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110_Cardiac > Cardiac Arrhythmias > Flashcards

Cardiac Arrhythmias Flashcards

1
Q

Sinus Brady

A
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2
Q

Sinus Brady Causes

A

Can occur in response to parasympathetic nerve stimulation and certain drugs

Also associated with some disease states
(Normal rhythm in aerobically trained athletes and during sleep)

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3
Q

Sinus Brady Manifestations

A

Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

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4
Q

Sinus Brady Treaments

A

Stop offending drugs
IV Atropine
Pacemaker
Dopamine or epinephrine infusion

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5
Q

Sinus Tachy

A
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6
Q

Sinus Tachy causes

A

Caused by vagal inhibition or sympathetic stimulation
Associated with physiologic and psychologic stressors
Drugs can increase rate

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7
Q

Manifestations of Sinus Tachy

A

Dizziness
Dyspnea
Hypotension
Angina in patients with CAD

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8
Q

Sinus Tachy treatment

A

Guided by cause (e.g., treat pain)
Vagal maneuver
β-blockers, adenosine, or calcium channel blockers
Synchronized cardioversion

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9
Q

A patient’s cardiac rhythm is sinus bradycardia with a heart rate of 34 beats/min. If the bradycardia is symptomatic, the nurse would expect the patient to exhibit:

Palpitations.
Hypertension.
Warm, flushed skin.
Shortness of breath.

A

SOB

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10
Q

Premature Atrial Contraction (1 of 4)

A
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11
Q

What is PAC?

A

Contraction starting from ectopic focus in atrium in location other than SA node
Travels across atria by abnormal pathway, creating distorted P wave
May be stopped, delayed, or conducted normally at the AV node

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12
Q

Premature Atrial Contraction Causes

A

Emotional stress
Physical fatigue
Caffeine
Tobacco
Alcohol
Hypoxia
Electrolyte imbalances
Disease states

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13
Q

PAC Manifestations

A

Palpitations
Heart “skips a beat”

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14
Q

Paroxysmal Supraventricular Tachycardia (PSVT) (1 of 4)

A
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15
Q

PSVT def

A

Reentrant phenomenon: PAC triggers a run of repeated premature beats
Paroxysmal refers to an abrupt onset and ending
Associated with overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity

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16
Q

PSVT Manifestations

A

Manifestations
HR is 151 to 220 beats/min
HR greater than 180 leads to decreased cardiac output and stroke volume
Hypotension
Palpitations
Dyspnea
Angina

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17
Q

PSVT Treatment

A

Vagal stimulation
IV adenosine
IV β-blockers
Calcium channel blockers
Synchronized cardioversion

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18
Q

Pulse pressure of Pt

A

SBP - DBP = 40 or greater

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19
Q

If pulse pressure is less than 40

A

Pt has decreased cardiac output

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20
Q

If pulse pressure greater than 60

A

Cause due to atherosclerosis

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21
Q

Propertis of cell:

A

Automaticity = Potassium in/out
Excitability = to electrically stimulate
Contractility = mechanically to impulse
Conductivity = Mechanical

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22
Q

SA node (Pacemaker) > AV node (Gatekeeper) > Bundle of HIS > Purkinje fibers of heart

A
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23
Q

Slide#4
ST segnment Repolarization

A
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24
Q

Depolarization

A

Contraction

25
Q

Repolarization

A

Relaxation

26
Q

EKG Placement
1 Pulse = PQRST
1 small box = 0.04
5 boxes = 0.2

A

1 stip = 6 sconds
Count HR by counting the R waves and x 10

27
Q

Slide#18

A

SA node, AV node = working good.

28
Q

Slide#19
SNB

A

IV Atropine for Bradycardia
Give Dopamine to increase BP

29
Q

Slide #25
SNT = 140 = HR

30
Q

Slide#27

A

Dizziness
Dyspnea
Hypotension
Angina in CAD

31
Q

Slide# 33
SVT is

A

150 bpm to 200 bpm and above

32
Q

Causes of SVT

A

Stress/ Exersion/ Stimulant. Dig toxicity

33
Q

With SVT

A

Cannot breathe anymore
Cardiac do not have enough o/p

34
Q

Slide# 36
Treatment SVT

A

Vagal Stimulation
Adenosine
Beta blockers
Calcium Channel Blocker
Synchronized Cardioversion

35
Q

Verpamil short hald life

A

Inject fast and raise hand immediately

36
Q

Atrial Flutter

A

Flutter is saw tooth

37
Q

CAD give

A
  • Beta blockers : metoprolol not converting then develop thrombosis so give
    Heparin or Coumadin
  • Cardioversion
  • Ablation
38
Q

Atrial fibrillation no P waves

A

P undistinguishable

39
Q

QRS not equal

A

too many Ps cannot identify Ps
but can be regular in between

40
Q

Treatment of a-fib

A

give anticoagulant (develop thrombosis)
cardioverson
RFA (Radio Frequency Ablation)
Cardiac Monitoring

41
Q

ROSC first identified monitor them by

A

EKG, count pulse

42
Q

a-fib question select

A

administer oxygen, IV access, monitor VS, ask hx before

43
Q

Identify ROSC what you have to do

A

EKG, Oxygen, anticoagulants, IV establish, medication , Teaching Pt.

44
Q

Slide $49
AV block 1

A

more than 0.12 - 0.20 PQ segment or P to Q distance

45
Q

Second degree HB

A

Progressive P
smaller-long-longer QRS dropped.

46
Q

Second deg HB give Morbitz 1 or Wenkcheback

A

Atropine (1) + Pace Maker (2) + EKG

47
Q

Second degree Morbitz 2

A

7 Ps seen and 5 QRS waver…PR interval consistent = but drops QRS in between with R irregular

48
Q

Morbitc type 2 associated with

A

Drug Toxicity
Heart Block

49
Q

Slide #55 : Final Examination
3rd degree HB

A

P no association with QRS
P regular and QRS regular
PR interval independent

50
Q

3rd degree HB s/s

A

decreased cardiac o/p > ischemia > develops shock.

51
Q

Ventricular Tachycardia

A

Lethal monomorphic
single firing site
Pacemaker not firing that is SA node not firing and AV node not firing = no pulse
this can kill a patient

52
Q

Beats in v-tach

A

200 - 280
Only ventricles are functioning
w/o pulse
QRS waves are wide.

53
Q

Slide#65
Torsades de Pointe

A

different sizes

54
Q

long QT, stable or unstable with pulseless ?

55
Q

Slide # 66
v-fib

A

give amiodrone
pulseless = pumping + defib

56
Q

v-tach cause is because

A

Hypoxia
CPR

57
Q

Slide #68
V-fib pt. dies

A

Give epinephrine for pulseless
Amiodarone

58
Q

Slide#69
SVT know meds

110_Cardiac (8 decks)

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