Download ALH 3205 Professor Cohen 9/02/2009 Cardiac Physiology Anatomy

ALH 3205
Professor Cohen
9/02/2009
Cardiac Physiology
 Anatomy of Heart
 Middle portion of inferior mediastinum
 Separates ant/post portions of inferior mediastinum
 Hollow organ
 Base- broadest part, superiodorsally directed
 On top and tipped towards back
 Apex – pointed end is inferioventral
 Bottom toward anterior wall of body
 Origin of great vessels enclosed in Pericardium
 **Know sections of Pericardium** Fibrous, Pericardial, Visceral…etc.
 Developed from a pair of blood vessels – embryologically
 Blood vessels have 3 layers: tunica adventitia, media, interna
 Therefore, heart has 3 layers: (inside  out)
 Endocardium (inside) – smooth, continuous with vessels that enter and leave
the heart
 To prevent clot formations
 Myocardium (middle): muscle of the heart, bulkiest layer
 Myocardium of left ventricle is 4-5x thicker than that of the right ventricle
 Cardiac muscle is closely related to skeletal muscle – a thicker muscle can
develop more force
 Force a muscle develops is directly related to its cross-sectional area
 Left ventricle has more force than right ventricle
 Left ventricle pumps blood to the entire system (thicker = greater
force)
 Right ventricle only pumps blood to lungs (thinner = less force)
 Epicardium (outer): attached to (and sometimes referred to as) parietal
pericardium
 Walls of heart:
 Lots of blood vessels, nerves and lymph vessels
 Collagen fibers w/in walls provide for attachment of cardiac muscles and valves
 RA  RV = tricuspid valve
 LA  LV = bicuspid valve
 RV and pulmonary trunk = pulmonary semilunar valve
 LV & aorta = aortic semilunar valve
 Entering RA = SVC & IVC
 Entering LA = 4 pulmonary veins
 Pulmonary trunk bifurcates into R/L arteries
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NO VALVES between SVC & IVC
NO VALVES between the 4 pulmonary veins and the LA
 Flow into upper chambers in directly related to pressure
 Pressure > in veins (entering chambers) than LA will enter the LA
 *If bicuspid valve has stenosed and blood pools in the LA, blood can back up
towards the lungs  pulmonary edema
Fibrous Skeleton –
 Made of collagen fibers – gives heart structure
 Electrically isolates the chambers from each other
 Any spontaneous electrical activity w/in a chamber is isolated in that chamber
Electrical Conduction System (in a healthy heart)
 Origin of heart beat:
 SA Node (in post. Wall of RA, adjacent to where SJV & IJV enter)
 Has its own intrinsic rhythm of depolarizing every 8/10 of a second
 Responsible for the resting heart rate (72 bpm)
 Some pathways go through interatrial septum: conduct message to the L side
of the heart  electrical message spreads across very quickly
 AV Node: ( in RA, near septum)
 Receives electrical signal from SA Node
 AV Node holds the electrical message momentarily and releases message
into the Bundle of His  R Bundle Branch & L Bundle Branch
 L Bundle Branch (divides into 2 smaller branches)  surround heart
giving off Purkinje fibers
 Purkinje fibers – extensions of electrical network on both sides that
help distribute electrical discharge through muscles of ventricles
when released by AV Node
Vasculature System:
 Capillaries are only exchange vessels in the system
 (From a classification standpoint) Arteries classified based on function
 Largest of the Arteries:
 Elastic arteries bc of high content of elastin in tunica media
 Closest to pumping action of the heart
 High content of elastin allows it the receive the high pressure of blood
flow directly from heart and rebound that flow further down
 Ex: Aorta
 Moving further away from pumping action of the heart = progression of less elastin
and more smooth muscle
 Transition gives rise to muscular arteries
 Less and less elastin + more smooth muscle (further down) = arteries distributing
into capillaries
Two major Vessels that supply Myocardium with O2 rich blood
 Coronary Arteries: L/R
