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Physiology > Test 1, Deck 2 > Flashcards

Test 1, Deck 2 Flashcards

1
Q

Refractory characteristics of slow vs fast APs

A

slow- time dependent- Ca2+ - longer

fast- voltage dependent- Na+

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2
Q

R on T phenomenon- PVCs

A

a premature beat (R wave) occurs during the relative refractory period of the previous beat (T wave)
aka premature ventricular contraction
- PVCs= polymorphic ventricular tachycardia

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3
Q

what is special about the refractory period of the AV node

A

have post-repolarization refractoriness

  • protects the ventricles during atrial fibrilation
  • depends on Ca2+ channels
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4
Q

In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation?

A

AV node refractory characteristics

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5
Q

How do you slow ventricular rate in patient with atrial fibrilation?

A

Calcium channel blocker or Beta blocker

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6
Q

as HR goes up, which part of the cardiac cycle shortens most

A

diastole

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7
Q

action potential duration equals what part of the cardiac cycle and what part of the EKG

A

systole

Q-T

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8
Q

what causes prolonged Q-T syndrome (T wave is super late)

A

acquired- bradycardia, hypokalemia, quindine
congenital- defects in sodium and potassium channels

e.g. Torsades (doesn’t repolarize normally is AP is too long, can be initiated by R on T)

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9
Q

hierarchy of cardiac pacemaker activity

A

arranged based on inherent beating rate:

SA node > latent atrial pacemakers > AV nodal/His bundle (junctional) > bundle branches > Purkinje’s

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10
Q

diastolic depolarization- SA node

A
  • T-type Ca current (at - voltages, Ca in)
  • hyperpolarization-activated inward current od sodium (funny channels)
  • deactivation of K+ current
  • inward Na/Ca exchanger
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11
Q

diastolic depolarization- Purkinje fibers

A
  • hyperpolarization-activated inward current of sodium (funny channels)
  • deactivation of K+ current
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12
Q

things that change heart rate

A

1- slope of diastolic depolarization
2- change in maximum diastolic potential (resting potential)
3- change in threshold
4- change of pacemaker

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13
Q

how would vagal nerve stimulation affect an EKG recording?

A

would have a longer R-R (less bpm)

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14
Q

what is sinus arrhythmia

A

variability in pacemaker cycle length caused by respiratory changes
inspiration- increase HR- inhibits PS nerve activity
expiration- decreases HR- stimulate PS nerve activity

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15
Q

heart rate is slower during expiration/inspiration

A

expiration

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16
Q

molecular reasons for cardiac arrhythmia

A

impulse formation, conduction, or both

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17
Q

electrical mechanisms responsible for dysrhythmias

A

altered automaticity, re-entry of excitation, triggered activity

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18
Q

causes of tachy-dysrhythmias

A

NE (sympathetics)
stimulants (caffeine)
stretching (aneurism)
sick sinus syndrome, fever, hyperthyroidism (BUSH)

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19
Q

causes of brady-dysrhythmias

A 
drugs (beta blockers, calcium channel blockers, digitalis) 
barbiturates, anesthetics
ishchmia/infarct
sick sinus syndrome
aging
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20
Q

causes of re-entry excitations

A

ischemia
infarction
congenital bypass tracts (WPW)

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21
Q

causes of DADs

A 
"Delayed afterdepolarization" 
digitalis
elevated catecholamines
rapid heart beat
EVERYTHING TOGETHER
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22
Q

causes of EADs

A 
"Early after depolarization" 
acidosis (ischemia) 
hypokalemia
quinidine
slow heart rates
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23
Q

3 requirements for re-entry of excitation

A

1- geometry for conduction loop
2- slow or delayed conduction
3- unidirectional conduction block

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24
Q

anti-arrhythmic therapies

A

1- drugs (Ca channel blockers, beta blockers)
2- radio frequency ablation
3- DC cardioversion
4- implantable cardioverter-defibrillator

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25
Q

PR interval length

A

0.12-0.2 seconds

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26
Q

QRS complex length

A

0.07-0.1 seconds

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27
Q

QT interval length

A

0.25-0.43 seconds

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28
Q

cardiac E-C coupling steps (CICR)

A

1) AP goes down into T-tubules
2) Depolarization activates L-type Ca2+ currents on sarcolemma & t-tubule membrane
3) Influx of Ca2+ binds to SR and opens Ryr channels
4) Released Ca2+ binds to troponin C
5) Relaxation occurs when Ca2+ is removed

