Physio Exam 3 (Muscles & CV) Flashcards
(152 cards)
1
Q
what is the control mode of skeletal, cardiac and visceral muscle
A
skeletal-voluntary
cardia & visceral - involuntary
2
Q
what is the appearance (histology) of skeletal, cardiac and visceral muscle
A
skeletal and cardiac - striated
visceral- smooth
3
Q
is skeletal muscle mono or polynucleated
A
polynucleated
4
Q
are skeletal muscles typically long or short?
A
long
5
Q
what is the epimysium and it’s structure?
A
- outermost sheath
- wraps around entire muscle
- supports
- made of connective tissue
- continuous and fuses with the tendon
6
Q
what is a fasicle and it’s structure?
A
- bundle of cells
- wrapped by perimysium
7
Q
what is the perimysium and it’s structure?
A
-wraps around each fasicle (cell bundle)
8
Q
what is the endomysium
A
-surrounds each fiber
9
Q
what is a muscle fiber and what surrounds each one? where are they located?
A
- muscle fibers are just what muscle cells are called
- the endomysium surrounds each fiber
- many fibers are located in each fasicle.
10
Q
what is the SR
A
- -wraps around the myofibril
- lacy network membrane-bound organelles
- ends in terminal cisterns
11
Q
What is the sarcolemma
A
- is like the plasma membrane around the muscle fiber
- continuous with the transverse tubules
12
Q
nuclei in skeletal muscle
A
- pushed off the the periphery
- reside just under the sarcolemma
13
Q
what is a myofibril
A
- several inside a muscle fiber
- contriactile elements of fiber
- made up of thick and thin filaments…sarcomere
14
Q
why are there mitochondria in skeletal muscle fibers
A
because they are very energy demanding cells
15
Q
transverse tubules and what fluid does it contain?
A
- region of the sarcolemma
- dives down into the muscle fiber
- contains interstitial fluid
- makes up the triad with terminal cisterns on both sides
16
Q
terminal cisterns and what fluid does it contain?
A
- swollen endings of the SR
- 2 of these: one on each side of the transverse tubule = triad
- contains SR fluid (very rich in Ca)
17
Q
what makes up the triad
A
- 1 transverse tubule
- 2 terminal cisterns (one on each side of the t-tubule)
18
Q
elastin (titin) fibers
A
- anchored to Z disk and to the M-line
- associated with the think myosin filaments
- functions as a spring and gives rise to elastic quality
19
Q
z-disk
A
- middle of the I band
- actin anchored to this and project outwards
20
Q
H-zone
A
- pale region
- M-line runs down the middle
- middle of the A-band
21
Q
M-line
A
runs down the middle of the H zone
22
Q
I band
A
- I=isotropic
- light band
- length of actin projecting from Z disk
23
Q
A-band
A
- A= anisotropic
- dark band
- length of myosin on both sizes of m line
24
Q
what is a sarcomere? what dictates the length
A
- functional unit of a muscle fiber
- runs from Z-disk to Z-disk
25
actin
- thin filament
- anchored to Z-disk
- projects toward m line
- I band is this length
26
myosin
- thick filament
- tails anchored to M line and project toward Z disk
- both sides of this is the A band
- so myosin is polarized and organized in a particular way
27
does the length of the sarcomere changes? if not what changes?
- the length doesn't change itself, but the relative position of the proteins is going to alters as a muscle contracts and relaxes
28
how does a sarcomere shorten?
- the Z-disks are pulled closer together bc that actin and myosin and sliding past each other
- that generates force
29
the pale portion of the H-zone is due to what?
no actin present, only myosin
30
what is the pale portion of the I band due to?
no myosin, only actin
31
T/F : the cross section along different points of the sarcomere whine's relaxed or starting to contract would look the same
false
- if we take it my the Z line we will see only actin filaments
- if we take it close to the M-line we will see only myosin filaments
- if we take it bw the Zline and M-line we will see both actin and myosin filaments, bc actin and myosin are overlapping with each other
32
does the length of the A band change during contraction?
