Venoarterial Extracorporeal Membrane Oxygenation Flow Research Articles

Timing of veno-arterial extracorporeal membrane oxygenation support in patients with cardiogenic shock.

The optimal timing for implementing mechanical circulatory support (MCS) in cardiogenic shock (CS) remains indeterminate. This study aims to evaluate patient characteristics and outcome associated with the time interval between CS onset and veno-arterial extracorporeal membrane oxygenation (VA-ECMO) implementation. In this study, patients with CS treated with MCS at 15 tertiary care centres in three countries were enrolled. Patients treated with MCS were stratified into early (<2 h), intermediate (2-12 h) and delayed (≥12-24 h) MCS implantation by using the time interval between CS onset and MCS device implementation. Adjusted logistic and Cox regression models were fitted to assess the association between timing of MCS implementation, patient characteristics and 30-day mortality. A total of 330 patients with CS treated with VA-ECMO and/or microaxial flow pump were included in this study; 20.9% received early, 55.8% intermediate, and 23.3% delayed MCS. Although crude 30-day mortality was slightly lower in patients with early MCS (58.1% vs. 64.7% vs. 64.3%), adjusted analyses showed no significant association between timing of MCS implantation and 30-day all-cause mortality (hazard ratio [HR] for early vs. intermediate MCS: 0.93, 95% confidence interval [CI] 0.59-1.46, p = 0.74; HR for early vs. delayed MCS: 1.29, 95% CI 0.78-2.13, p = 0.33). Moreover, the incidence of complications, related and unrelated to MCS, did not differ significantly among groups. In this exploratory study of patients with CS treated with MCS, the timing of device implantation within 24 h after CS onset was not associated with mortality. This supports a restrictive MCS approach, reserving its application for patients experiencing CS deterioration despite conventional therapy.

Systemic Hemodynamics, Cardiac Mechanics, and Signaling Pathways Induced by Extracorporeal Membrane Oxygenation in a Cardiogenic Shock Model.

Peripheral venoarterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly being used in patients suffering from refractory cardiogenic shock (CS). Although considered life-saving, peripheral VA-ECMO may also be responsible for intracardiac hemodynamic changes, including left ventricular overload and dysfunction. Venoarterial extracorporeal membrane oxygenation may also increase myocardial wall stress and stroke work, possibly affecting the cellular cardioprotective and apoptosis signaling pathways, and thus the infarct size. To test this hypothesis, we investigated the effects of increasing the peripheral VA-ECMO blood flow (25-100% of the baseline cardiac output) on systemic and cardiac hemodynamics in a closed-chest CS model. Upon completion of the experiment, the hearts were removed for assessment of infarct size, histology, apoptosis measurements, and phosphorylation statuses of p38 and protein Kinase B (Akt), and extracellular signal-regulated kinase mitogen-activated protein kinases (ERK-MAPK). Peripheral VA-ECMO restored systemic perfusion but induced a significant and blood flow-dependent increase in left ventricular preload and afterload. Venoarterial extracorporeal membrane oxygenation did not affect infarct size but significantly decreased p38-MAPK phosphorylation and cardiac myocyte apoptosis in the border zone.

Prognostic effects of microcirculation-assisted adjustment of venoarterial blood flow in extracorporeal membrane oxygenation: A prospective, pilot, randomized controlled trial

The study explored the clinical efficacy of microcirculation-assisted blood flow adjustment in patients receiving venoarterial extracorporeal membrane oxygenation (VA-ECMO). This prospective, pilot, randomized controlled trial was conducted from 2018 to 2021; enrolled patients were randomly assigned to the microcirculation or control group at a 1:1 ratio. Microcirculatory and clinical data were collected within 24h (T1) and at 24-48h (T2), 48-72h (T3), and 72-96h (T4) after ECMO initiation and were compared between the groups following the intention-to-treat (ITT) principle. The primary outcome was the Sequential Organ Failure Assessment (SOFA) score at T2. In addition to ITT analysis, analysis based on the as-treated (AT) principle was performed. A total of 35 patients were enrolled in this study. At T2, the SOFA score did not significantly differ between the microcirculation and control groups (16 [14.8-17] vs. 16 [12.5-18], P=0.782). Generalized estimating equation analysis demonstrated a significantly greater reduction in the SOFA score over time in the microcirculation-AT group than in the control-AT group (estimated difference:-0.767, standard error: 0.327, P=0.019). The lactate level at T2 was significantly lower in the microcirculation-AT group (2.7 [2.0-3.6] vs. 4.1 [3.0-6.6] mmol/L, P=0.029). No significant difference in the 30-day survival rate was noted between the groups. This prospective pilot study demonstrated the feasibility of microcirculation-assisted VA-ECMO blood flow adjustment despite no significant clinical benefit for critically ill patients. More efforts in personnel training and newer technologies may help achieve microcirculation optimization.

