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Central extracorporeal life support with left ventricular decompression for the treatment of refractory cardiogenic shock and lung failure
© Weymann et al.; licensee BioMed Central Ltd. 2014
Received: 13 January 2014
Accepted: 24 March 2014
Published: 29 March 2014
The purpose of this prospective study was to evaluate the effects and functional outcome of central extracorporeal life support (ECLS) with left ventricular decompression for the treatment of refractory cardiogenic shock and lung failure.
Between August 2010 and August 2013, 12 consecutive patients (2 female) with a mean age of 31.6 ± 15.1 years received central ECLS with left ventricular decompression for the treatment of refractory cardiogenic shock and lung failure. Underlying disease was acute cardiac decompensation due to dilated cardiomyopathy (n = 3, 25%), coronary artery disease with acute myocardial infarction (AMI) (n = 3, 25%), and acute myocarditis (n = 6, 50%). We routinely implemented ECLS by cannulating the ascending aorta, right atrium and inserting a left ventricular decompression cannula vent via the right superior pulmonary vein.
All patients were successfully bridged to either recovery (n = 3, 25%), long-term biventricular support (n = 6, 50%) or cardiac transplantation (n = 3, 25%). Seven patients (58.3%) were discharged after a mean hospital stay of 42 ± 11.9 days. The overall survival from ECLS implantation to the end of the study was 58.3%. The cumulative ICU stay was 23.1 ± 9.6 days. The length of support was 8.0 ± 4.3 days (range 3-17 days).
We strongly recommend left ventricular decompression in refractory cardiogenic shock and lung failure to avoid pulmonary edema, left heart distension and facilitate myocardial recovery.
Cardiogenic shock still has an unfavorable prognosis with a mortality rate of 50-80% [1–4]. The prognosis strongly depends on the delay between the compromise and reestablishment of adequate end-organ perfusion. Analysis of the Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) reveals that the proportion of INTERMACS level 1 patients (cardiogenic shock) undergoing long term VAD therapy has decreased from 42% in 2006 to 14% in 2012 due to poor outcomes. This has provided impetus to implement a more effective support strategy, which increasingly is taking the form of a bridge to bridge (salvage) approach using temporary extracorporeal devices in the first instance. Once the patient has been stabilised and has recovered end-organ function, replacement with a long-term support device can be considered .
Extracorporeal Life Support (ECLS) is an indispensable therapy for the acute treatment of patients with cardiogenic shock with or without lung failure. A common problem observed during ECLS is the absence of left heart decompression, which frequently leads to pulmonary edema and left ventricular distension which if untreated can cause subendocardial ischemia.
The purpose of our study was to objectively evaluate our institutional experience of left heart unloading during ECLS using a left ventricular vent with the aim of developing appropriate clinical management strategies and improving outcomes in this patient group.
Study design and patient cohort
n = 12
31.6 ± 15.1
Cardiovascular risk factors
Coronary heart disease
Pulmonary Hypertension > 60 mmHg sys.
LVEF before MCS, %
12.5 ± 5.4
Intra-aortic balloon pump
Cardiac arrest > 30 min
The ECLS weaning procedure consisted of intermittently reducing the blood flow rate, having ascertained that the left ventricle was not akinetic. This not only increased the left ventricular preload but also decreased its afterload, thereby facilitating left ventricle ejection. The feasibility of weaning from ECLS was evaluated by clinical judgment and transesophageal echocardiography at a reduced pump flow after a minimum of 48 hours’ support. All patients underwent daily TEE investigations, and procedural success was defined as a sustained reduction in left ventricular dimensions and an improvement in left ventricular contractility.
Prior to the initiation of ECLS, an unfractionated heparin bolus was administered i.v. at a dose of 300 IU/kg. A similar dose was given if the patient had previously been given heparin which had been fully reversed with protamine. If the patient was on cardiopulmonary bypass at the time ECLS was initiated, ECLS was instituted with full heparinisation. Further unfractionated heparin therapy was not administered in the first instance, and protamine sulphate was only administered if surgical bleeding could not be controlled. In the post-operative period, if bleeding was controlled, a continuous intravenous infusion of unfractionated heparin was initiated immediately. A target activated clotting time range of 130–160 seconds was selected, which was measured. For patients with persistent bleeding, for whom a surgical cause had been excluded, heparin was discontinued and not recommenced until the bleeding was under control.
Results of continuous variables are expressed as mean ± standard deviation. For discontinuous variables absolute and relative frequencies are reported. Statistical software SPSS for Windows 21.0 (SPSS Ing, Chicago, IL, USA) was used for data analysis.
