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The Cardiovascular System: The Heart (Functional differences between…
The Cardiovascular System: The Heart
Functional differences between cardiac and skeletal muscle
autorhytmicity
self-excitatory, don't need nervous input, depolarizes spontaneously (pacemaker potentials) and rhythmically
pacemaker cells
helps keep heart beating in a coordinated rhythm ~ effective pump
form the
cardiac conduction system
components of the cardiac conduction system/current movement
1)
sinoatrial (SA) node
- located in the right atrial wall just inferior to the entrance of the superior vena cava, it is the heart's pacemaker and its sinus rhythm determine heart rate
2)
atrioventricular (AV) node
- located in inferior part of the interatrial septum, slight delay in impulse conduction because very few gap junctions in the AV node ~ allows atria to finish contraction (push out blood) before ventricles contract
3)
Atrioventricular (AV) bundle
- located in the superior part of the interventricular septum, only electrical connection between atria and ventricles, impulse goes rapidly through bundle ~ big diameter fibers
4)
R & L bundle branches
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depolarization spreads through intermodal pathways and gap junctions
entire process lasts 220 ms
1) "funny" voltage-gated Na channel opens when membrane repolarizes to -60mV
allows slow leakage of Na across the membrane
2) When membrane depolarizes to -50 mV it triggers opening of T-type Ca channels
allows inward flow of Ca ions
3) at threshold (-40 mV) L-type Ca channels open, producing the upshot of the AP (called L-type because they're long lasting)
4) repolarization occurs when voltage-gated K channels open and L-type Ca channels simulaneously
syncytium (basic funct. unit for cardiac muscle) vs motor unit (basic funct. unit for skeletal muscle)
lengths of absolute refractory period (tetanic contractions cannot occur in cardiac muscles)
period of time when sodium-ion channels are closed, but still inactivated, can't fire another AP regardless of how powerful the stimulus
Skeletal = 1-2 ms, Cardiac = 250 ms (almost as long as the contraction period itself)
protects us, need to relax so can refill with blood
Action Potentials of Contractile Cardiac Muscle Cells
3 phases:
1)
rapid depolarization
- upshot caused by voltage -gated Na ion channels, aka "fast" Na ion channels
2)
Plateau phase
- due to Ca influx through slow Ca channels, keeps cell depolarized because most K channels are closed
3)
repolarization
- due to Ca channels inactivating and K channels opening, this allows K efflux, which brings the membrane potential back to its resting voltage
The refractory period (about 200 ms) - Na ion channels can't be triggered to open
absolute refractory period = cell cannot be excited at all
relative refractory period = cell needs a > than normal stimulus, 50 ms
prevents tetanic contractions
lasts 250-300 ms (30x longer than AP in skeletal muscle)
The Cardiac Cycle
all the events that occur in one complete heartbeat
0.8 sec
consists of 2 phase
systole - the contraction event
diastole - the relaxation
1)
atrial systole
100 ms
at the beginning of atrial systole, the ventricles are filled to about 70% of their normal capacity due to passive flow of blood through open AV valves
at end of atrial systole, ventricles hold approx. 120 ml of blood (= end diastolic volume/EDV)
atria relax and are in diastole for the rest of the cardiac cycle
2)
ventricular systole
begins as atrial systole ends, ventricles contract
AV valves close when ventricular pressure becomes greater than atrial pressure - marks beginning of isovolumic contraction
ventricular contraction continues - ult. ventricular pressure becomes greater than pressure in the large arteries leaving the ventricles
SL valves open - forces blood into aorta or pulmonary trunk
at end of ventricular contraction, the ventricles hold approx 50 ml of blood ~ end systolic volume (ESV)
3)
relaxation period
as ventricles relax, ventricular pressure falls --> SL valve closure --> isovolumic relaxation begins (period when all 4 valves are closed)
Cardiac Output
volume of the blood ejected from each ventricle per minute
determined by:
Stroke volume (SV) - the volume of blood pumped by each ventricle beat
EDV-ESV
3 factors regulate SV
2)
afterload
the pressure that must be exceeded before ejection of blood from the ventricles can begin
3)
contractility
the amount of force produced during a contraction at a given preload or afterload
positive inotropic agents - factors that increase contractility and HR
negative inotropic agents - factors that decrease contractility and HR
1)
preload
the degree of stretch on the heart muscle before it contracts
the more the heart is filled during diastole, the greater the force of contraction during systole
Frank-Starling law of the heart
- an increase in ventricular volume at the end of diastole has a direct increase on stroke volume
Factors the influence preload:
1) length of ventricular diastole - increased HR so less time in ventricular diastole --> less time for blood to return to the heart --> decreased EDV --> decreased preload --> decreased SV
2) venous return - increased venous return --> increased EDV --> increased stroke volume
heart rate (HR) - number of heart beats per minutes
CO = SV x HR
Cardiac reserve = the ratio between the maximum CO an individual can achieve and his/her resting CO
decreases with heart failure