28 A . Calhoun et al .: J Extra Corpor Technol 2025 , 57 , 24 – 31
Figure 1 . Pictorial representation of the four hemodynamic possibilities in patients supported by VA-ECMO with PAC and ALPP monitoring . Patients with adequate ALPP and low PAC-derived filling pressures do not require further unloading maneuvers . In the case of low ALPP and low PAC filling pressures , correction of hypovolemia and / or SVR will likely restore ALPP . Patients with adequate ALPP and elevated PAC filling pressures may likely require volume removal . In the case of low ALPP and elevated PAC filling pressures , the patient likely requires at a minimum non-invasive and failing that , invasive methods of LV unloading . ALPP : Arterial Line Pulse Pressure ; LV : Left Ventricle ; PAC : Pulmonary Artery Catheter ; SVR : Systemic Vascular Resistance ; VA-ECMO : Venoarterial Extracorporeal Membrane Oxygenation .
surrogate marker for LVD and reduced contractility . In the absence of clinical or radiographic indicators of LVD , hemodynamic surveillance for LVD may identify this pathologic state before clinical and radiographic findings . Thus , many publications in the literature recommend the use of invasive hemodynamic monitoring in patients with cardiogenic shock supported by VA-ECMO [ 3 , 5 ]( See Table 1 ).
While PAC surveillance of LVD is a very useful method of monitoring , there are drawbacks . For example , PAC positioning next to mechanical circulatory support devices ( such as cannulas ) can result in falsely low or high CVP readings depending on proximity to inflow or outflow ports of the drainage or return cannulas [ 41 ]. Additionally , patients with known long-standing heart failure may have elevated PAC-derived filling pressures without significant symptoms . Thus , it is difficult , if not impossible , to establish a single set of PCWP criteria to define the need for mechanical LV unloading . Finally , as an important caveat to PAC surveillance for LVD , care teams must have detailed knowledge of valvular and other cardiopulmonary abnormalities to properly interpret hemodynamic findings . For example , in patients with severe mitral stenosis , PCWP may be elevated despite normal or low left ventricular end-diastolic pressures . Additionally , in the rare case of patients with pulmonary vein stenosis , elevated PCWP does not imply increased left atrial or left ventricular pressures [ 42 ].
The use of ALPP monitoring for LV unloading is a basic method of surveillance for LVD . However , ALPP in patients supported by VA-ECMO can be altered for reasons other than LVD . For example , acute hypovolemia as frequently occurs with the initiation of VA-ECMO , often results in low flow through the pulmonary vasculature and thus a significant reduction in LV stroke volume . As a result , LVD can be misdiagnosed during the early stages of VA-ECMO . An acute reduction in systemic vascular resistance ( SVR ) can also be a cause of reduced ALPP . Other causes of acute hypovolemia such as hemorrhage or excessive diuresis may also reduce ALPP in the absence of LVD . Thus , while surveillance of ALPP is a straightforward monitoring method , it should not be solely relied upon to diagnose LVD ( See Fig . 1 ). An important differentiation must be made between arterial pulsatility ( or AV opening ) and adequate LV unloading . For example , while low ALPP does suggest that the AV is opening ( and aortic root thrombosis is unlikely ), AV opening may not be adequate to result in sufficient ejection of blood to reduce PCWP . Thus , the presence of AV openings does not fully exclude LVD .
ECHO markers of LVD include evidence of ventricular dilation , reduced LVOT VTI , lack of or reduced AV opening , echo contrast in the left atrium or LV thrombus formation in the left atrium or left ventricle , and blood stasis or thrombosis in the aortic root [ 2 , 5 ]. As with hemodynamic indicators of LVD , ECHO indicators may be misleading . For example , patients with known cardiomyopathy may appear to have LV dilation even in the presence of normal or low left heart pressures . Thus , subjective findings of LV dilation in patients supported by VA-ECMO do not always indicate the need for mechanical LV unloading . Additionally , as the LVOT VTI is a surrogate marker of stroke volume , this value can be low in the setting of hypovolemia and should not always prompt the initiation of mechanical LV unloading without further verification of the presence of LVD . The presence of echo contrast in the left atrium or LV often indicates LVD , though hypovolemia can mimic this as well . Finally , as with clinical and radiologic findings , thrombus is a late sign of LVD and while important to