Patient information: a 64-year-old man with past medical history of hypertension and end-stage renal disease on chronic hemodialysis presented with hypothermia, hyperkalemia (8.0 mmol/L), shock and delirium after missing dialysis for 3 weeks. He was noted to be in a wide complex tachycardia that was clinically a pulseless electrical activity (PEA) (Figure 1A). He received defibrillation shocks and advanced cardiovascular life support (ACLS) protocol ensued. He received calcium chloride, sodium bicarbonate, dextrose boluses and insulin. There was transient reappearance of p-waves after the administration of these temporizing therapies for hyperkalemia (Figure 1D), supporting a diagnosis of sinoventricular rhythm. However, the patient required emergent hemodialysis for a more definitive therapy and epinephrine drip for shock.
Clinical findings: physical exam was significant for an unresponsive patient with a thready pulse.
Timeline of current episode: the patient had previous history of missed hemodialysis with associated hyperkalemia and uremic encephalopathy, but this was the index event of an associated ventricular arrhythmia.
Diagnostic assessment: scheduled pulse checks were done during the ACLS resuscitation. Echocardiography images were obtained concurrently during the pulse check periods to rule out other acute structural cardiac anomaly.
Diagnosis: pulseless electrical activity with a wide complex tachycardia is considered as a cardiac arrest. Clinical considerations include ventricular tachycardia (VT), accelerated idioventricular rhythm, cardiac tamponade, hypovolemic shock, hyperkalemia, severe acidosis, hypothermia, hypoxia, pulmonary embolism, pneumothorax, and myocardial infarction.
Therapeutic interventions: CPR was resumed, and echocardiographic images were obtained intermittently during the pulse check intervals. The first images from standard apical 4-chamber view were recorded about 38 minutes before the patient was pronounced dead. The beginning images showed severe biventricular hypokinesis, LVEF approximately 20%, bi-atrial enlargement, severe mitral regurgitation, and moderate tricuspid regurgitation (Figure 2). There was only a trace of circumferential pericardial effusion and a subtle appearance of granularity of spontaneous echo contrast (SEC) noted in LV chamber only. As time progressed, there was progressive slowing of the heart rate with slightly increasing echogenicity within the LV chamber, and a nominal increase in pericardial effusion. These findings appeared unchanged until long tandem episodes of asystole heralded the last heart beats shortly thereafter. In the last 50 secs to the last heartbeat, continuous echo recording was obtained. We documented a rapid progressive echogenicity and dense thrombus formation in the LV chamber, cessation of cardiac wall motion and excursion of AV valves, followed instantaneously by the appearance of coagulation in all the other chambers (Figure 3). The AV valves appeared to be tethering with a fixed gap in mid annular-position, and an expanding rapid appearance of pleural effusion was appreciated at the end (Figure 4).
Follow-up and outcomes: the patient died during the ACLS interventions.
Informed consent: this case study is completely anonymized to protect the identity of the patient; thus, a formal informed consent was not obtained from this deceased patients.