Patient’s characteristics and support strategy
Support duration (d)
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
ECLS with LV vent
The survival on ECLS support was 100%. All patients were successfully bridged to either recovery (n = 3, 25%), long-term biventricular support (n = 6, 50%) or cardiac transplantation (n = 3, 25%) after mean ECLS support of 8.0 ± 4.3 days (range 3-17 days) (Table 2). The mean cumulative ICU stay (including the stay after ECLS explantation or upgrade) was 23.1 ± 9.6 days. Of all twelve cases, seven patients (58.3%) were discharged from hospital after a mean hospital stay of 42 ± 11.9 days and are currently alive. Three patients recovered on ECLS with no recurrence of cardiac decompensation. The overall survival from ECLS implantation to the end of the study was 58.3%. Four patients died in hospital on ongoing long-term BiVAD support after 60 ± 80.25 days. The cause of death was septic multi-organ-failure in two patients and severe refractory acute respiratory distress syndrome (ARDS) in two patients. One patient died of primary graft failure after successful bridging to transplantation with ECLS, resulting in the need for long-term biventricular assist device (BiVAD) support.
The most frequent postoperative adverse events during ECLS were: coagulation disorder (n = 8, 66.7%); refractory renal failure requiring hemodialysis (n = 6, 50%), surgical re-exploration due to bleeding (n = 5, 41.7%) and cerebrovascular event (ischemic stroke) (n = 1, 8.3%). One deep sternal wound infection at the ECLS side occurred during the postoperative course without affecting outcome.
ECLS provides immediate haemodynamic benefit, both in terms of increased mean and diastolic arterial blood pressure. However, this results in an increased systemic afterload, which in the context of poor left ventricular function may result in impaired left ventricular ejection and persistent aortic valve closure. Severe left ventricular distension can ensue which is potentiated by insufficient right atrial drainage, bronchial and Thebesian venous blood flow, aortic valve insufficiency, and extracardiac left to right shunting. This situation can induce a competitive flow and cause an impaired oxygen supply to the coronary arteries and the cerebral vessels. Elevated left ventricular end-diastolic volume and increased myocardial wall stress results in increased myocardial oxygen demand yet reduced perfusion of the coronary arteries. This mismatch can result in subendocardial ischemia, which can impair myocardial recovery [6, 7]. This pathophysiological mechanism can be ameliorated by adequate left ventricular decompression during ECLS.
Furthermore, the absence of direct left ventricular decompression during ECLS under conditions where left ventricular ejection is severely impaired can lead to intraventricular stasis of blood with a resultant risk of thrombus formation. None of our patients showed evidence of left ventricular thrombus during or after ECLS treatment in spite of left ventricular cannulation. Routinely transesophageal echocardiography demonstrated adequate decompression of the left ventricle in all study patients.
In the absence of left ventricular venting, inadequate left ventricular decompression during ECLS can remain undetected for prolonged periods resulting in an elevation of the left-atrial pressure, which can potentially lead to haemoptysis and pulmonary oedema . These complications were not observed in the study cohort. Another advantage of our technique is the ability to perform separate blood gas analyses from both the venous and left ventricular cannula. This allows the monitoring of both recovery of lung function and the timely detection of impaired coronary perfusion under conditions of improved left ventricular function. This problem occurs if, during ECLS the left ventricle starts to eject poorly saturated blood from the lungs into the aortic root resulting in inadequate coronary arterial oxygen saturation. In such circumstances, it is mandatory to increase ventilatory support. It has been shown in an animal model of ECLS with cannulation of the ascending aorta that an adequate oxygen supply of the coronary arteries could only be achieved with high ECLS blood flow rates (85% of calculated maximum) . For that reason, blood gas analysis samples from the left ventricular vent are more informative to those taken from the radial artery.
We believe that continuous monitoring of the cerebral arterial saturation by near-infrared spectroscopy is mandatory for monitoring cerebral perfusion during ECLS. It has been shown that an unregulated increase of the cerebral blood flow increases the risk of spontaneous cerebral haemorrhage during ECLS . Incorrect placement of the aortic cannula in the truncus brachiocephalicus can lead to impaired perfusion of the brain or, at worst, to cerebral oedema and haemorrhage.
Although there are alternative systems for left ventricular unloading like the axial flow Impella® system (Abiomed, Danvers, USA) and the Tandem Heart™ system (CardiacAssist, Pittsburgh, USA), they lack oxygenation capacity and only provide partial unloading of the congested left ventricle. They are deemed unsuitable for patients in refractory cardiogenic shock and respiratory failure [10, 11]. Although left ventricular decompression can be achieved via a percutaneous transaortic/transseptal catheter based system, because of the issues described above and the requirement for cannulae of relatively large diameter, central ECLS support with left ventricular decompression is preferred at our institution.
