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Biol 1190 > lecture 13 > Flashcards

lecture 13 Flashcards

1
Q

how many times a day does the heart beat?

A

100 000 times

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2
Q

study of the heart

A

cardiology

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3
Q

apex

A

pointed tip that rests on the diaphragm

formed by most inferior point of left ventricle

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4
Q

base

A

formed by the atria

opposite of apex

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5
Q

pericardium layers (make up, facts, positions) 3

A

fibrous
- inelastic dense irregular CT
- fused with central tendon
- prevents heart form overstretching, anchors heart in position

serous
- deep to fibrous
- two layers, parietal and visceral serous pericardium

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6
Q

pericardial cavity

A

space between parietal and visceral layers
- filled withs serous fluid that reduced friction between the heart and its layers

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7
Q

heart wall

A
  • deep to fibrous pericardium
  • 3 layers: epicardium, myocardium, endocardium
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8
Q

epicardium

A

most superficial layer of heart wall

AKA visceral pericardium
- serous membrane, holds fat
- thicker over ventricles (left especially)
- rich with vessels (blood/lymph)

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9
Q

myocardium

A

intermediate layer of the heart wall

  • made of cardiac muscle tissue
  • 95% of the heart wall
  • wrapped in endomysium and perimysium
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10
Q

endocardium

A

deepest layer of the heart wall
- made of endothelium
- lines chambers and valves
- continuous with blood vessel lining
- reduced friction

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11
Q

auricles

A

increase the volume of blood in each atrium

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12
Q

sulci

A

grooves that provide passage for the coronary arteries

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13
Q

right atrium receives blood from:

A

superior / inferior vena cava
coronary sinus

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14
Q

fibrous skeleton of the heart

A

four rings of dense CT encircle the heart valves and fuse at the interventricular septum

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15
Q

fibrous rings of the heart function

A
  • prevent overstretching
  • insertion points for cardiac muscles
  • electrical insulation between atria and ventricles
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16
Q

how do valves work?

A

blood moves from high to low pressure.

when ventricles contract, papillary muscles pull the chordae tendineae tight. pressure of blood pushes the valves closed

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17
Q

how do the semilunar valves work?

A

during contraction, blood moves from high to low pressure. after contraction, pressure is higher in the arteries, which pushes the valves closed

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18
Q

coronary vessels

A

blood vessels that service the heart

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19
Q

coronary arteries

A

blood from ascending aorta after contraction flows into these

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20
Q

coronary veins

A

drains into coronary sinus which empties to right atrium

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21
Q

cardiac muscle tissue facts

A
  • branched
  • mononucleated
  • striated
  • lots of mitochondria
  • intercalated discs
  • autorhythmic
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22
Q

cardiac muscle compared to skeletal

A

cardiac
- more/bigger mitochondria
- less but bigger t tubules
- smaller sarcoplasmic R
- make calcium from Interstitial fluid

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23
Q

cardiac conduction system formation

A

1% of cardiac muscle cells become autorhythmic

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24
Q

how does cardiac conduction work? 5 steps

A
  1. sinoatrial node
  2. atrioventricular node
  3. action potential
  4. signal travels branches
  5. signal reaches purkinjie fibres
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25
Q

sinoatrial node

A

pacemaker of the heart
- generates spontaneous action potentials
- stimulates synchronous contraction of the atria

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26
Q

atrioventricular node

A

in interatrial septum
- receives slowly transmitted signal from SA node

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27
Q

why is the signal between heart nodes delayed

A

high resistance between SA and AV nodes

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28
Q

purkinjie fibres

A

end of the electrical fibres in the heart

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29
Q

AV bundle

A

below AV node

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30
Q

cardiac action potential phases (3)

A

depolarization
plateau
repolarization

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31
Q

depolarization

A

opens voltage gated sodium channels, membrane becomes positive (actually positive not just less negative)

also opens voltage gates calcium channels

32
Q

plateau

A

unique to cardiac muscle
due to depolarization opening voltage gates calcium channels as well

rate of Ca2+ entry = rate of K+ exit = plateau of membrane potential

33
Q

repolarization

A

once signal has passes, sodium and calcium channels close, and K+ is transported out of the cell, restoring membrane potential

34
Q

refractory period

A

length of time that cell cannot response to another action potential

because at peak depolarization, sodium channels are plugged, even though the channel is open

longer than time of contraction to permit the heart to fill with blood before contracting again

35
Q

tetanus

A

sustained muscle contraction (eg, lockjaw)
individual twitch contractions are not distinguishable from one another

cause by bacterial infection that secretes a toxin that blocks the release of neurotransmitters that promote the relaxation of muscles

