Recent cardiogenic shock (CS) literature emphasizes early recognition, staging, and treatment to improve survival, highlighting the need for system-wide detection pathways and prompt shock team activation to enable timely intervention. We present a 26-year-old woman initially diagnosed with septic shock who deteriorated despite therapy. Ongoing reassessment led to reclassification as CS, prompting shock team activation and initiation of mechanical circulatory support, ultimately resulting in full recovery. CS is uncommon in young adults and may be misdiagnosed as distributive shock. Repeated evaluations with focused examinations, laboratory testing, and echocardiography are critical for early detection and proper diagnosis and management.

Mixed shock is common after cardiac arrest (CA), with dominant shock physiology sometimes changing over the course of hours. This article focuses on identifying dominant shock physiology in patients with refractory shock after CA and targeted strategies for resuscitation. The authors discuss approach to cardiogenic shock, including pharmacologic and mechanical support, as well as advanced pharmacologic therapies relevant to distributive shock.

Systemic capillary leak syndrome (SCLS) is a rare disorder characterized by acute episodes of hypotension, haemoconcentration, and hypoalbuminemia.

The classical concept of shunt confines the phenomenon to the pulmonary circulation, leaving microcirculatory flow maldistribution in distributive shock outside existing terminology. Tissue hypoxia can persist despite normal cardiac output; current hemodynamic stability criteria incorporate no microcirculatory dimension. This review addresses both gaps by proposing a unifying framework. We propose ineffective circulating volume (ICV) as blood flow that fails to achieve effective gas exchange, whether at the alveolar-blood interface (pulmonary shunt) or the blood-cell interface (systemic shunt). Pulmonary shunt and septic microcirculatory heterogeneity are established phenomena, whereas their unification as ICV-particularly the term systemic "functional shunt"-is a hypothesis requiring clinical validation. Anatomical shunt involves fixed structural bypasses correctable surgically; functional abnormalities reflect failure of active distribution mechanisms-hypoxic pulmonary vasoconstriction suppressed by inflammatory mediators, and conducted responses disrupted by endothelial injury. Supportive interventions may improve their physiological consequences, whereas durable reversal depends on resolution or treatment of the underlying disease. The ICV framework subdivides circulatory hypoxia into a macrocirculatory sublayer (global oxygen delivery insufficiency) and a microcirculatory sublayer (flow maldistribution), the latter potentially persisting even when macrocirculatory parameters are normalised. Acute respiratory distress syndrome and distributive shock may share three upstream molecular mechanisms-glycocalyx degradation, spatially heterogeneous inducible nitric oxide synthase overexpression, and neutrophil extracellular traps-that could impair regulatory systems at both interfaces. Changes in sepsis resuscitation targets are compatible with, but do not validate, the ICV framework's emphasis on macro-microcirculatory uncoupling. No study has simultaneously quantified shunt at both interfaces in the same patient cohort, and no randomised trial targeting the shared upstream mechanisms has used dual-interface ICV as a combined primary endpoint. Translating the ICV framework into prospectively defined clinical endpoints remains an open methodological challenge.

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract and are usually diagnosed before reaching an advanced size. Giant GISTs exceeding 20 cm are uncommon and are frequently associated with adverse pathological features, including high mitotic activity, necrosis, and metastatic dissemination, which together drive an aggressive clinical course and a poor prognosis. We report the case of a 57-year-old man with type 2 diabetes mellitus who presented with progressive abdominal distension, fatigue, early satiety, transfusion-dependent anemia, and general deterioration. Computed tomography demonstrated a 29 × 20 cm intra-abdominal mass occupying nearly the entire abdominal cavity, without radiologic evidence of major vessel invasion. Given the severity of the anemia and the rapid clinical decline, the multidisciplinary team proceeded directly to exploratory laparotomy without preoperative tissue diagnosis; the rationale for this decision is discussed. Complete macroscopic tumor resection was achieved together with resection of a densely adherent segment of ileum and mechanical side-to-side intestinal anastomosis, but the procedure was complicated by an estimated 3,000 mL of blood loss, attributed to tumor neovascularity and adhesiolysis, requiring massive transfusion. Histopathology confirmed a 30 cm mixed-type GIST weighing more than 5 kg, with diffuse CD117 positivity, a mitotic index of 18/5 mm², focal necrosis, negative surgical margins (R0), and metastatic implants in the omentum and parietal peritoneum, consistent with high-risk metastatic disease without transmural bowel-wall invasion -- a pattern more in keeping with a mesenteric/extraintestinal GIST closely applied to the ileum than a primary transmural ileal tumor. Despite maximal postoperative intensive care, the patient developed refractory distributive shock, severe metabolic acidosis, and progressive multiorgan failure, and died on postoperative day 1. This case illustrates the extreme end of the GIST clinical spectrum and underscores the importance of early diagnosis, prompt referral, and structured multidisciplinary planning, including a deliberate, documented decision process around preoperative biopsy and neoadjuvant therapy, before disease reaches this magnitude.

