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22 spring: Physiology > test 3: lecture 3 > Flashcards

test 3: lecture 3 Flashcards

1
Q

•Properties of cardiac muscle similar to skeletal muscle

A
  • Striated
  • Ca2+/troponin/tropomyosin regulation of crossbridge cycling
  • Sarcoplasmic reticulum stores and releases Ca2+
  • T tubules
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2
Q

how is cardiac and smooth muscle similar

A
  • Gap junctions
  • Extracellular Ca2+ required for contraction (Ca<u>2+ </u>induced Ca<u>2+</u> release)
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3
Q

why need ryanodine receptor and Ltype Ca receptor in cardiac muscle

A

Ltype Ca lets Ca into cell

will bind to ryanodine and ryanodine will let Ca from SR into the cell to trigger power stroke

Ltype and ryanodine not bound together like in the skeletal muscle

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4
Q

3 ways to get calcium out of the cell after power stroke

A

SERCA → calcium back into sarcoplasmic reticulum

Calcium ATPase: Ca pumped out of cell

sodium calcium exchanger (NCX): 3Na in = 1 Ca out

(3Na out/2K in to even out charges-maintain membrane potential)

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5
Q

why need extracellular Ca in cardiac cells

A

ryanodine receptor is different from RyR in skeletal (not bound)

needs Ca to trigger it to allow Ca out of the sarcoplasmic reticulum

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6
Q

the long plateau phase of cardiac contractile cells will prevent __

A

tetanus (summation)

1 AP= 1 beat

contraction same length as AP

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7
Q

how are cardiac and skeletal muscle different?

activity

neural input

gap junctions

A

cardiac : autorhythmic, autonomic innervation, yes gap junctions

skeletal: no autorhythmic activity needs to be innervated by somatic NS, no gap junctions

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8
Q

compare cardiac and skeletal

Ca source for contraction

Ca release from SR

Ca removal

A

cardiac: calcium from SR and ECF, Ca released from SR by CICR, Ca removed by SERCA back into SR, CA pump out of cell, NCX (1 Ca out/3Na) in

skeletal: Calcium from SR, Ca release from SR by foot processes, Ca removed by SERCA back into SR

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9
Q

compare cardiac and skeletal

ryanodine receptor

twitch duration

A

cardiac: RyR2 (needs Ca to trigger its release of Ca), 350 msec
skeletal: RyR1 (linked- will release Ca without binding to its own ECM Ca), 100 msec

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10
Q

systole

A

contraction of the ventricles (left)

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11
Q

diastole

A

relaxation of ventricles (left)

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12
Q

valves in heart open ___

A

passively

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13
Q

___ % of ventricle filling is due to AV contraction

A

20%

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14
Q

___ prevents signal from going from ventricles to atria

A

cardiac skeleton

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15
Q

if any conduction cell can initiate its own AP why is SA the hearts pacemaker?

A

hierarchy of normal automaticity

overdrive suppression

SA fires 70-80 AP a minute, which is faster then all of the other conduction cells

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16
Q

Draw wiggers

A
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17
Q

draw the pressure part of wiggers graph

A
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18
Q

draw the volume part of wiggers graph

A
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19
Q

what happens during mid to late diastole

A

ventricles filling

atria contracts (atrial depolarization)

aortic valve closed

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20
Q

what happens during systole

A

both set of valves closed during isovolumetric contraction

ventricles contract, and Aortic valves open

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21
Q

what happens during early diastole?

A

isovolumetric relaxation- both set of valves closed but no change in amount of blood

then AV valves open and ventricles begin filling

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22
Q

when does isovolumetric relaxation occur?

A

early diastole

both set of valves closed happens after ventricles contract-

happens when ventricles are relaxing- during repolarization

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23
Q

when does isovolumetric contraction occur?

