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Cardiovascular Physiology > L5/6 > Flashcards

L5/6 Flashcards

1
Q

autorhythmicity

A

built-in rhythm of action potentials -> heart contractions

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2
Q

autorhymic fibers function

A

non-contracting pace maker cells (inititate action potentials)

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3
Q

autorhymic fibers location

A
  • SA node
  • AV node
  • AV bundle
  • right/left bundle branches
  • Purkinje fibers
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4
Q

contractile fibers

A
  • delivers action potential via contractions but cannot initiate action potential
  • acts as pacemaker conduction system
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5
Q

propagation of cardiac action potential

A

depolarized SA node -(ap)-> both atria -> atria contraction -(ap)-> AV node -(ap)->AV bundle -(ap)->right & left bundle branches -(ap)-> Purkinje fibers -(ap)-> heart apex -(ap)-> ventircular myocardium -(ap)-> ventricle contraction -(blood)->semilunar valves

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6
Q

peacemaker potential is _mV

A

-60mV

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7
Q

peacemaker potential reaching threshold

A
  1. closed K+ channels & open F-type channels (Na+ permeable) -> almost at threshold
  2. F-type channels close & T-type voltage-gated Cas2+ channels open -> threshold reached
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8
Q

generation of action potentials in contractile fibers

A

opening L-type voltage-gated Ca2+ channels -> generates action potential -> causes contractile fibers to enter depolarizing phase

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9
Q

contractile fibers have a potential of _mV

A

-90mV

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10
Q

contractile fibers depolarizing phase

A

open fast voltage-gated Na+ channels -> +20mV

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11
Q

contractile fibers initial repolarizing phase

A

close fast voltage-gated Na+ channel and open fast voltage-gated K+ channels -> decreased from 20mV

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12
Q

contractile fibers plateau phase

A

close fast voltage-gated K+ channels and partially open slow voltage-gated K+ channels ->constant 10mV

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13
Q

contractile fibers final repolarizing phase

A

fully open slow voltage-gated K+ channels -> -90mV -> close channels

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14
Q

L-type voltage-gated Ca2+ channels close when

A

the final repolarizing phase of contractile fibers has been completed (-90mV)

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15
Q

Excitation-Contraction coupling in cardiac muscle

A

links cardiac action potential to cardiac contraction

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16
Q

calcium-induced calcium release

A

L-type voltage-gated Ca2+ -> increase extracellular calcium concentration (10% required) -> Ca2+ rleased from SR (other 90% required) -> contraction

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17
Q

graded contractions cardiac muscle

A

increase or decreasing contraction of syncytium muslce fibers by manipulating how much Ca2+ is in the sarcoplasm

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18
Q

relaxing cardiac muscle after contraction

A

decrease calcium concentration in the extracellular fluid with Ca2+-ATPase pump

> Ca2+ goes to SR

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19
Q

Cardiac muscle refractory period

A

-very long because of plateau phase

>helps with proper pumping (heart needs to relax and fill with blood)

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20
Q

ATP production

A

aerobic respiration

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21
Q

ECG P

A

atrial depolarization

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22
Q

ECG QRS

A

ventricular depolarizaiton

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23
Q

ECG T

A

ventricular repolairzation

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24
Q

ECG P-Q/P-R

A

atrial ventricular excitation conduction time

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25
Q

ECG S-T

A

Ventricular contractile fibers depolarize/pleateau phase

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26
Q

ECG Q-T

A

Ventricular depolarization to repolarization time

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27
Q

increase Q wave

A

myocardial infraction

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28
Q

increase R wave

A

enlarged ventricules

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29
Q

flat T wave

A

decreased O2 (ex: coronory artery disease)

30
Q

increased T wave

A

hyperkalemia (high K+ in blood)

31
Q

systole

A

phase of contraction

32
Q

diastole

A

phase of relaxation

33
Q

passive ventricular filling

A
  1. atria/ventricule(diastole)-(atria fills with blood from veins)-> atrial pressure > ventricular pressure
  2. AV valves open: atria -(blood)-> ventricules (80% capacity)
  3. SL valves close
    * no muscle contractions *
  4. SA node -(ap)-> atria -> depolaries
34
Q

atrial contraction

A
  1. atrial depolarization -> atrial systole -> contraction -> increased atrial pressure -> opens AV valves
  2. AV valves add remaining 20% of blood to ventricule
35
Q

isovolumetric ventricular contraction

A
  1. ventricules depolarized -> systole (atrial in diastole)-> increased ventricle pressure -> AV vavles close
  2. isovolumetric ventricular contraction when AV and SL vavles are closed
36
Q

ventricular ejection

A
  1. left ventricule > aortic pressure/right ventricle>pulmonary trunk -> SL valves open
    2a. left ventricle -(70mL blood) -> aorta
    2b. right ventricle-(70mL blood) ->pulmonary trunk
37
Q

