David Cohen, MD

Slideshows

Patient history includes right heart failure due to sinus venosus defect with anomalous right pulmonary venous return; surgical repair performed ca 2006.

Persistent Palpitations and Dyspnea in a Middle-aged Man

	An 83-year-old man with hypertension but who is otherwise healthy and very active for his age presents to your office for routine follow-up. He just returned from a trip out of the county where he was walking several miles per day and states he “feels like Tarzan.” His vitals are normal except his pulse is noted to be 45/beats min. He takes carvedilol 25 mg twice daily and losartan-HCTZ 40/25 mg once daily for hypertension. ECG is obtained and shown below (

	The ECG shows sinus rhythm at ~80 beats/min with 2:1 AV block for an effective ventricular rate of ~40 bpm. A cursory look at the rhythm strip lead II could lead one to identify this as marked sinus bradycardia. But note in V1 and V2 (

) that there are two clear p-waves (red lines) in between the QRS complexes (blue lines), with the sinus rate occurring at twice the ventricular rate.

What is the best next step in patient management?

	It is not possible to discern based on this single surface ECG if we are dealing with a Mobitz I (

) block. Determining the level of block is critical because asymptomatic Mobitz I or Wenkebach AV block is benign whereas Mobitz II AV block can progress to complete heart block and requires pacemaker implantation.

	Characteristics that differentiate this as proximal AV block include the narrow QRS, the absence of symptoms, and the patient’s high dose carvedilol as a possible causative agent. A simple non-invasive method to further demonstrate proximal vs distal AV block is to increase the sinus rate with exercise while performing continuous ECG monitoring and note whether AV conduction improves. A stress treadmill ECG is one option and having the patient perform leg lifts while supine and hooked up to telemetry or a rhythm strip is also sufficient.

 below shows a sample from leads V1 and V2 of the patient’s stress ECG at rest (left) and then 4 minutes into a standard Bruce exercise protocol (right).

	The baseline (rest, left) rhythm strip again shows 2:1 AV block with two p-waves in between each QRS complex while with exercise this becomes a 1:1 p-wave to QRS complex relationship. The presumed PR interval in the exercise strip, however, is very long (> 400 msec), and inspection of lead V2 shows it is inscribed 

the T-wave, therefore the rhythm with exercise likely is an accelerated junctional rhythm with 

Have we demonstrated a degree of nodal block significant enough to require pacemaker implantation?

	The exercise rhythm strip suggests intact retrograde AV node conduction but does not clearly reveal the status of antegrade AV node conduction. Reversible causes for AV nodal block must be addressed before pacemaker implantation is considered. Therefore the patient’s carvedilol was stopped and reassessment of AV node conduction was performed about 5 days after the initial visit with a repeat resting and stress ECG. Findings were essentially unchanged from the rhythm strips in the previous figures. The patient in the interim remained entirely asymptomatic and expressed an understandable reluctance to consider permanent pacemaker implantation.

Based on this new iformation, is pacemaker implantation now indicated?

	There still is no strict indication for pacemaker implantation primarily because the patient remains asymptomatic and also because the level of block has not been shown to be below the level of the AV node. The most recent (2012) 

 for Device-based Therapy of Cardiac Rhythm Abnormalities stress that:

Permanent pacemaker implantation is not indicated for asymptomatic type I second-degree AV block at the supra-His (AV node) level or that which is not known to be intra- or infra-Hisian

	The most accurate method to confirm the level of AV block is minimally invasive electrophysiologic (EP) evaluation of AV nodal physiology. This is performed by advancing a diagnostic pacing/mapping electrode catheter to the level of the AV node-HIS bundle region at the superior aspect of the tricuspid valve. Baseline conduction properties of the AV node and HIS bundle are then measured (in

below A, H and V represent depolarization of the atrium, HIS bundle, and ventricle, respectively).

	Advanced distal block is suggested if prolonged HIS to ventricular conduction times are noted (typically > 65 msec). An atrial pacing protocol at increasing rates is then performed with close evaluation of conduction to the ventricles to determine if AV block occurs below the level of the HIS (after the HIS signal) which would again demonstrate pathologic rather than physiologic AV block (before the HIS signal). Pathologic second-degree AV block at intra- or infra-His levels found on EP study is a Class IIB indication for pacemaker implantation in asymptomatic patients.

	The patient underwent diagnostic EP study as described above. Baseline H-V times were normal and atrial pacing performed at increasing rates demonstrated AV block occurring before the HIS bundle was activated. These conduction study findings were most consistent with type I second-degree AV block occurring at the supra-His (AV node) level without indication for pacemaker implantation. The patient subsequently underwent 4-week ambulatory rhythm monitoring that did not show evidence of high grade sinus or AV node dysfunction and has been happy with the deferral of permanent pacemaker implantation.

	Epstein AE, DiMarco JP, Ellenbogen KA, et al. 

2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society.

Articles

This 83-year-old man is treated only for hypertension and says he "feels like Tarzan." The routine ECG says otherwise.  