No because myosin isn't moving, it's not changing in length so the width of the A band stays constant, however the I band gets smaller bc of the increase bw the actin and myosin filaments. Actin doesn't change it's length either
33
if actin and myosin don't change their length during contraction, how does the muscle shorten?
actin and myosin change their position relative to each other in the sarcomere, so what changes is the degree of overlap bw the 2, pulling the Z lines closer together
34
when muscle is fully contracted what does it look like?
-Z-lines tugged in almost completely
-There is an A band present, but no apparent I-band nor H-zone bc the filaments are fully overlapped.
so, no matter where you take a cross section in a fully contracted muscle, it will be the same
35
why is elasticity important? how does it related to tension
- allows for structures to recoil spontaneously.
- muscle has natural passive elasticity
- when you stretch muscle, in generates passive tension
- increase stretch, increase T, increase want to recoil back to relaxed state
- serves structural role
36
what is nebulin and what is its function?
- wraps around thin actin filaments
- anchored at the Z line
- large protein
- length of nebulin is proportion to length of actin
- function: molecular ruler-- guiding the length of the thin filament.
- serves structural role
37
make up of myosin
- 2 heavy chains. the stem of the heavy chains wrap around each other like an alpha helix.
- the end of it (like the head in a golf driver-- huge head) is en in a globular protein
- 4 light chains
- there are essential light chains --stabilize the head region
- regulatory light chains --regulates the endogenous ATPase activity
- so it's heteromeric protein
38
make up of actin
- it is a polymer of these globular subunits
- single subunit that polymerize to form these filaments and 2 of these filaments wrap around each other.
- form like strands of pearls that twist around each other
39
tropomyosin- where is it positioned? what is it's job?
- a protein that is positioned along the grooves that form bw the two pearl strands of the actin
- it's a regulatory protein that regulates the binding of actin to myosin
40
what is troponin and that are it's 3 different subunits and their functions?
- troponin is a heterometic protein
- troponin T-- binds to tropomyosin (T=troponin)
- troponin C-- binds Ca (C=Ca), has 2 binding domains
- troponin I-- binds actin and inhibits contractions from taking place
41
how are the regulatory proteins positioned when the muscle is relaxed? and why?
- they are positioned in a way the prevent actin and myosin from interacting with each other, and therefore prevent contraction.
- this is when Ca is low since Ca is essential for contraction
- troponin I is covering the binding site on actin
- so tropomyosin is bound to the actin
42
what must interact in order for contraction to take place
actin and myosin
43
when Ca is high, how are the regulatory proteins arranged?
- it all shifts up and to the right
- triponin I is no longer covering the myosin binding site.
- 2 Ca bind to triponin C
- tropomyosin moves deeper into the actin groove
44
when actin and myosin interact with each other, what structure do they form? What is this structure essential in generating?
- they form a cross-bridge
| - essential to generate force
45
what happens when actin and myosin interact with each other in the presence of ATP
the myosin hydrolyzes ATP to give ADP + pi and in doing so, we generate force
46
what happens when actin and myosin interact with each other in the absence of ATP?
the actin and myosin combine to form a cross-bridge, so with no ATP we can't release this cross-bridge so we are licked in a state of rigor (locked in the tense state)-hard to the touch
47
what happens when myosin interacts with ATP on it's own, without actin?
myosin can hydrolyze ATP but no force bc force is due to the interaction of actin and myosin
48
what 2 things does ATP do in the muscle fiber?
1-provides the energy necessary to generate force
| 2-necessary in regulating the release of of the cross-bridge. so without ATP we are locked in a state of rigor
49
what's the order of the cross-bridge cycle
attached state --> released state --> cocked state -->cross-bridge state --> power stroke state --> back to attached when ADP released
50
where does the origin of command for contraction come from?
somatic motor neurons in the ventral horn of the spinal cord
51
what are collaterals?
the axon of the single motor neuron that innervates the single motor fibers that branches several time forming collaterals, enervating a single motor neuron several times.
