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Physio > Cardio Lec 6 > Flashcards

Cardio Lec 6 Flashcards

1
Q

Positive chronotropic agents do what

A

elevate hr (epi, norepi)

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2
Q

Negative chronotropic agents do what

A

lower hr (ach)

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3
Q

Heart beats independent of NS

A

t

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4
Q

At rest _NS dominates

A

PNS (keeps hr < 100bpm)

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5
Q

During exercise _NS dominates

A

SNS (hr > 100bpm)

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6
Q

What keeps hr < 100 bpm at rest

A

Ach

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7
Q

1 heart beat every time __ fires

A

SA node

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8
Q

Tachycardia factors

A

stress, drugs, heart disease, fever, caffeine, anemia, hyperthyroidism (very common)

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9
Q

Bradycardia factors

A

sleep, athletes, hypothermia

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10
Q

Intrinsic rate of SA node

A

100 bpm (but kept below this at rest by…)

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11
Q

Heart rate controlled by

A

pacemaker potential (rate of rise to threshold by nodal cells ANS affects this)

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12
Q

SNS makes pacemaker cells depolarize more

A

quickly

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13
Q

PNS makes pacemaker cells depolarize more

A

slowly

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14
Q

Main mediator of the PNS

A

vagus n.

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15
Q

If vagus n. severed & remove parasympathetic influences from the heart, hr would

A

go up bc PNS is what keeps hr down

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16
Q

How does the PNS affect the pacemaker cells?

A

Ach closes ca & na channels (doesn’t allow + ions in) -> opens k channels (allow + ions to exit) -> makes nodal cells take VERY LONG to DEPOLARIZE

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17
Q

How does the SNS affect the pacemaker cells?

A

norepi bind beta1 rs -> incr cAMP -> opens ca & na channels (+ ions enter cell) -> allow cells to DEPOLARIZE to threshold QUICKER

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18
Q

CO peaks at about __ & why

A

180 bpm bc anything greater -> filling time compromised bc diastole shortens so much & output will start to fall

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19
Q

EDV aka

A

preload

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20
Q

At rest, most blood is held on __ side

A

venous (capacitance vessels)

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21
Q

During exercise, venous return goes

A

up

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22
Q

When EDV/preload incr so too does

A

SV (Starling’s Law of the heart) HEALTHY HEART

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23
Q

Frank Staling’s Law

A

SV is directly proportional to EDV/preload

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24
Q

In a healthy heart, EDV is proportional to

A

SV

25
Q

In an unhealthy heart, as EDV increases or stretches too much, eventually

A

SV begins to fall bc some cross-bridges lost -> fibers not aligned -> can’t be used since binding sites on actin not aligned w/ myosin heads

26
Q

The more cross-bridges (actin & myosin interactions) the more

A

contractile force

27
Q

If EDV too low ->

A

ventricles not stretched enough -> actin filaments overlap one another -> can’t use binding sites -> can’t maximize cross-bridges -> can’t get max contractile force

28
Q

EDV changes commonly so have to match more blood in w/ more blood out

A

T

29
Q

Contractility refers to

A

greater contractile force at a CONSTANT EDV

30
Q

Contractility uses excess ___ to get more interactions for a greater force of contraction

A

calcium

31
Q

Starling’s Law vs Contractility

A

IN BOTH: greater contractile force due to more actin & myosin interactions. Starling’s more interactions due to: fibers align properly VENTRICLES MORE STRETCHED; Contractility more interactions due to: EXCESS CALCIUM (calcium moves tropomyosin & allows actin & myosin to interact)

32
Q

Inotropicity

A

by flooding more calcium -> more interactions -> bc inhibition relieved

33
Q

The only thing that can increase contractility is

A

an increase in intracellular calcium

34
Q

Starling’s Law relies on

A

STRETCH

35
Q

Ejection fraction refers to

A

% of EDV that is ejected at a given afterload

36
Q

After load refers to

A

load heart has to work AGAINST to eject blood

37
Q

Norm ejection fraction

A

65%

38
Q

Ejection fraction calc

A

EDV / SV

39
Q

ONLY factor that can increase ejection fraction is

A

increase in contractility

40
Q

Only thing that can increase contractility

A

calcium

41
Q

Aortic pressure is the

A

after load

42
Q

Only way semilunar valve opens

A

ventricular pressure must exceed aortic pressure

43
Q

We want after load to be low or high?

A

low so heart doesn’t have to work as hard

44
Q

Muscles isometric point

A

point at which muscle can only generate ISOMETRIC CONTRACTION bc after load is so great - heart cant contact against it

45
Q

If bp got so high that reached isometric point ->

A

Co would be 0 -> stay in isovolumetric phase -> wouldn’t enter ejection phase

46
Q

As you get to a higher EDV, isovolumetric point shifts

A

out bc heart can generate more forceful contraction bc fibers more aligned

47
Q

If nothing else changes, why would SV decrease as after load increases?

A

bc aortic semilunar valve will open LATER. (its spending more time generating PRESSURE, less time for blood to get EJECTED)

48
Q

Main determinant of after load

A

total peripheral resistance (TPR)

49
Q

TPR refers to

A

sum of all arterial resistance; determines bp & aortic pressure

50
Q

An increase in tpr result in an increase in

A

after load

51
Q

Venous return affects EDV

A

t

52
Q

Capacitance vessels

A

veins (store blood)

53
Q

Resistance vessels

A

arteries

54
Q

Venous side low press low resistance pathway

A

t

55
Q

Factors that aid venous return

A

valves, respiratory pump/breathing (by lowering r. atrial press), skeletal muscle pump, PRESSURE GRADIENT (high->low), exercise/MOVEMENT, sympathetic stimulation

56
Q

Anything that lowers r. atrial pressure will

A

improve press gradient -> aid venous return

57
Q

Anything that increases r. atrial pressure will

A

lowers press gradient -> retards venous return

58
Q

We want to keep r. atrial press __ so that __

A

minimized, blood can go from bottom up (high press -> low)

Physio (14 decks)

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