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Biol 1190 > lecture 13 > Flashcards

lecture 13 Flashcards

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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
sinoatrial node
pacemaker of the heart - generates spontaneous action potentials - stimulates synchronous contraction of the atria
26
atrioventricular node
in interatrial septum - receives slowly transmitted signal from SA node
27
why is the signal between heart nodes delayed
high resistance between SA and AV nodes
28
purkinjie fibres
end of the electrical fibres in the heart
29
AV bundle
below AV node
30
cardiac action potential phases (3)
depolarization plateau repolarization
31
depolarization
opens voltage gated sodium channels, membrane becomes positive (actually positive not just less negative) also opens voltage gates calcium channels
32
plateau
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
repolarization
once signal has passes, sodium and calcium channels close, and K+ is transported out of the cell, restoring membrane potential
34
refractory period
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
tetanus
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
how do cardiac muscle cells make ATP to contract and why
aerobic cellular respiration they have lots and fucking huge mitochondria
37
systole
when the atria or ventricles contract
38
diastole
when the heart is relaxed
39
cardiac cycle
repeated systole and diastole
40
ECG and what it does
electrocardiogram records changes in electrical currents due to action potentials in the heart muscles
41
ECG points of interest
P wave P-Q interval QRS complex T wave
42
P wave
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
P-Q interval
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
a longer P-Q interval could be due to:
heart damage
45
QRS complex
- measures rapid depolarization of ventricular muscle fibres - once signal has moved to the septum, Q wave starts - stimulates ventricular systole
46
T wave
- measures ventricular repolarization - starts at the apex - slower that depolarization - leads to ventricular diastole
47
blood pressure
The force of blood on the walls of the cardiovascular system
48
auscultation
act of listening for heart sounds using a stethoscope
49
4 major heart sounds
s1 - as AV valve closes s2 - as semilunar valve closes s3 - ventricular filling s4 - atrial filling
50
what are heart sounds?
blood turbulence
51
S1
Atrioventricular valve closing sound
52
S2
semilunar valves closing sound
53
S3
ventricular filling sound may to too quiet to hear
54
S4
atrial filling sound may be too quiet to hear
55
cardiac output
volume of blood pumped out of the ventricles per minute
56
stroke volume
volume of blood pumped by the ventricles per contraction
57
heart rate
the number of heart beats per minute
58
cardiac output (CO) calculation
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
cardiac reserve
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
the heart must response to signals coming from: (2)
higher brain centres like the limbic system sensory receptors - proprioreceptors - baroreceptors - chemoreceptors
61
proprioreceptors
sense body movement (eg. elevating heart rate during warm up)
62
baroreceptors
sense changes in blood pressure (eg. changes in elevation)
63
chemoreceptors
sense chemical changes in blood (eg. elevated CO2)
64
cardiac accelerator nerves
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
vagus nerves
stimulate acetycholine release output pathway to heart decreases rate of depolarization in SA/AV node - decreases heart rate
66
other things that effect heart rate (and therefore CO)
hormones (norepinephrine) cation availability (ones required for cardiac muscle contraction) age, gender, fitness, temperature
67
maximal heart rate formula
Max HR = 220bpm - age (years)
68
why is there a maximum heart rate at which CO stops increasing?
to allow the heart enough time to fill with blood
69
how is stroke volume regulated? (3)
preload contractility afterload
70
preload (and what effects it)
1 way SV is regulated measure of stretching as the heart fills two factors affect preload: - length of diastole - venous return
71
contractility
1 way SV is regulated strength of myocardial contraction, given a set preload two things change force of contractions: - positive inotropic agents - negative
72
positive inotropic agents
part of heart contractility promote Ca2+ entry during action potentials increase force of contractions
73
negative inotropic agents
part of heart contractility increases K+ leaving the cell or decreases Ca2+ entering decreases force of contraction
74
afterload
1 way SV is regulated the pressure of blood required in the ventricles to push the semilunar valves open
75
hypertension
high afterload and decreased SV blood left in the ventricles after systole
76
cardiac hypertrophy
enlarged heart
77
both athletes and fatasses may both experience cardiac hypertrophy, why?
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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