Clinical practice of emergency department-initiated extracorporeal cardiopulmonary resuscitation for cardiac arrest in adults.

Clinical practice of emergency department-initiated extracorporeal cardiopulmonary resuscitation for cardiac arrest in adults.

Postoperative prosthetic mitral valve occlusion due to left atrial thrombus during veno-arterial extracorporeal membrane oxygenation: a case report

BackgroundAnticoagulation using heparin is generally used to prevent thrombus formation during mechanical circulatory support, such as veno-arterial extracorporeal membrane oxygenation (VA-ECMO). However, during the early period following cardiac surgery, anticoagulation becomes more difficult due to the greater risk of critical bleeding complications.Case presentationA 71-year-old man presented with acute prosthetic valve occlusion caused by left atrial thrombus formation and bioprosthetic valve thrombosis during peripheral VA-ECMO following mitral valve replacement (MVR) despite continuous heparin administration and loading of antiplatelet agents. The VA-ECMO flow rate decreased 10 h after the intensive care unit (ICU) admission after MVR. Exploratory transesophageal echocardiography (TEE) examination revealed a left atrial thrombus, prosthetic valve obstruction by the thrombus, and an intrapericardial hematoma.ConclusionsIntracardiac thrombus formation might occur during VA-ECMO despite appropriate anticoagulation and loading of antiplatelet agents. Exploratory TEE examination was helpful in the detection of intra-atrial thrombus formation after cardiac surgery and surgical decision-making.

Aortic stenosis and mitral regurgitation modify the effect of venoarterial extracorporeal membrane oxygenation on left ventricular function in cardiogenic shock

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Eight female swine (45 kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure–volume catheter. Data are expressed as median (interquartile range). Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9–3.1) L/min and LV ejection fraction to 15.2% (10.5–19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2–34.9) to 56.0 (51.9–73.3) mmHg (P ˂ 0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2–40.0) to 19.1 (15.2–29.0) mmHg (P ˂ 0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0–53.4) to 72.5 (51.4–77.1) mmHg (P ˂ 0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7–19.1) to 20.8 (16.3–25.6) mmHg (P ˂ 0.01). Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.

Heart rate control and hemodynamic improvement with Ivabradine in cardiogenic shock patients on mechanical circulatory support

Abstract Background Cardiogenic shock (CS) is a life threatening condition due to primary cardiac dysfunction. First line therapy involves drug administration (including inotropes and/or vasopressors) up to mechanical circulatory support. Tachycardia is a compensatory mechanism in response to hypotension and low cardiac output or a side effect related to inotropic drugs. Ivabradine selectively acts on IKf channel in the sinoatrial node to reduce sinus heart rate without affecting inotropism. Its use in small non-randomized series of patients with CS was safe and well tolerated [1]. Methods We present the use of ivabradine in six patients with CS undertaking veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Data regarding haemodynamic and echocardiographic monitoring were collected before, at 12, 24 and 48 hours after ivabradine administration. Results Ivabradine was administered through naso-gastric tube with a median time of 23 hours [IQR 18–28] since VA-ECMO implantation at the starting dose of 2.5 mg twice a day. Haemodynamic and echocardiographic parameters are shown in table. Ivabradine was well tolerated and led to a significant reduction of heart rate after first administration (p&amp;lt;0.01) (Fig. 1, panel A). Echo-derived stroke volume increased significantly (p&amp;lt;0.001) (Fig. 1, panel B); so did cardiac index (p&amp;lt;0.001) and left ventricular cardiac power index (p 0.005) (Fig. 1, panel C). VA-ECMO rate pump and blood flow significantly decreased (respectively p 0.002, p 0.001). No significant changes were observed in arterial blood pressure (p&amp;gt;0.05). Norepinephrine was down-titrated in all patients (p 0.01). Patients presented with cardiac arrest died due to neurological injury whereas the others were weaned off VA-ECMO and discharged alive. Conclusions Ivabradine administration resulted in an effective reduction of heart rate leading to ventricular stroke volume allowing the reduction of extracorporeal flow support and vasopressors administration. Funding Acknowledgement Type of funding sources: None.

