Bleeding/Clotting risks and Anticoagulation
Bleeding and Clotting risks
Hemostasis during ECMO is profoundly altered by the simultaneous activation of prothrombotic and hemorrhagic pathways. Blood exposure to non-endothelialized biomaterials within the ECMO circuit initiates a host defense response that varies among patients but invariably leads to activation of coagulation, inflammation, and platelet pathways. Contact between blood and artificial surfaces promotes adsorption of plasma proteins, particularly fibrinogen, onto the circuit components and activates factor XII, thereby initiating thrombin generation through the intrinsic coagulation pathway. Simultaneously, the classical and alternative complement pathways are activated, resulting in the release of inflammatory cytokines that further amplify thrombin generation and platelet activation. Mechanical forces generated by pumps and turbulent flow contribute to platelet activation and consumption, while hemolysis releases free hemoglobin into the circulation. Free hemoglobin avidly binds vascular-derived nitric oxide (NO), leading to NO depletion, vasoconstriction, and a procoagulant state characterized by enhanced platelet activation and impaired regulation of vascular tone. Paradoxically, ECMO is also associated with a substantial risk of bleeding. Platelet counts frequently decrease because of consumption, hemodilution, and sequestration, while platelet function is impaired by both mechanical stress and inflammatory activation. Hemolysis, coagulation factor consumption, and the need for systemic anticoagulation further contribute to bleeding risk. One of the hallmark hemostatic abnormalities observed during ECMO is acquired von Willebrand syndrome. High shear stress generated by the ECMO circuit induces unfolding and elongation of von Willebrand factor (vWF) multimers, exposing the A2 domain to proteolytic cleavage by ADAMTS13. This process preferentially depletes high-molecular-weight vWF multimers, which are essential for platelet adhesion and aggregation, thereby exacerbating bleeding tendency. Acquired vWF deficiency can develop rapidly, often within the first 24 hours after ECMO initiation, and may persist throughout the duration of support. Consequently, the hemostatic profile of patients on ECMO reflects a dynamic and often unstable equilibrium between thrombosis and hemorrhage, requiring careful monitoring of platelet count and function, coagulation factors, fibrinogen, hemolysis markers, anticoagulation intensity, and circuit integrity to guide individualized management.
When severe bleeding occurs, teams may use factor VII or prothrombin complex concentrates like FEIBA to achieve hemostasis, though these interventions carry a risk of circuit thrombosis. FEIBA (Factor Eight Inhibitor Bypassing Activity) is an anti-inhibitor coagulant complex used to treat bleeding in patients with hemophilia A or B who have developed inhibitors (antibodies) against their factor replacement therapy. Because it works by forcing the blood to clot, thrombosis (the formation of unwanted blood clots) is a significant, well-documented risk associated with its use. In some instances, the risk of bleeding is so great that clinicians may choose to run the circuit without any anticoagulation for a short period, prioritizing the patient's survival over the integrity of the circuit.
Anticoagulation
Managing the delicate balance between bleeding and clotting is complicated by the systemic inflammation triggered by exposure to the artificial surfaces of the circuit. This immune hyper-response is particularly evident in patients who are septic or those transitioning directly from the operating room, as they have already undergone the inflammatory stress of bypass. Anticoagulation represents one of the most complex and incompletely resolved challenges in neonatal ECMO management. Exposure of blood to the artificial surfaces of the extracorporeal circuit activates coagulation cascades, platelet aggregation, inflammatory pathways, and fibrinolysis. Without anticoagulation, circuit and cannula thrombosis is inevitable; with anticoagulation, hemorrhagic risk increases substantially — a risk that is particularly consequential in neonates, postoperative patients, those undergoing CDH repair, and patients with neurologic vulnerability. Critically, anticoagulation practice remains highly variable across institutions. No universally accepted protocol exists, and available data are largely retrospective and confounded by heterogeneity in patient populations, circuit configurations, and monitoring strategies. This represents an area of acknowledged clinical uncertainty in which standardization is actively being pursued but has not yet been achieved. However, it is clear that maintaining appropriate anticoagulation is critical to prevent circuit thrombosis while minimizing bleeding. This is particularly challenging in neonates due to their immature hemostatic system and lack of reserve capacity.
