Electrical Properties of the Heart Flashcards Preview

LSS 1 - CVS - Laz > Electrical Properties of the Heart > Flashcards

Flashcards in Electrical Properties of the Heart Deck (19)

Explain the potassium hypothesis.

If a membrane is permeable to potassium and there is a higher concentration on one side of the membrane, the potassium will move down the concentration gradient and it will carry positive charge with it. As it carries positive charge with it, one side of the membrane will have a more positive charge than the other. This would mean that the electrochemical gradient opposes the concentration gradient. Eventually the electrochemical gradient will equal the concentration gradient that there would be no net movement of potassium. The cell membrane is more permeable to potassium ions than anything else, which is why the membrane potential is close to the equilibrium potential of potassium.


What are the intracellular and extracellular concentrations of potassium ions?

Inside = 120 mM
Outside = 5 mM


What value does the Nernst equation give when using potassium concentrations and what is its significance?

-80 mV - very close to the actual resting membrane potential of a ventricular myocyte hence meaning that potassium is the main determinant in the resting membrane potential


What value does the Nernst equation give when using sodium concentration and what is its significance?

+66mV - during the upstroke of an action potential, when the membrane is most permeable to sodium, the membrane potential will reach around +66 mV


What is the duration of an action potential in a nerve compared to a ventricular myocyte?

In a nerve = 2 ms
Ventricular myocyte = 200-400 ms


Describe and explain the cardiac action potential.

The cardiac action potential has a normal upstroke due to opening of sodium channels. Then there is a small repolarisation caused by transient outward potassium current. The membrane potential then plateaus for a long time due to the activation of long acting L-type calcium channels. Influx of calcium balances the efflux of potassium for a long while and hence maintains a constant membrane potential. Eventually, the membrane repolarises due to the inactivation of the L-type calcium channels.


What is the difference between absolute refractory period and relative refractory period?

During the absolute refractory period, the sodium channels cannot be reopened - this means that regardless of the stimulus strength, an action potential cannot be generated.
During the relative refractory period, an action potential can be generated, but only if there is a stimulus of greater than normal strength.


What is full recovery time?

The time at which a normal action potential can be elicited by a stimulus of normal strength.


What is the key difference between skeletal muscle and cardiac muscle in terms of excitation and tetanus?

With skeletal muscle, repolarisation occurs very early in the process of contraction. So the muscle can be re-stimulated very soon after the first action potential causing summation and tetany. The long absolute refractory period of cardiac muscle means that by the time the action potential has finished, the muscle is well into the process of contraction and hence action potentials can't be generated at a high enough frequency for them to summate and cause tetany.


What causes the early repolarisation in the cardiac action potential?

Transient outward potassium current


What causes the plateau in the cardiac action potential?

The opening of L-type calcium channels allows calcium influx, which just about balances the efflux of potassium so the membrane potential remains around 0 mV


State three drugs used in anti-hypertensive care and their targets.

These are all calcium channel antagonists


Describe the changes in ion channels that takes place during repolarisation.

The normal potassium channels open slowly starting repolarisation.
Then a weird potassium current (IK1) starts that is large and flows through diastole. This repolarises the membrane and helps to maintain resting membrane potential and reduce the risk of arrhythmia.


Different cells within the heart have different action potential shapes. What causes this difference?

Differences in the expression of ion channels


Why don't sinoatrial nodal cells have a stable resting membrane potential?

They don't have any IK1 potassium channels so they can't maintain a stable resting membrane potential.


What causes the upstroke in the action potential of sinoatrial nodal cell action potentials?

The upstroke is caused by calcium influx (there is very little sodium movement involved)


How does the autonomic nervous system control heart rate?

It alters the gradient of the pacemaker potential thus making it quicker or slower to reach threshold potential and generate an action potential.


Where are purkinje fibres found?

They run beneath the endocardium and penetrate about 1/3 of the way into the myocardium


What feature provides low resistance pathways between cells for impulse propagation?

Gap junctions