Venoarterial extracorporeal membrane oxygenation flow or dobutamine to improve microcirculation during ECMO for refractory cardiogenic shock.

Venoarterial extracorporeal membrane oxygenation (VA ECMO) effectively supports refractory cardiogenic shock (rCS), and sustains macro- and microcirculations. We investigated the respective impact of increasing VA ECMO flow or dobutamine dose on microcirculation in stabilized VA ECMO-treated patients with rCS. In this prospective interventional study, we included consecutive intubated patients, with ECMO-supported rCS and hemodynamic stability, able to tolerate stepwise incremental dobutamine doses (from 5 to 20 gamma/kg/min) or ECMO flows (progressive increase by 25% above baseline ECMO flow. Baseline was defined as the lowest VA ECMO flow and dobutamine 5 μg/kg/min (DOBU5) to maintain mean arterial pressure (MAP) ≥ 65 mmHg. Macro- and microcirculations were evaluated after 30 min at each level. Fourteen patients were included. Macro- and microcirculations were assessed 2 [2-5] days post-ECMO onset. Dobutamine-dose increments did not modify any microcirculation parameters. Only the De Backer score tended to be reduced (p = 0.08) by ECMO-flow increments whereas other microcirculation parameters were not affected. These findings did not differ between patients successfully weaned-off ECMO (n = 6) or not. When macrocirculation has already been restored in patients with ECMO-supported rCS, increasing dobutamine (above 5 μg/kg/min) or ECMO flow did not further improve microcirculation.

IMPACT OF EARLY APPLICATION OF VA-ECMO INTEGRATED CONTINUOUS CYTOKINE HEMOADSORPTION ON OUTCOME OF REFRACTORY CARDIOGENIC SHOCK

IMPACT OF EARLY APPLICATION OF VA-ECMO INTEGRATED CONTINUOUS CYTOKINE HEMOADSORPTION ON OUTCOME OF REFRACTORY CARDIOGENIC SHOCK

Secondary left heart failure occurred during VA-ECMO assistance for severe residual pulmonary hypertension after pulmonary endarterectomy: a case report

BackgroundIn patients of chronic thromboembolic pulmonary hypertension undergoing pulmonary endarterectomy, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides full haemodynamic support. However, during a rescue treatment of VA-ECMO for patients with difficulty weaning from cardiopulmonary bypass, a significantly increase left ventricular afterload through retrograde infusion of arterialized blood into the descending aorta may occur.Case presentationWe report a 70-year-old man who suffered severe residual pulmonary hypertension following pulmonary endarterectomy for chronic thromboembolic pulmonary hypertension. Preoperative echocardiogram showed a dilated and poorly functioning right ventricle, as well as a small left heart with normal function (TAPES9.6 mm, LVEF64%, average E/E′11.94, lateral E′12.1 cm/s, tricuspid regurgitation velocity 2.5 m/s), while postoperative echocardiography revealed a significant decrease of whole ventricular function on postoperative day 1(TAPES4mm, LVEF28%, average E/E′15, lateral E′6.7 cm/s, tricuspid regurgitation velocity 4.1 m/s), indicating the patient developed severe secondary left ventricular dysfunction on the basis of right ventricular dysfunction, during VA-ECMO support. Then comprehensive measures were adopted, such as down-regulating VA-ECMO flow rate, adjusting respiratory parameters, using vasoactive drugs, as well as prostacyclin. Eventually, the pulmonary hypertension decreased to moderate degree, and the heart function improved gradually.ConclusionsIn the face of severe residual pulmonary hypertension and sencondary left ventricular dysfunction associated with VA-ECMO, comprehensive measures described above may facilitate recovery. ECMO flow titration to maintain relatively low flow rate is very important to not only maintain systemic perfusion, but also reduce left ventricular afterload and ensure pulsatile perfusion of pulmonary artery.

Evaluation of the Oxiris Membrane in Cardiogenic Shock Requiring Extracorporeal Membrane Oxygenation Support: Study Protocol for a Single Center, Single-Blind, Randomized Controlled Trial.

Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is the rescue treatment proposed to patients with refractory cardiogenic shock. The VA-ECMO implantation promotes inflammation and ischemia-reperfusion injuries through the VA-ECMO flow, causing digestive mucosa barrier disrupture and inducing translocation of bacterial wall components—Lipopolysaccharides (LPS) with further inflammation and circulatory impairment. LPS is a well-studied surrogate indicator of bacterial translocation. Oxiris membrane is a promising and well-tolerated device that can specifically remove LPS. The main study aim is to compare the LPS elimination capacity of Oxiris membrane vs. a non-absorbant classical renal replacement (RRT) membrane in patients with cardiogenic shock requiring VA-ECMO.Methods: ECMORIX is a randomized, prospective, single-center, single-blind, parallel-group, controlled study. It compares the treatment with Oxiris membrane vs. the standard continuous renal replacement therapy care in patients with cardiogenic shock support by peripheral VA-ECMO. Forty patients will be enrolled in both treatment groups. The primary endpoint is the value of LPS serum levels after 24 h of treatment. LPS serum levels will be monitored during the first 72 h of treatment, as clinical and cardiac ultrasound parameters, biological markers of inflammation and 30-day mortality.Discussion: Oxiris membrane appears to be beneficial in controlling the VA-ECMO-induced ischemia-reperfusion inflammation by LPS removal. ECMORIX results will be of major importance in the management of severe cases requiring VA-ECMO and will bring pathophysiological insights about the LPS role in this context.Clinical Trial Registration: www.ClinicalTrials.gov, identifier: NCT04886180.

Effect of arterial oxygen partial pressure inflection point on Venoarterial extracorporeal membrane oxygenation for emergency cardiac support

BackgroundTemporary circulatory support is a bridge between acute circulatory failure and definitive treatment or recovery. Currently, venoarterial extracorporeal membrane oxygenation (VA-ECMO) is considered to be one of the effective circulatory support methods, although cardiac function monitoring during the treatment still needs further investigation. Inflection point of arterial oxygen partial pressure (IPPaO2) may occur at an early stage in part of patients with a good prognosis after VA-ECMO treatment, and the relationship between time of IPPaO2 (tIPPaO2) and recovery of cardiac function or prognosis remains unclear.MethodsTo investigate this relationship, we retrospectively analyzed the clinical data of 71 patients with different conditions after treatment with VA-ECMO in the emergency center of Jiangsu Province Hospital between May 2015 and July 2020. Spearman’s correlation analysis was used for the correlation between tIPPaO2 and quantitative data, and ROC curve for the predictive effect of tIPPaO2 on the 28-day mortality.ResultsThirty-five patients were admitted because of refractory cardiogenic shock (26 of 35 survived) and the remaining 36 patients due to cardiac arrest (13 of 36 survived). The overall survival rate was 54.9% (39 of 71 survived). Acute physiology and chronic health evaluation II, ECMO time, tIPPaO2, continuous renal replacement therapy time, mechanical ventilation time, and bleeding complications in the survival group were lower than those in the non-survival group, with length of stay, intensive care unit stay, and platelet levels were being higher. The tIPPaO2 was negatively correlated with ejection fraction, and the shorter tIPPaO2 resulted in a higher 28-day survival probability, higher predictive value for acute myocardial infarction and fulminant myocarditis.ConclusionsTherefore, tIPPaO2 could be a reliable qualitative indicator of cardiac function in patients treated with VA-ECMO, which can reveal appropriate timing for adjusting VA-ECMO flow or weaning.Trial registrationChiCTR1900026105.

Vortex dynamics of veno-arterial extracorporeal circulation: A computational fluid dynamics study

Veno-arterial extra corporeal membrane oxygenation (VA-ECMO) is a modified heart lung machine used for patients with both heart and lung failure. This results in retrograde supply of oxygenated blood through the femoral artery in which the unsteady pulsating antegrade flow from the aorta interacts with a steady, uniform, and retrograde flow from the femoral artery, creating a mixing zone. This work aims to provide a mechanistic interpretation of VA-ECMO by developing an in-silico framework using computational fluid dynamics. We performed several numerical simulations to investigate the effects of aortic geometry on VA-ECMO by implementing two idealized full aorta models and studied the formation of secondary flow features and vortices. We used vortex identification methods to capture the three-dimensional vortical structures formed under various ECMO support levels. Our results show that under pulsatile aortic flow and 80% of ECMO support, the streamwise vorticity and aortic arch geometry strongly influence the mixing zone. Furthermore, we found that pulsatility at the aortic inlet causes oscillation in secondary flow structures at the abdominal aorta leading to unsteadiness in ECMO flow and differential wall shear stress. We also examined the effects of VA-ECMO flow rates on secondary flow and vortical structures. We show that the location and complexity of secondary flows and vortical structures are affected by ECMO support levels and geometry of aortic segments. Together, we believe that this computational framework is a crucial step in understanding flow features and vortical structures formed during VA-ECMO administration, which can improve patient care and ECMO management.

