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Emergency Medicine: Cardiology 213

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  1. Acute Coronary Syndromes: A Focus on STEMI
    10 Topics
    3 Quizzes
  2. Acute decompensated heart failure
    10 Topics
    3 Quizzes
  3. Hypertensive Urgency and Emergency Management
    11 Topics
    3 Quizzes
  4. Acute aortic dissection
    9 Topics
    2 Quizzes
  5. Arrhythmias (Afib, SVT, VTach)
    10 Topics
    2 Quizzes

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  • April
  • Alyssa
  • Ashley
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  • Sherif
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Atrial Fibrillation

The diagnosis of AF requires documentation of the arrhythmia on ECG, which will show the characteristics of an irregularly irregular rhythm with no discernible P waves.

Additional diagnostic evaluation aims to determine the onset, type, underlying causes, and hemodynamic impact of AF. Key components include:

  • History and physical exam to elicit duration and nature of symptoms, precipitating factors, medical history, cardiovascular exam findings.
  • 12-lead ECG to confirm diagnosis and evaluate ventricular rate, intervals, preexcitation.
  • Assessment of vital signs including heart rate and blood pressure.
  • Lab tests:
    • Complete blood count, electrolytes, renal function tests, thyroid function tests, cardiac enzymes and BNP to uncover contributing factors
    • Coagulation studies if anticoagulation is being considered
  • Chest x-ray to evaluate heart size and pulmonary congestion
  • Echocardiography to evaluate chamber sizes, left ventricular function, valvular disease.
  • Additional cardiac imaging (eg, CT, MRI) may be warranted in certain cases to further evaluate anatomy and function.
  • Ambulatory ECG monitoring to document pattern (paroxysmal, persistent) and burden of AF

The evaluation aims to determine the type of AF (first detected, paroxysmal, persistent, long-standing persistent), identify reversible precipitating causes, assess stroke and bleeding risks using CHA2DS2-VASc and HAS-BLED scores respectively, and evaluate the need for further monitoring.

Supraventricular Tachycardia


On 12-lead ECG during AVNRT, the rhythm is regular with normal QRS complexes and ventricle rates typically between 140-250 bpm. The most characteristic ECG finding is RP interval (time from QRS to P wave) usually less than half the R-R interval, although not always. Retrograde P waves are typically not visible, buried in the QRS complex. Other findings may include pseudo r prime (r’) in V1, pseudo S waves in inferior leads, and pseudo Q waves in aVL. However, AVNRT ECG patterns have significant variability between patients and episodes.

Differential diagnoses to consider based on ECG include other SVTs like AVRT, atrial tachycardia, flutter or fibrillation. Adenosine can be diagnostic to help differentiate, as it will transiently block AV nodal conduction and terminate AVNRT. AVRT and atrial tachycardia will persist after adenosine.

Ambulatory Monitoring

Ambulatory ECG monitoring using Holter monitors or external loop recorders can help document tachycardia episodes. The advantage of ambulatory monitoring is ability to correlate timing of episodes with patient symptoms and activities. This can be useful in assessing frequency of recurrences, response to treatments, and triggering factors. Limitations include inconsistent patient compliance and short monitoring durations.

Electrophysiology Study

An electrophysiology study (EPS) involves catheter placement into the heart chambers to map electrical signals. Programmed electrical stimulation is used to induce AVNRT episodes in a controlled setting. EPS allows definitive diagnosis by directly assessing conduction through dual AV nodal pathways and mechanisms of tachycardia. It is also used to guide ablation therapy. However, EPS is an invasive procedure with some risks. It should be considered in patients when noninvasive methods fail to establish a clear diagnosis.

Ventricular Tachycardia

Monomorphic and polymorphic ventricular tachycardias (VT) share some similarities but have key differences in presentation and management.


  • Both originate from the ventricles
  • Wide QRS complex (>120 ms)
  • Potentially unstable depending on rate and duration
  • Risk of deteriorating to ventricular fibrillation 


  • Monomorphic VT has a regular rhythm with uniform QRS complexes suggesting a stable reentrant circuit
  • Polymorphic VT has an irregular rhythm with continuously varying QRS suggesting changing activation
  • Monomorphic VT is often due to scar from prior infarction
  • Polymorphic VT is often due to acute ischemia, bradycardia, electrolyte imbalance, or medication effect
  • Monomorphic VT management may involve IV antiarrhythmics, overdrive pacing, or catheter ablation
  • Polymorphic VT management centers on identifying and correcting any trigger plus IV antiarrhythmics
  • Monomorphic VT may be well tolerated if heart function is preserved
  • Polymorphic VT is unstable by definition and requires prompt termination
  • Monomorphic VT may be recurrent and require chronic management
  • Polymorphic VT may be a one-time event if the trigger is eliminated

In summary, the regular vs irregular QRS complexes help distinguish monomorphic and polymorphic VT. Therapy differs based on the underlying mechanism and stability.