Episode 15 – Atrial Fibrillation/Flutter

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

This week we review a post from Academic Life in Emergency Medicine, written by Brent Reed on selecting rate control agents in the management of atrial fibrillation.  This is a follow up post to Bryan Hayes’ summary of emergency department (ED) management of acute atrial fibrillation.  Both are high yield.

Acute Management:

  • No clear cut winner in the beta-blocker vs. calcium channel blocker battle

Long Term Atrial Fibrillation Management in General:

Avoid beta-blockers in:

  • Obstructive lung disease (asthma/COPD)
  • Peripheral vascular disease
  • Diabetics
  • Severe congestive heart failure (CHF)
  • Erectile dysfunction

Avoid calcium-channel blockers in:

  • Severe CHF and acute decompensated heart failure (ADHF)

Of note, in patients

The Maryland Critical Care Project has a great post with many of Dr. Amal Mattu’s key FOAM talks embedded on Tachydysrhythmias You Gotta Know.

The Bread and Butter

We summarize some key topics from the following readings, Tintinalli (7e) Chapter 280, 295 ; Rosen’s 8(e) Chapter  50 – a well written chapter, but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Atrial Fibrillation

Etiology

Screen Shot 2014-09-16 at 3.57.07 PM

Management

Unstable (hypotension, pulmonary edema, altered mental status, chest pain) – cardioversion.

  • Pads in either an anterior-lateral (AL) or anterior-posterior (AP) position followed by synchronized cardioversion at 100-200 J biphasic.  Current literature shows no significant difference in pad placement [1]
  • If cardioversion fails, try amiodarone load or diltiazem. Check out EMCrit on Crashing A Fib

Stable

  • Rate control. A target of <120 beats per minute is acceptable in the ED [2-3].  First line agents are nodal blocking agents such as diltiazem and metoprolol
    • Diltiazem 0.25 mg/kg IV over 2 minutes with a peak effect in 2-7 minutes. Can repeat at 0.35 mg/kg IV over 2 minutes.
    • Metoprolol 5-10 mg IV.
  • Rhythm control with cardioversion.  While there’s no proven benefit to rhythm control, many patients would prefer to be in sinus rhythm and ED cardioversion of stable new-onset atrial fibrillation is appropriate in a select population, notably, when the onset is <48 hours (or <72 hours per Rosen).  The pooled literature suggests a thromboembolism rate <0.8% [4].
    • Note: A recent article in JAMA by Nuotio et al found a higher rate of embolic events in patients who were electively cardioverted after >12 hours in atrial fibrillation.The 30 day risk of thromboembolism when cardioverted between 12-48 hours was 1.1%, compared to the ~2% risk if cardioverted after 48 hours. While the risk is still small, it is higher than the ~0.3% risk of thromboembolism with anticoagulation on board.
  • Treat the underlying cause (ex: sepsis, pulmonary embolism, hyperthyroidism, etc)
  • May also consider Amiodarone, Digoxin (mean >11 hours to rate control) [3]

In atrial fibrillation with pre-excitation (WPW), an often wide and irregular rhythm with different/changing morphologies to the QRS do NOT treat with an AV Nodal blocking agent as this may result in death (Adenosine, Beta-blocker, Calcium-channel blocker, etc). Treat with procainamide or shock

Disposition – Admit patients that present unstable, with underlying co-morbidities, or those that are not rate controlled.  Depending on the patient’s follow up and local practice patterns, the

Atrial Flutter

How to Avoid Misdiagnosing Atrial Flutter – Dr. Amal Mattu

Management – same as atrial fibrillation

  • More sensitive to electrical cardioversion, less sensitive to chemical cardioversion

Multifocal Atrial Tachycardia

Irregular narrow complex tachycardia with p waves of at least 3 morphologies (this can be difficult to see, so look in multiple leads, particularly V2)

 Etiology -often seen in advanced pulmonary disease

Management  – Treat the underlying cause, do NOT cardiovert MAT

 Learn from the master ECG educator, Dr. Amal Mattu

Generously Donated Rosh Review Questions (Scroll for Answers)

Question 1.  A 72-year-old man with a history of hypertension, diabetes, and congestive heart failure presents to the ED with heart palpitations for the past 4 days. He denies any chest pain, shortness of breath, abdominal pain, or history of similar palpitations. In the ED, his vital signs are BP 135/75, HR 138, RR 14, and oxygen saturation 98% on room air. His ECG is seen below. Which of the following is the most appropriate next step in management?