Impact of Venoarterial Extracorporeal Membrane Oxygenation Flow on Outcomes in Cardiogenic Shock.

Venoarterial extracorporeal membrane oxygenation (VA ECMO) is used to provide cardiopulmonary support in cardiogenic shock; however, high extracorporeal flow may increase left ventricular (LV) afterload leading to LV distention and intracardiac stasis. It is unclear how ECMO flow affects patient outcomes and complications related to ECMO. Retrospective review of patients at a single institution placed on VA ECMO from 2007 to 2018 was performed. Patients were divided into full flow (flow index > 2.2 L/min/m2) and partial flow (flow index < 2.2 L/min/m2) groups. In-hospital mortality and markers of end-organ perfusion were compared between groups balanced for risk factors using propensity score inverse probability of treatment weighting. ECMO-related complications such as LV distention, limb ischemia, and bleeding were recorded. There were 488 patients included, 405 (83%) in the partial flow group, and 83 (17%) in the full flow group. No major differences in age, gender, or comorbidities were found. There was no difference in in-hospital mortality between groups (51% vs. 55%, p = 0.59). At 72 hours post-ECMO initiation, there was no difference in the change in renal, hepatic function, or lactate from baseline nor in the rates of continuous venoveno hemofiltration initiation (p = 0.41). There was a trend towards the decreased incidence of LV distention requiring LV vent placement in the partial flow group (12% vs. 7%, p = 0.16). Compared with full flow VA ECMO, partial flow VA ECMO in carefully selected patients results in similar in-hospital mortality and provides similar end-organ perfusion for the treatment of refractory cardiogenic shock.

Prevention and treatment of pulmonary congestion in patients undergoing venoarterial extracorporeal membrane oxygenation for cardiogenic shock.

Cardiogenic shock is still a major driver of mortality on intensive care units and complicates ∼10% of acute coronary syndromes with contemporary mortality rates up to 50%. In the meantime, percutaneous circulatory support devices, in particular venoarterial extracorporeal membrane oxygenation (VA-ECMO), have emerged as an established salvage intervention for patients in cardiogenic shock. Venoarterial extracorporeal membrane oxygenation provides temporary circulatory support until other treatments are effective and enables recovery or serves as a bridge to ventricular assist devices, heart transplantation, or decision-making. In this critical care perspective, we provide a concise overview of VA-ECMO utilization in cardiogenic shock, considering rationale, critical care management, as well as weaning aspects. We supplement previous literature by focusing on therapeutic issues related to the vicious circle of retrograde aortic VA-ECMO flow, increased left ventricular (LV) afterload, insufficient LV unloading, and severe pulmonary congestion limiting prognosis in a relevant proportion of patients receiving VA-ECMO treatment. We will outline different modifications in percutaneous mechanical circulatory support to meet this challenge. Besides a strategy of running ECMO at lowest possible flow rates, novel therapeutic options including the combination of VA-ECMO with percutaneous microaxial pumps or implementation of a venoarteriovenous-ECMO configuration based on an additional venous cannula supplying towards pulmonary circulation are most promising among LV unloading and venting strategies. The latter may even combine the advantages of venovenous and venoarterial ECMO therapy, providing potent respiratory and circulatory support at the same time. However, whether VA-ECMO can reduce mortality has to be evaluated in the urgently needed, ongoing prospective randomized studies EURO-SHOCK (NCT03813134), ANCHOR (NCT04184635), and ECLS-SHOCK (NCT03637205). These studies will provide the opportunity to investigate indication, mode, and effect of LV unloading in dedicated sub-analyses. In future, the Heart Teams should aim at conducting a dedicated randomized trial comparing VA-ECMO support with vs. without LV unloading strategies in patients with cardiogenic shock.

Mechanical circulatory support in refractory cardiogenic shock due to influenza virus-related myocarditis.

