Group 6:

Drug-Induced
Arrhythmia
01
Pathophysiology
02
Patient
Presentation
Chief Complaint

“I was not feeling well,

and I think I passed out.”
 HPI
(History of Present Illness)
Julia Doellefeld is a 60-year-old woman who experiences a syncopal episode
while being evaluated in the emergency department. She reports being in her usual
state of relatively good health until she developed a “cold” approximately 4 days
before admission. She called her primary care physician complaining of her upper
respiratory tract symptoms, and the physician called in a prescription for
erythromycin 500 mg QID (for 10 days) to her pharmacy. She took the first dose on
the morning of admission. She started feeling worse approximately 1 hour after
taking the second dose of erythromycin. She reports feeling lightheaded and short
of breath. She experienced palpitations as well and eventually passed out for a few
minutes. She awoke on the floor of her living room and called for an ambulance. On
medic arrival, she was awake and alert but looked shaken. She was transported to
the ED without further events.

While being evaluated in the ED, she had another syncopal episode. ACLS
protocol was initiated, and a rhythm strip showed TdP.
 PMH SH
(Past medical history) (Social history)
❏ CAD S/P PTCA She lives with her husband
❏ Heart Failure (EF 30%) and does not smoke or
❏ Dyslipidemia drink alcohol
❏ Paroxysmal atrial
Fibrillation
 Medicines
❏ Carvedilol (Coreg) 3.125 mg po bid
❏ Pravastatin (Pravachol) 40 mg po daily
❏ Furosemide (Lasix) 40 mg bid (increased from 40 mg
po once a day due to increased edema)
❏ Warfarin (Coumadin) 4 mg po daily as directed
❏ Amiodarone 200 mg po bid
❏ Centrum Silver po daily
❏ Ranitidine (Zantac) 150 mg po daily
❏ Candesartan (Atacand) 8 mg po daily
❏ Aspirin 325 mg po daily
❏ Erythromycin 500 mg po QID, started day of
admission
 Allergies
NKDA (no known drug
allergies)

ROS (Review of
Symptoms)
The patient has no
complaints other than
those mentioned in the
HPI.
 Physical Examination
❏ Gen ❏ Lungs/Thorax
❏ The patient is awake on an ED ❏ CTA bilaterally
bed in moderate distress. ❏ Breasts
❏ VS ❏ Nontender
❏ BP : 104/50, P 98 (200 during ❏ CV
syncope) ❏ RRR ; with no murmurs
❏ RR : 30 or gallops
❏ T : 36.3°C ❏ Genit/Rect
❏ Ht : 5'7'' ❏ Deferred
❏ Wt : 90 kg ❏ Abd
❏ Skin ❏ NTND; no rebound or
❏ Warm and dry; no rashes seen guarding; (+) bowel
❏ HEENT sounds
❏ Normocephalic, atraumatic. ❏ MS/Ext
PERRLA. EOMI. Oropharynx is ❏ Trace edema in the lower
clear. extremities; pulses intact
❏ Neck/Lymph Nodes ❏ Neuro
❏ Supple; no JVD or bruits; no ❏ A& O×3
lymph nodes palpated
 Laboratories
❏ Na : 140 mEq/L ❏ Hgb : 12.1 g/dL
❏ K : 2.8 mEq/L ❏ WBC : 12 × 103/mm3
❏ Cl : 100 mEq/L ❏ Hct : 35%
❏ CO2 : 29 mEq/L ❏ RBC : 3.88 × 06/mm3
❏ BUN : 36 mg/dL ❏ Plt : 200 × 103/mm3
❏ SCr : 1.4 mg/dL ❏ MCV : 90.5 μm3
❏ Glu : 110 mg/dL ❏ MCHC : 34.4 g/dL
❏ Mg : 1.2 mg/dL ❏ INR : 2.3
 ECG (Electrocardiograph)

❏ NSR, QTc 605 ms; rhythm

strip from oscilloscope during
syncope:TdP
 Assessment

❏ 60-year-old woman S/P syncopal

episodes from drug-induced TdP
❏ Upper respiratory tract symptoms
❏ Drug-induced electrolyte imbalance
03
Questions
 Problem Identification
1.a. What risk factors predisposed the patient to drug-induced
arrhythmia?
❏ Feeling lightheaded
❏ Shortness of breath
❏ Palpitations
❏ Heart Failure
❏ Dyslipidemia
❏ Paroxysmal atrial fibrillation
 Problem Identification
1.b. What features of the patient’s ECG are characteristic of
TdP?
❏ The electrocardiogram showing torsades de pointes of 60-year-
old woman S/P syncopal episodes from drug-induced TdP
❏ Upper respiratory tract symptoms
❏ Drug-induced electrolyte imbalance
 Problem Identification
1.c. Discuss pharmacologic and nonpharmacologic factors that may have contributed
to drug-induced TdP in this patient.

