An Interactive Case Study of Transient Loss of Consciousness

Transient loss of consciousness due to syncope is a challenging and confusing problem to manage. As electrophysiologists, we are often asked for our opinion since syncope can be due to transient shifts in autonomic tone, blood pressure, and/or heart rate. Also, syncope can be associated with potentially life-threatening ventricular arrhythmias that may require interventional evaluation and treatment.

There is no standard evaluation for syncope other than directing testing based on a carefully and completely obtained history from the patient and observers, as well as evidence gleaned from medical records.

Here, I present a patient who exemplifies the complexities of the management of syncope. 

I caution you: the approach taken is not necessarily the way I would evaluate this patient, but this is the way this patient was managed.

There are various ways this case could have been handled. I encourage you to share your comments with us in an open dialogue format, by addressing the questions posed throughout the case on EP Lab Digest’s Facebook, Twitter, and LinkedIn pages. 

Case Presentation

The patient is a 68-year-old male found unresponsive by his wife while supine in an easy chair watching football. The patient had breakfast that morning and had one beer in the afternoon while watching the game. 

His eyes appeared to be partially open and when she shook him, he did not respond initially, so she called 911. When she returned to see him, he was awake and thought he might have fallen asleep. When paramedics arrived, he was awake and alert. His blood pressure was 160/90 and he had a regular pulse of 75 bpm. He was transported to the emergency department.

Two months before, he had an anterior wall myocardial infarction with an LAD occlusion and subsequent stent placement. His ejection fraction post infarction was 45% by MRI scan (Figure 1). It showed a left ventricular clot. He had New York Heart Association functional class II congestive heart failure symptoms, hypertension, insulin-dependent diabetes, and arthritis.

His medications included metoprolol 50 mg BID, lisinopril 10 mg BID, furosemide 40 mg a day, amlodipine 5 mg twice a day, aspirin 81 mg a day, clopidogrel, insulin, and warfarin. These medications had not changed for two months.
Physical examination showed a blood pressure supine of 160/95 with a heart rate of 70; upon 2 minutes of standing, his blood pressure was 120/80 with a heart rate of 75. He had had an S4 gallop and a grade 2/6 systolic murmur along with basilar râles. His electrocardiogram is shown in Figure 2.

Questions: 

• Did the patient have syncope in your opinion?
• What is the next step in his management?
• Laboratory values? Which? BNP? Troponin? When you measure a stool guaiac?
• What other tests are required? Echocardiogram? Cardiac catheterization?
• Would you admit the patient?

A stool guaiac was negative. The troponin was negative. The BNP was 800 pg/ml.

The patient was admitted. There was no evidence for an acute myocardial infarction by troponin values. A tilt table test was performed and considered “positive”, meaning that by tilting him, his blood pressure continued to drop and his heart rate did not increase to the point that he became very dizzy and lightheaded. He was thought to have a neurocardiogenic response, although it could have been consistent with neurogenic orthostatic hypotension. He was sent home with an event monitor.

Questions: 

• Is this reasonable?
• Does he need any adjustment in his medications? What adjustment?
• What is the next step? Pacemaker? Implantable loop recorder? Other testing?

Within one week, the patient’s event monitor noted a very long pause with paroxysmal AV block (Figure 3). This was not associated with symptoms.

The patient underwent electrophysiological testing. He had normal sinus node function and an HV of 85 ms. With pacing in the ventricle, he developed right bundle, superior axis, sustained monomorphic ventricular tachycardia with an abrupt drop in blood pressure initially from 140/90 to 100/60. The cycle length of the tachycardia was approximately 450 ms (Figure 4).

Questions: 

• What is the next step? ICD implantation? Ventricular tachycardia ablation? More aggressive electrophysiological testing? What is the best therapeutic approach?

Discussion

In summary, this is a 68-year-old male who had “collapsed” while supine in the chair. He had orthostatic hypotension, paroxysmal AV block, and slow ventricular tachycardia.