BackgroundThere is scarce evidence for mechanical circulatory support (MCS) in patients with influenza-related myocarditis complicated by refractory cardiogenic shock (rCS). We sought to investigate the impact of MCS using combined veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and micro-axial flow pumps (the ECMELLA concept) in influenza-related myocarditis complicated by rCS.MethodsThis is a prospective, observational analysis from the single centre HAnnover Cardiac Unloading REgistry (HACURE) from two recent epidemic influenza seasons. We analysed patients with verified influenza-associated myocarditis complicated by rCS who were admitted to our intensive care unit (ICU) on MCS. Subsequently, we performed a propensity score (PS) matched analysis to patients with acute myocardial infarction (AMI) complicated by rCS and non-ischaemic cardiomyopathy (DCM) related rCS.ResultsWe describe a series of seven patients with rCS-complicated influenza-related myocarditis (mean age 56±10 years, 58% male, influenza A (n=2)/influenza B (n=5)). No patient had been vaccinated prior to the influenza season. MCS was provided using combined VA-ECMO and Impella micro-axial flow pump. In two patients with out-of-hospital cardiac arrest, VA-ECMO had been implanted for extracorporeal cardiopulmonary resuscitation. All patients died within 18 days of hospital admission. By PS-based comparison to patients with AMI- or DCM-related rCS and combined MCS, 30-day mortality was significantly higher in influenza-related rCS.ConclusionDespite initial stabilisation with combined MCS in patients with rCS-complicated influenza-related myocarditis, the detrimental course of shock could not be stopped and all patients died. Influenza virus infection potentially critically affects other organs besides the heart, leading to irreversible end-organ damage that MCS cannot compensate for and, therefore, results in a devastating outcome.

Determining the impacts of venoarterial extracorporeal membrane oxygenation on cerebral oxygenation using a one-dimensional blood flow simulator

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is a mechanical system that provides rapid and short-term support for patients with cardiac failure. In many patients, pulmonary function is also impaired, resulting in poorly-oxygenated cardiac outflow competing against well-oxygenated VA-ECMO outflow, a condition known as North-South syndrome. North-South syndrome is a primary concern because of its potential to cause cerebral hypoxia, which has a critical influence on neurological complications often seen in this patient population. In order to reduce ischemic neurological complications, it is important to understand how clinical decisions regarding VA-ECMO parameters influence blood oxygenation. Here, we studied the impacts of flow rate and cannulation site on oxygenation using a one-dimensional (1D) model to simulate blood flow. Our model was initially tested by comparing blood flow results to those observed from experimental work in VA-ECMO patients. The 1D model was combined with a two-phase flow model to simulate oxygenation. Additionally, the influence of various other clinician-tunable parameters on oxygenation in the common carotid arteries (CCAs) were tested, including, blood viscosity, cannula position within the insertion artery, heart rate, and systemic vascular resistance (SVR), as well as geometrical changes such as arterial radius and length. Our results indicated that blood oxygenation to the brain strongly depended on the cannula insertion site and the VA-ECMO flow rate with a weaker but potentially significant dependence on arterial radius. During femoral cannulation, VA-ECMO flow rates greater than ~4.9L/min were needed to perfuse the CCAs. However, axillary and central cannulation began to perfuse the CCAs at significantly lower flow (~1L/min). These results may help explain the incidence of cerebral hypoxia in this patient population and the common need to change cannulation strategies during treatment to address this clinical problem. While this work describes patient-averaged results, determining these relationships between VA-ECMO parameters and cerebral hypoxia is an important step towards future work to develop patient-specific models that clinicians can use to improve outcomes.