-allows for muscles to contract in a coordinated way
52
what is a motor unit?
a group of muscles that are innervated by a single motor neuron
-so one motor neuron and all of the muscle fibers it innervates are a single motor unit..coordinated contraction
53
large muscle are innervated by multiple motor neurons. This entire population of motor neurons is called what?
motor neuron pool
54
a gentile contraction will need to call upon (few)/(many) motor neurons?
few
55
what is an innervation ratio?
number of neurons : number of muscle fibers
56
what are small innervation ratios? What is the relationship bw control and tension
- 1 motor neuron to every 1 to 2 to 3 muscle fibers...basically few to no collaterals
- we have very fine control over muscles with very small innervation ratios
- we can't generate a lot of tension, small force
57
large innervation rations? What is the relationship vw control and tension
- 1 motor nueron to hundreds of fibers.. basically many collaterals
- generate large forces, lots of tension
- coarse movement, bad control
58
where is the NMJ?
the point where the axon from the motor neuron is innervating the fiber.
59
describe the post synaptic side of the NMJ
- here is an expansion of the post-synaptic membrane
| - ruffled appearance which increases the SA and maximixes the expression of inotropic nicotinic Ach receptors
60
what is the motor neuron place
-the post synaptic side of the NMJ where the ionotropic nicotinic ACh receptors are located
61
describe the ionotropic N Ach receptors on the motor neuron plate on the post syn side to NMJ. What is the only thing that is regulated?
- when Ach binds it directly changes the permeability of the membrane
- N receptors are non-selective ion channels that let in all the small ions (Na, K, Ca, Cl) so the only thing that is regulated is the electrochemical gradient?
62
what is basically the epsp (although several differences) of the NMJ?
end plate potential
63
differences bw EPSO and end plate potential
1- every AP in the motor neuron produces AP in it's motor unit
2-all excitatory, none are in
64
we see disruption of function at the NMJ in a variety of diseases or as a result of a variety of drugs (ex-curare) what does it do?
what can also disrupt the NMJ
the ionic nervous system binds strongly to the receptor, preventing Ach from binding, and it leads to paralysis of the muscle
-inh the AChE would also disrupt. Think about not being able to clear the synapse of Ach. You have this continued contraction or excitation of the muscle in the absence of a stimulus.
65
What is used to target AChE to disrupt the NMJ? and why does it work?
- nerve gases are used
- they work bc when ion channels in the skeletal muscle are open for long periods of time, and sustained in a depolarized state, you are flooding the muscle with Na and you can no longer generate new APs-- bc the voltage gated Na channels are inactivated so the muscle is basically paralyzed
66
What does Botulinum toxin do? and how?
- it prevents the release of Ach from the pre synaptic terminal of the NMJ by breaking down the proteins interfering with proper communication.
67
what does curare do?
- disrupts the function of the NMJ, preventing Ach from binding so decreasing the Ach leads to paralysis
- it lowers the membrane potential, can't reach threshold to fire new AP
68
What happens to the Ca and tension when there are 2 APs at the end plate
- there is an increase in Ca before the cell can recover from the AP. The 2nd burst is longer and higher than the first
- for the tension: the 2nd wave develops since Ca can't recover. leads to a more sustained period of tension
69
what is a twitch?
change in muscle tension in response to an AP
70
What happens when 1 AP is fired in at the end plate
- cause increase in Ca which is larger but slower than the AP
- The Ca causes muscle contraction which is much slower than AP and a lot longer
71
describe single muscle twitches
- stim far apart enough in time that AP can go back to baseline before 2nd twitch.
- no summation bc stim is spreadout enough in time
72
describe temporal summation
- APs at greater frequency than for single muscle twitches, and close enough in time so can sum.
- when twitches summate they create longer anymore sustained changes in contraction
73
describe unfused tetanus
-APs arrive at a sufficient enough frequency that we see avg sustained tension, however there is a sawtooth appearance due to minute change still in Ca
74
describe fused tetanus
- even higher frequency stimulus than unfused tetanus
- no more sawtooth, we just see sustained tension
- there is enough Ca that levels never drop below a certain level to cause sawtooth appearance.
