Transient Bundle Branch Blocks
Written by: Alec Feuerbach, MD
Edited by: Robby Allen, MD; Antonia Quinn, DO
Remember our case: a woman 60 years of age presented with chest pain and an ECG with a left bundle branch block (1,2). She was placed in observation where her bundle branch block disappeared, only to return again a few hours later. After transferring her to a PCI-capable center where she had negative cardiac enzymes and a normal echocardiogram, she was started on anti-hypertensives, her symptoms resolved, and she was discharged.
Causes of Transient Bundle Branch Blocks
Transient bundle branch blocks like the one, in this case, were first described in 1913 in an address to the North-East London Post-Graduate College by Dr. Thomas Lewis. He described a 32-year-old bookbinder who “had been feeling more seedy than usual for some days”,(3) developed a bundle branch block along with a fever, and then returned to normal sinus rhythm the next day. In 1938, Comeau et al linked these transient blocks to a variety of significant heart diseases such as coronary and hypertensive heart disease, rheumatic heart disease, and acute infection; (4) though cases without any signs of heart disease have been described as well.(5)
Today we know that transient bundle branch blocks can occur for a variety of reasons. Far and away the most common trigger is heart rate.(6) Commonly referred to as exercise-induced bundle branch blocks, such rate-dependent blocks are reported in about 0.5% of all patients undergoing exercise stress tests.(7) They have been demonstrated with both tachycardia and bradycardia, though tachycardia is much more common; both right and left bundle branch blocks are observed, with right being more frequent.
It is thought that the bundle branch block in a tachycardia-dependent block occurs when an impulse arrives at tissue that is still refractory from incomplete repolarization.(6) In other words, when the atrial rate gets fast enough, conducting tissue within one bundle branch doesn’t have enough time to reset after being depolarized, and it is “blocked.” It is important to note that the rate at which the bundle branch block appears – the so-called critical heart rate – will be different for everyone and maybe at a rate that is not technically tachycardia. In a study of 50 patients with exercise-induced heart block (8), the rate at onset of bundle branch block ranged from 74 to 170/min with an average of 118/min. Thirteen patients in that study had onset below a rate of 100/min, and one case in another study (9) involved a critical rate of 60/min. Interestingly, the rate of offset (the rate at which the bundle branch block disappears) was slightly lower, ranging from 54 to 136/min with a mean of 89 bpm.
In reviewing the ECGs from our case, the patient was seen to have a bundle branch block at a rate of 97 and 87/min with normal conduction at 73 and 82/min. While these rates are below the average rate of onset in most studies, it is definitely possible that her left bundle was rate-dependent.
Still, there are numerous, other, documented causes of transient bundle branch blocks that we ought to consider. Most notably for our case, this phenomenon has been reported in cases of rapid increases in blood pressure.(10) Authors theorized that this could potentially be related to physical stretching of Purkinje fibers from increased left ventricular end-diastolic pressure (LVEDP) – which has been shown to slow conduction velocity in bench models.(11) Or, it may be related to increased LVEDP increasing intraventricular pressure and mechanical occlusion of an already diseased coronary artery – ultimately leading to temporary ischemia of the bundle branch.
In our patient, increases in heart rate were relatively mild but blood pressure fluctuated from 145/82 mm Hg on initial evaluation to 190/100 and 206/98 mm Hg. Furthermore, her symptoms and bundle branch block reportedly resolved once her blood pressure was controlled. Of course, this is speculative, based largely on chart review. And, unlike heart rate, blood pressure was not recorded at the time of ECG for review to see if all episodes of conduction block were related to elevated pressure.
Transient bundle branch blocks have been reported in other scenarios as well. Medications like lithium,(12) cardiotoxic drugs like lidocaine,(13) and antiarrhythmics like propafenone (14) have been reported to cause transient bundle branch blocks. This phenomenon has also been linked to toxins like mad honey (see above)(15) and procedures like anesthesia (6) and electroconvulsive therapy.(16) They have been reported in acute pancreatitis (17) and pulmonary embolism.(18) And if that’s not enough, one case report even described this with laughter (see below),(19) theorizing that changes in intrathoracic pressure led to decreased perfusion. Point being: keep the differential broad.
While that’s all interesting, we are still left with questions of what it means, and what we do with it. Unfortunately, the answers are not entirely clear.
Significance of Transient Bundle Branch Blocks
The majority of the research into the significance of episodic bundle branch blocks investigates rate-dependent blocks – those being the most common. When evaluating patients undergoing stress testing, the development of an exercise-induced (rate-dependent) bundle branch block has been correlated with higher all-cause mortality than those with normal stress tests.(6) Whether or not the exercise-induced bundle branch block, itself, has any independent prognostic significance is still up for debate.
