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Exam2 ECG/Basic Labs/Pharm > ECG I & II > Flashcards

ECG I & II Flashcards

1
Q

Aberrancy/Aberrant conduction

A

abnormal pathway of an impulse traveling through the heart’s conduction system

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2
Q

Arrhythmia

A

disturbance of the normal cardiac rhythm from the abnormal origin, discharge, or conduction of electrical impulses

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3
Q

automaticity

A

ability of cardiac cell to initiate an impulse on its own

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4
Q

Biphasic

A

Having an electrical impulse that is shown as deflections above and below the isoelectric line

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5
Q

chronotropy

A

neural, chemical, or physical factor that influences heart rate; referring to rate or time, such as the rate of cardiac contraction

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6
Q

positive chronotropic agent

A

increase heart rate

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7
Q

negative chronotropic agent

A

decrease heart rate

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8
Q

dromotropy

A

agent the affects the conduction speed of the AV node and subsequently the rate of electrical impulse; referring to the conductivity of a nerve fiber, such as the ability to conduct through the AV node

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9
Q

positive dromotropic agent

A

increase velocity

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10
Q

negative dromotropic agent

A

decrease velocity

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11
Q

inotropy

A

chemicals that influence contractility of the heart

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12
Q

positive inotropic agents

A

increase contractility

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13
Q

negative inotropic agents

A

decrease contractility

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14
Q

conductivity

A

ability of one cardiac cell to transmit and electrical impulse to another cell; the reciprocal of resistivity

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15
Q

depolarization

A

response of a myocardial cell to an electrical impulse that causes movement of ions across the cell membrane, which triggers myocardial contraction; the process or act of reversing the resting potential in excitable cell membranes when stimulated

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16
Q

deviation

A

major direction of the overall electrical activity of the heart. It can be normal, leftward (left axis deviation, or LAD), rightward (right axis deviation; RAD) or indeterminate (northwest axis). The QRS is the most important to determine; however, the P wave or T wave axis can also be measured

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17
Q

escape rhythm

A

a self-generated electrical discharge initiated by, and causing contraction of, the ventricles of the heart; this beat usually follows a long pause in ventricular rhythm and acts to prevent cardiac arrest

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18
Q

excitability

A

ability of a cardiac cell to respond to an electrical stimulus

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19
Q

infarction

A

tissue death due to inadequate blood supply to the tissue

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20
Q

intrinsic/inherent

A

naturally occurring electrical stimulus from within the heart’s conduction system

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21
Q

interval

A

duration of time that includes one segment and one or more waves

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22
Q

ischemia

A

local decrease in blood supply

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23
Q

monomorphic

A

form of ventricular tachycardia in which the QRS complexes have a uniform appearance from beat to beat

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24
Q

multifocal/multiform

A

type of premature ventricular contractions that have differing QRS configurations as a result of their originating from different irritable site in the ventricle

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25
Q

paroxysmal

A

episode of an arrhythmia that starts and stops suddenly

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26
Q

polymorphic

A

type of ventricular tachycardia in which the QRS complexes change from beat to beat

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27
Q

reciprocal leads

A

leads that take a view of an infarcted area of the heart opposite that taken by indicative leads

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28
Q

pre-excitation

A

an abnormal heart rhythm in which the ventricles of the heart become depolarized too early, which leads to their partial premature contraction

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29
Q

Threshold

A

the minimum level to which a membrane potential must be depolarized to initiate an action potential

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30
Q

ST segment

A

part of the ECG between the QRS complex and the T wave

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31
Q

sympathetic innervation “the gas pedal”

A

via thoracolumbar spinal nerve (T1-L2)

increase in SA nodal chronotropy (rate), AV nodal dromotropy (speed of AV node conduction) and myocardial intropy (contractility)

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32
Q

parasympathetic innervation “the break pedal”

A

via vagus nerve

Decreased SA nodal chronotropy and decreased AV nodal dromotropy

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33
Q

Reentry

A

normally impulse goes from AV to SA node but sometimes it turns around and goes backwards -reactivation of tissue by a returning impulse

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34
Q

accessory pathway

A

a form of reentry- a delayed or blocked impulse may travel through a different tract (no regulation)

35
Q

reentry-orthodromic-antidromic

A

the impulse may travel down the normal pathway and then back up the accessory pathway (orthodromic) or vice versa (antidromic)

36
Q

causes of reentry

A

myocardial ischemia
certain medications
hyperkalemia

37
Q

horizontal plane values

A

measures time
one small box-0.04 seconds
one large box-0.20 seconds

38
Q

p wave

A

atrial depolarization

electrical current generated by the SA node or atrial tissue

39
Q

duration of p wave

A

less than 0.12 seconds

40
Q

PR interval

A

impulse transmission time from SA node throughout the atria and to the AV node

41
Q

PR duration

A

range 0.12 to .20 seconds 3-5 small boxes

42
Q

QRS complex

A

depolarization of the ventricular myocardium

43
Q

QRS duration

A

less than 0.12 seconds

44
Q

Q wave

A

first downward deflection

45
Q

pathological q wave

A

can tell if it is pathological if you can drop a little box into it

46
Q

R wave

A

first positive upward deflection

more than one positive deflection noted as R’

