Wk4 - cardiac pacemakers Flashcards
What’re the 2 types of specialised myocardial fibres?
- contractile fibres
2. autorhymic cells
Structural features of myocardial cells.
- intercalated discs
- desmosomes
- gap junctions (increase cell to cell signal speed)
- many mitochondria
- large T tubules
Autorhythmic (AR) cells do not have a stable _____ ____ ____, and instead display _____ ______.
resting membrane potential; pacemaker activity (through repeated cycles of drift and fire)
What ionic events lead to the drifting of AR cell membrane potential toward threshold level, causing an action potential to subsequently “fire”?
(list these in chronological order)
- cyclical decrease K+ efflux
- Opening of I(f) channels - these are voltage gated and open when cell becomes very negative (depolarised), allowing influx of sodium.
- Opening of transient (T-type) calcium channels - allowing for increased influx of calcium
What accounts for the latter half of drift to threshold in AR cells?
Calcium influx through T-type (transient) calcium channels.
What ion passes through I(f) channels?
Na
What ion passes through transient “t-type” channels?
Calcium
Permeability to K+ decreases in between action potentials due to what?
inactivation of K+ channels
What causes the rising phase (depolarisation) of AR cells?
activation of voltage gated calcium channels (L-type, meaning latent). This causes a large amount of calcium to rush into the cell and thus it becomes more positive (depolarised)
What causes the falling phase (repolarisation) of AR cells?
the activation of voltage gated K+ channels. This causes a massive amount of K+ to rush out of the cell and thus it becomes more negative (repolarised)
Define influx.
substance moves into a cell
Definie efflux.
substance moves out of a cell
Summarise the effect of K+ on the resting membrane potential of AR cellls
K+ contributes to the drift toward threshold (first ionic event is a “cyclical decrease of K+ efflux”), and is also the cause of repolarisation or the falling phase due to the activation of voltage gated K+ channels and the subsequent efflux of K+ ions.
Where are AR cells located?
- SA node
- AV node
- Bundle of His (AV bundle)
- LBB and RBB
- Purkinje fibres
What’re the latent pacemakers of the heart?
The AV node and bundle of His.
This is as these autorhythmic cells have the next fastest inherent rate of sponatenous depolarisation, coming second only to the SA node.
What is the pacemaker of the heart? Why?
Sino-atrial node, as it has the fastest inherent rate of spontaneous depolarisation.
What happens should the SA node fail to operate?
The latent pacemakers of the heart take the role as pacemaker for the heart, however it would likely still be too slow and lead to heart problems.
Explain in detail the path an electrical impulse of the AR cells of the heart takes.
- AP originates in SA node
- AP spreads via gap junctions down internodal pathways, and across atrial myocardial cells (causing atrial contraction).
- AV nodal delay (pause…)
- Impulse travels through AV node to bundle of His, down bundle branches and into the purkinje fibres of the heart
Right and left ventricular contractions starts, and heads toward where?
ventricular contraction starts at the apex of the heart and heads toward the base
What is the point of electrical contact between the atria and the ventricles? (hint: there is only one point of electrical contact between these two places)
the AV node
What is the purpose of the AV nodal delay?
to allow for the completion of atrial contraction, before the commencement of ventricular contraction (maximising ejection of blood from the heart)
The bundle of His and purkinje fibres form a specialised system to ensure what functional property of the heart?
ensuring the heart contracts as a unit (ensuring ventricles contract simultaneously, and at the right point of time so as to make sure atrial ejection is complete)
How long is AV nodal delay?
0.1 seconds
The resting membrane potential (RMP) for AR cells is _____, whereas the RMP for contractile cardiac cells is _____.
unstable; stable
Explain the ionic events involved with the action potential (AP) of a contractile cardiac cell
- AP arrives at cardiomyocyte
- Electrical stimulus causes explosive increase in Na permeability, causing steep depolarisation as Na rushes into the cell
- Na permeability falls to low resting level (less Na influx)
- Membrane potential maintained in depolarised state for several hundred ms (Plateau phase). This is as explosive change in membrane potential (sharp depolarisation) decreases K+ permeability and induces opening of “slow” calcium channels. Thus this plateau phase consists of mostly just a slow efflux (leak) of calcium
- Inactivation of calcium channels and activation of K+ channels occurs, sharp repolarisation occurs due to fast efflux of K+
What is a cardiomyocyte?
contractile cardiac cell (cardiac muscle cell)
What’re the 2 voltage dependant permeability changes which occur in a cardiomyocyte, due to the sharp depolarisation following an action potential?
What do these changes permit, and why?
- activation of slow calcium channels
- decrease of permeability to K+
these changes permit the plateau phase of a cardiomyocyte, which basically adds to the length of the refractory period of cardiac muscle. Thus, it helps to ensure tetanus of the heart can not occur.
How do the T-tubules of cardiac cells compare to sk muscle cells?
cardiac cells T-tubules much larger and branch inside the cell more extensively
How does the sarcoplasmic reticulum (SR) of cardiac cells compare to sk muscle cells?
cardiac cells SR is very reduced compared to skeletal muscle
what is the consequence of cardiac muscles having a reduced SR?
cardiac muscle relies on the ECF for its calcium supply, which is why these cells have an extensive T-tubule system. Calcium diffuses directly from the T-tubules into the cytosol (sarcoplasm) of the cardiac muscle cell.
The extra amount of calcium which is supplied by the T-tubules to cardiac muscle cells, is largely responsible for what phase in the AP of a cardiomyocyte?
the plateau phase; as this phase involved the slow leaking of calcium through “slow calcium channels”
Which muscle presents a longer refractory period, skeletal or cardiac? How long is cardiac muscles refractory period?
cardiac, it’s refractory period (250ms) is nearly as long as the period of contraction (300ms)
Skeletal fibres are able to be re-stimulated again in a process known as _____.
summation
What is the chief factor responsible for the large refractory period of cardiac muscle?
The inactivation of Na channels is the main point which enables the refractory period (and thus plateau phase) to occur. Remember, it is the influx of Na into the cardiac muscle cell which causes it’s depolarisation in the first place
When do sodium channels become active again (post depolarisation) in a cardiomyocyte?
when the RMP returns to normal resting levels (-90mv)
Define ‘graded contraction’ in the context of cardiac muscle?
the strength of contraction is proportional to the number of crossbridges formed within the muscle
How is it the strength of contraction may be increased in cardiac muscle?
increase in [Ca+2] leads to an increase in the number of crossbridges formed and thus, an increased strength of contraction
How is contraction of the heart modulated (by what)?
by the ANS and circulating adrenaline
Briefly explain the physiological events which lead to a greater force of contraction of the heart? (note: this question refers to the effect of cAMP).
- Phosphorylated protein kinase (cAMP) activates regulatory protein phospholamban
- Phospholamban enhances the calcium ATPase activity in the SR
- This increases amount of calcium sequestered into the SR
- Upon stimulation there is a greater [Ca+2] available and thus, a greater force of contraction
Effect of the SNS on HR?
- increase HR
- done by increasing the amount of I(f) channels and thus, increasing the calcium influx and the speed at which an AR cell drifts toward threshold
Effect of PNS on HR?
- slows HR
- done by increasing K+ efflux and decreasing calcium influx, thus decreasing the speed at which AR cells drift toward threshold
