It Must be Cardiac

by 12leadekg on March 4, 2011

81 year of Female altered mental status
What is going on with this patient?

Press CTRL and + putton on keyboard to zoom in on EKG strip to get a better look

Ok here is a folow up for It Must be Cardiac  Here is a Head CT



The patient's ECG demonstrated a sinus rhythm at a rate of 60 bpm, with a markedly prolonged QT interval of 680 msec (normal range for females, 70% left anterior descending coronary artery stenosis at angiography.[9] Despite the association of this ECG pattern with significant coronary artery disease, in the setting of acute stroke this ECG pattern can be present without preexisting coronary artery disease.[1]

The determination of the causality of ECG changes seen in the patient described above requires careful attention to the neurologic and cognitive examination. Since patients who present with acute stroke also frequently have risk factors for the development of coronary artery disease, this ECG pattern can present a diagnostic dilemma. CNS-derived cardiac conditions can present with ECG changes mimicking cardiac ischemia and/or injury, focal wall motion abnormalities on echocardiography, and elevated biomarkers for cardiac injury. Therefore, these tests provide little diagnostic differentiation. Consequently, it is imperative to perform a rapid, but detailed, neurologic examination in patients who present to the ED with an ECG as described above in order to identify patients whose ECG changes may be related to an ongoing acute stroke. If the examination or clinical judgment warrants, rapid noncontrast CT scanning of the head or a magnetic resonance imaging (MRI) scan of the brain should be performed to evaluate for a CNS process.[1,2,3,4,6,10]

Once a patient has been identified as having ECG changes resulting from an acute stroke, it is reasonable for clinicians to perform echocardiography and serum biomarker analysis in order to potentially identify patients at a higher risk for cardiac adverse events. At a minimum, the presence of ECG changes during a CNS event warrants the placement of the patient on telemetry monitoring; however, given the frequency of ventricular arrhythmias (including ventricular tachycardia and fibrillation) in patients with acute stroke, placement of the patient in an intensive care unit solely for cardiac monitoring provides the highest level of safety. Treatments aimed at limiting adrenergic stimulation to the heart (beta-adrenergic receptor antagonists) can be given if the patient manifests evidence of cardiac dysfunction or injury. In cases of severe systolic dysfunction, supportive measures such as loop diuretics, supplemental oxygen, and/or endotracheal intubation may be necessary. While no randomized data support their use in stroke-mediated cardiac dysfunction, angiotensin-converting enzyme inhibitors (ACEI) and statin therapy are also reasonable options.[3,10]

Because of the overlapping risk profiles in patients with cerebrovascular and cardiovascular disease, once an acute CNS event has been treated, cardiac risk stratification with myocardial perfusion imaging may be performed. This serves to evaluate for potential underlying coronary artery disease that was "unmasked" by the stress of the CNS event. In the majority of patients with CNS-mediated ECG changes and cardiac dysfunction, however, the cause of their cardiac abnormalities is not significant coronary artery disease. Therefore, proceeding directly to coronary angiography in the absence of other compelling indicators is probably unwarranted.[10]

Despite the sometimes dramatic cardiac presentations in patients with acute stroke, the majority of these patients recover their cardiac function with supportive care. Patients should be monitored on telemetry until the ECG normalizes and the acute stroke symptoms stabilize. In patients with cardiac regional wall motion abnormalities, repeat echocardiography may be performed following normalization of the ECG to document resolution of the cardiac dysfunction.[10]

The patient in this case was admitted to the intensive care unit for cardiac monitoring, serial neurologic examinations, and further testing. An MRI of the brain confirmed a right-sided acute ischemic stroke, but the presence of the small subdural hemorrhages (likely the result of the patient's recurrent falls) prevented the use of antiplatelet therapy in this patient. The ECG changes normalized within 2 days and the cardiac enzymes remained within normal limits. An echocardiogram was performed on hospital day 2 which demonstrated moderate diastolic dysfunction, with no focal wall motion abnormalities. A repeat CT scan of the head on hospital day 4 showed no progression of the small subdural hemorrhages. The patient's neurologic exam did not change from her initial presentation and she was discharged to a skilled nursing facility on hospital day 5.

Special thanks are extended to Dr. John Vozenilek, MD, FACEP, for his contributions to the publication of this case
courtesy of Medscape