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Physiology 1 > 15&16 Cardiac Electrophysiology > Flashcards

15&16 Cardiac Electrophysiology Flashcards

1
Q

What connects cardiac muscle fibers together?

A

Intercalated discs

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2
Q

What are the two types of membrane junctions in intercalated discs and what are their functions?

A

Desmosomes hold the cardiac cells together (mechanically important)

Gap junctions link the cells of each chamber into a functional syncytium (electrically important)

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3
Q

What is a syncytium? What is a functional syncytium?

A

A syncytium is a network of electrically connected cells. A functional syncytium creates a wave on contraction (this allows the heart to work as a unit and begins with pacemaker cells)

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4
Q

How does the action potential in cardiac cells get to the sarcoplasmic reticulum?

A

Down the t-tubules, similar to skeletal muscle

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5
Q

Do gap junctions connect the atria to the ventricles?

A

No, the gap junctions are specific to each chamber

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6
Q

What is the sequences of electrical events in the heart?

A

SA node -> AV node -> bundle of his -> bundle branches -> Purkinje fibers

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7
Q

What is the pathway of communication between the atria and ventricles?

A

The AV node to the bundle of his

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8
Q

Why is there a delay in the AV node firing?

A

The delay ensures that atrial contraction precedes ventricular contraction to allow for complete ventricular filling

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9
Q

What do the purkinje fibers do?

A

They rapidly spread impulse throughout much of the left and right ventricles, which allows for efficient contraction and ejection of blood

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10
Q

What drives the heart rate?

A

The SA node

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11
Q

Why does the SA node drive the heart rate?

A

It suppresses the other latent pacemakers by a phenomenon called overdrive suppression.

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12
Q

What is ectopic pacemaker?

A

When the latent pacemakers have an opportunity to dive the heart rate ONLY when the SA node is suppressed or if the intrinsic firing rate of the latent pacemaker become faster than the SA node

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13
Q

What cells have slow action potential?

A

Pacemaker (nodal) cells such as the SA and AV node

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14
Q

What cells have fast action potentials?

A

Conductile (bundle of his and purkinje fibers) and contractile cells (ventricular and atrial cells)

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15
Q

What causes the upstroke (phase 0) in a fast action potential?

A

Fast inward Na+ current

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16
Q

What causes early depolarization (Phase 1) in fast action potential?

A

Activation of some transient K+ channels to flow out of the cell (sodium channels closed at this point)

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17
Q

What is responsible for the plateau phase (Phase 2) of the fast action potentials?

A

L-type Ca2+ channels open for inward current and outward current on K+ through both transient and leaky channels (they are beginning to close however)

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18
Q

What causes repolarization (phase 3) of fast action potentials?

A

Closure of Ca2+ channels and further increase i K+ flowing out of the cell by ordinary voltage gated channels (transient channel is closed at this point)

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19
Q

What causes resting potential (phase 4) in a fast action potential?

A

Back ground k+ currents through ordinary voltage gates and leaky gates

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20
Q

Why do fast action potentials last longer than a neuron action potential?

A

The plateau phase prolongs it

21
Q

What causes the upstroke (phase 0) in slow action potentials?

A

It is a gradual upstroke due to inward, long-lasting Ca2+ current (L-type channel)

22
Q

What causes repolarization (phase 3) in slow action potentials?

A

Ca2+ channels close and k+ channels open and k+ flows out

23
Q

What is responsible for pacemaker potential (phase 4) in slow action potentials?

A

“Funny” Na+ current in and transient Ca2+ current in (T-type channel)

24
Q

What does the “funny” Na+ channel do?

A

It slowly leaks sodium which contributes to the transient slow depolarization and “drifting”. This eventually triggers the opening of transient calcium current, and combined, threshold is reached.

25
Q

Why is it a good thin that the refractory period of the action potential and the contractile response in cardiac muscle line up?

A

It makes summation and tetanus of cardiac muscle impossible -no other action potential to pump the heart can be elicited during the contractile phase.
-Ensures periods of contraction and relaxation which are essential for pumping blood

26
Q

Where does the Ca2+ come from in cardiac muscle excitation-contraction coupling?

A

Both the SR and from the outside.