 Each has a unique distribution

Both arise from ascending aorta
 ONLY blood vessels that come off ascending aorta
 These arteries arise BEHIND the cusps of the aortic semi-lunar valve
 When Left Ventricle is in systole and blood is exiting the L ventricle through
aortic semilunar valve (semilunar valve is open bc blood is leaving)
 Openings to coronary arteries are BLOCKED by the aortic valve
 When left ventricle is in diastole (relaxed)- aortic semilunar valve is closed
 Coronary arteries are profuse with blood
 Cardiac Muscle Tissue
 Similar to Skeletal Muscles
 Striated, composed of sarcomeres
 Sarcomeres contain all the same contractile proteins as skeletal muscle
 Troponin, tropomyosin, actin, myosin
 Troponin (slightly diff. in cardiac muscle, than skeletal muscle) – used to
determine whether cardiac damage is present
 MAJOR DIFFERENCE: (from skeletal mm)
 Skeletal muscle stores all calcium it needs to initiate contractile process
 Cardiac muscle relies (to some degree) on extracellular calcium to excite
contractile process
 IN BOTH: T/T complex blocks active site on actin – takes ionic Ca+ to move T/T 
sliding filament theory
 Ca+ channel blockers – reduce force at which the heart contracts, reduces
contractile of vascular smooth muscle
 Both have Sarcomeres (Z Line to Z Line): thin & thick filaments (and cross
bridges)
 Thick and thin filaments must interact
 Myosin cross bridges must be able to interact
 Length Tension Relationship – must be a certain length of a sarcomere to
produce a contraction
 IN skeletal: sarcomere is longer
 Can’t stretch sarcomere out very long or else contraction will not occur
 DIFFERENCES: (from skeletal mm)
 Cardiac muscles are short, branched and interconnected
 Intercalated discs (Gap Junctions) – located between adjacent cells
 Have electrical resistance about 400 times less than electrical resistance that
exists between cells where there is no Gap Junction
 As a result: electrical impulse can spread quickly across all cells
interconnected by Gap Junctions (no delay)
 Starts in SA Node
 *Cardiac muscle functions as a syncitium – one large cell*
 No motor units in Cardiac Muscle
 Either ALL cells get the signal to contract or none – ALL OR NONE
 Hearts can contract w/various amounts of force: Can vary the force by
changing the thickness of the walls  athletes have a thicker left ventricle =
slower Stroke Volume
 Resting sarcomere is must shorter!
 Can stretch the sarcomere of a cardiac muscle out further and still get a
contraction
 EDV (end diastolic volume):
 If increased volume in ventricle (before it contracts) it stretches out the
walls a little  have a greater distance to contract = greater force of
contraction
 All areas of heart are auto-rhythmic –
 SA Node is spontaneously active
 Pacemaker Potential – bc membranes of cells that make up the SA Node are
not effective at keeping NA+ ions out
 When NA+ ions enter a cell – change transmembrane potential
 (In skeletal muscle and in nerve tissue – membrane can keep ions out)
 Cells of SA Node cannot keep the NA+ out – gradually leak in
 At Threshold – Fires an action potential
 Tries to recover (resting membrane potential) – but Na+ is still leaking
in so action potential gets fired again  what produces the hearts’
beating
 All cells of heart do this, but SA Node does it at a faster rate
 Atrial tissue is spontaneously active approx. 60x per min (every 1 sec)
 As you get further down the heart the rate of action gets lower
 Action potential
 Skeletal mm
 Cardiac mm
 Rises to about +20 to +30 mv
 after initial spike exhibits a plateau that lasts bw .25 and .3 seconds
 the presence of the plateau causes the muscle contraction to have a duration
that is somewhere bw 20 and 50 times longer in cardiac mm than in skeletal
mm.
 then rapid repolarization
 Major differences bw cardiac and skeletal muscle that is responsible for the
prolonged muscle contraction and the plateau in the cardiac mm.
