First experiences with a combined usage of veno-arterial and veno-venous ECMO in therapy-refractory cardiogenic shock patients with cerebral hypoxemia

Abstract

The use of extracorporeal membrane oxygenation (ECMO) is becoming a popular tool in the treatment of cardiogenic shock. We present two case reports where classical veno-arterial peripherally cannulated ECMO therapy proved insufficient with profuse cerebral hypoxemia. After augmenting the setting into veno-veno-arterial ECMO, we achieved a remarkable improvement of all oxygenation parameters. The simultaneous use of veno-venous and veno-arterial ECMO might display as a novel strategy to counteract the coronary and cerebral hypoxemia in veno-arterial ECMO therapy in patients with therapy-refractory cardiogenic shock or in combined cardiopulmonary failure. In this manuscript, the veno-veno-arterial ECMO setup is described in full detail and different venous cannulas are discussed.

Keywords

veno-arterial ECMO veno-venous ECMO veno-veno-arterial ECMO combined ECMO ECMO bypass cardiopulmonary failure cardiogenic shock ECMO cerebral hypoxemia

Introduction

Cardiogenic shock complicates approximately 5% to 8% of ST segment elevation myocardial infarction (STEMI) and 2.5% of non-STEMI cases.¹ Despite current advances in medicine and the implementation of state-of-the-art management guidelines, cardiogenic shock remains the leading cause of death in hospitalized patients, regardless of etiologies.^2-9 Mortality remains high, approaching 70% in some settings. Recent management strategies have incorporated the use of mechanical circulatory support, which has been associated with better survival in non-randomized trials. Mechanical circulatory support (intra-aortic balloon counterpulsation [IABP], left ventricular assist device [LVAD], extracorporal membrane oxygenation [ECMO]) is increasingly used in the acute setting and has become an important treatment modality for cardiogenic shock.¹⁰ IABP Shock II trial results, however, suggest that the use of IABP did not significantly reduce 30-day mortality in patients with cardiogenic shock due to acute myocardial infarction.¹¹ Additionally, despite non-pulsatile LVAD being reported as providing superior hemodynamic support compared with IABP for cardiogenic shock,^12-16 it is costly and requires cardiopulmonary bypass and ventriculotomy for implantation. Besides, the complexity and prolonged duration of the procedure also limits its application as an emergent life-saving device in patients with cardiogenic shock. Of importance is the fact that the potential risk of right heart failure with LVAD use is also a challenge, especially in high-risk candidates for LVAD.^17-19

In contrast, ECMO provides immediate and adequate systemic circulation and oxygenation while being much simpler and requiring less time to complete compared with LVAD.^8,9,20 ECMO is not a cure, it is a life-support system that creates time for evaluation, diagnosis and treatment of the condition that caused the heart, lung or combined organ failure. Hill et al. reported the first successful ECMO case in an adult patient with respiratory failure in 1972.²¹ Resurrection of interest in ECMO therapy in acute respiratory distress syndrome (ARDS) was due to a worldwide epidemic of H1N1 from the year 2009. As the authors of the latest randomized controlled trial CESAR (conventional vs. ECMO Therapy in ARDS) conclude, transferring adult patient with severe, but potentially reversible, respiratory failure to centers specializing in the treatment of severe respiratory failure for consideration of ECMO significantly increased survival without severe disability. The academic proof was furnished that ECMO therapy in trained hospitals improves the outcome of severely ill patients. Furthermore, the use of ECMO is likely to be cost-effective when compared with other technologies currently competing for health resources.²²

The classification of ECMO implementation contains, on the one hand, central cannulation and, on the other hand, peripheral cannulation. The results of a retrospective study comparing peripheral versus central cannulation in ECMO, carried out by Kanji et al., suggests that there is comparable tissue perfusion and limb ischemia with both cannulation techniques. Central cannulation is associated with a higher incidence of bleeding due to the need of sternotomy, higher transfusion rates, a greater possibility for re-operation and greater resource utilization due to the need of a cardiac surgeon, an operating theatre and perfusionists.²³ Therefore, peripheral cannulation is safe and advantageous, especially during emergency scenarios.^24-26 (Table 1). Apart from lower limb ischemia, the essential disadvantage of peripheral cannulation is supracoronary and coronary hypoperfusion (despite adequate positioning of the cannula in the aortic vessel), leading, consecutively, to hypoxemia and ischemia in the brain and heart due to insufficiently oxygenated reversed blood flow being generated by the extracorporal pump, which is contrary to the physiological bloodstream. Even though animal studies report about adequate oxygenation of cerebral and coronary tissue by peripherally cannulated ECMO systems,²⁷ clinical experience showed the opposite results with strokes and postapoplectic intracerebal bleeding or large myocardial necrosis.²⁸

Table 1.

