Electrical activity of the heart Flashcards

1
Q

what does the term ‘functional syncytium mean’

A

cardiac muscle is a fusion of lots of cells to make one big cell with lots of nuclei. It isn’t a true syncititium because it still has one nuclei per cell but it acts as if it was (functional)

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2
Q

gap junctions between membrane of cardiac muscle cells

A

protein channels that connect the membranes. Allow small signaling cells through and electrical current – hence why one cell contracting will make next cell contract

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3
Q

Desmosomes between membrane of cardiac muscle cells

A

physical connection between cells that keep cells together throughout contraction and so cells contract as one big muscle cell

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4
Q

How does the action potential differ to that in skeletal muscle

A

Cardiac muscle has a longer AP than skeletal muscle.

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5
Q

non- pacemaker action potential

A

PINK LINE ON GRAPH

at rest, starts at -90 mV. When AP starts there is initial rapid depolarisation. Rapid increase to permeability of Na+ so it moves in and cell depolarises to threshold. After Ca2+ channels (L-type) open up and Ca2+ moves in contributing to plateau. Leaky K+ channels shut - during plateau. Eventually Ca2+ channels shut and there is an increase in permeability to K+ again REPOLARISATION

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6
Q

What is different between cardiac and skeletal muscle excitation-contraction coupling (3)

A
  1. Structure - cardiac is a functional syncitium 2. Action potential 3. Refractory period
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7
Q

describe the excitation-contraction coupling in cardiac muscle

A

sodium and calcium enter during action potential. Ca2+ can be used for triggering excitation-contraction coupling. In cardiac muscle you can vary how much Ca2+ is coming in from outside the cell (not all troponin binding sites are saturated) and so you can also regulate the strength of contraction ie make the heart beat stronger or weaker (Can’t do that with skeletal as Ca2+ that is released is always enough to activate all sites)

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8
Q

where is Ca2+ stored?

A

sarcoplasmic reticulum

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9
Q

Describe cardiac muscle refractory period

A

long A.P, long refractory period. Muscle has to relax before it can contract again – no sustained contraction. Can’t stimulate cardiac muscle soon after a previous contraction as it is still in its refractory period. Don’t want sustained contraction in heart – need repetitive contraction and relaxation. NO TETANUS

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10
Q

what do pacemakers do

A

spontaneously bring the cell to threshold

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11
Q

how is equilibrium reached between electrical and concentration gradients?

A

at rest K+ is continuously leaking out due to leaky K+ channels. K+ brings positive charge with it and so builds up an electrical gradient If Na+ and Ca2+ channels open then they would depolarise cell and conc gradient is set up. Over time this becomes equal

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12
Q

what is an L- type channel

A

large type - let a lot of current in

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13
Q

Describe the pacemaker action potential

A

Once the cell has reached threshold - normal events occur- voltage gated Ca2+ channels open and lots of Ca2+ flows in and depolarise cell – reason for AP.

The cell reaches threshold in a more complex way in pacemaker cells. however.

  1. During depolarising phase non-pacemaker cells are held at -90mV due to leaky K+ channels, if you close these it would depolarise to threshold as K+ wouldn’t be leaking out.
  2. PF weird sodium current – not like normal Na+ channels – open by repolarising phase of previous AP - let a bit of Na+ in at the start of pacemaker potential.
  3. T-type – voltage gated Ca2+channels that open at more hyperpolarised levels – let in a tiny amount of Ca2+ - does the last little bit of pacemaker potential

N.B. Don’t need to know this in depth - just know that reaching threshold in pacemaker cells is more complex.

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14
Q

What is the sinoatrial (SA) node?

A

Also called the sinus node. Cluster of cells that are situated in the upper part of the wall of the right atrium. A.P generated here due to pacemaker cells spontaneously reaching threshold. The depolarisation spreads through the walls of the atria and causes them to contract. This forces blood into the ventricles.

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15
Q

What are the bundle of His and Purkinje fibers?

A

Part of the special conducting system of the Heart. Conducts the depolarisation from the atrioventricular node in the inferior part of the interatrial septum to the septum between the ventricles and then to the left and right ventricles.

Bundle of His is larger and so faster conduction occurs here than in the tiny Perkinje fibers.

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16
Q

Which drugs can modulate the electrical activity of the heart?

A
  1. Ca2+ channel blockers - decrease the force of contraction as reduce amount of Ca2+ getting into the cell so reduce cross bridge formation and reduce force of contraction. Get them for L or T type.
  2. Cardiac glycosides - increase the force of contraction - not used much anymore - increase the amount of Ca2+ being released from stores
17
Q

How can temperature modulate the electrical activity of the heart?

A

Big effect on the flow of ions - increase by 1 degrees can mean 10 more beats per min

18
Q

How does hyperkalemia modulate the electrical activity of the heart?

A

Cell depolarises - ventricular cells depolarise to threshold spontaneously - uncoordinated contraction of ventricles - fibrillation and heart block (block of AP getting from atria to ventricle)

19
Q

How does hypokalemia (low plasma K+) modulate electrical activity?

A

Has same effect as hyperkalemia which is unexpected - not known why. Causes Fibrillation and heart block.

20
Q

How does hypercalcemia (high plasma Ca2+) modulate the electrical activity of the heart?

A

increased heart rate and force of contraction (lots of Ca2+ moves in and rapid depolarisation of cell)

21
Q

How does hypocalcemia (low plasma Ca2+) modulate the electrical activity of the heart?

A

decreased Heart Rate and force of contraction

22
Q

Difference between L and T type channels?

A

L-type voltage gated Ca2+ channels are clearly the primary channel type. T-type are low voltage ie they have a low threshold of activation.

L-type take more to reach threshold - longer lasting however.

23
Q

Describe the special conducting system?

A

In a healthy heart, the fastest pacemaker is in the sinoatrial SA node in the upper part of the R atrium. When the AP is evoked it is spread through gap junctions. Spreads slowly across the atria. The wave of depolarisation moves down the atria and therefore a wave of contraction moves down the atria too - blood is pushed into ventricles.

Atrioventricular node (inferior part of septum between atrium and ventricle) conducts AP really slowly – long time for AP to get from atria to the ventricle. This delay allows for atria to fully expell blood into ventricles before ventricular contraction.

Bundle of His and purkinje fibres work as rapid conducting system – make sure AP reaches ventricles at the same time so get strong ejection of blood.

24
Q

What is the annulus fibrosis?

A

Annulus fibrosis makes up the parts of the heart that are not connected by gap junctions and so it’s called a non-conducting region.

25
Q

How come you can feel/hear the heart beating from the periphery (skin)?

A

Lots of cells in atria and ventricles contracting at the same time can summate to large extracellular electrical waves, hence why you can feel it at periphery – record this on skin with ECG (electrocardiogram)

26
Q

On an ECG what does the P wave correspond to?

A

atrial depolarisation

27
Q

On an ECG what does the T wave correspond to?

A

ventricular repolarisation

28
Q

What does the QRS complex correspond to?

A

Ventricular depolarisation