Unfractionated Heparin (UFH): The most commonly used anticoagulant. It has a short half-life and is reversible with protamine. However, its efficacy can be limited by low antithrombin (ATIII) levels in neonates, sometimes requiring ATIII replacement (e.g., with FFP). As such, unfractionated heparin has historically been the standard anticoagulant for ECMO. It acts by potentiating antithrombin, which in turn inhibits thrombin and other coagulation factors. However, in the neonatal population, this mechanism is inherently limited by developmental hemostatic particularities. Antithrombin levels are physiologically reduced in neonates, resulting in relative heparin resistance. This can lead to a clinical scenario in which escalating heparin doses fail to achieve adequate anticoagulation, while simultaneously increasing hemorrhagic risk. Monitoring heparin effect is further complicated by the imprecision of available assays; the activated partial thromboplastin time (aPTT), though widely used, is not linearly correlated with heparin concentration and is susceptible to interference from numerous confounding variables present in critically ill neonates.
Direct Thrombin Inhibitors (DTIs): Such as bivalirudin, are gaining use. They do not depend on ATIII and can inhibit clot-bound thrombin. Their short half-life is an advantage, but they lack reversal agents and require careful management, especially during weaning or in areas of blood stasis. Clot may formed if there is stasis (example: left atrial stasis).
Bivalirudin is a direct thrombin inhibitor (DTI) that does not require antithrombin as a cofactor, thereby circumventing the problem of neonatal antithrombin deficiency. Because it acts directly and independently, its anticoagulant effect is theoretically more predictable and easier to titrate. Its plasma half-life is approximately 20 minutes, offering a meaningful practical advantage: upon discontinuation of the infusion, anticoagulant activity dissipates rapidly without requiring reversal agents. This contrasts favorably with heparin, for which protamine reversal carries its own hemodynamic and immunologic risks and does not guarantee immediate hemostatic restoration. Monitoring of bivalirudin presents its own challenges. The aPTT, while used at some centers, is not an ideal assay for DTIs and lacks linearity across the therapeutic range. The dilute thrombin time (dTT) is emerging as a preferred monitoring tool and is being adopted at an increasing number of centers, though institutional availability and standardization remain obstacles. Thromboelastography (TEG) and rotational thromboelastometry (ROTEM) can be used adjunctively to assess global coagulation status, platelet function, and fibrinolysis, and are increasingly integrated into ECMO anticoagulation protocols alongside platelet aggregation assays. An important pharmacokinetic limitation of bivalirudin is its partial degradation by plasma esterases. In regions of circulatory stasis — such as within dysfunctional ventricles (or distended LA/LV) intracardiac thrombus, or poorly flowing circuit segments — local enzymatic degradation may render bivalirudin ineffective precisely where anticoagulation is most needed. This property makes bivalirudin less ideal for patients with significant ventricular dysfunction, intracardiac stasis, or myocarditis, where thrombus formation within cardiac chambers is a primary concern.
In the CDH population, Bivalirudin represents a potentially favorable use. These patients are neonates with the well-described antithrombin deficiency that limits heparin efficacy, yet they typically maintain preserved or near-normal ventricular contractility without significant intracardiac stasis. This hemodynamic profile reduces the risk associated with bivalirudin's susceptibility to esterase-mediated degradation. Some high-volume CDH and ECMO centers have transitioned to bivalirudin as the primary anticoagulant for CDH patients on ECMO. An additional rationale for avoiding heparin in this population derives from preclinical data suggesting that heparin may inhibit angiogenesis and pulmonary vascular development in animal models. While these findings are derived from a limited number of studies and have not been definitively validated in human neonates, they provide a biologically plausible mechanistic reason to prefer a non-heparin anticoagulant in a condition defined by abnormal pulmonary vascular growth.
Monitoring: A combination of tests is often used, as no single test is ideal. These include Activated Clotting Time (ACT), activated Partial Thromboplastin Time (aPTT), Anti-Xa assay, and viscoelastic tests like Thromboelastography (TEG) or Rotational Thromboelastometry (ROTEM). These tests can be affected by factors like hemolysis and hyperbilirubinemia.
Anticoagulation targets during ECMO are increasingly individualized according to the patient's thrombotic and hemorrhagic risk profile. Standard-risk patients are often managed with an aPTT target of approximately 80–100 seconds and anti-factor Xa levels between 0.3 and 0.7 IU/mL, while maintaining platelet counts above 80,000/μL, fibrinogen concentrations above 1 g/L, and hemoglobin levels above 80 g/L.