75
where (in what structure) are the electrochemical gradients in the muscle fiber
transverse tubules
76
What is the AP dependent upon
relationship bw the interstitial fluid in transverse tubules and intracellular fluid in terminal cisterns
77
what enables the AP to drive deep into the fiber
it goes alone the transverse tubules which diver down deep into the muscle fiber
78
What that the AP activate in the fiber and where?
-activates voltage gates Ca channels that are present on the SR (t tubule)
79
Steps in terminating contraction
1- Na-Ca exchanger and Ca pump in the plasma membrane both extrude Ca from the cell
-via primary and secondary active transport
2- Ca pump, pumps in Ca to the SR
3-Ca is bound in the SR by calreticulum and calsequesterin
-as soon as Ca levels have returned to normal, no longer sufficient Ca conc to bind to troponin C. so troponin-tropomyosin complex resides in it's inhibitory conf and triponin 1 will interfere with actin and main binding
80
what does the Ca in the SR bind to
calreticulum and calsequesterin
81
what is isotonic contraction
- muscle only fixed at one end (like lifting a weight)
| - muscle can contract and shorten and can do external work
82
isometric contraction
- 2 ends of the muscle are fixed (like trying to lift a wire with both ends fixed to the ground)-- basically when you're trying to lift an immovable object
- when stimulated the muscle can contract but it can't shorten.
- does no external work because no observable work is being done
- but Z disks are pulling close to each other as a result of ongoing cross-bridge cycling, and we're stretching the elastic elements, we're overall increasing tension inside
83
if you increase the amount to stretch the muscle, what happens to tension?
in increases
84
muscle has passive tension when unstimulated because?
-muscle not contracting, no cross-bridge cycle taking place, it's passively producing tension
85
muscle has active tension when stimulated bc?
we are actively developing tension from cross-bridge cycle.
86
what does the length-tension relationship depend upon?
anatomy of the muscle
87
3 functions of ATP in skeletal muscle?
1- hydrolysis of ATP by myosin energizes the cross-bridge, providing the energy needed to generate force
2-binding of ATP to myosin dissociates the cross-bridge bound to actin, allowing the cross-bridge cycle to proceed
3-hydrolysis of ATP by the Ca ATPase in the SR provides energy required for the active transport of Ca into the SR therefore ending contraction
88
How do we generate ATP?
```
anaerobic pathway (2 pathways)- faster metabolically, during periods of high intensity activities sustained for short periods of time.
aerobic- during periods of activity where you're doing a lot of work, but not really intense work, for long periods of time.
```
89
what are 3 energy sources in working muscle?
1-phosphocreatine stores
2-oxphos in mt
3-phosphorylation of ADP by cytosolic glycolytic pathways
90
describe slow twitch (type I)
- fatigue resistant
- red (myoglobin)- so muscle is rich in O2 storage
- oxidative
- high mt
- low glycogen- bc not relying on glycolytic pathways
91
describe fast twitch (type IIa)
- fatigue resistant
- red (myoglobin)
- oxidative
- high mt than slow twitch
- abundant glycogen
92
describe fast twitch (type IIb)
- fatiguable
- white (low myoglobin)
- glycolytic
- few mt
- high gly - bc relies on glycolytic pathways.
93
semilunar valves include. are they inflow or outflow
pulmonary valve (R) and aortic valve (L). outflow valves
94
atrioventricular valves include? which is on the right and which on the left
tricuspid (R) and bicuspud (L)
95
describe cardiac muscle
- striated
- involuntary
- fatigue resistant
- many mt that allow muscle fibers to engage in continuous aerobic respiration
- rich in myoglobin
- robust blood supply
- short branched fibers
- 1 centrally located nucleus
- connected by intercalated disks
- slightly different form of the triad
- can contract on it's own (intrinsic activation). but there is extrinsic innervation to modulate the contractility of the heart but.
