CV 1 Flashcards

1
Q

Inotropy definition

A

Strength of contraction

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2
Q

Chronotropy definition

A

rate of contraction

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3
Q

Lusitropy definition

A

Relaxation

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4
Q

Dromotropy definition

A

Conduction

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5
Q

Bathmotropy definition

A

Excitability

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6
Q

The heart pumps how much blood

A

6 L/min
8640 L/day
2282. Gallons/day

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7
Q

CO =

A

CO = HR x SV

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8
Q

SV =

A

SV = EDV - ESV

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9
Q

MAP =

A

MAP = CO x TPR
MAP = 2x DBP + SBP / 3

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10
Q

F ( Tissue Blood flow ) =

A

F = MAP / VR

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11
Q

of Nucleus in cardiac myocytes

A

1 per myocyte

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12
Q

Titin

A

~ Giant Protein
~ Bungee cord of the heart
~ molecular spring that functions as passive elasticity for the muscle (striated muscle)

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13
Q

What are Titans made of

A

Immunoglobulins

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14
Q

Intercalated disks are comprised of:

A

Fascia Adherens
Desmosomes
Gap Junctions

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15
Q

What do Fascia Adherens do

A

~ Anchoring sites for myocyte
~ Connect to the closest myocyte

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16
Q

What do Desmosomes do

A

~ Specialized for cell to cell adhesion
~ Resist searing forces

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17
Q

What do Gap Junctions do

A

~ Think electrical
~ Allow Ads to spread between cardiac cells - permits ion passages
~ Connexons: specialized tunnels

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18
Q

What separates the Atrial syncytium and Ventricular syncytium?

A

Thick fibrous connective tissues

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19
Q

What is the Cardiac Muscle controlled by

A

ANS

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20
Q

length of cardiac action potential

A

200 msec

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21
Q

Resting membrane potential of cardiomyocyte is

A

-90 mV

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22
Q

What maintains -90mV of the cardiiomyocyte?

A

constant outward leak of K+ through - inward rectifier channels

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23
Q

Phase 0

A

Depolarization
~ Threshold is reached at -70 mV activating fast Na+ channels
~ Rapid depolarization
~ L-type Ca+ channels open at -40 mV
~ Overshoot to +30

24
Q

Phase 1

A

Early repolarization
~ Some K+ channels open briefly and outward flow of K+ returns TMP to 0 mV

25
Q

Phase 2

A

Plateau phase
~ L-type Ca2+ channels are still open - small constant influx of Ca2+. Becomes significant in the *** excitation contraction coupling process
~ K+ leaks out - delayed rectifier K+ channels
~ K+ permeability decreases x5
~ Two currents are electrically balanced at 0 mV

26
Q

Phase 3

A

Repolarization
~ Ca2+ channels gradually inactivate
~ K+ outflow exceeds Ca2+ inflow.
~ Membrane ionic concentrations are restored by
- Na+ - Ca2+ exchanger,
- Ca2+ ATPase
- Na+ - K+ Atpase

27
Q

Phase 4

A

Resting membrane potential

28
Q

Number of cardiac T-tubules

A

1 tubule to 1 SR ( Diad )
( Triad in skeletal )

29
Q

DHP receptor differences

A

Electrochemical in cardiac
Electromechanical in skeletal

30
Q

Cardiac T tubules

A

5x diameter in skeletal

31
Q

What does phospholamban do

A

inhibits re-uptake of calcium into the SR

32
Q

What happens when phospholamban is phosphorylated

A

When phosphorylated it becomes inactive (disinhibition) increasing Ca++ uptake by the SR (enhances lusitropy)

33
Q

Normal mitral annulus

A

3 - 3.5 cm

34
Q

Normal aortic annulus

A

1.8 - 2.3 cm

35
Q

AV valve properties

A

~ Thin, flimsy, low pressure valves
~ Papillary muscles
~ Chordae Tendinae
prevents bulging into atria during contraction

36
Q

Semilunar valve properties

A

~ Strong yet pliable fibrous tissue
~ Smaller diameter compare to AV valves
~ More rapid ejection and valve closure
~ Prone to mechanical abrasions

37
Q

Total duration of cardiac cycle

A

70 bpm; 1/70 = 0.014 min/beat or 0.84 sec

38
Q

What is the delay between atria and ventricular contraction? Why?

A

~ 0.1 seconds
~ To allow for ventricular filling

39
Q

Atria contract ______ second ahead of the ventricles

40
Q

Resting membrane potential of SA nodal fibers

A

-55 to -60 mV

41
Q

Why isn’t the SA node depolarized all the time?

A

Ca++ channels become inactive after about 150ms of opening

42
Q

Atrial muscle velocity

43
Q

Specialized conduction fiber velocity

44
Q

What 4 Specialized conduction fibers are in the Atria

A

~ Anterior Interatrial band (Bachman’s Bundle) Right atrium to Left Atrium
~ Anterior Internodal Pathway
~ Middle Internodal Pathway
~ Posterior Internodal pathway

45
Q

AV node delay

A

0.09 sec delay in node

46
Q

AV node location

A

Posterior wall of right atrium behind tricuspid valve

47
Q

AV bundle delay

A

0.04 sec delay

48
Q

Conduction travels through the AV node then through the AV bundle what are the associated delays?

A

~ AV node - 0.09 sec
~ AV bundle - 0.04 sec

49
Q

What causes delay at the AV node and AV bundle

A

reduction in number of gap junctions between the AV node and the AV bundle (resistance to conduction = slow excitation)

50
Q

Purkinje conduction velocity

A

1.5 - 4 m/sec ( 6x ventricular muscle conduction velocity)

51
Q

Purkinje fibers are

A

Large fibers ( larger than ventricular muscle fibers )

52
Q

Conduction velocity from bundle branches to terminating purkinje fibers

A

0.03 seconds

53
Q

Conduction velocity from endocardium to epicardium

A

0.03 seconds

54
Q

Conduction velocity from bundle branches to contraction

A

0.06 seconds

55
Q

What happens with PNS stimulation

A

ACh is released which increases membrane permeability to K+

This causes hyper-polarization = less excitability ( SA node -65 to -75mV )

56
Q

What happens with SNS stimulation

A

Release of NE stimulates B1 adrenergic receptors

increased membrane permeability of Na+ and CA++ ions ( closer to threshold - decreasing conduction times )

~ increases nodal discharge
~ increases chronotropy
~ increases isotropy
~increases overall heart activity

57
Q

At rest, O2 consumption by beating heart =

A

9mL / 100g / min