ECG Challenge: It's the Level of the Block that Counts

: A 51-year-old man with a history of chronic methamphetamine abuse presents to the emergency department with leg swelling, dyspnea, and near-syncope with exertion, symptoms that have been getting progressively worse for about two weeks.  He denies fever, cough, chest pain, or other complaints. He is otherwise healthy.

: Vital signs are normal except for a pulse of 110 beats/min.  His lungs are clear and his heart is tachycardic without murmurs. His legs have 1-2+ bilateral symmetric pitting edema. The rest of the physical exam is normal.

: Congestive heart failure (CHF), pulmonary embolism (PE), pneumonia.

: Chest x-ray, duplex ultrasound of the legs, and CT angiography chest are negative for pneumonia, DVT, and PE; ECG tracing is shown below.

Please click here for answer and discussion.

	The ECG shows sinus tachycardia, a right bundle branch block, right atrial enlargement (P-pulmonale), right axis deviation, and possible right ventricular hypertrophy, all consistent with cor pulmonale.  The next day an echo showed severe pulmonary hypertension. The cause was determined to be methamphetamine abuse.

	Cor pulmonale is right sided CHF, usually caused by obstructive lung disease, which can also be caused by pulmonary hypertension. Symptoms typically include dyspnea on exertion, fatigue, and exertional syncope.  Unlike left sided CHF, examination shows clear lungs. ECG findings are the result of hypertrophy of both the right ventricle and right atrium; these are listed in the tables below.

	The diagnosis of cor pulmonale or pulmonary HTN is confirmed by echocardiogram. Treatment depends on severity. Initial emphasis is on control of causative factors or diseases, but in severe cases a variety of medications may be used. See second chart below for medications. For this patient abstinence from methamphetamine abuse was the key component of therapy.

For addtional details, click on image below. 

A 51-year-old man is seen in ED for progressive dyspnea, near syncope on exertion, bilateral edema. What does the tracing tell you? 

ECG Challenge: Leg Swelling, Short of Breath

	A 77-year-old woman with longstanding paroxysmal atrial fibrillation (PAF), hypertension, hyperlipidemia, and coronary artery disease presents to your office for follow-up one month after undergoing coronary artery bypass grafting (CABG) with concomitant left atrial maze ablation. She feels well without angina but describes persistent dyspnea on exertion and fatigue since the operation. She denies any palpitations or dizziness consistent with her prior episodes of PAF.  She was discharged home on post-operative day 7 on metoprolol succinate 50 mg daily for presumed persistent sinus tachycardia. Her pre- and post-operative ECGs are shown in 

ECG 1. Pre-operative 12-lead ECG, above

	ECG 2. Post-operative 12-lead ECG, below

Does the post-operative ECG represent sinus tachycardia as thought or an arrhythmic process?

The post-operative ECG shows a narrow complex tachycardia at ~110 beats/min with P-waves preceding each QRS complex that are upright in leads II, III and avF. These surface ECG characteristics are consistent with sinus tachycardia. However, considering that the patient's preoperative baseline ECG showed a significantly slower, normal heart rate in the 60 beats/min range and she is status post left atrial maze ablation, a persistent atrial arrhythmia should be suspected. Electrical reentry may occur around the linear atrial scars created by maze ablation leading to refractory left atrial arrhythmias, specifically atrial flutter (AFL) and atrial tachycardia (AT). Closer comparison of the two ECGs 

 reveals broad, biphasic P-waves in lead V1 of the pre-operative ECG (Figure 2- 

) versus narrow, entirely positive P-waves in lead V1 of the post-operative ECG (Figure 2- 

The sinoatrial (SA) node is located at the junction between the right atrium (RA) and superior vena cava (SVC), therefore SA node activation is seen on the surface ECG as positive P-wave deflections in the inferior leads (high to low activation 

 deflections in lead V1 (anterior to posterior activation 

). The subtle finding of entirely positive P-waves in lead V1 of the postoperative ECG likely represents activation of a left atrial focus posterior to the SA node (

. The right superior pulmonary vein (RSPV) is typically located just posterior to the SA node and a microreentrant circuit at the region of the RSPV may occur post left atrial maze ablation. 

What is the next step in managing the patient?

Recall that persistent, rapid AFL and AT, in addition to causing symptoms of palpitations, dyspnea, and fatigue, may lead to tachycardia-induced systolic heart failure. It is not uncommon for anti-arrhythmic drug therapy to be ineffective with left atrial arrhythmias, as in this patient’s arrhythmia which slowed to an average heart rate in the 90s-100s but nevertheless persisted despite attempted treatment with sotalol. She ultimately underwent electrophysiology study with 3-dimensional intracardiac activation mapping during ongoing tachycardia.

 displays the detailed electro-anatomic map of the anterior right atrial 

 chambers. A micro-reentrant AT was mapped to the RSPV, which is seen in the electro-anatomic map to traverse just posterior to the SA node at the RA-SVC junction.  Circumferential radiofrequency ablation around the RSPV (represented by light blue dots) terminated the tachycardia to sinus rhythm. Post-ablation, she has remained free of recurrent atrial arrhythmias.

