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492 Cards in this Set
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what are eletrical activties of the heart important?
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important for activation of the contraction of the heart mm
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NAME
this is ability of the heart is important bc it helps w the to active the heart mm to contract |
electrical activities of the heart
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why are the mechanical activity of the heart and control of this important?
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necessary to pump blood out to the heart to vessels for distb
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what are the fxs of the heart?
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(1)recieve blood (de O2) into the R side of the heart (R atrium) (2)receive oxygenaed blood from the lungs and pump it to all tissues
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why is it important for the heart to receive blood into the R side of the heart?
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because ensures that the blood gets to the right ventricle which pumps the blood to the lungs for o2
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why is it important for the heart to receive O2 blood?
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to pump to rest of boy to supply O2 and nutrients
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what do the valves in the heart aid in?
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ensure the blood moves in a one way direction into/out of the heart
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the pumping of the heart is carried out by the (1)
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cardic mm (contraction)
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NAME
these ensure that the blood enters and leaves the heart |
valves
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describe the pumping of the heart mm
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heart mm relaxes and contracts
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what are (2) fxs of the heart that enable it to pump blood to the body?
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(1)exictability (2)contractility
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what is exictability ?
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ability of the heart to respond to electrical stimulation and generate action potential
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NAME
this is the ability of the heart mm to respond to eletrical stim and generate action potentials |
exictabiltiy
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what is the contraclitiy?
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ability to contract respond to eletrical stimulation and generate F required to pump blood out of the heart
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NAME
this is the ability of the heart to contract an respond to eletrical stim and generate F required to pump blood out of the heart |
contractility
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why is the contracility and exictability of the heart important?
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allows the heart to pump blood to the body
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why is it important to understand the concepts of contraciltiy and excitability?
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there fx ensures that blood is pumped to the heart through the vascular system
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what is the relationship btwn exicatbiltiy and contrctabiltiy?
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see ch 7
excitation/cotraction coupling |
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the key to understanding the speacil fx of the heart?
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lies the knowledge of the eletric exicaory /conductrry tissues and heartmm
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eletrical activitvy of the heart allows for (1)
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sequential contraction of the atria and ventricles
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(1)of the heart allows for sequential contraction of the atria and ventriales of the heart
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electrical activity
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what is the origin of the cardaic excitation?
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the pacemaker cells
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NAME
these allow the heart to have the fx of cardaic excitabiltiy |
pacemaker cells
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what allows the heart to have cardiac excitation?
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the pacemaker cells
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the pacemakers cells allow the heart to have the fx of (1)
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cardaic exication
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where are the pacemakers located?
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sino-atrial node of the R atrium
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the (1)are located in the sino-atrial node of the R atrium
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pacemakers cells
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the pacemaker calls are located in the (1)
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sino-atrial node of the R atrium
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NAME
these are known are the true pacemaker of the heart |
pacemaker cells
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what are pacemaker cells?
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are specilzied exictiarty tissue that allow the heart to have cardaic excitation
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describe the fx of pacemaker cells, how do they all give the heart cardiac excitation?
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have intrinsic ability to generate action potential which starts the process of exciation of the heart
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NAME
these have the ability to inherent ability to generate action potential which starts the process of exication of the heart |
pacemaker cells
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how does
the activity of the pacemaker cells affect the heart? |
(1)the rate of exictiation and contraction of the heart (aka heart rate) (2)brings about a wave of depolorization that spreads through the atriamm, reaches the ventrical mm
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NAME
these brings about a wave of depolorization that spreads through the atrium and reaches the ventrical mm |
pacemaker cells
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NAME
this determines the rate of exication and contraction of the heart |
pacemaker cells
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NAME
this determine the heart rate |
pacemaker cells
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the pacemaker cells determine a person's (1)
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heart rate
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the heart rate is just the rate at which the heart (1)
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of exication and contraction of the heart
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NAME
is just the rate of exication and contraction of the heart |
heart rate
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the activity of the pacemaker cells brings about a wave of (1)that spreads to the (2) and reaches (3)
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(1)depoloratzation (2)atria mm (3)ventricle mm
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what does SA node stand for?
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sino-atrial node
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where does the exication of the pacemakers start?
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in the SA node
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how does the excitation generated of the SA node reach the atrial and ventricular mm?
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(1)direct path to the atrial mm(2)through specialized conducting tissues to the ventrical mm
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describe the speaclized conducting tissue system that allows the generatiion of exciation by the SA node? (6)
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action potential travels from the SA node to the (2)inter-nodal tract to the (3)AV node (4)the AV bundle through the (5)HIS-Purkinje System to the (6)ventricle system
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are there other parts that can act as the orgin of excitation? if yes, what are they?
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yes, the AV node and purkinje fibers
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T or F
the pacemakers cells are the only parts of the heart that can act as in orgin of exication |
false- av node and his-purkinje fibers
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what parts of the heart can act as an orgin for exication? (3)
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pacemaker cells (2)AV node (3)Purkinje fibers
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the pacemaker cells, AV node, and purkinje fibers can all act as (1)
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orgin of exictation
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what is the differ btwn the exication that occurs at the pacemaker cells vs the AV node of the HIS-purkinje fibers?
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rate of d/c is slower than the SA node
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T or F
the AV node and the HIS-purkinje fibers and pacemakers can all generate an action potential at the same rate |
false-av node and his-purknje cells slower
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the AV node an the HIS-purknje fibers are also called the (1)
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latent pacemakers
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these are called the latent pacemakers?
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AV node and the purkinje fibers
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why are the AV node and the purkinje fibers also called the latent pacemaker?
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bc when SA node is active they are slient...only serve as a conducting tissue
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when the SA node is active, what is the fx of the AV node and HIS-purkinje fibers?
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serve as conducting tissue ONLY do not generate action potential-slient
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what is the only time that the AV node and the HIS-purknje cells become active /generate a action potential?
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when nodal d/c from SA node is lost
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what happens when other parts of the heart are inapporietaely activated? despite the presnce of SA excitation?
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arrhythmia
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what is arrhythmia?
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loss of rhytm of the heart and subsequent uncoordinate contraction of the heart
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NAME
this is the loss of rhytm of the heart and uncoordinated subsequent contraction of the heart |
arrhytmia
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what is the general cuases of arrhythmia, what is happen to the heart at the time?
