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Physio Exam 3 (Muscles & CV) > Physio Exam 3 (Muscles & CV) > Flashcards

Physio Exam 3 (Muscles & CV) Flashcards

1
Q

what is the control mode of skeletal, cardiac and visceral muscle

A

skeletal-voluntary

cardia & visceral - involuntary

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2
Q

what is the appearance (histology) of skeletal, cardiac and visceral muscle

A

skeletal and cardiac - striated

visceral- smooth

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3
Q

is skeletal muscle mono or polynucleated

A

polynucleated

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4
Q

are skeletal muscles typically long or short?

A

long

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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
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6
Q

what is a fasicle and it’s structure?

A
  • bundle of cells

- wrapped by perimysium

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7
Q

what is the perimysium and it’s structure?

A

-wraps around each fasicle (cell bundle)

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8
Q

what is the endomysium

A

-surrounds each fiber

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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.
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10
Q

what is the SR

A
  • -wraps around the myofibril
  • lacy network membrane-bound organelles
  • ends in terminal cisterns
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11
Q

What is the sarcolemma

A
  • is like the plasma membrane around the muscle fiber

- continuous with the transverse tubules

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12
Q

nuclei in skeletal muscle

A
  • pushed off the the periphery

- reside just under the sarcolemma

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13
Q

what is a myofibril

A
  • several inside a muscle fiber
  • contriactile elements of fiber
  • made up of thick and thin filaments…sarcomere
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14
Q

why are there mitochondria in skeletal muscle fibers

A

because they are very energy demanding cells

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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
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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)
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17
Q

what makes up the triad

A
  • 1 transverse tubule

- 2 terminal cisterns (one on each side of the t-tubule)

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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
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19
Q

z-disk

A
  • middle of the I band

- actin anchored to this and project outwards

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20
Q

H-zone

A
  • pale region
  • M-line runs down the middle
  • middle of the A-band
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21
Q

M-line

A

runs down the middle of the H zone

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22
Q

I band

A
  • I=isotropic
  • light band
  • length of actin projecting from Z disk
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23
Q

A-band

A
  • A= anisotropic
  • dark band
  • length of myosin on both sizes of m line
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24
Q

what is a sarcomere? what dictates the length

A
  • functional unit of a muscle fiber

- runs from Z-disk to Z-disk

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25
Q

actin

A
  • thin filament
  • anchored to Z-disk
  • projects toward m line
  • I band is this length
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26
Q

myosin

A
  • 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
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27
Q

does the length of the sarcomere changes? if not what changes?

A
  • the length doesn’t change itself, but the relative position of the proteins is going to alters as a muscle contracts and relaxes
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28
Q

how does a sarcomere shorten?

A
  • the Z-disks are pulled closer together bc that actin and myosin and sliding past each other
  • that generates force
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29
Q

the pale portion of the H-zone is due to what?

A

no actin present, only myosin

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30
Q

what is the pale portion of the I band due to?

A

no myosin, only actin

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31
Q

T/F : the cross section along different points of the sarcomere whine’s relaxed or starting to contract would look the same

A

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
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32
Q

does the length of the A band change during contraction?

A

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

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33
Q

if actin and myosin don’t change their length during contraction, how does the muscle shorten?

A

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

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34
Q

when muscle is fully contracted what does it look like?

A

-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

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35
Q

why is elasticity important? how does it related to tension

A
  • 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
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36
Q

what is nebulin and what is its function?

A
  • 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
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37
Q

make up of myosin

A
  • 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
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38
Q

make up of actin

A
  • 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
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39
Q

tropomyosin- where is it positioned? what is it’s job?

A
  • 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
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40
Q

what is troponin and that are it’s 3 different subunits and their functions?

A
  • 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
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41
Q

how are the regulatory proteins positioned when the muscle is relaxed? and why?

A
  • 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
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42
Q

what must interact in order for contraction to take place

A

actin and myosin

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43
Q

when Ca is high, how are the regulatory proteins arranged?

A
  • 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
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44
Q

when actin and myosin interact with each other, what structure do they form? What is this structure essential in generating?

A
  • they form a cross-bridge

- essential to generate force

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45
Q

what happens when actin and myosin interact with each other in the presence of ATP

A

the myosin hydrolyzes ATP to give ADP + pi and in doing so, we generate force

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46
Q

what happens when actin and myosin interact with each other in the absence of ATP?

A

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

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47
Q

what happens when myosin interacts with ATP on it’s own, without actin?

A

myosin can hydrolyze ATP but no force bc force is due to the interaction of actin and myosin

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48
Q

what 2 things does ATP do in the muscle fiber?

A

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

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49
Q

what’s the order of the cross-bridge cycle

A

attached state –> released state –> cocked state –>cross-bridge state –> power stroke state –> back to attached when ADP released

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50
Q

where does the origin of command for contraction come from?

A

somatic motor neurons in the ventral horn of the spinal cord

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51
Q

what are collaterals?

