Cardio Lec 6 Flashcards

(58 cards)

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

25
In an unhealthy heart, as EDV increases or stretches too much, eventually
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
The more cross-bridges (actin & myosin interactions) the more
contractile force
27
If EDV too low ->
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
EDV changes commonly so have to match more blood in w/ more blood out
T
29
Contractility refers to
greater contractile force at a CONSTANT EDV
30
Contractility uses excess ___ to get more interactions for a greater force of contraction
calcium
31
Starling's Law vs Contractility
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
Inotropicity
by flooding more calcium -> more interactions -> bc inhibition relieved
33
The only thing that can increase contractility is
an increase in intracellular calcium
34
Starling's Law relies on
STRETCH
35
Ejection fraction refers to
% of EDV that is ejected at a given afterload
36
After load refers to
load heart has to work AGAINST to eject blood
37
Norm ejection fraction
65%
38
Ejection fraction calc
EDV / SV
39
ONLY factor that can increase ejection fraction is
increase in contractility
40
Only thing that can increase contractility
calcium
41
Aortic pressure is the
after load
42
Only way semilunar valve opens
ventricular pressure must exceed aortic pressure
43
We want after load to be low or high?
low so heart doesn't have to work as hard
44
Muscles isometric point
point at which muscle can only generate ISOMETRIC CONTRACTION bc after load is so great - heart cant contact against it
45
If bp got so high that reached isometric point ->
Co would be 0 -> stay in isovolumetric phase -> wouldn't enter ejection phase
46
As you get to a higher EDV, isovolumetric point shifts
out bc heart can generate more forceful contraction bc fibers more aligned
47
If nothing else changes, why would SV decrease as after load increases?
bc aortic semilunar valve will open LATER. (its spending more time generating PRESSURE, less time for blood to get EJECTED)
48
Main determinant of after load
total peripheral resistance (TPR)
49
TPR refers to
sum of all arterial resistance; determines bp & aortic pressure
50
An increase in tpr result in an increase in
after load
51
Venous return affects EDV
t
52
Capacitance vessels
veins (store blood)
53
Resistance vessels
arteries
54
Venous side low press low resistance pathway
t
55
Factors that aid venous return
valves, respiratory pump/breathing (by lowering r. atrial press), skeletal muscle pump, PRESSURE GRADIENT (high->low), exercise/MOVEMENT, sympathetic stimulation
56
Anything that lowers r. atrial pressure will
improve press gradient -> aid venous return
57
Anything that increases r. atrial pressure will
lowers press gradient -> retards venous return
58
We want to keep r. atrial press __ so that __
minimized, blood can go from bottom up (high press -> low)