Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Exam1Lec6CardiacMusclePhysiology > Flashcards

Exam1Lec6CardiacMusclePhysiology Flashcards

1
Q

The 2 pumps of the heart is comprised of _ _ and separated by _

A
  • Muscular chambers
  • Valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Left or right ventricle has more myocardium? Why?

A

Left because it pumps blood against a higher resistance (compared to the right) so it needs more muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What muscle allows the valves to open and close

A

Chonde teni with papillary muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does muscle contraction closely follow?

A

the wave of depolatization (excitation) throughout the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is Cardiac output and what contributes to it?

A
  • the amount of blood pumped by the heart minute and is the mechanism whereby blood flows around the body
  • Stroke volume and heart rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is end diastolic vol and end systolic vol

A

The EDV is the filled volume of the ventricle prior to contraction and the ESV is the residual volume of blood remaining in the ventricle after ejection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does end diastolic and systolic volume contribute to

A

Stroke vol
EDV-ESV= SV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do we calculate cardiac output and stoke vol

A

CO=HR * SV-> in ml so you might have to convert to Liters
SV=EDV-ESV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is venous return?

A

Amount of blood returning to the righ atrium/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When valves are closed (filling artria/ventricle), what happens to pressure during myocardial contraction?

A

Pressure develops

this is isovolumetric contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What needs to happen for aortic valve to open

A

To exceed the aortic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does blood move?

A

according to the pressure gradient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Explain the graph with isovolumic contraction/relaxion and opening/closing of valves

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Striated muscle with _ and _ filaments

A

thin and thick

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • where are interacalated discs
  • what do they contain
A
  • betwenn cardiac cells that contain both the mechanical (fascia adherens and desmosomes) and electrical connections (gap junctions) between cells (permits function as a syncytium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

T-tubule of cardiac lie along what?

A

Z line and not the I bands like skeletal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the difference of SR in cardiac then skeletal muscle

A

not as dense as in skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In the SR of cardiac cells, what is the calcium reuptake pump and what is it inhibited by

A
  • SERCA2a
  • Phospholamban inhibits it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is abundant and occupies 305 of heart volume

A

Mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What prevents the reupture and overstretching of heart

A

abundance of connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the z line

A

point of attachment of the thin filaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does thin filaments contain

A
  • Actin
  • Troponin
  • Tropomysosin
  • Nebulin-scaffold for thin filament
  • alpha actinin- anchors actin to z line
  • Tropomodulin (regulates length of thin filament)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does thick filaments contain

A
  • myosin
  • meromysoin
  • C-protein (scaffolds for thick filament)
  • Titan
24
Q

What does titin tethers and what is it

A
  • tethers myosin to Z-line
  • Stretch-sensor, signal transducer and involved in increasing force in response to stretch
25
Q

What does depolarization causes

A

calcium entry via voltage-gated calcium channels

26
Q

Calcium entry triggers what

A

calcium release from the SR via ryanodine receptors

27
Q

Explain what increases intracellular calcium

A
  • influx through voltage gated L type calcium channels
  • release from theSR via Ca- induced ca release channels (majority)
28
Q

What plays a role in relaxation of calcium

A
  • intracellur Ca pumped back into SR
  • Ca pumped out of the myocyte via CaATPase pumps and a Na/Ca exchanger
29
Q

What does Ca binding enable

A

teh mechanical force to be generated through cross bridge cycling event

30
Q

Go through the cross bridge cycle (ratchet machanism)

A
  1. Bound ATP causes conformation change in hinge region of myosin and promotes binding to actin
  2. Hydrolysis of ATP causes a conformational change in the hinge region of myosin, causing movement of the thin filament and shortening of the sarcomere
  3. After mvt, ADP dissociated from myosin
  4. myosin actin remain bound with no ATP (rigor mortis state)
  5. ATP binding to myosin
  6. ATP binding causes dissociation of myosin (ATP) from actin
31
Q

What is the difference of sacromers in cardiac and sketeal muscle

A

sacromers in cardiac are not going to produce the same degree of stretch and length

32
Q

Force (tension) produced with increase of what?

