Point-of-care ultrasound (POCUS) is now routine during resuscitation, and clinicians may interpret a single intra-arrest finding, such as cardiac standstill, pseudo-pulseless electrical activity (PEA), or organized motion, as a fixed description of the patient's physiological state. This perspective argues that this assumption deserves scrutiny. The physiological state during cardiac arrest may evolve over time; cardiac mechanical activity may follow a trajectory that unfolds over minutes or a longer resuscitation. Published intra-arrest POCUS protocols generally define when and how imaging should be performed during brief interruptions in cardiopulmonary resuscitation (CPR) but do not provide a standardized framework for interpreting findings according to elapsed time from arrest recognition. Accordingly, the same ultrasound finding may represent different points in the resuscitation. Existing prognostic and diagnostic reviews of intra-arrest ultrasound have documented substantial variation in the timing of image acquisition without resolving what that variation means for interpretation. We propose that ultrasound findings are better interpreted as points along a trajectory than as isolated, static observations. This may provide additional temporal context for interpreting prognostic findings and help avoid overinterpretation of a single early intra-arrest observation. We translate this concept into five practical considerations: recording elapsed arrest time at acquisition, avoiding premature futility judgments from early standstill, interpreting pseudo-PEA as a potentially transitional state, considering repeat scanning where feasible without prolonging interruptions in high-quality CPR, and using ultrasound as an adjunct to established clinical assessment and resuscitation decision-making. This framework is conceptual rather than a demonstrated physiological model; available evidence does not currently establish whether observed differences reflect distinct physiological phenotypes, timing effects, or both. This hypothesis could be evaluated through prospective studies that record the timing of clinically obtained ultrasound examinations and, where serial imaging is clinically indicated, assess changes over the course of resuscitation without prolonging interruptions in CPR. Studies incorporating standardized acquisition timing and blinded interpretation of stored recordings could help determine whether acquisition timing contributes to the interpretation and prognostic value of intra-arrest ultrasound findings. Until then, clinicians should interpret intra-arrest ultrasound with attention to when a finding occurred, not only what it showed.

Amniotic fluid embolism (AFE) is a rare and life-threatening obstetric emergency characterized by sudden cardiopulmonary collapse and coagulopathy. Diagnosis remains clinical, and one of exclusion, as presentation may overlap with other causes of maternal cardiovascular collapse and hemorrhage. Here we present a 34-year-old woman, gravida 7 para 2133, at 33 weeks and one day gestation with known complete placenta previa who presented with vaginal bleeding and painful uterine contractions. Ultrasound performed two weeks prior demonstrated complete placenta previa without sonographic evidence of placenta accreta spectrum (PAS). Following cesarean delivery, the patient developed acute respiratory distress and pulseless electrical activity (PEA) arrest requiring cardiopulmonary resuscitation with return of spontaneous circulation after approximately 10 minutes. Massive transfusion protocol was initiated, and cesarean hysterectomy was performed after the identification of an abnormally adherent placenta. Final pathology demonstrated PAS grade 3D (previously known as placenta percreta), a condition associated with an increased risk of AFE, with extensive myometrial invasion and serosal disruption. The operative course was further complicated by disseminated intravascular coagulopathy, massive hemorrhage, acute respiratory distress syndrome, and severe urologic injury. Despite substantial postoperative morbidity requiring later urinary diversion surgery, both maternal and neonatal survival were ultimately achieved. This case highlights the diagnostic complexity of AFE occurring concurrently with catastrophic hemorrhage from previously undiagnosed PAS and emphasizes the importance of rapid multidisciplinary management and evidence-based protocols in optimizing outcomes.

Pseudo-pulseless electrical activity (p-PEA) is a clinical condition where cardiac output drops severely enough to produce a non-palpable pulse in the setting of organized electrical activity of the heart, but imaging or monitors display evidence of cardiac motion. It may be seen in shock states such as anaphylactic shock. We describe a case where a previously healthy teenage patient presenting for operative removal of orthopedic hardware developed p-PEA after anaphylaxis to antibiotics. Despite loss of pulses and severe mottling of the skin, the patient's pulse oximetry (plethysmography) and capnometry (measurement of end-tidal carbon dioxide) displayed visually normal, reassuring waveforms. The condition responded to chest compressions and administration of epinephrine and vasopressin; the patient was ultimately able to be discharged home on postoperative day (POD) 2. Prompt recognition, diagnosis, and clinical management of p-PEA and anaphylaxis are key to good patient outcomes. Epinephrine is the mainstay of treatment for anaphylactic reactions and is indicated during cardiopulmonary resuscitation (CPR) for p-PEA.