96
what are myocytes
- force generating
- make up the mass of the body of the heart
- excitable cells
97
cardiac myocyte AP vs nerve cell AP
cardiac AP is much slower repolarization
98
phase 4 in cardiac AP
- resting membrane potential
| - k dominates bc they are the only channels that are open. so it's very close toe equal pot for K, very neg about -90 mV
99
phase 0 in cardiac AP
- rapid depolarization
- increase Na
- decrease K
100
phase 1 (upstroke) in cardiac AP
initial repolarization
- decr Na
- incr K
101
phase 2 (plateau phase) in cardiac AP
-incr in slow Ca channels
102
phase 3 in cardiac AP
repolarization
- decr Ca
- incr K
103
absolute refractory period
- period where most of the Na channels are inactivating
- it includes phase 1, 2 and part of 3
- insufficient Na channels available to support another AP
104
effective refractory period. why is it a protective mechanism
- a little longer than abs refractory
- still can't fire AP even though some Na channels have recovered.
- includes phases 1, 2, 3
- protective mech bd prevents multiple APs from invading the myocytes. by limiting the freq of depolarization, we are limiting the HR. Important bc arrhythmias that take place are elevations of HR, and at very high rates of contraction, the heart is unable to fill efficiently with blood, so we no longer have efficient pumping of blood.
- so many anti-arrhythmic drugs alter cellular excitability and target the effective refractory period
105
reflective refractory period
- you have seen enough repolarization that a portion of the channels have recovered enough from inactivation.
- if a sufficiently strong sim occurs during this period, we can generate AP
106
Supra-Normal period
- from the end of the RRP until phase 4 is resumed.
- brief period in time where entire pop of voltage gated Na channels have recovered from inactivation but membrane pot has not quite returned to rest...so a smaller than usual stimulus would be able to generate an AP bc the membrane is already slightly depolarized
107
describe the refractory period in skeletal muscle in comparison to the twitch (contraction)
the refractory period is very short compared with the amount of time required for the development of tension
-skeletal muscles that are stimulated repeatedly will have summation and then tetanus. NEVER seen in the heart
108
describe refractory period in cardiac muscle in comparassion to the twitch (contraction)
- the refractory period lasts almost as long as the entire muscle twitch
- long refractory period in cardiac muscle prevents tetanus bc no summation
109
describe Ca signaling in cardiac muscle during systole. and what is this affected by?
- AP enters from adjacent cell via gap junctions at intercalated disks
- Ca channels open and Ca enters cell vis DHPR from t- tubules.
- Ca induces Ca release from SR through ryanodine-receptor channels.
- local release causes Ca spark
- summed Ca sparks create Ca signal
- Ca ions bind to troponin to initiate contraction
affected by incr pi and dec Ach
110
describe Ca signaling in cardiac muscle during diastole. and what is this affected by (what inhibits it?
- relaxation occurs when Ca unbinds from troponin
- some Ca is pumped back into the SR for storage
- other Ca is exchanged with Na in Na/Ca pump
- 1 Ca out for 3 Na in
inhibited by digitalis and ouabain
-they indirectly dear the Na/Ca exchange which leads to an incr in Ca
111
what are the 2 collections of conducting cells collected together in nodes?
SA and AV node
112
bundle of his
-initial segment that leaves AV node, it bifurcates and descents through the ventricular septum and invests the entirely of the ventricular wall and they are called parking fibers
113
purkinje fibers
bifurcationsof the bundle of his
| -invest entirely the ventricular wall
114
why are the nodes called pace-maker cells
- they are auto-rhythmic
| - they initiate the cycle of contraction without any input from the NS
115
SA node.
1st pacemaker cell- sets HR
116
what happens if SA node is damaged and we need a secondary/ectopic pacemaker? if it were in the atria can we tell it's there if we are only looking at HR?
-if in the atria we cannot tell it was there if we were only looking at HR bc their rate of discharge is close to that of the SA node
117
what would happen if there was a disruption in the AV node?
