It’s around 4 a.m. and staff members hear the telltale “thud” of someone falling onto the floor. It’s not unusual in the dementia unit of this extended care facility, and they quickly find the 80-year-old female patient on the floor alert and oriented. She says she’d been sleeping and rolled out of bed and onto her nightstand. She complains of minor eye pain, but appears unhurt. At her own insistence, she’s helped back into bed.
Several hours later, the staff members discover her eye and the bridge of her nose are swollen and red. The pain has increased, so they call 9-1-1.
Upon arrival, the patient is alert and oriented, but lethargic and somewhat somnolent. Staff members report no mental status changes. She states the reason she rolled out of bed earlier was she hadn’t slept well the previous night.
She has no specific complaints other than pain around her eye and nose. Although she’s able to answer all of the crew’s questions appropriately, she still seems a bit too lethargic. A Cincinnati stroke assessment was negative.
Initial vital signs are strong/slightly irregular pulse of 90, blood pressure of 112/90, oxygen saturation of 88% on room air and a respiratory rate of 24. Blood glucose is 120 mg/dL and oral temperature is 98.5 degrees F. Her lungs are clear in all fields and air movement is good. The patient is placed on oxygen at 2 L/min via nasal cannula and her saturation quickly rises to 98%.
She most likely could’ve been taken to the hospital as a BLS patient with no issue, but her lethargy causes the crew to suspect other possibilities, particularly since her symptoms started the night before. An IV is established and a 12-lead captured. However, the patient is jittery, and a stable 12-lead is difficult to obtain.
The 12-lead shows widespread depression with hyperacute T waves throughout. (See Figure 1 below.) The patient has no chest pain, but since she’s elderly, some of her subtle symptoms are reason for concern. The crew is also concerned with the 12-lead as it raises the possibility of cardiac ischemia and a possible occlusion of the left anterior descending artery. The crew is less than three minutes from a percutaneous coronary intervention-capable hospital, and on arrival, shows the 12-lead to the attending physician.
Figure 1: 12-lead ECG showing hyperacute T waves
Although the patient didn’t present with classic cardiac symptoms, her lethargy and alarming 12-lead caused the patient to be evaluated for cardiac issues. Troponin was zero and a cardiology consult revealed that the patient’s 12-lead was an indication of cardiac memory and was a result of a recent pacemaker implantation.
Just as the name implies, cardiac memory is the heart’s tendency to remember the electrical pathways it previously traveled. Consider this similar phenomenon: city workers are replacing the sidewalk on your street, and in order to walk to your house, you have to cut through the grass. Since it takes a while to complete the replacement sidewalk, you eventually wear a pathway on the lawn down to bare dirt. After a few weeks, the sidewalk is replaced, but the dirt pathway remains.
On your way home, every once in a while, you inadvertently follow this path instead of the sidewalk. You have a habit (or memory) of the old pathway and you occasionally use it. The dirt path is still clear in your mind and once the grass grows back, you’ll probably never use it again, preferring the sidewalk instead. In the case of this patient, her pacemaker had caused her heart to beat with hyperacute T waves—a fairly normal occurrence. This was a new pathway her heart learned. After the pacing stopped, her heart continued to remember this electrical pathway.
If a paced rhythm had been shown, the electrical morphology in the 12-lead would’ve looked fairly normal. Instead, when the pacing stopped, her heart continued to follow the same electrical pathway. Since she’d only just received her pacemaker several months earlier, her heart hadn’t returned to its normal electrical pathway for non-paced beats due to scar tissue at the site of the pacemaker. The scar tissue and necrotic tissue had caused a more permanent change to the electrical morphology, and because she’d been paced for so long (at least initially), this unusual electrical pathway persisted.
Table 1: North American Society of Pacing and Electrophysiology pacemaker classifications
Pacemakers are fairly widespread, and are becoming more commonplace as their size, durability and functionality improves. They’re usually titanium coated and about the size of a pack of matches. They have a battery that can last up to 10 years, and several wires that both detect as well as initiate cardiac beats in the upper and lower chambers. They’re classified according to the North American Society of Pacing and Electrophysiology (NASPE)1 table above. Based on this classification method, up to five properties of the pacemaker can be easily represented, with each placeholder indicating a certain characteristic:
1. The first column represents which area of the heart will be paced. This is an indication the pacemaker is able to generate an electrical impulse to the specific chamber(s). Either the atria, ventricles or both (dual) can receive the pacemaker’s electrical signal.
2. The second column is what area of the heart the pacer is looking for a spontaneously generated electrical signal in. The pacer can look for a generated signal from either the atria, ventricles or both (dual).