Patients at high risk of bleeding, such as those with severe acidosis, pre-existing coagulopathy, prematurity, recent surgery, or abnormal viscoelastic testing, may require lower anticoagulation targets, typically an aPTT of 60–80 seconds and anti-factor Xa levels of 0.3–0.5 IU/mL, coupled with higher thresholds for platelet count and fibrinogen replacement.
Conversely, patients at high thrombotic risk, characterized by hypercoagulable viscoelastic profiles, elevated inflammatory markers, or clinical evidence of thrombosis within the patient or circuit, may warrant more aggressive anticoagulation with higher aPTT and anti-factor Xa targets.
Ultimately, anticoagulation management during ECMO should integrate conventional coagulation tests, viscoelastic assays, clinical assessment of bleeding and thrombosis, and ongoing evaluation of circuit integrity to maintain the optimal balance between hemorrhagic and thrombotic complications.
When CDH repair is performed while the patient remains on ECMO, anticoagulation management requires careful perioperative planning. Given bivalirudin's short half-life, the infusion is typically discontinued at surgical timeout. By the time the repair is underway, residual anticoagulant activity has largely dissipated, facilitating surgical hemostasis during patch repair and closure. Following completion of surgery, anticoagulation is restarted according to the institutional protocol, with the timing and target range guided by the degree of surgical bleeding and the state of the circuit. During periods when the circuit must be clamped — such as during trial-off assessments or weaning maneuvers — bivalirudin's susceptibility to stasis-related degradation within the circuit becomes relevant. To address this, some centers administer low-dose heparin directly into the circuit during clamped intervals, while continuing bivalirudin systemically for the patient. This combined approach attempts to maintain circuit patency during periods of reduced or absent flow without exposing the patient to the limitations of systemic heparin.
Tranexamic acid (TXA) is used as an adjunctive hemostatic agent in patients with significant bleeding risk on ECMO, particularly in the perioperative CDH repair period. Inhaled TXA has been employed specifically for pulmonary hemorrhage. This application remains largely institutional and is not yet standardized.
In rare circumstances of life-threatening hemorrhage that cannot be controlled despite conventional measures, some centers have run the ECMO circuit temporarily without systemic anticoagulation, accepting the risk of circuit thrombosis in order to prioritize patient survival. This is a last-resort decision requiring careful judgment and close circuit surveillance. Prohemostatic agents such as recombinant factor VIIa or prothrombin complex concentrates — including FEIBA (Factor Eight Inhibitor Bypassing Activity), an anti-inhibitor coagulant complex — may be used to achieve hemostasis in refractory bleeding, though both carry a significant risk of accelerating circuit thrombosis and systemic thromboembolism. Their use therefore requires coordinated decision-making between the ICU team, hematology, and the perfusionist, with circuit exchange on standby if needed.
Ultrasfiltration and CRRT
Fluid overload is common in patients receiving veno-arterial (VA) ECMO and may arise from capillary leak, renal dysfunction, inflammation, transfusion requirements, or the need to administer large volumes of medications and nutritional support. One of the major advantages of the ECMO circuit is that it provides a platform for extracorporeal fluid management through ultrafiltration and, when indicated, continuous renal replacement therapy (CRRT). Ultrafiltration is typically performed using a hemoconcentrator or hemofilter integrated into the circuit and allows clinicians to remove excess fluid, reduce central venous pressure, and optimize hemodynamics while maintaining adequate organ perfusion. This approach is particularly useful when patients require high fluid intakes, such as total parenteral nutrition or blood product administration, which may otherwise exceed their optimal fluid balance. When renal dysfunction is present or solute clearance is required, CRRT can be incorporated into the ECMO circuit to provide continuous management of fluid, electrolytes, and metabolic waste products. Nevertheless, some centers prioritize preserving native renal function and reserve ultrafiltration or CRRT for patients with persistent fluid overload or overt renal failure, aiming to avoid excessive volume depletion and additional prerenal kidney injury. Beyond volume control, extracorporeal filtration techniques may also modulate the inflammatory response associated with ECMO. Blood exposure to artificial surfaces activates inflammatory pathways and leads to the release of cytokines and other mediators. Modified ultrafiltration (MUF), originally developed in cardiopulmonary bypass, has been shown to remove some of these inflammatory mediators and may help attenuate the systemic inflammatory response associated with extracorporeal support, although the clinical significance of cytokine removal in ECMO continues to be investigated.
