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FHB exam one > Heart 2 > Flashcards

Heart 2 Flashcards

1
Q

Intercalated disc

A

Specialized region of intercellular connections between cardiac cells

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2
Q

Three types of adhering junctions within an intercalated disc

A

Fascia adherens, macula adherens, and gap junctions

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3
Q

Fascia adherens

A

Anchoring sites for actin that connect to the closest sarcomere

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4
Q

Macula adherens

A

Holds cells together during contraction by binding intermediate filaments, joining the cells together (desmosomes)

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5
Q

Gap junctions

A

Low-resistance connections that allow current (AP’s) to conduct between cardiac cells

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6
Q

How close are cell membranes in heart cells?

A

2-4 nanometers

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7
Q

Connexon channels

A

Create intracellular connections

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8
Q

Primary determinant of internal resistance in cardiac tissue

A

Gap junctions

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9
Q

“Healing over”

A

Increase in internal resistance that results from a decrease in the number of open gap junctions

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10
Q

What causes healing over?

A

Increase in intracellular (cytosolic) calcium and/or hydrogen ions

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11
Q

Clinical application of healing over

A

Damaged tissue from a myocardial infarction will become electrically isolated

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12
Q

Three factors that determine cardiac conduction

A

Length constant, and rate of rise AND amplitude of action potential

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13
Q

Membrane resistance is inversely related to __ __.

A

potassium permeability

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14
Q

Internal resistance is inversely related to . . .

A

the number of gap junction connections AND to cell diameter

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15
Q

What is shown on a graph showing the relationship between the number of available fast Na+ channels and the membrane potential before stimulation of an action potential?

A

Shows that all the sodium channels have already been activated during depolarization and are no longer open to continue working. The number hits zero around -50mV, which is right about where the depolarization happens

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16
Q

Conditions that influence the AP upstroke due to changes in the RMP

A

Hyperkalemia, premature excitation during relative refractory period, ischemia/myocardial injury

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17
Q

What effect does hyperkalemia have on the upstroke of the AP waveform?

A

The fast upstroke will not be present, as the sodium channels have been deactivated already from the membrane potential being so close to threshold. Creates a slow waveform

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18
Q

Other than elevated blood levels of potassium, how else can hyperkalemia be stimulated?

A

If there is an infarct in an area of the heart, the injured cells can leak out potassium and increase the concentration of potassium in the local ECF

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19
Q

During infarction, how high can the local potassium concentration reach?

A

Up to 20 mEq/L

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20
Q

P-R interval

A

Conduction time from atria to ventricular muscle

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21
Q

QRS interval

A

Intraventricular conduction time (i.e., conduction through ventricles)

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22
Q

Why does the AV node delay?

A

To allow time for optimal ventricular filling

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23
Q

Why is AP slow at the AV node

A

Due to slow inward calcium current

24
Q

How is the long refractory period of the AV node beneficial?

A

Protects the ventricles from abnormally high atrial rates (i.e., atrial fibrillation or atrial flutter)

25
Q

Clinical determinant of AV nodal conduction time

A

P-R interval

26
Q

First degree heart block

A

Abnormal prolongation in P-R interval greater than 0.20 seconds

27
Q

Second degree heart block

A

Some atrial impulses fail to activate ventricles; not all P waves are followed by a QRS complex

28
Q

Third degree heart block

A

Complete AV nodal block; no consistent P-R interval

29
Q

Typical method of travel through the His-Purkinje system

A

Rapid conduction that brings the electrical impulse to the endocardial surface, resulting in endocardial and epicardial activation of the ventricles

30
Q

How long is the QRS complex normally?

A

Less than 100 msec in duration; narrow

31
Q

Clinical determinant of intraventricular conduction time

A

Duration of QRS complex

32
Q

Why does the QRS complex need to be so short?

A

Syncrhonized ventricular activation to give a concise and strong contraction

33
Q

Possible causes of slurred QRS complexes

A

Hyperkalemia, ischemia, ventricular tachycardia

34
Q

Notched QRS complex

A

Indicates asynchronous electrical activation of the left and right ventricles

35
Q

Possible causes of a notched QRS complex

A

Right and/or left bundle branch blocks

36
Q

Supraventricular tachycardia

A

Conduction through the ventricles is normal, just rapid; the impulse still comes from the atria and travels through the AV node into the His-Purkinje system.

37
Q

Ventricular wall motion and QRS during supraventricular tachycardia

A

QRS duration is normal because ventricles are firing normally, just more frequently. Ventricular wall motion is normal

38
Q

Ventricular tachycardia

A

Conduction through the ventricles is not normal, because the impulse originates within the ventricular muscle and not through the His-Purkinje system

39
Q

EKG findings and ventricular wall motion during ventricular tachycardia

A

QRS duration is prolonged (slurred) and the wall motion is abnormal. This causes a compromise in stroke volume

40
Q

What determines atrial conduction?

A

The shape of the P wave of an EKG

41
Q

Which is more fatal: a-fib or v-fib?

A

V-fib, since that is what is responsible for getting the blood oxygenated and perfused to the body. Atrial dysrhythmia will still get enough blood through to sustain life

42
Q

What is the life-threatening secondary effect of atrial fibrillation?

A

Clotting due to pooling of blood in the atrial appendages, increasing potential for stroke, MI, or PE

43
Q

How does acetylcholine act in the heart?

A

Via muscarinic receptors

44
Q

What is the effect of the ACh release in the heart?

A

Increases K permeability directly via G-proteins, hyperpolarizing the membrane and decreasing the chance for action potential

45
Q

What is the other secondary effect of ACh release on the heart?

A

Inhibition of adenylate cyclase activity and cAMP synthesis, decreasing slow inward calcium current indirectly

46
Q

ACh directly inhibits these structures in the heart

A

Atrial muscle, SA node, and AV node

47
Q

What are the effects of ACh on an EKG?

A

Lengthened P-R interval, lengthened R-R interval

48
Q

What does ACh not directly effect?

A

Basal ventricular muscle function

49
Q

Atropine

A

Pharmaceutical agent that blocks the muscarinic ACh receptors

50
Q

What areas of the heart does norepinephrine affect?

A

All areas

51
Q

What is the primary receptor acted on by norepinephrine in the heart?

A

Beta-1 adrenergic receptors

52
Q

When NE binds its receptors, what intracellular signal is released?

A

cAMP

53
Q

On what gradient does NE have an effect?

A

Positive effect on slow inward calcium current

54
Q

EKG changes seen after NE release

A

Decreased R-R interval, decreased P-R interval

55
Q

Inotropic effect

A

Hormonal reaction that changes contractility of the heart

FHB exam one (23 decks)

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