7. Electrical Properties of the Heart Flashcards
What is the Potassium Hypothesis?
- The membrane is more permeable to potassium ions than anything else
- As K+ moves to one side, that side becomes more positive and the side it leaves becomes more negative
- The “electrical gradient” opposes the concentration gradient - moves in the opposite direction
- Equilibrium: electrical gradient = concentration gradient
- Ions can move back and forth - no net movement
What can you predict using the Nernst Equation and how is this used with K+ concentrations?
- Resting Membrane Potential
- Potassium concentration: inside = 120 mM, outside = 5 mM
- Plug into the Nernst Equation => equilibrium potential of around -80 mV
- Close to the RMP of a ventricular myocyte
- Established by the movement of potassium through channels, but maintained by the sodium-potassium pump
What is the equilibrium potential with Sodium in the Nernst Equation?
+66 mV
Why is the Goldman-Hodgkin-Katz equation a better way to calculate the RMP?
Takes into account the relative permeabilities of the membrane to different ion
How do action potentials differ between nerves and the heart?
- Nerve APs last about 2ms
* Heart APs last 200-400ms
Describe the cardiac action potential in detail
- Upstroke - same as nerve, opening of sodium channels
- Sodium channels start to inactivate - membrane potential starts to recover and repolarise slightly
- Brief increase in potassium permeability due to the opening of transient outward channels - repolarises the membrane
- Influx of calcium due to open L-type Calcium Channels balances efflux of potassium - plateau around 0 mV
- Absolute refractory period caused by inactivation of sodium channels for a long time
- This period is long - can’t re-stimulate for a long time - doesn’t tetanise
- Inactivation of LTCCs and opening of another subtype of potassium channel causes eventual repolarisation
- Relative refractory period - after absolute refractory period - AP can be elicited with a larger stimulus strength
- Sodium channels recover from inactivation
What determines the membrane potential at rest?
Potassium
What is the full recovery time?
The time at which a normal action potential can be elicited with a normal stimulus
What are the 5 phases of the cardiac action potential? (0 to 4)
- Phase 0 = upstroke
- Phase 1 = early repolarisation
- Phase 2 = plateau
- Phase 3 = repolarisation
- Phase 4 = resting membrane potential (diastole)
Name 3 dihydropyridine calcium channel antagonists and how they work?
- Nifedipine
- Nitrendipine
- Nisoldipine
- Bind to LTCCs
- Block calcium entry
What is the potassium channel that switches on/off during depolarisation/repolarisation?
- IK1
- Switches off during depolarisation
- Switches on as the membrane repolarises
- IK1 current is large and flows during diastole
- Stabilises the RMP and reduces the risk of arrhythmia
Why do different parts of the heart have different action potentials?
- Different expression of ion channels
* Different ionic currents flowing
Why is there no IK1 in SA node cells
- IK1 is needed to maintain a stable membrane potential
* SA node cells do not have this - no resting potential - constantly depolarising
Describe how the SA node cell is different to other cardiomyocytes
- Very little sodium influx
- Upstroke caused by calcium influx, not sodium
- T-type channels, which activate at more negative potentials than LTCCs
- Unstable membrane potential - constantly oscillating
- First upward slope on graph = pacemaker potential (PF)
What effect does sympathetic and parasypathetic stimulation of the heart have on the pacemaker potential?
Sympathetic
• Steeper
• Threshold potential reached more rapidly - increases heart rate
Parasympathetic
• Decreased gradient
• Longer to reach threshold potential - decreases heart rate