EDV

A

the filled volume of the ventricle prior to contraction

38
Q

ESV

A

is the residual volume of blood remaining in the ventricle after ejection

39
Q

stroke volume

A

stroke volume = EDV-ESV

volume of blood ejected from each ventricle/contraction

40
Q

ejection fraction

A

ejection fraction = SV/EDV x 100%

percentage of the end-diastolic volume that is ejected with each stroke volume

41
Q

isovolumetric ventricular relaxation

A
  1. ventricular repolarization -> diastole -> relexation -> decreased pressure
  2. vavle cusps collect backflow -> close SL valves
  3. ventricule pressure < atrial pressure -> A.V valves open -> repeat
42
Q

Heart beat steps

A
  • passive ventricular filling
  • atrial contraction
  • ventricular ejection
  • isovolumetric ventricular relaxation
43
Q

lubb & dupp

A

lubb: AV valves closing (louder)
dupp: SL valves closing

44
Q

cardiac output

A

volume of blood ejected from each ventricle/minute

45
Q

heart rate definition

A

number of beats per minute

46
Q

cardiac reserve

A

maximum cardiac output-cardiac output at rest

47
Q

stroke volume preload

A

degree of stretch on heart before it contracts

48
Q

frank-starling law

A

increased stretch leads to increased contraction

49
Q

increased EDV causes

A

increased filling time and increased venous return

50
Q

stroke volume contractility definition

A

forcefulness of contraction of individual ventricular msucle fibers

51
Q

inotropic effects

A

alter contractility
>postivie: increases
>negative: decreases

52
Q

positive inotropic effect mechanisms

A
  1. NE + B1-adrenergiic receptor (sarcolemma)
  2. Gs activates -(stimulates)-> adenylyl cyclase -(produces)-> cAMP
  3. cAMP + protein kinase -> phosphorylates:
    - L-type voltage gated Ca2+ channels -> increased Ca2+ in sacroplasm
    - Ca2+ release channels -> release Ca2+ from SR lumen into sacroplasm
    - phospholamban -> reuptake Ca2+ to SR lumen after contraction to preserve Ca2+ supply
    - myosin heads -> increases rate of crossbridge cycling
  4. increases contractivity
53
Q

negative inotropic effect mechanisms

A

decreases Ca2+ in sarcoplasm to decrease contractility

54
Q

stroke volumme afterload definition

A

pressure that must be exceed before ejection of blood from ventricles
>must open SL vavles

55
Q

increased afterload causes

A

decreased velocity of ventricular muscle fiber shortening

56
Q

chronotropic effects

A

+ -> increases heart rate

- -> decreases heart rat

57
Q

cardiac accelerator nerves and heart rate regulation (ANS)

A

cardiac accelerator nerves: connect sympathetic NS with SA node, AV node and ventricular myocardium

58
Q

Vagus X nerves and heart rate regulation (ANS)

A

connect parasympathetic and heart wall (AV and SA nodes)

59
Q

NE and increased heart rate via SA node increased ap mechanism

A

NE + B1-adrenergic receptors in sarcolemma -> Gs -> increased adenyly cyclase -> increased cAMP + F-type NA+ channels -> Na+ enters cell -> depolarziation -> SA node generate action potentials

60
Q

NE and increased heart rate sympathetic or parasympathetic?

A

sympathetic

61
Q

increasing heart rate via increasing action potential conduction (atria->ventricules) mechanism

A

F-type Na+ channels -> Na+ influx -> depolarize AV node -> fires AP

62
Q

increasing heart rate via increasing action potential conduction (atria->ventricules) sympathetic or parasympathetic?

A

sympathetic

63
Q

increasing heart rate by increasing contractility mechanism

A

NE + B1-adrenergic receptors -> G protein -> increased Ca2+ -> increased contractility

64
Q

increasing heart rate by increasing contractility mechanism sympathetic or parasympathetic?

A

sympathetic

65
Q

decreasing heart rate via Ach mechanism

A

Ach + Gi -> decreased cAMP

Ach + Gi -> opens K+Ach channels -> K+ outflux -> hyperpolarizes -> SA node decreases Ap

66
Q

decreasing heart rate via Ach sympathetic or parasympathetic?

A

parasympathetic

67
Q

decreasing heart rate via decreasing conduction (atria -> ventricles) mechanism

A

K+Ach open -> K+outflow -> hyperpolarizes AV node -> decreases action potentials

68
Q

decreasing heart rate via decreasing conduction (atria -> ventricles) mechanism sympathetic or parasympathetic?

A

parasympathetic

69
Q

heart rate chemical regulation via hormones

A

E and NE

70
Q

heart rate chemical regulation via ions

A

Na+, K+ and Ca2+

71
Q

heart rate chemical regulation via no ions and no hormones

A

age, gender, physical fitness and body temperature

Cardiovascular Physiology (14 decks)

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