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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
where are pacemaker cells mainly found?
in SA node. | have natural automacity = can gen impulses themselves
26
Pacemaker cells have an unstable what potential, and what is this also known as?
have an unstable resting potential, AKA pacemaker potential = slow depol towards threshold
27
The rate of decay of resting potential determines what?
Rate of decay of the SA node resting potential determines the rate of AP, and hence HR heart rate.
28
When does the pacemaker potential occur?
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
29
What is "cardiac muscle excitation-contraction coupling?"
the process whereby AP triggers myocyte to contract
30
how does AP travel through cardiac myocyte?
AP conducted through gap junctions of cardiac myocyte - each has filament for contraction
31
1st step in cardiac muscle excitation-contraction coupling? (3)
- Na enters into cytosol via channel (red dots) - increase in AP - Initiates beginning of depolarisation phase
31
2nd step in cardiac muscle excitation-contraction coupling? (5)
- 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
32
3rd step in cardiac muscle excitation-contraction coupling?
contractions take place, Ca released from myofilament after it binds
33
4th step in cardiac muscle excitation-contraction coupling?
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
34
5th step/ ending summary in cardiac muscle excitation-contraction coupling?
cell wants to return to normal AP. using the ATP on surface, 3Na leave, 2K enter. helps resting MP. contract, relax = 1 HR/beat :)
35
conduction pathway in the heart (5 steps)? | leading to contraction and one elec signal in ECG
``` SA node AV node Bundle of His Bundle branches Purkinje fibres ```
36
general features of ECG trace: | whats happening in P wave?
atria depolarise in response to triggering SA node. first little bump
37
general features of ECG trace: | whats happening in PR interval?
delay of AV node to allow filling of ventricles. line between P bump and QRS complex
38
general features of ECG trace: | whats happening in QRS complex?
venticle depolarisation, triggers main pumping contractions up down up (peak)
39
general features of ECG trace: | whats happening in ST segment?
beginning of ventricle repol, should be flat line right after QRS
40
general features of ECG trace: | whats happening in T wave?
ventricular repolarisation last bump
41
how will ST segment change in myocardial infarction?
should be a flat line between QRS complex and final T wave. increased in MI
42
what does an ECG measure and how?
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
how can ECG be used as diagnostic tool? what can it detect?
- arrythmias - conduction disturbances e.g. left bundle block - marked LV hypertrophy - MI e. g. ST elevation MI (STEMI)
44
purpose of the PR interval?
atrial depol + delay in AV junction (AV node/bundle of His) delay = time for atria to contract before ventricles contract
45
whats a bundle branch block?
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
Podcast 1: summary of prev 4 stages of cardiac conduction?
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
how to diagnose normal sinus rhythm?
P-QRS-T deflections
48
5 abnormalities of impulse generation/conduction (arrhythmias)
sinus: - bradycardia - tachycardia heart block: - first degree - second - third
49
sinus bradycardia - values and possible cause?
less than 60/min consequence of inc vagal/parasymp tone depressed SA node/function
50
sinus tachycardia values and possible cause?
100/min or higher rhythm physiol response to: - physcial exercise/stress - result from congestive HF
51
heart block: first degree
AV block, abnormal slow conduction in AVN= incomplete heart block. = extended PR interval of more than 0.2s/ one big ECG box!
52
heart block: second degree | what is it and how identified?
heart block when fraction of impulses from atrua are conducted. QRS sometimes present/absent PQ interval longer
53
heart block: third degree | what is it and how identified?
atria and ventricles depolarising independantly no association between atria and ventricles complete heart block
54
podcast 2: cardiac cycle 2 basic phases on one cardiac cycle?
diastole- vents relaxed | systole- vents contract, eject blood-> aorta and pulmonary artery
55
4 things/mechanisms that happen during single heart beat
- elec activity - mechanical activity - pressure changes - volume changes
56
4 phases of cardiac cycle? 2-4: systole (inc in pressure, dec in volume) 5-7: diastole (dec pressure, inc volume)
1: atrial contraction 2: isovolumetric contraction 3: rapid ejection 4: reduced ejection ... 5: isovolumetric relaxation 6: rapid filling 7: reduced filiing
57
What is heart failure?
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
What are the causes of heart failure?
coronary artery disease high BP previous heart attack valve disease, thyroid disease, kidney disease, diabetes, or heart defects present at birth
59
Podcast 3: physiol factors that regulate CO whats CO and how calculated?
amount blood pumped by heart/min ``` CO= HR x SV CO= HR x (EDV-ESV) ```
60
whats normal CO in 70kg man?
5L/min CO=70kg x (120-50) = 70min-1 x 70ml = 5Lmin-1
61
how much can exercise inc CO to?
normal: 5L.... inc to 25L/min
62
why do ventricles contract?(SV in CO)
= sufficient pressure to eject blood-> aorta
63
2 things involved in regulation of HR? | and affect?
1. autonomic- on SA node: sympathetic = ⬆ HR (faster depol) parasymp = ⬇ HR (slower depol) 2. excitation-contraction (EC) coupling
64
what are chronotropic agents?
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
2 types of chronotropic agents and role and examples?
positive: increase contractility - digoxin negative: decrease contractility - B blockers (propanolol)
66
affect of Ca binding to myofilament/ cardiac myocyte?
negative chronotropic effect | decr HR
67
what does EC coupling procedd trigger?
whereby AP triggers myocyte to contract
68
wheres Ca2+ stored in cardiomyocyte? | and where released to?
SR released into cytosol (RyR2 channel), can go back into SR (SERCA pump)
69
another factor role in EC coupling? hormones?
``` bind to B receptor, cAMP cAMP dependant phosphokinase A phosphorylation Troponin I ... Troponin C-> complex, Ca into something via ATP... ```
70
SV=...?
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
what factors influence SV?
preload.... then afterload
72
whats - preload - afterload?
- vol blood entering ventricles | - resistance- in arteries as blood leaves left venticle
73
What is after load? simply
pressure in the wall of the ventricle during ejection
74
What is another term given to contractility?
inotropy
75
What is contractility determined by?
contractile machinary of myocardial striated muscle
76
when may preload increase?
hypervolaemia- fluid overload in blood- due to inc body Na contract- initial prior to contraction inc venous pressure, dec inotropic effect, dec HR
77
when may afterload increase?
during hypertension, vasoconstriction affect: inc aortic pressure= inc afterload of LV.
78
Factors influencing SV: what does frank starling mechanism describe? whats effect due to?
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
whats force of ventricular muscle fibres dependant on?
length of ventricular muscle fibres in diastole inc EDV= inc muscle fibre length inc ventricle contractility (inc Ca2+ sensitivity) and SV
80
frank starling mechanisms- requirement for greater SV?
increase EDV= inc SV vent contract more forcefully= eject more
81
What can a QRS duration greater than 0.12 seconds indicate?
bundle branch block
82
What can the PR interval reveal?
AV conduction problems i.e. heart block
83
what happens to frank starling curve (ventricular EDV/ stroke vol)(ml) in a- exercise b- HF patient
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
podcast 4: CO changes in exercise, hypertension, HF what factors control CO?
HR * parasymp - * symp + SV * symp + * EDV+ from venous return +
85
exercise and CO look at goodnotes diagrams | page 46,48 on s1w7
86
what drugs are vasodilators and decrease BP?
ACE1 act on RAAS | alpha blockers inhib vasoconstriction from symp tone
87
what drugs increase BP?
B blockers- symp + chronotropy diuretics- inc Na+ reabs= inc CO and bp CCB- inc vasoconstriction, TPR, BP

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