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Arrythmias Flashcards

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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
# AFib Rate control who and Rx
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
26
# Afib rhythm control
Young, symptomatic, EF < 45%, HOCUM, new onset OACtx (oral anticoag therapy) Anti Arrhythmic Drugs: flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone Cardioversion ablation
27
Anti Arrhythmic Drugs: | 6
flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone
28
Cardioversion
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
29
# Atrial Fibrillation Management options
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**
30
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- 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
31
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
they have mechanical valve, they need a bridge (says we dont need to know difference between hep and lov)
32
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
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
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?
amiodarone tox VELCRO lung sounds maybe thyroid bc hair
34
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
D. direct current cardioversion they are hemodynamically unstable need help naow
35
Atrial Flutter
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
37
AFlutter Tx
OAC for 21 days think about cardioversion or ablation
38
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. OACTx she is stable next treatment would be Cardioversion
39
Supraventricular Tachycardia (SVT)
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
Supraventricular Tachycardia (SVT)
41
Supraventricular Tachycardia (SVT)
42
# Supraventricular Tachycardia (SVT) Tx
43
# Supraventricular Tachycardia (SVT) prevention
Radiofrequency catheter ablation- Preferred approach to patients with recurrent symptomatic reentrant PSVT
44
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. ablation - if stable first try if unstable then cardioversion first then ablation
45
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
Vasovagal maneuver is first step adenosine is second step cardioversion is third step (if hemodynamically unstable then this is 1st)
46
Conduction Abnormalities
First Degree Heart Block Second Degree Heart Block Mobitz type I Mobitz type II Third Degree Heart Block
47
First degree heart block
no intervention just monitor Causes: medications, ischemia, Lyme disease
48
Second Degree Heart Block Mobitz type I Tx
no intervention
49
Second Degree Heart Block Mobitz type II Tx
Pace maker and or atropine
50
First Degree AV Block | no intervention just monitor
51
What is treatment for 1’ AVB? A) external pacemaker B) permanent pacemaker C) atropine 1mg IVP D) epinephrine gtt E) monitor
**E monitor** C-for brady D- for shock Vfib or VT
52
# Second Degree AV Block Mobitz Type I (Wenckebach)
Progressive PR interval prolongation with each beat until a P wave is not conducted Irregular R-R interval
53
Mobitz Type I (Wenckebach) Second Degree AV Block
54
# Second Degree AV Block Mobitz Type II Tx and progression
Treatment: Atropine and/or Pacemaker Usually progresses to 3’AVB
55
# Second Degree AV Block Mobitz Type II
Extra P waves with dropped QRS Usually associated with bradycardia PR interval may be normal or prolonged
56
Second Degree AV Block Mobitz Type II
57
Qualifiers for permanent pacemaker
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
Premature Ventricular Contractions (PVC) | general and charecteristics
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
Premature Ventricular Contractions (PVC) | more info
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
# PVC Symtomatic Tx
If symptomatic, beta-blockers or non-dihydropyridine CCB are first-line therapy
61
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
unifocal PVC no treatment needed unless pt wants it, if so ditiazem
62
# Ventricular Tachycardia general
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
# VTACH Initial Treatment – determined by the degree of hemodynamic compromise and duration
Urgent direct current cardioversion Intravenous amiodarone +/- short acting beta-blocker or verapamil
64
# Vtach Long-Term Management
Reverse precipitating causes Beta-blockers in those with structural heart disease Catheter ablation Implantable cardioverter-defibrillator
65
# Vtach Polymorphic ventricular tachycardia (Torsades de Pointes) Tx
Treat with IV magnesium Clinical Pearl Patients with a prolonged QT interval have a higher risk of developing polymorphic VT
66
What electrolyte disturbance is most associated with torsades de pointes? Hypomagnesemia Hypermagnesemia Hyperkalemia hypocalcemia
Hypomagnesemia
67
Ventricular Fibrillation general and Tx
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
VFib
69
What is primary treatment for Vfib? 1) shock 2) amiodarone
SHOCK
70
# Asystole general and Tx
No electrical activity of the heart Tx: high-quality CPR, epinephrine FLATline
71
NOT Asystole
72
Hypokalemia
- u wave
73
Hyperkalemia 4
Peaked T waves Widening of the QRS Increase in PR interval Bradycardia
74
Calcium
75
Long QT Syndrome What can cause it
May lead to potentially fatal arrhythmia polymorphic ventricular tachycardia (torsades de pointes) S/Sx Palpitations, fainting, sudden death Normal Range: < 0.440 sec
76
Prolonged QT Interval Causes
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
Brugada Syndrome
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
Wolff-Parkinson-White (WPW)
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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