Episode 63 – Bradycardia

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Emergent transvenous pacing is a crucial skill for emergency physicians. It may be daunting due to the pacing box and various catheters. We have found that routinely rehearsing the procedure, reviewing where pacing equipment is in our departments, and where

In this episode we review the following videos:

Practical Pointers for Pacemaker Placement by Dr. Jason Nomura
Transvenous pacing video by Dr. Al Sachetti
Pacing 101 (Transcutaneous is Just Stupid) by Dr. Joe Bellezo on the Ultrasound Podcast
- This podcast lays down the argument that transcutaneous pacing is stupid. Transcutaneous pacing is difficult – patients are diaphoretic, capture rates may be 40%, and it takes a significant amount of energy. Further, it hurts.
  - However, in our opinion, there may be a role. In this talk, Dr. Bellezo quotes a 1981 study, in which emergent pacers were placed in “6 minutes.” Review of this study finds that this was actually 6 minutes, 45 seconds (closer to 7 minutes) [1]. This likely does not reflect the majority of emergency providers experience, certainly not ours, where the range is more often 15-30 minutes for the procedure. Thus, transcutaneous pacing may be a temporizing measure as one locates the ultrasound, gathers the supplies, and prepares for transvenous pacing in the unstable patient.

Core Content

We delve into core content on bradycardias and heart blocks using Rosen’s Emergency Medicine (8th edition) Chapter 79 “Dysrthymias” and Tintinalli’s Emergency Medicine (8th edition) Chapter 18 “Cardiac Rhythm Disturbances” as a guide.

Rosh Review Emergency Board Review Questions

Question 1a.

A 71-year-old woman presents after a fall at home. Her electrocardiogram is shown below.

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Third Degree Heart block.

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Question 2.

A. Administration of epinephrine

B. Defibrillation

C. Observation

D. Placement of transcutaneous pacer pads

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D. The patient has third degree heart block. In third degree atrioventricular (AV) block, also known as complete heart block, there is no conduction through the AV node, and an escape pacemaker is responsible for the ventricular rate. On electrocardiogram, P waves occur at regular intervals, and QRS complexes occur at regular intervals, but there is no association between the P waves and QRS complexes. When the block occurs in the AV node, a junctional escape pacemaker takes over with a rate of 40-60 beats/minute, and the QRS complex is narrow. If the block occurs at the infranodal level, a ventricular escape pacemaker paces at a rate of 40 beats/minute or less. Infranodal blocks results in a wide QRS complex. Patients with third degree heart block require cardiac pacing, as the slow escape rhythm is rarely adequate to maintain cardiac output and tissue perfusion. Transcutaneous pacing should be initiated while arrangements for transvenous pacing are made. Third degree blocks are commonly associated with cardiac ischemia or infarction. A nodal third degree block (narrow QRS complex) is a complication of acute inferior wall myocardial infarction, and may last for several days. Extensive acute anterior wall infarction is associated with infranodal third degree blocks (wide complex QRS), indicating damage to the infranodal conduction system. When a third degree heart block is seen with acute myocardial infarction, mortality is increased.

Administration of epinephrine (A) is incorrect. Defibrillation (B) the treatment for cardiac arrest from ventricular fibrillation or pulseless ventricular tachycardia. Observation (C) is incorrect since the patient’s slow heart rate is likely not adequate to maintain cardiac output.

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Question 3.

A 56-year-man presents to the ED with right arm pain and some chest discomfort. The day prior to arrival, he tried using heavier weights at the gym. He has a history of hypertension, hyperlipidemia, and COPD. In the ED, his vital signs are BP 136/90, HR 60, RR 16, and oxygen saturation 97% on room air. His rhythm strip is seen below. Which is the most appropriate management for this rhythm?

