25, 15, 13
A low arterial pulse pressure most often does NOT indicate left ventricular distension. The commonest phenotype is low pulsatility without distension, caused by reduced transpulmonary flow from right ventricular failure - and unloading that ventricle removes preload from one already underfilled. The discriminating measurement is the pulmonary artery diastolic pressure and pulsatility, which is frequently not being made because pulmonary artery catheters are often omitted on venoarterial support.
The simulation prediction that venoarterial ECMO uniformly produces left ventricular distension
DOI 10.14814/phy2.70961
Measurement of left ventricular end-diastolic pressure, arterial pulse pressure, pulmonary artery diastolic pressure and pulmonary artery pulse pressure, with cluster analysis
Phenotypes derived by cluster analysis without external validation; clinical arm sampled only within the first two hours; outcomes inextricably linked to the underlying cause of shock. Indexed passage only, no full text. [VERIFICATION REQUIRED]
Three phenotypes in both arms. Animal centroids for change in end-diastolic pressure and pulse pressure: Cluster 1 +4.99 and -1.85 mmHg; Cluster 2 +0.02 and -5.57 mmHg; Cluster 3 +1.31 and +15.5 mmHg. Clinical phenotypes: pulsatile 26% (highest arterial pulse pressure); low pulsatility 52% (low arterial AND low pulmonary artery pulse pressure); left ventricular distension 22% (elevated pulmonary artery diastolic pressure). Acute myocardial infarction was commoner in the distension phenotype; the low-pulsatility phenotype had a larger right ventricular diameter and more tricuspid regurgitation. The distension phenotype also had higher TAPSE, a smaller right ventricle and higher pulmonary artery pulse pressure - better right ventricular function and higher transpulmonary flow into a ventricle that could not empty.
58 pigs with cardiogenic shock at two levels of ECMO flow, and 128 patients with cardiogenic shock sampled within 2 hours of venoarterial ECMO