Vomiting… and a fortuitous identification of fluctuating AV block

A 65-year-old male with history of diabetes mellitus type 2, hypertension, and hypothyroidism presented to the ED with nausea and vomiting that began that morning. He also reported generalized weakness and decreased exercise tolerance. Upon initial presentation, the patient had a heart rate of 109 per minute, blood pressure 107/68 mm Hg, temperature 97.8 degrees Fahrenheit, respirations 22 per minute, and pulse oximetry of 97% on room air. The patient was actively vomiting and somewhat ill-appearing but alert and oriented. His chest was clear to auscultation, heart rate was regular and tachycardic without murmur, and extremities were well-perfused. There were normoactive bowel sounds, and his abdomen was soft, non-distended, and non-tender.

The initial ECG is Figure 1:

Figure 1. Initial ECG

Lets look at the rhythm strip from the initial ECG:

Sinus tachycardia with 1st degree AV block.
Red arrow: P; red bracket: P-P interval; blue bracket: PR interval

The ED provider administered 4 mg ondansetron and one liter of crystalloid intravenously, and the patient’s symptoms improved. Upon reassessment, the ED provider noted a change in rhythm to irregular with more apparent P waves and a ventricular rate of approximately 50 per minute.

A repeat ECG is Figure 2:

Figure 2. ECG #2

The rhythm strip from ECG #2:

Normal sinus rhythm with occasionally increased P-P interval, unifocal junctional escape complex with slurred S due to synchronous P, 2:1 AV block, 2nd degree AV block Type 1
Red bracket: P-P interval; blue bracket: PR interval; green asterisk: junctional escape complex with synchronous P

An ECG fifteen minutes later is Figure 3:

Figure 3. ECG #3

The rhythm strip from ECG #3:

Normal sinus rhythm with irregular, occasionally increased P-P interval, 2:1 AV block, 3rd degree AV block with junctional escape rhythm with occasional slurred S due to synchronous P
Red bracket: P-P interval; blue bracket: PR interval; green asterisk: junctional escape rhythm with occasional synchronous P

A chest radiograph did not reveal any abnormalities. The blood test results were unremarkable including potassium 4.4 mmol/L, glucose 100 mg/dL, troponin less than 0.010 mg/mL, thyroid-stimulating hormone 1.40 µU/L, and total thyroxine (T₄) 1.26 µg/dL which was mildly low. The cardiology consultant recommended further monitoring and evaluation in the coronary care unit. Serial troponin levels remained undetectable. On hospital day 1, transthoracic/transesophageal echocardiography demonstrated normal ejection fraction and valves and no intracardiac thrombus. After shared decision-making that included consideration of the symptoms (perceived by the patient to be debilitating) and documented, contemporaneous intervals of 3rd degree AVB, the cardiologist implanted a pacemaker on hospital day 2. The patient remained in sinus rhythm until being discharged home the following day. At follow-up one month later, his pacemaker had recorded no further episodes of AVB.

Vagally-mediated AVB is infrequently described in the literature, but its prevalence may be underestimated as it may often occur without recognition. Vagally-mediated AVB has been found incidentally upon Holter monitoring during sleep (1) and in the conditioned athlete (2). Talwar et al (3) and Mehta et al (4) have previously reported cases similar to ours in which AVB was induced by nausea and vomiting. Mehta et al (4) reproduced the conduction block with esophageal balloon inflation within the esophagus, and in both reports, the AVB was either prevented (4) or abolished (3) by administration of atropine. Sleep and vomiting are associated with increased parasympathetic tone, and vagal hypertonia is one of the mechanisms involved in reflex syncope (5). Increased vagal tone slows conduction in the sinus and AV nodes but does not affect His-Purkinje (infranodal) conduction. Therefore, the mechanism underlying vagally-mediated AVB is situated proximally to the cardiac conduction system, and the site of the block is within the AV node.

Vagally-mediated AVB must be differentiated from paroxysmal, bradycardia-dependent AVB, because bradycardia-dependent AVB may progress to persistent AVB (6,7). Depression of both sinus and AV node conduction must be present to diagnose vagally-mediated AVB (5,6). 

