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october exam > cardiac > Flashcards

cardiac Flashcards

1
Q

properties of cardiac muscle

A

-have properties of both skeletal and neural tissue
-when presented with electrial stimulus, cardiac myocytes contract in a coordinated way contributing to pumping mechanism of the heart

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2
Q

automaticity

A

ability to generate an AP spontaneously. cardiac conduction cells (SA node) display this when they set the HR

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3
Q

excitability

A

ability to respond to an electrical stimulus by depoloraizing and firing AP

cardiac cells are excitable b/c they can respond (depolarize) when presented with an electrical stimulus

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4
Q

conductance

A

the ability to transmit electrical current

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5
Q

can ions pass through cell membrane

A

no- they are charged

ion needs an open channel to cross from one side of the membrane to the other

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6
Q

what does open channel vs closed channel do

A

open channel- increases conductance of the ion

closed channel- reduces conductance of the ion

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7
Q

chronotropy is in reference to

A

HR

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8
Q

dromotropy

A

describes conduction velocity through the heart

(velocity= distance/ time)

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9
Q

lusitropy

A

describes rate of myocardial relaxation during diastole

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10
Q

RMP

A

electrical potential across a cell membrane at rest

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11
Q

what determine RMP (3 things)

A

chemical force (chemical gradient), electrostatic counterforce, na/k atpase

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12
Q

at rest nerve cell continious leaks __

A

k (loses pos charges)

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13
Q

what is primary determinant of RMP

A

K

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14
Q

decreased vs increased K

A

decreased K = rmp becomes more neg- cells more resistance to depolarization
increased K= rmp becomes more pos- cells depolarize more easily

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15
Q

threshold potential

A

voltage change that must occur to iniate depolorarization

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16
Q

what is the prime determinent of threshold potential

A

serum ca

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17
Q

decreased vs increased ca

A

decreased ca= tp becomes more neg

increased ca= tp becomes more pos

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18
Q

depolarization

A

movement of a cells membrane potential to a more pos value (less of a charge difference between inside and outside of the cell)

a cell depolorizes when na or ca enters the cell

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19
Q

can depolorization be stopped

A

no depolorization is all or none- once it begins it cannot be stopped

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20
Q

ability of a cell to depolarize is determined by the difference of

A

rmp and TP

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21
Q

when RMP is closer to TP..

A

earier to depolarize

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22
Q

when RMP is further from TP

A

harder to depolarize

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23
Q

repolarization

A

return of cells membrane potential to more neg value after depolarization

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24
Q

cell repolarizes when ___ or ___

A

k leaves cell or cl enters cell

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25
Q

during the refractory period can the cell depolarize

A

cell is resistance to depolarization- this is b/c RMP is further from TP

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26
Q

hyperpolarization

A

movement of cells membrane potential to a more neg value beyond baseline RMP

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27
Q

when does hyperpolarization happen

A

after repolarization cell typically hyperpolarizes for short time

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28
Q

in excitable tissue what restores the ionic balance towards RMP

A

na- k atpase restores ionic balance

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29
Q

what is the purpose of na- k atpase

A
  • removes na that entered the cell during depolarization
    -returns k that has left the cell during repolarization
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30
Q

for every 3 na ions it removes, it brings __ k ions into the cell

A

2

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31
Q

does na- k atpase turn on and off

A

always on!!

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32
Q

is na- k atpase active

A

active! - needs atp- duh

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33
Q

how is na- k atpase inhibited

A

inhibited by digoxin

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34
Q

what happens with severe hyperkalemia

A

serum k very high- inactives na channels (they arrest in their closed inactive state)

ex: K+ in cardioplegia solution arrests the heart in diastole during CPB, K concentration does not allow the cells to repolarize)

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35
Q

decreased serum ca

A

TP becomes more neg
cells depolarize more easily

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36
Q
A
36
Q

hypercalcemia

A

tp increases
cells more resistant to depolarization

ex: IV calcium is given to reduce risk of dysrthyhmias in pt with hyperkalemia (increase gap between RMP and TP)

37
Q

unlike neurons, cardiac myocytes AP have

A

a plateua phase where depolarization is prolonged. this gives cardiac myocytes time to contract, so the heart has enough time to eject stroke volume

38
Q

what nodes do not have a plateau phase

A

SA and AV node

39
Q

5 phases of cardiac AP

A

phase 0= depolarization: Na in
phase 1= inital repolarization: Cl in and K out
phase 2= plateau: ca in and k out
phase 3= repolarization: K out
phase 4= maintence of transmembrane potential: k out and na/k atpase function

40
Q
A
41
Q

how does conduction move

A

sa- intenodal tracts- av- bundle of his- L and R bundle branches- purkinje fibers

42
Q

sa node action potential characteristics

A

3 phases (phase 1 or phase 2)
rmp is higher
na/ k atpase re-establishes na and k gradients after repolarization

43
Q

what cells in myocardium are capable of automaticity

A

all cells! but they all have a diff rate of spontaneous depolraization

44
Q

at rest which autonomic tone takes over

A

pns>sns

45
Q

pns tone uses what nerves

A

vagus nerve (CN 10)

