Lecture 6: Cardiac Muscle, Excitation and Signaling Flashcards Preview

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Flashcards in Lecture 6: Cardiac Muscle, Excitation and Signaling Deck (26):

What are the fundamental characteristics of the heart beat?

1. heart beat is myogenic, but can be influenced by nervous and hormonal factors
2. myocardial contraction is all-or-none (every cell beats together)
3. Atria contract first, and after a small delay, the ventricles contract next


What is a key difference between cardiac muscle and skeletal muscle?

Every myocyte contracts for every beat (all or non TISSUE response)
Skeletal muscles have altering number of cells that contract


What are the phases of the cardiac action potential?

Phase 0 = Upstroke (Na channels or T-type Ca in SA/AV nodes)
Phase 1 = repolarization (inactivation of Na and opening of transient outward K)
-spike is an overshoot seen in ventricular and purkinje fibers but not in SA/AV nodes
Phase 2 = plateau (Ca slowly inactivating while K+ channels slowly activating)
-protects heart from extra excitation (tetany)
-due to calcium channels
-not seen in skeletal muscle
Phase 3 = rapid repolarization (inactivation of Ca and activation of K)
Phase 4 = Resting potential (inward rectifier)


What is the significance of phase 2?

Controls contraction and guards against dangerous arrhythmias


What dictates the membrane potential?

By whichever ion is most permeable at rest
As determined by the Nernst equation…
E = (61.5/z)*log (Io/Ii)


How many ways can the channels get blocked?

In two ways
1. The channel can be physically closed
2. An inactivation gate (the ball and chain) could close in on it as well


What are the key characteristics of the Na+ channel ?

It mediates the upstroke (stage 0)
Has two gates (an activation and inactivation gate)
Inactivation gates are closed as you get more depolarized
Na channel gets blocked by tetrodotoxin


What does tetrodotoxin do?

They block Na channels


What are the consequences of a raised extracellular K+?

More positive the membrane potential = more inactivation gates that are CLOSED so therefore the upstroke is shorter because less Na channels would be open
Shorter upstroke = slower conduction and possibly no contraction (see curve f)
Causes arrhythmias and perhaps death


What are the key characteristics of the T-type Ca channel?

Stands for “Transient” type calcium channel
Activates between -80 to -40mV
Found only in SA and AV nodal cells that help generate spontaneous action potentials
So t-type Ca channels are crucial to generation of phase 0 in SA and AV nodal cells
Blocked by Amiloride
Less sensitive to dihydropyridine blockers


What are the key characteristics of the L-type Ca channel?

Stands for “Long” lasting type calcium channel
Activates between -30mV to 0 mV
Responsible for the PLEATEAU (phase 2) of the cardiac action potential
Blocked by the following antagonists:
i. Nifedipine (dihydropyridine)
ii. D600
iii. diltiazem


What are the key characteristics of the INWARD RECTIFIER K+ current?

It is called “inward” because under EXPERIMENTAL conditions, K+ was able to be carried inwards...but this would never occur PHYSIOLOGICALLY
In physiologic conditions, K moves out of the cell


What is the significance of the inward rectifier K+ channel?

Responsible for the major proportion of RESTING potential
Stage 4
Channel deactivates at potentials above -20mV (so it is off during the plateau


What are the key characteristics of the DELAYED K+ channel?

Activates very slowly during positive potential
Responsible for gradual repolarization during plateau
Stage 2 to Stage 3!


What is the point of the transient outward current?

Produces a little dip between phase1 and 2
Potassium type channel


Is the fast or slow response sensitive to TTX? D600?

Fast response is sensitive to TTX (Na)
Slow response is sensitive to D600 (Ca)


What happens if you block Na channels with TTX? Ca channels with D600?

If you block Na, Ca can carry the AP
If you block Ca, Na can carry the AP
Calcium and sodium channels are both capable of generating an AP alone
So depending on the tissue, you can have different channels generating an AP
This is why different tissues have different looking AP’s!!


What is the difference between the Na and Ca current?

Na is FAST (“rapid”)
Ca is slow


In what myocytes are the slow Ca channels responsible for upstroke (stage 0)?

SA and AV nodes
Na current is not operative in SA and AV nodes because potentials are not sufficiently negative


In which myocytes are the rapid Na channels mainly responsible for upstroke?

Purkinje fibers
Bundle of His
Ca can also contribute but are overshadowed by the speed of the Na channel


What are the causes of Long QT syndrome?

What are the causes of Long QT syndrome?
Genetic (K+ channels are blocked)
Drug induced (K+ channels are blocked)
Too many sodium channels
Prolongs the Ventricular depolarization
If the plateau lasts too long, repolarization can be adversely affected and torsades de pointes could occur


What two categories can the action potentials of the heart be divided into?

1. Contractile AP (atrial and ventricular)
2. Conduction AP (SA node)


What are the currents responsible for SA node?

1. DIASTOLIC potential = I_k (as the K+ channels switch off, this shit depolarizes)
2. I_f = funny current (both K and Na are permeable) and also depolarizes
3. I_ca = depolarization


What is diastolic potential?

The term for the “resting” potential of SA nodes but as Goldman states, stage 4 is not flat, so diastolic is used instead


What is one way to change the identity of the pacemaking myocyte?

By inactivating some K+ channels to make ventricle myocytes contract the fastest


How does AP propagate?

Through gap junctions
Cardiac muscle = functional syncytium (or functionally share the same cytoplasm, even each cell have own nuclei, so not true syncytium)