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Health.2 > Elec Activity Of The Heart, Regulation Of CO 🫀 > Flashcards

Elec Activity Of The Heart, Regulation Of CO 🫀 Flashcards

1
Q

What is a cardiac muscle cell called?

A

myocyte

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2
Q

What is meant by autorhythmic?

A

myogenic/ self-excitable - cells generate an APl throughout myocardium causing heart to contract as a single unit

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3
Q

What do APs/ current pass through to be conducted to the next myocytes?

A

gap junctions

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4
Q

What are the key organelles within a cardiomyocyte? (7)

A
  • contractile myofilaments
  • T-tubules containing:
  • Na/Ca exchanger
  • L-type Ca2+ channel
  • RyR receptors
  • SERCA pump
  • sarcoplasmic reticulum
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5
Q

role of gap junctions in cardiac myocyte?

A

help generate elec activity of heart = 1 contraction/heart beat
impulses between myocytes

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6
Q

role of calcium stored in the cardiac muscle cell- sarcoplasmic reticulum (SR)?

A

helps contraction of the myofilament

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7
Q

What is an action potential?

A

transient depolarisation as a result of ion channels

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8
Q

What are the 3 broad cardiac action potential patterns?

A
  • SA and AV node AP
  • Atrial muscle AP
  • Purkinje fibres & ventricular muscle AP
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9
Q

Through what 3 characteristics do the 3 broad cardiac action potential patterns differ by?

A
  • duration
  • shape
  • ionic basis
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10
Q

What are the 5 phases of ventricular action potential?

A

1) phase 0: depolarisation
up
2) phase 1: partial repolarisation

3) phase 2: plateau

4) phase 3: repolarisation
down
5) phase 4: resting membrane potential

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11
Q

In phase 0 of ventricular action potentials, what occurs in terms of ion movement? (hint: Na)

A

depolarisation: rapid influx of Na due to opening of Na ion channels

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12
Q

In phase 1 of ventricular action potentials, what occurs in terms of ion movement? (hint: Na, K)

A

repolarisation: closure of Na+ channels, small efflux of K+

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13
Q

In phase 2 of ventricular action potentials, what occurs in terms of ion movement? (hint: Ca, K)

A

plateau phase sustained by :

  • influx of Ca into myocyte
  • efflux of K
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14
Q

In phase 4 of ventricular action potentials, what occurs in terms of ion movement?

A

nothing - this is a stable state with no alteration

resting membrane potential

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15
Q

In phase 3 of ventricular action potentials, what occurs in terms of ion movement? (hint: Ca, K)

A

rapid repolarisation: fast efflux of K, due to closure of Ca channels

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16
Q

how does SA node fiber AP graph differ to ventricular muscle fiber graph?

A

SA: only has 0, 3, 4 phase
learnt in year 1

Ventricular has 0,1,2,3

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17
Q

In phase 0 of SA node action potentials, what occurs in terms of ion movement? (hint: Ca)

A

depolarisation:
VG Ca channels open, fast VG Na are inactivated due to less negative resting potential of these cells = slow conduction velocity used by SA node

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18
Q

In phase 3 of SA node action potentials, what occurs in terms of ion movement? (hint: Ca, K)

A

repolarisation:

inactivation of Ca channels but increase activation of K channels so increase K efflux

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19
Q

In phase 4 of SA node action potentials, what occurs in terms of ion movement? (hint: Ca, K)

A

slow, spontaneous depolarisation due to ‘funny current’ channels: responsible for slow K and Na inward current, different from Na in phase 0 in ventricular AP

fall below threshold

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20
Q

What phase of what type of action potential determines the heart rate?

A

phase 4 of SA node action potentials
slope of repolarisation.
catecholamines more = higher HR

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21
Q

how does atrial muscle depolarisation compare with SA and AV nodes depol?

A

atrial muscle: fastest depol

SA and AV: slow depol

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22
Q

what happens to VG K+ channels in SA node AP when resting potential = -.

A

become permanently inactivated. slow velocity conduction by SA nodes

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23
Q

upstroke in SAN compared with ventricular?

A

upstroke in SAN much slower.

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24
Q

what is rhythm of heart determined by and what is this?

A

pacemaker cell:

excitable cells that generate electrical impulses (autorhythmic) to set the heart rhythm

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25
Q

where are pacemaker cells mainly found?

A

in SA node.

have natural automacity = can gen impulses themselves

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26
Q

Pacemaker cells have an unstable what potential, and what is this also known as?

A

have an unstable resting potential, AKA pacemaker potential

= slow depol towards threshold

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27
Q

The rate of decay of resting potential determines what?

A

Rate of decay of the SA node resting potential determines the rate of AP, and hence HR
heart rate.

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28
Q

When does the pacemaker potential occur?

A

at the end of 1 AP and before the start of the next one - this is the slow depolarisation of pacemaker cells (e.g. SA cells) towards the threshold

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29
Q

What is “cardiac muscle excitation-contraction coupling?”