This case highlights some of the complexities of the management of a patient with apparent transient loss of consciousness. To start, it is unclear if the patient actually lost consciousness. 

Addressing the Questions: 

• Did the patient have syncope in your opinion?
• Would you admit the patient?

Ultimately, the symptom itself is rather unclear. The patient awoke clearheaded, making it unlikely that this was hypoglycemia in a diabetic. The position under which the condition occurred makes it also unlikely that orthostatic hypotension, even if present, was the cause of the problem. It is unlikely that a seizure caused the problem, but it is certainly possible that the patient simply drifted off to sleep after a beer. This raises issues regarding how aggressive to be with management of this patient. Nevertheless, because of the apparent unarousability in this patient, and due to his underlying structural cardiac disease, hospital admission to evaluate his condition made sense.

If he had lost consciousness, the cause for the episode is still not clear. While he does have orthostatic hypotension, the episode occurred in a semi-supine position, making it an unlikely cause for his episode.  

Addressing the Questions: 

• What is the next step in his management?
• Laboratory values? Which? BNP? Troponin? When you measure a stool guaiac?
• What other tests are required? Echocardiogram? Cardiac catheterization?

From the emergency department’s point of view, a specific battery of tests is often considered based on several large clinical trials. The ROSE (Risk Stratification of Syncope in the Emergency Department) Study1 would suggest that measuring a BNP and even a stool guaiac may be predictive of outcomes in 30 days, but measuring a BNP here or even a stool guaiac would not tell us the cause for syncope and would not help in terms of longer short-term predictions of risk. 

Tilt table testing makes little sense in this particular circumstance; it would not be unusual for a patient with orthostatic hypotension and no increase in heart rate at 2 minutes to have a similar response on a tilt table test. The patient likely has some type of a dysautonomic condition associated with diabetes. Aggressive treatment of this problem, which may prevent  orthostatic hypotension, will not necessarily prevent syncope (which occurred in the semi-supine position) in this patient. 

Addressing the Questions: 

• Does he need any adjustment in his medications? What adjustment?
• What is the next step? Pacemaker? Implantable loop recorder? Other testing?

Adjustment of his medications may help prevent orthostatic hypotension, but may also worsen the patient’s hypertension and create new risks. Furthermore, there is no evidence that prevention of orthostatic hypotension in this patient would prevent any symptomatic episode, since the patient never had such a complaint and the symptom that did occur was unrelated likely to orthostatic hypotension.

The pause that was seen on the monitor was asymptomatic, but concerning. Paroxysmal AV block could be due to a dysautonomic condition related to the positive tilt table test, or could be related to a block in the His-Purkinje system in a patient with an anterior wall myocardial infarction. Even though the transient paroxysmal AV block was unrelated to syncope or other any other symptoms, it is certainly concerning and a reason to consider a pacemaker, since the apparent syncopal episode that occurred may have been related to transient asystole. 

Addressing the Questions: 

• What is the next step? ICD implantation? Ventricular tachycardia ablation? More aggressive electrophysiological testing? What is the best therapeutic approach?

The monitor showed a markedly prolonged period of asymptomatic asystole; while it is reasonable to consider this a likely cause for his event, and thus making a pacemaker reasonable, the patient has impaired left ventricular function. However, the ejection fraction is not impaired enough and the timing is wrong to consider an ICD for primary prevention purposes; even with the episode of suspected syncope, with this ejection fraction alone, an ICD is still not indicated.  

There is a disconnect between what the MRI scan and the electrocardiogram show. The electrocardiogram displays a fairly extensive myocardial infarction, and therefore, transient loss of consciousness in the face of this particular circumstance is highly concerning for the long-term risk of sudden cardiac death. 

