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FA17 Cardio 2 > Arrythmia > Flashcards

Arrythmia Flashcards

1
Q

ectopic beats

A

potentials reached by myocardial cells outside normal conduction system

spontaneously depolarize

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2
Q

escape rhythm

A

SA node fails and latent pacemakers take over

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3
Q

PAC

A

increased sympathetic activity depolarizes atria outside SA node

typically asymptomatic, may have palpitations

early beat on an otherwise normal rhythm

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4
Q

causes of PAC symptoms

A

EtOH
caffeine
emotional stress

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5
Q

bradycardia arrhythmia causes

A

issue is with the SA node

  1. sinus bradycardia
  2. sick sinus syndrome
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6
Q

sinus bradycardia

A

heart rate slowed bc of decreases SA node firing

intrinsic issue or extrinsic

often benign, only treat if symptoms

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7
Q

intrinsic causes of sinus bradycardia

A

aging

ischemic heart disease

cardiomyopathy

athletes

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8
Q

extrinsic suppression of SA node causes

A

pharm (beta blockers)

metabolic causes (thyroid, DM)

vasovagal PNS stimulation (fear, pain)

secondary to shock (hemorrhagic or neurogenic)

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9
Q

symptoms of bradycardia

A 
fatigue
light headedness
syncope
change in mental staus 
chest pain
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10
Q

tx of bradycardia

A

atropine 0.5 mg IV (temp. speeds up HR)

transcutaneous or transvenous pacing (central line)

definitive tx is implantation of pacemaker

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11
Q

Paces of SA node, AV node, ventricular escapes

A

SA: 60-100

AV: 40-60

ventricular escape: 20-40

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12
Q

junctional escape rhythm

A

arises from AV node or His

narrow QRS no P wave

HR 40-60

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13
Q

ventricular escape rhythm

A

HR 20-40

wide QRS

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14
Q

tx of escape rhythms

A

same as bradycardia

  1. atropine
  2. transcutaneous or transvenous pacemaker
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15
Q

first degree AV block

A

prolonged PR

P wave for each complex

transient or fixed

no need for tx, but can progress

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16
Q

transient first degree AV block causes

A

vagal tone increase

transient local ischemia

drugs that depress conduction

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17
Q

fixed first degree AV block causes

A

MI and or degeneration due to age

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18
Q

second degree AV block

A

intermittent failure of AV node conduction

two types (Wekenbach/Mobitz I and Mobitz II)

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19
Q

Mobitz I

A

AV delay gradually increases until impulse is blocked

PR segment increases between each beat until blockage and then is reset

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20
Q

population with Mobitz I

A

type I 2nd degree AV block

children, athletes, increased vagal tone, during sleep

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21
Q

2nd degree AV block Type I treatment

A

almost never needed

can be benign but also could be due to MI

if symptomatic treat like bradycardia (atropine, transcutaneous pacer/transvenous pacer, permanent pacemaker)

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22
Q

Mobitz II

A

PR interval is unchanged prior to a P wave with no QRS

predictable cadence

treatment regardless of symptoms is pacemaker

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23
Q

3rd degree AV block

A

complete heart block

no association between atrial contraction and ventricular contraction

SA node passes to AV node but doesnt get to ventricle - escape beat controls ventricles

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24
Q

common causes of 3rd degree AV block

A

MI
drug toxicity
chronic degeneration

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25
Q

third degree AV block symptoms

A 
lightheadedness 
syncope
chest pain
hypotension 
AMS

Completely unstable

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26
Q

sick sinus syndrome

A

intrinsic SA node dysfunction

brief periods of episodic bradycardia

decreased CO = sx of bradycardia

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27
Q

sick sinus syndrome symptoms + treatment

A

dizziness, confusion, syncope, altered mental status

treatment: transcutaneous pacemaker + permanent pacemaker

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28
Q

tachycardia mechanisms

A

HR >100

  1. enhanced cellular automaticity
  2. triggered activity
  3. unidirectional block and re-entry
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29
Q

factors to consider with tachycardia

A

is it above ventricle (narrow QRS) ?
P wave association with QRS complex
P wave morphology

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30
Q

sinus tachycardia

A

100-160 bpm

p wave for every QRS (can be difficult)

secondary to increased sympathetic tone and decreased vagal stimulation

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31
Q

probably causes of sinus tachycardia

A

exercise
fever
dehydration
hypoxemia

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32
Q

atrial flutter

A

fast atrial rate (250-350) with different ventricular rate

“saw tooth pattern”

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33
Q

causes of atrial flutter

A

re-entry impulse

saw tooth P waves (atria depolarized thru out cycle)

pre existing heart condition

can be transient, persistent, permanent

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34
Q

symptoms of atrial flutter

A

palpitations
SOB
generalized weakenss
vague (feel ill, nausea)

35
Q

atrial flutter tx

unstable

A

synchronized cardioversion

36
Q

atrial flutter tx

asymptomatic but stable

A

pharmacological

Non-DHP CCB

anti-arrythmics

consider synchronized cardio version

37
Q

atrial fibrillation

A

very common

atrial quiver or anarchy in atria

atrial rate 350-600

very erratic baseline w.o. recognizable p waves

38
Q

atrial fibrillation symptoms

A

palpitations
SOB
weaknesss
chest pain

39
Q

atrial fibrillation common in its with

A 
HTN 
CAD 
EtOH intoxication 
thyrotoxicosis 
pulmonary disease
40
Q

atrial fibrillation is dangerous bc

A
  1. decreased CO

2. blood stasis, causing increased clot risk

41
Q

unstable AFib with RVR tx

A

systolic BP less than 90
chest pain
altered mental status

synchronized cardio version

42
Q

tx of stable AFib with RVR

A

control ventricle rate to restore sinus rhythm

CCB (BB if needed)