Successful weaning from ECMO begins well before the actual trial-off. Prior to any attempt at reducing support, reversible factors that may impair native cardiorespiratory performance should be optimized, including sedation and analgesia, body temperature, ventilator settings, fluid status, and vasoactive support. In selected patients with severe pulmonary hypertension or excessive respiratory effort, temporary neuromuscular blockade may be considered to reduce oxygen consumption and facilitate assessment of intrinsic organ function. The expected timeline of recovery should also be considered, as acceptable ECMO duration varies substantially according to the underlying diagnosis. For example, neonates with meconium aspiration syndrome typically recover within several days, whereas patients with congenital diaphragmatic hernia or complex postoperative cardiac disease may require support for several weeks (2 to 4 weeks). Consequently, ECMO weaning should be viewed as a physiologic stress test designed to determine whether native cardiac and pulmonary function can sustain adequate oxygen delivery and end-organ perfusion in the absence of extracorporeal support.
Weaning is a gradual process that involves reducing ECMO support as the patient's native organ function recovers. When a patient exhibits signs of recovery, the team must assess their readiness for decannulation. There are no strict criteria, but typically the underlying cause of cardiac/respiratory failure must be resolving, and the patient should demonstrate optimized hemodynamics, including resolved lactic acidosis, normal gas exchange, and adequate blood pressure on minimal vasopressor support. A weaning trial is conducted by slowly decreasing the circuit flow while observing the capacity of the heart and lungs to resume their functions. If the patient shows evidence of uncompensated respiratory or hemodynamic deterioration during this trial, ECMO flow is increased to restore stability.
Timing and Duration: Average ECMO run times vary by diagnosis (e.g., Meconium Aspiration Syndrome: 5-6 days; Congenital Diaphragmatic Hernia: median 2-3 weeks, but can be longer). Longer runs (beyond 4-6 weeks for CDH) may have limited benefit, but universally accepted limits are not established.
Signs of Recovery:
Respiratory: Improved lung compliance, clearing chest X-ray, good lung expansion on low ventilator settings (e.g., PEEP 10, Delta 10, RR 10 for "rest settings" - highly variable by center and individualized to the patient), and reduced oxygen requirements.
Cardiac: Development of a pulsatile arterial trace (if previously flat), signs of intrinsic cardiac output, improving ventricular function on echocardiography, decreasing left atrial pressures, and minimal or no need for inotropes/vasopressors.
Weaning Strategies:
Gradual Flow Reduction: ECMO flows are progressively decreased (e.g., from 90-100 mL/kg/min down to 50 mL/kg/min or less) while conventional support is increased.
Clamp Trial: The classic method involves clamping the cannulae proximal to the patient and opening a bridge to recirculate blood within the circuit. This allows complete separation of the patient from the circuit for a trial period (15 minutes to 2 hours) to assess their tolerance without ECMO support. Adequate anticoagulation must be maintained in the circuit during the clamp trial to prevent thrombosis.
During a clamp trial, ECMO flows are first progressively reduced to minimal support, often to approximately 50% of baseline flow or to 50–60 mL/kg/min (if achievable), while conventional cardiopulmonary support is increased. Of note, in a neonate, minimal flow may still be significant! In centrifugal pumps, a minimum pump speed (typically 1000–1500 rpm) is maintained to preserve circuit flow and prevent retrograde blood movement. The arterial cannula, venous cannula, and any left atrial vent are clamped proximal to the patient, while the bridge is opened to allow blood recirculation within the circuit (to avoid clotting within the system). To minimize thrombosis, the patient and cannulae may be briefly reconnected at regular intervals, although practices vary among centers. Throughout the trial, tolerance should be assessed continuously using clinical examination, invasive hemodynamics, arterial blood gases, mixed venous oxygen saturation, lactate trends, and, when available, near-infrared spectroscopy and echocardiography. The objective is not simply to maintain normal oxygen saturation or blood pressure, but rather to demonstrate that oxygen delivery remains adequate and that the patient can sustain end-organ perfusion without extracorporeal support.