Cardiogenic shock (CS) is the most serious heart failure manifestation, characterised by a significant risk of morbidity and mortality despite improving diagnosis and treatment: early recognition and accurate hemodynamic phenotypization are crucial to improve its poor prognosis. Recently, point-of-care ultrasound (PoCUS) has evolved as a key method in emergency settings for fast shock assessment. Evidence indicates that PoCUS improves the clinician's diagnostic accuracy by identifying ventricular dysfunction, valvular disease, complications of myocardial infarction, loading conditions, and systemic congestion. Multiorgan protocols that combine cardiac, pulmonary, and vascular assessments enable differentiation among cardiogenic, obstructive, hypovolemic, and distributive shock. Echocardiographic parameters-including ventricular function, volume indices, and dynamic measures such as stroke volume and cardiac output-can guide fluid management, vasoactive therapy, and circulatory support. Limitations include operator dependence and potential imaging challenges due to patient factors. When combined with clinical and laboratory data, PoCUS is a fundamental tool for early CS assessment. With this paper, we aimed to describe the role of PoCUS in the differential diagnosis of undifferentiated shock, confirming or ruling out CS, assessing CS prognosis, guiding appropriate treatment and enabling hemodynamic monitoring. Integrating PoCUS elements with validated classifications, such as the Society for Cardiovascular Angiography and Interventions (SCAI) CS stages, can be useful for improving CS management. This review highlights validated PoCUS markers, practical PoCUS applications within the SCAI framework, and areas for further research, emphasising the increasing role of PoCUS in personalised, physiology-guided management of CS in the emergency department.

Vasoplegia remains one of the most challenging and incompletely understood complications across the spectrum of mechanical circulatory support (MCS). Initially described following cardiopulmonary bypass, it is increasingly recognized in patients supported with veno-arterial extracorporeal membrane oxygenation (V-A ECMO) and combined unloading strategies such as ECPELLA (ECMO and Impella support) as well as in patients bridged to heart transplantation with temporary or durable mechanical circulatory support (MCS). Despite occurring in different clinical settings, these syndromes share common pathophysiological features, including systemic inflammation, endothelial dysfunction, glycocalyx degradation, dysregulated nitric oxide signaling, neurohormonal imbalance, microcirculatory impairment and severe vasomotor dysregulation. Although vasoplegia is commonly considered a technology-specific complication, growing evidence suggests that CPB-associated vasoplegia, postcardiotomy vasoplegic syndrome, ECMO-related vasodilatory shock and distributive shock during ECPELLA may represent distinct manifestations of a common pathobiological process driven by blood-artificial surface interactions, ischemia-reperfusion injury, hemolysis and immune activation. This narrative review proposes a unified framework of vasoplegia across the continuum of MCS. Key mechanistic pathways and current therapeutic strategies, including catecholamines, vasopressin, angiotensin II, methylene blue and hydroxocobalamin, are discussed. By integrating evidence from cardiac surgery, critical care and mechanical circulatory support, vasoplegia is presented as a unifying syndrome of extracorporeal circulation. This perspective may support earlier recognition, phenotype-based management and the development of more targeted therapeutic strategies in a clinically significant yet underexplored area of cardiovascular critical care.

We present the case of a 52-year-old man with a history of diabetes mellitus who presented with altered mental status following acute cocaine use. Initial evaluation revealed severe hyperglycemia (1655 mg/dL), profound metabolic acidosis, hyperkalemia, and severe hypernatremia consistent with mixed diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). The patient required endotracheal intubation, mechanical ventilation, continuous insulin infusion, aggressive fluid resuscitation, and electrolyte correction. His intensive care unit course was complicated by distributive shock requiring norepinephrine, phenylephrine, and vasopressin support. He subsequently developed transient cardiomyopathy with a left ventricular ejection fraction of 35% and marked transaminitis. Right upper quadrant ultrasonography and computed tomography demonstrated gallbladder sludge and borderline wall thickening, raising concern for acute cholecystitis. However, hepatobiliary scintigraphy was negative for cystic duct obstruction, and liver enzymes improved rapidly following hemodynamic stabilization. These findings supported a diagnosis of ischemic hepatitis secondary to shock and cocaine-induced vasoconstriction rather than primary biliary pathology. The patient's clinical status improved with supportive management, and he was discharged with outpatient endocrinology and cardiology follow-up. This case highlights the potential for cocaine-associated mixed DKA-HHS to present with profound metabolic derangement and multisystem organ dysfunction while mimicking acute biliary disease, emphasizing the importance of careful diagnostic evaluation to avoid unnecessary surgical intervention.

