Foundations EKG I

Unit 5 Instructor—Approach to Tachyarrythmias

Timeline:
• Divide learners into 4 groups at different tables (this approach is suggested for groups of 8 or more
learners and should be modified to 1 or 2 groups so sites with lower numbers of learners)
• 5 min large group review of the Unit 5 Summary “Approach to Bradyarrythmias”
• Give each group 2 copies of the Unit 5 EKG Challenges Packet (merged challenge EKG content for EKGs 1-
4), this allows learner groups to all review content and record their group's answers to the interpretation
and questions for each EKG
• Allow 20 minutes for groups to complete the 4 challenges (give updates at 5min increments)
• 20 minutes large group discussion of answers to challenges. May consider asking each group to present
their responses to a different EKG

Meeting Resources:
• Notify learners in advance of the session that they need to review the unit summary and challenge EKGs
• Before the session, have a few copies of the unit summary (pages 2-6 of this document) printed to give to
learners who forgot their copies/devices and copies of the Unit 5 EKG Challenges Packet to give to groups
• Before the session, make sure to print this document for your own reference during the group discussion
• After the meeting, send out the answer document to learners for independent review
 Foundations EKG I
Unit 5 Instructor—Approach to Tachyarrythmias
Unit 5, Case 17—35yM with history of HTN and anxiety c/o palpitations which started
HR: 170 BP: 110/70
15 minutes prior to arrival. No CP but does feel very tired and SOB since onset. No
history of similar symptoms. RR: 22 O2 Sat: 97%
What treatment options do you have for this patient?

Unit 5, Case 18—57yM with PMH of HL, DM2 c/o palpitations and SOB for the past 72
hours. Sent to the ED from PMD’s office for an abnormal EKG. HR: 146 BP: 101/78
What is your diagnosis?
RR: 18 O2 Sat: 98%
How would you manage this patient in the ED?
What diagnostics would you order in the ED?

Unit 5, Case 19—44 y/o M with a history of a “heart problem” presents with palpita- HR: 150 BP: 120/86
tions. He reports he has been “shocked” before and is prescribed rivaroxaban.
RR: 14 O2 Sat: 99%
What are your management options for this patient?

Unit 5, Case 20—73yoF with a 50 pack year smoking history is admitted for shortness of
breath and increased sputum production. She reports many prior hospitalizations for HR: 115 BP: 120/70
similar symptoms.
RR: 22 O2 Sat: 90%
What underlying conditions are associated with this rhythm?
What electrolyte abnormalities should be evaluated for and corrected in patients with
this rhythm?
 Foundations EKG I - Unit 5 Summary
Approach to Tachyarrhythmias
Narrow Complex

When evaluating a tachyarrhythmia one should first evaluate whether the QRS is a narrow complex or a
wide complex. Next one should determine if the rhythm is irregular or irregular, as this will help narrow
down your differential diagnosis of possible causes. Supraventricular tachycardia (SVT) refers to any tach-
yarrhythmia that arises from above the Bundle of His. To further classify SVT one can distinguish between
regular and irregular rhythms.

Regular Irregular

Narrow Sinus tachycardia Atrial fibrillation

AVNRT MAT
Orthodromic AVRT
2:1 atrial flutter
Wide Ventricular tachycardia Atrial fibrillation with aberrancy
Antidromic AVRT
 AV Nodal Re-entry Tachycardia (AVNRT) is the most common re-entrant rhythm seen in the ED. Common
causes include caffeine ingestion, exertion, or other drug ingestions in patients with structurally normal
hearts. Note the regular narrow complex tachycardia (typically 140-280 bpm).

Treatment includes:
• Vagal Maneuvers to increase vagal tone
• Adenosine to block transmission through the AV node
• Synchronized cardioversion (especially for hemodynamically unstable or refractory SVT)
• Beta/calcium channel blockers can be considered but caution should be used as their effects can
last long after conversion of rhythm

AVRT is an anatomic re-entry circuit (Bundle of Kent) within the heart.

