Brainscape's Knowledge GenomeTM

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


See full index

Physiology > B1W3: Cardiac Muscle > Flashcards

B1W3: Cardiac Muscle Flashcards

1
Q

AV Valves

A

LAB RAT bicuspid/mitral tricupid Chordae tendae pull back Between atria and ventricles

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

Aortic/pulmonary valves

A

Prevent backflow from aorta/pulmonary artery into ventricles

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

Prolapsed valve

A

Mitral valve that accidently lets blood leak through backwards

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

Rheumatic fever

A

Causes high instance of valvular stinosis (interferes with transfer of blood)

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

Mitral regurgitation

A

Elevates arterial pressure because blood is not moving forward, staying put

This elevates the atrial pressue a little more each cycle, messing up end diastolic volume and diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

S1 heart sound

A

the “lub”

  • marks beginning of systole/end of diastole
  • closure of mitral/tricuspid valves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S2 heart sound

A

The “dub”

End of systole/beginning of diastole

Closure of aortic/pulmonary valves

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

Additional heart sounds

A
  • swishing means there’s a problem with laminar flow
  • 3rd sound=increased atrial pressur
  • 4th sound=stiffened left ventricles

It is important to listen to the nature and timing of the sound

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

Three different types of cells in myocardium

A
  • Myocardial muscle: in atria and ventricles, generates force
  • Conducting: bundle of His, purkinje fibers; coordinates contraction
  • Pacemaker: SA node and AV node; initiates heart-beat, and control of heart beat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cardiac muscle ccomponents

A
  • actin/myosin
  • intercalated disks, i.e. gap junctions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Major conducting pathways

A
  1. Atrial syncytium
  2. AV node
  3. Bundle of His
  4. Ventricular syncytium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Action potential in cardiac muscle
A
  • due to influx of Na+ and Ca2+
  • Calcium causes plateau phase, where calcium enters and binds to troponin
  • Abslutely refractory period and relative refractory period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Cardiac excitation-contraction coupling

A

Needs external calcium to contract–DEPENDENT ON IT

  • Ca2+ enters cell via L type Ca2+ channels during plateau for calcium-induced-calcium released
  • T tubule helps Ca2+ released from SR using RyR receptors
  • Ca2+ also stays in T tubules!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

End diastolic volume

A

Volume of blood filling the ventricle during rapid filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Stroke volume

A

Volume of blood ejected as the ventricles contract during systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

End-Systolic Volume

A

Volume remaining in each ventricle after contraction

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

Ejection fraction

A

Fraction of the end-diastolic volume that is ejected; will be reduced in people at end stage of heart disease

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

Equation for Stroke Volume

A

Stroke Volume=EDV - ESV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Calcium’s role in contraction

A

Binds to Troponin C once released from SR, T-tubules or extracellular fluid

Troponin C does conformation chainge on tropomyosin

Active sites on actin are uncovered for myosin to bind

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

Ejection fraction equation

A

EF=SV/EDV

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

Volume-Pressure Relationship

A

As you fill heart, pressure increases

Just adding volume generates pressure

This works to a point until you pass the Frank-Starling relationship

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

Stroke work

A

Output of heart

(work=force x distance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Chronotropic action

A

effecting the heart rate

24
Q

inotropic

A

effecting the strength of cardiac contraction

25
Q

lusitropic action

A

effect on rate of relaxation

26
Q

preload

A

The load in heart before systole (i.e. EDV)

27
Q

afterload

effects ESV

A

resistance in aorta against ventricular pumping

28
Q

determinants of stroke volume

A

preload

contractility

afterload

29
Q

length tension relationship in cardiac muscle

A

Tension of heart increases, length will increase too

30
Q

What affects EDV

A

Ventricular performance increases as we increase EDV

  • venous tone
  • total blood volume
  • body position
  • pumping of skeleatl muscle
  • atrial contribution to ventricular filing
  • intrathoracic pressure
  • intrapericardial pressure, ventricular compliance
31
Q

Effect on preload of compliance

A

Compliance of ventricles

If they’re stiff, more pressure at less volume

If too compliant, more volume out with little pressure

  • extrinsic compression (pleural pressure, tumor), thickness of LV wall (edema, muscle) and elasticity due to cross-bridges will all affect
32
Q

How is contraction measured?

A

Using isovolumic pressure-volume curve

Clamp aorta, fill ventricle with varying amounts, can see the max amount of tension heart can have at any volume

33
Q

factors affecting myocardial contractility

A
  • sympathetic/parasympathetic impulses/hormones circulating
34
Q

Role of sympathetic on heart

A

Chronotrophic and inotrophic (increases heart rate and stroke volume)

SA node discharge rate increased

35
Q

Role of parasympathetic on heart

A

Innervates only nodes, not ventricles (unlike sympathetic)

Slows heart rate

SA discharge rate decreased

36
Q

Catecholamines on heart contractility

A

increases

37
Q

B blockers on contractility

A

block stimulation of Ca2+ channels and Na+/Ca2+ exchangers

Constant depolarization

38
Q

Ca2+ channel blockers

A

Block L-type Ca2+ channels

39
Q

Digitalis glycosides

A

Inhibit Na/K pump and Ca channels; increases cytosolic Ca2+

40
Q

Cardiac output and arterial pressure

A

Cardiac output not affected by increases in afterload until over 160 (hypertension)

–CO is determined almost entirely by ease of blood flow

41
Q

Increase in afterload on volume/pressure curve

A

Narrows and moves upward

42
Q

Volume/pressure curve under increase of volume

A

widens

43
Q

Increase in contractile state on volume/perssure curve

A

Widens; pushes up isovolumetric-volume curve (makes line steeper)

44
Q

Sinus nodal fiber compared to ventricular muscle fiber

A
  • no plateau
  • looks like “normal” action potential
45
Q

Purpose of AV node

A

Delays transmission from SA node to ventricles

Allows time for atria to empty

46
Q

Pacemaker Node Contraction

A

No plateau

Unstable resting potential–Funny Na+ channels (IF) slowly open until threshold, then Ca2+ channels open

47
Q

Pulmonary system

A

low resistance/pressure

48
Q

Systemic system

A

high resistance/pressure

49
Q

increase in preload causes…

A

increase in stroke volume

thick and thin filaments stretch, overlap, more cross bridges

50
Q

positive inotropic effect

A

increase contractility

51
Q

negative inotropic effect

A

decrease contractility

52
Q

increasing contractility means…

A

greater stroke volume

Frank Starling curve becomes near vertical…for that given EDV, more blood will be pumped out

53
Q

Cardiac output equation

A

CO=HR x SV

54
Q

if afterload increases:

A

higher pressure needed to open aortic valve

ejection phase shortened

stroke volume decreases

55
Q

if preload increases

A

stroke volume increases

end systolic volume does not change

56
Q

Accumulation of what solute is responsible for tetanus?

A

Ca2+

Physiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions