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BRS Cardiology > Cardiac muscle and cardiac output > Flashcards

Cardiac muscle and cardiac output Flashcards

1
Q

What is the contractile unit in myocardial cell?

A

sarcomere

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2
Q

what is the length of the sarcomere

A

from Z line to Z line

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3
Q

what does sarcomere contain?

A

thick filaments (myosin) and thin filaments (actin, troponin, tropomyosin)

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4
Q

how is cardiac muscle contract?

A

thin filaments slide along thick filaments by forming and breaking cross bridges between actin and myosin

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5
Q

what are intercalated disks

A

ends of the cells

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6
Q

fxn of intercalated disks

A

maintain cell-cell adhesion

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7
Q

fxn of gap junctions

A

low restance path btwn cells for rapid electical spread of AP

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8
Q

because of gap junctions, heart behaves as an ___

A

electrical syncytium

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9
Q

more mitochondria in cardiac or skeletal muscle?

A

cardiac

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10
Q

what are T tubules

A

invaginate cells of Z lines

carry AP into cell interior

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11
Q

Are T tubules more developed in ventricles or atria

A

ventricles

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12
Q

What is the SR

A

storage and release of Ca2+ for EC coupling

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13
Q

Steps in EC coupling

A

Page 77

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14
Q

What is contractability/inotropy?

A

intrinsic ability of cardiac muscle to develop force at a given muscle length

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15
Q

____ is the intrinsic ability of cardiac muscle to develop force at a given muscle length

A

contractability/inotrophy

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16
Q

Contractability/inotropy can be estimated by the ____

A

Ejection fraction

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17
Q

equation for ejection fraction

A

EF = stroke volume/ end diastolic volume

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18
Q

How does heart rate affect contractility

A

More AP per unit time –>
more Ca2+ enter myocardial during AP plateaus –>
more Ca2+ in SR and released from SR
more tension produced during contraction

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19
Q

What is a positive staircase

A

Incr HR, incr force of contraction in stepwise as intracellular [Ca2+] incr cumulatively

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20
Q

What is postextrasystolic potentiation?

A

beat after an extrasystolic beat has incr force of contraction

extra Ca2+ enter cells during extrasystole

21
Q

how does sympathetic stimulation (catecholamines via B1 receptors) affect contractility

A

incr inward Ca2+ current during plateau of cardiac AP,
incr activity of Ca2+ pump of SR
more Ca2+ in SR
more Ca2+ available for release

22
Q

How does cardiac glycosides (digitalis) affect contractility

A

incr force of contraction by inhibit Na+/K+ ATPase in membrane
incr intracellular Na+, decr Na+ gradient
decr Na+ Ca2+ exchange, so more Ca2+ inside cell

23
Q

How does parasympathetic stimulation (ACh via muscarinic receptors) affect contractility

A

decr inward Ca2+ current during plateau

decr force of contraction in atria

24
Q

___ is the end-diastolic volume = Right atrial pressure

A

Preload

25
Q

Preload is the ___

A

EDV = Right atrial pressure

26
Q

When venous return incr, end diastolic volume ____ and stretches the ventricular muscle fibers

A

increases

27
Q

When venous return incr, end diastolic volume increases and _____ the ventricular muscle fibers

A

stretches

28
Q

____ for the LV is the aortic pressure

A

Afterload

29
Q

Afterload for the LV is the ___

A

aortic pressure

30
Q

Increases in aortic pressure cause ___ in afterload on the LV

A

increase

31
Q

____ for the RV is pulmonary artery pressure

A

Afterload

32
Q

Afterload for the RV is ____

A

pulmonary artery pressure

33
Q

Sarcomere length determines the ____

A

max # of cross bridges between actin and myosin

34
Q

Sarcomere length determines ____

A

the max tension or force of contraction

35
Q

When is velocity of contraction (at a fixed muscle length) MAX?

A

when afterload = 0

36
Q

Decr in velocity of contraction, ____ in afterload

A

increases

37
Q

Frank Starling relationship

A

describes incr in SV and CO in response to incr in venous return or EDV

38
Q

Frank Starling relationship is based on ____ relationship. Why?

A

length-tension relationship in the ventricle

incr in EDV, incr ventricular fiber length, incr tension

39
Q

What is the mechanism that matches CO to venous return

A

Frank starling relationship,

greater venous return, greater CO

40
Q

Incr in contractility shift Frank Starling curve ____

A

shift upward, increasing CO for any RA pressure or EDV

41
Q

Diastolic/systolic pressure Curve is the relationship between ____

A

diastolic/systolic pressure and diastolic/systolic volume in the ventricle

42
Q

LV cycle loop

1–> 2 (isovolumetric contraction)

A

1) LA fills LV with blood (~140 mL= EDV)
low LV pressure because muscle is relaxed

2) on excitation, LV contracts and ventricular pressure incr
Mitral valve closes (LV pressure > LA pressure)

Since no blood ejected from ventricle= isovolumetric

43
Q

LV cycle loop

2–> 3 (ventricular ejection)

A

3) Aortic valve opens when LV pressure > aortic pressure
blood eject into aorta and LV volume decr
–> STROKE VOLUME (LV ejected)

4) volume leftover in LV = end systolic volume

44
Q

How do you measure stroke volume

A

width of the Pressure volume loop

45
Q

LV cycle loop

3 –> 4 (isovolumetric relaxation)

A

5) LV relaxes
Aortic valve closes because LV pressure < aortic pressure

6) since all valves closed, LV volume constant

46
Q

LV cycle loop

4–> 1 (ventricular filling)

A

7) when LV pressure < LA pressure, mitral valve opens and LV fills
8) LV fills to 140 mL (end-diastolic volume)

47
Q

Changes in LV cycle loop

Increased preload

A

INCR WIDTH OF P-V LOOP

Increased EDV (incr venous return b/c incr blood volume or decr venous capacitance)

incr Stroke volume (more blood ejected from LV)

48
Q

Changes in LV cycle loop

Increased afterload

A

DECR WIDTH OF P-V LOOP

due to increased aortic pressure
so LV ejecting blood against higher P –> decr in stroke volume

increased end-systolic volume

49
Q

Changes in LV cycle loop

Increased contractility

A

LV has greater tension during systole
incr stroke volume

decrease in end-systolic volume

BRS Cardiology (9 decks)

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