Positive (+) and negative (-) aspects of peripheral vs. central cannulation in ECMO.

Peripheral cannulation	Central cannulation
+ cannulation through the Seldinger technique	+ antegrade Flow
+ anywhere implantable	+ homogenous blood flow distribution
+ easy explantation	+ mobilization possible
+ fast implantation
- retrograde flow in the aortic vessel (CAVE: ARDS)	- sternotomy and re-sternotomy inevitable
- danger of limb/arm ischemia	- dangerous bleeding
- non-homogenous blood flow distribution	- arrhythmias
- danger of arterial vessels injury	- aortic wall damage
- mobilization very limited

Here, we present two case reports reflecting our experience and clinical approach to ECMO therapy in patients with therapy refractory cardiac and pulmonary failure without the possibility of sternotomy (due to highly unstable medical condition) where a peripherally cannulated veno-arterial ECMO system brought no improvement.

Postulation

– By additionally attaching a venous cannula aligned away from the pump in the vena subclavia or jugularis interna, venous blood will be more sufficiently oxygenated. In consequence, oxygenation of pulmonary artery blood will decrease hypoxia-induced vasoconstriction and pulmonary artery pressure, thus, achieving a very positive effect in the therapeutic strategy, especially in patients with ARDS, pulmonary hypertension and right heart failure.

– Moreover, by enriching venous blood with oxygen via veno-veno-arterial ECMO, ventilator strategies with high peak and mean pressures can be avoided. Therefore, v-v-a ECMO facilitates a reduction in intrathoracic pressure through a reduction in mechanical ventilation, which may also improve right ventricular function.

– Through streaming oxygenated blood into the heart, we also presumably achieve an adequate oxygenation supply to the myocardium and supracoronary vessel via increasing perfusion of oxygen-rich blood through the coronary arteries and arteriae carotides communes and vertebrales, thus, improving the cardiovascular function and neurologic outcome of the patient.

Case Reports

Case 1

A female patient of 74 years of age was admitted to a primary hospital with dyspnoea and a worsened general state of health. In her medical history, we discovered a pulmonary fibrosis (with pulmonal hypertension) that was neither fully diagnosed nor treated. Prior to current conditions, the patient lived alone, capable of managing her household on her own.

This patient was diagnosed and treated for pneumonia, but developed a general septic state with refractory septic shock, thus, complete respiratory, as well as circulatory, failure. Our ECMO center was contacted and, after verifying the diagnosis and excluding contraindications, the decision was made to implant a peripheral veno-arterial ECMO (due to refractory shock with very high doses of catecholamines: norepinephrine at a rate of 1.2 µg/kg/min combined with dobutamine at 6.0 µg/kg/min) on site, at the intensive care unit (ICU) of the primary providing hospital. After transferring the patient to our ICU at the University Hospital in Halle/Saale, she developed a steady state of gas exchange and intracerebral perfusion saturation of oxygen measured through the near-infrared spectrum (right 67%/left 66%) at a ventilator FiO₂ of 0.6 (ECMO FiO₂ 0.6). Arterial blood gases (A.radialis dextra) showed PaO₂10.5 kPa/PaCO₂ 5.3kPa, with a peripheral saturation of oxygen 94-95%. On the 3^rd ICU day, a worsening of oxygenation, measured by near-infrared spectrography, right 43%/left 44%, pulse oxymetry on the right hand 89%, and also in the blood gas analysis (PaO₂7.2 kPa/PaCO₂ 4.5 kPa) under the ventilator FiO₂ 1.0 and ECMO FiO₂ 1.0, took place (Figures 1, 2). Due to a largely compromised coagulation and a highly unstable cardiovascular situation, we decided to modify the v-a ECMO to “shunt” the circulation and augment the v-a ECMO - at the same time and with the same machine - into a veno-veno-arterial ECMO via a “ductus” (see Method/system setup below for explanation) as an ultima ratio decision to allow adequate oxygen supply to the myocardium and supracoronary vessels. What we achieved was a spectacular improvement of all oxygenation parameters, as follows: peripheral saturation of 99%, near-infrared spectrum (right 73%/left72%), PaO₂ 13.5kPa/PaCO₂ 4.6 kPa and a reduction of ventilator FiO₂ to 0.5, as well as pressure support as seen in the Figures 1 and 2 (Peak pressure 36 cmH₂0 → Peak pressure 22 cmH₂O). This improvement remained constant for the rest of the patient’s treatment; the ventilator support did not need to be escalated.