Transcranial Doppler is an effective method in assessing cerebral blood flow patterns during peripheral venoarterial extracorporeal membrane oxygenation.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) can be life-saving in refractory cardiogenic shock but carries a risk of neurologic complications such as stroke and hemorrhage. As little is known about the effects of different peripheral VA-ECMO cannulation sites on cerebral blood flow (CBF), transcranial Doppler (TCD) was used to determine whether the cannulation site affects CBF. Thirty-seven patients receiving VA-ECMO for cardiogenic shock via axillary or femoral artery cannulation were prospectively enrolled. Measured bilateral middle cerebral artery (MCA), mean flow velocities (MFV), and pulsatility indices (PI) were the primary outcomes and adverse neurologic events were secondary outcomes. The median age was 58 years (IQR 51-66) with 26 (70%) males. Median VA-ECMO flow was 3.8 L/min (IQR 3.2-4.9) with mean arterial pressures of 80 mm Hg (IQR 75-86). Nineteen patients received right axillary artery cannulation while 18 underwent femoral cannulation. Compared with the femoral group, MFV was higher in the axillary group in the right MCA (46 cm/s [IQR 26-57] vs 27 [17-36], P = 0.03) and left (43 [IQR 35-60] vs 29 cm/s [16-48], P = 0.05). Axillary PI was significantly lower compared with the femoral group (right: 0.48 cm/s [0.25-0.65] vs 0.83 [0.66-0.93], P = 0.02; left: 0.41 cm/s [0.29-0.63] vs 1.02 [0.7-1.3], P = 0.004). One axillary patient experienced a stroke with deficits. TCD appears to be an effective tool for indirect monitoring of CBF in patients withECMO with limited pulsatility. Axillary artery cannulation seems to provide higher cerebral flow rates without any difference in neurologic outcomes. Future studies may incorporate TCD into regulating ECMO flows to achieve physiologic CBF.

Detection of microembolic signals in the common carotid artery using Doppler sonography in the porcine model of acute heart failure treated by veno-arterial extracorporeal membrane oxygenation.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a method used for the treatment most severe cases of decompensated heart failure. The purpose of this study was to evaluate the risk of the formation of microembolisms during VA-ECMO-based therapy. Heart failure was induced with simultaneous detection of microembolisms and the measurement of blood flow rate in the common carotid artery (CCA) without VA-ECMO (0 l/min) and at the VA-ECMO blood flow rate of 1, 2, 3 and 4 l/min. If embolisms for VA-ECMO 0 l/min and the individual regimes for VA-ECMO 1, 2, 3, 4 l/min are compared, a higher VA-ECMO flow rate is accompanied by a higher number of microembolisms. The final microembolism value at 16 min was for the VA-ECMO flow rate of 0 l/min 0.0 (0, 1), VA-ECMO l/min 7.5 (4, 19), VA-ECMO 2 l/min 12.5 (4, 26), VA-ECMO 3 l/min, 21.0 (18, 57) and VA-ECMO 4 l/min, 27.5 (21, 64). Such a comparison is statistically significant if VA-ECMO 0 vs. 4 l/min p<0.0001, 0 vs. 3 l/min p<0.01 and 1 vs. 4 l/min p<0.01 are compared. The results confirm that high VA-ECMO flow rates pose a risk with regards to the formation of a significantly higher number of microemboli in the blood circulation and that an increase in blood flow rates in the CCA corresponds to changes in the VA-ECMO flow rates.

Coronary arterial perfusion during venoarterial extracorporeal membrane oxygenation

The effects of venoarterial extracorporeal membrane oxygenation on left ventricular performance have not been studied in detail. Coronary arterial flow obtained by direct measurement with an electromagnetic flowmeter and blood gas analysis from the aortic root were tabulated during venoarterial extracorporeal membrane oxygenation in 14 puppies, and these parameters were evaluated with respect to changes in the venoarterial extracorporeal membrane oxygenation flow. Unique automatic blood pumps generating pulsatile flow were used for the venoarterial extracorporeal membrane oxygenation bypass. Coronary arterial flow decreased as the extracorporeal membrane oxygenation flow increased (106 ± 26 ml/min per 100 gm of left ventricle at 20 ml · min -1 · kg bypass flow to 71 ± 17 ml/min per 100 gm of left ventricle at 100 ml · min -1· kg bypass flow, p < 0.01). There were no significant changes in the mean or diastolic pressures in the ascending aorta despite changes in the extracorporeal membrane oxygenation flow. Arterial oxygen tension in the ascending aorta was not increased even under high-flow venoarterial extracorporeal membrane oxygenation. This result indicates that oxygenated blood from the extracorporeal membrane oxygenation circuit does not pass in a retrograde fashion into the aortic root and thus does not perfuse the coronary arteries. The diastolic aortic pressure did not correlate with the changes in extracorporeal membrane oxygenation flow. The decrease in coronary arterial flow is therefore predominantly caused by increased coronary arterial resistance. Tension-time index, an indicator of myocardial oxygen consumption, did not decrease with venoarterial extracorporeal membrane oxygenation. In conclusion, high-flow venoarterial extracorporeal membrane oxygenation causes undesirable hemodynamic effects on the left ventricle. (J T HORAC C ARDIOVASC S URG 1996;111:630-6)