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SA node is generating action potential along with other parts of the heart such as as the AV node and HIS-purjine celsl
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describe the flow of the eletrical conduction of the heart (15)
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(1)SVC (2)SA node (3)IVC (4)membranous septum (5)AV node (6)right AV valve (7) R ventricle (8)ventricular branch (9)papillary mm (10)bundles of HIS (11)trabeculae cornae (12)papillary mm (13)left AV valve (14)aortic valve (15)aorta
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describe the eletrical conduction of the heart (pathway) (15)
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(1)SVC (2)SA node (3)IVC (4)membranous septum (5)AV node (6)right AV valve (7) R ventricle (8)ventricular branch (9)papillary mm (10)bundles of HIS (11)trabeculae cornae (12)papillary mm (13)left AV valve (14)aortic valve (15)aorta
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describe the eletrical conduction of the heart (pathway) (15)
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(1)SVC (2)SA node (3)IVC (4)membranous septum (5)AV node (6)right AV valve (7) R ventricle (8)ventricular branch (9)papillary mm (10)bundles of HIS (11)trabeculae cornae (12)papillary mm (13)left AV valve (14)aortic valve (15)aorta
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where are the location of the excitory and conducting tissue? (3)
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(1)SA node pace maker cells (3)latent pacemakers (AV and HIS-purknje fibers (4)the conducting tissues-internodal tracts, the av nodes, and purknje fibers when SA node is active
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how does the activty of the SA node determine the heart rate?
aka how does it infleunce the heart rate? |
(d/c oustide of all ext influences per action potential per min)
SA nodes=100-120 AV node= 80 HIS purkinje fibers =30-50 |
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the inherent rate of d/c of (1)is about 100-120
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SA node
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the inherent rate of d/c of the (2)is about 80
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AV node
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the inherent rate of d/c of the (1)is about 30-50
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HIS-purkinje fibers
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the inherent rate of d/c of the HIS-purknjie fibers is about (1)
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30-50
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the inherent rate of d/c of the SA node is (1)
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100-120
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the inherent rate of d/c of the AV node is (1)
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80
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usually the (1)determines the heart rate
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SA node
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which rate inherent d/c is used to determine the heart rate?
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the fastest one usualy the SA node
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what are the implications of the different intrinsic rate of d/c of the pacemakers?
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the fastest rate of exictation determines the rate of excitation for whole heart (2)when the fastest is non fx the next fastest takes over the pace-making of the heart
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the rate of excitation is also called (1)
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inherent or instrinic rate of d/c
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the inherent or intrinsic rate of d/c is also called the (1)
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rate of excitation
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what happens when the pacemaker w the fastest d/c rate is non-fx?
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the next fastest pacemkaer takes over pace making of the heart
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what will be the heart rate when the SA node is non-fx?
describe process how doe sit occur (3) |
latent pacemakers take overs over. hwoever, before occurs thre is a intial lag period of 4 to 10 sds of no exciatio nor contraction (2) during this period, the latent pacemaker is uses the overdrive to supression of self-exictabiltiy (3)when the latent pacemaker takes over, it drives the heart to its own intrinsic rate
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when the SA node fails, how long the the intial lag period
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4 to 10
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when the SA node fails and the latent pacemakers can take over, there is a (1), in which the latent pacemaker are (2)
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(1)intial lag period of 4 to 10 sd (2)they are over driving the supression of the self-excitiabiltiy of the heart
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excitation of the heart can also be called (1)
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atrial depolarization
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(1)of the heart can also be called atrial depolarization
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exicitation
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exication and contraction of the heart just refers to (1)
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atrial depolarization and contraction followed by ventricular depolarization and contraction
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how is the rthym of exication and contraction established in the heart ?
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by the v of conduction of the exicatory and conduction of tissues and that of the heart mm
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what are some implications for slow conduction of the AV node? what does it allow for?
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allows time for the atrium to be completely deplorarized followed by contraction before the ventricles are depolarized thus allowing time for the atria to empty the blood into the ventricles before ventricular contraction begins. the slow rate of conduction of the av node
thus, conduction of the av node is curcial to the establishment of the rhhym of the hearat |
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NAME
this is crucial to the establishment of the rhytm of the heart |
av node conduction
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av node conduction is vital to he establishment of the (1)
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rhytm of the heart
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except for abnormal states, the direction of conduction in the heart btwn the atria and ventricles in a (1)direction through the AV bundles
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foward
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normal, what direction is the conduction of the heart in?
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btwn atria and ventricles through AV in a foward direction
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conduction is from the (1) to the (2) (GENERAL Not specfic)
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atrial region to the ventricular region
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T or F
conduction only occurs throug hthe AV bundle |
true
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conduction ONLY occurs throug the (1)
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av bundle
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Can conduction occur somewhere else other than the av bundle?
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no
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what prevenst conduction from occuring in other areas of the heart?
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prvendetd by a cont fibrious barrier
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conduction through the mm of atria and ventricles is prevented by a (1)
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fibrious barrier
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how long is the delay at the AV node?
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p 119
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what cuases the delay in the AV region?
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p 119
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why do the whole atria and the whole ventricles contract as a single unit when they receive electrical stimualtion?
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when the action potential reach the mm cells, they conduct ery rapidly from mm to mm in which all cells are deplorized at the same time
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the heart mm is described as a (1)
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functional synctium
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the (1)can be described as a functional synctium
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heart mm
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how is possible, that all the mm cells of the heart deplorize at the same time?
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(1)cells are joined together by intercalated discs that have a low resistance compared to reg cardaic mm (2)the mm membranes have a gap junction at the intercalated dics btwn the sucessive cells. (ions are transmitted easily from one cell to another
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NAME
these two attributes allow current to rapidly flow through the heart mm and allow them heart them all contract as if they have been depolorized at the same time |
(1)the cells have intercaclualed dics that have a lower R comapred to reg cardiac mm cells (2)mm membranes have gap junction ta the intercalated discs...that enhance the v of conduction
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what are intercaluatd dics?
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special electrical conducting dics that have extremely rate of low electrical R compared to reg cardiac mm cells
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NAMe
these are special electrical conducting dics that have extremely rate of low electrical R compared to reg cardiac mm cells |
intercalated discs
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what is the low electrical R of the intercaled discs comapred to reg cardaic cells?
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1/400th of the reg cardaic cell
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the intercalated disc have a rate (1)of that of the reg cardaic mm cells
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1/400th
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what allows for increased v of conduction of the heart mm?
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gap junctions btwn the intercalatud discs btwn the next cells
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the mm membranes have a (1)at the intercalated discs btw nthe sucessive cells that increase the v of conduction btwn celsl
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gap junctions
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the mm membranes have a gap junction t the intercalated discs btw nthe sucessive cells that (1)
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increase the v of conduction btwn cells
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is functioanl synctium and anatomical synctium the same thing ?
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no
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T or F
the heart is considered a anatomical syncitium |
false-functioanl syncitum
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T or F
each heart chamber is exicted as if it was one unit |
true
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T or F
the heart contracts as a single unit |
true
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rapid contraction of the HIS purkinje fibers allows for (1)
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rapid implulses throughout the ventricular mm allowing them to contract as single unit
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how do the HIS purkinje fibers also help w allowing the heart to contract as one unit?
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allow for rapid impulses throughout the ventriclar mm
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conduction in the ventricles is from the (1)to the (2)tissue
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endocadium to the epicardium
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the electrical activity clinically recorded for the heart is the (1)
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electrical activity of the cardiac cell mass (the atria mm and ventricle) mm
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what does EKG stand for?
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electrocardiogram
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the EKG is also called (1)
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ECG
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the (1)is also called a EKG
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ECG
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when the electrically activity of the heart is recorded on paper or oscilloscope the recording is called (1)
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ECG
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what does the ECG represent?
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the electrical activity of the atrial and ventricular mm mass
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why do you need to record the electrical activity of the heart?
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to determine if the heart mm are receiving and responding to the electrical activity generated in the SA node
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the heart mm refers to the (1)and (2)mm
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atria and ventricles
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NAME
this is done to determine if the heart mm are recieving and responding to the electrical activiy generated in the SA node |
ECG
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the electrical activity that gives rises to the EKG is the cummulation of the (1)
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electrical activity of the invdl heart cell mm
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how do you record the electricay activity of the heart mm?
