Despite advances in cardiac arrest management, survival with favorable neurological outcomes remains limited. Physiological monitoring may complement standardized resuscitation by providing real-time information about circulatory effectiveness, reversible causes, and treatment responses. However, whether physiology-guided interventions improve patient-centered outcomes remains uncertain. This narrative review examines the current evidence and clinical applicability of physiological monitoring during resuscitation, physiology-informed rescue strategies, and individualized post-cardiac arrest care. During cardiopulmonary resuscitation, invasive arterial pressure monitoring, waveform capnography, and echocardiography provide complementary information about the circulation generated by chest compressions and potential mechanisms of resuscitation failure. Although observational and experimental studies support their physiological relevance, no adult diastolic pressure target or pressure-guided vasopressor strategy has been validated to improve survival or neurological recovery. Recent randomized trials of transesophageal echocardiography have demonstrated physiological or procedural effects without establishing clinical benefit. Among rescue strategies, extracorporeal cardiopulmonary resuscitation has yielded inconsistent results across randomized trials, with potential benefits dependent on patient selection, intervention timing, and system capabilities. Resuscitative endovascular balloon occlusion of the aorta has not improved clinical outcomes in randomized evaluation, while head-up resuscitation remains investigational. Following the return of spontaneous circulation, randomized trials have challenged the benefits of uniformly higher blood pressure and oxygenation targets, mild hypercapnia, and deeper or prolonged temperature control. Individualized approaches incorporating cerebral autoregulation, venous congestion, and cardiopulmonary physiology are physiologically appealing but lack prospective validation. Physiological assessment may complement established resuscitation algorithms by refining clinical decisions during and after cardiac arrest. However, improvements in physiological measurements should not be equated with improved patient outcomes. Future trials should determine whether predefined, physiology-guided treatment strategies improve survival and neurological recovery.
Serotonin syndrome (SS) typically presents with altered mental status, autonomic dysfunction, and neuromuscular abnormalities. We report an atypical case of perioperative tramadol-induced serotonergic toxicity in an adolescent characterized by isolated neuromuscular symptoms with completely preserved consciousness and stable autonomic function, challenging the established paradigm that altered mental status and hyperthermia are obligatory for diagnosis. A 13-year-old girl (weight 54 kg, height 152 cm, BMI 23.4 kg/m²) underwent arthroscopic meniscus repair under general anesthesia with fentanyl. One hour postoperatively, tramadol 50 mg (0.93 mg/kg) was administered intravenously. Ten minutes later, she developed right-hand tremor progressing to bilateral paroxysmal convulsions. Crucially, she remained fully conscious, coherent, and oriented throughout, accurately recalling the convulsive process. Continuous monitoring revealed stable hemodynamics without hyperthermia (maximal temperature 37.2 °C). Emergent non-contrast head CT and MRI revealed no structural abnormalities. Blood gas analysis showed metabolic acidosis (lactate 6.0 mmol/L) and electrolyte disturbances, including hypomagnesemia (0.68 mmol/L preoperatively). After midazolam sedation, electrolyte correction, and magnesium supplementation, symptoms recurred. Multidisciplinary consultation and Hunter criteria application confirmed probable serotonergic toxicity. Treatment included tramadol discontinuation, midazolam infusion, and supportive care, leading to symptom resolution within 3 days. Three-month follow-up confirmed no recurrence of neurological symptoms. This case represents a rare abortive form of serotonergic toxicity characterized by isolated neuromuscular manifestations without autonomic or mental status changes, possibly unmasked by pre-existing hypomagnesemia. Anesthesiologists should not exclude serotonergic toxicity based on intact mental status or normothermia; Hunter criteria should be applied immediately when abnormal neuromuscular symptoms occur postoperatively in patients with recent serotonergic drug exposure and metabolic predispositions. Not applicable
Severe tetanus causes autonomic dysfunction and generalised muscle spasms, which can produce marked haemodynamic swings that may injure the aortic wall. Aortic dissection complicating tetanus is nevertheless extremely rare, and its clinical course is poorly documented. A 58-year-old man with severe tetanus (Ablett grade IV) developed an acute Stanford type B aortic dissection during recurrent episodes of autonomic instability and generalised muscle spasms. The primary intimal tear lay at the T4–T5 vertebral level, corresponding anatomically to concurrent acute compression fractures of T2–T6. He was treated with mechanical ventilation and thoracic endovascular aortic repair (TEVAR). His only intensive-care complication was ventilator-associated pneumonia, which resolved with treatment. He was discharged in stable condition and at 3 months was free of pain, with good functional status, blood pressure well controlled without antihypertensive medication, and no reintervention; he declined follow-up computed tomography angiography, so aortic remodelling could not be assessed. The association we describe is temporal only and does not establish that tetanus caused the dissection. We offer a speculative “biomechanical stress–neuroendocrine storm” hypothesis to frame this rare complication and to alert clinicians to potentially life-threatening vascular events in severe tetanus.
Acute high-risk abdominal surgery (AHA) comprises a population of patients with perforated hollow viscus, intestinal obstruction or intestinal ischemia and carry high mortality and morbidity. With a coordinated effort it has been shown that the 30-day mortality can be reduced to 11,8
The purpose of this study was to evaluate a revised stroke 25 protocol in Manitoba, which integrated Stroke Team Activation by the Virtual Emergency Care and Transfer Resource Service (VECTRS), and to determine whether its implementation reduced time to acute stroke treatment compared to the previous protocol. This retrospective chart review utilized Emergency Medical Services (EMS) data from the Winnipeg Fire Paramedic Service (WFPS) and hospital electronic medical records from the Winnipeg Health Sciences Centre (HSC), comparing 12 months before and 12 months after implementation of the revised Stroke 25 protocol. For each patient, the interval from EMS arrival at HSC to initiation of acute stroke treatment was calculated. Mean times to thrombolysis and EVT were compared between pre- and post-implementation cohorts. In the pre-intervention cohort, 757 patients with suspected stroke were triaged to HSC, of whom 131 received Alteplase or Tenecteplase (TNK) and 33 underwent EVT. In the post- intervention group, 717 patients were triaged, with 110 receiving Alteplase/TNK and 30 undergoing endovascular thrombectomy (EVT). Mean time to thrombolysis decreased from 59.1 min pre- intervention to 52.8 min post- intervention, while mean time to EVT decreased from 92.2 min to 84.1 min, respectively. Implementation of the revised Stroke 25 protocol was associated with modest reductions in absolute time to treatment for patients with acute ischemic stroke; however, while these differences were not statistically significant, the impact for these patients may still be clinically significant.