In this case, three ECG characteristics are demonstrative:

1) An irregularly and subtly lengthened (by 40 milliseconds (8)) P-P interval with delayed Ps that are occasionally synchronous with junctional escape complexes (Figures 2 and 3)

2) Heterogeneous presentation of AVB including 1st degree (Figure 1), 2nd degree Type 1 (Figure 2), 2:1 (Figures 2 and 3), and 3rd degree (Figure 3)

3) Resumption of AV conduction upon sinus acceleration (shortened P-P interval) with significant PR prolongation (Figure 1).

In comparison, bradycardia-dependent AVB will typically demonstrate unchanged P-P intervals, constant PR intervals, additional conduction abnormalities such as bifascicular or bundle branch block, and initiation by premature complexes or tachycardia (7,9) – all features that are absent from the ECGs in this case. When ECG monitoring is non-diagnostic, electrophysiology study may help differentiate the two types of AVB. In patients with bradycardia-dependent AVB, His-Purkinje (infranodal) conduction may be decreased upon provocative testing (a specific, but insensitive criterion) (5,6,10), whereas in those with vagally-mediated AVB, both AV nodal and His-Purkinje conduction are usually normal or only minimally decreased (5,6). According to current guidelines (11), pacemaker placement is contraindicated if vagally-mediated AVB is asymptomatic. However, if symptoms are clearly attributable to vagally-mediated AVB, pacemaker placement may be reasonable (12).

Summary:

1. Vagally-mediated AV block may occur in settings of increased parasympathetic tone.
2. The diagnosis of vagally-mediated AV block requires simultaneous depression of sinus and AV node conduction that may be demonstrated by ECG as irregularly increased P-P intervals and varying degrees of AV block.
3. Vagally-mediated AV block must be differentiated from paroxysmal, bradycardia-dependent AV block which may progress to persistent AV block and require pacemaker placement.
4. In an asymptomatic patient with vagally-mediated AVB, pacemaker placement is contraindicated. When symptoms are clearly attributable to vagally-mediated AV block, pacemaker placement may be reasonable.

This case report was also written by Monisha Dilip MD.

References:

1. Butta C, Tuttolomondo A, Di Raimondo D, et al. A second-degree atrioventricular block with double escape rhythm secondary to paroxysmal vagal hypertonia. J Cardiovasc Med (Hagerstown) 2017;18(10):822-3.
2. Vidal A, Agorrody V, Abreu R, et al. Vagal third-degree atrioventricular block in a highly trained endurance athlete. Europace 2017;19(11):1863.
3. Talwar KK, Edvardsson N, Varnauskas E. Paroxysmal vagally mediated AV block with recurrent syncope. Clin Cardiol 1985;8(6):337-40.
4. Mehta D, Saverymuttu SH, Camm AJ. Recurrent paroxysmal complete heart block induced by vomiting. Chest 1988;94(2):433-5.
5. Aste M, Brignole M. Syncope and paroxysmal atrioventricular block. J Arrhythm 2017;33(6):562-7.
6. Alboni P, Holz A, Brignole M. Vagally mediated atrioventricular block: pathophysiology and diagnosis. Heart 2013;99(13):904-8.
7. Lee S, Wellens HJ, Josephson ME. Paroxysmal atrioventricular block. Heart Rhythm 2009;6(8):1229-34.
8. Lange HW, Ameisen O, Mack R, et al. Prevalence and clinical correlates of non-Wenckebach, narrow-complex second-degree atrioventricular block detected by ambulatory ECG. Am Heart J 1988;115(1 Pt 1):114-20.
9. Shohat-Zabarski R, Iakobishvili Z, Kusniec J, et al. Paroxysmal atrioventricular block: clinical experience with 20 patients. Int J Cardiol 2004;97(3):399-405.
10. Twidale N, Heddle WF, Tonkin AM. Procainamide administration during electrophysiology study–utility as a provocative test for intermittent atrioventricular block. Pacing Clin Electrophysiol 1988;11(10):1388-97.
11. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. Circulation 2018:CIR0000000000000628.
12. Shen WK, Sheldon RS, Benditt DG, et al. 2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation 2017;136(5):e60-e122.

The following two tabs change content below.

• Bio
• Latest Posts

deSouza

Latest posts by deSouza (see all)

• Diagnosis of a Supraventricular Tachydysrhythmia During Ketamine Infusion - July 14, 2023
• A previously unknown etiology of acute pancreatitis - January 19, 2021
• Vomiting… and a fortuitous identification of fluctuating AV block - March 22, 2019