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use a EKG
this is done by placing electrodes placed on the heart surface or on the body....it records the electrical activity of the atrial and ventricular mm giving/action potential |
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where can the eletrcodes for the EKG be placed?
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on the skin--see pic
in notes (1)RA, LA, and LL (2)right arm (wrist), left arm (wrist), and L ankle |
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what is the theory of recording behind the EKG?
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trans-membrane action potential occuring during each heart beat in all of the cardaic cells
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it is beleived that (1)occurs during each heart beat in all cardaic cells
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trans-membrance action potential
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does every cardaic cell produce a trans-membrance action potential during each heart beat?
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yes
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the mebrance electrical changes summate (1) that (2)
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several complex electrical fields (2)conduct to the body surface
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why are the electricodes placed on the skin? why is this able to generate a accurate example of the electrical activity of the heart?
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its beleived that each cadiac mm producs a trans-membrance action potential. These changes produce electrical fields that are conducted to the body's surface
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do the electric fields conduct with equal intensitory simuatenously to all point on the body surface?
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n
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T or F
the elctrical fields conduct with equal intensity to all points on the body surface |
f-no
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the electrical fields in conducted in the body develop (1)
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PD
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what does PD stand for?
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potenital differenc
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what is PD?
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the different electrical fields conducted to the differ regions of the body surface during each beat
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NAME
this refers to the different electrical fields conducted to the differ regions of the body surface during each beat |
PD
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how can PDs be detected?
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electrocardiograph
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what is the purpose of the electrocardiograph?
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to detect PD
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what is electrocardiograph?
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a voltage detecting device that to detects PDs
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NAME
this is a a voltage detecting device that to detects PDs |
electrocardiograph
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why considerable amplification needed with a elctrcocardiograph?
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bc the PDs are small
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what are the size of the PDs?
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small-no larger than 2 or 3 mv
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the PDs are (1)in size....being no larger than (2)
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(1)small (2)2 or 3 mv
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what kind of useful info is obtained by a ECG? (6)
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(1)heart rate- (atrial and ventricular rate) (2)site of orgin of the pacemaker for any single beat (3)the sequence and time for conduction to occur throughout the whole heart (4)any abnormaility in site of origin or sequence of conduction can be detected and analzyed and specfic treatment divsed and applied (5)the effectiveness of therpeautic maneuvers designed to correct distrubances in the cardaic rhytm can be eval by sequential monitoring of the ECG (6)various abnormal conditions can pin point these-
a)abnormal enlargement of the one or another cardiac chamber of the heart b)inadequate blood flow through coronary arteries c)changes in the ionic composition of blood plasma d)certain drugs alter the ECG in specfic ways |
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what are (2)types of heart rate?
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(1)atrial heart rate (2)ventricular heart rate
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NAME
these are some of the things this can be used to determine (1)heart rate- (atrial and ventricular rate) (2)site of orgin of the pacemaker for any single beat (3)the sequence and time for conduction to occur throughout the whole heart (4)any abnormaility in site of origin or sequence of conduction can be detected and analzyed and specfic treatment divsed and applied (5)the effectiveness of therpeautic maneuvers designed to correct distrubances in the cardaic rhytm can be eval by sequential monitoring of the ECG (6)various abnormal conditions can pin point these- a)abnormal enlargement of the one or another cardiac chamber of the heart b)inadequate blood flow through coronary arteries c)changes in the ionic composition of blood plasma d)certain drugs alter the ECG in specfic ways |
EKG
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the electrical activity of the indvl mm cells is the jsut the (1)
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action potential generated/intialized by the pacemaker cells and conducted to the mm cells
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for an action potential to occur, what ions are involved? (4)
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Na++, K+, Ca+, Cl-,
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the movement of what ions brings about the generation of an action potential? (4)
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Na++, K+, Ca+, Cl-,
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what bring about the depoloarization of the cell?
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movement of ions in and out of the cell spec...Na, K, Ca, and Cl
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(1)this most occur before a action potential can be generated
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depolarization of the cell
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why is important to have an understanding of the action potential? (2)
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helps to understand the importance of appropriate levels of ions in our bodies (2)helps to understand the reason for certian therpeautic measures aimed at influencing the rate at which the heart delivers the electrical activity
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the details of the effects of ions (charge flow in the generation of electrical activity can be learned by studying the (1)
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recording of the elctrical activity
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how is the recording of action potentials on the nodal and mm cells done?
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inserting electrodes into single cells of the SA node as well as the ventricular mm.and recording action potential
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recording the eletrical activity of single NA nodal and single ventrical mm is done by (1)
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inserting electrodes into single cells of the SA node as well as the ventricular mm.and recording action potential
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action potetnial can also be called (1)
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trans-membrane potential
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(1)can also be called trans-membrane potential
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action potential
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when learnign about action potetnial, are you looking at the activity of every heart mm or just the single cell (in the EKG?
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single cell
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what does AV node stand for?
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atrioventr node
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in the EKG, where are the trans-membrance action potential recorded for, what cells? (6)
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(1)SA node pacemaker cells (2)Atrial mm (3)AV node (4)av bundle branch (5)purkinje fibers (6)ventricular mm
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the trans-membrane potentials of the (1)and (2)give rise to the EKG results
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atrial and ventricular mm
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in the EKG, what waves are recorded? (2)
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P and T waves and QRS waves
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what are P waves?
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the trans-membrane potential changes of the atrial mm
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NAME
this just refers to the the trans-membrane potential changes of the atrial mm |
P wave
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what are the QRS and T waves?
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trans-membrane potential changes of the ventricular mm
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NAME
these are the trans-membrane potential changes of the ventricular mm |
QRS and T wves
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what is the differ btwn the P and T and QRS waves?
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P waves- changes in potential of the atrial mm
T and QRS waves- changes in the action potential of the ventricular mm |
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what do you pronounce
purkinje fibers? |
purr-ken-ge
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how many phases are there in the electrical activity of the nodal cells and mm cells?
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5
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what is diastolic potential ?
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is the resting mebrane potential in the heart
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NAME
this just refers to the resting membrane potential in the heart |
diastolic potential
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what causes each of the phases of an action potetnial?
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by the movement of specific ions across membrane
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each of the phases of electrical activity of nodal and cardaic mm cells is brought about by (1)
|
movement of specfic ions across the membrane
|
|
|
describe the phases of electrical activity at the SA nodes
|
starts C
phase 4- -cell is at diastolic potential (cell maintians resting potential til activated) phase 0- pacemaker cells generate action potential (cell membrane becomes more positive)...upstroke of action potetnial once thereshold of -40 is reached phase 1- the cell membrane become more postive (repolarization) ...does not occur in nodal cells phase 2- plateua- maintains state of deplorization (cell rests cannot repoloraization )....little repolorization occurs phase 3- repolarization occurs ( cell becomes more negative and returns to its resting membrance potential or disatolic potential until pacemaker cells are activated again) |
|
|
T or F
during the generaizatio of an action potetnial, nodal cells go through phase 1 |
false
|
|
|
do nodal cells when generating an actoin potential go through phase 1?