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29
Q

structure-function EC coupling: sarcolemma

A
  • propagates action potentials

- controls Ca2+ influx via slow inward Ca2+ current

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30
Q

structure-function EC coupling: T-tubules

A
  • transmits electrical activity to cell interior

- located at Z-lines

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31
Q

structure-function EC coupling: SR, terminal cisternae

A
  • where Ca2+ influx triggers opening of Ca2+ release channels
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32
Q

structure-function EC coupling: SR, longitudinal cisternae

A
  • cite of Ca2+ re-uptake to initiate relaxation
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33
Q

structure-function EC coupling: troponin C

A
  • Ca2+ receptor on actin (contractile protein)
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34
Q

cardiac vs skeletal muscle: size, connection, activation

A

size: cardiac are much smaller
connection: cardiac are electrically coupled (syncytium) vs individual muscle cells
activation: cell to cell conduction vs Ach transmission at NMJs

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35
Q

cardiac vs skeletal muscle: contraction, contraction amplitude, summation, metabolism

A

contraction: CICR vs voltage-sensors on Ca2+ channels
amplitude: Ca2+ influx and SR content vs frequency of APs
summation: no summation vs tetanus
metabolism: aerobic (35%mit) vs anaerobic (2% mit)

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36
Q

what is contractility, and can you change the strength of a contraction without changing it?

A

contractility- the inherent ability of actin and myosin to form cross-bridges and generate contractile force; determined by intracellular Ca2+
YES

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37
Q

what are catecholamines

A

NE (neurotransmitter) and E (hormone)

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38
Q

mechanism of catecholamines

A

1) bind to Beta1 receptors on sarcolemma
2) activation adenyl cyclase to increase cAMP
3) cAMP activates PKA
4) PKA phosphorylates lots of stuff

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39
Q

what does PKA phosphorylate in the catecholamine cascade?

A

1- Ca2+ channels- increases calcium influx
2- phospholamban- increases SRCA rate (relaxation)
3- troponin I- reduces troponin C’s affinity for calcium

1&2 increase strength of contraction
2&3 decrease time course of relaxation

40
Q

mechanism of calcium channel blockers

A

1- plugs up Ca+ influx
2- decreases SR release of Ca2+- leads to less contraction (VASODILATION)
3- inhibition of slow inward Ca2+ channel inhibits conduction of AV node, blocks SVT

41
Q

3 factors that change muscle contraction via a change in contractility

A

1) catecholamines- sympathetics
2) cardiac glycosides (dig)
3) Ca2+ channel blockers (vasodilator, blocks SVT)

42
Q

Cycle length influences contraction amplitude by altering _______ by altering the time available for intracellular Ca2+ handling

A

contractility

43
Q

positive staircase- as heart rate increases, the strength of the contraction ____

A

increases

- greater Ca2+ influx at higher HR, less time for Ca2+ efflux; increased SR content and release

44
Q

premature beat results in a ___ than normal contraction

A

smaller

  • less time for recovery of slow inward Ca2+ current & SR release channels & re-organization of terminal cisternae
  • gives you a smaller CICR release
45
Q

what is a PESP

A

post-extrasystolic potentiation

  • stronger than normal contraction of the heart following a premature beat
  • more time for recovery of Ca2+
46
Q

signs of A-fib w/ radial pulse

A

fast heart rate (tachycardia), irregular speed of heart rate, force for each beat is different

    • because of force-frequency relationship, different amounts of Ca2+ causing different forces of contraction
    • skipped beat is b/c not enough pressure to open aortic valve
    • thumping is a PESP
47
Q

contractility of the heart is ____ with a premature beat

A

reduced

48
Q

turn on an electric stimulator (in a lab) to increase heart rate, what does it look like?

A

premature beat (but think stair-case effect- slowly recovers)

49
Q

four factors that determine cardiac output

A

1) heart rate
2) myocardial contractility
3) preload
4) afterload

50
Q

what is preload dependent on?

if preload were low, what would the treatment be?

A
  • end-diastolic volume (the amount of ventricular filling)
  • generates passive tension
  • give more volume
51
Q

afterload is any force that _____

A

resists muscle shortening e.g. arterial pressure

the load on the muscle after contraction is initiated

52
Q

a premature beat is a _____ contraction

A

isometric

53
Q

if compliance is low, the tissue is _____; aka _____

A

stiff; heart

54
Q

the slope of the resting tension curve is primarily determined by

A

muscle compliance

55
Q

the slope of the active tension curve is primarily determined by

A

muscle contractility

56
Q

what is resting diastolic tension

A

the amount of tension that develops passively by stretching the muscle (increasing preload)

initial myocardial fiber length= EDV

57
Q

what is active systolic tension

A

the amount of isometric tension that is developed by muscle contraction at a particular preload

58
Q

stretching cardiac muscle …

A

a) creates more optimal overlap between the thick and thin filaments
b) increases Ca2+ sensitivity of myofilaments

