A 68yr long-term care inmate presented to nursing with an altered level of consciousness, chest pain, and bradycardia. Paramedic services were called to the scene for transport and found the nursing staff encouraging the pt to walk back and forth across the exam room to, “help bring his pulse up.” The following EKG was recorded. Note that voltage enhancement has been maximized in the rhythm strip to 2cm/mv, while the 12-lead is displayed with the standard gain of 10mm/mv.
As this is a third party case, little direct clinical or situational information is available to contextualize this EKG or the surrounding events. Objectively speaking, a markedly bradycardic junctional rhythm can be appreciated with retrograde conduction of p-waves, seen inverted, buried 160ms into the QRS complex. Net positive QRS deflections in I-III, avL and avF, and negative in avR indicate an axis in the lower left quadrant. Close examination reveals a 0.1mv electrical alternans, perhaps most evident in the limb leads, but also apparent (~0.05mv) in V5 and V6. Explicitly pathological features include subtle precordial T-wave inversions in V1-3 and conspicuous low voltage QRS amplitude in all leads.
Regarding this latter subject, numerous criteria have been suggested as to what constitutes abnormally low voltage; a consensus approach would consider either the sum of the QRS voltages in all 12 leads as necessarily less than 12mv, or a combined judgment requiring the average of QRS voltages in the limb leads as less than 5mm and that in the precordial leads less than 10mm.
The typical differential diagnosis associated with low voltage QRS includes etiologies of increased impedance (such as obesity, hyperinflative lung disease, and pericardial/pleural effusion), etiologies of infiltrative disease (such as hemochromatosis, amyloidosis, and neoplasm), and metabolic or toxicological causes (such as hypothyroidism and alcoholism). Low voltage has also been associated with both chronic and acute ischemic heart disease. An exhaustive review of the DDx can be found here.
While neither the clinical nor the electrocardiographic features of this case are sufficiently specific to seal any one diagnostic verdict, there are nonetheless some possibilities here worthy of note. Exogenous toxicological etiologies should be ruled out; hypotension with a slow junctional escape could be linked to digitalis, beta and calcium channel blockers, or other readily available pharmaceuticals. Of particular interest, the possibility of RCA associated ischemia must also be entertained. The pt’s clinical picture, low voltage QRS amplitude, and junctional bradycardia are strongly suggestive in this direction. Similar presentations with more explicit pathological substrates can be seen on this site in case nos. 4A- 4D, particularly the slow junctional STEMI of no. 4D.
Lastly, the subtle finding of electrical alternans forces a compelling consideration of pericardial effusion. Were the heart indeed spatially shifting within the pericardium from beat to beat, one would anticipate a greater shift of axis in the frontal, limb-lead plane than the transverse plane of the precordial leads, just as is present on this tracing. Alternating junctional foci or an artifact of physical positioning could produce a similar bigeminal effect, yet when this alternans is seen in the context of low voltage, the finding commands greater attention.
Paramedic services successfully temporized this pt’s status with atropine and supportive care until he reached the emergency department; there, after 20 minutes, he receded into semi-consciousness. No follow-up could be done.