|
no
|
|
|
NAME
these are the true pacemakers that determine the overall electrical activity of the heart |
SA nodal pacemakers
|
|
|
describe the order in which the phases at the nodal cells (SA)
|
phase 4
phase 0 phase 1 phase 2 phase 3 |
|
|
what is the normal resting membrane potential of SA node cell?s
|
-55 mv to -60 mv
|
|
|
the normal RMP is (1)for SA node cells
|
-55 mv and -60 mv
|
|
|
what does RMP stand for?
|
resting membrane potential
|
|
|
is the RMP steady ?
|
no.
|
|
|
does the RMP undergo spontaneous deploarization?
|
yes...the cell membrances are unstable...this means some passive ions channels open w.out an stimulis..allowing ions to flow into cell
|
|
|
T or F
the RMP is steady |
False...is unstable and undergoes spotaneous deplorization
|
|
|
what triggers deplorization of cells?
|
the flow of postively charged ions into the cell
|
|
|
NAME
this is triggers by the depolorization of the cell |
inflow of postive ions into the cell
|
|
|
what causes depolarization?
|
the inflow of positive ions into the cell
|
|
|
when does depolarization occur in cardiac cells?
|
phase 4
|
|
|
depolorization occurs during phase (1)
|
4
|
|
|
phase 4 is called (1)
|
disatolic deplorization
|
|
|
NAME
this phase is often called diastolic depolarization |
phase 4
|
|
|
deplorization occurs when the cell is (1)
|
resting or in the resting phase/ distole of the cardiac contraction
|
|
|
NAME
this occurs during the resting phase or diastole of the cardaic contraction and |
depolarization
|
|
|
depolarizatio initiates the (1)
|
the generation of an action potetnial
|
|
|
the generation of an action potetnial starts the (1)of the heart
|
exication
|
|
|
what is the basis of the automaciticty of the heart?
|
automatic depolarization and generation of the action potetnial by the nodal cells
|
|
|
NAME
this phase is called diastolic deplorization |
phase 4
|
|
|
describe the generation of an action potential of cardaic cells in DETAIL
|
see sheet
|
|
|
what brings about depolarization of cell?
|
positive inflow of K+ and Na+
(1) (DIRECTLY) START HERE (1)progressive increase in permeability of passive Na channels of the nodal membrane to the Na+ (Na+ gates open) LEADS TO (2)increase of Na+ entering the cell...resulting in a more positive charge of inside the cell and more negative charge outside the cell LEADS TO (3) increased positive charge in cell LEADS TO (INDIRECTLY) (4)increase k+ in cell (RETENTION-stays in cell) LEADS TO (5)decrease in K+ leaving cell LEADS TO (6) progresive decline in K+ permeability of the nodal tissue (K2 channels close) LEADS to more slow Ca channels opening and more Ca channels and further depolarization |
|
|
(1) and (2)
these both activties cause slow Ca channels to open and slow increase of Ca in the cell...accerlating the deplorization process (influz of Ca |
(1)progressive decline in permeabiltiy of K+ and rentention of K+ in cells (K+ gates close)
(2)opening of Na gates into cell |
|
|
what is thereshold for generating action potential?
|
-40 mv
|
|
|
the result of the entry of postive charges ino the cell is the deplorizatio to the (1)
|
thershold of -40 mv
|
|
|
what happens once thereshold potential is reached?
|
voltage gated ions open tremdously increasing permeabiltiy of the ion across the membrane
|
|
|
phase 0 is called the (1)
|
upstroke
|
|
|
NAMe
this phase is called the upstroke of action potential |
phase 0
|
|
|
when does phase 0 begin?
|
once thereshold of -40 is reached
|
|
|
the full upstroke is brought about by the (1)
|
slow entry of Ca into the cell
|
|
|
T or F
the full ustroke is brought about by the Na and K |
no..CA false
|
|
|
what brings about phase 0?
|
predominatly entry of Ca into the cells
|
|
|
what drugs can block phase 0?
|
(1)verapamil (2)nifedipine (3)diltazine (4)
|
|
|
what do these drugs do
(1)verapamil (2)nifedipine (3)diltazine (4) |
block phase 0-
(block the Ca channels) |
|
|
phase 0 is only present in (1)
|
mm cells
|
|
|
is phase 0 present in nodal celsl?
|
no only mm cells
|
|
|
T or F
phase 0 is only present in mm cells |
true
|
|
|
what bring about repolorization?
|
(1)increased permeabiltiy of K+ 9 (leave cell)
cell becomes more negative |
|
|
what happens at the end of repolorization? (2)
|
a. increase activity of Na pump helps to return the Na and K back to their normal locations (aka….high level increase of pereambiltiy of mm the K+ channels open, K+ leaves the cell-leading to negative cell inside and return to resting membrane potential)
b. increased activity of Ca pump helps bring Ca back to normal levels |
|
|
draw a pic of the eletrical events at the SA node
|
see pic
|
|
|
draw a pic describing the electrical activity events in detail at the SA node
|
see pic
|
|
|
what is the RMP for the ventricular mm cell noramlly?
|
-85 mv - 95 mv
|
|
|
RMP for the ventricular mm cell is (1)
|
-85 m to -95 mv
|
|
|
the RMP for the (1)is generally -85mv to -95 mv
|
ventricualr mm cell
|
|
|
draw a pic that illustrates the eletrical activity changes that occur in the ventricular mm cell when an actoin potential is generated
|
see pic
|
|
|
the action potential in the cardaic mm is genearted only when teh (1)
|
the mm is stimualted by the electrical current from the SA node
|
|
|
when is the action potetnial for the cardaic mm (ventricualr mm cell) generated?
|
only when teh mm is strimualted by the eletrical current from the SA node
|
|
|
the action potenial is brought about by change in (1)
|
permabiltiy of ions (inflow of postive inons)
|
|
|
describe in DETAIIL the phases that occur for the eletrical activity of the ventricular mm cells
|
see notes
|
|
|
the RMP is brought about in the (ventricular mm cells) by mainly by (1)and it is also aided by the (2)
|
(1)mainly by the - steady high increase of permeabiltiy of K+ and k+ leaving the cell
(2)slowly by increase in membrane permeailtiy of Ca and K causes increase in positve charges inside of the membrane and helps to prevent hyperpolarization by the increase of k efflux |
|
|
NAMe
this helps to prevent the hyperolorizarion by the increase of K efflux |
permeabiltiy of the Na and Ca
|
|
|
in normal mm cells, the RMP is dominated by the (1)
|
K enflux
|
|
|
can phase 0 in reg mm cells be blocked?
|
yes b drugs that block Na channels such as Tetrodotoxin (poison
|
|
|
what does tetrodotoxin do (posion)
|
blocks phase 0- inflow of na+ into cell/ cant deplorize cell and no action potenial genertaed by ventricular mm cells
|
|
|
why can the heart NOT undergo tetanic contractions?
|
bc the of hte long refractory period in the pahse 2- plateau
|
|
|
is the heart rate constant or does it go up and down?
|
goes up and down bc changes according to the needs of the body
|
|
|
why does the heart rate go up/down?
|
changes according to the needs of the body
|
|
|
what controls the heart rate?