Rosh Review
Rosh Review

A. Chemical cardioversion

B. Rate Control

C. Synchronized cardioversion

D. Warfarin

Question 2.  When do you worry about giving calcium channel blockers, beta-blockers, or digoxin in a patient with atrial fibrillation?

Question 3. An 18-year-old woman presents with palpitations and near syncope. Her vitals are T 98.7F, HR 199, BP 113/66, RR 32, and oxygen saturation 94%. Her ECG is shown below. What treatment is indicated?

Rosh Review
Rosh Review

A. Administer adenosine 6 mg IV

B. Administer diltiazem 10 mg IV

C. Administer lopressor 10 mg IV

D. Administer procainamide 100mg IV

References

1.  Kirkland S, Stiell I, AlShawabkeh T, Campbell S, Dickinson G, Rowe BH. The Efficacy of Pad Placement for Electrical Cardioversion of Atrial Fibrillation/Flutter: A Systematic Review. Acad Emerg Med. 2014;21(7):717–726.

2. Chapter.  Rosen’s Emergency Medicine, 8e.

3.Chapter.  Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011

4. Cohn BG, Keim SM, Yealy DM. Is Emergency Department Cardioversion of Recent-onset Atrial Fibrillation Safe and Effective? J Emerg Med. 2013;45(1):117–27.

Answers

1.  B. Atrial fibrillation is caused by chaotic, disorderly firing from a second focus within the atria, resulting in uncoordinated atrial contractions. Patients with atrial fibrillation may present with palpitations, chest pain, shortness of breath, or they may be asymptomatic. Atrial fibrillation can be classified as chronic or paroxysmal, with paroxysms lasting minutes to days. On ECG, there are irregularly irregular narrow QRS complexes. In addition, no discernible p-waves are noted, rather fibrillatory waves are seen. Unless the patient is hemodynamically unstable, the mainstay of therapy is rate control. This is achieved through medications that act on the AV node such as calcium channel blockers (eg diltiazem or verapamil), beta-blockers, or digoxin. Due to digoxin’s slow onset of action and side effects, it is considered a second line medication.

If atrial fibrillation has been present for >48 hours, there is an increased risk of atrial thrombus formation. An echocardiogram should be obtained in these patients to exclude thrombus formation prior to rhythm control. Patients with chronic atrial fibrillation usually are placed on warfarin (D) or a similar anticoagulant to prevent thromboembolism.Chemical cardioversion (A) (amiorodone, procainamide or flecainide) can be attempted in patients with paroxysmal atrial fibrillation for less than 48 hours. Synchronized cardioversion (C) is used in patients who are hemodynamically unstable. This can be achieved by administering 50 – 100 J of electricity in synchronization mode.

2.  If a patient has an accessory pathway, such as Wolff-Parkinson-White Syndrome.

3. D. This patient presents with near syncope in the setting of atrial fibrillation with abberant conduction most likely secondary to Wolff-Parkinson-White (WPW) syndrome and should be chemically or electrically cardioverted. WPW syndrome refers to the presence of an accessory pathway between the right atrium and right ventricle. This accessory pathway has a shortened refractory period and can bypass normal conduction down the AV node. Because of the shortened refractory time, the accessory pathway in WPW can conduct atrial impulses much faster than the AV node can allowing for a ventricular rate between 150 and 300 beats per minute. Any tachycardia greater than 200 beats per minute in an adult should raise suspicion for an accessory pathway.

Patients with WPW can be asymptomatic or may present with severe tachydysrhythmias. The most common presenting dysrhythmia is reentrant tachycardia (70-80%) and second is atrial fibrillation (10-30%). In these tachydysrhythmias, the patient can conduct orthodromically (down the AV node and back up the accessory pathway), antidromically (down the accessory pathway and up the AV node) or in both directions. Patients who have any antidromic conduction will present with wide complex tachycardias. In patients with irregularly irregular wide-complex tachycardias, atrial fibrillation with WPW is the most common diagnosis. If the patient is unstable, electrical cardioversion should be pursued immediately as these patients run the risk of degrading into ventricular tachycardia and ventricular fibrillation. If the patient is stable, procainamide can be administered for chemical cardioversion. Procainamide is a class Ia anitdysrhythmic agent. The dose of procainamide (D) is 18-20 mg/kg administered at a rate of 20-30 mg/min.

