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CVR Lectures > Electrical activation of the heart > Flashcards

Electrical activation of the heart Flashcards

1
Q

What is the membrane of heart muscle cell permeable to?

A
  • Normally only K+
  • The potential is determined only by ions that can cross membrane
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2
Q

How does the heart muscle produce a negative membrane potential?

A
  • K+ ions diffuse outwards (high to low)
  • Anions can not follow
  • Excess of anions in the cell
  • Generates negative potential inside the cell
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3
Q

What are myocyte membrane pumps transferring?

A
  • K+ pumped in to cells
  • Na+ and Ca2+ pumped out of cells by myocyte
  • Against their electrical and concentration gradients (active transport)
  • Therefore requires a Na+/ K+ pump
  • And requires ATP for energy
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4
Q

What is a cardiac action potential?

A

Brief change in voltage across the cell membrane. Normally shown in a graph form

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5
Q

What is happening in the first stage of the cardiac action potential?

A
  • 4: resting potential
  • The resting cardiac myocyte membrane (sarcolemma) is much more permeable to K+ (since K+ channels are open meaning K+ is leaving the cell - RESTING POTENTIAL IS MAINTAINED BY NA+ & K+ ATPase PUMPS, pumping 3Na+ ions OUT for every 2K+ ions pumped IN) than to Na+ - meaning the resting membrane potential is much closer to the K+ equilibrium potential (-90mV) than to the Na+ equilibrium potential (+60mV)
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6
Q

What is happening in the second stage of the cardiac action potential?

A
  • 0: Rapid depolarisation
  • When an action potential arrives, Na+ voltage gated ion channels are OPENED, and Na+ entry depolarises the cell, triggering more Na+ channels to open - positive feedback effect
  • The charge increases from -90mv to +20mv
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7
Q

What is happening in the third stage of the cardiac action potential?

A
  • 1: small repolarisation
  • When potential in cell is positive (+52mV) then voltage gated Na+ channels CLOSE, at the same time voltage gated K+ channels OPEN - partially REPOLARISING the
    cell
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8
Q

What is happening in the fourth stage of the cardiac action potential?

A
  • 2: maintain depolarised state
  • Calcium channels open causing calcium to enter the cell and maintain a depolarised state for a long period of time
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9
Q

What is happening in the fifth stage of the cardiac action potential?

A
  • 3: re-polarisation back to resting potential
  • Re-polarisation eventually occurs due to the eventual closure of the L-type Ca2+ channels, and the reopening of the K+ channels (the
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10
Q

What mechanism returns the voltage to normal?

A

ATP-ase returns it to normal

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11
Q

How is an action potential created?

A

Local depolarisation activates nearby voltage gated Na+ channels to open and influx of sodium ions enters the cell, which causes a wave of depolarisation across the membrane

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12
Q

How does an action potential spread across the membrane?

A

Gap junctions allow cell-to-cell conduction and propagation of action potential through the whole myocardium

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13
Q

Why do we need so much electrical activity?

A
  • End goal is all about calcium
  • Contraction of the heart muscle requires (appropriately-timed) delivery of Ca2+ ions to the myocyte cytoplasm
  • If a cell is excited electrically it causes contraction
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14
Q

What is the first stage of excitation-contraction coupling?

A

When the action potential is generated, there is an influx of Ca2+ via the T-tubules via L-type Ca2+ voltage gated channels

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15
Q

What is the second stage of excitation-contraction coupling?

A
  • The small amount of Ca2+ ions that influx (too small to be able to initiate muscle contraction) bind to ryanodine receptors on the sarcoplasmic reticulum - this binding causes the sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell - this initiates cardiac muscle contraction - the start of the CROSS-BRIDGE CYCLE
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16
Q

What is the third stage of excitation-contraction coupling?

A
  • Ca2+ binds to the Ca2+ binding site on the troponin protein on actin filament
  • This causes the troponin to change shape and thus displace the tropomyosin protein on the actin filament, exposing the myosin binding sites
17
Q

What is the fourth stage of excitation-contraction coupling? (myosin head)

A
  • The myosin head on the myosin filament then binds to the actin filament via the myosin binding site, the inorganic phosphate is dropped in order for the myosin head to bind to the actin, the ADP still remain attached to the head - this is known as cross-bridge formation
  • The myosin head then drops the ADP to contract and pull the actin filament OVER the myosin filament - thereby decreasing the Z lines resulting in muscle contraction - this is know as the power stroke
  • ATP then binds to the myosin head, detaching the head from the actin filament, and moving the head to its start position
  • The ATPase in the myosin head then hydrolyses the ATP into ADP & Pi ready for the next contraction IF THE MYOSIN BINDING SITES REMAIN OPEN
18
Q

What is the comparison to skeletal muscle?

