cardiology

Episode 47 – Left Bundles and Implantable Cardiac Devices

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The Free Open Access Medical Education (FOAM)

We cover a post from Dr. Smith’s ECG blog investigating ways to read ischemia on a ventricular paced ECG.  In A Patient with Ischemic symptoms and a Biventricular Pacemaker, Dr. Smith asserts that the modified Sgarbossa criteria may work in ventricular paced rhythms as well as Left Bundle Branch Blocks (LBBB).

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@FOAMpodcast

Core Content

We delve into core content on implantable cardiac devices using Rosen’s (8th edition), Chapter 80 and Tintinalli (8th edition)

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Generously Donated Rosh Review Questions

Question 1.  A 44-year-old man with an automatic implantable cardioverter-defibrillator (AICD) in place presents with weakness and palpitations. Vitals are HR 180, BP 83/53, RR 28. His ECG is shown below.  

rosh review

Question 2.  A 76-year-old woman presents to the Emergency Department with generalized weakness and fatigue. She had a pacemaker placed one month ago. 

rosh review

Answers

  1. Electrical cardioversion.  This patient presents with unstable ventricular tachycardia and should immediately be electrically cardioverted. AICDs are placed for a number of indications but the goal is the treatment of ventricular dysrhythmias, particularly ventricular tachycardia (VT) and ventricular fibrillation (VFib). All AICDs have a right ventricular lead that is used for sensing. During insertion, the cardiologist determines the parameters for the device to deliver a shock. Despite the presence of these devices, patients may still present in ventricular dysrhythmias that have not been shocked if the device is malfunctioning. Patients may also experience inappropriate shocks. Regardless of the presence of the device, if a patient presents in an unstable dysrhythmia,electrical cardioversion or defibrillation (depending on the circumstance) should still be performed. This patient presents with ventricular tachycardia and hypotension and device failure. It is recommended that if a shock is to be delivered in a patient with an AICD that the pads not be placed over the device site. Otherwise, the presence of a device is not a contraindication to external electrical cardioversion/defibrillation.
    Amiodarone (A) and procainamide (D) are antidysrhythmic agents that can be used in the treatment of stable ventricular tachycardia. Placing a magnet over the AICD site (C) may be beneficial in treating patients who are receiving inappropriate shocks.
  2. A. Failure to capture can range from complete absence of pacemaker activity to pacemaker spikes being seen but not resulting in depolarization of the myocardium. Complete absence of activity can be due to battery depletion, fracture of the pacemaker lead (which is uncommon with today’s technology) or disconnection of the lead from the generator. Intermittent failure to capture is commonly due to lead displacement and is most likely to happen within the first month of placement. Failure to pace can also be due to impaired endocardium, which despite an intact and normally functioning pacemaker, will not depolarize properly. Causes include ischemia or infarction, hyperkalemia or use of class III antiarrhythmic drugs. Overpacing (B) can occur when atrial flutter develops during dual chamber pacing. The pacemaker may sense the atrial flutter waves resulting in a rapidly paced ventricular rate. A “runaway pacemaker”, a pacemaker that causes extreme increases in pacing rates due to malfunction, is very unlikely with current pacemaker technology. In both of these cases, placing a magnet over the pacemaker will switch it from demand to fixed mode and may terminate the tachycardia. Oversensing (C) occurs when the pacemaker senses electrical activity that is not of cardiac origin and erroneously inhibits the generator. This may result in bradycardia. Undersensing (D) occurs when the pacemaker can not adequately sense the intrinsic electrical activity of the heart. If the pacemaker is in an inhibit mode, this can result in the pacemaker firing inappropriately.

References:

1. Sgarbossa EB, Pinski SL, Barbagelata et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996 Feb 22;334(8):481

2.  Smith SW, Dodd KW, Henry TD et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Ann Emerg Med. 2012 Dec;60(6):766-76.

3.Cai Q, Mehta N, Sgarbossa EB, Pinski SL, Wagner GS, Califf RM, Barbagelata A. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013 Sep;166(3):409-13. doi: 10.1016/j.ahj.2013.03.032.

