Cardio Lecture 3: MP and AP (Finished) Flashcards

Contraction , which is initiated by an action potential

a transient change in the polarization of the resting membrane potential that is transferred from the cell to cell based on ionic differences

electrical potential difference

microelectrodes

Negatively

-90 mV, 0mV

polarized

1. Na
2. K
3. Ca
4. Cl

ions

Potassium

Voltage difference between 2 points in a material are directly proportional to the current (I) and the Resistance (R)

Inverse of the resistance; notated as g

big resistance = small conductance // small resistance= large conductance

1. Cell type
2. Ionic concentration differences (chemical gradient/electrochemical forces)
3. Permeability of the cell membrane (high conductance for K⁺= high permeability for K to flow in and out)
4. Electrogenic pumps

Concentration for K is higher inside than outside; wants to move DOWN it's concentration gradient

Concentrations for both are higher OUTSIDE the cell; want to flow against their gradients to go inside the cell

Entropy effects

Nernst Equation

IS NOT THE SAME

• The E_m is LESS NEGATIVE than E_k (~90mV compared to -96mV) .....therefore the negative voltage required to stop the outward flow of K⁺ is NOT STRONG ENOUGH.....SOOO there's a small net electromotive driving force resulting in a steady and slow leakage of K⁺ from the intracellular phase to the extracellular phase in the resting non pacemaker cardiomyocyte (inward rectifier potassium channel, K₁₁)

All of the ions will contribute to the E_m , so the Em will NOT BE EQUAL to the chemical potential for a resting membrane.

**in contrast, the reason for the resting membrane potential of a non pacemaker cardiac myocyte being so close to Ek is because it's significantly more permeable to K⁺ than Na⁺, Ca⁺⁺ or the Cl^- ions**

Permeability and conductance

• higher the permeability = higher the conductance >> meaning greater the solute transport across the cell membrane

Goldman-Hodgkin-katz Equation, this equation is fundamental to cardioelectrophysiology and for understanding the action potential

**not responsible for this, just know there is a better model than Nernst*

Ion pumps which are couples with ATP hydrolysis to drive the pumps

Na⁺/K⁺- ATPase pump

intracellular Na⁺ increases

• Ions are able to cross the sarcolemma via specialized ion channels or pores that penetrate the phospholipid bilayer.
• The ion channels are protein structures that are selective for specific ions. These protein structures adjust their shape/conformation so ions can flow in, out, or not at all.
• Ions can have more than one channel.

• Flux of + charge into the resting cells = inward current and depolarization (reducing the - charge/neutralizing charges)
• Flux of + charge out of the resting cells = outward current and hyperpolarization
• If the cell is depolarized, the outward flux causes depolarization (loosing + charges and becoming more -)

****Opposite effects for flux of - charge into and out of the cell****

• The ion channels are glycosylated proteins with repeating domains.
• Each domain consists of 6 transmemb rane segments.
• The K+ channels has 4 domains that are not bonded together by peptide bonds, in comparison to the Na⁺ and Ca⁺⁺ channels
• The Na+ channel have a loop between domains 3 and 4 that is believed to be the inactivation gate

• Fast Na+ channel has 2 gate; inner H gate and outer M gate
• Channel is closed at the normal resting membrane potential
• When depolarized, the M gate rapidly opens and Na+ flows in
• The H gate starts to close when the M gate starts to open, then completely closes in a few milliseconds when the cell starts to undergo depolarization.
• Flow of Na+ into cell stops
• Neat the completion of depolarization, the H gate opens and the M gate closes.

membrane potential (E_m)

1. Nonpacemaker APs (fast response)
2. Pacemaker APs (slow response)

Triggered by APs in adjacent cells (gap junctions) with depolarizing currents

Spontaneously generates their own APs simultaneously

Shape and duration

4 - Resting/polarized (true resting potential, maintained by the inward rectifying Channel I_k1)

0 - Depolarization as a result of temporal increase in Na+ conductance (gNa⁺) >> resulting in a rush of Na+ from extracellular to intracellular

1 - Repolarization as a result of the opening of the transient outward K+ channel (I_to) and the inactivation of the Na+ channel >> gCa++ increases and slow movement of Ca++ into cardiomyocyte via the L-type calcium channel (I_ca, aka the slow, inward, long-lasting current)

2 -

3 - Still depolarization but the downward slope is the result of gK⁺ increases which initiates an outward K+ current through the potassium delayed rectifier (I_kr) >> gCa⁺⁺ decreases

4 - Resting/poplarzied

• Ventricular cells are unexcitable (refractory)during phases 0, 1, and 2
• No new propagation AP are generated because Na+ channels are closed

• Includes ARP and some of phase 3
• Only localized action potentials can be generated, but they cannot be propagated , they are weak af and can't go anywhere

• Weaker than normal APs ay be generated and conducted

weaker than normal stimuli

To allow the heart to go through a full/complete cycle

If the fast response Na⁺ channels are blocked pharmacologically or inactivated by depolarization >> the AP upstroke is reduced

Spontaneous depolarizations called afterdepolarizations can be generated by non pacemaker cells during phase 3 or early phase 4; from slow Ca⁺⁺ channels if the fast response Na⁺ channels are closed

It will take more time for the ion current to travel through the tissues >> depression of the slop of phase 0

**when the membrane potential rises to ~55mV= essentially all of the fast Na⁺ channels are inactivated by the closure of the H gate**

Drugs that inhibit the K⁺ current through the Potassium Delayed Rectifier (I_kr) leading to cardiotoxicity and dangers arrhythmia's

**Terfenadine

• Rapid (K_r)
• Slow (K_s)

4 - no true resting potential = what's happening here is the gK⁺ decreases, gCa⁺⁺ increases due to transient Ca⁺⁺ channels, pacemaker current (funny current, I_f), and the L-type Ca⁺⁺ ion channels open

0 - Depolarization ,slope is softer than phase 0 some of nonpacemaker APs

3 - Repolarization due to decrease in gCa⁺⁺ and increase in gK⁺

The higher intrinsic "firing" rate of the SA node controls the there nodes.

**the others can't keep up!

SA Node

**SA node > AV node > Bundle of His > Purkinje Fubers

Ectopic Focus

1. Change slope of Phase 4
2. Alter the threshold voltage
3. Change the hyperpolarization

More quickly reaches threshold and has the AP kick in

Takes longer to reach threshold and have the AP kick in