Brainscape's Knowledge GenomeTM

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


See full index

Physiology > Cardiac Muscle > Flashcards

Cardiac Muscle Flashcards

1
Q

how is cardiac muscle similar to skeletal

A

-striated
-same mechanics of skeletal muscle
however, there is a simultaneous contraction of all fibers

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

intercolated junctions

A

mechanically and electrically connected at these spots

-connected by gap junctions and desmosomes

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

types of contractions

A
  • twitches
  • variable force (not all or nothing)
  • no fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

excitation contraction coupling in cardiac muscle

A

cardiac action potential

  • voltage gated Na+, Ca++, K+ channels
  • calcium plateau, causes ca++-stimulated Ca++ release from SR through ryanodine receptors
  • very long refractory period-no tetanus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

cardiac output equation

A

CO (liters/min)=Heart Rate (beats/min)X Stroke Volume (liters/beat)

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

average CO

A

5L/min (resting)

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

average HR

A

93 bpm

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

average stroke volume

A

.07L/b

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

calculating max heart rate

A

220-age

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

Heart rate: pacemaker potential

A

a different type of voltage-gated Na+ channels: pacemaker channels (If channels)

  • open by hyperpolarization
  • cause slow depolarization when cell returns to resting potential
  • AP shuts If channels
  • gets closer to ENa+ when open
  • open slowly
  • controlling how fast channels open back up controls HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pacemaker potential

A

-controls heart rate
-changes in rate are called chronotropic effects
-sympathetic response: epinephrine/norepinephrine
B-adrenergic receptors->increased cAMP->increased rate of pacemaker channel opening
-parasympathetic response: acetocholine
muscarin Ach receptors-> Gk protein-> opens K+ channel-> slows pacemaker potential

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

Stroke volume

A

force development depends on cytoplasmic [Ca++] and on preload of the muscle

  • changes in force of contraction are known as inotropic effects
  • increased force of contraction results in an increased stroke volume (volume of blood pumped per beat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

chronotropic effects

A

changes in heart rate

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

inotropic effects

A

changes in force of contraction

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

Frank starling law of the heart

A

change in force development as a function of preload

  • really the length-tension relationship of cardiac muscle
  • resting length of cardiac muscle is such that increases in preload (filling) cause increased force and therefore increased ejection of blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

change in contractility

A

change in contraction strength by control of Ca++

  • changes are usually caused by increasing th eamount of Ca++ loaded into the sarcoplasmic reticulum
  • changes in contractility change the ejection fraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ejection fraction

A

fraction of the blood in the ventricle that is ejected into the artery

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

control of contractility

A
  • troponin/tropmoyosin controls activity of the myosin ATPase (like skeletal muscle)
  • Ca++ enters cell through plasma membrane during action potential and also comes from SR, as a result of calcium induced calcium release from the SR through RyR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does Ca++ leave the cytoplasm

A

leaves between beats

  1. Ca-ATPase pumps it back into the SR
  2. A Na?Ca-exchanger (countertransport) system moves calcium out of the cell by secondary active mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

staircase effect

A

change in contractility

  • at high heart rates, the Na/Ca-exchanger cannot extrude all of the calcium that enters during the AP
  • the excess calcium that builds up in the cell is taken up the SR, since the Ca-ATPase is not as limited as the Na/CA exchanger
  • known as calcium loading of the SR
  • calcium loading leads to increased contractility, which is an increase in the force produced at any given preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do catecholamines cause in increase in contractility

A
  • they interact with B-adrenergic receptors
  • increased [cAMP] activates protein kinase A which phosphorylates multiple target proteins
    1. voltage gated calcium channels of the plasma membrane
    2. Ca-atpase of sarcoplasmic reticulum
    3. troponin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

voltage gated calcium channels of the plasma membrane

A
  • increased inward calcium flow during the action potential leads to increased [calcium] and also to calcium loading of the SR
  • the channels then close more quickly, leading to a shorter action potential, shorter contraction, and increased filling time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Ca-ATPase of sarcoplasmic reticulum

A

increased rate of this pump causes SR loading

-it also decreases the time needed to relax between beats. this increases filling time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

troponin

A

causes troponin to release its calcium more quickly, again leading to increased filling time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

digitalis

A

a drug that increases contractility

-causes the Na/Ca-exchanger to work more slowly, thus promoting Ca++-loading of the SR

26
Q

control of HR through sympathetic

A

nor/epinephrine

  • B-adrenergic
  • Gs increases cAMP
  • phosphorylates If channels, open faster, less time to get back to threshold
27
Q

control through parasympathetic

A

slow HR

  • acetylcholine (muscarinic receptors
  • alpha subunit: GI protein decreases cAMP, fewer phosphorylated If channels
  • B subunit: Gk open K+ channels, extra hyperpolarization
28
Q

pacemaker of the heart

A

SA node

29
Q

what happens to smooth muscle tension when HR increase

A

it decreases in the blood vessels, allows greater ouput

30
Q

what connects the para/sympathetic to the heart

A

the vagus nerve

31
Q

stroke volume

A

higher pressure=higher stroke volume

  • contract more forcefully, increase pressure, increase stroke volume
  • need each cell to contract more strongly (already have 100% recruitment)
  • frank starling law (increased filling increases SV)
32
Q

preload

A

fill heart more, increase volume, stretches chamber more

  • more blood, stronger contraction

- heart only ejects half of whats in it

33
Q

ejection fraction

A

EF=SV (what leaves heart)/EDV (end diastolic volume, filling of heart)
ex= 70/135=.52

