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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
Complete Block
3rd degree | complete disruption of conduction btwn atria and ventricles
26
Incomplete block
1st - all atrial impulses reach bent ricks but its slow | 2nd- some atrial impulse reach ventricle
27
Many P wave with occasional QRS
EKG of 3rd degree black
28
Elongated PR interval
EKG of 1st degree block
29
3:1 block- 3 P follow by 1 QRS
EKG of 2nd degree block
30
During a complete block what is the pacemaker of the heart
Ventricles | sustain 35-45 bpm
31
Less deadly that ventricular tachy/fib
Atrial tachycardia (tach)
32
atrial flutter speed
200-350 action potential (HR) per minute
33
Atrial flutter risk of _____ from ____
CVA | stasis- clot formation
34
Atril fibrilation speed
>300-350 action potentials per minute
35
EKG characteristics of A-fib | dr stowell had a-fib
chaotic P wave morphology | uncoordinated depolarization
36
MC arrhythmia encountered in clinical practice
A-fib
37
AV node and ventricles _____ keep up and __________
CAN NOT | they max out around 200 bp
38
Ventricular Tach speed
> 100 bpm and > 3 irregular beats (PVCs) in a row
39
Ventricular Fibrillation
functionally heart can't act as a pump | MEDICAL EMERGENCY
40
MC cause of death in MI
V-fib
41
Cardiac AP- slow response
unstable resting membrane potential | pacemaker cells
42
Cardiac AP- fast response
stable resting membrane potential | contractile cells
43
Phase 4 (slow depolarization) driving force- (slow depolar)
inc. Na+ into cell, depolarizes membrane via "slow Na+ channels" at -50mV - inc. Ca++ into cell via "transient Ca++ channels"
44
``` Phase 0 (upstroke) (slow depolar) ```
inc Ca++ into cell
45
``` Phase 3 (repolarization) (slow depolar) ```
inc. K+ out of cell
46
``` Phase 0 (upstroke) (fast response) ```
rapid inc. Na+ into cell
47
``` Phase 2 (plateau) (fast response) ```
initial inc. K+ out of cell
48
``` Phase 3 (repolarization) (fast response) ```
Inc. K+ out of cell
49
``` Phase 4 (resting membrane potential) (fast response) ```
K+ maintain resting membrane potential
50
Fast response AP exhibit prolonged positive phase with prolonged _____________
period of contraction
51
Fast response AP exhibit prolonged positive phase with prolonged _____________
period of contraction (ensures adequate ejection time)
52
Parasymp. response on nodal cells in Atria
promote/prolong K+ efflux out and inhibit Na+ and Ca++ influx into pacemaker cells
53
Decrease slope/increase duration of phase 4
Primary effect of parasymp. in Atria
54
Sympathetic action on the heart
Inc. HR, Inc. Contratilit, Inc. relaxation rate | aka less relaxation time
55
Prolong/ increase Ca++ influx
Sympathetic stimulation
56
Pacemaker cells
increase slope/decrease duration of phase 4
57
Vaughan William Classifications: | Class 1
Sodium Channel blockade
58
Class 1A 1B 1C
Moderate Weak Strong
59
Class 2
Beta Blockade
60
Class 3
Potassium channel blockade
61
Class 4
Calcium channel blockade
62
Elevated K+ levels and cardiac APs result:
Bradycardia | severe hyperK can be rapidly fatal
63
Elevated K+ levels and cardiac APs result:
Bradycardia | severe hyperK can be rapidly fatal
64
Phase 2 and 3 (fast response)
hyperkalemia causes and INCREASE in efflux on potassium out of myocardium during repolarization result= shortened repolarization
65
Elevated K+ levels and cardiac APs result: | EKG changes
Slowing of conduction: peaked T waves- initial progression: Widening of QRS interval and ventricular arrhythmias develop terminal: sine wave pattern
66
Decrease K+ levels and Cardiac APs result:
result is Tachycardia/arrhythmias
67
Hypokalemia in ECF will
hypopolarize cell (hard to excite) but the OPPOSITE happens in CARDIAC CELL. they HYPEREXCITE
68
Hyperexcite Phase 2 and 3 (fast response)
increase ECF will prolong or slow repolarization
69
EKG changes Dec Potassium
Initial: depression of T wave, elevated U wave
70
EKG changes Dec Potassium | with marked hyopkalemia
t wave becomes progressively smaller, u wave becomes increasingly bigger
71
EKG changes Dec Potassium further
ventricular and atria tach, potential v fib
72
Calcium in cardiac muscle increased then
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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