A. Aspirin

B. Cardioversion

C. Observation

D. Temporary pacing

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D. This ECG demonstrates type II second-degree heart block. Second-degree heart block is defined by one or more impulses not reaching the ventricles and is classified as type I and type II. Type II second-degree heart block, also known as Mobitz II, is caused by an infranodal conduction abnormality, most commonly in the bundle of His or the purkinje fibers. ECG findings demonstrate random dropped QRS complexes without any changes in the PR interval. Type II second-degree heart block carries a worse prognosis than type I second-degree heart block and necessitates treatment. Unlike type I, atropine has no effect on the His-Purkinje system and may worsen conduction. Temporary pacing is critical in this case because this rhythm can devolve to complete heart block. In the ED, transcutaneous or transvenous pacing should be instituted if the patient is symptomatic and there should be immediate consultation with a cardiologist. Patients with Mobitz II in the setting of an acute myocardial infarction should be treated with temporary pacing and revascularization; following revascularization most conduction abnormalities will improve or resolve and will not require permanent pacing.

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Question 4.

A man who presents with syncope is placed on the cardiac monitor. On the monitor you note a repeating trend of 6 P waves, 5 of which are followed by a narrow QRS complex and 1 of which is not followed by a QRS complex. The PR interval during this trend progressively increases. Which of the following is the most likely diagnosis?

A. First-degree AV block

B. Third-degree AV block

C. Type I second-degree AV block

D. Type II second-degree AV block

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C. A key distinction between first-degree and second-degree heart block is that in first-degree block the P wave is always followed by a QRS complex. In other words, the ratio of P waves to QRS complexes is 1:1, or, the electrical signal from the atria always passes to the ventricles. In second-degree AV block, the electrical impulse sometimes gets to the ventricles. There are two main types of second-degree AV block. In Mobitz type I, or Wenckebach, second-degree block, there is a progressive beat-to-beat lengthening of the PR interval until a P wave does not conduct through the AV node. The absent conduction and resultant “missing” QRS complex is called a “dropped” QRS, which represents an absent beat of ventricular contraction. First-degree AV block (A) has a 1:1 ratio of P waves to QRS complexes. Mobitz type II second-degree heart block (D) is characterized by a nonconducted P wave which is not preceded by progressive PR interval prolongation. AV dissociation, or third-degree AV block (B), occurs when none of the P waves conduct through the AV node. This complete AV block occurs with separate atrial and ventricular rates. There is no discrete correlation or trend between P waves and QRS complexes.

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References:

Lang R, David D, Klein HO, et al. The use of the balloon-tipped floating catheter in temporary transvenous cardiac pacing. Pacing Clin Electrophysiol. 1981;4(5):491-6.
Roberts J and Hedges J. “Emergency Cardiac Pacing.” Roberts and Hedges’ Clinical Procedures in Emergency Medicine

Episode 59 – Syncope (and the PESIT study)

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The PESIT study in the New England Journal of Medicine stirred up controversy in the FOAM world earlier in October 2016. In this episode we cover the following posts on this article on pulmonary embolism in syncope:

Core Content

We delve into core content on syncope usingRosen’s Emergency Medicine (8th edition) and Tintinalli’s Emergency Medicine (8th edition) Chapter 52

Rosh Review Emergency Board Review Questions

An 83-year-old is being evaluated in the emergency department after an episode of syncope. The woman was preparing dinner when she felt her heart start to race. The next thing she remembers is waking up on the floor. She experienced a similar episode about three weeks ago. She has never had anything like this before. Her past medical history is remarkable for hypertension, hyperlipidemia and hypothyroidism. Her medications include lisinopril, atorvastatin and levothyroxine. On physical exam her blood pressure is 142/83, heart rate 76/min, and respiration rate 13/min. Cardiac auscultation reveals no murmur. The remainder of her physical exam is normal. Electrocardiogram reveals normal sinus rhythm with left axis deviation. No cardiac rhythm abnormalities are detected. What is the most likely etiology of this patient’s syncope?

A. Aortic stenosis

B. Cardiac dysrhythmia

C. Orthostatic hypotension

D. Vasovagal

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B. Cardiac dysrhythmia is the most likely cause of this woman’s syncope. Cardiac dysrhythmias are a common cause of syncope in the elderly population. It is characterized by a brief or absent prodrome and palpitations immediately preceding the event. Several episodes over a short period of time in someone with no history of syncope suggest a dysrhythmia. Given this patient’s short prodrome, palpitations and history of a previous similar event makes a cardiac dysrhythmia the most likely etiology.

