Cardiac cycle and its control Flashcards

1
Q

Function of the cardiac cycle

A
  • Transport nutrients, oxygen and waste products around body
  • Transport hormones (e.g. adrenaline from adrenals)
  • Transfer heat, usually from core to skin
  • Buffer body pH
  • Assist in response to infection
  • Assist in formation of urine-filtration and circulation
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2
Q

Sequences of cardiac cycle:

A
  1. Diastole: AV valves open, blood pools into atria from SVC, IVC and coronary sinus (right) and pulmonary veins (left), flows directly into ventricles
  2. Atrial systole: SAN initiates action potential causing contraction of atria forcing residual blood into ventricles, increases ventricular pressure so AV valves shut
  3. Ventricular contraction: AV and semilunar valves shut as ventricles contract (isovolumetric contraction), rise in pressure causes SL valves to open and blood forced out outflow tract
  4. Both valves close again, ventricles relax reducing pressure causing AV valves to open and filling stage begins again
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3
Q

Define end-diastolic volume or preload

A

Total volume of blood present in ventricles at end of diastole

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4
Q

Define isovolumetric contraction

A

Contraction of ventricle when both valves are shut causing a rise in pressure

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5
Q

Define end-systolic volume (how much is it?)

A

Blood remaining in ventricles at end of ventricular systole
Around 40-50ml

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6
Q

Define stroke volume output

A

Volume of blood ejected from ventricles during ventricular systole

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7
Q

What is the ejection fraction?

A

Ratio of stroke volume output to end-diastolic volume

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8
Q

Define isovolumetric relaxation

A

Both sets of valves closed but area in ventricles increases during diastole causing pressure to decrease, allows AV valves to open

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9
Q

Role of chordae tenidiae and papillary muscles

A

Orientate the AV valves and prevents them from becoming inverted during ventricular systole

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10
Q

What determines opening and closing of valves?

A

Pressure gradient across the valves

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11
Q

Sequence of intitation and conduction of impulse through the heart:

A

SAN -> AVN -> bundle of his -> left/ right bundle branch -> purkinje fibres

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12
Q

What are the pacemaker cells of the heart?

A

SAN = primary pacemaker as has fastest intrinsic rate so determines heart rate
AVN = slows condution and acts as a secondary pacemaker

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13
Q

Describe the sequence of events involved in contraction of cardiac muscle:

A
  • Calcium enters into cardiac muscle from exterior by voltage gated channels which have been opened by depolarising impuse of purkinje fibres
  • Caclium binds to receptors on SR causing more calcium to be release (calcium-induced calcium release) - amplified calcium
  • Calcium binds to troponin C and cardiac muscle sarcomeres contract in same mechanism as skeletal muscle
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14
Q

Describe the phases of an action potential in the heart:

A

Phase 4 (baseline):
- K+ channels open at rest so K+ moves inwards and membrane potential is negative

Phase 0 (fast depolarisation):
- Voltage gated Na+ channels open in response to depolarisation from gap junctions
- Influx of Na+ depolarises cell further causing more Na+ channels to open = steep depolarisation
- Na+ channels inactivated almost immediately and can’t reopen

Phase 1 (notch):
- Reopening of K+ ion channels causes some rapid repolarisation

Phase 2 (plateau):
- Inwards movement of Ca2+ balances outward movement of K+ so no change in membrane potential

Phase 3 (repolarisation):
- Ca2+ channels close, K+ currents repolarise
- Na+ channels recover as membrane potential becomes more negative
- Cycle can now restart

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15
Q

How can heart rate be altered?

A

Action of ACh from vagus nerve increases K+ permeability so takes longer time to reach threshold potential = less BPM

Action of NA: increases Ca2+ permeability, shorter time to threshold = more BPM

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16
Q

What do the different parts of an ECG represent?

A

P wave: atrial depolarisation (contraction of Atria)
QRS complex: ventricular depolarisation (contraction of V)
T wave: ventricular repolarisation (start of ventricular diastole)
P-R interval: delay through AVN
ST interval: plateau pahse of AP, important at allowing tissues to relax and not be reactivated

17
Q

What abnormalities are visible on ECG?

A

Sinus bradycardia
Atrial fibrillation
Ventricular fibrilation
STEMI

18
Q

What determines cardiac output?

A

Heart rate x stroke volume

19
Q

What is Startling’s law?

A

Force of contraction is increases as muscle is stretched in response to filling of chambers
(more blood returning to heart -> more full atria -> increased cardiac output)

20
Q

What adrenoreceptors are mainly found on heart? What binds to them? What are the effects?

A

Mainly B1 receptors which are found on nodal tissue, conduting system and myocardium
Noradrenaline (released by sympathetic nervous system) and adrenaline bind to them
Effects:
- Positive inotropy (force)
- Positive chronotropy (rate)
- Positive lusitroy (speed of relaxation)
- Positive dromotropy (speed of contraction)

21
Q

Role of vagus nerve in altering cardiac output?

A

Terminates on nodal tissue (right vagus on SAN and L vagus on AVN)
Releases ACh which activates M2 receptors which reduce heart rate due to increased K+ permeability.