LV distension can be defined as a pathological increase in LV end-diastolic pressure (LVEDP) or volume (LVEDV) caused or exacerbated by VA ECMO. There are two overlapping mechanisms (see diagrams):
- Insufficient LV cardiac output to equal the volume of blood entering the LV from the right ventricle (via the pulmonary circulation), the bronchial arteries and Thebesian veins [A]
- ECMO pump driven aortic regurgitation (with competent pulmonary valve) [B]
In regard to the first mechanism, VA ECMO lowers right heart and pulmonary blood pressure but tends to increase systemic arterial blood pressure. It does not provide specific LV unloading. In the setting of relative left heart failure, left heart congestion is gradually, but progressively, exacerbated with VA ECMO (LV distension syndrome) as arterial blood pressure rises. Medical management of this form of LV distension syndrome is vasodilation and application of PEEP. Untreated, this form of LV distension syndrome can progress to the second form. Inotropic support may exacerbate this form of LV distension (as a result of preferential RV effect of inotropes).
Pump-driven LV distension occurs with any degree of aortic valve regurgitation if LV ejection is absent during VA ECMO support. Provided a competent pulmonary valve, it results in rapid and progressive LV distension, severe pulmonary congestion and reduction in blood volume in the systemic circulation (Access Insufficiency). This is also true whenever regurgitant volume is greater than ejected volume. Thus, patients with known aortic valve regurgitation must receive early partial VA ECMO support and maintain sufficient LV ejection at all times.
As the complications of LV distension are severe or fatal, the prevention of the syndrome is a primary aim during VA ECMO. Management consists of detecting the at-risk population, providing timely medical management to optimize LV load, and employing mechanical decompression therapies if warranted in a timely manner.
LV distension may result in the following spectrum of adverse clinical outcomes
Increased LV wall tension (increased oxygen consumption/myocardial ischaemia)
- Pulmonary and pleural oedema (exacerbate lung shunt, increase the risk of pneumonia)
- Pulmonary haemorrhage
- Left heart and aortic thrombus (increase CVA risk or complete left heart obstruction)
- Impaired VA ECMO blood flow (Access Insufficiency/inability to maintain oxygen delivery)
Often, after these complications have occurred, salvage LV decompression options have limited utility. Therefore it is important to first screen patients in a timely manner after ECMO initiation, and secondly recognise high risk clinical features of LV distension so early and effective LV decompression can be implemented.
Implementation of medical (high PEEP, low BP) or surgical intervention where physiology does not lead to LV loading may be harmful. Conditions where LV distension does not typically occur:
- Primary cardiac graft failure
- Pulmonary hypertension
- All patients after being established on VA ECMO should have an echocardiogram performed within 2 hours if their pulse pressure is < 10 mmHg (despite inotropes), or there is pulmonary oedema on CXR (despite high PEEP i.e. 15 cmH20).
- All other patients should have an echocardiogram within 24 hours
Note: TTE is a superior modality for identifying LV thrombus and assessing LV function if adequate windows are available in comparison to TOE.
Pre ECMO Risk Factors for LV distension
- Predominant left heart failure physiology (e.g. LV AMI)
- Advanced cardiomyopathy
- Pre-existing aortic or mitral valve regurgitation
- Prolonged cardiac arrest (ECPR) cases
Post ECMO Features of LV Distension
- Arterial line pulse pressure < 10 mmHg despite inotropic support (post ECMO)
- Elevated pulmonary artery diastolic pressure > 25mmHg
- CXR: progressive pulmonary oedema
- Echocardiogram features (despite inotropic support):
- Moderate to severely dilated left ventricle (note: a normal LV size does not exclude LV distension).
- Very severely reduced LV ejection fraction (i.e. LVEF <10%, LVOT VTI < 5 cm)
- No aortic valve opening
- Aortic regurgitation
- Mitral regurgitation
- Spontaneous LV echo contrast, or LV thrombus
Where high risk clinical features of LV distension are present, medical management should be optimised and immediate discussion regarding options for LV decompression should occur between the ICU consultant and ECMO consultant and where necessary the cardiothoracic surgeon and on-duty heart failure cardiologist.
Medical management is appropriate for patients at risk or with mild forms of LV distension where recovery of LV function is anticipated. It is not a long term strategy and prevents extubation.
- Lower MAP to 60-70mmHg
- High PEEP (15 to 25 cmH20)
- Inotropic support for maintenance of pulsatility
Note: inotropes may exacerbate LV distension if LV is non-responsive to inotropes by primarily increasing RV output
- Volume state reduction (fluid removal) if blood pressure and venous pressures adequate
- Increasing VA ECMO flow
Note: In particular, where RV systolic function is better than LV systolic function reducing pulmonary blood flow by increased ECMO blood flow can be effective. The afterload, however, needs to be controlled to MAP target with systemic vasodilators as required.
Intra-aortic balloon pumping (IABP) may provide additional afterload reduction in patients at risk of LV distension. Previously inserted IABP support should be maintained following VA ECMO initiation in patients at risk for LV distension in the absence of IABP complications (leg ischaemia or bleeding).
Mechanical LV Decompression Interventions
Where medical management is insufficient to allow recovery from VA ECMO support or there is associated access insufficiency (unstable or inadequate circuit blood flow), immediate consideration should be given to provision of mechanical decompression. Mechanical decompression options provide benefit if they result in stable VA ECMO blood flow, reduce LV and pulmonary congestion and promote recovery or facilitate transition to longer term forms of mechanical cardiac support. Patients unlikely to recover or, unsuitable for longer term support, should not be offered mechanical LV decompression.
Intra-aortic balloon pump provides afterload reduction and therefore may assist patients at risk of LV distension, however, it is NOT considered a treatment for progressive forms of LV distension that is not controlled by medical management.
Mechanical options for LV distension, described in the literature such as atrial septostomy, or trans-atrial LA catheterisation that are not immediately accessible and therefore not used at Alfred Health are not included in this guide.
Potential consideration is given to the following options:
- Trans-apical surgical LV vent cannula
- Trans-aortic LV ‘pigtail’ catheter
- Pulmonary arterial drainage via single lumen cannula
- Pulmonary venous drainage in conjunction with central VA ECMO cannulation
First line: insertion of an LV apical vent via a left anterolateral thoracotomy. Other options required expert opinion and discussion at the bedside.
LV decompression interventions may be performed as a bridge to recovery, a bridge to more durable mechanical support devices e.g. VAD, and very rarely as a bridge to heart transplantation. Patients who are not candidates for escalation of treatment (to a VAD or transplant), who are unlikely to wean off ECMO should not undergo a LV decompression intervention.
Trans-aortic LV ‘pigtail’ catheter
Placement of a small lumen catheter in the mid-LV cavity can be performed in the cardiac cath lab. Advantages include the direct drainage of blood out of the LV as a percutaneous intervention. The potential risk of arterial embolism and fairly low flow rates represent the main disadvantages.
This approach is routine in low or non-pulsatile ECPR cases. ECPR patients are at high risk of developing LV distension syndrome. Further description of the patient selection and practical procedures is provided in the according sections.
Central VA ECMO
This option is usually reserved for post cardiac surgical patients. A second venous access cannula is inserted via a mid-line sternotomy into one of:
- The right superior pulmonary vein into either LA or LV
- Directly in the pulmonary trunk
- Cannula insertion directly in the left atrium