|
sa node
|
|
|
the heart rate is controlled by the (1)
|
sa node
|
|
|
NAME
this is the source of exication and determines the heart rate |
SA node
|
|
|
NAME
this the source of delay and determines the rhythm of exication and contraction of the heart |
AV node
|
|
|
the AV node determines the (1)while the SA node determines the (2)
|
(1)rhytm of exication and contraction of the heart (2)heart rate (rate of exication)
|
|
|
AV node is the source of (1)
|
delay that determiens the rhytm of the heart (contraction/exication)
|
|
|
the SA node is the source of (1)that determines the heart rate
|
exication
|
|
|
what are some EXTERNAL infleunces that can affect the rate and rhythm of the heart?
|
(1)the auto nerve fibers that (2)blood levels of circulating hormnes such as ephinephrie (3)plasma electrolyte concentrations
|
|
|
NAME
all of these factors affect this?? (1)the auto nerve fibers that (2)blood levels of circulating hormnes such as ephinephrie (3)plasma electrolyte concentrations |
the rhtym/heart rate
|
|
|
when refering to auto fibers you are refering to (1) and (2)
|
parasympathetic and sympathetic fibers
|
|
|
the auto fibers control the fx of the (1) and (2) of the heart
|
SA and AV nodes
|
|
|
T or F
the auto fibers are the primary cuase of cardaic exication |
false
|
|
|
are the auto fibers that are the primary cuase of cardaic exiciation?
|
no
|
|
|
can auto fibers affect the force of contraction?
|
yes
|
|
|
the auto fibers only serve to regulate the (1)
|
already existing intrinsic automaticity
|
|
|
the auto fibers that innervate the heart are innervated by the (1)
|
(vagus nerve
|
|
|
descibre the how the auto fibers innervate the heart?
|
(1)parasympathethic- innervate only the SA and the AV nodes
sympathethic fibers-innervate the node and ventricular mm |
|
|
the parasymapthic fibers innerveate the (1) and (2)of the heart
|
SA and AV
|
|
|
the sympathethic fibers innervate only the (1) and (2)
|
nodes and ventricular mm
|
|
|
the sympathetic nerve innervate the (1)of the heart while the parasympathethic nerves innervate the (2)of the heart
|
(1)ONLY the SA and NA nodes (2)ventricular and atrial mm
|
|
|
T or F
the parasympathetic nerves innervate both the ventricular and atrial mm |
false - only the sa and na nodes
|
|
|
how does the control of the heart rate by the auto fibers nerves take place?
|
(1)at rest, there is a tonic d/c of the efferent (parasymapthic)via the vagus nerve
at rest the parasympathic system is active sending action potetnials to the sa and av nodes (2)the effects the parasympathitc to decrease the (heart rate) intrinsic rate of d/s of the sa node aka.... the parasympathetic nerves to the heart (by way of the efferent motor vagus nerve) constitute the dominant regulatory influence on the Sa node at rest |
|
|
efferent fiber are also calld (1)
|
motor fibers
|
|
|
(1)fibers are also called motor fibers
|
efferent
|
|
|
afferent fibers are also called (1)
|
sensory fibers
|
|
|
(1)are also called the sensory fibers
|
afferent
|
|
|
how does the parasympathic influence the heart at rest?
|
the parasympathic nerve to the heart (by way of the efferent motor vagus nerve)......is active at rest, decreases the heart rate (intrinsic rate of the d/c of the sa node)
|
|
|
at rest the parasymapthic nerve influences the SA node by (1)
|
decreasing the intrinsic rate of d/c of the SA node (decreases the heart rate)
|
|
|
when is the parasympathic fibers noraml active in the heart?
|
at rest
|
|
|
at rest, the the parasympathic system decreases the intrinsic rate of d/c of the Sa node by (1) to (2)
|
(1)100-120 (2) 70 min
|
|
|
at rest, the the parasympathic system decreases the intrinsic rate of d/c of the Sa node by (1) to (2)
|
(1)100-120 (2) 70 min
|
|
|
NAME
this constitutes the dominant regulatory influence on the SA node at rest |
parasympathetic fibers
|
|
|
parasymapthethic fibers primarly regulatory influence on teh (1)of the heart
|
SA node at rest
|
|
|
what nerve supplies the parasympathetic nerve to the heart?
|
vagus nerve
|
|
|
vagus nerve is also called the (1)
|
CN X
|
|
|
the parasymapthic nerve (1)the heart rate while the symapathic nerve (2)heart rate
|
(1)decreases (2)increaeses
|
|
|
how does the parasympathetic nerve increased activity of the vagus nerve wil slow the heart down? (2)
|
(1)decreased rate of SA nodal d/c (2)decreasesd exicitabiltiy of the A-V junction fibers leads to d/c rate of conduction to slow conductio nof cardaic impulse to the ventricles leads to decreased heart rate
|
|
|
NAME
this refers decreased heart rate |
bradycadia
|
|
|
the parasympathetic slows down the heart rate by (1) and (2)
|
decreased rate of intrinsic d/c at the sa node (2) decreased exictabiltiy at the av (leads to decreased conduction and heart rate
|
|
|
decreased exictabiltiy at the av node leads to (1) and (2)
|
decreased conduction leads to slower conduction of cardaic impulses to the ventricles leads to decreased heart rate
|
|
|
what is the negative chrontropic effect?
|
is the slowing down of the heart by the stimulation of the vagus nerve
|
|
|
NAME
this refers to the is the slowing down of the heart by the stimulation of the vagus nerve |
negative chrontropic effect
|
|
|
what is the ventricular escape?
|
when the sa node is blocked or non-functional..conduction does not reach the av junction then
the purkjue fibers develop and rhytm that takes over the pacemaker fxs, sending action potetnial to the ventricle mm which will contract in response to the exication despite the absenece of the sa node alka ventricle escapes the block |
|
|
when the sa node is nonfx, how does ventricular mm escape the block?
|
when the sa node is blocked or non-functional..conduction does not reach the av junction then
the purkjue fibers develop and rhytm that takes over the pacemaker fxs, sending action potetnial to the ventricle mm which will contract in response to the exication despite the absenece of the sa node VENTRICULAR ESCAPE |
|
|
HAVE NOT ADDED FLASHCARDS
|
see notes
|
|
|
the mechanical activity of the heart just involves the (1)
|
contraction of the atrial and ventricular mm
|
|
|
the contraction of the heart is initated by the (1) followed by (2)
|
atrial mm depolarization (2)ventricular mm depolarization
|
|
|
what happens w each beat of the atria?
|
sends blood to vessels
|
|
|
what happens we each beat of the ventricles?
|
sends blood to either lungs (for the R ventricl) and or the systemic circulation of the (left ventricle
|
|
|
each beat of the atria sends blood to the (1) and each beat of the ventricle sends blood to (2)
|
(1)blood vessels (2)blood to eitehr hte lungs via R ventricle or systematic circulation (L ventricle)
|
|
|
what is the stroke vol?
|
vol of blood ejected by the ventricles per beat
|
|
|
NAME
this is the vol of blood eject by the ventricles per beat |
stroke vol
|
|
|
what is the cardaic out put?
|
the vol of blood jected per min
|
|
|
NAME
this is the vol of blood ejected per min |
cardaic output
|
|
|
what is the differ btwn the stroke vol and cardaic output?
|
(1)cardiac output- vol of blood ejected per min (2)stroke vol-vol of blood ejecte by the ventricles per beat
|
|
|
what conditions must be met for the heart to contract? (5)
|
(1)sa nodes d/c ap (2)conducting tissue are conducting the ap to the heart (3)the heart mm is intact and is able to conduct ap (4)the enough Ca released into the heart cytoplasm (5)the contractile elements of the heart mm cells are intact and wll positoned for F generation
|
|
|
Can the heart contract w.out Ca?
