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Pathophysio 1 Final > Module 2 > Flashcards

Module 2 Flashcards

1
Q

bradycardia

A
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2
Q

tachycardia

A

> 100 bpm

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3
Q

Spread of electrical excitation

A
  1. SA node
  2. Internodal pathway
  3. AV node
  4. bundle of his
  5. right and left bundle branches
  6. Purkinje fibers
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4
Q

time of electrical conduction

A

0.2-0.3 seconds

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5
Q

Increase temp
Various drugs
inspiration
all act to ____ the heart rate

A

increase

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6
Q

Respiratory sinus arrhythmia

A

normal occurrence, as a result of inspiration/vagus reflex

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7
Q

Increase parasympathetic influence
decrease sympathetic influence
meds- digitalis
all act to _____ the heart rate

A

decrease

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8
Q

how does inspiration affect the heart rate?

A

brief decrease in vagus tone thus increases the heart rate

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9
Q

time for atria to depolarize

A

0.1 sec

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10
Q

Bachmann bundle aka

A

anterior pathway- transmits directly to left atria

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11
Q

length of delay at AV node

A

0.1 sec

fxn to allow atrial kick

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12
Q

Sympathetic NS will ______ delay at AV node

A

Shorten

S S

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13
Q

Parasympathetic NS will ______ delay at AV node

A

lengthen

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14
Q

time for ventricle depolarization

A

0.1 sec

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15
Q

P wave

A

SA node is depolarized, sends AP throughout atria via internal atrial pathways
1/10 second (wow 0.1 for everything)

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16
Q

conduction delay at AV node

A

0.1 sec. “PR” or “PQ” INTERVAL- from start of atrial contract to start of ventricle contraction

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17
Q

Q wave

A

septal depolarization

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18
Q

R wave

A

ventricular depolarization

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19
Q

S wave

A

depolarization of pukinje fibers

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20
Q

ST SEGMENT

A

NO electrical activity

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21
Q

T wave

A

ventricular repolarization

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22
Q

Segment vs interval

A 
Segment = between waves
Interval = include one of both waves
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23
Q

ELEVATED ST segment

A

potential acute MI, ischemia

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24
Q

DEPRESSED ST segment

A

potenial ischemia, acute posterior MI

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25
Q

Complete Block

A

3rd degree

complete disruption of conduction btwn atria and ventricles

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26
Q

Incomplete block

A

1st - all atrial impulses reach bent ricks but its slow

2nd- some atrial impulse reach ventricle

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27
Q

Many P wave with occasional QRS

A

EKG of 3rd degree black

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28
Q

Elongated PR interval

A

EKG of 1st degree block

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29
Q

3:1 block- 3 P follow by 1 QRS

A

EKG of 2nd degree block

30
Q

During a complete block what is the pacemaker of the heart

A

Ventricles

sustain 35-45 bpm

31
Q

Less deadly that ventricular tachy/fib

A

Atrial tachycardia (tach)

32
Q

atrial flutter speed

A

200-350 action potential (HR) per minute

33
Q

Atrial flutter risk of _____ from ____

A

CVA

stasis- clot formation

34
Q

Atril fibrilation speed

A

> 300-350 action potentials per minute

35
Q

EKG characteristics of A-fib

dr stowell had a-fib

A

chaotic P wave morphology

uncoordinated depolarization

36
Q

MC arrhythmia encountered in clinical practice

37
Q

AV node and ventricles _____ keep up and __________

A

CAN NOT

they max out around 200 bp

38
Q

Ventricular Tach speed

A

> 100 bpm and > 3 irregular beats (PVCs) in a row

39
Q

Ventricular Fibrillation

A

functionally heart can’t act as a pump

MEDICAL EMERGENCY

40
Q

MC cause of death in MI

41
Q

Cardiac AP- slow response

A

unstable resting membrane potential

pacemaker cells

42
Q

Cardiac AP- fast response

A

stable resting membrane potential

contractile cells

43
Q

Phase 4 (slow depolarization)
driving force-
(slow depolar)

A

inc. Na+ into cell, depolarizes membrane via “slow Na+ channels”
at -50mV - inc. Ca++ into cell via “transient Ca++ channels”

44
Q 
Phase 0 (upstroke) 
(slow depolar)
A

inc Ca++ into cell

45
Q 
Phase 3 (repolarization)
(slow depolar)
A

inc. K+ out of cell

46
Q 
Phase 0 (upstroke)
(fast response)
A

rapid inc. Na+ into cell

47
Q 
Phase 2 (plateau)
(fast response)
A

initial inc. K+ out of cell

48
Q 
Phase 3 (repolarization)
(fast response)
A

Inc. K+ out of cell

49
Q 
Phase 4 (resting membrane potential)
(fast response)
A

K+ maintain resting membrane potential

50
Q

Fast response AP exhibit prolonged positive phase with prolonged _____________

A

period of contraction

51
Q

Fast response AP exhibit prolonged positive phase with prolonged _____________

A

period of contraction (ensures adequate ejection time)

52
Q

Parasymp. response on nodal cells in Atria

A

promote/prolong K+ efflux out and inhibit Na+ and Ca++ influx into pacemaker cells

53
Q

Decrease slope/increase duration of phase 4

A

Primary effect of parasymp. in Atria

54
Q

Sympathetic action on the heart

A

Inc. HR, Inc. Contratilit, Inc. relaxation rate

aka less relaxation time

55
Q

Prolong/ increase Ca++ influx

A

Sympathetic stimulation

56
Q

Pacemaker cells

A

increase slope/decrease duration of phase 4

57
Q

Vaughan William Classifications:

Class 1

A

Sodium Channel blockade

58
Q

Class 1A
1B
1C

A

Moderate
Weak
Strong

59
Q

Class 2

A

Beta Blockade

60
Q

Class 3

A

Potassium channel blockade

61
Q

Class 4

A

Calcium channel blockade

62
Q

Elevated K+ levels and cardiac APs result:

A

Bradycardia

severe hyperK can be rapidly fatal

63
Q

Elevated K+ levels and cardiac APs result:

A

Bradycardia

severe hyperK can be rapidly fatal

64
Q

Phase 2 and 3 (fast response)

A

hyperkalemia causes and INCREASE in efflux on potassium out of myocardium during repolarization
result= shortened repolarization

65
Q

Elevated K+ levels and cardiac APs result:

EKG changes

A

Slowing of conduction: peaked T waves- initial

progression: Widening of QRS interval and ventricular arrhythmias develop
terminal: sine wave pattern

66
Q

Decrease K+ levels and Cardiac APs result:

A

result is Tachycardia/arrhythmias

67
Q

Hypokalemia in ECF will

A

hypopolarize cell (hard to excite) but the OPPOSITE happens in CARDIAC CELL. they HYPEREXCITE

68
Q

Hyperexcite Phase 2 and 3 (fast response)

A

increase ECF will prolong or slow repolarization

69
Q

EKG changes Dec Potassium

A

Initial: depression of T wave, elevated U wave

70
Q

EKG changes Dec Potassium

with marked hyopkalemia

A

t wave becomes progressively smaller, u wave becomes increasingly bigger

71
Q

EKG changes Dec Potassium further

A

ventricular and atria tach, potential v fib

72
Q

Calcium in cardiac muscle increased then

A

if large amount of Ca++ was released in cardiac muscle it would be unable to relax

Pathophysio 1 Final (2 decks)

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