A

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

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52
Q

what is a motor unit?

A

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

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53
Q

large muscle are innervated by multiple motor neurons. This entire population of motor neurons is called what?

A

motor neuron pool

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54
Q

a gentile contraction will need to call upon (few)/(many) motor neurons?

A

few

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55
Q

what is an innervation ratio?

A

number of neurons : number of muscle fibers

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56
Q

what are small innervation ratios? What is the relationship bw control and tension

A
  • 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
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57
Q

large innervation rations? What is the relationship vw control and tension

A
  • 1 motor nueron to hundreds of fibers.. basically many collaterals
  • generate large forces, lots of tension
  • coarse movement, bad control
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58
Q

where is the NMJ?

A

the point where the axon from the motor neuron is innervating the fiber.

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59
Q

describe the post synaptic side of the NMJ

A
  • here is an expansion of the post-synaptic membrane

- ruffled appearance which increases the SA and maximixes the expression of inotropic nicotinic Ach receptors

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60
Q

what is the motor neuron place

A

-the post synaptic side of the NMJ where the ionotropic nicotinic ACh receptors are located

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61
Q

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?

A
  • 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
Q

what is basically the epsp (although several differences) of the NMJ?

A

end plate potential

63
Q

differences bw EPSO and end plate potential

A

1- every AP in the motor neuron produces AP in it’s motor unit
2-all excitatory, none are in

64
Q

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

A

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
Q

What is used to target AChE to disrupt the NMJ? and why does it work?

A
  • 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
Q

What does Botulinum toxin do? and how?

A
  • it prevents the release of Ach from the pre synaptic terminal of the NMJ by breaking down the proteins interfering with proper communication.
67
Q

what does curare do?

A
  • 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
Q

What happens to the Ca and tension when there are 2 APs at the end plate

A
  • 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
Q

what is a twitch?

A

change in muscle tension in response to an AP

70
Q

What happens when 1 AP is fired in at the end plate

A
  • 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
Q

describe single muscle twitches

A
  • 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
Q

describe temporal summation

A
  • 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
Q

describe unfused tetanus

A

-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
Q

describe fused tetanus

A
  • 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
Q

where (in what structure) are the electrochemical gradients in the muscle fiber

A

transverse tubules

76
Q

What is the AP dependent upon

A

relationship bw the interstitial fluid in transverse tubules and intracellular fluid in terminal cisterns

77
Q

what enables the AP to drive deep into the fiber

A

it goes alone the transverse tubules which diver down deep into the muscle fiber

78
Q

What that the AP activate in the fiber and where?

A

-activates voltage gates Ca channels that are present on the SR (t tubule)

79
Q

Steps in terminating contraction

A

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
Q

what does the Ca in the SR bind to

A

calreticulum and calsequesterin

81
Q

what is isotonic contraction

A
  • muscle only fixed at one end (like lifting a weight)

- muscle can contract and shorten and can do external work

82
Q

isometric contraction

A
  • 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
Q

if you increase the amount to stretch the muscle, what happens to tension?

A

in increases

84
Q

muscle has passive tension when unstimulated because?

A

-muscle not contracting, no cross-bridge cycle taking place, it’s passively producing tension

85
Q

muscle has active tension when stimulated bc?

A

we are actively developing tension from cross-bridge cycle.

86
Q

what does the length-tension relationship depend upon?

A

anatomy of the muscle

87
Q

3 functions of ATP in skeletal muscle?

A

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
Q

How do we generate ATP?

A 
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
Q

what are 3 energy sources in working muscle?

A

1-phosphocreatine stores
2-oxphos in mt
3-phosphorylation of ADP by cytosolic glycolytic pathways

90
Q

describe slow twitch (type I)

A
  • fatigue resistant
  • red (myoglobin)- so muscle is rich in O2 storage
  • oxidative
  • high mt
  • low glycogen- bc not relying on glycolytic pathways
91
Q

describe fast twitch (type IIa)

A
  • fatigue resistant
  • red (myoglobin)
  • oxidative
  • high mt than slow twitch
  • abundant glycogen
92
Q

describe fast twitch (type IIb)

A
  • fatiguable
  • white (low myoglobin)
  • glycolytic
  • few mt
  • high gly - bc relies on glycolytic pathways.
93
Q

semilunar valves include. are they inflow or outflow

A

pulmonary valve (R) and aortic valve (L). outflow valves

94
Q

atrioventricular valves include? which is on the right and which on the left

A

tricuspid (R) and bicuspud (L)