In recent years, portable miniaturized cardiopulmonary bypass/ECMO devices providing up to 10 l/min of blood flow with gas exchange have become available for the treatment of acute cardiogenic shock. The Lifebridge™ (Lifebridge, San Antonio, USA) and CardioHelp™-System (Maquet, Rastatt, Germany) are compact portable ECMO systems. According to the latest AHA-guidelines, these devices are recommended for patients with cardiogenic shock after STEMI who fail to stabilize rapidly with pharmacological therapy alone (class 1/Level of Evidence B) . Two of our study patients were transported to our centre whilst supported with one of these systems (CardioHelp™-System). Support is implemented by puncturing the groin vessels for peripheral veno-arterial ECMO whilst maintaining external cardiac compression. Patients attached to the emergency system can be haemodynamically stabilized thereby allowing diagnostic imaging or can be transferred to specialized centers . A recent meta-analysis of studies using percutaneous circulatory support during high-risk revascularization procedures showed a marked reduction in death of patients in cardiogenic shock (45%) as well as in those who has sustained a cardiac arrest refractory to therapy (40%) . Despite achieving good blood flow rates through these compact systems, some patients do not regain function of either the left ventricle or the edematous lung and this is likely to be attributable, at least in part, to the absence of effective left ventricular decompression.
In the case of peripheral veno-arterial ECMO, if the left ventricle ejects deoxygenated blood into the aorta, there is a risk of cerebral and myocardial hypoxia as a result of the left ventricle selectively perfusing the heart, head and upper limbs whilst the peripheral ECMO perfuses the lower limbs and abdominal organs with oxygenated blood . Myocardial and cerebral hypoxia can go unrecognized  and it has been shown that peripheral cannulation is associated with a higher risk of thrombus formation in the aortic root .
Peripheral support also necessitates arterial access, with the potential danger of vessel injury and occlusion, which can result in ischemia of the extremities. Cannulation of the neck vessels can lead to injury of the jugular vein or the carotid artery. Foley demonstrated a 21% incidence of extremity ischemia with cannulation of the femoral vessels. These patients were treated with fasciotomy and in one case an amputation had to be conducted [15, 16]. Limb ischaemia occurred in none of our patients. The risk of inadequate distal limb perfusion in patients undergoing peripheral cannulation is elevated in those with comorbidities such as peripheral arterial disease and in children [15–17]. Consequently, alternative cannulation sites such as central aortic cannulation and axillary or subclavian artery cannulation should be considered early, to avoid distal limb ischemia.
The fourth annual INTERMACS report  revealed that the proportion of INTERMACS level 1 patients has dropped from 42% in 2006, when the database was implemented, to 14% in 2012. Of these patients, only less than 50% of were alive after 12 months . Hence INTERMACS level 1 status (cardiogenic shock) is the greatest risk factor for mortality in VAD therapy . Our study details a patient cohort with severe lung edema and end-organ failure from within and outside the catheter laboratory who were deemed to be candidates for temporary circulatory support. They were not considered suitable for long-term support as weaning from cardiopulmonary bypass would have carried a high risk due to respiratory failure. These patients did not even qualify as INTERMACS level 1 for immediate long-term VAD therapy.
The novel technique described here is believed to confer a significant survival advantage given the dismal prognosis of the study cohort at presentation to our institution. Also important is the timing of device insertion, but this is largely influenced by the timing of referral. Some poor outcomes following ECLS therapy are due to delay in commencing support. Ideally, ECLS should be considered prior to the onset or aggravation of end-organ failure. After initial end-organ recovery with the presented novel technique total artificial hearts with portable consoles may be suitable devices for these patients in future [19, 20].
Our technique highlights the potential use of central ECLS with direct left ventricular decompression in patients with refractory cardiogenic shock and lung failure to facilitate myocardial recovery and prevent pulmonary congestion. Separate blood gas analyses from the venous cannula and the left ventricular vent allow monitoring of pulmonary recovery and facilitate the early detection of coronary hypoxia when the left ventricle begins to recover. Moreover, this strategy is particularly suitable for patients in extremis whose neurologic status is questionable and thus candidacy for cardiac transplantation or long-term support is uncertain. The novel technique described is best suited to centers with established ECLS infrastructure and activity levels, which maintain competency [21–28], . For this reason, regionalization is recommended to ensure that adequate volumes are present at each ECMO center. Given the acuity of care and the risk of sudden decompensation if the circuit fails, intensive specialized staff training is mandatory.
Written informed consent was obtained from the patients for publication of this report and any accompanying images.
The expert technical assistance of Dirk Fischer (Media Centre University of Heidelberg) for 3-D reconstructions in Figure 3 is gratefully acknowledged.
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