|
no needs to generate ap
|
|
|
how do you know the heart is pumping adequate amount of blood into circualtion?
|
measure the quanity of blood pumped from each ventricle to circulation per min
|
|
|
NAME
this the quanity of blood pumped from the ventricle per min |
cardaic output
|
|
|
what determines the cardaic output?
|
(1)stroke vol (2)heart rate
|
|
|
the cardaic output is determined by (1)and (2)
|
stroke vol (2)heart rate
|
|
|
NAME
this is determined by heart rate and stroke vol |
cardaic output
|
|
|
what is the heart rate?
|
the number of times the heart contracs per beat
|
|
|
NAME
this is just the number of times the heart contracts per min |
heart rate
|
|
|
how do you find the cardiac output?
|
stroke vol (heart rate)
|
|
|
NAME
this is the stroke vol multipled by the heart rate |
cardaic output
|
|
|
what is the average heart rate?
|
72
|
|
|
the average heart rate is (1)
|
72
|
|
|
what determines the charactiscs of the heart rate?
|
the rate of the pacemaker activity
|
|
|
what regulatse the heart rate?
|
Auto system
|
|
|
what is the average stroke vol?
|
70 o 80 ml/s per beat
|
|
|
the average stroke vol is (1)
|
70 to 80 m/s per beat
|
|
|
what determines the stroke vol?
|
the contractiltiy of the heart
|
|
|
NAME
this just refers to the contractility of the heart |
myocardial performance
|
|
|
what regulates stroke vol?
|
intrinsic/ extrinsic factor
|
|
|
what does C.O. stand for?
|
cardaic output
|
|
|
what does b/min stand for?
|
heart rate per min
|
|
|
the 72 b/m and the stroke vol is 70 ml/beat, what is the cardaic output?
|
51/min
72 b/m (70) |
|
|
how does cardaic output change w age?
|
decreases w age
|
|
|
T or F
the cardaic output decreases w age |
true
|
|
|
T or F
the cardiac output is the same for men and women |
false-women 10 to 20
|
|
|
the cardiac output is (1) when compared in women vs men
|
10-20 % less in females
|
|
|
how does body size affect cardiac output?
|
varies w size......
|
|
|
what is the cardiac index?
|
co per sq meter of body s.a.
|
|
|
NAMe
this is the co per sq meter of body surface area |
cardaic index
|
|
|
what is a more accurate measure of co?
|
cardiac index
|
|
|
the stroke vol depends on the(1)
|
myocardial performance
|
|
|
the mycocardial perforance is just hte (1)
|
contracbiltiy of the heart
|
|
|
what can affect the stroke vol?
|
(1)amount of Ca in the cells (2)the number of ap overlap points btwn the actin active sites and the mysoin heads prior to the start of contraction
|
|
|
the stroke vol depends on (1) and (2)
|
intrinsic mechanism- amount of ca (2) extrinsic reg mechaism- the overlap btw the actin and mysoin heads prior to the start of contraction
|
|
|
intrinsic regulation is directed at the interaction of the (1)
|
part of the mm cells and F generated by the mm, the actin and myosin filaments
|
|
|
what are the active sites?
|
active sites-are specfic locations that the mysoin heads interact w for the F to be generated following the stimulation of mm
|
|
|
NAME
these are the sites where the myosin filaments interact |
active sites
|
|
|
the mysoin heads interact at the (1 to produce the F needed to generate the stimulation of the mm
|
active sites
|
|
|
what is the intrinsic mechanism used to control stroke vol?
|
is how stroke vol decreases/increases by controling the number of ap points btwn the actin active sites an the myosin heads prior to the site of contraction
|
|
|
NAME
this refers to the bodies ability to control the stroke (increase or decrease) by controling by the number of ap points btwn the actin active sites and the mysoin heads prior to mm contraction |
intrinsic mechanism
|
|
|
the greater the extent of interaction btwn the actin active sites and the heads of the myosin filaments the (1)
|
greater the F of contraction generated by the mm stimualted
|
|
|
the greater the (1)the greater the F of contraction by the mm stimulated
|
the extent of interaction btwn teh actin active sites and the myosin filament heads
|
|
|
what conditions bring about changes in the extend of overlap btwn the actin active sites and the myosin heads in the ventricular mm?
|
change in length of the ventricular mm
|
|
|
what is the length-tension relationship?
|
the stretching of the mm determines the amount of F generated to to the extent of the interaction btwn the actin active sites and the mysoin heads
|
|
|
what is the length-tension relationship?
|
the stretching of the mm determines the amount of F generated to to the extent of the interaction btwn the actin active sites and the mysoin heads
|
|
|
the stretching of the mm (in the heart) determines the (1)
|
amount of F generated (aka the extent of interaction btwn the actin active sites and he mysoin heads)
|
|
|
what determines the the extent of interaction btwn the actin active sites and the myosin heads?
|
the stretching of the mm
Ex)greater stretching tells them to generate more ap causing more F of contraction |
|
|
what happens when the cardaic mm stretches? (2)
|
the numberof ap at the actin active site and the mysion heads increases
(2)the F generated by stimulation increases |
|
|
can mm contract if not stimuilated?
|
no
|
|
|
does the length tension relationship apply all the time?
|
no-- to much stretching beyond optium length can cause loss of possible interaction points and decreased F
|
|
|
the length of the mm determines the (1)
|
number of interaction points (aps)generated btwn the actin active sites and the myosin heads
|
|
|
the interaction of (1)is resp for the F of contraction
|
the length of mm (stretch) (2)generation of ap at the actin active sites and the myosin heads
|
|
|
what does VEDV stand for?
|
ventricular end diastolic vol
|
|
|
VEDV is also called (1)
|
preload
|
|
|
(1)is also called preload
|
VEDV
|
|
|
what is preload?
|
changes in the vol of blood in the ventricles at the end of ventricular filling
|
|
|
NAME
this refers to changes in the vol of blood in the ventricles at the end of ventricular filling |
prelaod
|
|
|
what determines VEDV?
|
s veneous return?
|
|
|
VEDV is determined by the (1)
|
veneous return
|
|
|
NAME
this is determined by the venous return |
VEDV
|
|
|
what is venous return?
|
the amount of blood returning per min
|
|
|
NAME
this is the amount of blood returning per min |
venous return
|
|
|
how does the increases in vol of blood in the ventricles have an effect on the F of contraction?
|
increase in VEDV leads to
(1)increase in the length of the cardaic mm causing (2) increase in extent of interaction points at the actin and myosin heads (3)this causes in in F of contraciton of heart mm (4)increase in the SV (5)increase in CO |
|
|
in short, VEDV in the end leads to (1)
|
increase in co
|
|
|
what is the Frank Starling Mechanism relationship?
|
relationship btwn the stretch of the cardaic mm and F of contraction generated upon stimulation of the heart
|
|
|
NAME
this just refers to the relantionship btwn the stretch of the cardaic mm and the F of contraction generated upon stimulation |
Frank Starling Mechanism
|
|
|
what are the benefits of the Frank Sterling Mechanism?