Genvoya is a fixed-dose antiretroviral medication commonly used in the treatment of human immunodeficiency virus (HIV) infection and is generally well tolerated. Severe toxicity following Genvoya overdose has not been well described, and currently available reports generally describe mild clinical courses managed with supportive care alone. We present the case of a 35-year-old male with HIV, hypertension, and amphetamine use who presented after intentional ingestion of approximately 90 tablets of Genvoya in a suicide attempt. He was initially awake, alert, and hemodynamically stable. Over the next 24 hours, however, he developed distributive shock requiring vasopressor support, acute hypoxic respiratory failure requiring high-flow nasal cannula oxygen therapy, metabolic acidosis, QTc prolongation, mild acute kidney injury, and newly reduced systolic cardiac function with an estimated ejection fraction of 25-35%. Chest imaging demonstrated pulmonary edema and volume overload. Infectious workup remained negative throughout admission. The patient was managed with supportive care in the medical intensive care unit and gradually improved over the following days. This case adds to the limited literature describing severe multisystem complications following large-volume Genvoya overdose.

Severe quetiapine overdose may lead to central nervous system depression and cardiovascular instability; however, refractory distributive shock is an uncommon and life-threatening presentation. Intravenous lipid emulsion has emerged as a potential adjunctive therapy in intoxications caused by highly lipophilic drugs, although evidence remains limited. We report the case of a 25-year-old woman with intentional ingestion of approximately 4.5 g of quetiapine, who developed progressive neurological deterioration and refractory distributive shock despite mechanical ventilation and dual vasopressor support. Laboratory findings showed severe metabolic acidosis with hyperlactataemia, and echocardiography revealed a hyperdynamic profile with reduced systemic vascular resistance. Given the persistence of haemodynamic instability and neurological impairment, a 20% intravenous lipid emulsion was administered as rescue therapy. Within three hours, the patient exhibited marked neurological improvement, with recovery of consciousness (Glasgow Coma Scale score 14/15), along with progressive haemodynamic stabilization allowing discontinuation of vasopressors. Lactate levels normalized within 9 h, and the patient was successfully extubated at 24 h, with no treatment-related adverse events. This case highlights the potential role of intravenous lipid emulsion as an adjunctive rescue therapy in severe quetiapine intoxication with refractory haemodynamic and neurological compromise. Although causality cannot be definitively established, the temporal association and rapid clinical response support its consideration when conventional supportive measures are insufficient.

Carcinoid syndrome is characterized by the presence of a carcinoid tumor that can release chemical mediators that, if not adequately controlled, can even lead to carcinoid crisis. In this condition occurs hemodynamic instability, with distributive shock, bronchospasm, and cardiac arrhythmias. Carcinoid tumors have an incidence of 1-2 cases per 100,000 patients, and 20-30% of them present episodic vasomotor symptoms such as bronchospasm, hypotension and diarrhea secondary to therelease of vasoactive amines. Because it is an infrequent situation, we present the anesthetic management of a patient withcarcinoid syndrome undergoing surgery for tricuspid and pulmonary valve replacement, where we indicate the procedure forinduction, maintenance and termination of anesthesia without any reported events. The risk of a carcinoid crisis must beconsidered, in conjunction with a multidisciplinary approach to ensure effective surgery.

Point-of-care ultrasound (POCUS) has emerged as an essential bedside tool for the rapid assessment and management of critically ill patients. This review outlines the evolution of POCUS from a focused, rule-in/rule-out modality to an advanced, integrative diagnostic approach capable of supporting complex haemodynamic evaluation. Technological advances, including handheld devices and artificial intelligence, have enhanced accessibility, diagnostic accuracy, and training efficiency. In the intensive care setting, echocardiographic interpretation must be contextualised within dynamic physiological variables such as preload, ventilation, vasoactive support, and metabolic status. POCUS plays a pivotal role in differentiating shock phenotypes-cardiogenic, distributive, hypovolaemic and obstructive-by integrating structural and functional cardiac assessment with lung and systemic venous ultrasound findings. Key haemodynamic parameters, including left ventricular outflow tract velocity time integral (LVOT VTI) and Doppler-derived indices, enable evaluation of cardiac output and fluid responsiveness, while dynamic tests such as passive leg raising further refine management decisions. The review also highlights the role of POCUS in assessing hypoxaemia through combined cardiopulmonary evaluation and introduces the 'POCUS pyramid' framework, integrating cardiac, pulmonary, and venous domains into a unified physiological model. Ultimately, when performed by appropriately trained clinicians, POCUS and critical care echocardiography enhance diagnostic precision, guide therapy, and improve bedside decision-making while recognising inherent limitations and the need for structured training and governance.