Pump-Controlled Retrograde Trial-Off: A newer technique that uses the patient's native cardiac output to maintain circuit integrity, acting as a "stress test" without clamping the circuit. Pump-controlled retrograde trial-off is an emerging ECMO weaning strategy increasingly explored in neonatal and pediatric ECMO programs as an alternative to traditional clamp trials. Instead of fully clamping the circuit, ECMO pump flow is progressively reduced to very low levels, allowing the patient’s native cardiac output to generate retrograde blood flow through portions of the ECMO circuit while maintaining circuit continuity and minimizing stasis. In this configuration, the ECMO circuit essentially becomes a passive conduit, and the patient’s cardiovascular system is “stress tested” under near-decannulation physiology without abrupt interruption of the circuit. This approach may reduce the risks associated with clamp trials, including thrombus formation, sudden preload/afterload shifts, hemodynamic instability, and emergent recannulation if the patient deteriorates. In neonates, this strategy can provide a more physiologic assessment of myocardial recovery, pulmonary vascular adaptation, oxygen delivery, and end-organ tolerance while maintaining a safety margin for rapid reinstitution of support if needed. Continuous monitoring during pump-controlled retrograde trial-off can include invasive hemodynamics, arterial blood gases, lactate trends, cerebral and somatic NIRS, echocardiography, and assessment of ventilatory reserve and pulmonary hypertension physiology. The technique has been studied primarily in pediatric populations. However, the original feasibility study noted a practical limitation in the smallest neonates: PCRTO was unsuccessful in a patient weighing 2.2 kg, whose cardiac output was insufficient to perfuse both the body and the ECMO circuit simultaneously, though it was tolerated from 2.8 kg upward. Two conversions from PCRTO to AV bridging also occurred in small neonates (2.2 kg and 2.9 kg). Pandya et al. found that PCRTO resulted in significantly shorter trial-off durations (median 88 vs. 197 minutes, P < 0.001) compared to AV bridging, with comparable safety. However, no randomized controlled trial has directly compared complication rates between PCRTO and clamp trials, so these advantages remain largely theoretical and observational rather than definitively proven.
Post-Weaning Considerations: If successful, decannulation follows. If unsuccessful, the patient can return to full ECMO support, and further investigations for the cause of weaning failure (e.g., residual cardiac lesions, pulmonary issues) are pursued.
Following successful decannulation or a trial-off, some centers elect to leave the cannulas in place for 24–48 hours in case reinstitution of ECMO becomes necessary. During this period, strategies to minimize thrombus formation within the cannulas are essential. Approaches vary among institutions and may include intermittent flushing with heparinized saline or maintaining a continuous low-rate infusion through the cannulas, effectively using them as large-bore central venous access devices. Regardless of the strategy employed, close surveillance for thrombosis, bleeding, and vascular complications is required, and cannulas should be removed promptly once the likelihood of ECMO reinstitution is deemed low.
The decision to decannulate is rarely based on a single parameter. Instead, it integrates the underlying diagnosis and expected recovery trajectory, evidence of cardiorespiratory recovery, the patient's performance during a trial-off, and the balance between the risks of ongoing ECMO support and the risks associated with decannulation.
The "clamping of the bridge test" is a classic approach used to assess a patient's readiness for weaning off support. It is often referred to as a clamp trial.
Outcomes, Complications and Prognosis
Overall survival to hospital discharge for neonates on ECMO for respiratory disease is around 73%. For cardiac indications, survival is typically lower, around 40%. Survival rates vary significantly by specific diagnosis (e.g., Meconium Aspiration Syndrome: 92%; Congenital Diaphragmatic Hernia: ~50%; Cardiac Diagnoses: 35-45%). Longer ECMO runs are associated with increased risk of complications and generally lower survival. Survivors of neonatal ECMO, particularly those with CDH, are at increased risk for long-term morbidities, including chronic lung disease and neurodevelopmental delay. For more in-depth information and specific guidelines, the Extracorporeal Life Support Organization (ELSO) website (www.elso.org) is an invaluable resource, offering comprehensive practice guidelines and registry data.
While ECMO provides a vital bridge to recovery or further intervention, it is associated with significant morbidity and mortality risks that require constant mitigation. Bleeding is among the most frequent complications, often arising from anticoagulation, sepsis, or disseminated intravascular coagulation. Because neurologic or gastrointestinal bleeding may present late, clinicians must monitor for unexplained decreases in hematocrit and regularly track laboratory markers such as fibrinogen and PTT. Migrating or dislodged cannulas can also cause bleeding or hemorrhagic shock, making it essential to verify cannula positions through physical measurements and routine imaging. In some cases, severe bleeding may even necessitate the temporary discontinuation of anticoagulation.