|
ensures that
(1)venous return is pumped out of the heart (2)ensures that output of both ventricles are matched (3)co is maintined despite changes in the aortic or pumonic pressure |
|
|
NAME
some benefits of this include ensures that (1)venous return is pumped out of the heart (2)ensures that output of both ventricles are matched (3)co is maintined despite changes in the aortic or pumonic pressure |
frank sterling mechanism
|
|
|
what ensures that the output of by both ventricles matches?
|
the frank sterling mechanism
|
|
|
what ensures that the venous return is pumped out?
|
the frank sterling mechanism
|
|
|
what ensures that the co remains the same despite changes in the aortic or pulmonic pressure?
|
frank sterling mechanism
|
|
|
what is the average co of the ventricles?
|
L- 5 L /m
R- 5-L/m |
|
|
T or F
the average co of the L ventricle is differ thnat the R Ventricle |
false
|
|
|
is the a differ btwn the average co in the R vs L ventricle?
|
no should be same
|
|
|
does the co changes if the aortic or pulomonic pressure change?
|
no bc of the frank sterling mechanism
|
|
|
T or F
changes in the pulomonic or aortic pressure can affect teh co of the heart |
false- frank sterling mechanism
|
|
|
what happens if the Ventricles had differ co?
|
the blood would accumualte in the lungs
|
|
|
in hypertension pt, what role does the Frank Sterling mechism play?
|
ensures the co remains normal up to 170 mm hg
|
|
|
how long will the frank sterling mechanism take place w hypertension?
|
170 mg hg above normal
|
|
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preload can cause changes in the (1)
|
length of caradic mm
|
|
|
if VESV increases enough the (1
|
the pump will fail
|
|
|
what is ext regulation of the ext regulation of the stroke vol?
|
involves the reg of stroke vol by system or agents outside the heart
those agents include hormones and auto system |
|
|
NAME
this involves the reg of the stroke vol by the auto system and the agents (actions of chemicls in teh blood) to control stroke vol |
extr regulation of stroke vol
|
|
|
what is the differ btwn instrinic mechanis and ext regulation of stroke vol?
|
(1)instrinic reg
stroke vol controlled by the interaction of the myosoin and action active sites to control F of contraction of the mm (2)ext regulation- mechanism-reg of stroke vol bu auto system and the chemicals agets in the blood |
|
|
increased Ca in crypolams will (1)
|
increase opening btwn the mypsoin and active sites -resultingin a generation of ap
AND increased F of contraction |
|
|
does the parsymp s have an direct afffect on stroke vol on contractibiliyy of the heart
|
no INDIRECT
|
|
|
T or F
the paraspym ns has a direct effect on the contractibility of the heart |
false- NO- affects symp fibers to reduce their effectinvess when active
|
|
|
NAME
when active this system will work to reduce the affects of the sympath fibers and their effectvness |
parasymp ns
|
|
|
what hormone directly affects the heart?
|
catecholamines
|
|
|
what are catecholamines?
|
refers to epinephrine and noneprinephrine
|
|
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NAME
this just refers to epinephrine and some nonepinephrine |
catechalmines
|
|
|
cateacholamines come from the (1)
|
adrenal medulla
|
|
|
epinephrine and norepeinephrine come from the (1)
|
aderenal medulla
|
|
|
what affects do teh catecholamines have on the heart?
|
have a inotropic effect - of stim the symp ns
|
|
|
NAME
this hormone will stimulate the symp ns |
catceholamines
|
|
|
catecholamines will stim the (1)
|
symp ns
|
|
|
how are drugs used to affect the heart rate, what is there role?
|
drugs are used either block the receptors involved in teh auto response or (2)ehance or block the Ca availability to the cytoplasm
to increase/decrease the contracibiltiy of the heart |
|
|
how does the heart rate affect co?
|
increase in heart rate causes increase in co up to a limit of 179 beat/min
afterwhich increase in heart will cause decrease in co |
|
|
what is the limit at which the heart rate will cause the co do decrease
|
170 beat/min
|
|
|
When the heart rate reaches (1), the co will decrease
|
,170
|
|
|
what happens to the co, if the heart rate is greater than 170?
|
co will decrease
|
|
|
why does a increase in the heart rate above 170, lead to decrease heart rate/
|
leaves decreased time for ventricular filling and inadequate time for complete filling during diastole
(2)this causes decreased venous return, and (3)decrased stroke vol (4) decrease cardaic output |
|
|
increase in the heart rate above 170, will lead to (1) which causes (2) leading to (3)eventually leading to (4)
|
(1)decreased time for the ventricular to fill and empty all the blood during diastole (2)decrease venous return (3)decreased stroke vol (4)decrease co
|
|
|
in short, increased hr will in the long run (1)
|
derease co
|
|
|
what mechanical events take place to ensure that the heart
does the following (1)the ventricles fill w blood (2)the do2 is ejected from the ventricle (3)O2 goes into general circulation for each beat of the heart |
the cardiac cycle
|
|
|
each cardaic cycle result ins (1)
|
ejection of a certain vol of blood from eac ventricle into circulation
|
|
|
describe the cardiac cycle? (5)
|
(1)the atria is first filled w blood coming from the SVC and IVC (2)blood enters the ventrciles through the AV node (3)the enetry of the blood is aided by the ventricular mm (small way)
(4)after the ventricles are filled, the ventricles contract to send the blood to the circulation R-heart through the pulmonic valves to the pulmonary circulation L- ventricle through the aortic valuve to systematic circulation |
|
|
From R heart blood is sent to (1)
|
Pulmonary circulation
|
|
|
the left ventricle through the aortic valves to the (1)
|
systemic circulation
|
|
|
the R heart blood is sent to (1) the when the blood is in L ventricle is sent to the (2)
|
(1)pulomary ciculation (2)systematic circulation
|
|
|
what are some points you should look at (Important) to the cardiac cycle ?
|
(1)atrial filling (2)ventricular and diastolic vol (3)ventricular contraction (4)POSITION OF AV VALVES, aortic and pumonic valves-which one opens/closes (5)end systolic vol (6)stroke vol
|
|
|
what is the ventricular and diastolic vol?
|
vol in the ventricle at the end of filling and before contraction
|
|
|
NAME
this refers to teh vol in teh ventricle at the end of filling and before contraction |
ventricular and diastolic vol
|
|
|
what is the end systolic vol?
|
the vol of blood in the ventricles after contraction of ventrciular
|
|
|
NAME
this is the amount of blood in the ventrciles after contraction |
end systolic vol
|
|
|
what is the differ btwn
ventricular and diastolic vol and end systolic vol? |
(1)ventricular and diastolic vol- amount of blood vol in the ventricle (when filling) prior to contraction (2)systolic vol- amount of blood vol in the ventricles after contraction
|
|
|
what conditions can cause changes in the Heart rate and have an effct on co?
|
look up
|
|
|
how do measure the heart rate?
|
asuculation and ECG
|
|
|
what are the (2)cylces of the cardaic cylce?
|
daistole (2)systole cycle
|
|
|
what is the diastole cycle?
|
period of relaxation of the ventricles..(the heart is being filled w blood at the time
|
|
|
NAME
this is the period in the cardaic cycle when the heart relaxes and the ventrciles fill w blood |
diastole cycle
|
|
|
what is teh systole cycle?