What cause of persistent DOE, fatigue in this patient who is s/p CABG and maze ablation? Your ECG read?

ECG Challenge: Subtle but Significant

	A 66-year-old woman presents to the ED with a 3-day history of generalized weakness, malaise, recurrent near-syncope, nausea, and occasional vomiting. She denies chest pain, fever, difficulty breathing, diarrhea, and fainting. Her history includes diabetes, end-stage renal disease, coronary disease, and complete heart block after pacemaker implantation.

	She is afebrile. Pulse is 126 beats/min; blood pressure, 81/53 mm Hg; and oxygen saturation, 100% on room air. She appears adequately hydrated as evidenced by a moist oropharynx. There is no jugular venous distention or thyroid mass. Heart rate is regular and rapid without murmur, and lungs are clear. She has weak peripheral pulses and mild bilateral pitting edema, which she states is of recent onset. Other physical findings are unremarkable.

	Laboratory results, including a CBC count, metabolic panel, and troponin I level, are normal. Urinalysis shows 25 white blood cells per high-power field with few bacteria.

	Antibiotic treatment was initiated for possible urosepsis despite the lack of fever and leukocytosis. Although there was no clear evidence of dehydration, IV fluids were administered because of the hypotension, history of vomiting, and possible sepsis. When the patient’s blood pressure remained unchanged, pacemaker interrogation was expedited for possible pacemaker-mediated tachycardia (PMT), which turned out to be the correct diagnosis. The unit was reprogrammed, and all vital signs immediately normalized.

	Pacemaker-mediated tachycardia (PMT) is rare, especially with modern pacemakers, in which a perpetual activation loop occurs between the atrial and ventricular leads. The ventricular rate is typically under 130 beats/min, which represents the upper programmed set rate limit of the pacemaker. Nevertheless, hemodynamic compromise, namely hypotension, may still occur. As in this case, PMT is often not considered until other, more common conditions have been ruled out and no other explanation seems plausible.

	Symptoms typically include generalized weakness and syncope or near-syncope. Palpitations and chest pain may occur. Blood pressure is often low, and the pulse is typically between 110 and 130 beats/min. Neither hypotension nor tachycardia is usually responsive to fluids in patients with PMT, which is one clue to the diagnosis.

	Once the diagnosis of PMT is suspected, a cardiologist should be consulted and a representative from the pacemaker company called to interrogate the pacer. Pacer interrogation can confirm the diagnosis and can be followed by pacer reprogramming to terminate the tachycardia. If the patient is unstable, application of a magnet to the pacemaker should break PMT by switching to a non-synchronous present rate (usually between 60 and 100 beats/min). If a magnet is not available, atrioventricular nodal blockers can be tried, but caution should be used if the diagnosis is uncertain because in other conditions they may worsen hypotension.

	For more information on PMT, see the chart below.

Excerpt on PACEMAKER MEDIATED TACHYCARDIA (PMT) 

Her history includes diabetes, ESRD, coronary disease, and complete heart block after pacemaker implantation. What's your ECG read? 

Hypotension and Near-syncope in a 66-year-old Woman

	A 72-year-old woman presents to the ED for a wrist injury sustained after a fall. She states she fell because she lost her balance and did not feel weak or light-headed prior to the fall. She also states that she did feel “woozy” after she fell, but currently she denies any symptoms other than right wrist pain. She denies any chest pain, trouble breathing, or other complaints.

	Her examination is unremarkable except for a systolic murmur and a mild deformity and tenderness to her right wrist. Her skin is intact, her compartments soft, and distal neurovascular status is within normal limits. You administer 4 mg of morphine IV for pain and initiate a near-syncope work up because of her age just in case something else is going on.

	Laboratory results, including a CBC, metabolic panel, and cardiac enzymes are normal except for a white blood cell count of 11.3 x 10

/µL. A wrist X-ray shows a distal radius fracture, which you splint and sling.

	Note the ST-elevation in V4-V6, which was markedly changed from the baseline ECG. Troponins became positive at 8 hours.

	In addition to clinical skills, careful ECG interpretation is critical to avoid errors in management of patients with acute coronary syndrome (ACS). ST elevation can be subtle early during a STEMI, especially if changes are in the inferior or lateral leads. T-waves tend to be smaller and benign early repolarization less pronounced in the lateral leads. When the lateral leads look like anterior leads, STEMI should always be considered, especially if there is more ST elevation or larger T-waves in the lateral leads than is present in the anterior leads, as in this case.

	It is also essential to keep in mind that an ECG can be normal during an ACS, especially early on. Comparison with an old ECG and serial ECGs can be critical. Remember, the most recent ECG may have been recorded during an acute MI, so just because the current one looks the same does not rule out ACS. See page shot below for more information on EKG changes in ACS.

Page capture on ECG findings in ISCHEMIA from the 

QUICK ESSENTIALS Emergency Medicine 1-Minute Consult pocketbook

A 72-year-old woman sustains a distal radius fracture during a fall after losing her balance. She denies syncope. What's your ECG read?