 In skeletal mm. the spike is due to the rapid opening of fast sodium channels
 Na+ ions rush in a produce
 Channels close very quickly and Na+ pumped out
 In cardiac muscle, this electrical activity is due to the opening of TWO type of
channels
 First type are responsible for the upward movement are the same as the
open Na+ channels
 Second type of channels, slow Na+ Ca+ channels open up as soon as the fast
Na+ channels begin to close
 Open later but they stay open longer
 During this time lasrge amounts of Ca+ and Na+ enter the cell prolonging
the depolarization
 Positives rushing in keeping it in depolarized state
 At the same time, these Ca+ ions are exciting the contractile process by
affect the sarcomeres
 Immediately after the beginning of the depolarization, the permeability of
cardiac muscle cell membrane to K+ decreases about 5 fold
 At rest more Na+ outside than more K+ inside
 When you prevent K+ from leaving you trap K+ inside
 Also contributes to plateau and preventing early recovery
 When slow Ca+ channels do close, there is a stop to the influx of those ions and the
permeability of the membrane returns to normal
 Refractory period
 Absolute
 An excitable tissue when it is absolutely refractory it will not respond to
another stimulus
 Membranes potential is reversed
 During cardiac plateau it is absolute refractory
 Relative
 Membrane will respond to another stimulus iF it is stronger than the normal
stimulus
 Membrane potential is blow zero and returning to -80
 The absolute refractory period of ventricular tissue is bw .25 and .3 seconds which
is directly equal to the duration of the action potential
 Due to the calcium channels and the plateau
 The relative refractory period of ventricular tissue is approx .05 seconds
 When it can respond to a stronger than normal stimulus
 Tetanus refraction: short absolute refractory and relative refractory longer where
skeletal mm can respond to a stronger and stronger stimulus but in cardiac muscle
there is long absolute refractory due to low Na+ Ca+ channels that stay open longer
and decreased permeability of K+
 Cardiac cycle
 Repeating pattern of contraction and relaxation of the heart
 Consists of electrical, mechanical, and acoustical events in that order
 Electrical always preceeds mechanical, has to be stimulated before an action, then
mechanical produces sounds
 Contraction- systole not depolarization
 Depolarization results in systole
 Relaxation- diastole
 Repolarization leads to diastole
 Atrial systole occurs is ventricular diatole and ventricular systole occurs during atrial
diastole
 The upper chambers and lower chambers not in systole at the same time
 CAN be in diastole at the same time
 Atrial and ventricular diastole
 Venous return of blood (SVC & IVC into right atrium or pulmonary vein into LA) fills
the atrium and bc the AV valves are open fills the ventricles
 Ventricles are 80% filled with blood due to venous return before atrial systole
 Atrial systole adds final amount of blood ventricle produce the end diastolic
volume [EDV]
 Volume of blood in the ventricle following atrial systole
 Contraction of the ventricles at rest ejects about 2/3 of the EDV laving 1/3
behind called the end systolic volume[ESV]
 Amount left after ventricular systole
 EDV – ESV= stroke volume
 The amount of blood left after each beat
 100mL – 34mL= 66 mL being ejected from the heart
 Ejection fraction = SV/EDV= 66%
 number may be decreased in myopathies
LOOK AT THE CHART ON CARDIAC CYCLE!!!!!!!!!
QuickTime™ and a
decompressor
are needed to see this picture.

Remember if a pressure above a valve is higher above it opens, if higher below its
closed
 When ventricles loaded with EDV
 Phase 1: Isovolumetric contraction
 The volume in the ventricle not changing but it is contracting
 No blood is moving so AV valves and semilunar valves are closed
 The pressure inside the ventricle is building bc there is contraction
 The pressure below the valves is higher so valves stay closed
 Phase 2: Ejection
 The moment the pressure in the ventricle exceeds the pressure in the aorta bc
then the semilunar valve will open and blood will start to flow out
 The pressure in the ventricle will reach 120 mmHg even as the ventricular
volume decreases and blood is leaving
 Phase 3:
 As the pressure of the ventricle eventually starts to falls, back pressure in the
aorta closes the semilunar valves and the pressure in the aorta falls to 80 mmHg
which the pressure in the ventricle continues to decline all the was to 0mmHg

Phase 4: Isovolumetric relaxation
 All valves closed again and ventricle is relaxing
 Phase 5: rapid filling
 Occurs when pressure in the ventricle falls below the pressure in the atrium
allowing the bicuspid valve to open and venous return will fill atria and fall
through the open AV valves into the ventricles
 Phase 6: Atrial systole