A

during systole

atria have contracted and both set of valves closed, ventricles are filled with blood and ventricle contraction has started but it isnt strong enough to open aortic valve yet

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24
Q

EDV

A

end diastolic volume

•Volume of blood in ventricle at the end of diastole

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25
Q

ESV

A

End-systolic volume (ESV)

•Volume of blood in ventricle at the end of systole

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26
Q

SV

A

Stroke volume (SV)

•Volume of blood ejected from ventricle each cycle

SV = EDV – ESV

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27
Q

EF

A

Ejection fraction (EF) measures heart efficiency

•Fraction of EDV ejected during a heartbeat

EF = SV/EDV

EF= (EDV-ESV)/(EDV)

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28
Q

CO

A

cardiac output

measures blood output per minute

CO = SV × HR

CO =( EDV=ESV) x HR

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29
Q

____ measures heart efficiency

A

ejection fraction

EF= SV/EDV

(EDV-ESV)/(ESV)

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30
Q

___ measures blood output per minute

A

cardiac output

CO= SV x HR

CO= (EDV-ESV) x HR

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31
Q

____ is volume of blood ejected from ventricle each cycle

A

stroke volume

SV = EDV – ESV

32
Q

volumes and blood flow rates are similar for the left and right sides of the heart, what differs?

A
  • Systolic pressure on left ventricle: ~120 mm Hg
  • Systolic pressure on right ventricle: ~20 mm Hg

(left side has to pump blood to everywhere, there is more resistant therefore left side of the heart is much thicker)

33
Q

Lub S1

A

“Lub” S1: backflow hitting AV valves after they close at the start of ventricular systole

hearing turbulence

isovolumic contraction

34
Q

dub S2

A

backflow hitting the aortic and pulmonary valves at the start of diastole

•Usually briefer, sharper, and higher pitched•Normally the valves close at the same time

isovolumic relaxation

35
Q

split S2

A

Split second heart sound (split S2): the second heart sound (“dub”) is split into two sounds

•Can be normal (during inspiration) really dead breathe= more venous blood into right side of heart → right has more blood then left, takes longer to empty- therefore a second dub sound

•Can be pathological

•Wide splitting •Reverse splitting •Fixed split

36
Q
A

C point A marks the beginning of isovolumetric contraction

37
Q

preload

A

happens during diastole (heart not actively contracting)

resting/stretched

the tension in the wall of the ventricle produced by the end-diastolic pressure

loosely: the end diastolic pressure

preload is not a measure of volume

38
Q

___ the tension in the wall produced by the end-diastolic pressure

A

preload

39
Q

___ the tension in the wall produced at the time of the opening of the aortic valve (during systole)

A

afterload

loosely: the pressure at the time of the opening of the aortic valve

40
Q

afterload

A

Strictly: the tension in the wall produced at the time of the opening of the aortic valve (during systole)

Loosely: the pressure at the time of the opening of the aortic valve

during ejection, when ventricle is active and shortening

41
Q

Frank starling relationshi[

A

In a healthy heart:

  • Increased volume (pressure) results in increased force of contraction
  • Stroke volumes of the left and right ventricles remain balanced•

Clinical Relevance: If balance were not maintained: blood accumulation in pulmonary or systemic circulation can result (edema)

42
Q

passive tension

A

rubber band

the more you stretch it, the more passive tension it supplies

43
Q

explain passive vs active

A

cardiac muscle

  • Wide dynamic range to take advantage of the increased active tension at longer lengths (greater heart filling produces more force of contraction).
  • Significant passive tension at peak active tension lengths
  • Passive tension tends to limit the degree of heart filling
44
Q
A

skeletal muscle: passive restricted by skeleton

•Relatively short length changes over the dynamic range due to muscle attachment near the joints of bones.

Works over the range of the peak active force

•Very little passive tension at peak active tension lengths

cardiac

  • Wide dynamic range to take advantage of the increased active tension at longer lengths (greater heart filling produces more force of contraction).
  • Significant passive tension at peak active tension lengths
  • Passive tension tends to limit the degree of heart filling
45
Q

why does cardiac muscle have such a larger working range?

A

passive tension adds to work range

46
Q

two ways to increase the force of contraction (tension)

A

increase length

adjust contractility (Calcium concentration and sensitivity)

47
Q

what part of the ANS impacts contractility

A

sympathetic increases contractility (will influence contractile cells in the heart)

Parasympathetic does not effect contractility

48
Q

what does parasympathetic do to heart

A

decrease HR

does not impact contractility

49
Q

what does sympathetic do to heart?

