Hence, further cardioversion was avoided. Cardioversion restored sinus rhythm but with generally little impact on hemodynamics and with continued recurrence of dysrhythmias. Ventricular ectopy and sustained arrhythmias persisted despite treatment with intravenous amiodarone. Incessant dysrhythmias continued, including progressive atrioventricular (AV) conduction delay, left axis deviation in beats conducting with variable QRS morphologies including left bundle branch block (LBBB), RBBB ventricular ectopy, nonsustained monomorphic ventricular tachycardia (VT) ( Figure 1, bottom), sustained monomorphic VT ( Figure 2, top), and bidirectional VT characterized by RBBB morphology and alternating QRS axis ( Figure 2, bottom). Blood cultures were drawn and empiric antibiotics initiated. The patient was intubated for impending respiratory failure. Poor response to fluids necessitated hemodynamic support with intravenous pressors and intraaortic balloon pump. Ventriculography confirmed echocardiographic findings, demonstrating hyperdynamic left ventricular function with no wall motion abnormalities. Concern for coronary ischemia and lactic acidosis prompted urgent coronary angiography, which demonstrated nonobstructive coronary atherosclerosis with slow coronary flow.
There were no findings of Takotsubo cardiomyopathy. Bedside echocardiography demonstrated hyperdynamic left ventricular function with no regional wall motion abnormalities and no evidence of pericardial effusion. Troponin T (<0.01 ng/mL) and digoxin levels (0.1 ng/mL) were not elevated. Initial blood tests revealed hypokalemia (2.9 mmol/L) and acidosis (pH 7.21) with increased anion gap (17) and elevated lactate levels (9.7 mmol/L). Both ECGs also demonstrate ventricular ectopy. Presenting electrocardiogram (ECG) ( top) and ECG showing progressive changes in atrioventricular conduction ( bottom).
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