- SA node continues to pace the atria, but secondary/ectopic pacemaker will emerge that will pace the ventricles-- these will have a very low rate of discharge (30-40 bpm), the atria will be contracting at a different rate which would cause arrhythmias
- since the AV node itself discharges AP that isn't paced by the SA node at a rate of 40-60 bpm
118
what happens if the SA node fails and there isn't another atrial pacemaker?
the HR would fall to 40-60 bpm (rate of AV node) because it would pick up the role as the pace maker
119
describe why it's important that the conduction velocity for the AV node is slow? what would happen if there was no delay of AP?
- the delay of AP allows for proper filling of the ventricles.
- if no delay of AP, then the ventricles would contract before they were filled, and you would not have an efficient pump
120
what happens to the rate of conduction once the signal exits the AV node?
it's extremely rapid through the rest of the conduction system of the ventricle. this gives a nearly simultaneous contraction of the ventricle
121
what is normal sinus rhythm?
the pattern and timing of the electrical signals is normal
122
what are the 3 main criteria of normal sinus rhythm?
1-APs originate in SA node
2-bundle of conductive tissue in SA node is discharging APs in a cyclical way at a reg rate of discharge bw 60 and 100 APs per min
3- activation of the myocardium (force generating cells) occur in the proper sequence and with the correct timing and delays necessary for coordinating an affection contraction
123
describe the SA node AP
- very different than cardiac myocytes/
- phase 4 is anything but stable, it is what sets the HR
- funny current- due to slowly activating NA channels that maintain slow depolarization
- slower due to Ca entering nodal tissue through T-type channels
- there is no phase 1 or 2
- ONLY phases 4, 0 , 3
124
how do the nodal tissues synchronize contractions with the adjacent cardiac myocytes?
once the pacemaker is discharging these APs, the wave of depolarization invades the cardiac myocytes and is spread from cell to adj cell through gap junctions with the APs fired by the cells being synchronized so the cells shorten and operate as a unit
125
what innervates the SA node?
large number of sympathetics and parasympathetics from vagus
126
what innervated the adrenal medulla? what does it do?
sympathetics
| -releases pi and norepi that interact with receptors in the SA node
127
what does sympathetics stimulation cause in the heart?
incr contractality, freq, conduction velocity and irritability
overall effect is to incr HR
128
what does incr of norepi and epi(symp transmitters) do?
| in terms of inotropic, chronotropic and dromotropic states
```
positive inotropic state (myocardium- atrial and ventricular muscle)- increase contractility
positive chronotropic (SA) state-increased frequency of AP- so increases discharge
positive dromotropic (AV) state- increased conduction velocity
```
129
what does incr of Ach (parasymp transmitter) do?
| in terms of inotropic, chronotropic and dromotropic states
```
negative inotropic state (myocardium atrial and ventricular muscle)- decreased contractility-- not sig
negative chronotropic (SA)- reduced frequency of APs- so slows discharge
negative dromotropic (AV)- reduced conduction velocity
```
*vagal innervation of ventricular and atrial myocardium is sparse and makes only minor contributions
130
what happens if you increase the discharge from the SA node but you don't enhance the conduction velocity from the AV node?
- you won't be able to coordinate contraction of the atria with the contraction of the ventricles, that will amount of a block through the AV node
131
how do the sympathetics and parasympathetics work together in the heart?
they work to balance contractility, discharge from Sa node, and conduction velocity of the electrical signals in order to coordinate HR and contractility-- to meet ongoing demands placed on the heart as a pump
132
How does the membrane potential change in the nodal tissues over time?- pacemaker potentials. how does it change with parasymp or simp sim
- with parasymp or symp sim, we see the most change in the slope of phase 4.
- slope of phase 4 incr with symp sim--so rate of depolarization increased so we reach threshold more quickly
- slope of phase 4 dear with parasymp sim-- when vagal stim dominates, so it takes longer for the cells to reach threshold, takes longer for depolarization
133
what can the EKG diagnose?
cardiac arrythmias
- electrolyte disturbances
- conduction abnormalities
- eschemic heart disease
- helps in identifying the source of pathology that is not coming from the heart
134
U-wave in EKG
- very tiny
- follows the T wave
- due to repolarization of papillary muscle or purkinje fibers but bc of the size of the muscle that is reflecting it, it gets varied often.