Thrombosis remains a constant threat as the foreign surfaces of the circuit naturally activate the coagulation cascade. Clots forming on the arterial side of the circuit are particularly dangerous because they can dislodge and travel to the brain, resulting in a debilitating stroke, or to other organs like the kidneys. Routine neurological checks are necessary to assess for new-onset seizures or changes in status that might indicate an embolic event. Clots on the venous side or within the oxygenator, while less likely to reach the patient, can lead to oxygenator failure and may require a circuit change. To prevent such formations, systemic anticoagulation with agents like heparin or bivalirudin is maintained, though this requires a delicate balance to avoid exacerbating the risk of hemorrhage.
Mechanical and environmental factors also introduce risks, such as air emboli and limb ischemia. Because the venous limb of the circuit operates under negative pressure, air can be entrained through any disruption or open access point. While small amounts of air are often vented by the oxygenator, large volumes can cross into the arterial side and cause organ damage or neurologic injury. Limb ischemia is another concern, particularly with femoral cannulation, where the cannula position or compartment syndrome can compromise distal blood flow. Furthermore, the continuous compression of tubing in roller head pumps can lead to tubing rupture over time; clinicians mitigate this through the practice of walking the raceway to distribute mechanical strain.
Outcomes for pediatric cardiac ECMO vary based on the patient's age and underlying condition. The mean duration of support is approximately seven days, and patients who require longer support often accumulate more complications and have lower survival rates. Survival to hospital discharge is generally lower for neonates, patients with congenital heart disease, or those placed on ECMO during cardiac arrest (ECPR), where the predicted survival is less than 50 percent. For specific conditions like acute viral myocarditis, registry data suggests a survival chance of about 50 percent. Successful cases often involve transition to oral heart failure medications and eventual transfer to lower levels of care after decannulation and extubation.
ECMO Programs and Multidisciplinary Care
The structure of pediatric ECMO programs varies significantly across medical centers, often depending on the size of the staff and the specific expertise available. In most institutions, the program is primarily operated by a dedicated team of nurses and respiratory therapists, with the perfusion team serving in a supportive and consultative role. In contrast, other centers may have more overlap between perfusion and ECMO specialists, especially when managing complex devices like ventricular assist devices (VADs) that require integrated oxygenators. Regardless of the specific staffing model, the trend in modern programs is toward high levels of interdisciplinary collaboration, where perfusionists, nurses, and physicians act as a unified resource for troubleshooting and education. One of the most critical moments for this collaboration occurs in the operating room when a patient fails to come off cardiopulmonary bypass and must be transitioned to ECMO. This transition is typically a highly coordinated "dance" that can take as little as ten seconds once the decision is made to disconnect the bypass tubing and connect the primed ECMO circuit. A major concern during this phase is the timing of heparin reversal agents; if protamine or other reversal agents are administered too early or without clear communication, the ECMO circuit can clot almost instantly, leading to catastrophic failure. Success in these high-stakes moments relies on the ECMO team and the perfusionists working in tandem to ensure the circuit is ready before the patient's native circulation is compromised. The design and maintenance of the ECMO circuit have evolved toward a philosophy of simplification and miniaturization. Clinicians have found that reducing the number of connectors, pigtails, and stopcocks significantly lowers the risk of thrombosis and unexpected mechanical failures. The introduction of advanced technology, such as integrated pressure sensors and digital oxygenator readouts, further assists in this effort by eliminating the need for external transducers and stagnant fluid lines that can harbor clots. This "less is more" approach is driven by the recognition that every additional component in the circuit provides a surface for clot formation or a potential point of entry for air entrainment.
The human element of ECMO care is as important as the mechanical components, necessitating robust education and simulation programs. Annual "wet labs" and crisis management simulations allow the multidisciplinary team to practice responses to rare but high-stress events, such as cannula dislodgement or massive air entrainment. These simulations are vital for developing a shared mental model and improving communication between team members who may be "siloed" in their respective roles. By spending time in different clinical environments, such as ICU staff visiting the operating room to observe complex procedures like the Norwood, team members gain a deeper appreciation for the pressures and expertise of their colleagues. This mutual understanding fosters a culture where expertise is shared freely, ensuring that the most knowledgeable person can "fill the gaps" in patient management during a crisis.