Episode 34 – Tachyarrhythmias

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The Free Open Access Medical Education (FOAM)

The St. Emlyn’s team ran a post on the REVERT trial, which added a new spin to the traditional (and traditionally ineffective) Valsalva maneuver for stable supraventricular tachycardia (SVT). In this post, Dr. Rick Body goes through the trial covering not only the results but also drops pearls on methodology.

  • Randomized 433 patients with SVT to one of the following:
    • “Modified” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec and then placed supine with passive leg raise immediately after procedure (see video)
    • “Standard” Valsalva maneuver: patient sitting up performs Valsalva using a syringe to maintain 40 mm Hg for 15 sec while maintaining upright position
  • 43% of the patients in modified Valsalva group versus 17% in the standard technique achieved sinus rhythm at one minute yielding an absolute risk reduction of 26.2% (p<0.001) with a number needed to treat of about 4 (3.8).

Core Content – Supraventricular Tachycardia (SVT) and Ventricular Tachycardia (VT)

Tintinalli (7e) Chapter 22;  Rosen’s Emergency Medicine (8e) Chapter 79

SVT 

Broad term referring to tachycardias originating above the ventricles, including the regular rhythms of sinus tachycardia, AV nodal reentrant tachycardia, AV reentrant tachycardia, and the irregular rhythms of multifocal atrial tachycardia, atrial fibrillation, and some forms of atrial flutter.

Diagnosis: JACC algorithm

Treatment:

  • Unstable patients – electrical cardioversion at 0.5-1 J/kg (100J for an adult) + ABCs!
  • Stable patients-
    • Valsalva maneuver – we like this method of having a patient blow on a syringe. Unfortunately, prior to the REVERT trial, the valsalva maneuver success rate has been documented ~19% [3].
    • Adenosine (0.1mg/kg or 6 mg in adult; 2nd dose 0.2 mg/kg or 12 mg in adult, with occasional dose adjustments) – administration can be tricky because of the drug’s short half life, necessitating proximal administration, elevation of the arm, and a quick saline flush afterwards. You can combine the adenosine IN the flush as detailed in this post, meaning no stopcock.
    • Calcium channel blockers or beta-blockers (verapamil, diltiazem or even metoprolol, esmolol) – Recently the calcium channel blockers have increased in popularity in the FOAM world and these are Rosenalli approved [4,5].

VT

Diagnosis: Typically wide QRS complex (95% with QRS >120 ms) and fast (150-200 beats per minute).

  • SVT with abberency can have a wide complex but this should be treated as VT [4,5] (see this video)
  • Monomorphic – complexes have same morphology
  • Polymorphic – complexes of various morphologies, associated with poor prognosis [4,5]

Treatment:

  • Unstable patients – electrical cardioversion at 0.5-1 J/kg (100J for an adult) + ABCs!
  • Stable patients with monomorphic VT
    • Electrical cardioversion
    • Procainamide – Level B recommendation for first line treatment of monomorphic VT[6].
    • Amiodarone – common in the US but per the AHA guidelines “reasonable in patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C)” [6].
      • Note: Dangerous if prolonged QT [6]
    • Lidocaine – “may be reasonable” [6]
  • Stable patients with polymorphic VT
    • Electrical cardioversion
    • Beta-blockers (particularly if ischemic)
    • Amiodarone
    • Cardiac catheterization if potentially ischemic cause [6]
  • Torsades de Pointes – withdraw offending agent, magnesium sulfate IV if “a few episodes” per the AHA

Generously Donated Rosh Review Questions 

Question 1. A 26-year-old woman presents with dizziness and palpitations. She reports episodes of these symptoms beginning about 1 week ago, which initially only lasted a few minutes. However, for the past two days, she has had about 4 episodes a day which last about 20 minutes each. Her social history is significant for heavy caffeine intake. Her pulse is 166 bpm and her blood pressure is 140/70. Her rhythm strip is seen below. 

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Question 2. A 33-year-old woman with chronic persistent asthma presents with palpitations. Her vital signs are HR 210, BP 118/73, and pulse oxygenation of 97% on room air. An ECG is shown below. 