Aortic stenosis (A) is unlikely the cause of her syncope. Aortic stenosis is associated with a crescendo-decrescendo systolic ejection murmur. Syncope related to aortic stenosis typically occurs during exertion and is associated with very severe disease. This patient’s syncopal episode occurred while stationary. Additionally, she has no systemic symptoms of aortic stenosis.Vasovagal (D) is the most common cause of syncope in the general population. It is usually triggered by provoking factors such a blood draw or an intense emotion. Prodromal symptoms include feeling warm, sweating, nausea, and pallor. This woman does not report any of these symptoms. Orthostatic hypotension (C) causes syncope upon assuming an upright position from supine or sitting. It is often caused by hypovolemia, medications or autonomic nervous system disorders. This woman was standing while preparing dinner making orthostatic hypotension unlikely.

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An 18-year-old woman presents after having a syncopal episode. She is complaining of a 2-day history of lower abdominal pain and vaginal spotting. Her BP is 86/42, HR is 128, RR is 18 breaths, and oxygen saturation is 99% on room air. She is drowsy, but answers questions appropriately. What is the most appropriate next step in management?

A. Establish large-bore IV access and administer an IV fluid bolus

B. Initiate rapid sequence induction and orotracheal intubation

C. Perform a bedside urine pregnancy testing

D. Perform an ultrasound of the abdomen to assess for free fluid

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A. The patient is hypotensive and tachycardic. She is suffering from hypovolemic shock secondary to a ruptured ectopic pregnancy. Therefore she requires immediate intravenous access and volume resuscitation with Lactated Ringer’s or normal saline. Emergency Department management of unstable patients includes rapid assessment of the ABC’s (Airway, Breathing, Circulation). This patient is phonating, has a respiratory rate of 18 breaths per minute and an oxygen saturation of 99% on room air. There is no concern that her airway or breathing is in immediate jeopardy, therefore she would not require immediate rapid sequence induction and orotracheal intubation (B). Although a bedside pregnancy test (C) and abdominal ultrasound (D) would help make a diagnosis of ruptured ectopic pregnancy, the next step would be to resuscitate the patient.

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References

De Lorenzo RA. “Syncope.” Chapter 15. Rosen’s Emergency Medicine (8 ed). pp 131-145
Chapter 52. Tintinalli’s Emergency Medicine: A Comprehensive Review (8 ed).
Serrano LA, Hess EP, Bellolio MF et al. Accuracy and Quality of Clinical Decision Rules for Syncope in the Emergency Department: A Systematic Review and Meta-analysis. Annals of Emergency Medicine. 56(4):362-373.e1. 2010.

Episode 54 – The Pericardium

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We cover ultrasound guided pericardiocentesis using the posts from EMin5, CoreEM, and the Ultrasound Podcast.

Historically, pericardiocentesis is taught using a landmark based method; however, use of ultrasound guidance may increase success. Experts recommend an approach wherever the largest pocket of fluid exists and each location has particular downsides to be aware of.

Core Content

We delve into core content on the pericardium using Rosen’s (8th ed) Chapter 82 and Tintinalli (8th ed) Chapter 55.

Generously Donated Rosh Review Questions

1.A 25-year-old man presents to the ED with chest pain, shortness of breath, and fever. Vital signs include BP 98/50 mm Hg, HR 136 beats/minute, RR 26 breaths/minute, and T 102.4°F. On auscultation, you hear rales to the mid-thorax bilaterally. Bedside cardiac ultrasound shows global hypokinesis and a small pericardial effusion. Which of the following organisms is the most common cause of this condition worldwide?

