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Physiology Exam 2 (Lauren) > Cardiac Electophysology > Flashcards

Cardiac Electophysology Flashcards

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1
Q

What are the two connections between cardiac muscle cells?

A

Gap junctions

Desmosomes

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2
Q

What is the function of desmosomes?

A

Hold the cardiac muscle cells together

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3
Q

What allows the cardiac muscle tissue to function as a syncytium?

A

Gap junctions

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4
Q

Does the heart rely on outside innervation to initiate action potentials?

A

No the SA node is self-depolarizing

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5
Q

What isolates the electrical current of the atria from the ventricles?

A

A band of electrically nonconductive fibrous tissue

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6
Q

Why cant the atria and ventricles contract at the same time?

A

The ventricles wouldn’t be able to fill with blood if they did

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7
Q

Which parts of the heart have their own special kind of action potential?

A

SA node

AV node

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8
Q

Where are the fastest action potentials?

A

The ones between the bundle of his and the purkinje fibers

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9
Q

Where is there the longest delay in the conduction?

A

AV node to bundle of his

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10
Q

Why is there a delay between the AV node and bundle of his?

A

Very slow conduction through the AV node.

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11
Q

What is the benefit of having a delay between the AV node and the bundle of his?

A

Allows adequate time for ventricular filling between beats**

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12
Q

What is meant by overdrive suppression?

A

The phenomenon bu which the SA node drives the heart rate and suppresses the latent pacemakers (AV node, bundle of His, purkinje fibers)

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13
Q

What is ectopic focus/ectopic pacemaker?

A

When the latent pacemakers have an opportunity to drive the heart rate.
(SA node firing rate decreases- ex fatal stimulation

SA node stops firing completely-damage

Intrinsic firing of latent pacemakers becomes faster

Conduction of APs form the SA node is blocked due to disease)

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14
Q

What would happen if the AV node failed?

A

The atria would be driven by the SA node, and the ventricles would be driven by the much slower Purkinje fibers

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15
Q

What is another name for nodal cells?

A

Pacemaker cells

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16
Q

What kind of action potentials for conductyile and contractile cells do?

A

Fast action potentials

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17
Q

What channels cause phase 0 Upstroke in fast action potential?

A

Voltage gated Na+ channels

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18
Q

What channels cause Phase 1 (early depolarization) in fast action potentials?

A

Transient K+ channels

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19
Q

What channels cause phase 2 (plateau phase) in fast action potential?

A

L-type Ca+ channels (voltage gated)

K+ channels

They are fighting

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20
Q

What channels cause phase 3 (reploarization) in fast action potential?

A

Ca+ channels closing, and K+ current increasing

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21
Q

Why isn’t there a hyperpolariation in fast action potentials?

A

Because the resting membrane potential of cardiac muscle is close to -90mV already, so background K+ current will keep it close to it’s resting membrane potential

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22
Q

Why is the resting membrane potential of fast action potential cells -90mV?

A

Because of the high permeability of the membrane to K+ at rest

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23
Q

WHere do the inactivation gates on the sodium channels close in fast action potentials?

A

at the peak of phase 0

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24
Q

What phases are missing in the slow action potential?

A

1 (early depolarization) and 2 (plateau)