59
Q

_____ increases the max slope of the systolic tension curve, and _____ decreases it

A

sympathetics; heart failure

60
Q

an increase in preload ____ the amount of muscle shortening

A

increases

61
Q

an increase in afterload ___ the amount of muscle shortening

A

decreases

62
Q

A positive increase in contractility changes what? (tension, relaxation, muscle shortening, velocity of shortening)

A
  • raises peak isometric tension
  • enhances the rate of relaxation (sympathetics)
  • increases the amount of muscle shortening
  • increases the velocity of shortening
63
Q

afterload is synonymous with what

A

force

64
Q

increasing afterload

A

decreases the velocity of muscle shortening

decreases the amount of muscle shortening

65
Q

at a given afterload, an increase in preload

A

shifts the curve right; increases the velocity of shortening and the max isometric force

66
Q

at a given afterload, an increase in contractility

A

shifts the curve up and to the right; increases the velocity of shortening and the max isometric force

67
Q

EKG inferior view of the heart

A

leads 2, 3 and aVF

68
Q

EKG lateral view of the heart

A

leads 1, aVL, V5, V6

69
Q

EKG anterior view of the heart

A

leads V3, V4

70
Q

EKG septal view of the heart

A

leads V1, V2

71
Q

which electrode is most parallel to mean frontal plane vector? and which direction is it in?

A

II, down and left

72
Q

order of ventricular depolarization

A

interventricular septum (down-right), apical depolarization (down-left), endocardial surface (down-left)

73
Q

why is the vector of repolarization the same as depoarlization?

A
  • repo starts where depo ends

- repo goes from positive to negative, so vector is switched

74
Q

what is the last part of the heart to depolarize?

A

epicardial surface of the left ventricle

75
Q

where is the AP slower- endo or epi- and why?

A

endocardial surface- it has less Ito K+ channels, repolarization takes longer

76
Q

normal angles for Einthoven’s triangle

A

-30* - 105*

77
Q

if the mean frontal plane vector is more negative than -30, which kind of deviation is it?

A

left axis

78
Q

how to use hexaxial reference to approximate the MFPV

A

1- pick smallest recording of the 12
2- take line perpendicular to that
3- see if that line is + or - (pointing right or left)
4- use that line to approximate vector

79
Q

einthoven triangle method

A

1- sum blocks up and down for q+rs+t for two leads (1+3=2)

2- plot value on triangle

80
Q

things that skew MFPV

A

left ventricular hypertrophy
pulmonary hypertension
bundle branch block (right deviation w/ right block)

81
Q

which part of conduction does hypokalemia affect most and what happens?

A

Purkinje fibers- AP lengthens and u wave pops out

U wave- after T, repolarization of purkinjes

82
Q

if all the QRS complexes are taller, what do you suspect?

A

hypertrophy- more cells= more current

83
Q

phases of the cardiac cycle

A 
atrial systole (last squeeze)
isovolumic contraction (**all valves closed)
ejection- rapid and reduced
isovolumic relaxation
filling- rapid & reduced
84
Q

units for pressure, aortic blood flow, ventricular volume, time

A

mm Hg (0-120)
L/min (0-5)
ml (20-38)
0-0.8 seconds

85
Q

ACV waves

A

A- atrial contraction
c- ventricular contraction
v- filling & emptying of atrial chamber

86
Q

3rd heart sound

A

rapid filling of blood into a heart that dilated

87
Q

4th heart sound

A

vigorous contraction of atria pumping into ventricle

88
Q

systolic murmur

A
  • stenosis of aortic/pulmonic valve
    or
  • insufficient/incompetent mitral/tricuspid valve
89
Q

diastolic murmer

A

-stenosis of mitral/tricuspid valve
or
-insufficient aortic/pulmonic valve

90
Q

physiological splitting

A

Aortic valve followed by pulmonic valve during inspiration (negative pressure caused by inspiration pulls right ventricle out, filling takes longer- negative pressure differential; more preload)

91
Q

paradoxical splitting

A

Pulmonic followed by aortic due to left bundle branch block (come closer together during inspiration)

92
Q

persistent splitting

A

right bundle branch block- becomes exaggerated with inspiration

93
Q
  • cardiac index and units

- venous pressure

A
  • 2.5-4.0 (3.1)
    litres/min/sq m
  • 3-8 mm Hg
94
Q

right atrial pressure
right ventricle pressure (systolic)
right ventricle pressure (end-diastolic)

A

-2-5 (2)
18-30 (25)
-5-5 (2)

95
Q

Pulmonary artery systolic, diastolic, mean

A

18-30 (25)
6-12 (10)
10-20 (15)

96
Q

Pulmonary wedge pressure

left atrial pressure

A

0-12 (6)

97
Q

left ventricle- systolic

left ventricle- diastolic

A

100-140 (120)

85-105 (95)

Physiology (22 decks)

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