43
Q

stable asymptomatic persistent AFIB tx

A

CCB
Beta blocker
Start on anticoagulant

44
Q

MAT

A

stimuli does not come from one foci from several foci

isoelectric baseline which is more discernible between P waves (can see the P wave)

45
Q

MAT commonly associated

A

Pulmonary disease

Hypoxemia

46
Q

MAT tx

A

non-DHP

47
Q

two types of re-entrant tachycardias

A

AV nodal reentrant Tachycardia

AVRT

48
Q

Paroxyxsmal SVT

A

sudden onset and termination

atrial rates b/t 160-180

narrow QRS

49
Q

PSVT symtoms and epidemiology

A

mc effects young adults, if elderly will have syncope

palpitations, light headedness, SOB, can be asymptomatic

50
Q

PSVT treatment

non pharm

A

vagal maneuvers

  • carotid massage
  • Ice pack to the face

valsalva maneuvers
-classical and REVERT techniques

51
Q

PSVT tx pharm

A

adenosine (adenocard) 6mg IB fish

theophylline may inhibit adenosine

52
Q

mc form of AV nodal re-entrant tachycardia

A

PSVT

53
Q

AVRT Ventricular pre-excitation syndrome

A

only one bypass tract (typically bundle of kent)

impulses travel to ventricles thru accessory pathway AND AV node

AKA WPW

54
Q

distinct EKG of wolfe parkinson white syndrome

A

shortened PR
delta wave
widened QRS

55
Q

WPW orthodromic conduction tx

A

narrow QRS, more common

vagal maneuvers, adenosine and procanamide if stable

synchronized cardio version if stable

56
Q

WPW Antidromic conduction

A

wide complex QRS

less common

tx with procainamide

DONT GIVE CCB, BB, adenosine

57
Q

PVCs origination and EKG shows

A

ectopic ventricular foci

widened QRS complex (No P wave)

58
Q

PVCs are issue

A

not dangerous in those W/O heart disease

increased risk of VTach or VFib in those WITH heart disease

commonly follows MI

increased risk if >10/min or couplet/triplet

59
Q

Bigeminal PVCs

A

when every alternate beat is a PVC

60
Q

trigeminy PVCs

A

two normal beats precede a PVC

PVC every third beat

61
Q

PVC tx

A

reassurance, BB if >10/min

62
Q

V Tach

A

> 3 + consecutive beats

HR > 100-250

63
Q

Non-sustained V Tach

A

3 or more PVCs, last less than 30 seconds, self-limiting

dont usually treat (anti-arrythmics can cause VFib)

consider beta blocker for tx

64
Q

sustained V Tach

A

lasts > 30 seconds and requires termination

can be stable or unstable

65
Q

stable V Tach vitals + tx

A

Pt has: Pulse, normal BP, no chest pain, normal mental status

tx with: 
1. IV access 
2. EKG 
3. Cardio consult 
consider anti-arrhythmic (Procainamide)
66
Q

unstable VTach vitals + tx

A

1 of: pulseless, chest pain, hypotension, LOC

WITH Pulse: tx is synchronized cardio version + ICD

NO pulse: defibrillation

67
Q

defibrillation steps in unstable V Tach

A

PULSELESS

  1. CPR + defibrillate
  2. CPR 2 min, IV/IO access
  3. defibrillate again
  4. Epinephrine + CPR 2 min
  5. Defib (3rd time)
  6. Amiodarone + CPR
  7. Defibrillation
68
Q

monomorphic V Tach

A

rate is regular and QRS complexes are the same

single origin of arrhythmia in ventricle

69
Q

polymorphic V Tach

A

rate is irregular and QRS complexes are variable in shape

cyclic alteration of impulse from ventricle

gives appearance of twisted QRS - TORSADES

70
Q

Torsades des Pointes

A

long QT syndrome is a cause (can be congenital)

can be caused by underlying metabolic abnormalities (hypo-K, Mg) or medications

71
Q

initial tx of Torsades des Pointes

A

CPR
non synchronized cardio version
amiodarone and Epi
Mg 2gm IV drip over 5-15 min while treating

long term: BB + ICD

72
Q

definitive pharm tx of Torsades

A

Mg IV drip

73
Q

how is V Tach differentiated from SVT

A

wide QRS in v tach

74
Q

most life threatening form of arrhythmia

A

V Fib

severe drop in cardiac output that leads to death

75
Q

treatment of VFib

A

electrical defibrillation

CPR + Defib between Epi and Amiodarone

76
Q

pulseless electrical activity

A

presence of rhythm without a pulse or electrical activity without perfusion

77
Q

PEA treatment

A

CPR + Epi + H&Ts

success depends on patient’s baseline and speed when started

78
Q

what do we do for patients who have ROSC following V Tach, V Fib, or PEA

A

RAVEL

fluid management
airway management
vasopressors
evaluate H & T

79
Q

H & Ts

A

H: hypovolemia, Hypoxia, Hyponatremia, Hyperkalemia, Hypothermia

T: thrombosis, tension pneumothorax, tamponade, toxins

80
Q

RAVEL

A 
Responsive 
Airway
Vitals
Ekg 
Labs

done after return of SR in Vtach/VFib

81
Q

Asystole management

A
  1. CPR
  2. 1 Epi ever 3-5 min
  3. H & Ts
82
Q

physiological monitoring during CPR

A

PeTCO2 (end tidal CO2 device connected to endotracheal tube, measures CO2 exhalation)

Arterial one (radial artery, monitors BP and ABG)

83
Q

when an IV site is not available in cardiac arrest…

A

IO

can give drugs, fluids, all ages, quick

found in PROXIMAL TIBIA, distal femur, proximal humors, distal tibia)

FA17 Cardio 2 (10 decks)

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