Arrythmias Flashcards
with inferior wall mi be cautious giving
nitroglycerin
bc can make r vent hypotensive
instead give lots of fluid to increase preload
amiodarone
class 3 BB
has iodine, can be toxic
cannot miss signs of tox
for atrial or ventricular arrythmia
prevents VT, AFib, VF
amiodaron Adverse Effects
Hypotension
Corneal micro-deposits
Thyroid dysfunction
Hypothyroidism > Hyperthyroidism
Pulmonary Fibrosis- velcro lungs
Blue-gray skin discoloration
Sinus Tachycardia
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
Sinus tach
Sinus Brady
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
Sinus Bradycardia
work up
Tx
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
Premature Atrial Contractions (PAC)
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
- They arepremature. That is they occur earlier than you would expect if you were to measure the previous P to P intervals.
- They areectopic. Meaning originating outside of the SA node. Thus the P wave morphology would be different than the normal sinus P wave.
- 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.
- 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.
Multifocal atrial tachycardia (MAT)
3 or more distinct P wave morphologies on EKG
Seen with severe COPD
Atrial Fibrillation (AF or A.Fib.)
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
review
how do you treat HOCUM?
BB and CCB
to lower Hr
bc they have hypertrophy an less space in ventricle
which lead do you look for P wave?
lead 2
AFIB with RPR (rapid vent response) rate above 100
AFIB with normal vent rate 60-100
AFib with slow ventricular rate less than 60
AFIB RF
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
AFib
S/Sx
Asymptomatic, palpitations, fainting, SOB, chest pain, stroke
AFib
classifications
Paroxysmal
Recurrent episodes < 7 days
Persistent
Recurrent episodes > 7 days
Longstanding, persistent
>12 months
Permanent
Strategy is to cease efforts to maintain NSR
purpose of HAS-BLED
assess risk of bleeding
purpose of CHADS-VAS
asses risk of stroke
if 2 or more should be on anticoag
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
C. Stroke
Left Atrial Appendage Occlusion
to prevent Afib from atrial appendage
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
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
Anti Arrhythmic Drugs:
6
flecainide, propafenone, sotalol, dofetilide, amiodarone, dronedarone
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
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
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
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)
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
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
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
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
AFlutter Tx
OAC for 21 days
think about cardioversion
or ablation
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
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
Supraventricular Tachycardia (SVT)
Supraventricular Tachycardia (SVT)
Supraventricular Tachycardia (SVT)
Tx
Supraventricular Tachycardia (SVT)
prevention
Radiofrequency catheter ablation- Preferred approach to patients with recurrent symptomatic reentrant PSVT
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
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)
Conduction Abnormalities
First Degree Heart Block
Second Degree Heart Block
Mobitz type I
Mobitz type II
Third Degree Heart Block
First degree heart block
no intervention just monitor
Causes: medications, ischemia, Lyme disease
Second Degree Heart Block
Mobitz type I
Tx
no intervention
Second Degree Heart Block
Mobitz type II
Tx
Pace maker and or atropine
First Degree AV Block
no intervention just monitor
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
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
Mobitz Type I (Wenckebach) Second Degree AV Block
Second Degree AV Block Mobitz Type II
Tx and progression
Treatment: Atropine and/or Pacemaker
Usually progresses to 3’AVB
Second Degree AV Block
Mobitz Type II
Extra P waves with dropped QRS
Usually associated with bradycardia
PR interval may be normal or prolonged
Second Degree AV Block
Mobitz Type II
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
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
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
PVC
Symtomatic Tx
If symptomatic, beta-blockers or non-dihydropyridine CCB are first-line therapy
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
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
VTACH
Initial Treatment – determined by the degree of hemodynamic compromise and duration
Urgent direct current cardioversion
Intravenous amiodarone
+/- short acting beta-blocker or verapamil
Vtach
Long-Term Management
Reverse precipitating causes
Beta-blockers in those with structural heart disease
Catheter ablation
Implantable cardioverter-defibrillator
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
What electrolyte disturbance is most associated with torsades de pointes?
Hypomagnesemia
Hypermagnesemia
Hyperkalemia
hypocalcemia
Hypomagnesemia
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)
VFib
What is primary treatment for Vfib?
1) shock
2) amiodarone
SHOCK
Asystole
general and Tx
No electrical activity of the heart
Tx: high-quality CPR, epinephrine
FLATline
NOT Asystole
Hypokalemia
- u wave
Hyperkalemia
4
Peaked T waves
Widening of the QRS
Increase in PR interval
Bradycardia
Calcium
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
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
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
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
