Heart Flashcards

1
Q

Automatism and Rythmicity

A

Capacity to generate rhythmic electric signals by itself. FREQUENCY OF CONTRACTION

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2
Q

Excitability

A

Ability to respond to effective stimuli, generating action potentials.

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3
Q

Conductivity

A

Ability to conduct the cardiac stimulus in a controlled and organized way to the neighbouring
cells.

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4
Q

Chronotropism

A

Modification of the heartbeat through external influence

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5
Q

Inotropism

A

Contractility: Each cell’s ability to contract with more or less intensity. Depends on the amount of Ca2+ entering the cells and the length of the fibre before
contraction, Contraction strength

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6
Q

Myogenic

A

the stimulation signal

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7
Q

Modified specialised fibres (4)

A
  • Auto rhythmic cells
  • Sinoartrial node
  • AV node
  • AV bundel of His
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8
Q

Autorythmic cells

A

Fire action potentials spontaneously, act as pacemaker and form the conduction system of the heart.

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9
Q

Sinoartrial (SA) node

A
  • Cluster of cells in the wall of right atrium (anterior to opening of vena cava).
  • Begins heart activity that spreads to both atria.
  • Excitation spreads to atrioventricular (AV) node as well.
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10
Q

AV node

A

Within interatrial septum, transmits signal to the bundle of His.

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11
Q

AV bundle of His

A
  • The connection between atria and ventricles.
  • Divides into bundle branches (right and left) and then into Purkinje fibers, large diameter fibers that quickly conduct signals.
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12
Q

Pacemaker cells

A

Within SA node and AV node

Very small cells capable of generating electrical signals and lack contractile fibres.

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13
Q

Steps of heartbeat

A
  1. SA node connects with the atrial muscle
  2. then spread towards the AV node through the internal pathway
  3. towards atrial myocardium via gap junction
  4. Transmission slows down from atria to ventricle through the bundle of His
  5. this allows for the time- frame between atrial contraction- emptying and ventricular contraction
  6. Signal reaches the Purkinje fibres through subendocardium
  7. this fibres transmit to all cells in ventricular walls
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14
Q

Prepotential (pacemaker potential)

A
  • slow depolarisation
  • opening of Na+ channels
  • Transient ca2+ channels are open: entry of ca2+
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15
Q

DEPOLARIZATION

A
  • Fast depolarization
  • Long-lasting(L-type) Ca2+channels are open:
    fast entry of Ca2+
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16
Q

REPOLARIZATION

A

Opening of slow K+ channels

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17
Q

Which one is the fastest and the real pacemaker of the heart?

A

SA node= Hearts pacemaker

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18
Q

Sympathetic

A
  1. Binding to β1 receptors in pacemaker cells. If channels open for longer time
  2. Na release
  3. increase Na+
  4. increase Ca2+

= faster depolarisation speed, cardiac rate increases

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19
Q

Parasympathetic

A
  1. Binding to ACh receptors (M2) in pacemaker cells
  2. Ach release
  3. increased K+ (Kathi)
  4. decreased Ca2+ (Clari)

= slower depolarisation speed, cardiac rate decreases

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20
Q

TRANSMISSION of AP

A

Contractile cells need a stimulus to generate an action potential.
The stimulus is transmitted from the pacemaker cells through GAP junctions.

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21
Q

Skeletal muscle: potential

A

stable at -70mV (in Form von Arm)

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22
Q

Contractile myocardium: potential

A

stable at -90mV (9 in Form von Herz)

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23
Q

Autorythmic myocardium: potential

A

unstable pacemaker potential, usually starts at -60mV

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24
Q

Skeletal muscle. threshold potential

A

net Na+ entry through Ach channels

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25
Contractile myocardium: threshold potential
Depolarization enters via gap junction (contract/ weitergeleitet über gap junction)
26
Autorythmic myocardium: threshold potential
net Na+ entry through I-funny channels, reinforced by ca2+ entry
27
skeletal muscle: action potential
Na+ entry (Natalia)
28
Contractile myocardium. action potential
Na+ entry (Natalia)
29
Autorythmic myocardium: action potential
ca2+ entry (auto- Clarissa)
30
skeletal muscle: repolarization phase
rapid, caused by k+ (Kathi)
31
contractile myocardium: reploraization phase
extended plateau cause by ca2+ entry, rapid phase caused by k+
32
autorythmic myocardium: depolarisation phase
rapid caused by K+
33
skeletal muscle: hyperpolarization
due to excessive K+ Hugh k+ permeability when k+ channels close, leak of k+ and Na+ restores potential to resting state
34
Contractile myocardium: Hyperpolarization
none: resting potential is -90mV the equilibrium potential for k+
35
Autorythmic myocardium: hyperpolarization
none, when depolarisation hits -60mV the funny channels open again
36
skeletal muscle: duration of action potential
short 1-2 sec
37
Contractile myocardium: duration of action potential
extended 200+ msec
38
autorythmic myocardium: duration of action potential
variable, generally 150+ msec
39
Skeletal muscle: refractory period
generally brief
40
Contractile myocardium: refractory period
Long cause preexisting of Na+ channels gates delayed until end of action potential
41
Autorythmic myocardium: refractory period
none
42
Internodal pathway
Propagation of the AP from the SA node to the atrioventricular (AV) node (100 ms delay) and from there to the bundle of His to the Purkinje fibres: excitation of the myocardium in the ventricle
43
Action potential:
The influx of Ca2+ lengthens the total duration of a myocardial AP. Due to the plateau phase, repolarization in cardiac muscle lasts longer than in neurons or skeletal muscle fibres.
44
Contraction:
Refractory period: time interval during which a second contraction cannot be triggered. In cardiac muscle, the refractory period is longer than contraction. Tetanus (maintained contraction) cannot occur in cardiac muscle.
45
Energy production
The ATP production is mainly aerobic from oxidation of fatty acids and glucose (during rest) and also lactic acid (during exercise).
46
What does prevent cardiac muscle fibres from suffering tetanus?
a longer refractory period
47
On what does the strength of contraction depend on?
on the intracellular calcium
48
p- wave
atrial depolarization
49
PQ or PR segment
conduction through AV node and A-V bundle
50
PQ or PR segment
Conduction continues through the atrioventricular (AV) node and the bundle of His
51
QRS complex
Represents the rapid ventricular depolarisation It starts in the atrioventricular (AV) node - interventricular septum – apex - ventricular layers (from endocardium- pericardium)
52
ST segment
ventricles contract
53
T wave
ventricular repolarization
54
Large P wave
enlargement of an atrium.
55
Large Q wave
could indicate myocardial infarction
56
Large R wave
enlarged ventricle
57
Flat T wave
insufficient oxygen reaching the heart
58
Longer P-Q segment:
presence of scar tissue probably due to coronary artery disease.
59
Elevated S-T segment
acute myocardial infarction
60
Longer Q-T segment
myocardial damage, ischemia (low blood flow).