47
Q

S wave

A

first downward deflection after the R wave

48
Q

ST segment

A

excited state of the ventricular myocardium
follows QRS
ventricular contractility starts here

49
Q

j point

A

landmark for MI to measure elevation or depression

50
Q

t wave

A

electrical repolarization of the ventricular myocardium

following the QRS complex

51
Q

QT interval

A

represents the return of stimulated ventricular myocardium to a resting state

52
Q

normal QT

A

normal if QT interval is less than half distance of R-R interval

53
Q

U wave

A

repolarization of the purkinje system

54
Q

causes of prominent U wave

A

profound bradycardias
hypokalemia
hypothermia

55
Q

Define Bachman’s bundle.

A

The anterior tract that divides and extends into the LA.

56
Q

Where is the triangle of Koch located?

A

In the floor of the right atrium superior to the septal leaflet of the tricuspid valve.

57
Q

What is the only pathway to the ventricles called (in a normal person)?

A

Triangle of Koch

58
Q

Why is the AV node delayed?

A
  1. to allow for atrial contraction (increase preload and subsequent contraction due to Frank-Starling mechanism)
  2. protects the ventricles from inappropriate high atrial rates (ie atrial fibrillation and flutter)
59
Q

Is the refractory period longer for the SA or the AV node?

A

The AV node refractory period is longer.

60
Q

Why is Ca++ important for electrical conduction in the heart?

A

Calcium is the major ion responsible for the action potential.

61
Q

Define automaticity

A

Self-excitation
(accomplished by P cells which are located in the SA node, atrial tissue, AV node, and ventricular tissue —they have different rates bc different refractory periods)

62
Q

What maintains the negative resting potential?

A

The sodium-potassium ATPase pump

63
Q

How does the ATPase pump reset the membrane to pre-depolarizing electrolyte levels?

A

It exchanges 3 Na+ ions OUT of the cell for

2 K+ ions INTO the cell

64
Q

Using the sodium-potassium ATPase pump is an active process. What does it require?

A

Magnesium and ATP(energy)

65
Q

Which phase of the action potential plot corresponds with the resting membrane potential?

A

Phase 4

66
Q

Describe phase 4 of the action potential

A

resting membrane potential (-80 to -90mV)
negativity maintained by the sodium/potassium pump
sodium out/potassium in
(corresponds with the baseline between the T and P wave)

67
Q

Where happens during phase 0 of the action potential?

A

Rapid depolarization of the cell (stimulus applied)
Sodium rushes out of the cell making it less negative
(Potassium leaks out of the cell)

68
Q

In what phase do the drugs lidocaine and procainamide work?

A

Phase 0

69
Q

Describe phase 1 of the action potential.

A

(Brief rapid initiation of repolarization)
(closure of the sodium channels)
Chloride ions enter the cell (makes it more negative)

70
Q

Describe Phase 2 of the action potential.

A

“Plateau” phase
Slowing of repolarization
Calcium enters the cell, leading to contraction of the muscle in a sustained, slower manner

71
Q

Which class of antiarrhythmics work at phase 2 of the action potential?

A

Class IV antiarrhythmics (calcium channel blockers)

Verapamil, Diltiazem

72
Q

Describe Phase 3 of the action potential.

A

Sudden acceleration in the rate of repolarization.
Potassium movement into the cell causes this rapid return in intracellular negativity
Sodium-potassium pump operates at this phase

73
Q

What class of antiarrhythmics work in phase 3?

A

Class III

Amiodarone, sotalol (by prolonging the return to a resting potential)

74
Q

Bachman’s bundle

A

anterior tract divided and extends into L atrium (near intra-atrial pathways)

75
Q

intra-atrial pathway

A

conduct impulse through atria from SA–> AV

76
Q

triangle of koch

A

septal leaflet of the tricuspid valve (below AV node)

77
Q

major ion responsible for AP

A

Ca

78
Q

orthodromic

A

AV node cycling

79
Q

antidromic

A

down AV node then backup through accessary pathway

80
Q

conduction velocity

A

necessary for synchronized myocardial contraction

81
Q

funny channels (If)

A

unstable membrane potential (-60mV) gradually drifts toward threshold due to opening of ___

82
Q

what ion do funny channels (If) permeable to?

A

K+ and Na+

83
Q

absolute refractory period

A

cell can’t depolarized again, no matter how strong the impulse
AP: phase 0- mid-phase3
ECG: QRS-to peak of T wave

Exam2 ECG/Basic Labs/Pharm (5 decks)

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