Pulmonary infarction (PI) is a recognized but relatively uncommon complication of pulmonary embolism (PE). Because its clinical presentation and imaging findings often overlap with those of community-acquired pneumonia (CAP), PI is frequently misdiagnosed. Progression to cavitation is exceedingly rare and typically reflects extensive, irreversible parenchymal necrosis. We describe a 66-year-old woman with heart failure with reduced ejection fraction (HFrEF) and coronary artery disease (CAD) who initially presented with symptoms consistent with CAP. Although she initially improved, she re-presented ten days later with acute hypoxemic respiratory failure and a newly developed smooth-walled cavitary lung lesion. Chest computed tomography confirmed a submassive PE complicated by necrotizing PI and secondary abscess formation. Given the failure of conservative management and evidence of parenchymal gangrene with the need for source control, she underwent urgent right lateral thoracotomy with bilobectomy for source control. The post-operative course was complicated by refractory shock and pulseless electrical activity (PEA) arrest. Following goals-of-care discussions, the family elected to pursue comfort-focused care. This case shows the importance of systemic-to-pulmonary collateral circulation in preserving lung parenchymal viability. In patients with limited cardiovascular reserve, failure of bronchial arterial compensation can precipitate catastrophic necrotizing infarction. Clinicians should maintain a high index of suspicion for PI in cases of "nonresolving pneumonia," as early recognition may be critical in preventing progression to cavitary disease.

Massive pulmonary embolism (PE) is a life-threatening emergency often presenting with hemodynamic collapse or cardiac arrest. Despite advances in resuscitation and reperfusion therapies, outcomes remain poor. We report the case of a 74-year-old man with a history of hypertension, hyperlipidemia, and diabetes mellitus who presented with acute severe dyspnea leading to pulseless electrical activity (PEA) cardiac arrest. Return of spontaneous circulation was achieved with advanced cardiac life support, but he subsequently experienced recurrent PEA arrest requiring intubation, vasopressors, and antiarrhythmic therapy. Electrocardiography showed sinus tachycardia with right bundle branch block and repolarization abnormalities. Laboratory evaluation revealed marked troponin elevation, leukocytosis, thrombocytopenia, and hypokalemia. Duplex ultrasound demonstrated bilateral lower extremity deep vein thromboses. Echocardiography showed preserved left ventricular function with an enlarged, hypokinetic right ventricle and apical sparing. Chest computed tomography angiography revealed a large burden of bilateral pulmonary emboli with right ventricular strain and wedge-shaped pulmonary infarctions. The patient was treated with systemic thrombolysis (tenecteplase), complicated by transient oral and urinary bleeding that resolved spontaneously. Over several days, he stabilized, was weaned from vasopressors and mechanical ventilation, and discharged on full anticoagulation to outpatient follow-up. This case highlights the diagnostic challenge of massive PE, the value of bedside echocardiography, and the importance of prompt reperfusion therapy in unstable patients.

Pulseless electrical activity (PEA) arrest in patients with end-stage heart failure with reduced ejection fraction (HFrEF) most commonly reflects profound circulatory collapse rather than a primary arrhythmogenic event. Although post-resuscitation encephalopathy often prompts early neurologic prognostication, myocardial dysfunction and refractory shock frequently dominate outcomes in this population. We report the case of a 59-year-old woman with end-stage HFrEF, severe multivessel coronary artery disease, chronic lung disease, HIV infection, and active cocaine use who presented with acute hypoxic respiratory failure and decompensated heart failure and subsequently developed prolonged PEA arrest. Her post-arrest course was complicated by refractory cardiogenic shock, focal cerebellar infarction with delayed MRI due to hemodynamic instability and vasopressor dependence, and multisystem organ failure. Taken together, these findings underscore an important post-resuscitation diagnostic pitfall: neurologic abnormalities may coexist; however, refractory hemodynamic collapse often predominates. An integrated framework incorporating shock physiology, substance-associated cardiotoxicity, and competing neurologic injury is essential for accurate clinical assessment and informed goals-of-care discussions.