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Year : 2017  |  Volume : 5  |  Issue : 3  |  Page : 127-129

Intermittent complete heart block presenting as recurrent pulmonary edema

Department of Cardiology, Government Medical College, Calicut, Kerala, India

Date of Web Publication12-Sep-2017

Correspondence Address:
S Sulaiman
30/1277D Dream Land, Medical College PO, Calicut - 673 008, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/heartindia.heartindia_1_17

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A middle-aged female presented with recurrent flash pulmonary edema. On evaluation, the patient had apparently stable 2:1 atrioventricular block and a good left ventricular systolic function. Holter recordings revealed intermittent episodes of complete heart block (CHB) precipitating pulmonary edema. The patient underwent permanent pacemaker implantation with complete resolution of symptoms. Isolated recurrent pulmonary edema in CHB is a rare manifestation and has never been reported before.

Keywords: Atrioventricular block, complete heart block, conduction defects, recurrent pulmonary edema

How to cite this article:
Sulaiman S, Rajesh G N, Vellani H. Intermittent complete heart block presenting as recurrent pulmonary edema. Heart India 2017;5:127-9

How to cite this URL:
Sulaiman S, Rajesh G N, Vellani H. Intermittent complete heart block presenting as recurrent pulmonary edema. Heart India [serial online] 2017 [cited 2022 Jan 21];5:127-9. Available from: https://www.heartindia.net/text.asp?2017/5/3/127/214421

  Introduction Top

Complete heart block (CHB) is commonly encountered in clinical practice. While reversible causes of CHB include myocardial ischemia, drug toxicity and electrolyte abnormalities among others, the common causes of permanent CHB include degenerative disease, previous infarction, and congenital. These patients usually present with symptoms of low cardiac output such as giddiness, presyncope, or syncope and less commonly with dyspnea. We describe a patient with intermittent CHB with an unusual manifestation (isolated recurrent pulmonary edema).

  Case Report Top

We had a 56-year-old female patient with history of diabetes mellitus and hypertension for 15 yrs. She was on regular treatment and her blood sugars and pressure had been well controlled. She had left facial nerve palsy of lower motor neuron type (Bell's palsy) 20 years before. Two years before presentation, the patient was found to have 2:1 atrioventricular (AV) block with a P rate of 90/min and a constant PR interval of 200 ms. On treadmill, her maximum workload was 13 METS attaining a maximum heart rate of 79/min (47% of max. predicted rate). She had two episodes of acute pulmonary edema [Figure 1] of 25 days just before visiting our institution. Both episodes occurred while at rest (the second episode while sleeping). Hospitalization records revealed that her blood pressure (BP) was within normal limits during both admissions and electrocardiogram showed 2:1 AV block with a ventricular rate of 52/min and without any ischemic changes [Figure 1]. She was never documented to have any tachyarrhythmias. She denied symptoms of effort angina, palpitations, presyncope, or syncope anytime in the past. There was no history of acute coronary syndrome in the past. Her regular medications included atorvastatin, losartan, metformin, aspirin, and hydrochlorothiazide. Her laboratory parameters are listed in [Table 1].
Figure 1: (a) Chest X-ray taken during first episode of pulmonary edema. (b) Chest X-ray showing pulmonary edema during second hospitalization. (c) Electrocardiogram showing 2:1 AV block with a “P” rate of 100/mt and ventricular rate of 50/mt. PR interval is 200 ms

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Table 1: Laboratory parameters for evaluation of flash pulmonary edema

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The patient was a moderately built and well-nourished female. She had left hemifacial spasm. All peripheral pulses were well palpable. Her BP was 150/90 mmHg in both upper limbs and 160/90 mmHg in lower limb. Precordial examination was normal and there was no mass or bruit on abdominal examination. Echocardiography showed good left ventricular (LV) function with an ejection fraction of 72%. Two-dimensional speckle tracking longitudinal strain analysis showed preserved LV strain. No significant obstructive lesions were found in coronary angiography [Figure 2]. Renal angiogram showed normal vessels. Left ventricular end-diastolic pressure by catheterization was 4 mmHg. Common causes of flash pulmonary edema were ruled out [Table 1]. Subsequently, Holter monitoring was done in two settings. Although the rhythm was 2:1 most of the time, Holter recordings revealed that the rhythm degenerates slowly into a low ventricular rate of 31/min and subsequently developing complete AV dissociation with a junctional escape rhythm [Figure 3]. This was correlated temporally with patient's symptoms. Since the patient definitely required a permanent pacemaker implantation (PPI), an electrophysiological study (EPS) was deferred. Her functional status improved and she remains absolutely symptom-free after PPI.
Figure 2: (a) Coronary angiography showing left coronary system and right coronary artery (b). No significant obstructive disease noted. Renal angiogram showing normal right (c) left and (d) renal arteries