3. The third column indicates the type of response that will occur when a signal by the heart is generated, and is specifically related to column 2. Inhibited indicates that the pacemaker will not (it will be inhibited) generate a signal if it senses an intrinsically generated electrical signal from the heart. So, if the pacemaker senses an atrial/ventricle beat, it will not generate an atrial/ventricle beat. The inhibited mode is usually used for either pacing atrial or ventricle beats—not both. Dual is used for the coordination of atrial and ventricle beats. If the column specifies dual, then when the pacer senses an atrial signal from the heart, it won’t generate an atrial beat. Instead, a timer starts that will cause the pacemaker to generate a ventricular beat after a certain interval. If the patient has a ventricular beat during this interval, the pacemaker won’t generate a ventricular beat. So, if column 3 has a mode of response of inhibited, it usually means the patient’s heart is reliably generating either atrial or ventricle beats, and that the unreliable chamber must be watched and paced. Column 3 is set to trigger during testing and diagnostics.
4. This column indicates how the pacemaker responds to an increase in patient activity. Rate-modulated pacemakers are responsive to changes in patient activity. This means the pacemaker can be programmed to respond to changes in rate, sensing, refractory periods, mode, hysteresis or others.
5. The fifth column indicates whether the pacemaker generates electrical signals in one or more locations in the different chambers. Ventricles indicate several stimulation sites in the ventricles, whereas atrium refers to a pacemaker that has several stimulation sites in the atria. Dual indicates that both chambers have multiple sites.
For example, a pacemaker labeled as “DDDRO” would indicate that the pacemaker will both sense and generate an electrical signal in both chambers if it doesn’t detect the heart’s own electrical beat. After the atrial beat (whether generated by the pacemaker or by the patient’s own heart), the pacemaker will start a timer, and generate another electrical signal if and only if the ventricle doesn’t beat on its own. The pacemaker will respond to changes in the patient’s activity, and it contains only one stimulation area in the atria and ventricles.
In the case of this patient, she had several concerning issues during presentation. Namely, she had weakness and mild hypoxia along with a possible syncopal episode. Considering her age (> 80), she was less likely to experience the hallmark chest pain and dyspnea of a younger patient.2 She was a candidate for possible ST segment elevated myocardial infarction (STEMI) and so a 12-lead was clearly in order. (See Figure 2 below.)
Figure 2: Chief complaints of STEMI patients by age1
Unfortunately, when she was discussing her medical history, the paramedics were less concerned about when she had received a pacemaker than the fact she had one. The crew was familiar with what paced rhythms looked like, and how they can be diagnosed to reveal a STEMI (Modified Sgarbossa Rule), but her 12-lead didn’t seem to meet that criteria.3
Although cardiac memory was documented several decades ago, its physiology and significance is still being researched because it can be caused by many etiologies. The important ramification for the prehospital environment is that it can mimic an acute myocardial infarction. Cardiac memory is characterized by persistent but reversible T-wave changes on the ECG caused by abnormal electrical activation patterns.
In this case, it was brought on by ventricular pacing, but cardiac memory has also been recorded in intermittent left bundle branch block, pre-excitation observed in Wolff-Parkinson-White syndrome, and episodes of tachycardia.4–7
The duration and direction/magnitude of the T-wave deflection depends on the type of abnormal stimulus and the duration. It can persist for several days or weeks.
1. Bernstein AD, Daubert JC, Fletcher RD, et al. NASPE position statement: The revised NASPE/BPEG generic code for antibradycardia, adaptive-rate, and multisite pacing. Pacing Clin Electrophysiol. 2002;25(2):260–264.
2. Glickman SW, Shofer FS, Wu MC, et al. Development and validation of a prioritization rule for obtaining an immediate 12-lead electrocardiogram in the emergency department to identify ST-elevation myocardial infarction. Am Heart J. 2012;163(3):372–382.
3. Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified sgarbossa rule. Ann Emerg Med. 2012;60(6):766–776.
4. Chatterjee K, Harris A, Davies G, et al. Electrocardiographic changes subsequent to artificial ventricular depolarization. Br Heart J. 1969;31(6):770–779.
5. Rosenbaum MB, Elizari MV, Lazzari JO, et al. The mechanism of intermittent bundle branch block: Relationship to prolonged recovery, hypopolarization and spontaneous diastolic depolarization. Chest. 1973;63(5):666–677.
6. Kalbfleisch SJ, Sousa J, el-Atassi R, et al. Repolarization abnormalities after catheter ablation of accessory atrioventricular connections with radiofrequency current. J Am Coll Cardiol. 1991;18(7):1761–1766.
7. Kernohan RJ. Post-paroxysmal tachycardia syndrome. Br Heart J. 1969;31(6):803–806.