In 1998, Grady et al linked exercise-induced bundle branch block with a 29% higher risk of death and 19% higher risk of major cardiac events.(20) When controlled for age and previously documented coronary artery disease, Grady et al(20) reported a relative risk of 2.73 for reaching a composite primary endpoint when comparing exercise-induced LBBB with a cohort of patients with normal stress tests. The primary endpoint included all-cause mortality, percutaneous coronary intervention, open heart surgery, nonfatal myocardial infarction, documented symptomatic or sustained ventricular tachydysrhythmia, or implantation of a permanent pacemaker or an implantable cardiac defibrillator. Though the authors note that not all of these patients had coronary angiography, and that the average timing of angiography was 3.5 years before the trial, they concluded that exercise-induced LBBB has an independent contribution to prognosis. They then went on to hypothesize, however, that this phenomenon’s clinical significance may be as a sign of underlying coronary artery disease or ischemic burden, somewhat contradicting their conclusion that an exercise-induced LBBB is an independent prognostic factor. Perhaps it could be argued, though, that this phenomenon is an early marker of CAD not seen on prior angiography, or that it is a marker of more clinically significant CAD.
A more recent study, however, was unable to establish exercise-induced LBBB as an independent prognostic factor. Stein et al(7) completed a prospective cohort study of 9,623 patients undergoing exercise stress testing; 6,922 had normal stress tests and only 38 had exercise-induced blocks. Those with the exercise-induced blocks had significantly higher all-cause mortality than patients with normal stress tests and patients with exercise-induced ST-depressions; however, this predictive ability disappeared when controlling for the presence of CAD or heart failure. Therefore, Stein et al(7) concluded that the finding of an exercise-induced LBBB should serve as a prompt to further investigate for evidence of CAD.
Implications for the Emergency Department
The reasonable approach when treating a patient with a transient bundle branch block in the ED is focusing, first and foremost, on excluding an acute coronary syndrome.
Complicating this determination is the fact that angina-like chest pain with an episodic bundle branch block does not necessarily signify the presence of CAD. A variety of case reports and studies have identified individuals with episodic bundle branch blocks, chest pain, and clean coronaries.(21, 22) Indeed this a common enough occurrence to be described in the literature as “painful bundle branch block syndrome”.(23) It is thought that the pain is a result of dyssynchronous cardiac contraction caused by abnormal conduction.
Furthermore, ischemic-like T waves on the “normal-conduction” ECG in a patient with an episodic bundle do not necessarily indicate ischemia. A phenomenon called cardiac memory can lead to short- and long-term changes in T wave morphology after a period of abnormal conduction (such as a bundle branch block). The mechanism of this phenomenon in the short-term involves modifications of protein and channel trafficking, and in the long-term, changes in gene transcription and protein synthesis (24) – both well beyond the scope of this post (and well over my head).
This can lead to T wave inversions mimicking ischemia (25) and even a Wellens-like pattern.(26) You may remember that one of the main reasons our patient was transferred to a PCI-capable center was the presence of a Wellens pattern on her “normal-conduction” ECG. While impossible to say for sure, it is possible this was simply an example of cardiac memory. Research is ongoing to develop diagnostic tools to help differentiate ischemia from cardiac memory.(24)
Perhaps of some theoretical use in risk stratification, there is some evidence that the critical heart rate (the rate of bundle block onset) itself may be an indicator of CAD. Two small studies have found that a critical heart rate less than 125/min is more likely to indicate coronary artery disease, and thus, a worse prognosis, while an onset greater than 125/min is associated with normal coronaries.(27,28) Theoretically, this may make sense considering that one proposed mechanism for this phenomenon is that damage to bundle branch tissue from ischemia slows its repolarization – leading it to be refractory at faster heart rates. Could more damage equal slower repolarization? It is important to note, however, that these studies are small – 11(27) and 28 patients(28) – and the potential of this as a risk stratification tool is far from established.
Clearly, determining the significance of a transient bundle branch block is a difficult, if not, an impossible task in the ED. For us, however, approaching this condition is not unlike anything else we treat. Rule out the most dangerous conditions first – is this an acute coronary occlusion? Maintain a broad differential – is this a pulmonary embolism? Mad Honey Poisoning? Drug toxicity? And, remember that a benign episodic bundle branch block is a diagnosis of exclusion.
References:
feuerbacham
Latest posts by feuerbacham (see all)
- Characteristics of Typical Atrial Flutter - October 6, 2022
- Interpreting a Paced Electrocardiographic Rhythm - August 18, 2022
- Understanding Right Bundle Branch Block Morphology - July 26, 2022
2 Comments
RICHARD PARKER · April 17, 2023 at 11:39 am
Many thanks for this article – we have exactly this patient sat in resus in ED in London right now. Serial ECGs flipping between a Wellen’s pattern and LBBB. We’re all scratching our heads as to what on earth is happening… Getting cardiology involved for a decision re: PCI but may well be a case of “cardiac memory.” Interesting. Thanks again.
Alec Feuerbach · April 17, 2023 at 2:56 pm
Glad to hear this was helpful! Would love to hear how the case resolves
-Alec