Lecture 7: Afib/Aflutter + Stroke. Lecture 8: OTHER ARRHYTHMIAS

Question 1

Scoring Systems for Stroke Risk (we use a scoring system b/c not everyone who has AFib is gon have stroke!)

Answer 1

A variety of systems have been published
– CHADS2
– CHA2DS2-VASc
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All use selected clinical characteristics to predict the risk of stroke
All scores provide a rough estimate of risk of thrombosis in a population at similar risk as patient being reviewed

Question 2

Answer 2

Question 3

Meta-analysis of Efficacy and Safety of New Oral Anticoagulants. What did these study find? what’s the final recommendation?

Answer 3

Newer agents like dabigatran, rivaroxaban, and apixaban are better at preventing stroke than warfarin! However the newer agent can cause more GI bleed! Usually recommend new agent over warfarin! Unless patient have a mechanical heart value !

Question 4

When is it ok to omit DOAC in AFib patient?

Answer 4

Question 5

IV – PO transition

Answer 5

• Need to covert patients from IV to PO prior to discharge
• Different anticoagulants will have different approaches
  – Want to start warfarin while on heparin since it takes days for warfarin to work – don’t want to increase hospital stay
  – Transition to NOAC’s is much different often include stopping IV heparin and starting NOAC at same time. Check your drug information sources.

Question 6

Sinus Bradycardia: General, Causes: Physiologic, Pharmacologic, Pathologic, prognosis, treatment

Answer 6

Impulse originate at SA node is slowed. On ECG - all complex looks normal…it’s just wide and spread out! HR at less than 60 BPM.
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CAUSES
-Physiologic: Athletes, Valsalva Maneuver
-Pharmacologic: Beta blockers, Calcium channel blockers, Amiodarone (class III)
- Pathologic: Acute MI, especially inferior MI’s, Hypothermia, Hypertension
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Prognosis: We do not worry too much about bradycardia unless the HR is v low! Rate at 60-50 is well tolerated and if tolerated? DO NOT need treatment! 40 BPM will start experiencing symp of hypotension, syncope, and confusion…then we will give med!
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Treatment: Atropine, artificial pacemaker

Question 7

Sinus Tachycardia: General, Causes: Physiologic, Pharmacologic, Pathologic, prognosis, treatment

Answer 7

Impulse originate at SA node is too fast! On ECG - all complex looks normal…it’s more narrow! HR over 100 BPM
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CAUSES
- Physiologic: infant, exercise, stress
- Pharmacologic: sympathomimics, anticholinergic, xanthine
- Pathologic: hypotension, hypovolumic, anemia, CHF, fever

Question 8

AV and AV NODAL RE-ENTRANT TACHYCARDIAS symptoms and treatment?

Answer 8

Symptoms: Palpitations, dizziness, dyspnea, chest pain, fatigue, syncope
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Treatment Approaches – AV node ablation (slow pathway- AV node ablation of one of the pathways today is very common and most effective. Often recommended to patients

Question 9

AV and AV NODAL RE-ENTRANT TACHYCARDIAS Flowchart/ Algorithm

Answer 9

Question 10

Wolff-Parkinson-White Syndrome: Symp and treatment

Answer 10

-Most patients will have accessory pathway ablated (destroyed)
-Flecainide, propafenone, amiodarone, dofetilide, sotalol
-AV blocking drugs (class 2 BB and 4 CCB) must be used with caution or avoided in patients with associated atrial fibrillation. Using AV blocking drugs in these cases may cause rapid VRR with atrial fibrillation (300-500 beats/min)

Question 11

1st Degree AV-Block: ECG, causes, prognosis/ TX?

Answer 11

Question 12

2nd degree AV-Block and 3rd degree AV-Block….what is it? what to do?

Answer 12

2nd degree AV-Block: Two types – Mobitz Type I and II
-Treatment if symptomatic – acutely atropine, chronically pacemaker.
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3rd degree AV-Block -No atrial depolarizations reaches the ventricular
Ventricular pacemakers take over (junctional escape rhythm – 30 to 60 beats/min), ECG: P wave have no relationship with QRS. QRS is slower than P. Usually very symptomatic – including loss of consciousness
Treatment: Pacemaker!!!

Question 13

Ventricular Dysrhythmias: Premature ventricular contractions (PVC’s)

Answer 13

PVCs in the absence of heart disease
-Usually asymptomatic, but may be symptomatic
-Do not require treatment unless bothersome to the patient, in which case β-blockers or IC agents may be used.

Question 14

Ventricular Dysrhythmias: Ventricular Tachycardia: general/ symp/ etiology

Answer 14

The symptoms of VT (monomorphic VT or TdP), if prolonged (i.e., sustained), can vary from nearly completely asymptomatic to pulseless, hemodynamic collapse. Fast heart rates and underlying poor LV function will result in more severe symptoms. Symptoms of nonsustained, self-terminating VT also correlate with duration of episodes (e.g., patients with 15-second episodes will be more symptomatic than those with three-beat episodes).
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Etiology
-Ischemia
-Post MI – acute (24hrs) and chronic
-Electrolyte disturbances (e.g. hypokalemia)
-Structural heart disease (e.g. heart failure)
-Catecholamines
-Digitalis toxicity

Question 15

Ventricular Tachycardia: sustain vs non-sustained/ un-sustained

Answer 15

Question 16

Ventricular Tachycardia: non-sustained/ un-sustained TREATMENT

Answer 16

Question 17

Ventricular Tachycardia: non-sustained/ un-sustained TREATMENT Flowchart form

Answer 17

Question 18

Ventricular Tachycardia: ICD

Answer 18

-Electricity is most effective therapy
-Patients with EF < 40% need to be considered for ICD placement (follow guidelines)
-Patients with ICD and frequent shocks need antiarrhythmic therapy to suppress arrhythmia formation

Question 19

IN HOSPITAL
Sustained Ventricular Tachycardia –Hemodynamically Stable. Patient is consciousness and decent BP …what to do

Answer 19

Stable? look at picture.
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Unstable?…nonresponsive? ACLS protocol-> SHOCK DEFIBRILLATION

Question 20

CHRONIC THERAPY for Life Threatening Arrhythmia

Answer 20

Question 21

Antiarrhythmic Agents: Amiodarone - dosing, excretion, side effect

Answer 21

Dosage range (chronic)
-Atrial arrhythmias, AV block: 100-200 mg/day
-Ventricular arrhythmias: 400 mg/day
May or may not do a loading dose when treating Afib, loading is often used when treating v. arrhythmias
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Excretion
t1/2 is dependent on chronicity of dosing:
single dose (oral): 18-36 hrs.
chronic therapy: 20-60 days
-Dosage adjustments not necessary for renal, hepatic, disease
-Inhibits most drug metabolizing enzymes
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Side effects
-Early: bradycardia
-Long term: pulm fibrosis, photosensitivity, pigment blue, hepatox/ elevated enzymes
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Amiodarone potentially has a number of significant adverse effects and drug interactions BUT is our most effective AA agent and has low proarrythmic potential. So it is often used!

Question 22

Amiodarone monitoring

Answer 22

Question 23

Common Amiodarone and Digoxin DDI

Answer 23