|
when ventricles contract to eject the blood
|
|
|
NAME
this part of the cardaic cycle is when the ventricles are contracting to eject the blood |
systole period
|
|
|
what is the differ btwn the diastole and systole period?
|
diastole-heart relaxes as the ventricles fill w blood
(2)systole- ventricales contract to eject the blood |
|
|
give an outline of the cardaic cycle? (2)
|
(1)diastole
a) isovulmic relaxation b)ventricular filling (2)systole period a) isovolumic contraction b)period of ejection |
|
|
NAME
during this cycle, this occur isvolumic relaxation and ventricular filling |
diastole
|
|
|
NAME
during this cycle, the subphases are isovolumic contraction and period of ejection |
systole period
|
|
|
what are the sub period of the diastrolic cycle?
|
(1) isovolumi relaxation (2)ventricular filling
|
|
|
what are the sub periods during the systole period?
|
(1)isovolumic contraction (2)ejection of blood
|
|
|
when does the diastole cycle begin?
|
at the end of the ventricular ejection
|
|
|
NAME
this begins at the end of ventricular ejection |
diastole cycle
|
|
|
describe in detail what happens during the diastole cycle
|
see notes
|
|
|
NAME
this begins at the end of isovolumic relaxation |
ventricular filling
|
|
|
when does ventricular filling occur?
|
at the end of of the isovolumic relaxation
|
|
|
what is teh diastasis?
|
slow filling of the ventrcile
|
|
|
NAME
this is when the ventricle slowly fills |
diastasis
|
|
|
describe the ventricular filling process
|
stage 1- rapid filling of 30% of ventricle
stage 2-slow filling (60%) stage 3- 10% filling bc of atrial contraction (atrial kick) |
|
|
the atrial contraction is iniated by the (1)
|
atrail deplorization
|
|
|
what is the effect of the ventricular filing?
|
vol of blood in ventricualr rissing
|
|
|
what is the end diastolic pressure?
|
pressure on the ventricualar walls at the end of ventricular filling
|
|
|
NAME
this is the pressure at the end of diastole |
end diastolic pressure
|
|
|
when does the ventricular systole begin?
|
at the end of the diastole cycle (ventriculars are full)
|
|
|
what iniaites the ventricualr systole?
|
ventricualr depolarization
|
|
|
what does VESV stand for?
|
ventricular end systolic vol
|
|
|
what is VESV?
|
the vol at the end of the systole
|
|
|
what is VEDV?
|
vol at the end of the diastole period
|
|
|
what is the differ btwn
VESV and VEDV? |
(1)VESV-vol at the end of the systole (2)VEDV=vol at the end of the cycle
|
|
|
NAME
this is the vol at theend of the systole cycle |
VESV
|
|
|
NAME
this is the vol at the end of the diastolic cycle |
VEDV
|
|
|
when does the diastole cycle begin?
|
at the end of the ventricular ejection
|
|
|
NAME
this begins at the end of ventricular ejection |
diastole cycle
|
|
|
describe in detail what happens during the diastole cycle
|
see notes
|
|
|
NAME
this begins at the end of isovolumic relaxation |
ventricular filling
|
|
|
when does ventricular filling occur?
|
at the end of of the isovolumic relaxation
|
|
|
what is teh diastasis?
|
slow filling of the ventrcile
|
|
|
NAME
this is when the ventricle slowly fills |
diastasis
|
|
|
describe the ventricular filling process
|
stage 1- rapid filling of 30% of ventricle
stage 2-slow filling (60%) stage 3- 10% filling bc of atrial contraction (atrial kick) |
|
|
the atrial contraction is iniated by the (1)
|
atrail deplorization
|
|
|
what is the effect of the ventricular filing?
|
vol of blood in ventricualr rissing
|
|
|
what is the end diastolic pressure?
|
pressure on the ventricualar walls at the end of ventricular filling
|
|
|
NAME
this is the pressure at the end of diastole |
end diastolic pressure
|
|
|
when does the ventricular systole begin?
|
at the end of the diastole cycle (ventriculars are full)
|
|
|
what iniaites the ventricualr systole?
|
ventricualr depolarization
|
|
|
what does VESV stand for?
|
ventricular end systolic vol
|
|
|
what is VESV?
|
the vol at the end of the systole
|
|
|
what is VEDV?
|
vol at the end of the diastole period
|
|
|
what is the differ btwn
VESV and VEDV? |
(1)VESV-vol at the end of the systole (2)VEDV=vol at the end of the cycle
|
|
|
NAME
this is the vol at theend of the systole cycle |
VESV
|
|
|
NAME
this is the vol at the end of the diastolic cycle |
VEDV
|
|
|
what is the differ
btwn the VESV and teh VEDV |
VESV= vol at the end of systolic cycle
VEDV=the vol at the end of the diastolic cycle |
|
|
NAME
this is the vol at the end of the diastolic cycle |
VEDV
|
|
|
NAME
this is the blood vol at the end of the systole cycle |
VESV
|
|
|
is all of the vedv ejected per beat?
|
no
|
|
|
T or F
all of the vedv is ejected per beat |
false
|
|
|
T or F
the stroke vol only consistute a small fraction of the vedv |
true
|
|
|
what is the ejection fraction?
|
amount of blood vol left over after the stroke vol
|
|
|
NAME
this refers to the amount of blood vol lefter over after the stroke vol |
ejection fraction
|
|
|
the ejection fraction is noramlly?
|
60%
|
|
|
how do you find the ejection fraction?
|
stroke vol/ (VEDV)
|
|
|
the R heart sends blood to the (1)
|
Left heart
|
|
|
the L heart sends blood to the (1)
|
body
|
|
|
what is the cytoplasmic rectum?
|
stores Ca in the cell
|
|
|
NAME
this stores Ca in teh cell |
cytoplasmia rectum
|
|
|
draw pic of concentrations levels in the cell
|
see notes
|
|
|
what kind of gated channels are there?
|
(1)voltage- electrical (2)passive (3)chemical (ions)
|
|
|
what is diffusion?
|
movement from a high concentration ot a low concentration
|
|
|
what happens if the Na and K def?
|
heart would stop- no exciation/contraction
|
|
|
what happens if use agents that blocks the voltage Ca channels/
|
no ap at SA node or mm...comp blocked heart stops
|
|
|
All mm need (1) to generate ap
|
Ca
|
|
|
what might you do to increase the heart rate?
|
block the symp or stimualte parasymp
|
|
|
what might you do decrease the heart rate?
|
block parasymp and stimualte symp
|
|
|
for the heart,
the symp fibers innervate (1) |
ventricular mm
|
|
|
for the heart,
the parasymp fibers innervate the (1) |
AV and SA node only
|
|
|
for the heart,
the symp ns innervate teh (1)while the symp ns innervates teh (2) |
(1)ventricular mm (2)AV and SA node
|
|
|
NE opens (1)channels while Ach opens (2)channels
|
(1)Na and Ca (2)K
|
|
|
NE leads to the opening of (1)channels
|
Na and Ca
|
|
|
Ach leads to the opening of (1)
|
K channels
|
|
|
what can a block of the valve and HTN Do?
|
prevent blood from being ejected
|
|
|
what is going on w people with CHF?
|
receiving overload from ventricles ...more than can accept
|
|
|
anything that blocks the ventricles will cause (1)
|
CHF
|
