Loss of arterial pulsatility

Arterial pulsatility reflects native cardiac function on ECMO support. Maintenance of native cardiac function is a primary aim of VA ECMO support.

Causes and consequences

Causes of loss of pulsatility on the arterial line trace include

• Artifact
• Inadequate preload (e.g. excessive VA ECMO flows, haemorrhage)
• Mechanical obstruction (e.g. tamponade, tension pneumothorax, RVOT, LVOT obstruction, pulmonary embolism). Intrathoracic bleeding causing cardiac compression is a common cause immediately following intrathoracic surgery.
• Arrhythmias
• LV failure
  • Poor LV contractility e.g. ischaemia / infarction
  • Excessive afterload: typical MAP target 65-70 mmHg
  • Valvular regurgitation: Aortic or Mitral regurgitation (see LV Failure)

Consequences of loss of pulsatility

Thrombosis

• Stagnating or low flow across the left ventricle and aortic root
• Echocardiographically this may manifest as spontaneous echo contrast (SEC) which may progress to manifest thrombus
• Massive intracardiac thrombosis: generally lethal
• Thromboembolism with potential cerebral, limb, kidney or gut ischaemia / infarction.

Increased left ventricular filling pressure/High LV load

• Loss of left ventricular ejection (forward flow) can increase the risk of pump driven LV distention (Left Ventricular Failure). Avoiding high LV afterload is a primary concern during VA ECMO.

Further consequences

• Impaired coronary perfusion and further ischaemic damage to the myocardium
• Mitral regurgitation with resultant left atrial hypertension, pulmonary oedema, pulmonary capillary rupture and haemorrhage.

Assessment

Clinical assessment should consider following causes:

• Artifact: check for damping of waveform and palpable peripheral pulses. Replace arterial line if required
• Arrhythmia: exclude non-perfusing rhythms
• Console: check flow and pump speed setting. Assess for signs of Access Insufficiency and perform dynamic assessment
• Hb: exclude clinically apparent bleeding (retroperitoneal, pleural, GIT), downward trend on ABG or FBE
• Tension pneumothorax: palpate, Auscultate and consider CXR
• Tamponade: bedside Echo, measure CVP and assess for Access Insufficiency
• Pulmonary oedema: ETT (frothy secretions +- haemorrhage) or on CXR.

Echocardiographic assessment is essential, looking for features of:

• Tamponade
• Right heart failure
  • RV: size, function, compression/obstruction (e.g. in severe RVOT hypertrophy), SEC or thrombosis
  • valves: valvular regurgitation (may be continuous)
• Left heart failure
  • LV: size (LVEDD), function, compression / obstruction, SEC or thrombosis
  • valves: mitral or aortic regurgitation (may be continuous), frequency and adequacy of aortic valve opening

Note: In ECPR and more severe forms of acute cardiac failure, it is common to lose pulsatility immediately after commencing VA ECMO. As VA ECMO is always combined with cardiac ultrasound assessment, in this setting, it is not necessary to repeat cardiac ultrasound examinations.

Additional eFAST assessment may be performed concurrently where appropriate (e.g. assessing for haemothorax / substantial intraperitoneal fluid).

Management

Management depends on the underlying cause found on assessment, and may include:

• Inadequate preload: consider volume loading (including blood / blood products). NOTE: LV failure with LV distention syndrome is usually associated with a “sucked down” RA and IVC. Volume loading will not correct this problem. The “need” for volume loading in VA ECMO should always prompt a search for LV failure and bleeding.
• Mechanical obstruction: usually surgical management with adjunctive medical management (e.g. volume loading as temporising measure; correcting coagulopathy preoperatively in tamponade)
• Poor contractility: treat underlying cause (e.g. angiography for ischaemia) and optimize temperature, acidosis, pO₂ and pCO₂.
• Arrhythmia: aim for K+ > 4.5 and Mg > 1 (or higher) in ventricular arrhythmias and consider amiodarone / direct current cardioversion (DCR). β blockade may be instituted after senior consultation. Consider cardiology referral.
• RV / LV failure: consider inodilators or constrictors (e.g. milrinone, adrenaline) as dictated by MAP, with pulmonary vasodilators (e.g. iNO) if required.
• Excessive afterload: review MAP targets and consider inodilators / vasodilators. PEEP application. Aggressive afterload control cannot be underestimated in these situations.

In the absence of pulmonary oedema, with adequate systemic perfusion and MAP, managing inadequate preload and / or excessive afterload may resolve the loss of pulsatility.

Measures to combat the consequences of loss of pulsatility

Anticoagulation

Increased anticoagulation, particularly in the setting of SEC or thrombus, should be considered in the context of other clinical priorities (e.g. haemostasis).

LV decompression is described in the next section