46
Q

what nodes to the R and L vagus nerve innervate

A

R innervates SA
L innervates AV

47
Q

sns tone comes from what nerves

A

cardiac accelerator fibers (t1-t4)

48
Q

what is the intrinsic firing rate of SA

A

70-80 (faster in denervated heart)

49
Q

what is the intrinsic firing rate of AV node

A

40-60

50
Q

what is the inrinsic firing rate of purkine fibers

A

15-40

51
Q

what 3 ways can you alter the HR

A
  1. rate of spontaneous phase 4 depolarization
  2. threshold potential
  3. resting membrane potential
52
Q

what situations (slope changes) increase HR

A
  1. slope of phase 4 depol increases
  2. slope of phase 4 depol remains constant but TP becomes more neg
  3. slope of phase 4 deol remains constant but RMP becomes less neg- shortens distance between RMP and TP so cells reach threshold faster
53
Q

what catecholamine and receptor increases HR by sns tone

A

NE stimulates B1 - increases HR by increasing na and ca conductance - increasing slope of phase 4 (steeper slope)

54
Q

what receptor slows HR (pns activation)

A

acetacholine stimulates m2 receptor- increases k conductance and hyperpolarizes SA node

decrease RMP and reduces slope of spontaneous phase 4 depolariazation (less steep slope)

55
Q

look into oxygen delivery equation

A

dont know

56
Q

what does cao2 tell us

A

oxygen content in the blood- how many grams of o2 is in decileter of arterial blood

most o2 is bound to hgb- small amount is dissolved

57
Q

what law does the amount of gas dissolved in a solution follow

A

henrys law- at a constant temp the amount of gas that dissolves in a solution is directly proportional to partial pressure of that gas

58
Q

whats ohms law

A

forms the basis for understanding hemodynamics

map=( co x svr)/ 80 + cvp

59
Q

poiseullies law

A

an adaptation of ohms law- incorporates vessel diameter, viscosity and tube length

look up formula

60
Q

flow describes

A

movement of liquid, electrict or air per unit time

61
Q

what is the greatest impact on flow

A

altering radius of tube- raises radius to 4th power

62
Q

vascular resistance is primarily determined by

A

radius of arterioles- small changes in vessel diameter can yield big impacts on tissue blood flow

63
Q

what is reyonlds number used for

A

can be used to predict if the flow will be laminar or turbulent

64
Q

what are the numbers to determine reynolds number

A

re < 2,000 predicts that flow will be mostly laminar

re >4000 predicts that flow will be mostly turbulent

re= 2,000- 4,000 suggests transitional flow

65
Q

whats the issue with turbulent flow

A

a lot of energy is lost to heat and vibration

66
Q

vibrations occuring with turbulent flow can produce

A

a murmur (valvular ht disease) or bruit (carotid stenosis)`

67
Q

viscosity

A

result of friction from intermolecular forces as fluid passes through a tube. blood viscosity is determined by hct and body temp

68
Q

viscosity is inversely proportional to

A

temp. a cooler temp increases viscosity and resistance

69
Q

how does viscosity relate to administering rbcs

A

can improve flow- can dilute the unit with normal saline (decreased hct) by running it through fluid warmer (inc temp)

70
Q

CO

A

hr x sv

5-6 L/min

71
Q

CI

A

co/ bsa

2.8-4.2 L/min

72
Q

sv

A

edv- esv

50-110 ml/beat

73
Q

sv index

A

sv/ bsa

30-65 ml/beats per min2

74
Q

ejection fraction

A

edv- esv / edv x 100
60-70%

75
Q

normal map

A

70-110

76
Q

pulse pressure

A

sbp-dbp

40

77
Q

svr

A

map- cvp/ co x 80

800-1500 dynes x sec x cm5

to do svr index just replace co with ci

78
Q

pvr

A

mpap - paop / co x 80

150-250 dynes x sec x cm5

79
Q

sarcomere

A

the functional unit of contractile tissue in the heart. the amount of tension that each sarcomere can generate is directly r/t the number of cross brides that can be formed before contraction

80
Q

the greater the tension the ___ the force of contraction

A

greater- up to a point!

81
Q

preload

A

ventricular wall tension at end of diastole (just before contraction

often interchangable with ventricular end diastolic volume

82
Q

what curve tells reltionship between ventricular volume and ventricular output

A

frank starling

83
Q

is contractility dependent on PL and AL

A

no

inc PL= inc force of contraction (starlings law) not the same as increased contractility!

contractility is the ability of myocardial sarcomeres to perform work (shorten and produce force)

84
Q

atrial kick contributes to __ % of CO

A

20-30

85
Q

when would you be reliant on atrial kick

A

a non compliant stiff ventricle

86
Q

conditions associated with reduced myocardial compliance

A

myocardial hypertrophy, HF with pEF, fibrosis, aging

more likely to see lower CO, cardiac rhythm disturbances, afib, junctional rhythm

87
Q
A

october exam (12 decks)

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