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Figure 3: (a) Holter tracing showing 3:2 atrioventricular conduction with wenckebaching (Arrows green-conducted P waves with normal PR; blue-conducted with prolonged PR, red-nonconducted P waves). (b) 3:2 atrioventricular conduction. Lowest-recorded heart rate (31/min). (c) Holter recordings showing complete atrioventricular dissociation with a constant ventricular rate of 44/min

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  Discussion Top

The conduction disturbances in the AV node are classified by severity into first-, second-, and third-degree heart blocks. Second-degree heart block can be of Mobitz type I or type II. 2:1 AV blocks are distinct and do not truly belong to any of the above types since there are no consecutively conducted impulses. A 2:1 AV block can be a form of type I or type II AV block. If the QRS complex is normal and the PR interval is increased, the block is more likely to be at the nodal level while a wide QRS complex indicates a infranodal block. Our patient had a normal QRS complex with a normal PR interval suggesting an intrahisian AV block. CHB commonly presents with symptoms of low cardiac output. This includes giddiness, blackouts, presyncope, or frank syncope. Unlike in sick sinus syndrome, low ventricular rate in CHB is an ominous sign and requires emergent intervention. Suprahisian CHBs are generally considered to be less dangerous than infrahisian blocks. Although paroxysmal AV block can occur secondary to hyperresponsiveness of the AV node to vagotonic reflexes, sudden deterioration of an apparently stable 2:1 rhythm may indicate an infranodal block. Our patient developed two episodes of life-threatening pulmonary edema, in the absence of LV dysfunction, requiring intensive care. Pulmonary edema develops in CHB as low ventricular rate elevates the left atrial and subsequently the pulmonary venous pressures. However, such manifestation is more likely to occur when the ventricular rate rapidly falls, as the case in our patient, than in a patient with persistently low rate. Our patient had a baseline ventricular rate of 52/min which dropped to 34/min with worsening of the conduction block. Further, recurrent pulmonary edema as an isolated presenting manifestation of CHB is seldom seen in clinical practice. This is so, because these patients would have developed symptoms of low cardiac output well before symptoms of backward failure emerge. An extensive search of literature yielded one case report in which the patient with CHB and thrombosis of sinus of Valsalva presented with pulmonary edema.[1] This patient also had diastolic heart failure and other comorbidities such as polycystic kidney disease (autosomal dominant polycystic kidney disease) which might have contributed to the manifestation. To the best of our knowledge, this is the first report of intermittent CHB (masquerading as 2:1 AV block) presenting with recurrent episodes of isolated pulmonary edema.

In our case, the CHB was identified by Holter recordings. However, in patients with infrequent symptoms, Holter may not reveal the worsening conduction. In these patients, a comprehensive electrophysiology (EP) study is to be considered. Since the PR interval in our case is within normal limits, the atrio hisian (AH) and His - ventricular (HV) intervals are expected to be normal at baseline. The presence or absence of his potential in the alternately nonconducted beats will help localize the site of block. The CHB may be unmasked by various EP protocols.

Our case is important in two aspects. First, symptoms in patients with an apparently stable 2:1 AV block should not be taken lightly. Continuous rhythm monitoring/EPS has to be carried out to identify the true nature of the disease. Second, CHB might present with symptoms of isolated pulmonary edema without any symptoms of low cardiac output, especially if it occurs intermittently. This has to be suspected in a patient with AV block and an apparently stable rhythm presenting with disproportionate symptoms. Strictly speaking, this is not true LV backward failure as the diastolic function is usually normal or only mildly impaired. It is the sudden fall in ventricular rate that precipitates pulmonary edema.

  Conclusion Top

Conduction defects of the heart usually cause symptoms of low cardiac output secondary to bradycardia. Some patients with AV blocks and apparently stable rhythm might develop intermittent high degree blocks. Such patients might present with symptoms of isolated, backward failure without symptoms of low cardiac output and can confuse the clinical picture. Continuous rhythm monitoring helps in identifying the true nature of the disease.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Eltawansy SA, Amor MM, Thomas MJ, Daniels J. Complete heart block with diastolic heart failure and pulmonary edema secondary to enlarging previously diagnosed thrombosed aneurysm of sinus of valsalva in a patient with history of autosomal dominant polycystic kidney disease. Case Rep Cardiol 2015;2015:281716.  Back to cited text no. 1


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1]


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