 Final volume of blood into ventricles
 Back at EDV
 Waves associated with
 P wave
 Atrial depolarization
 Atrial systole after depolarization
 QRS complex
 Ventricle depolarization
 Larger because ventricle is larger than the atria
 Ventricular systole after depolarization
 T wave
 Ventricular repolarization
 Ventricular diastole after repolarization
 ST segment is critical
 During this time is when the ventricles are contracting
 If there is an ischemic attack then there will be an abnormality in the ST segment
 Isoelectric: in normal EKG the base line will be fairly even but if problem wont be
 ELECTRICAL ACTIVITY BEFORE MECHANICAL
 5 things you can determine from and EKG
 Rate
 Rhythm
 Axis
 Electrical position of the heart
 Depends on circmstance
 Pregnancy- large abdomen pute pressure on diaphragm and tips heart
slightly
 Hypertrophy
 Athletic vs clinical
 Athletes heart thicker due to its working harder
 Clinical heart is getting thinner even though it looks bigger
 MI- infarction
 Acousticals
 Produced by closing of valves not opening
 “Lub Dupp”
 Heart sound number one caused by the closing of the AV valves
 Ventricles are contracting in systole

Heart sound number two caused by closing in semilunar valved
 Associated with ventricular diastole
 Sounds of heart bounch of bones and muscles
 Murmurs- abnormal heart sounds:
 Produce an abnormal flwo of bloos and an abnormal sound upon auscultation
 Graded on a 1-6 scale
 One= nonsignificant
 6= extreme
 Stenosis
 Valve doesn’t open properly
 Regurgitation
 Valve doesn’t close properly
 Cardiac output= stroke volume [mL/beat] x HR [bpm]
 Volume of blood ejected by the heart each minute
 Measured in mL/min
 Average HR= 72 bpm
 Average SV = 70-80 mL/beat
 Average CO = 5000 mL/min
 Can change
 Any increase of decrease correlated to a change in HR and/or SV
 Regulating heart rate
 Normally both division of the ANS are continuously active to the heart
 If the nerves are cut completely the heart would continue to beat on own
 Has auto-rhymicity
 NE and E:
 Both increase the rate of the SA node hence they are said to be + chronotropic
agents
 Inc the rate of diastolic repolarization
 Increase conduction rate through the AV node
 These same agents also increase the force of both atrial and ventricular
contraction making them + inotropic agents
 Increasing EDV
 ACH [parasympatheric]
 Hyperpolarizies the cells of the SA node
 Decreases the rate
 Brings further way from threshold
 Decreases the rate of diatoic repolarization
 Decreases the rate through the AV node
 Negative chronotropic agent and negative inotrope
 Decreases the force of atrial contraction but have no significant effect on the
ventricles
 Regulation of stroke volume
 EDV: referred to as the preload
 The volume of blood the ventricle has to work against when it become active
SV is directly proportional to preload
 More blood in ventricle before it contracts the more blood it will be able to
pump out
 SV directly related to contractility
 Inc blood in ventricle before it contracts the more force it will contract with
 To effect blood: pressure generated but eh L ventricle must be greater than the
average pressure in the arterial system
 That pressure is a blockade working against ejection bc it is holding the aortic
semilunar valve closed
 Afterload- pressure in the aorta placed on ventricle after they begin to contract
 SV indirectly proportional to afterload: greater afterload less SV
 Venous return is important to everything
 EDV, SV, and Q are all associated with this
 The mean [average] venous pressure is about 2 mmHg but the pressure at the
junction of the SVC and IVC is about .5-0 mmHg
 Pressure lowest near the right atrium and blood flows from high pressure to
low so will move into atrium
 ANS contracts smooth mm in the walls of large veins
 Venous pressure will increase facilitation venous return
 Large veins run through muscles  when feeling faint can do muscle
exercises to facilitate venous pumping
 Flow dynamics
 Flow= change in pressure [P]/resistance [R]
 Directly related to the change in pressure and indirectly related to its resistance
 Narrow tube= more resistance=decreased flow
 Pasallies equation:
 As the length of a blood vessel increases, we increase the resistance to flow
 As resistance increases, flow decreases
 The value cant change
 Lambda=viscosity of a fluid
 As viscosity increases  the resistance increases  flow decreases
 This value can change bc it is homeostatically regulated
 Radius of a blood vessel
 As radius increasesthe resistance will decrease  the flow will increase
 Variable and exponential so has a HUGE effect on the flow
 The single most powerful flow regulatory mechanism we have is
vasoregulation [constriction or dilation]
 Done by ANS
 Flow regulated and shunted to necessary areas
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