The patient was successfully weaned off ECMO, however, died a short time later due to the general health condition of lung fibrosis and septic pneumonia.

The patient had been treated for 9 days with ECMO therapy.

Case 2

A 54-year-old male patient was admitted to a secondary hospital with a gradually worsening dyspnoea. The patient had no cardiac history. Transesophageal echocardiogram (TEE) at admission showed a highly pathological left ventricular ejection fraction of 10-15% and the left ventricle was massively dilated. The patient was obese (134 kg), a heavy smoker and a former alcohol abuser. Chronic obstructive pulmonary disease (COPD) and sleep-apnoea syndrome were also in the history.

Since the heart enzymes were also elevated (electrocardiogram (ECG) with no signs of a transmural lesion), a heart catheter examination was performed, during which the patient decompensated and needed to be resuscitated (10 minutes). The examination showed no relevant coronary vessel stenosis and an IABP was implanted. Our ECMO center was contacted and decided to implant a v-a ECMO due to a high-grade cardiomyopathy of yet unknown origin. The patient was then transferred to the University Hospital under nor-adrenergic and adrenergic circulatory support (epinephrine 0.1µg/kg/min, norepinephrine 0.3µg/kg/min) and ECMO therapy.

On the 3^rdday, the general state of the patient deteriorated drastically and it was impossible to secure sufficient oxygenation, measured on the right hand (A.radialis dextra). Pulse oximetry showed a drop to 86% and a respective worsening in blood gas analysis was detected; PaO₂ of only 6.0 kPa despite maximum ECMO support and an FiO₂ of 1.0 on ECMO, as well as on the ventilator. The PaCO₂ remained oscillating at 5.5 kPa. Unfortunately, this patient did not have near-infrared INVOS measuring, but, based on the values of the arterial blood gases, we could assume cerebral and coronary hypoxia, so we decided again, as an ultima ratio, to use the additional “ductus” and create a veno-veno-arterial ECMO system. The improvement in oxygenation was immediate and long-lasting (Figures 3 and 4). Peripheral oxygen saturation showed 100%, the PaO₂ increased to 12.4 kPa, and the PaCO₂ remained stable at 4.5kPa, so that we were able to reduce the FiO₂ values on the ventilator as well as on ECMO and we could significantly reduce the ventilatory pressure support, as can be seen in Figure 4. ECMO therapy with the v-v-a setup continued for four days, was then switched back to v-a setup for an additional six days, after which it was then weaned off without any complication. This patient recovered fully, with no functional neurological deficits, and was discharged from the hospital after eight weeks of additional supportive therapy.

Method

System Setup

In order to avoid sternotomy and possible complications with the central cannulations, we decided to leave the peripheral arterial cannula in situ and created an extra shunt from the arterial line of the existing ECMO system to a larger-bored Shaldon catheter (Vygon Trylise Expert Highflow Catheter, VYGON GmbH & Co. KG, Aachen, Germany) already placed in a jugular internal vein for hemofiltration (Figures 5, 6). The aim was to increase the flow of oxygenated blood in the pulmonary circulation, thus, boosting the central venous oxygen saturation and reducing the pulmonary hypoxic vasoconstriction and afterload of the right ventricle and also to augment the oxygen supply of the coronary arteries and supracoronary branches.

Indeed, implementing an additional oxygen-rich tube in a central vein spectacularly and directly improved peripheral saturation in the right arm, cerebral oxygen saturation and PaO₂ as well as PaCO₂ removal and reduced invasivity and inspiratory oxygen supply of the ventilator. This ultima ratio decision secured sufficient cerebral and coronary oxygenation, enabled the restricted and congested heart to recover by unloading the right ventricle, reduced hypoxic pulmonary vasoconstriction and facilitated the de-escalation of ventilation strategies.