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25
What causes the phase 0 (upstroke) in slow action potential?
L-type Calcium channels
26
How can pacemaker cells induce their own spontaneous action potentials?
The funny Na+ channels start opening as soon as they become negative, and once they hit a certain voltage, the voltage gated/L-type Ca+ channels start opening
27
Why can’t the heart muscle reach tetany?
The plateau phase (in fast action potentials) is so long that it guarantees that the muscle will relax before another action potential can be fired
28
Why is it a good thing that tetany of heart muscle is impossible?
It ensures alternate periods of contraction and relaxation which are essential for pumping blood
29
Instead of DHP receptors in the T-tubules of heart muscle, what do we have instead?
L-type Calcium channels
30
What happens when the action potential reaches the voltage gated/L-type calcium channels in the t-tubules?
They open and a small amount of Calcium from the ECF enters, and then the small amount of calcium tells the RYR channels to release a lot of calcium from the SR
31
During what phase of the fast action potential do the L-type Ca+ channels open?
Plateau
32
What is the result of Calcium induced calcium release from the SR
cytosolic calcium levels increase | Calcium binds to troponin and allows the formation of cross bridges
33
A decrease in contractile force occurs when the concentration of intracellular calcium______
Decreases
34
What are the 3 mechanisms of decreasing intracllular calcium?
SERCA (primary active transport) Sarcolemmal Na+/Ca+ exchanger (secondary active transport) Sarcolemmal Ca+ ATPase
35
The mechanisms for removing intracellular calcium in cardiac muscle is most similar to smooth muscle or skeletal muscle?
Smooth
36
What gives the sarcolemmal Na+/Ca+ exchanger the energy to do what it does?
Na+/K+ ATPase that makes the sodium gradient
37
Does cardiac muscle exhibit summation or recruitment?
No
38
Why doesn’t cardiac muscle do recruitment?
Because there are no motor units. The gap junctions make it all one unit
39
Is cardiac muscles at Lo (optimal length) when the heart chamber is empty?
No, it reaches Lo when it is stretched by the filling of the atrium/ventricle
40
Stretching cardiac muscle (increases or decreases) contraction?
Increases
41
What is a positive inotropic effect?
Something that increases the contractility of the heart (Involves an increase in the amount of tension developed and also an increased rate of tension development at a given fiber length)
42
What is a negative inotropic effect?
Anything that decreases the contractility of the heart | Decrease in tension development and a decrease in the rate of tension development at a given fiber length
43
What ion mostly determines the inotropic state of the heart?
Calcium
44
What is the inotropic state?
Contractility state
45
Where does the intracellular calcium come from? What causes it’s release?
Comes from the SR Calcium coming through L-type calcium channels triggers its release
46
How do you regulate the inotropic state of the heart?
Regulate the L-type calcium channels
47
A single action potential provides sufficient free cytoplasmic Ca+ to activate what percentage of the cross bridges?
50%
48
Which nerve carries parasympathetic impulses to the heart?
Vagus
49
What parts of the heart are under parasympathetic innervation?
SA node and AV node
50
Which parts of the heart are under sympathetic innervation ?
SA node AV node Contractile tissues of the ventricles
51
What is the term for heart rate?
Chronotropy
52
What is modulated to change the conduction velocity?
Dromotropy
53
What do you change to modulate the contractility
Inotropy
54
What causes the drifting rise of the voltage of the slow action potential?
Funny sodium channels
55
What is the target of sympathetic and parasympathetic innervation to speed up or slow down the heart
The funny sodium channels | Letting in more or less sodium
56
Sympathetic innervation involves norepinephrine binding to ___ receptors on the heart, which are coupled via ____receptors to ______. This causes an (increase/decrease) in cAMP. cAMP then activates ________ which leads to (increased/decreased) phosphorylation of ________ and _______
``` B1, Gs Adenylate cyclase Increase Protein Kinase A Increased Sarcolemmal L-type Calcium channels Phospholamban ```
57
What are the 3 important features of the positive inotropic effect?
Increased peak tension Increased rate of tension Faster rate of relaxation
58
Phosphorylation of the sarcolemmal L-type calcium channels causes what?
Increased Ca-induced Ca release from the SR
59
What enzyme phosphorylates the sarcolemmal L-type Ca+ channels?
Protein kinase A
60
What is phospholamban coupled to?
SERCA
61
What is the result of phosphorylation of phospholamban (PLB)?
Increased uptake of calcium into SR | Faster relaxation, plus more calcium in SR for contraction next time
62
Parasympathetic innervation to the heart involves ____ binding to _____ receptors which are coupled to ______ proteins which cause an (increase/decrease) in contractility
ACh Muscarinic Gi Decrease
63
How does parasympathetic innervation cause a decrease in contractility
1. ) Decreased calcium flowing through sarcolemmal L-type calcium channels 2. ) increased K+ current which keeps the voltage more negative and shortening the plateau phase
64
What is the overall effect of parasympathetic innervation?
Decreased amount of Ca+ entering atrial cells during the action portential, decrease the trigger Ca+, and decreased amount of Ca+ released from the SR
65
A positive inotropic effect will (increase/decrease) cardiac output
Increase
66
A negative inotropic effect will (increase/decrease) cardiac output?
Decrease
67
Increased heart rate will cause an (increase/decrease) in tension/contractility (Tension is a measure of contractility)
Increase
68
What parts of the heart are affected by sympathetic stimulation?
SA Node AV Node Atrial muscle Ventricular muscle
69
Which parts of the heart are affected by parasympathetic stimulation?
SA node | AV node
70
Sympathetic stimulation will always cause (constriction/dilation) of vessels excpet for skeletal muscle vessels which will (constrict/dilate)
Constriction Dilate
71
What type of receptors are on the arterioles supplying skeletal muscle? What about the arterioles that supply the rest of the body?
Skeletal- B2. (Dilate) All other arterioles- a1 (constrict)
72
A drug that blocks the Na-K ATPase pump will have what effect?
It will block the pump that creates the gradient that allows the other pump to reduce intracellular calcium. Calcium will accumulate in the cytosol, and contractility will increase.
73
What are examples of drugs that block the Na+/K+ ATPase pump?
Digitalis Digoxin
74
What are the effects of calcium channel blockers on the heart?
1. ) decreased contractility( negative inotropy) 2. ) decreased heart rate (negative chronotropy) 3. ) Decreased conduction velocity (negative dromotropy)
75
What are some examples of calcium channel blocker drugs?
Verapamil diltiazem
76
What will B-agonists do?
They will mimic sympathetic stimulation. Calcium will accumulate and increase the force of contraction
77
What is an example of a B-agonist and why would we give it to someone?
Isoproterenol for heart attack or congestive heart failure

Physiology Exam 2 (Lauren) (5 decks)

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