A

the process whereby AP triggers myocyte to contract

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30
Q

how does AP travel through cardiac myocyte?

A

AP conducted through gap junctions of cardiac myocyte - each has filament for contraction

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31
Q

1st step in cardiac muscle excitation-contraction coupling? (3)

A
  • Na enters into cytosol via channel (red dots)
  • increase in AP
  • Initiates beginning of depolarisation phase
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31
Q

2nd step in cardiac muscle excitation-contraction coupling? (5)

A
  • Depolarisation phase= Ca enters myocyte through L-type channels, stimulating RyR receptor on SR
  • Ca released from SR via RyR into cytosol =plateau phase of ventricular AP
  • Also increase of [Ca], then binds to myofilament
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32
Q

3rd step in cardiac muscle excitation-contraction coupling?

A

contractions take place, Ca released from myofilament after it binds

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33
Q

4th step in cardiac muscle excitation-contraction coupling?

A

repolarisation
decreased Ca and contractions. (relaxation)

Ca leaves via:

  • goes to SR - via SERCA//PLB
  • Na-K (Na-CaX) exchanger. 3 Na come in for 1 Ca out
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34
Q

5th step/ ending summary in cardiac muscle excitation-contraction coupling?

A

cell wants to return to normal AP.
using the ATP on surface,
3Na leave, 2K enter.
helps resting MP.

contract, relax = 1 HR/beat :)

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35
Q

conduction pathway in the heart (5 steps)?

leading to contraction and one elec signal in ECG

A 
SA node
AV node
Bundle of His
Bundle branches
Purkinje fibres
36
Q

general features of ECG trace:

whats happening in P wave?

A

atria depolarise in response to triggering SA node.

first little bump

37
Q

general features of ECG trace:

whats happening in PR interval?

A

delay of AV node to allow filling of ventricles.

line between P bump and QRS complex

38
Q

general features of ECG trace:

whats happening in QRS complex?

A

venticle depolarisation, triggers main pumping contractions

up down up (peak)

39
Q

general features of ECG trace:

whats happening in ST segment?

A

beginning of ventricle repol, should be flat

line right after QRS

40
Q

general features of ECG trace:

whats happening in T wave?

A

ventricular repolarisation

last bump

41
Q

how will ST segment change in myocardial infarction?

A

should be a flat line between QRS complex and final T wave.

increased in MI

42
Q

what does an ECG measure and how?

A

hearts electrical conduction system
detects by electrodes attached under surface of skin

  • elec impulses gen by polarisation and depolarisation of cardiac tissue picked up.
    current transformed to waveforms
43
Q

how can ECG be used as diagnostic tool? what can it detect?

A
  • arrythmias
  • conduction disturbances e.g. left bundle block
  • marked LV hypertrophy
  • MI
    e. g. ST elevation MI (STEMI)
44
Q

purpose of the PR interval?

A

atrial depol + delay in AV junction (AV node/bundle of His)

delay = time for atria to contract before ventricles contract

45
Q

whats a bundle branch block?

A

delay/ blockage along pathway that electrical impulses travel to make your heart beat= harder for heart to pump blood efficiently through body.

greater than 0.12seconds QRS duration

46
Q

Podcast 1: summary of prev

4 stages of cardiac conduction?

A
  1. elec impulse gen at SA node stims atria to contract
  2. impulse-> AV node, brief delay
  3. goes to bundle of his then divides to L and R bundle branches
  4. conduction-> purkinje fibres= contraction of vents
47
Q

how to diagnose normal sinus rhythm?

A

P-QRS-T deflections

48
Q

5 abnormalities of impulse generation/conduction (arrhythmias)

A

sinus:

  • bradycardia
  • tachycardia

heart block:

  • first degree
  • second
  • third
49
Q

sinus bradycardia - values and possible cause?

A

less than 60/min

consequence of inc vagal/parasymp tone

depressed SA node/function

50
Q

sinus tachycardia values and possible cause?

A

100/min or higher rhythm

physiol response to:

  • physcial exercise/stress
  • result from congestive HF
51
Q

heart block: first degree

A

AV block, abnormal slow conduction in AVN= incomplete heart block.
= extended PR interval of more than 0.2s/ one big ECG box!

52
Q

heart block: second degree

what is it and how identified?

A

heart block when fraction of impulses from atrua are conducted.
QRS sometimes present/absent
PQ interval longer

53
Q

heart block: third degree

what is it and how identified?

A

atria and ventricles depolarising independantly
no association between atria and ventricles

complete heart block

54
Q

podcast 2: cardiac cycle

2 basic phases on one cardiac cycle?

A

diastole- vents relaxed

systole- vents contract, eject blood-> aorta and pulmonary artery

55
Q

4 things/mechanisms that happen during single heart beat

A
  • elec activity
  • mechanical activity
  • pressure changes
  • volume changes
56
Q

4 phases of cardiac cycle?

2-4: systole (inc in pressure, dec in volume)
5-7: diastole (dec pressure, inc volume)

A

1: atrial contraction
2: isovolumetric contraction
3: rapid ejection
4: reduced ejection
…
5: isovolumetric relaxation
6: rapid filling
7: reduced filiing

57
Q

What is heart failure?