135
P-wave
depolarization of both atria
| -relationship bw P and QRS helps distinguish arrhythmias
136
PR interval
- from onsert of P wave to onset of R (of QRS complex)(ventricular depolarization)
- normal duration 0.12-2.0 sec
- represents atria to ventricular conduction time (through bundle of his)
- prolonged PR interval could indicate 1st degree blockage
137
QRS complex
ventricular depolarization
- large than P wave bc greater muscle mass of ventricles
- normal duration 0.08-0.12 seconds
- Q wave greater than 1/3 height of R is abnormal and could be MI
138
ST segment
- connects QRS complex and T wave
| - duration 0.08 -0.12
139
T wave
- repolarization or recovery of ventricles
| - interval from beginning of QRS to apex of T is absolutely refractory period
140
QT interval
-beginning of QRS to end of T
141
sinus bradycardia on EKG
- slow HR bc dominating sym outfow, still considered normal.
- reg r-r intervales
- less than 60 but above 40
- not unusual in highly trained athletes
142
premature vetricular contractions (PVCs) in EKG
normal sinus rhythm interrupted by unexpected wave form. everything up until this point is normal, normal r-r interval.
- but no P wave proceeding this contraction bc the contraction originated within the ventricles themselves
- not unusual for this to happen on occasion but we don't want like 6 in a row
143
1st degree block in EKG
- at first it looks normal, just elongation of p to r interval which tells us theres some delay in conductance
- overall rhythm ok just elongated
144
2nd degree block EKG (mobits II)
- there is consistent conduction but some p wave are independent of successive QRS
- conduction failure through AV node entirely
- we can only measure p-r interval when we have successive conductance
145
3rd degree block EKG
-the atria are essential being paced by the SA node but complete failure of conduction through AV node, so we have p waves occurring at expected rate of 60-100 bpm but ventricles being paced by pacemakers independently from atria in range of 20-40 bpm, atria and ventricles acting as separate entities.
146
atrial flutter EKG
- discharge is regular but atria beating insufficiently
- contraction of atria is independent to a certain extent of ventricles, not due to conduction failure-- it's just that the P waves are going to be very rapid
147
atrial fibrilation EKG
-r-r intervals are very irregular, rhythm highly irregular, no normal p waves, atria unable to pump blood to ventricles in efficient manner, blood can clot in atria
148
ventrical tachycardia EKG
-reg r-r intervals but we can't see atrial wave bc pattern of ventricular discharge is so great, can't see p waves
149
v-fib
ventricles unable to pump blood in any coordinated passion, they are fluttering, basically no discernible HR
150
what is the cardiac cycle
seq of mechanical and electrical events that repeat with every heartbeat
151
how to calculate duration of a single cardia cycle?
Duration (sec/beat) = 60 (sec/min) / HR (beat/min)
152
describe the events in the cardiac cycle
1-late diastole-- both sets of chambers are relaxed and ventricles fill passively
2-atrial systole -- atrial contraction forces a small amount of additional blood into ventricles
3- isovolumetric ventricular contraction- first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
4-ventricular ejection -- as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected
5-isovolumetric ventricular relaxation -- as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed
easier this way
1-opening of AV valves (tricuspid and mitral)
-fill R and L ventricles. includes contraction of atria squeezing out blood to fill the ventricles. Ventricles are in diastole, the ventricle must be relaxed in order to be filled.
2-closing diastole of AV valves (tricuspid and mitral)
-isovolumetric ventricular contraction (all valves closed). beginning of systole
-since all valves closed, no change in blood vol in ventricles.
3-opening of semilunar valves
-rapid ventricular ejection
-decreased ventricular ejection
systole
4-closing of semilunar valves
-isovolumetric ventricular relaxation (all valves closed) diastole and back to phase 1