  • There is a small amount of Ca2+ entry from the ECF through L-type channels. This leads to calcium induced calcium release because the calcium from the ECF acts as a second messenger for RYR receptors of the SR, which ultimately results in a large amount of Ca2+ release from the SR.
27
Q

What are the 3 ways that calcium is removed from the cell?

A
  • SERCA (active transport)
  • Na+/Ca2+ exchanger (secondary active)
  • Ca2+ ATPase (active transport)
28
Q

An increase in contractility means that there has also been an increase in what else?

A

Tension develops at a given fiber length- fiber length is not changing.

29
Q

What is a positive ionotropic effect?

A

Increase in contracility that involves an increase in the amount of tension developed and also an increased rate of tension development at a given fiber length

30
Q

What is a negative ionotropic effect?

A

A decrease in contractility that involves a decrease in tension development and a decrease in the rate of tension development at a given fiber length.

31
Q

The ability to alter the contracility in any muscle is primarily relegated to the regulation of ***

A

Ca2+ influx

32
Q

Which cranial nerve carries parasympathetic impulses to the heart?

A

Vagus

33
Q

What are chronotropic effects?

A

Effects that change the heart rate

34
Q

What is a dromotropic effect?

A

Something that affects the conduction speed in the AV node and subsequently, the rate of electrical impulses in the heart

35
Q

What is an ionotropic agent?

A

Something that alters the force or energy of muscular contractions

36
Q

What kind of effect does the sympathetic NS have on contractility or ionotropy?

A

Positive ionotropic effect, which has 3 features:

1) Increased peak tension
2) Increased rate of tension development
3) and a faster rate of relaxation

37
Q

The sympathetic effect of heart rate is mediated by activation of what? What happens when this is activated?

A

Mediated by activation of B1 receptors, which are coupled to G proteins and adenylate cyclase = increased production cAMP, activation of PKA, and phosphorylation of proteins that produce physiological effect of increased contractility

38
Q

What are the two proteins that are phosphorylated to produce the increase in contractility?

A
  • The sarcolemmal Ca2+ channel: These carry more Ca2+ in
  • Phospholamban, the protein that regulates the Ca2+ ATPase in the SR. Results in greater uptake and storage of Ca2+ by the SR
39
Q

What are the two effects of increased Ca2+ uptake by the SR?

A

1) causes faster relaxation

2) Increases the amount of stored Ca2+ for release on subsequent beats

40
Q

What kind of effect does the parasympathetic NS have on contractility or ionotropy?

A

Negative ionotropic effect

41
Q

The parasympathetic effect on heart rate is mediated by what? What happens when this is stimulated?

A

Mediated by muscarinic receptors coupled to Gi coupled proteins and adenylate cyclase.

42
Q

What are the two factors responsible for the decrease in atrial contractility caused by parasympathetic stimulation?

A

1) ACh decreases inward Ca2+ current during AP plateau
2) ACh increases K permeability (it flows out) thereby shortening the duration of AP and indirectly decreasing inward Ca2+ current

43
Q

How does heart rate effect contractility?

A

The Ca2+ released from the SR can be cumulative when the HR is fast enough because there is less time to pump Ca2+ back into the SR. That can cause the staircase effect- with every single bout of activation, you have a larger amount of Ca2+ which means the tension of the heart contraction is stronger

44
Q

What effects does the parasympathetic NS have on the atrial and ventricular muscle?

A

No significant effects

45
Q

What effects does the sympathetic NS have on atrial and ventricular muscle?

A

Increased strength of contraction

46
Q

How do Na-K ATPase blockers work?

A

They inhibit the Na-K ATPase which increases the ICF Na+ concentration, thereby revering the Na+/Ca+ exchanger leading to higher intracellular Ca2+. This results in enchanced contractility (Positive ionotropy)

47
Q

What are the vascular effects that calcium channel blockers have?

A

Smooth muscle relaxation (vasodilation)

48
Q

What are the cardiac affects of calcium channel blockers?

A

Decreased contractility, decreased heart rate, and decreased conduction velocity

49
Q

What are the effects of B-agonists on contractility?

A

Positive Inotropy via the cAMP-pathway

Physiology 1 (6 decks)

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