A

inability of heart to supply adequate blood flow + oxygen delivery to peripheral tissues and organs.
Under perfusion of organs -> reduced exercise capacity, fatigue, and shortness of breath.
can also-> organ dysfunction (e.g., renal failure) in some patients.

58
Q

What are the causes of heart failure?

A

coronary artery disease
high BP
previous heart attack
valve disease, thyroid disease, kidney disease, diabetes, or heart defects present at birth

59
Q

Podcast 3: physiol factors that regulate CO

whats CO and how calculated?

A

amount blood pumped by heart/min

CO= HR x SV
CO= HR x (EDV-ESV)
60
Q

whats normal CO in 70kg man?

A

5L/min

CO=70kg x (120-50)
= 70min-1 x 70ml
= 5Lmin-1

61
Q

how much can exercise inc CO to?

A

normal: 5L…. inc to 25L/min

62
Q

why do ventricles contract?(SV in CO)

A

= sufficient pressure to eject blood-> aorta

63
Q

2 things involved in regulation of HR?

and affect?

A
  1. autonomic- on SA node:
    sympathetic = ⬆ HR (faster depol)
    parasymp = ⬇ HR (slower depol)
  2. excitation-contraction (EC) coupling
64
Q

what are chronotropic agents?

A

influence currents and slope of pacemaker, thus HR

e.g. NE (peak to left) increases slope of pacemaker potential
ACh (peak to right) reduces slope of pacemaker potential

65
Q

2 types of chronotropic agents and role and examples?

A

positive: increase contractility
- digoxin

negative: decrease contractility
- B blockers (propanolol)

66
Q

affect of Ca binding to myofilament/ cardiac myocyte?

A

negative chronotropic effect

decr HR

67
Q

what does EC coupling procedd trigger?

A

whereby AP triggers myocyte to contract

68
Q

wheres Ca2+ stored in cardiomyocyte?

and where released to?

A

SR
released into cytosol (RyR2 channel),
can go back into SR (SERCA pump)

69
Q

another factor role in EC coupling? hormones?

A 
bind to B receptor,
cAMP
cAMP dependant phosphokinase A
phosphorylation
Troponin I
...
Troponin C-> complex, Ca into something via ATP...
70
Q

SV=…?

A

SV = EDV (120ml) - ESV (50ml)

amount blood pumped by vent during each heart beat = filled vol of vent before contraction - vol blood left after ejection

71
Q

what factors influence SV?

A

preload…. then afterload

72
Q

whats

  • preload
  • afterload?
A
  • vol blood entering ventricles

- resistance- in arteries as blood leaves left venticle

73
Q

What is after load? simply

A

pressure in the wall of the ventricle during ejection

74
Q

What is another term given to contractility?

A

inotropy

75
Q

What is contractility determined by?

A

contractile machinary of myocardial striated muscle

76
Q

when may preload increase?

A

hypervolaemia- fluid overload in blood- due to inc body Na contract- initial prior to contraction

inc venous pressure, dec inotropic effect, dec HR

77
Q

when may afterload increase?

A

during hypertension, vasoconstriction

affect: inc aortic pressure= inc afterload of LV.

78
Q

Factors influencing SV: what does frank starling mechanism describe?
whats effect due to?

A

relationship between EDV and SV

effect due to heart muscle fibres responding to stretch by contracting more forcefully
NOT DUE to ELASTIC effect but due to IND EXPOSURE of ATP energy

79
Q

whats force of ventricular muscle fibres dependant on?

A

length of ventricular muscle fibres in diastole

inc EDV= inc muscle fibre length
inc ventricle contractility (inc Ca2+ sensitivity) and SV

80
Q

frank starling mechanisms- requirement for greater SV?

A

increase EDV= inc SV

vent contract more forcefully= eject more

81
Q

What can a QRS duration greater than 0.12 seconds indicate?

A

bundle branch block

82
Q

What can the PR interval reveal?

A

AV conduction problems i.e. heart block

83
Q

what happens to frank starling curve (ventricular EDV/ stroke vol)(ml) in
a- exercise
b- HF patient

A

a- inc symp tone= inc SV, inc B receptors stim= inc contractility
b- inc EDV dec SV dec cardiac function and contractility. inasequate for tissues

84
Q

podcast 4: CO changes in exercise, hypertension, HF

what factors control CO?

A

HR

  • parasymp -
  • symp +

SV

  • symp +
  • EDV+ from venous return +
85
Q

exercise and CO look at goodnotes diagrams

page 46,48 on s1w7

A
86
Q

what drugs are vasodilators and decrease BP?

A

ACE1 act on RAAS

alpha blockers inhib vasoconstriction from symp tone

87
Q

what drugs increase BP?

A

B blockers- symp + chronotropy
diuretics- inc Na+ reabs= inc CO and bp
CCB- inc vasoconstriction, TPR, BP

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