36
Q

how do cardiac muscle cells make ATP to contract and why

A

aerobic cellular respiration

they have lots and fucking huge mitochondria

37
Q

systole

A

when the atria or ventricles contract

38
Q

diastole

A

when the heart is relaxed

39
Q

cardiac cycle

A

repeated systole and diastole

40
Q

ECG and what it does

A

electrocardiogram

records changes in electrical currents due to action potentials in the heart muscles

41
Q

ECG points of interest

A

P wave
P-Q interval
QRS complex
T wave

42
Q

P wave

A

triggers atrial systole
- atrial muscle cells are in depolarization after being signalled by the SA node
- contraction of atria occurs AFTER the P wave

43
Q

P-Q interval

A

time between P wave and QRS complex
- the time for action potential to travel from SA node to the AV node
- atrial systole is happening here

44
Q

a longer P-Q interval could be due to:

A

heart damage

45
Q

QRS complex

A
  • measures rapid depolarization of ventricular muscle fibres
  • once signal has moved to the septum, Q wave starts
  • stimulates ventricular systole
46
Q

T wave

A
  • measures ventricular repolarization
  • starts at the apex
  • slower that depolarization
  • leads to ventricular diastole
47
Q

blood pressure

A

The force of blood on the walls of the cardiovascular system

48
Q

auscultation

A

act of listening for heart sounds using a stethoscope

49
Q

4 major heart sounds

A

s1 - as AV valve closes
s2 - as semilunar valve closes
s3 - ventricular filling
s4 - atrial filling

50
Q

what are heart sounds?

A

blood turbulence

51
Q

S1

A

Atrioventricular valve closing sound

52
Q

S2

A

semilunar valves closing sound

53
Q

S3

A

ventricular filling sound

may to too quiet to hear

54
Q

S4

A

atrial filling sound

may be too quiet to hear

55
Q

cardiac output

A

volume of blood pumped out of the ventricles per minute

56
Q

stroke volume

A

volume of blood pumped by the ventricles per contraction

57
Q

heart rate

A

the number of heart beats per minute

58
Q

cardiac output (CO) calculation

A

CO = SV x HR

cardiac output = stroke volume x heart rate

L/min = L/beat x beats/min

do not forget to convert units if needed

59
Q

cardiac reserve

A

difference between max cardiac output and cardiac output at rest in on person

avg = 4-5x resting value
elite = 7-8x resting

mainly controlled by heart rate (autonomic nervous system)

60
Q

the heart must response to signals coming from: (2)

A

higher brain centres like the limbic system

sensory receptors
- proprioreceptors
- baroreceptors
- chemoreceptors

61
Q

proprioreceptors

A

sense body movement
(eg. elevating heart rate during warm up)

62
Q

baroreceptors

A

sense changes in blood pressure
(eg. changes in elevation)

63
Q

chemoreceptors

A

sense chemical changes in blood
(eg. elevated CO2)

64
Q

cardiac accelerator nerves

A

stimulate norepinephrine release

output pathway to heart
- increase rate of depolarization in SA/AV nodes - increases heart rate

or

increases contractility of atria and ventricles - increasing stroke volume

65
Q

vagus nerves

A

stimulate acetycholine release

output pathway to heart

decreases rate of depolarization in SA/AV node - decreases heart rate

66
Q

other things that effect heart rate (and therefore CO)

A

hormones (norepinephrine)
cation availability (ones required for cardiac muscle contraction)

age, gender, fitness, temperature

67
Q

maximal heart rate formula

A

Max HR = 220bpm - age (years)

68
Q

why is there a maximum heart rate at which CO stops increasing?

A

to allow the heart enough time to fill with blood

69
Q

how is stroke volume regulated? (3)

A

preload
contractility
afterload

70
Q

preload (and what effects it)

A

1 way SV is regulated

measure of stretching as the heart fills
two factors affect preload:
- length of diastole
- venous return

71
Q

contractility

A

1 way SV is regulated

strength of myocardial contraction, given a set preload

two things change force of contractions:
- positive inotropic agents
- negative

72
Q

positive inotropic agents

A

part of heart contractility

promote Ca2+ entry during action potentials

increase force of contractions

73
Q

negative inotropic agents

A

part of heart contractility

increases K+ leaving the cell or decreases Ca2+ entering

decreases force of contraction

74
Q

afterload

A

1 way SV is regulated

the pressure of blood required in the ventricles to push the semilunar valves open

75
Q

hypertension

A

high afterload and decreased SV

blood left in the ventricles after systole

76
Q

cardiac hypertrophy

A

enlarged heart

77
Q

both athletes and fatasses may both experience cardiac hypertrophy, why?

A

athletes = training = sigma

fucking fat people = low cardiac reserve , heart has to work harder to keep their lazy asses alive because daily tasks are somehow difficult

Biol 1190 (31 decks)

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