A. Coxsackievirus B

B. Mycobacterium tuberculosis

C. Plasmodium falciparum

D. Trypanosoma cruzi

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[toggle title=”Answers” state=”closed”]D. Trypanosoma cruz. This patient presents with signs and symptoms of myocarditis accompanied by pericarditis. Myocardial injury results from inflammation of the myocardium. The most common etiology worldwide is Chagas disease, caused by the protozoan Trypanosoma cruzi. The protozoan is spread by the reduviid bug, also known as the kissing bug as it feeds on the faces of those affected. Unfortunately, in many patients, the cause of myocarditis is idiopathic. Other noninfectious causes include connective tissue disorders such as scleroderma, toxins such as chemotherapy, cocaine, and heavy metals, and peripartum myocarditis. Symptoms often include a viral prodrome with fever, myalgias, and generalized weakness. Patients may present with chest pain, symptoms of acute heart failure, tachycardia, dysrhythmias, syncope, cardiogenic shock, or even sudden cardiac death. Diagnosis can be very difficult and patients often present to the ED multiple times prior to being diagnosed. An ECG may show global or segmental ST elevation, nonspecific ST segment and T wave changes, dysrhythmias, or conduction delays. Troponin and creatinine phosphokinase are often elevated. Echocardiography classically shows global hypokinesis. Management is primarily supportive; however, patients with new left bundle branch block or low ejection fraction may require a left ventricular assist device as a bridge to cardiac transplantation in some cases as these are poor prognostic indicators. The most common long-term sequelae of myocarditis is dilated cardiomyopathy.[/toggle]
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2.A 56-year-old woman with a history of lymphoma presents to the Emergency Department at the recommendation of her primary care physician. During a routine visit, she had a chest X-ray that showed a “big heart.” She denies chest pain, shortness of breath, leg swelling, cough, orthopnea, or lightheadedness. Her vital signs include temperature 98.6 ºF, HR 88 beats/minute and regular, RR 14 breaths/minute, BP 121/89 mm Hg, and oxygen saturation 98% on room air. Her cardiac and neck exams are within normal limits. A bedside ultrasound reveals a small pericardial effusion. Which of the following is the next best step in management?

A.Lower extremity ultrasound

B. Pericardiocentesis

C. Reassurance and close follow up

D. Thoracic Surgery consultation

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[toggle title=”Answers” state=”closed”] C. Reassurance and close follow up. The patient likely has a malignant pericardial effusion secondary to her known malignancy. Pericardial effusions are accumulations of fluid in the pericardial space that occur rapidly or gradually. Rapid accumulation of pericardial effusion can produce tamponade physiology and hypotension. This requires pericardiocentesis for emergent decompression of the effusion. Pericardial effusions that develop gradually often occur secondary to cancer (e.g. lymphoma, lung cancer, breast cancer, melanoma) or as the result of cancer treatment (e.g. radiation). Clinical signs or symptoms are determined by the rate of fluid accumulation. Asymptomatic pericardial effusions require no immediate treatment. Echocardiography is the diagnostic tool of choice. Chest X-ray may show a large cardiac silhouette indicating gradual fluid accumulation within a stretched pericardium. Malignant pericardial effusions can be managed in a variety of ways, including systemic or intrapericardial chemotherapy, or a pericardial window with pericardial resection. Lower extremity venous ultrasound (A) is an imaging modality to evaluating and diagnosing a deep venous thrombosis (DVT). This patient has no clinical features suggesting a DVT. Pericardiocentesis (B) is indicated in patients with symptomatic pericardial effusions or those who are experiencing tamponade physiology with hypotension. Thoracic surgery consultation (D) is not indicated since the patient is asymptomatic and hemodynamically stable.

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3. A 4-year-old girl is brought to the ER by her parents due to lethargy. A week prior the girl had a cough and colds. Later symptoms progressed to include fever and malaise. She has been less active with decreased appetite. A few hours prior to arrival in the ER, she has been having difficulty of breathing. On exam, temperature is 38.3°C, respiratory rate of 35, heart rate of 126, blood pressure of 90/60, clear breath sounds, hepatomegaly, and poor pulses. Which of the following is the most likely diagnosis?

