Cardiology 6.2 Electrical Activity Of The Heart

Front 1

What is a functional syncytium and why is it important in the heart?

Back 1

Cardiac cells beat together without innervation. This is important since the heart must provide coordinated, pulsatile, contraction for efficient movement of blood. Streamlines AP mechanism to not need as many motor neurons.

Front 2

Know the major differences between initiation of contraction in skeletal muscle and cardiac muscle.

Back 2

1) Spontaneous depolarization
2) AP spreads cell to cell
3) Long AP (100 to 250x longer)
4) Slow Ca channels

Front 3

Compare and contrast the AP in a pacemaker cell and a ventricular cell.

Back 3

Slow APs in pacemaker (mostly slow Ca channels) also no fast Na channels.
"funny" Na channels close during AP; open once AP finished.
K channels closed during phase 4.

Ventricular have 0 - 5 stages, fast Na channels allow for undefined 0 slope.

Efflux of K balances the influx of Ca during phase 2 of ventricular AP.

Front 4

What conditions are responsible for and what is the purpose of the prolonged phase of depolarization in cardiac muscle cells; i.e. the plateau of the action potential?

Back 4

Allows ventricles to refill (arrested depolarization).

Ca/K influx and efflux are balanced.

Front 5

Fusion and temporal summation are the mechanisms that permit graded and prolonged tension development in skeletal muscle. Why doesn't this happen in the heart?

Back 5

Absolute refractory period.
Na channels become inactivated at the peak of the cardiac AP and can't pass through channel.
As long as Na channels stay inactivated

Front 6

What causes spontaneous depolarization in pacemaker cells?

Back 6

Funny Na channels are open and K channels are closed during "rest".

Front 7

What effect do sympathetic and parasympathetic nerves have on cardiac pacemaker cells? What neurotransmitters mediate these effects?

Back 7

Sympathetic is NE (B adrenergic) - speeds up (higher shorter AP and shorter quicker contraction)
Parasympathetic is E (muscarinic cholinergic) - slows down (ion channel changes)

Sympathetic nerves act on the SA node pacemaker cells to increase HR, on the AV node cells to increase cond vel and shorten AV delay, and on all cardiac cells to shorten refractory period and make each cardiac contraction stronger and quicker, yo.

Pare influences SA node (decrease HR) and AV node (slow conduction and lengthen refractory period) and on all suprventricular cells (lengthen refractory period and make their contractions weaker and slower).

Front 8

Be able to trace an AP in the SA node through the specialized conducting system of the heart to the ventricular muscle cells.

Back 8

not yet answered

Front 9

What is the purpose of the slow conduction of APs through the AV node?

Back 9

Electrically isolates ventricles from being stimulated to contract at rates too rapid for efficient pumping.

Front 10

Compare the intrinsic pacemaker activity of the SA and AV node.

Back 10

SA is 70 to 160
AV is 40 to 60

Front 11

What is the importance of the long refractory period in AV node cells?

Back 11

Filling of ventricles.
So that it doesn't override the SA node pacemaker.

Front 12

Arrhythmias may be due to a problem in AP formation or AP conduction. Name an example of each.

Back 12

AP formation - sick sinus syndrome (SA fails to form AP).

AP conduction - AV node blocks.

Front 13

Understand the three degrees of severity of AV node block.

Back 13

3rd degree is worst - total block
2nd degree is sporadic blockage (parasympathetic can exaggerate)
1st degree; every AP propagates, but is really slow

Front 14

What kind of disorders cause supraventricular tachyarrhythmias? Ventricular tachyarrhythmias?

Back 14

Atrial fib or flutter
V. Fib.

Front 15

Explain what is meant by a re-entrant arrhythmia.

Back 15

AP spreads through one part of heart then circles back to depolarize the part of the heart from which it began.

Front 16

Understand how the antiarrhythmic drugs in the following categories work: lidocane, cardiac glycosides (digitalis), Ca channel blockers, beta adrenergic antagonists (Propanolol)

Back 16

Lidocane - bind to some fast Na channels and prevent from opening. Raise threshold for AP.

Ca Channel Blockers - decreases Ca entry during AP. Makes pleateau less positive and lengthens AP and lengthens refractory period. Protect ventricles from rapid flutter and decreases strength of contraction.

Cardiac Glycosides - inhibits Na/K ATP-ase. Some Na channels remain in an inactive state. Resting membrane not as negative. Makes cells somewhat refractory.
Increase parasympathetic tone.
Allow more Ca in (Ca/Na exchanger and Na/K exchanger - need Na to ship out Ca) Increased contractility.

Beta Blockers - Prevent sympathetic tone. Decreases contractility.

Automaticity - the ability to create an AP.

Front 17

What conditions could casue an increase in heart rate?

Back 17

Premature beat, ectopic pacemaker, reentry

Front 18

What conditions could cause more atrial BPM than ventricular beats?

Back 18

atrial flutter, AV node block, atrial fib, any supraventricular tachycardia

Front 19

Know the concentrations of Na, K, and Ca in the intracellular, extracellular, and plasma fluids.

Back 19

Na intra 15
extra 140
plasma 142

K intra 150
extra 5
plasma 4

Ca intra .0001
extra 1
plasma 2.5

Front 20

What factors are responsible for maintenance of the membrane potential?

Back 20

See above
Na/K ATP ase pump (3/2)
Na/Ca antiport (3/1)
Ca ATP-ase on SR

Front 21

Explain how a cardiac AP leads to a contractile event.

Back 21

Na channels open. Depolarization.
Slow Ca channels open.
Ca triggered Ca release.
Troponin/Troplmyosin shit and boo-yah! Contraction!

Phospholamban and ATP Ca pump put Ca back into SR.

Front 22

What is meant by the period of supernormal excitability?

Back 22

During repolarization after an AP, the period where the cell can be easily depolarized. From the end of the relative refractory period to the end of the repolarization period and is associated w/the very beginning of phase 4.

The cell is most readily depolarized during this period and hyperexcitable because only a small reduction in the membrane potential is required during this time to reash threshold potential. The membrand can be depolarized by a stimulus that is smaller than normal. The membrane is thus more vulnerable during this period.

Front 23

What is an auxiliary or subordinate pacemaker cell?

Back 23

AV node, bundle branches, perkinje fibers. Beat slower than SA node and can take-over if the conducting body above it.

Front 24

Understand how Ca moves in response to the AP.

Back 24

Ca becomes more permeable during the AP (upon threshold).

Pacemaker - Ca causes depolarization
Ventricular - Ca enters after threshold

Front 25

What is meant by postextrasyystolic potentiation?

Back 25

The increased ventricular contraction that occurs after a supranormal contraction. Ventricles take longer to fill, get more Ca, and contract harder!