34
Q

2 ways to increase contractility

A
  1. staircase effect
  2. epinephrine (B receptor increases cAMP, phosphorylates SR ca++atpase, loads up SR with ca++, increases contractility)
    - also phosphorylates ca++ channel of plasma membrane (AP channel, lets more ca++ in, plateau gets taller)
35
Q

ways that epinephrine effects contractility

A
  1. If channels increase rate
  2. phosphorylate SR ca++ atpase (makes it faster)
  3. phosphorylates ca++ channel of plasma membrane (AP channel)
  4. troponin
    first 3 affect contractility
    -3+4 make relaxation faster
36
Q

what makes the SA node different from the hearts other myocytes

A

it contains specialized autorhythmic cells that control the overall cardiac rhythm

37
Q

from the SA node, where do the AP go

A

conducted from cell to cell through the gap juncitons thorugh the atrial contractile cells and also through an internodal pathway to the AV node
-depolarization occurs slowly across atria, conduction slows through AVn ode

38
Q

from the AV node, where do the AP go

A

the AV node delays the AP, then conducts it through the bundle of His, bundle branches, and purkinje fibers to the ventricular contractile cells`

  • moves rapidly through ventricular conducting system to the apex of the heart
  • spread upward from apex, FAST
39
Q

what does the AV node do

A

controls the rate of AP and sends signal out after receiving it

40
Q

ECG/EKG

A

a recording of the spread of the action potential across the heart. The recording shows an upward deflection if the action potential is moving toward the positive electrode

41
Q

P wave

A

result of atrial depolarization

42
Q

PR interval

A

result of the delay of the action potential by the AV node

43
Q

QRS wave

A

result of depolarization of the ventricles

44
Q

QRS interval

A

tells us how long it takes for the AP to spread across the the ventricles

45
Q

QT interval

A

recorded while the ventricles are depolarized

-calcium plateau, all contracting

46
Q

T wave

A

result of repolarization of the ventricles

47
Q

flat lines

A

all contracting, no movement

48
Q

atrial systole

A

atria contract, completing ventricular filling

-correlates with the P wave of the ECG

49
Q

diastole

A

atria and ventricles are at rest, ventricles are filling

50
Q

ventricular systole

A

ventricles contract, ejecting blood into aorta and pulmonary arteries

51
Q

steps of ventricular systole

A
  1. AV valves (bicuspid/tricuspid) close producing first heart sound. correlates with QRS wave of ECG. ventricles are done filling and contain the end diastolic volume
  2. isovolumic contraction: both AV valves and both semilunar valves (aortic and pulmonary) are closed, so the ventricle builds up pressure without any change in volume. the semilunar valves will not open until ventricular pressure exceeds arterial pressure. this is analogous to the isometric phase of a skeletal muscle mixed contraction
  3. ejection phase: (ventricular systole) begins when semilunar valves open. during this phase, the ventricular pressure is approximately equal to arterial pressure. the pressure increases as more blood is forced into the elastic arteries. ventricular volume decreases to end systolic volume as the cardiac muscle fibers shorten. this is analogous to the isotonic phase of a skeletal muscle mixed contraction
  4. semilunar valves close when the cardiac contraction begins its isovolumic relaxation phase. this produces the second heart sound. it correlates with the T wave of the ECG
  5. AV valves open when the pressure in the ventricle drops below the atrial pressure. this marks the beginning of diastole, and the ventricles begin to fill again
52
Q

what is the afterload

A

pressure preventing valves from opening (diastolic arterial pressure)

53
Q

arteriole pressure determined by?

A

the volume of blood contained in the arteries

54
Q

arterial pressure (ejection phase)

A
  • arterires are elastic, so more blood they contain the more their walls are stretched, and greater the pressure on the blood
  • during the ejection phase, more blood is being forced into the arteries by the heart. during this phase the arterial pressure is approximately the same as ventricular pressure. the highest pressure attained during this time period is systolic pressure
55
Q

arteriole pressure (diastole)

A

the pressure in the arteries is driving the blood through the arterioles and into the capillaries and veins

  • as blood leaves the arteries, the arterial pressure falls
  • this occurs until the semilunar valves open to begin the next ejection phase.
  • the lowest pressure attained, just before the SL valves open is diastolic pressure
56
Q

diastolic pressure

A
  • says what the arteries are doing
  • easy blood flow=open arteries and lower diastolic pressure
  • constricted=higher diastolic pressure
  • also tells time between heart beats
57
Q

cardiac output equation

A

CO=HRXSV

58
Q

stroke volume calculation

A

end diastolic volume-end systolic volume

59
Q

what happens as end diastolic volume increases

A

the preload on the cardiac muscles increase. the frank-starling law tells us that as preload increases, contraction force increases and therefore stroke volume increases
-EDV increases if venous return to the heart increases

60
Q

how does contractility affect SV

A

it changes the ejection fraction (EF=SV/EDV)

-affected by staircase effect, B-adrenergic receptors, and digitalis

Physiology (11 decks)

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