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References:

  1. Whinnett ZI, Sohaib SM, Davies DW. Diagnosis and management of supraventricular tachycardia. BMJ (Clinical research ed.). 345:e7769. 2012
  2. Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. The New England journal of medicine. 367(15):1438-48. 2012.
  3. Smith et al. Effectiveness of the Valsalva Manoeuvre for reversion of supraventricular tachycardia. Cochrane Database Syst Rev. 2013 Mar 28;3:CD009502. doi: 10.1002/14651858.CD009502.pub2
  4. ”Cardiac Rhythm Disturbances.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide.  7th ed. pp 136-146.
  5. “Tachyarrhythmias.” Rosen’s Emergency Medicine. 8th ed. Chapter 79.
  6. Zipes DP, Camm AJ, Borggrefe M et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death. Journal of the American College of Cardiology. 48(5):e247-e346. 2006

Episode 20 – Anticoagulation

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The Free Open Access Medical Education (FOAM)

We review Dr. Rory Spiegel’s, A Case of Identity Part Two, post on EMNerd which is essentially a take down of dual antiplatelet therapy (DAT) in acute coronary syndrome (ACS).  The bottom line?  There’s no demonstrable and clinically significant benefit from DAT as demonstrated in the trials below.

CURE trial – composite endpoints of questionable clinical significance and an enormous sample size.

  • 2.1% absolute decrease in cardiovascular death and myocardial infarction (MI), completely powered by the 1.5% absolute difference in MIs. Almost all of these MIs were Type IV and peri-procedural. Mortality between groups was identical at 30 days and end of follow up (1.0% vs 1.1% and 2.3% vs 2.4%, respectively).

ACCOAST – RCT of prasugrel or placebo prior to angiography

  • No difference in cardiovascular death, myocardial infarct, stroke, urgent revascularization or glycoprotein IIb/IIIa rescue therapy (10.8% vs 10.8%)
  • Approximately 1% increase in major bleeding

CREDO – RCT with placebo or clopidogrel 3-24 hours prior to urgent cardiac catheterization

  • No statistical difference  in the rates of death, stroke or MI at 28 days
  • Statistical significance of a secondary endpoint of the 1-year outcomes with a 2% absolute reduction in the rate of death, MI, and stroke, largely the result of a 1.9% reduction of MIs.
  • 1% increase in major bleeding events

Thienopyridine Meta-Analysis

  • In patients with non-ST elevation ACS, pretreatment with thienopyridines is not associated with reduced mortality but comes at a cost of a significant excess of major bleeding.

Composite endpoints are problematic (see this post, “Would You Rather“) and statistical significance claimed in these trials is largely a product of composite outcomes rather than patient oriented measures.

The Bread and Butter

We summarize some key topics from the following readings, Goldfrank (10th ed) Chapter 60, EMPractice October 2013 (there’s almost nothing in Rosenalli on this topic) but, the point isn’t to just take our word for it.  Go enrich your fundamental understanding yourself!

Aspirin

  • Irreversibly inhibits platelets (for the duration of platelet’s life)

Ibuprofen

  • Reversibly inhibits platelets

Novel Oral Anticoagulants (NOACs)

NOACs have gained increased popularity and are slowly supplanting warfarin for common anticoagulation indications such as non-valvular atrial fibrillation (NVAF) as well as treatment of venous thromboembolisms such as pulmonary embolism (PE) and deep venous thrombosis (DVT).

Direct thrombin inhibitor – dabigatran (Pradaxa).  This drug was the first to supplant warfarin for NVAF in the United States, billed as more patient friendly given the lack of purported need for routine monitoring.  Recent investigations by Cohen et al, however, demonstrate that monitoring may, in fact, be safer.  Further, in a real world, retrospective cohort of Medicare beneficiaries given either dabigatran or warfarin for atrial fibrillation, major bleeding of the dabigatran cohort was higher than in the warfarin cohort 9.0% (95% CI 7.8 – 10.2) versus 5.9% (95% CI 5.1 – 6.6) after propensity matching [Hernandez].  For more on the problems with dabigatran, check out Emergency Medicine Literature of Note.

  • Predominantly renal excretion
    • Caution with impaired renal function (can cause dabigatran to stick around longer)
    • Hemodialysis an option in acute overdose; however, most people would probably not want to put a dialysis catheter in a coagulopathic patient.
  • Half-life ~ 15 hours
  • Can elevate the PTT. If the PTT is normal, likely not coagulopathic secondary to dabigatran [Dager et al].
  • No reversal agent

Factor XA inhibitors – these have XA in the name….rivaroXAban, apiXAban, edoXAban.