A
  • Contraction lasts LONGER than in skeletal muscle - up to 15 times longer in duration; this is due to the slow
    calcium channels
  • Decreased permeability of membrane to potassium after action potential
19
Q

What does the sinoatrial node do?

A
  • Normally determines the rate the heart beats at - the number of times the heart contracts per minute
  • Resting membrane potential of -55 to -60 mV - this is closer to the threshold of depolarisation thus it depolarises first, it is closer to the depolarisation threshold due to its slow Na+ inflow not found anywhere else in the body
20
Q

What does the Atrioventricular node do?

A
  • Located at the base of the right atrium - transmits cardiac impulse from atria to ventricles
  • Consists of modified cardiac cells that have lost contractile capability but conduct action potentials with LOW RESISTANCE
  • After the AV node has been excited, the action potential progresses down the interventricular septum - this pathway of conducting fibres is called the bundle of His
  • The AV node and the bundle of His constitute the ONLY electrical connection between the atria and ventricles - except from THIS PATHWAY the atria are completely
    isolated from the ventricles by a layer of nonconducting connective tissue
  • Delays impulse so atria can empty blood into ventricle, fewer gap junctions.
21
Q

Does the SA node have a steady resting potential?

A
  • The SA node does not have a steady resting potential, instead it undergoes SLOW DEPOLARISATION - this is known as the pacemaker potential; it brings the membrane potential to a threshold, at which point an action potential occurs
22
Q

What three ion channel mechanisms contribute to the pacemaker potential?

A
  • The first is the progressive reduction in K+ permeability. The K+ channels that opened during the repolarisation phase of the previous action potential gradually close due to the membranes return to negative potentials
  • Second, pacemaker cells have a unique set of channels that, unlike most voltage gated channels, open when the membrane potential is at NEGATIVE values - these non-
    specific cation (positive ions) conduct mainly an inward Na+ current, since this is not normal these channels are
    referred to as “funny” and are thus called F-type channels
  • The third channel is a Ca2+ channel that opens VERY BRIEFLY but contributes to an inward current of Ca2+ which acts as an important final depolarising boost to the
    pacemaker potential. Since the channel is only opened briefly it can be called transient so these channels are known as T-type Ca2+ channels
23
Q

What is sympathetic stimulation?

A
  • Sympathetic postganglionic fibers innervate the entire heart
  • Controlled by adrenaline & noradrenaline
  • Increases heart rate (positively chronotropic)
  • Increases force of contraction (positively inotropic)
  • Increases cardiac output (by up to 200%)
  • Decreased sympathetic stimulation will result in decreased heart rate & force of
    contraction and a decrease in cardiac output by up to 30%
24
Q

What is parasympathetic stimulation?

A
  • Fibers are transmitted via the vagus nerve (CN10)
  • Controlled by acetylcholine which bind to muscarinic receptors
  • Decreases heart rate (negatively chronotropic)
  • Decreases force of contraction (negatively inotropic)
  • Decreases cardiac output (by up to 50%)
  • Decreased parasympathetic stimulation will result in an increased heart rate
25
Q

What are the velocities of conduction?

A
  • Faster in specialised fibres
  • Atrial and ventricular muscle fibres: 0.3 to 0.5 m/s
  • Purkinje Fibres: 4m/s
26
Q

What is the His-Purkinje system?

A
  • AV node to the ventricles
  • There is a rapid conduction:
    Which allows coordinated ventricular contraction, very large fibres and high permeability at gap junctions
  • These fibres in turn make contact with Purkinje fibers, large-diameter conducting cells that rapidly distribute the impulse throughout much of the ventricles
  • Finally the Purkinje fibres make contact with ventricular myocardial cells - which spread the action potential through the rest of the ventricles
  • The conduction from the AV node to the ventricles is RAPID to enable coordinate
    ventricular contraction
27
Q

What is automaticity?

A
  • The ability for spontaneous, rhythmic self-excitation
  • Spontaneous discharge rate of heart muscle cells decreases down the heart
  • SAN (usually) fastest
  • Ventricular myocardium slowest
28
Q

What is the refractory period?

A
  • Lasts approx 0.25 s
  • The refractory period is the period of time after an action potential where second impulse CANNOT cause a
    second contraction of cardiac muscle:
  • This is to prevent excessive FREQUENT contraction
  • To allow adequate filling time
29
Q

What is Long QT syndrome?

A
  • Abnormal K+ channels causes loss of function so delays in repolarisation

CVR Lectures (28 decks)

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