A

muscle length (stretch)

33
Q
  • Resting Tension:
  • Active tension:
  • Total tension:
  • Lmax:
A
  • Resting Tension: produced by the resting biomechanical properties of the cardiac tissue (no cross bridge cycling)
  • Active tension: produced by cross bridge cycling
  • Total tension: RT+AT
  • Lmax: Length at whcih active force is maximal

MEASURED IN PAPILLARY MUSCLES

34
Q

Stretching the heart increases what?

A

the force of contraction

35
Q

What does not increase the force of contraction?

A

Not by increases ca2+ or increase filament overlap

36
Q

What is frank-Starling law of the heart?

A
  • The force of contraction of the heart is proportional to the initial fiber length
  • Fiber length is the amount of force that your going generate from the heart is going to be proportional to the fiber length
37
Q

The length dependent increases in force following stretch may be due to what?

A
  1. Decreased interfilament spacing between actin and myosine, brought about by titin, which binds both of the filaments
  2. Increase in sensitivity to calcium or the actin-myosin complex
38
Q

What is the role of titin and how does stretch affect this

A
  • Titin binds both actin and myosin
  • Stretching brings the two dilaments closer together
39
Q

What is one mechanism to explain how preload influecnes contractile force

A

increaseing the sarcomere lenth increases troponin C calcium sensititvity, which increase the rate of cross brigde attachment and detachment and the amount of tension developed by the muscle fiber

40
Q

What increases the sensitivity of cardiac muscle to calcium

A

stretching

41
Q

Explain this graph with stretching and sensitivity to calcium

A
42
Q

What will happen when there is an increase in venous return

A

greater force of contraction, resulting in a greater cardiac ejection

43
Q

Venous return=

A

cardiac output
* The heart pumps what is gets

44
Q

Less blood= _ stretch= _ pumping out
More blood= _ stretch= _ pumping out

A

Less and less
more and more

45
Q

the vigor of contraction is determined by what?

A

The afterload and the autonomic N.S

46
Q

How does the Autonomic NS regulate the heart

A
  • Para: with the vagus nerve will contril the HR at the SA node
  • Sym: regulate pacing activity, HR and force of contraction
47
Q

Explain this picture

A
48
Q

Epi and NE bind to what receptor
Ach binds to what receptor

A

Epi +NE: beta one adrengeric
Ach: muscarinic receptor

49
Q

What does the activation of Gs do

A

increase cAMP which activates PKA to phosphorylate VDCC, RYR, phospholamban and troponin I

50
Q

What are the effects when these molecules are phosphoralated:
* VGCC
* RYR receptor
* Phospholamban
* Troponin I

A
  • VGCC: increase calcium entry
  • RYR: increase intracellular calsium release from SR
  • Phospholamban: removing its inhibition of CaATPase allow for increase of uptake of Ca by CaATPase which shortends contraction and increase rate of relaxation (lusitropic effect) due to the rapid accumulation of calcium which also increases ca stores for next contraction
  • Troponin I: makes Ca dissocaite from myofialments to decrease myofulament sensitivity to Ca++ to cause relaxation
51
Q

What does Vagal stimulation cause?

A

ACh-> M2-> activation of Gi-> decrease cAMP so decrease in phophoration

52
Q

Explain the difference between the two graphs

A

B-Adrenergic stimulation enhances contraction and accelerates relaxation

53
Q

What is the difference between preload and after load

A
  • Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling from venous return
  • Afterload is the force or load against which the heart has to contract to eject the blood.
54
Q

What are factors that affect EDV/preload

A
  • Ventricular compliance: if vents are stiff, as blood is returning/filling the vents are not going to strech as much or change in length (impact starling laws)
  • Filling time (HR): increase HR will decrease time for filling which will imact end diastolic volume by decreasing it thus decreases the stretch or length. ~also decrease SV~
  • Venous return: increase return, increase length, increase force
55
Q

What happens when you change afterload and its effect on cardiac output

A
  • Increasing aortic pressure does not decrease cardiac output unctil MAP>160 mmHg
  • Increasing the afterload, will cause the heart to have to pump more so it is more work for the heart

Physiology (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions