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CMT-uno > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

with inferior wall mi be cautious giving

A

nitroglycerin
bc can make r vent hypotensive

instead give lots of fluid to increase preload

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2
Q

amiodarone

A

class 3 BB
has iodine, can be toxic
cannot miss signs of tox

for atrial or ventricular arrythmia
prevents VT, AFib, VF

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3
Q

amiodaron Adverse Effects

A

Hypotension
Corneal micro-deposits
Thyroid dysfunction
Hypothyroidism > Hyperthyroidism
Pulmonary Fibrosis- velcro lungs
Blue-gray skin discoloration

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4
Q

Sinus Tachycardia

A

Upright P wave in lead II preceding every QRS with a ventricular rate is greater than 100/min

Causes / Treatment
Exercise, Anemia, Dehydration or shock, fever, sepsis, infection, hypoxia, chronic pulmonary disease, hyperthyroidism, pheochromocytoma, medications/stimulants, heart failure, pulmonary embolus

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5
Q
A

Sinus tach

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6
Q

Sinus Brady

A

Upright P wave in lead II preceding every QRS with a ventricular rate less than 60/min

Causes / Treatment
AV blocking medications
Heightened vagal tone
Sick sinus syndrome
Hypothyroidism
Hypothermia
Obstructive sleep apnea
Hypoglycemia

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7
Q

Sinus Bradycardia
work up
Tx

A

Work up: TSH, holter, echo
Treatment: dc av nodal slowing agents, r/o underlying disease;

if symptomatic
Atropine- first line in hosptial
External pacing
Permanent pacemaker- HR 35 or less

if HR 40 or higher and aSx, NO treatment given

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8
Q

Premature Atrial Contractions (PAC)

A

Occurs when a focus in the atrium (not the SA node), generates an action potential before the next scheduled SA node action potential

Characteristics
Premature
Ectopic
Narrow complexes
Compensatory pause

  1. They arepremature. That is they occur earlier than you would expect if you were to measure the previous P to P intervals.
  2. They areectopic. Meaning originating outside of the SA node. Thus the P wave morphology would be different than the normal sinus P wave.
  3. They arenarrow complexes. Since they come from the atrium, they will eventually travel through the AV node and use the normal conduction system to spread to the ventricles. Unlike a premature ventricular contraction, which is wide-complexed since it does not use the normal ventricular conduction system. Less commonly, a PAC can conduct aberrantly in a right or left bundle pattern which can make distinguishing from a prematureventricularcontraction difficult.
  4. There is acompensatory pauseafter the PAC. The extra atrial action potential causes the SA node to become refractory to generating its next scheduled beat. Thus it must “skip a beat” and it will resume exactly 2 P to P intervals after the last normal sinus beat.
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9
Q
A

Multifocal atrial tachycardia (MAT)

3 or more distinct P wave morphologies on EKG
Seen with severe COPD

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10
Q

Atrial Fibrillation (AF or A.Fib.)

A

Occurs when action potentials fire very rapidly within the pulmonary veins or atrium in a chaotic manner resulting in a VERY fast atrial rate (300-600 beats per min)
Ventricular rate is usually 100-200 due to the AV node that becomes intermittently refractory

NO P waves will be seen on EKG with varying RR intervals

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11
Q
A
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12
Q

review

how do you treat HOCUM?

A

BB and CCB

to lower Hr
bc they have hypertrophy an less space in ventricle

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13
Q

which lead do you look for P wave?

A

lead 2

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14
Q
A

AFIB with RPR (rapid vent response) rate above 100

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15
Q
A

AFIB with normal vent rate 60-100

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16
Q
A

AFib with slow ventricular rate less than 60

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17
Q

AFIB RF

A

Hypertension, valvular heart disease, CAD, cardiomyopathy, COPD, obesity, sleep apnea, excessive ETOH, DM, thyrotoxicosis

*look for left atrial enlargement +/- mitral disease on echo ( means theyve had AFIB for a while)

YOU ARE AT RISK OF STROKE

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18
Q

AFib

S/Sx

A

Asymptomatic, palpitations, fainting, SOB, chest pain, stroke

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19
Q

AFib

classifications

A

Paroxysmal
Recurrent episodes < 7 days

Persistent
Recurrent episodes > 7 days

Longstanding, persistent
>12 months

Permanent
Strategy is to cease efforts to maintain NSR

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20
Q

purpose of HAS-BLED

A

assess risk of bleeding

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21
Q

purpose of CHADS-VAS

A

asses risk of stroke

if 2 or more should be on anticoag

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22
Q

Which of the is given a score of 2 on the (CHA2DS2-VASc score) and if present, automatically required anticoagulation?
A. Congestive heart failure
B. Diabetes
C. Stroke
D Hypertension

A

C. Stroke

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23
Q
A
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24
Q

Left Atrial Appendage Occlusion

to prevent Afib from atrial appendage

A
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25
Q

AFib

Rate control
who and Rx

A

Old, asymptomatic, preserved EF

OACtx (oral anticoag therapy)

People who are hard to rhythm control like obese, sleep apnea, underlying lung disease, longer time with Afib burden

Rx: beta blockers, calcium channel blockers

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26
Q

Afib

rhythm control

A

Young, symptomatic, EF < 45%, HOCUM, new onset

OACtx (oral anticoag therapy)

Anti Arrhythmic Drugs: flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone

Cardioversion
ablation

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27
Q

Anti Arrhythmic Drugs:

6

A

flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone

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28
Q

Cardioversion

A

synchronized vs unsynchronized
unsynch is just zap em without lining up
synch you zap with ecg hooked up, make sure theyre on blood thinners for 3 week and still are

Requires conscious sedation
Unless hemodynamically unstable- patient should be on full anticoagulation therapy > 21 days prior, or duration of afib < 48 hours

Post “stunning” phenomenon- increase CVA risk for 30 days post therefore MUST take OACtx

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29
Q

Atrial Fibrillation

Management options

A

Replace K+ and Mg++ (and check TSH)

Rate control – BB, CCB, digoxin

Rhythm control-Amiodarone, ibutilide, flecainide, propafenone, dofetilide

Anticoagulation (CHA2DS2-VASc score)
Dabigatran, rivaroxaban, apixaban, edoxaban, warfarin, heparin

Cardioversion
Electrical or chemical (amiodarone, etc.)

Ablation
Pulmonary vein isolation / MAZE procedure

if a patient is unstable the treatment is direct current cardioversion

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30
Q

58 yo male w a history of paroxysmal Afib presents for clearance colonoscopy. He takes apixaban 5 mg po bid
A) stop apixaban 48 hours prior to the procedure and resume per instructions post scope
B) stop apixaban 72 hours before and start lovenox bridge
C) stop apixaban and take asa 325 mg while off apixaban

A

A- stop apixaban 48 hours prior to the procedure and resume per instructions post scope
B- does not have mechanical bridge so does not need bridge
C- asa does not help prevent strokes from Afib

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31
Q

Patient with a mechanical mitral valve and permanent afib on warfarin presents for clearance colon resection
A. Dc warfarin and start lovenox bridge
B. DC warfarin and start heparin bridge
C. Dc warfarin 5 days pre op and resume post op day 1

A

they have mechanical valve, they need a bridge (says we dont need to know difference between hep and lov)

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32
Q

80 yo male presents for routine ov. No PMHx. No complaints. You detect irregular heart tones on PE. This is ECG

A) start OACTx
B) start Oactx and BB
C) start OACTx, and ccb
D) start asa
E) start asa and bb

A

AFib Asx

needs OACTx bc CHADVAS score (80 y)

No BB or CCB bc rate is controlled and ASx

No asa bc no benefit for AFib

33
Q

48 yo M PMHX: PAF presents with fatigue, malaise, and doe. Rx: amiodarone 200 mg po BID (x years), Eliquis 5 mg bid. VSS. On PE “Velcro” lung sounds. Thinning hair, eyebrows. Ecg 3 months ago showed NSR (normal sinus rythm).
What is most likely differential?

A

amiodarone tox
VELCRO lung sounds
maybe thyroid bc hair

34
Q

A 72 year old presents to ED with palpitations, CP, diaphoresis, and SOB x 13 hours. PMHX: Mitral Regurgitation ( moderate), HTN, OSA. No daily medications. Vs: 80/40- HR 130’s, RR 20, O2 sat 90% on RA. Which of the following interventions is correct?
A. start metoprolol 25 mg po BID
B. start apixaban 5 mg po BID
C. both A and B
D. direct current cardioversion

A

D. direct current cardioversion

they are hemodynamically unstable need help naow

35
Q

Atrial Flutter

A

Occurs when a “reentrant circuit” is present causing a repeated loop of electrical activity to depolarize the atrial at a fast rate of ~300 beats per minute

Produces a classic “sawtooth” pattern of the atrial activity with lack of P waves

Clinical Pearl
A narrow complex tachycardia at a ventricular rate of exactly 150 beats per minute is very commonly atrial flutter

36
Q
A
37
Q

AFlutter Tx

A

OAC for 21 days

think about cardioversion
or ablation

38
Q

48 yo female presents with fatigue. PMHX: HTN, HLP, CKD, obesity. stable. PE: unremarkable.
A. Start OACTX
B. Send for cardioversion
C. Start asa 81 mg daily
D. Start asa 81 md daily and clopidogrel 75 mg daily

A

A. OACTx she is stable

next treatment would be Cardioversion

39
Q

Supraventricular Tachycardia (SVT)

A

Definition – rapid rhythm disturbances originating from the atria or the atrioventricular node (narrow complex)
Paroxysmal supraventricular tachycardia (PSVT)

Mechanisms
Reentry – follow a revolving pathway
Automaticity – spontaneous and repetitive firing from a single focus

EKG
Narrow QRS complex tachycardia
Usually 160-220 bpm
Rate does not vary

40
Q
A

Supraventricular Tachycardia (SVT)

41
Q
A

Supraventricular Tachycardia (SVT)

42
Q

Supraventricular Tachycardia (SVT)

Tx

A
43
Q

Supraventricular Tachycardia (SVT)

prevention

A

Radiofrequency catheter ablation- Preferred approach to patients with recurrent symptomatic reentrant PSVT

44
Q

What is most successful treatment of SVT?
A. ablation
B. Anti-arhythmic drug therapy
C. Beta blocker therapy
D. Calcium Channel blockers
E. Vasovagal maneuvers

A

A. ablation - if stable first try

if unstable then cardioversion first then ablation

45
Q

Patient presents in ED with “heart flying” acute onset for last 20 min. PT is hemodynamically stable with ECG showing tachycardia narrow complex arrythmia rate 170. which is most appropriate action?
Vasovagal maneuver
Adenosine
Cardioversion
IV betablocker

A

Vasovagal maneuver is first step

adenosine is second step

cardioversion is third step (if hemodynamically unstable then this is 1st)

46
Q

Conduction Abnormalities

A

First Degree Heart Block

Second Degree Heart Block
Mobitz type I
Mobitz type II

Third Degree Heart Block

47
Q

First degree heart block

A

no intervention just monitor
Causes: medications, ischemia, Lyme disease

48
Q

Second Degree Heart Block
Mobitz type I
Tx

A

no intervention

49
Q

Second Degree Heart Block
Mobitz type II
Tx

A

Pace maker and or atropine

50
Q
A

First Degree AV Block

no intervention just monitor

51
Q

What is treatment for 1’ AVB?
A) external pacemaker
B) permanent pacemaker
C) atropine 1mg IVP
D) epinephrine gtt
E) monitor

A

E monitor

C-for brady
D- for shock Vfib or VT

52
Q

Second Degree AV Block

Mobitz Type I (Wenckebach)

A

Progressive PR interval prolongation with each beat until a P wave is not conducted
Irregular R-R interval

53
Q
A

Mobitz Type I (Wenckebach) Second Degree AV Block

54
Q

Second Degree AV Block Mobitz Type II

Tx and progression

A

Treatment: Atropine and/or Pacemaker
Usually progresses to 3’AVB

55
Q

Second Degree AV Block

Mobitz Type II

A

Extra P waves with dropped QRS
Usually associated with bradycardia
PR interval may be normal or prolonged

56
Q
A

Second Degree AV Block
Mobitz Type II

57
Q

Qualifiers for permanent pacemaker

A

Pauses > 3.0 seconds ( +/- symptoms)
Sinus brady <35 bpm
Sinus brady 36-40 bpm and symptomatic
Chronotropic incompetence
2’AVB type II
3’AVB/complete heart block

58
Q

Premature Ventricular Contractions (PVC)

general and charecteristics

A

Occurs when a focus in the ventricle generates an action potential before the next scheduled SA nodal action potential

Characteristics
Premature
Ectopic
Wide complexes
Compensatory pause

59
Q

Premature Ventricular Contractions (PVC)

more info

A

Most patients are asymptomatic

May be associated with energy drinks, electrolyte abnormalities and hyperthyroidism

If more than 10,000 per day (per ambulatory EKG monitoring) or 30% total heart beats; echocardiogram is recommended

60
Q

PVC

Symtomatic Tx

A

If symptomatic, beta-blockers or non-dihydropyridine CCB are first-line therapy

61
Q

44 yo presents with reports of occasional heart “flop”. No pmhx, no rx. IRR with Mid systolic click on physical exam.
What is treatment of PVCs?
No treatment needed
Metoprolol 25 mg po BID
Diltiazem 120 mg po bid
Amiodarone 200 mg daily

A

unifocal PVC

no treatment needed unless pt wants it, if so ditiazem

62
Q

Ventricular Tachycardia

general

A

Wide QRS complex (>120 ms) originating in the ventricles at a rate greater than 100 beats/min
Often underdiagnosed or misdiagnosed

Can be associated with
Degenerating into ventricular fibrillation
Presenting as syncope
+/- hemodynamical stability

63
Q

VTACH

Initial Treatment – determined by the degree of hemodynamic compromise and duration

A

Urgent direct current cardioversion
Intravenous amiodarone
+/- short acting beta-blocker or verapamil

64
Q

Vtach

Long-Term Management

A

Reverse precipitating causes
Beta-blockers in those with structural heart disease
Catheter ablation
Implantable cardioverter-defibrillator

65
Q

Vtach

Polymorphic ventricular tachycardia (Torsades de Pointes)
Tx

A

Treat with IV magnesium

Clinical Pearl
Patients with a prolonged QT interval have a higher risk of developing polymorphic VT

66
Q

What electrolyte disturbance is most associated with torsades de pointes?
Hypomagnesemia
Hypermagnesemia
Hyperkalemia
hypocalcemia

A

Hypomagnesemia

67
Q

Ventricular Fibrillation
general and Tx

A

Quivering of the ventricles with virtually NO forward cardiac output
Main cause of sudden cardiac death (SCD) in patients with myocardial infarction

Tx: ACLS (defibrillation, epinephrine, antiarrhythmics)

68
Q
A

VFib

69
Q

What is primary treatment for Vfib?
1) shock
2) amiodarone

A

SHOCK

70
Q

Asystole

general and Tx

A

No electrical activity of the heart
Tx: high-quality CPR, epinephrine

FLATline

71
Q
A

NOT Asystole

72
Q

Hypokalemia

A
  • u wave
73
Q

Hyperkalemia
4

A

Peaked T waves
Widening of the QRS
Increase in PR interval
Bradycardia

74
Q

Calcium

A
75
Q

Long QT Syndrome
What can cause it

A

May lead to potentially fatal arrhythmia polymorphic ventricular tachycardia (torsades de pointes)

S/Sx
Palpitations, fainting, sudden death

Normal Range: < 0.440 sec

76
Q

Prolonged QT Interval Causes

A

Congenital
Acquired
Medications
Macrolides, Fluoroquinolones, Antifungal, Antidepressants, Antipsychotics, Ondanstron , Antiarrhythmics, Methadone
Disease states
Intracranial hemorrhage
Electrolyte abnormalities
Hypocalcemia, hypomagnesemia, hypokalemia
Treatment : treat underlying cause, ICD

77
Q

Brugada Syndrome

A

Genetic disorder that results in sudden cardiac death from polymorphic ventricular tachycardia or ventricular fibrillation in the setting of a structurally normal heart
Most commonly from a mutation in the sodium channel gene SCN5A

QT interval is normal*
Treatment is ICD

the most common cause of sudden death in young men without known underlying cardiac disease in Thailand and Laos

78
Q

Wolff-Parkinson-White (WPW)

A

Accessory pathway that connects the electrical system of the atria directly to the ventricles allowing conduction to avoid passing through the AV node

Shortened PR interval

Delta wave
Treatment: ablation

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