95
Q

describe cardiac muscle

A
  • 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
Q

what are myocytes

A
  • force generating
  • make up the mass of the body of the heart
  • excitable cells
97
Q

cardiac myocyte AP vs nerve cell AP

A

cardiac AP is much slower repolarization

98
Q

phase 4 in cardiac AP

A
  • 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
Q

phase 0 in cardiac AP

A
  • rapid depolarization
  • increase Na
  • decrease K
100
Q

phase 1 (upstroke) in cardiac AP

A

initial repolarization

  • decr Na
  • incr K
101
Q

phase 2 (plateau phase) in cardiac AP

A

-incr in slow Ca channels

102
Q

phase 3 in cardiac AP

A

repolarization

  • decr Ca
  • incr K
103
Q

absolute refractory period

A
  • 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
Q

effective refractory period. why is it a protective mechanism

A
  • 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
Q

reflective refractory period

A
  • 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
Q

Supra-Normal period

A
  • 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
Q

describe the refractory period in skeletal muscle in comparison to the twitch (contraction)

A

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
Q

describe refractory period in cardiac muscle in comparassion to the twitch (contraction)

A
  • the refractory period lasts almost as long as the entire muscle twitch
  • long refractory period in cardiac muscle prevents tetanus bc no summation
109
Q

describe Ca signaling in cardiac muscle during systole. and what is this affected by?

A
  • 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
Q

describe Ca signaling in cardiac muscle during diastole. and what is this affected by (what inhibits it?

A
  • 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
Q

what are the 2 collections of conducting cells collected together in nodes?

A

SA and AV node

112
Q

bundle of his

A

-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
Q

purkinje fibers

A

bifurcationsof the bundle of his

-invest entirely the ventricular wall

114
Q

why are the nodes called pace-maker cells

A
  • they are auto-rhythmic

- they initiate the cycle of contraction without any input from the NS

115
Q

SA node.

A

1st pacemaker cell- sets HR

116
Q

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?

A

-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
Q

what would happen if there was a disruption in the AV node?

A
  • 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
Q

what happens if the SA node fails and there isn’t another atrial pacemaker?

A

the HR would fall to 40-60 bpm (rate of AV node) because it would pick up the role as the pace maker

119
Q

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?

A
  • 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
Q

what happens to the rate of conduction once the signal exits the AV node?

A

it’s extremely rapid through the rest of the conduction system of the ventricle. this gives a nearly simultaneous contraction of the ventricle

121
Q

what is normal sinus rhythm?

A

the pattern and timing of the electrical signals is normal

122
Q

what are the 3 main criteria of normal sinus rhythm?

A

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
Q

describe the SA node AP

A
  • 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
Q

how do the nodal tissues synchronize contractions with the adjacent cardiac myocytes?

A

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
Q

what innervates the SA node?

A

large number of sympathetics and parasympathetics from vagus

126
Q

what innervated the adrenal medulla? what does it do?

A

sympathetics

-releases pi and norepi that interact with receptors in the SA node

127
Q

what does sympathetics stimulation cause in the heart?

A

incr contractality, freq, conduction velocity and irritability
overall effect is to incr HR

128
Q

what does incr of norepi and epi(symp transmitters) do?

in terms of inotropic, chronotropic and dromotropic states

A 
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
Q

what does incr of Ach (parasymp transmitter) do?

in terms of inotropic, chronotropic and dromotropic states

A 
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
Q

what happens if you increase the discharge from the SA node but you don’t enhance the conduction velocity from the AV node?

A
  • 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
Q

how do the sympathetics and parasympathetics work together in the heart?

A

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
Q

How does the membrane potential change in the nodal tissues over time?- pacemaker potentials. how does it change with parasymp or simp sim

A
  • 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
Q

what can the EKG diagnose?

A

cardiac arrythmias

  • electrolyte disturbances
  • conduction abnormalities
  • eschemic heart disease
  • helps in identifying the source of pathology that is not coming from the heart
134
Q

U-wave in EKG

A
  • 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
Q

P-wave

A

depolarization of both atria

-relationship bw P and QRS helps distinguish arrhythmias

136
Q

PR interval

A
  • 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
Q

QRS complex

A

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
Q

ST segment

A
  • connects QRS complex and T wave

- duration 0.08 -0.12

139
Q

T wave

A
  • repolarization or recovery of ventricles

- interval from beginning of QRS to apex of T is absolutely refractory period

140
Q

QT interval

A

-beginning of QRS to end of T

141
Q

sinus bradycardia on EKG

A
  • 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
Q

premature vetricular contractions (PVCs) in EKG

A

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
Q

1st degree block in EKG

A
  • 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
Q

2nd degree block EKG (mobits II)

A
  • 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
Q

3rd degree block EKG

A

-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
Q

atrial flutter EKG

A
  • 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
Q

atrial fibrilation EKG

A

-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
Q

ventrical tachycardia EKG

A

-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
Q

v-fib

A

ventricles unable to pump blood in any coordinated passion, they are fluttering, basically no discernible HR

150
Q

what is the cardiac cycle

A

seq of mechanical and electrical events that repeat with every heartbeat

151
Q

how to calculate duration of a single cardia cycle?

A

Duration (sec/beat) = 60 (sec/min) / HR (beat/min)

152
Q

describe the events in the cardiac cycle

A

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

Physio Exam 3 (Muscles & CV) (1 decks)

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