Conduction of AVRT may be orthodromic (traveling down the normal direction of the nerve fibers) or antidromic
(opposite to the normal conduction pathway). Antidromic conduction tends to cause a wide QRS complex whereas
orthodromic often causes a narrow complex .
Atrial fibrillation is an irregularly irregular rhythm with variable conduction through the AV node. In evaluation of a
patient with atrial fibrillation with RVR or atrial flutter, first clinicians must determine whether a patient is
hemodynamically stable or not. In unstable patients treatment is immediate synchronized cardioversion.
For stable patients with atrial fibrillation over 48 hours, rate control is the primary focus as rhythm control risks
thromboembolism.
Rate control can be achieved with beta blockers (for example metoprolol 2.5-5 mg IV bolus over 2 minutes up to 3
doses), calcium channel blockers (diltiazem 0.25 mg/kg IV bolus over 2 minutes with a second bolus if needed), or
digoxin (0.25mg IV every 4-6 hours up to 1mg)
All patients with atrial fibrillation should have their thromboembolic risk assessed by using the CHA2DS2-VASc score.
This accounts for the patient’s age, sex ,and history of CHF, hypertension, stroke/TIA, vascular disease, or diabetes.
A score greater than or equal to 2 should prompt consideration of anticoagulation.
For hemodynamically stable patients with onset of atrial fibrillation less than 48 hours ago the following treatments
may be considered:
• Elective synchronized cardioversion
• Medication for rhythm control (amiodarone, flecainide, ibutilide, etc)
Atrial flutter is a re-entry tachycardia in the right atrium which causes an atrial rate of 300 bpm. The actual ventricular
rate is determined by the degree of the AV block (how often the atrial impulse results in ventricular conduction). For
example, in atrial flutter with 2:1 block the EKG would show a regular rate of about 150 bpm as every other atrial
impulse results in ventricular conduction. Atrial flutter with 3:1 block would have a rate of about 100 bpm. Flutter
waves are usually best seen in leads II, III, and aVF.

When approaching a narrow complex rhythm, some sources suggest unmasking flutter waves with adenosine (AVNRT/
AVRT will often convert to sinus rhythm whereas atrial flutter should show flutter waves). Suspect atrial flutter with a
2:1 block if you see a very regular narrow complex rhythm at 150 bpm.

Rate controlling medications can be used to attempt to control atrial flutter (as you would use in atrial fibrillation).
Unlike atrial fibrillation, atrial flutter is often responsive to synchronized cardioversion at low voltages.
The other “irregularly irregular” rhythm is multifocal atrial tachycardia (MAT). MAT is most often seen in pa-
tients with severe lung disease. The criteria for diagnosing MAT are at least 3 different P wave morphologies
typically with slightly different PR intervals. Varying P wave morphologies and PR intervals are the result of
different ectopic foci. Treatment of MAT is not usually necessary—treating the underlying disease will treat the
MAT, however keep in mind that hypokalemia and hypomagnesemia can exacerbate MAT.

Created by Ashley Deutsch, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd
 Foundations EKG I - Unit 5, Case 17
35yM with history of HTN and anxiety c/o palpitations which HR: 170 BP: 110/70
started 15 minutes prior to arrival. No CP but does feel very tired
RR: 22 O2 Sat: 97%
and SOB since onset. No history of similar symptoms.

What is your interpretation of the EKG?

History/Clinical Picture
Rate What treatment options do you have for this patient?
Rhythm
Axis

P Waves
Q/R/S Waves
T Waves
U Waves

PR Interval
QRS Width
ST Segment
QT Interval
Triage EKG—Unit 5, Case 17
 Unit 5, Case 17—Supraventricular Tachycardia
What is your interpretation of the Triage EKG?
History/Clinical Picture—Sudden onset palpitations
Rate—168
Rhythm—Supraventricular Tachycardia given the rhythm is regular, no P waves are visible, and QRS complexes are narrow
Axis—Normal
P Waves—None apparent
Q, R, S Waves—Q wave in aVL. Normal R/S waves.
T Waves—Normal
U Waves—None apparent
PR Interval—No clear PR interval
QRS Width—Narrow
ST Segment—ST depression V2-5. No ST elevation
QT Interval—Normal. QTc 400ms (R-R 360ms, QT 240ms)
Diagnosis—Supraventricular Tachycardia is a catch-all term for a variety of reciprocating rhythms. It is important to scruti-
nize the post-cardioversion EKG for signs of an accessory pathway in your patients with SVT.