A. Bronchiolitis

B. Dysrhythmia

C. Myocarditis

D. Pneumonia

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[toggle title=”Answers” state=”closed”]The girl demonstrates signs and symptoms that are suspicious for myocarditis which is a condition that results from inflammation of the heart muscle. Majority of children present with acute or fulminant disease. Myocarditis can be caused by infectious, toxic, or autoimmune conditions. Common causes of viral myocarditis include enterovirus (coxsackie group B), adenovirus, parvovirus B19, Epstein-Barr virus, cytomegalovirus, and human herpes 6 (HHV-6). The presentation of the disease is variable and patients can present with broad symptoms that range from subclinical disease to cardiogenic shock, arrhythmias, and sudden death. There is usually a history of a recent respiratory or gastrointestinal illness within the previous weeks. There is a prodrome of fever, myalgia, and malaise several days prior to the onset of symptoms of heart dysfunction. Then patients present with heart failure symptoms that include dyspnea at rest, exercise intolerance, syncope, tachypnea, tachycardia, and hepatomegaly. Testing is focused on determining the severity of cardiac dysfunction and these include electrocardiography (ECG), cardiac biomarkers, chest radiography, and echocardiography. Confirmation of myocarditis is generally made by cardiac magnetic resonance imaging or endomyocardial biopsy.

Dysrhythmia (B) usually presents with palpitations, syncope, chest pain. In the vignette, the girl’s symptoms are more consistent with a myocarditis. A primary dysrhythmia resulting in myocardial injury is differentiated from myocarditis by an endomyocardial biopsy. Bronchiolitis (A) is typically a disease in children younger than two years of age. It is diagnosed clinically with the characteristic findings of a viral upper respiratory prodrome followed by increased respiratory effort. Pneumonia (D) usually presents with respiratory complaints, particularly cough, tachypnea, retractions, and abnormal lung examination which were not present in the vignette.

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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).

Core Content

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

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. [polldaddy poll=9378494]

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. [polldaddy poll=9378495]

Answers

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.
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 47 – Left Bundles and Implantable Cardiac Devices

(ITUNES OR LISTEN HERE)

The Free Open Access Medical Education (FOAM)

Core Content

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

Generously Donated Rosh Review Questions

[expand title=”Answer”]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” [/expand]

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. [polldaddy poll=9378495]

[expand title=”Answer”] 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. [/expand]

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

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].
  - The Pros – RAGE podcast, ERcast (bonus)
  - The Cons – Dr. Minh Le Cong’s RAGEback

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. [polldaddy poll=9061960]

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. [polldaddy poll=9061966]

References:

Whinnett ZI, Sohaib SM, Davies DW. Diagnosis and management of supraventricular tachycardia. BMJ (Clinical research ed.). 345:e7769. 2012
Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. The New England journal of medicine. 367(15):1438-48. 2012.
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
”Cardiac Rhythm Disturbances.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. pp 136-146.
“Tachyarrhythmias.” Rosen’s Emergency Medicine. 8th ed. Chapter 79.
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 34 – Tachyarrhythmias

(ITUNES OR Listen Here)

The Free Open Access Medical Education (FOAM)

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

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].
  - The Pros – RAGE podcast, ERcast (bonus)
  - The Cons – Dr. Minh Le Cong’s RAGEback

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

References:

Whinnett ZI, Sohaib SM, Davies DW. Diagnosis and management of supraventricular tachycardia. BMJ (Clinical research ed.). 345:e7769. 2012
Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. The New England journal of medicine. 367(15):1438-48. 2012.
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
”Cardiac Rhythm Disturbances.” Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th ed. pp 136-146.
“Tachyarrhythmias.” Rosen’s Emergency Medicine. 8th ed. Chapter 79.
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

(ITUNES OR LISTEN HERE)

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.

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

ER Cast

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. [polldaddy poll=8501352]

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. [polldaddy poll=8505511]

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

(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

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?

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?

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 15 – Atrial Fibrillation/Flutter

(iTunes or listen here)

The Free Open Access Medical Education (FOAM)

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

Atrial Fibrillation

Etiology

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]

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)

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?

A. Administer adenosine 6 mg IV

B. Administer diltiazem 10 mg IV

C. Administer lopressor 10 mg IV

D. Administer procainamide 100mg IV

References

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

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

FOAMcast

An Emergency Medicine Podcast

Episode 63 – Bradycardia

Episode 59 – Syncope (and the PESIT study)

Episode 54 – The Pericardium

Episode 47 – Left Bundles and Implantable Cardiac Devices

Episode 47 – Left Bundles and Implantable Cardiac Devices

Episode 34 – Tachyarrhythmias

Episode 34 – Tachyarrhythmias

Episode 20 – Anticoagulation

Episode 15 – Atrial Fibrillation/Flutter

Episode 15 – Atrial Fibrillation/Flutter