A

increase HR

increase contractility (only sympathetic will travel to contractile cells in heart)

50
Q

____ binds to β-adrenergic receptors and causes ___ HR

A

norephinephrine

Sympathetic response increases HR

51
Q

norepinephrine released by the ___ nervous system __HR

A

sympathetic

increases

52
Q

____ binds to muscarinic cholinergic receptors

A
  • Acetylcholine binds to muscarinic cholinergic receptors
  • Parasympathetic response decreases HR
53
Q

acetylcholine produced by ___ nervous system ___ the heart rate

A

parasympathetic

decreases

54
Q

sympathetic innervation of the heart channels

A

Increased sympathetic activity
(norepinephrine or epinephrine)

β1 receptors in SA node

Increased permeability to sodium and Ca2+ (funny channel and T type calcium channel)

Increased rate of spontaneous depolarization

Increased heart rate and contractility (L type calcium channel and ryanodine Ca receptor)

55
Q
A

(norepinephrine or epinephrine)

this binds to Beta1 G protein receptor and causes down stream activity

activates L-type Ca channels and Ryanodine Receptors on the SR to increase intracellular Ca and increase contractility

will increase Calcium sensitivity of troponin

will also increase SERCA (reabsorption of Ca back into the SR) (decreases time it takes for muscle to relax)

56
Q
A

sympathetic (norepinephrine or epinephrine) release and bind to Beta 1 g protein receptor in SA node

this causes increased function of the funny channel (Na in) and the T type calcium channel (Ca in)

this increases spontaneous depolarization

57
Q

parasympathetic activity of the heart

A

Increased parasympathetic activity
(acetylcholine)

Muscarinic cholinergic receptors in SA node

Increased open state of K+ channels and closed state of Ca2+ channels

Decreased rate of spontaneous depolarization; hyperpolarization

Decreased heart rate

58
Q

two ways parasympathetic effects heart channels

A

acetylcholine binds to G protein receptor

increases activity of K channel (K out of cell→ repolarization)

makes it harder for T-type calcium channels to meet threshold

59
Q

three things EDV is affected by:

A

venous return

ventricular compliance

diastolic filling time

60
Q

ESV is affected by ____ and ____

A

ventricular contractility

afterload

61
Q

ventricular volume of stiff heart vs normal heart

A

stiff can’t hold as much (noncompliant)

not stretchy (during diastole → relaxation)

takes more pressure to get the same amount of volume

62
Q

increased contractility will cause

A

larger stroke volume

(systole→ ventricle contract)

increase contractility can move more blood then a normal heart

63
Q

which line is heart disease

A

decreased contractility (can not pump as much)

64
Q

what impacts cardiac output

A
65
Q

explain pace maker curve

A

in normal heart→ sympathetic innervation causes the systolic to decrease

the pacemaker did not allow that, it kept systolic the same and only decreased the diastolic (relaxation time)

66
Q

____ are abnormal disruptions in flow (turbulence) that can be auscultated

A

murmurs

•Can occur during diastole, systole, or be continuous

67
Q

____ describes a valve that fails to close completely

A

Incompetent or insufficient

•Regurgitation describes the backflow across the incompetent valve

68
Q

___ describes the backflow across the incompetent valve

A

•Regurgitation

69
Q

____ occurs when a valve fails to open widely enough

A

stenosis

70
Q

when the murmur is so extreme that it can be palpated

A

thrill

71
Q

defects that cause a murmur can lead to ___

A
  • Abnormal blood flow to a region of the body
  • Abnormal blood pressure in a region of the body
  • Cardiac hypertrophy
72
Q

MR causes

A
73
Q

patent ductus causes

A
74
Q

mitral stenosis leads to

A
75
Q

when would you hear tricuspid or mitral incompetence

A

lub S1= backflow hitting the AV valves after they close at the start of the ventricular systole

TI and MI do not close all the way and allow back flow, lub would not be as loud??

would hear a continuous murmur as blood leaks back and forth??

22 spring: Physiology (34 decks)

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