heart Flashcards

myocardial control mechanisms: explain the mechanisms regulating heart rate, contractility and myocardial oxygen supply

1
Q

primary pacemaker cells in heart

A

SAN (sino-atrial node)

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2
Q

key features of SAN cells

A

no true resting potential, so instead generate regular, spontaneous action potentials

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3
Q

speed at which depolarising current is carried into SAN cell primarily, and method

A

relatively slow by Ca2+ currents as opposed to fast Na+ currents

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4
Q

3 channels regulating heart rate

A

I f (“funny” hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels), I Ca (repolarising transient T-type Ca2+ channel or repolarising long lasting L-type Ca2+ channels), I K (K+ channels)

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5
Q

processes of heart rate action potential generation, and SNS and PSNS influences on cAMP and channels

A

HCN channels switch on during hyperpolarisation, utilising cAMP and drive Na+ influx to initiate depolarisation -> as current rises, T-type then L-type Ca2+ channels open (predominant driver) -> K+ channels open, initating repolarisation -> spontaneous depolarisation that triggers action potential; SNS increases cAMP, I f and I Ca; PSNS decreases cAMP (by I f) and increases I K

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6
Q

electrical excitation causing cardiac contraction in cardiac myocytes pathway

A

action potentials from SAN -> membrane depolarisation of myocytes -> VGCC open -> small release of Ca2+ into cytoplasm -> induces release of Ca2+ from SR by depolarisation or ryanodine receptors (RyR2; Ca-induced Ca-release) -> promotes troponin to initiate contraction

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7
Q

% of free Ca2+ in a cardiac twitch necessary for cardiac contraction from induced influx of Ca2+ current (I Ca) through L-type channels vs Ca-induced Ca-release

A

20-25% vs 75-80%

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8
Q

how is repolarisation of cardiac tissue achieved

A

Na+/Ca2+ provides Ca2+ efflux and Na+ influx, meaning Na+ can efflux in exchange for a K+ influx via Na+/K+-ATPase

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9
Q

2 components of increased myocardial oxygen supply

A

increased coronary blood flow, increased arterial O2 content

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10
Q

4 components of increased myocardial oxygen demand (for myocyte contraction)

A

increased HR, increased preload, increased afterload, increased contractility

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11
Q

which component increases number of contractions

A

increased HR

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12
Q

which components increase force of contraction most

A

afterload and contractility (preload only causes a small increase in force of contraction)

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13
Q

how does afterload increase work of heart

A

increased resistance in system means heart has to work harder

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14
Q

how does preload increase work of heart

A

Starling’s law; high blood return so dealing with more volume (stroke volume), so heart works harder

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