events as
seen in skeletal muscle – troponintropomyosin “shift”
– 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!
– elevated ECF Ca+ can increase the strength of
contraction
• refractory period of cardiac muscle is
longer than skeletal muscle (250msec)
– allows for the emptying of the chambers
20-25
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 the EKG 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 on the website
20-26
Electrocardiogram---ECG or EKG
• P wave (80msec) = atrial depolarization
– SA to AV node and right atrium to left
atrium
– absence: atrial fibrillation and SA blocks
– increased amplitude = hypokalemia (low
K+)
• PR (PQ) interval (120-200msec) = SA
node through the AV node and into
ventricles
– AV node function and coordination
between atrial and ventricular conduction
systems
– long interval –AV block
http://www.ecglibrary.com/ecghist.html
http://www.anaesthetist.com/icu/organs/heart/ecg/Findex.htm
20-27
Electrocardiogram---ECG or EKG
• QRS complex (80-120msec) = rapid
depolarization of ventricles
– used to diagnose: cardiac arrhythmias,
conduction abnormalities, ventricular
hypertrophy and myocardial infarctions
• QT interval = depolarization and
repolarization of the ventricle
– measures electrical conduction/activity of
the entire ventricle
– lengthened QT interval could be a sign of
sudden cardiac death
• ST segment (80-120msec) = end of QRS
to the start of the T wave
-period when ventricles are depolarized
20-28
Cardiac Cycle – for Anatomists
2 Atrial systole and ventricular
diastole
• diastole – rest period
–
chambers are filling with blood
• systole – pumping period
–
1 Atrial and
ventricular diastole
cardiac muscle contraction forces blood
out under pressure
• 1. Atrial and ventricular diastole
0.1
sec
0.4
sec
0.3 sec
– atria and ventricles are filling with blood
– muscle is relaxed
• 2. Atrial systole/ventricular diastole
– contraction of atria forces blood into
ventricles
• 3. Ventricular systole/atrial diastole
3 Ventricular systole and atrial
diastole
– ventricular contraction forces blood out of
lungs and body
– atria start to fill again
20-29
Here’s your
cardiac cycle!
AHHHH!
20-30
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 before the onset
of atrial contraction (2)
20-31
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
20-32
Cardiac cycle
• 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
20-33
Cardiac cycle
• D. Start of ventricular systole
– at the start 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 =
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
20-34
Cardiac cycle
• E. isovolumetric ventricular
contraction
– just after the closing of the AV and
opening of the SL valves 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)
– ventricular pressure opens the
semilunar valves
20-35
Cardiac cycle
• F. Ventricular ejection
– ventricular pressure will now exceed
aortic pressure as the ventricle
continues is contraction (12)
– the 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)
20-36
Cardiac cycle
• F. End of ventricular systole
– the ventricular volume drops
– BUT ventricular pressure continues to
rise for a short period of time as the
contraction increases its force (red
line)
– pressure 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)
20-37
Cardiac cycle
• G. Ventricular
repolarization
– T wave – (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)
20-38
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) but
ventricular pressure drops
sharply (19)
20-39
Cardiac cycle
• I. Ventricular
filling/MidVentricular Diastole
– as the atria fills from blood from the
pulmonary veins (lungs) it increases
atrial pressure
– as atrial pressure exceeds ventricular
pressure – the AV valve opens again
(21)
– ventricular filling starts again
increasing ventricular volume (blue
line)
– 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
– a new SA depolarization
20-40
• 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
20-41
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
• Cardiac reserve is the ratio of the maximum output to normal
cardiac output at rest
– average is 4-5 while athlete is 7-8
20-42
20-43
Stroke volume
• SV = end-diastolic volume - end-systolic
volume SV = EDV- ESV
– ESV –amount of blood left in a ventricle after
systole)
• measured by EKG – end of the T wave
– EDV –amount of blood in a ventricle after filling
• measured using MRI, CT scan or a ventriculography
(catheter in the ventricle and injection of an X-ray visible
dye)
20-44
Stroke volume
• two components influence SV
• 1. intrinsic control: heart’s inherent ability to vary SV
– as more blood returns to the heart, the heart pumps out more blood
– for skeletal muscle –when muscle length is less than or greater than
optimal length/lo– muscle contraction is weak
– for cardiac muscle – resting cardiac muscle length is already less than
lo
• SO - increasing cardiac muscle length towards lo increases
contractile tension
• therefore filling the ventricle with more blood stretches the
cardiac muscle and increases the resultant force of contraction
• as the cardiac cell is stretched - myofilaments are pulled closer
together
• allows more cross-bridge formation
• 2. extrinsic control
– sympathetic and parasympathetic control
20-45
EXTRINSIC
EXTRINSIC
+
INTRINSIC
20-46
Regulation of Heart Rate
• Nervous control from the cardiovascular center in the medulla oblongata
– 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
20-47
Sympathetic Regulation of Heart Rate
– Sympathetic impulses increase heart rate and force of
contraction
• supplies the atrial and ventricular musculature PLUS the SA
and AV nodes
• speeds up contraction rate by
• 1. speeding up the rate of depolarization of the autorhythmic
cells of the SA node
– decreases K+ permeability by inactivating K+ channels
– swifter drift towards threshold
• 2. reduces the AV delay
– by activating the L-type Ca+ channels
• 3. speeds the rate of conduction through the Bundles and
Purkinje fibers
20-48
Parasympathetic Regulation of Heart Rate
– parasympathetic impulses decrease heart rate through
the vagus nerve
• primarily supplies the SA and AV nodes – no musculature
• little effect on ventricular conduction system or ventricular
contractile cells
• 1. hyperpolarizes the SA node – slows APs - release of AcH
by the vagus binds to muscarinic receptors on the
autorhythmic cells of the SA node
• 2. decreases the excitability of the AV node – increases AV
delay (hyperpolarizes the AV node)
• in contractile cells of the atria – reduces the inward Ca+ flow
shortening the plateau phase – weakened atrial contraction
20-50