In patients with WPW, antidysrhythmic agents that block the AV node are contraindicated. Blocking the AV node causes unopposed electrical conduction down the accessory pathway. This can lead to ventricular dysrhythmias. Additionally, the accessory pathway in WPW responds paradoxically to AV nodal blocking agents by further decreasing its refractory time. Adenosine (A), beta-blockers (C), calcium-channel blockers (B) and digoxin all block the AV node.

Episode 7 – Heart Failure

Episode 7 (iTunes or Listen Here)

The Free Open Access Medical Education (FOAM)

We review RAGE Podcast Episode 4 that awesomely covers nearly everything under the sun. A few of our favorite pearls:

Impact apnea –people who sustain traumatic brain injury often have associated apnea.  Support their airway because this could lead to arrest. Bystander support is crucial.

Right Ventricular Myocardial Infarction (RVMI)– Think about this in any inferior MI situation. Give fluids, these patients are preload dependent and need the cath lab.

Right Ventricular Heart Failure – OH CRAP.

  • Optimize Oxygenation, Hemodynamics, Contractility, Rate/rhythm, Afterload, and Preload
  • Give fluids, but not too much. Inotropes and vasopressors are often necessary. These guys like milrinone and epinephrine.

The Bread and Butter

We summarize some key topics from the following readings,  Tintinalli (7e) Chapters 53, 57; Rosen’s (8e) Chapters 78, 81…but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

RVMI – often associated with inferior MIs and can carry increased morbidity/mortality.

ECG pearls –

  • look for ST elevation in lead III greater than lead II or lead V1 (especially with ST depression in V2.
  • Right sided leads – elevation in V4R most specific but elevation in V3R-6R are indicative of RVMI.  Keep V1 and V2
025_ECG_12leads
http://www.elin.ttu.ee/mesel/Study/Courses/3240BME/Content/1_Bioelectricity/BME_2_bioelectric_signals.htm

Treatment – RVMI is preload dependent so they need fluid.  Too much fluid may cause the RV to impinge on the LV.

Acute Heart Failure (WikEM)

  • Give nitrates, which decrease preload, before diuretics.  Diuretics are only indicated in volume overloaded patients, and many patient simply have fluid shifts and are overall euvolemic or have decreased plasma volume.  Thus, in some patients, diuretics may be harmful.
  • Use non-invasive ventilation
  • BNP.  The boards and ACEP recommend it but randomized clinical trials have not consistently demonstrated a benefit in the Emergency Department (Carpenter et al)

Right vs Left Sided Heart Failure – this distinction is someone artificial as chambers are interdependent in series.

  • Left-sided failure – pulmonary symptoms (dyspnea and orthopnea)
  • Right-sided failure have systemic venous congestion(pedal edema and hepatomegaly)

High Output Failure – conditions with excess cardiac output

  • Causes – increased preload (excess mineralocorticoids, fluid/salt retention), decreased systemic vascular resistance (pregnancy, cirrhosis, severe anemia, beriberi, thyrotoxicosis, Paget’s disease, or vasodilator medications), or tachycardia and persistent beta-adrenergic stimulation.
  • Treatment – correct underlying cause

Generously donated Rosh Review questions (scroll for answers)

Question 1.  [polldaddy poll=8168396]

Question 2. A 73-year-old man presents to the ED with progressive shortness of breath for two days without chest pain. The patient has a history of hypertension controlled with hydrochlorothiazide, but has been noncompliant with his medications. In the ED, his vital signs are BP 186/102, HR 108, RR 34, and oxygen saturation 90% on room air. On exam, the patient has pulmonary crackles midway up both lung fields, jugular venous distension, and pitting edema of his lower extremities. A chest X-ray depicts increased interstitial markings and an enlarged cardiac silhouette. An ECG shows sinus tachycardia. [polldaddy poll=8168406]

Question 3.  [polldaddy poll=8169897]

References:

O’Brien JF.  Heart Failure.  Rosen’s Emergency Medicine (8e).  Chapter 81, 1075-1090.e7

Hollander JE, Diercks DB.  Chapter 53:  Acute Coronary Syndromes: Acute Myocardial Infarction and Unstable Angina.”Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011. p 367-385

Peacock WF.  Chapter 57: Congestive Heart Failure and Acute Pulmonary Edema. Failure. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7e. New York, NY: McGraw-Hill; 2011  p 404-414

 

Answers:

Question 1.  D. This patient presents with symptoms of acute decompensated heart failure (ADHF) and should be started on nitroglycerin therapy immediately. Patients with ADHF present with shortness of breath, increased work of breathing, tachycardia, hypoxia, crackles on lung examination and jugular venous distension. These patients experience acute worsening of left ventricular function and output secondary to a number of mechanisms including increased systemic vascular resistance. Therapy focuses on reduction of preload to decrease the flow of blood into the lungs and afterload reduction to increased the effectiveness of the left ventricle. Both of these goals can be accomplished through the administration of nitroglycerin. At lower doses, nitroglycerin acts as a peripheral vasodilator and increases venous capacitance leading to decreased preload. At higher doses, nitroglycerin causes arterial vasodilation leading to decreased afterload. Because of its rapid onset of action, nitroglycerin is the first line medication in patients with ADHF. Furosemide (A) may be useful in patients with volume overload and ADHF but this represents less than half of patients with ADHF. Additionally, the effects are delayed. Heparin (B) can be given in cases of ischemia induced ADHF but will not yield any immediate benefits. Morphine (C) was historically used as a preload reducer but has been associated with increased morbidity in patients with ADHF and is no longer recommended.

Question 2.   A .  This patient is in acute heart failure with pulmonary edema. The clinical presentation of heart failure includes shortness of breath, jugular venous distension, crackles and rales, peripheral edema, S3 gallop, orthopnea, and paroxysmal nocturnal dyspnea. A chest X-ray may show an enlarged cardiac silhouette, Kerley B lines suggesting pulmonary edema, and pulmonary vessel cephalization. Labs may show an elevated plasma brain natiuretic peptide (BNP). Management of heart failure with acute pulmonary edema begins with addressing the ABCs.Noninvasive respiratory therapy, such as bilevel positive airways pressure (BiPAP) or continuous positive pressure airway (CPAP) is the most appropriate next step in management. Noninvasive positive pressure ventilation increases oxygenation, decreases the worth of breathing, and decreases preload and afterload. In addition to BiPAP, adjunctive medications include nitrates, diuretics, morphine sulfate, and position the patient sitting up. Nitrates act as venous and arterial vasodilators and help to reduce preload and afterload. Morphine sulfate is thought to decrease oxygen consumption by decreasing catecholamines, decrease preload from mild vasodilator effects and decreases pain and anxiety. However, there are some studies that link the use of morphine sulfate to an increased mortality. Furosemide can be used in patients with evidence of fluid retention (JVD, extremity edema). Pulmonary edema secondary to heart failure usually responds well to preload and afterload reduction with noninvasive ventilation and nitroglycerin. If the patent continues to deteriorate then intubation (C) may be necessary. A myocardial infarction is less likely given the lack of chest pain and ECG that does not reveal ST-segment elevations. Therefore, activation of the cath lab (B) is unnecessary. Hydrochlorothiazide (D) has no role in the acute management of pulmonary edema. Once stabilized, the patient can resume his daily medications.

 

Question 3.  Correct Answer ( C ) Atrioventricular (AV) conduction blocks occur in 25%–30% of patients with acute myocardial infarction. A narrow complex third-degree AV block in the setting of an inferior wall MI is usually transient and resolves spontaneously. Other AV blocks associated with a favorable prognosis include first-degree heart block and second-degree Mobitz type I (Wenckebach). Patients with a new left bundle branch block (A) in the setting of an acute MI are more likely to develop CHF, AV block, and ventricular fibrillation and have an overall increased mortality. Left posterior hemiblock (B) is associated with a large infarct size, increased risk of cardiogenic shock, and increased mortality. A new right bundle branch (D)in the setting of an anterior wall MI is associated with an increased risk of developing complete AV block and cardiogenic shock.