SVT Types:
AVNRT (AV nodal re-entrant tachycardia): a functional re-entry circuit that is within the AV node. There are a few sub-types
but distinguishing those is beyond the scope of this discussion. This is the most common re-entrant rhythm seen in the ED.
AVRT can occur randomly or as a result of exertion, caffeine or other ingestions in patients with structurally normal hearts.
AVRT (AV re-entrant tachycardia): an anatomical re-entry circuit that can manifest itself in two primary ways—orthodromic
or antidromic (below).
Orthodromic (Narrow) — 95%, clockwise conduction pathway. The first phase of conduction is fast—atria to ventricle
through the AV node. The second phase of conduction is slow—through an accessory pathway like a WPW tract.
Antidromic (Wide)— 5%, counterclockwise conduction pathway. The first phase of conduction is slow—through an
accessory pathway like a WPW tract. The second phase of conduction is fast—atria to ventricle through the AV node.
 Unit 5, Case 17—Supraventricular Tachycardia

What treatment options do you have for this patient?

Vagal Maneuvers—Increasing vagal tone can break re-entrant supraventricular tachycardias
Adenosine—Breaks re-entrant SVT by blocking transmission through the AV node.
Cardioversion—Synchronized cardioversion is very effective at converting refractory SVT
Beta/Calcium Channel Blockers—Verapamil, Metoprolol, Esmolol, Diltiazem, and Labetalol are all effective but due
to their half- lives they may remain active for long after the patient has converted

Resource Links: Life in the Fast Lane Dr. Steve Smith’s Blog

Created by William Burns, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd
 Foundations EKG I - Unit 5, Case 18
57yM with PMH of HL, DM2 c/o palpitations and SOB for the past HR: 146 BP: 100/70
72 hours. Sent to the ED from PMD’s office for an abnormal EKG.
RR: 18 O2 Sat: 98%

What is your interpretation of the EKG?

History/Clinical Picture
Rate
What is your diagnosis?
Rhythm
Axis
How would you manage this patient in the ED?
P Waves
Q/R/S Waves What diagnostics would you order in the ED?
T Waves
U Waves

PR Interval
QRS Width
ST Segment
QT Interval
Triage EKG—Unit 5, Case 18
 Unit 5, Case 18—Atrial Fibrillation with RVR
What is your interpretation of the EKG?
History/Clinical Picture— middle aged woman presents with palpitations for 72 hours
Rate— 140-160
Rhythm— atrial fibrillation
Axis— normal
P Waves— absent
Q, R, S Waves— normal
T Waves— no notable abnormalities
U Waves— absent
PR Interval— not applicable
QRS Width— normal
ST Segment— no notable deviation
QT Interval— difficult to assess given degree of tachycardia but grossly normal
Diagnosis: Atrial fibrillation with rapid ventricular rate

Discussion: Atrial fibrillation is characterized by chaotic, disorganized atrial activity with variable conduction through the
AV node. ECG findings include an irregularly irregular ventricular rate with no organized atrial activity. Rapid ventricular
rates may be poorly tolerated and should be treated with rate or rhythm control. In the hemodynamically unstable
patient, synchronized cardioversion should be done emergently. Hemodynamically stable patients may be managed
medically. Rhythm control with medications (amiodarone, flecainide, ibutilide, among others) or with elective synchronized
cardioversion can be considered in patients who have been in atrial fibrillation for ≤ 48 hours. In patients in whom the
duration of atrial fibrillation is ˃ 48 hours or unknown, rhythm control should be avoided due to the risk of
thromboembolism. In these patients, the focus should be on rate control with beta-blockers (generally metoprolol) or non-
dihydropyridine calcium channel blockers (diltiazem or verapamil). The ED physician should search for an underlying cause
for the atrial fibrillation (PE, hyperthyroidism, medication side effect) with appropriate diagnostics. All patients in atrial
fibrillation should have their thromboembolic risk assessed in the ED using the CHA2DS2-VASc score and anticoagulation
should be started for a score ≥ 2, assuming no contraindications.

Resource Links: Life in the Fast Lane — great overview Dr. Steve Smith’s Blog – great lecture
Created by Duncan Wilson, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd
 Foundations EKG I - Unit 5, Case 19
44 y/o M with a history of a “heart problem” presents with HR: 150 BP: 120/80
palpitations. He reports he has been “shocked” before and is
RR: 14 O2 Sat: 99%
prescribed rivaroxaban.