Measuring cerebral oxygen saturation by near-infrared spectrum is considered to be the best method to investigate cerebral tissue oxygenation and to define critical hypoxemia of the brain in patients with ECMO, because its usefulness in monitoring cerebral hypoxia was reported recently and allows continuous monitoring.^29-32

To create the shunt (“ductus”) mentioned above, we connected an extra 3/8” line via a Y-connector with the pre-existing arterial line of our ECMO system (Figure 8). The 3/8” line was then reduced to a Luer-lock, using the special perfusion adapter (CalMed^® Perfusion Adapter, CalMed Laboratories, MediMark Europe, Grenoble Cedex2, France), and was subsequently connected to a max-flow 4-way stop-cock (Medfusion^®, Smith Medical Deutschland GmbH, Grasbrunn, Germany) of the large-bored catheter (Shaldon catheter, see Figure 8). In order to use the second lumen of the Shaldon catheter, we connected a 3/16” line to this lumen. In both cases, a 12Fr Vygon Trilyse Expert^® Highflow catheter was used, which is specially designed to master high flows and pressures up to 1000 mmHg.³³ To prevent the arterialized blood being siphoned back through the venous 24Fr cannula placed in the vena cava superior (of the ECMO system), we pulled this venous cannula a few centimeters (10cm) caudally and positioned it in the vena cava inferior (10cm caudally of the atriosuperior vena caval junction). The position of the cannula was detected by X-ray (Figure 7). Alternatively, TEE guidance could be used. To assure that the ECMO venous line aspirated no arterialized blood, blood gas analysis before and after perfusing the extra line was carried out (samples taken from the arterial line before the oxygenator) and the oxygen saturations were compared.

Using the 3/8” line enabled us to measure simultaneously the exact flow in the Shaldon catheter, as well as in the arterial line, so that we could state and quantify the actual lung and heart support. We measured flow to the femoral artery (5 liters per minute [LPM]) with the integrated flow meter of the Levitronix system (Thoratec Europe Limited, Huntingdon, Cambridgeshire, UK) and placed a second flowmeter on the “ductus” line (measured flow of 1.2 LPM) to the Shaldon catheter. Another advantage of using the 3/8” line was the reduction in flow resistance and the optimal inflow of a rather small lumen Shaldon catheter. In this matter, a flow of up to 1.2 LPM and a pressure of 260 mmHg could be achieved through the Vygon^® catheter.

Discussion

Circulatory supporting devices, such as an IABP and an LVAD, counteract the effects of cardiogenic shock. The IABP is fast and simple to apply and increases coronary blood flow. However, its effectiveness was challenged in cases of cardiac arrest or ventricular arrhythmia.^11,34,35 The LVAD can also be effective, but requires an additional surgical procedure, more time and is, therefore, unsuitable in cases of emergency. Recently, an LVAD that can be applied percutaneously has become available; however, additional equipment and procedures are required in order to apply the LVAD.³⁶ Although percutaneous LVAD provides superior haemodynamic support in patients with cardiogenic shock compared with IABP, the use of these more powerful devices did not improve early survival. Therefore, these results do not yet support percutaneous LVAD as the first-choice approach in the mechanical management of cardiogenic shock. Since the advent of the percutaneous approach for ECMO, it has shown good results and shown that it can be applied quickly. Recent trials reported that cardiopulmonary resuscitation (CPR) with ECMO showed better results than CPR without ECMO when CPR was required for over 10 minutes.^9,38

The comparison between the central and peripheral cannulation, as well as the pros and cons of the two cannulation techniques, were described above. The essential disadvantage of peripheral cannulation in v-a ECMO setup is possible supracoronary and coronary hypoperfusion, leading consecutively to hypoxemia and ischemia in the brain and heart.²⁸ In order to solve these complications occurring in our case reports, we searched for a different, less-invasive solution to enhancing cerebral and coronary oxygenation.

The modified design of a veno-veno-arterial ECMO allows adequate oxygenation supply, especially to the myocardium and brain, in cardiogenic shock patients with otherwise no further opportunity to improve cerebral and coronary oxygenation. Furthermore, v-v-a ECMO enabled the restricted heart to recover, reduced hypoxic pulmonary vasoconstriction and facilitated ventilation strategy de-escalation. It is of utmost importance to prevent the arterialized blood being siphoned back through the venous cannula placed in the superior vena cava (of the ECMO system). The position of the cannulas has to be checked by X-ray or, alternatively, by TEE guidance.