Rivaroxaban – approved for NVAF and treatment of DVT/PE.  Half life approximately 6-9 hours.

Apixaban – approved for NVAF and treatment of DVT/PE. Half life about 12 hours.

Edoxaban – approved for NVAF. Half life about 10-14 hours.

Bleeding Duration from ACCP

Bleeding Duration from ACCP

  • Cleared by liver and kidneys.
  • Can elevate the prothrombin time (PT), but not reliably. Specific assays exist but are not widely available and are expensive.
  • No specific reversal agent although andexanet alfa is in the pipeline.  It’s a Factor Xa decoy (Andexanet Alfa) that binds up the F10A inhibitors like a sponge. Read more here.
  • In the setting of major bleeding, guidelines recommend 4 factor PCCs.  A recent study demonstrates reduction in bleeding using 4 factor PCCs on healthy patients given edoxaban [Zahir et al, EMLitofNote].  The benefit of 4 factor PCCs is predominantly based on improvement in numbers, not patient oriented benefit and is discussed in these posts by Dr. Spiegel The Sign of Four, The Sign of Four Part 2.

More FOAM on Anticoagulation Reversal

Generously Donated Rosh Review Questions 

Question 1. A 65-year-old man with a metal aortic valve presents with hematemesis. His vitals are BP 95/50 and HR 118. The patient is on warfarin and has an INR of 7.3. 

Question 2. A 66-year-old woman with atrial fibrillation on warfarin presents with dark stools for 2 days. Her vitals are T 37.7°C, HR 136, BP 81/43, RR 24, and oxygen saturation 94%. Her labs reveal a hematocrit of 19.4% (baseline 33.1%) and an INR of 6.1. 

 

Answers.

1. D.  The patient presents with life-threatening bleeding and an elevated INR from warfarin use requiring immediate anticoagulant reversal regardless of the indication for anticoagulation. Warfarin acts by inhibiting vitamin K recycling thus limiting the effectiveness of vitamin K dependant clotting factors (factors II, VII, IX and X). The effect of warfarin can be measured using the prothrombin time or the INR. Warfarin is indicated for anticoagulation for a number of disorders including the presence of a metal valve. Patients with metal valves are at a higher 1-year risk of clot formation around the valve and subsequent embolic stroke. The therapeutic goal of warfarin in a patient with a metallic valve is usually between 2.5 –  3.5 or 3.0 – 4.0. Despite the increased stroke risk, patients with life-threatening bleeding should always have their warfarin reversed by administration of vitamin K and fresh frozen plasma (FFP). Alternatively, prothrombin complex concentrates can be given instead of FFP.

Warfarin is not amenable to hemodialysis (A) for removal or reversal. Although patients with a mechanical valve are at an increased stroke risk (increased 1 year risk) reversal should not be delayed (B), as the patient is more likely to die in the immediate situation from their gastrointestinal bleed. Platelet transfusion (C) will not help, as warfarin does not inhibit platelet function.

2. C.  The patient has a life-threatening gastrointestinal bleed in the setting of anticoagulation with warfarin, a vitamin K antagonist. Warfarin acts by inhibiting the synthesis of vitamin K-dependant factors in the coagulation cascade (II, VII, IX, X, protein C, and protein S). The anticoagulant effect of warfarin should be reversed as part of the patient’s emergent treatment. Fresh frozen plasma (FFP) contains all factors in the coagulation cascade and should be given in patients with major bleeding and elevated INR. Vitamin K should be given IV in critically ill patients with elevated INR because it shortens the time to effect.

Vitamin K should not be given intramuscularly (B) because absorption via this route is highly variable. Vitamin K should also not be given orally (D) in critically ill patients because the onset of action will be delayed. Additionally, absorption in patients with gastrointestinal bleeding may be variable. Vitamin K should be given along with FFP (A) because the factors inhibited rely on vitamin K for function.

Episode 15 – Atrial Fibrillation/Flutter

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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

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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

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.  

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. 

Question 3.  

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.