Therefore, before a pacemaker is implanted, an electrophysiology test is warranted to evaluate the possibility of inducible ventricular tachycardia. In a patient with this type of structural heart disease, it becomes important to also rule out the possibility of ventricular tachycardia. Electrophysiologic testing is justified in this patient; it should have been considered earlier in his management. While the test showed inducible sustained monomorphic ventricular tachycardia, it was rather slow and well-tolerated.  Did it cause his purported transient loss of consciousness? Is it a premonitory risk factor for sudden cardiac death? Neither of these may be the case.

As mentioned, the induced ventricular tachycardia was sustained but was rather slow and well-tolerated, and it did not cause syncope. Further, a slower, well-tolerated induced ventricular tachycardia is not necessarily predictive of sudden cardiac death. Nevertheless, based on the available information for this patient, an ICD was reasonable. A properly programmed ICD may treat associated bradyarrhythmias and tachyarrhythmias that could cause syncope in this patient.  

Despite the fact that the electrophysiology test showed no serious hemodynamic change with this ventricular tachycardia, this was a sustained monomorphic ventricular tachycardia and it does indicate the possibility of a reentry circuit. While a slow ventricular tachycardia like this may not necessarily be associated with sudden cardiac death, it is concerning. Furthermore, the electrophysiology study is often stopped once a monomorphic ventricular tachycardia is initiated, even if it is not poorly tolerated. Perhaps extending the electrophysiologic test until a faster ventricular tachycardia is initiated may make some sense, but this also puts the patient at risk without necessarily increasing the benefit of the test. Induction of ventricular fibrillation may also be a false positive.

In this particular instance, there is no clear-cut answer as to what caused this patient’s witnessed episode; nevertheless, because of the test results, implantation of an ICD made the most sense, and this was true even with a well-tolerated induced ventricular tachycardia that occurred during a time period that a primary prevention ICD would not be considered. 

On the other hand, ablation of ventricular tachycardia may also make sense, but it would not necessarily mean that all ventricular tachycardia is eliminated or that the syncope is treated, and may not affect the long-term risk of sudden cardiac death. 
An implantable defibrillator was ultimately placed. Programming of the device was complicated by the rate of the tachycardia, as it was rather slow. While the slow rate needed to be programmed to treat this slower ventricular tachycardia, the patient may end up getting inappropriate shocks for sinus tachycardia, which may create more problems in this patient who is thought to have a secondary prevention indication for an ICD.

Join the conversation! Answer these questions and discuss how you would have handled this case on EP Lab Digest’s social media sites. 

References

1. Reed MJ, Newby DE, Coull AJ, et al. The ROSE (Risk Stratification of Syncope in the Emergency Department) Study. J Am Coll Cardiol. 2010;55(8):713-721. 
2. Olshansky B, Sullivan RM. Syncope in Patients with Organic Heart Disease. Cardiol Clin. 2015 Aug;33:449-463. 
3. Olshansky B, Sullivan RM. Sudden death risk in syncope: the role of the implantable cardioverter defibrillator. Prog Cardiovasc Dis. 2013;55(4):443-453. 
4. Morady F, Shen EN, Bhandari A, Schwartz AB, Scheinman MM. Clinical symptoms in patients with sustained ventricular tachycardia. West J Med. 1985;142:341-344. 
5. Krol RB, Morady F, Flaker GC, DiCarlo LA, Jr., Baerman JM, Hewett J, de Buitleir M. Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome. J Am Coll Cardiol. 1987;10:358-363.
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11. Calkins H, Shyr Y, Frumin H, Schork A, Morady F. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med. 1995;98:365-373.
12. Olshansky B, Poole JE, Johnson G, et al. Syncope predicts the outcome of cardiomyopathy patients: Analysis of the SCD-HeFT study. J Am Coll Cardiol. 2008;51:1277-1282.
13. Militianu A, Salacata A, Seibert K, et al. Implantable cardioverter defibrillator utilization among device recipients presenting exclusively with syncope or near-syncope. J Cardiovasc Electrophysiol. 1997;8:1087-1097.