In our two case reports, we used a Shaldon (Vygon Trilyse Expert^®) catheter as the bypass line. Prospectively, we plan to test more large-bored catheters with a bigger internal diameter of the lumen (Edwards AVA Highflow catheter^®), but with a smaller external diameter (9 French). In preliminary experiments, we achieved 60% higher flow rates compared to the catheter mentioned above. In the above cases, we consciously decided against the special perfusion single-lumen cannulas, as by using the multi-lumen catheter (Vygon^®) parallel to the ECMO therapy, additional drug application or even dialysis could be performed simultaneously.

During the therapy with the new setup, we could only observe minor system vulnerabilities on the max-flow stop-cocks which, in spite of the pressure limitations of 2 bar (according to the manufacturer), showed small leakages and they had to be exchanged at 48-hours intervals. However, another great advantage of the Shaldon catheter is the self-limiting maximum flow of 1.2 LPM through the bounded lumen without the need of any additional (regulatory) device. However, in specific situations, higher veno-venous blood flow rates are necessary to ensure adequate oxygenation and perfusion. Therefore, in each patient, an individual perfusion strategy should be considered. Treating patients with hypercapnia-associated problems and exorbitantly elevated ventilatory peak pressures, implementation of an additional veno-venous bypass with a Shaldon catheter is, in our point of view, satisfactory. In contrast, dealing with a preferentially oxygenation problem, veno-venous blood flow rates of 1.2 LPM or less could be insufficient, so that large-bored catheters (e.g. a 16 French perfusion cannula) are required to guarantee sufficient oxygenation.

So, in patients with a high cardiac output, a flow of 1.0 - 1.5 LPM would not suffice; in this case, we recommend the implantation of a 16 Fr. cannula in the vena subclavia instead of a Shaldon catheter; we carried it out in a 3^rd patient where we had increased the flow up to 2.5 LPM by using the following cannulas:

venuous femoral: 24 Fr. (total 6.5. LPM), arterial femoral: 19 Fr. (4LPM), venous subclavian: 16 Fr. (2.5 LPM).

This patient was successfully weaned off after 12 days and was discharged from the hospital 3 weeks later.

However, increasing the blood flow via the additional shunt is fraught with possible problems as, firstly, right ventricular dysfunction can develop by the increasing right ventricular preload, secondly, venous cerebral drainage could be encumbered and thirdly, the blood volume of the arterial line of the ECMO system could become insufficient to ensure an adequate perfusion.

An extremely important supportive procedure in the therapy for the compromised lungs is the patient’s positioning.

Another option to the approach of this problem, presented in both case reports above, would be the cannulation of the subclavian or axillary artery, thus, achieving sufficient perfusion and oxygenation of the supracoronary vessels. Sufficient coronary artery supply, however, is not guaranteed. Moreover, hyperperfusion of the arm and, possibly, of the head when simultaneously compromised venous drainage is present, could lead to interstitial edema with congestion, as proved in the axillary artery side graft study by Chamogeorgakis et al.³⁸ This technique also presents a potential risk of vessel damage, the possibility of a steal phenomenon and is mostly engineerable by additional surgery through inserting a tubular prosthesis on the subclavian/axillary artery to connect the ECMO tube.^39-41

Taken together, v-v-a ECMO is neither the “magic bullet” for the treatment of therapy-refractory cardiogenic shock nor the unique potential to guarantee adequate cerebral and cardiac oxygenation without causing further ventilator-associated lung damage. However, v-v-a ECMO creates an appropriate treatment option and offers these patients more time to recover without triggering organ damage or failure. However, currently, the European Society of Cardiology/European Association for Cardio-Thoracic Surgery (ESC/EACTS) guidelines recommend a consideration of ECMO implantation for temporary support only in patients continuing to deteriorate after IABP implantation where adequate circulation cannot be maintained.⁴² The American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines published in 2011 and the Society for Cardiovascular Angiography and Interventions (ACCF/AHA/SCAI) guidelines even advise a hemodynamic support device if the patient does not stabilize quickly with pharmacological therapy; however, with no recommendation for ECMO systems (only the Impella, the TandemHeart and the IABP).⁴³ Though these strong recommendations are not substantiated by any robust clinical evidence and should, therefore, be re-evaluated, in the future, large randomized trials need to show the effect of different percutaneous mechanical assist devices on mortality in cardiogenic shock patients.⁴⁴

Footnotes

Declaration of conflicting interest

The authors have no conflicts of interest to declare.

Funding

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

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