What is your interpretation of the EKG?

History/Clinical Picture
Rate
What are your management options for this patient?
Rhythm
Axis

P Waves
Q/R/S Waves
T Waves
U Waves

PR Interval
QRS Width
ST Segment
QT Interval
Triage EKG—Unit 5, Case 19

EKG courtesy of Shanna Jones, MD

 Unit 5, Case 19—Atrial Flutter
What is your interpretation of the EKG?
History/Clinical Picture—a young man with a history of a recurrent tachycardia for which he has been cardioverted in
the past. The fact that he is anticoagulated makes atrial fibrillation or atrial flutter most likely
Rate— ~150
Rhythm— Aflutter with 2:1 conduction
Axis— normal
P Waves— present, upright P wave in V1
Q, R, S Waves— Q wave in III, delayed R wave progression
T Waves— difficult to assess secondary to interference from the flutter waves
U Waves— none apparent
PR Interval— normal
QRS Width— narrow
ST Segment— difficult to assess, but no obvious ST elevation or depression
QT Interval— normal

Diagnosis: Atrial Flutter with 2:1 Conduction

Discussion: This patient presents with rapid, symptomatic atrial flutter with stable hemodynamics. Atrial flutter is very
responsive to synchronized cardioversion, and assuming he has been compliant with his rivaroxaban, it may be reasonable to
perform elective synchronized cardioversion. If the patient were not anticoagulated, elective cardioversion may need to be
deferred until an echocardiogram can be performed to rule out intra-atrial thrombus. Rate control with calcium channel
blockers (diltiazem, verapamil, etc) or beta blockers (metoprolol, esmolol, etc) would also be appropriate.

Resource Links: Life in the Fast Lane — great overview Dr. Steve Smith’s Blog – in depth video lecture

Created by William Burns, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd
 Foundations EKG I - Unit 5, Case 20
73yoF with a 50 pack year smoking history is admitted for short- HR: 115 BP: 120/70
ness of breath and increased sputum production. She reports
RR: 22 O2 Sat: 90%
many prior hospitalizations for similar symptoms.

What is your interpretation of the EKG?

History/Clinical Picture
Rate
What underlying conditions are associated with this
Rhythm
rhythm?
Axis

P Waves
Q/R/S Waves
What electrolyte abnormalities should be evaluated for
T Waves
and corrected in patients with this rhythm?
U Waves

PR Interval
QRS Width
ST Segment
QT Interval
Triage EKG—Unit 5, Case 20

Courtesy of Edward Burns of Life in the Fast Lane

Creative Commons License
 Unit 5, Case 20—Multifocal Atrial Tachycardia
What is your interpretation of the EKG?
History/Clinical Picture— elderly woman with significant smoking history presents for COPD exacerbation
Rate— 115-120
Rhythm— multifocal atrial tachycardia
Axis— right axis deviation
P Waves— P-waves of alternating and varied morphology suggesting rhythm is driven by multiple ectopic foci throughout
the atria
Q, R, S Waves— no pathologic Q-waves, S-waves laterally due to axis deviation, early R-wave progression
T Waves— inversions anteroseptal leads
U Waves— none
PR Interval— varied but not prolonged
QRS Width— normal
ST Segment— normal
QT Interval— normal
Diagnosis: multifocal atrial tachycardia

Discussion: Multifocal atrial tachycardia is generally associated with severe lung disease. It is generally seen in patients hos-
pitalized for COPD exacerbations and may be associated with WHO group III pulmonary hypertension and cor pulmonale.
Treatment involves treating the underlying lung disease. Hypokalemia and hypomagnesemia can exacerbate MAT and
should be corrected. Theophylline toxicity is also associated with MAT, and should be considered in patients on this
medication. Beta-blockers and calcium channel blockers can be considered if tachycardia is severe, though it should be
noted that beta-blockade may worsen bronchospasm in patients with acute flairs of obstructive lung disease.

Resource Links: Life in the Fast Lane — great overview

Created by Duncan Wilson, MD Edited by Nick Hartman, MD; Shanna Jones, MD; & Kristen Grabow Moore, MD, MEd