❏ Pharmacologic Treatment
❏ The most effective antiarrhythmic medication for AF and VT is amiodarone, but
due to serious ADRs and unfavorable pharmacokinetics, it must be used with
extreme caution. The cardiologist should be in charge of writing prescriptions
for antiarrhythmic medications. Drugs used for a variety of purposes may
produce TdP by blocking potassium repolarizing channels. Quick IV. Risk
factors for TdP include injection, electrolyte imbalances, eating disorders,
chemotherapy with CYP inhibitors, liver illness, and kidney disease.
 Problem Identification
1.c. Discuss pharmacologic and nonpharmacologic factors that may have contributed to drug-induced TdP
in this patient.

❏ Non-Pharmacologic Treatment
❏ The atrial appendages are isolated, and the atrial walls are sliced in a precise pattern to
carry out the Maze treatment. The atrial contraction will be organized as a result of forcing
the depolarization wave front to go along a particular path from the sinus node to the
atrioventricular node. Reentry is not possible because the area of continuous atrial
myocardium is too tiny in relation to the "wavelength" of atrial fibrillation.
❏ Through the use of ablation catheters, high-frequency (radiofrequency) alternating current
can be used to precisely generate tiny lesions inside the heart at the anatomical source of
various arrhythmias. Patients with atrioventricular reentry (overt or covert Wolff-
Parkinson-White syndrome) or atrioventricular nodal reentry tachycardias may find relief
using this technique.
 Desired Outcome
2. What are the short-term goals of pharmacotherapy for this patient?
❏ The patient was treated with magnesium infusion, and she converted to
normal sinus rhythm. The erythromycin was stopped. Potassium and
magnesium were replaced, and the patient was admitted for further
electrophysiology workup. Erythromycin cannot be prolonged for used
because it may cause prolongation of the QT interval, arrhythmias (i.e.,
ventricular tachycardia, Torsades de Pointes, ventricular fibrillation, and
heart block), may be observed after rapid intravenous administration and
coincident with high, peak erythromycin plasma concentrations.
 Therapeutic Alternatives
3.a. What nonpharmacologic therapies may be useful for this patient?
❏ Nonpharmacologic therapies that may be useful for this patient include:
❏ Avoiding trigger factors for her arrhythmia such as smoking, caffeine,
alcohol, and strenuous exercise.
❏ Maintaining a healthy lifestyle by eating a healthy diet, exercising
regularly, managing stress, and compliance with her medication
regimen.
❏ The patient may also benefit from nonpharmacologic therapies such as
avoiding trigger foods and beverages and maintaining a healthy
weight., and avoiding smoking and alcohol.
 Therapeutic Alternatives
3.b. What pharmacotherapy options are available for acute treatment of TdP?
❏ There are a few different pharmacotherapy options for acute treatment of TdP. These
include:
❏ Beta blockers: Beta blockers can help to slow down the heart rate and decrease the
risk of further TdP episodes.
❏ Examples of beta blockers include propranolol, atenolol, and metoprolol.
❏ Calcium channel blockers: Calcium channel blockers can also help to slow down the
heart rate and decrease the risk of further TdP episodes. Some examples of calcium
channel blockers include amlodipine, diltiazem, and verapamil.
❏ Antiarrhythmics: Antiarrhythmics can help to stabilize the electrical activity of the
heart and prevent further TdP episodes.
❏ An example of an antiarrhythmic drug is antiarrhythmic agents.
 Optimal Plan
4. Design a pharmacotherapeutic plan for the treatment of acute drug-induced TdP for
this patient.
❏ As a relatively new kind of therapy for torsade de pointes, intravenous magnesium
sulphate. The preferred medication for reducing early afterdepolarizations (EADs) and
ending the arrhythmia is magnesium. Magnesium accomplishes this by reducing the
calcium influx, which lowers the amplitude of EADs. Magnesium can be administered
intravenously (IV) at 1-2 g initially in 30-60 seconds, and again in 5-15 minutes.
Magnesium is effective even in patients with normal magnesium levels. Because of
the danger of hypermagnesemia (depression of neuromuscular function), the patient
requires close monitoring.
 Outcome Evaluation
5. What monitoring parameters should be used to assess
efficacy and toxicity of treatment?
❏ Check EKG or ECG for Cardiac Rhythm normalization
❏ Serum magnesium is check as per doctor orders
❏ Monitor for s/sx of magnesium sulfate toxicity (ie;
hypotension, Areflexia, respiratory depression, oliguria, SOB,
etc.)
 Patient Education
6. What medication counseling should be provided for the
patient to prevent recurrence?
❏ Explaining the cons and pros of treatment and making sure to
present all medication taking before incorporating another
type of medication, this is to increase pharmacovigilance
especially to outpatient clients.
 Clinical Course
The patient was treated with magnesium infusion, and
she converted to normal sinus rhythm. The
erythromycin was stopped. Potassium and magnesium
were replaced, and the patient was admitted for
further electrophysiology workup.
 Clinical Pearl
There is a need for increased pharmacovigilance
regarding drug-induced arrhythmias in the outpatient
setting because a large number of pharmacologic
agents and/or conditions that cause QT prolongation
and TdP are present in the outpatient population.
Thank You!