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Cardiovascular Physiology Lecture 4 (Objective 1 (Depolarization->…
Cardiovascular Physiology Lecture 4
Objective 1
Understand the
contractile mechanisms
of cardiac muscle
Mechanical events lag behind electrical events: contraction follows depolarization
-ECG begins with atrial depolarization (P wave): atrial contraction
occurs at the end of the P wave
-
P-R segment
: electrical signal slows as it moves through AV node and AV bundle
-
QRS complex: ventricular depolarization: ventricular contraction
begins shortly after Q wave and continues through T wave
Depolarization-> Contraction by Excitation Contraction Coupling of Cardiac Muscles
L-type Ca 2+ channels open: Ca2+ flows into cell
Ca 2+ induces Ca 2+ release by ryanodine receptor channels (RyR)
Action Potential enters from adjacent cell
Local release causes Ca 2+ spark
Summed Ca 2+ sparks causes Ca 2+ signal
Ca 2+ binds to troponin which initiates contraction
Relaxation occurs when Ca 2+ releases from troponin
Ca 2+ is pumped back into the sarco.retic. for storage
Ca 2+ is exchanged with Na + by the NCX antiporter
Na = gradient is maintained by the Na + K + ATPase pump
Objective 2
Recognize the
mechanical events
of the cardiac cycle
3. Isovolumic Ventricular Contraction:
first phase of ventricular contraction ->AV valves close-> not enough pressure yet to open semilunar valves (SHORT)
Ventricular ejection:
as ventricular pressure rises and exceeds arteries, semilunar valves are pushed open and blood flows through (LONG)
Atrial Systole:
atrial contraction pushes a little more blood into ventricles
Isovolumic Ventricular Relaxation:
Pressure drops in ventricles as they begin to relax, blood flows back in the semilunar cusps, snaps the valves shut. (SHORT)
1.
Late Diastole:
both sets of chambers are relaxed and ventricles fill passively (LONG)
Wiggers Diagram
Aortic Pressure
Atrial Pressure
Ventricular pressure
Ventricular Volume
Electrocardiogram
Phonocardiogram
Right after P-wave-> Atrial contraction: atrial pressure increases a little, when it goes back down mitral valve closes to prevent flow into atria
End of Q-wave -> starts ventricular contraction (QRS complex through end of t wave=ventricular depol.) huge spike in ventricular pressure...when this rises above aortic pressure semilunar valves open to let blood flow through to body
From end of t-wave to start of p-wave-> ventricular pressure drops, relax, begin to fill. Mitral valve opens to let blood flow from atria to ventricles
S-wave Once full=end diastolic volume -> end systolic volume = stroke volume
Cardiac Output:
The volume of blood pumped by one ventricle in one minute.
CO=HR (beats/min.) x SV (mL per beat)
SV= EDV-ESV (avg. at rest 70 mL)
Ejection fraction: (SV/EDV)*100%
-% of EDV "ejected" during each contraction
Objective 3
Understand the role of the
autonomic nervous system
in determining the rate and force of contraction
HR is initiated by SA node, but modulated by input from the
autonomic nervous system RATE
-Parasympathetic branch: slows HR
-Sympathetic branch: speeds up HR
CV control center in medulla oblongata
Sympathetic neurons (NE)
Beta 1 receptors of autorhythmic cells
Increase Na + and Ca 2+ influx
Increase rate of depolarization
Increase HR
CV control center in medulla oblongata
Parasympathetic neurons (ACh)
Muscarinic receptors of autorhythmic cells
increase K+ efflux; decrease Ca 2+ influx
Hyperpolarizes cell and decrease rate of depolarization
Decrease HR
Regulation of Stroke Volume
SV= volume of blood pumped by one ventricle in one contraction
Directly related to
FORCE
generated by cardiac muscle during contraction
Contractility
: the intrinsic ability of a cardiac muscle fiber to contract at a given fiber length
Length
of muscle fibers at beginning of contraction
Length tension Relationship
Initial sarcomere length->indicator of stretch
Small changes in length large change in force/tension
Objective 4
Understand the mechanistic relationship between venous return and stroke volume ("
Frank-Starling Law
of the heart")
Force
: Indicated by SV
Stretch
: indicated by ventricular end-diastolic volume (how much blood before it contracts)
"The heart pumps the blood it receives"
If it pumps more blood it will contract more to eject more blood
EDV= "preload" determines the stretch of fibers before contraction
EDV is determined by Venous Return
Venous Return:
the amount of blood that enters the heart from the venous circulation.
Respiratory pump: reduction in intra-thoracic pressure during inspiration draws blood towards the heart
Inhale, drop in intra thoracic pressure, diaphragm collapses, blood moves superiorly because increase in abdominal pressure, increased blood flow through thoracic veins
Constriction of veins via increased sympathetic activity
Skeletal muscle pump: compression of veins pushes blood towards the heart
Muscles contract, squeezes blood through veins
Contractility ("Ionotropy")
-Any chemical that affects contractility is an ionotropic agent
->
Increased contractility
= "positive inotropic effect" i.e Epi and NE
->
Decreased contractility
= "negative ionotropic effect" i.e. beta blockers, calcium channel blockers
Catecholamines Increase Cardiac Contraction
Epi: hormone released from medulla
NE: released by SNS neurons
Bind to beta receptors on cardiac cells
Activates cAMP
Phosphorylation
More Calcium channels open
Increased Ca stores in SR
More forceful Contraction
Or Phospholambin
Increase Ca-ATPase on SR
Ca removed faster
Shortens Ca-troponin binding
Shorter duration of contraction