Abstract:The PAPi is a simple, invasive hemodynamic measure that may help identify high-risk patients with acute IWMI with severe RVD. Earlier identification of this high-risk population may improve clinical outcomes.
“…The pulmonary artery pulsatility index (PAPi), defined as [(systolic pulmonary artery pressure -diastolic pulmonary artery pressure)/central venous pressure], is a novel hemodynamic index that predicts severe RVF in the setting of acute inferior wall myocardial infarction 15 and was developed with the goal of identifying patients who will require percutaneous mechanical RVAD support. Its utility has not been studied to predict RVF after LVAD implantation.…”
“…The pulmonary artery pulsatility index (PAPi), defined as [(systolic pulmonary artery pressure -diastolic pulmonary artery pressure)/central venous pressure], is a novel hemodynamic index that predicts severe RVF in the setting of acute inferior wall myocardial infarction 15 and was developed with the goal of identifying patients who will require percutaneous mechanical RVAD support. Its utility has not been studied to predict RVF after LVAD implantation.…”
“…Procedural data were extracted from the catheterization reports and included the following parameters: RAP, PCWP, pulmonary artery (PA) systolic, diastolic, and mean pressures, systemic arterial systolic, diastolic, and mean pressures, cardiac output, pulmonary vascular resistance, systemic vascular resistance, PAPi, transpulmonary gradient (TPG), and DPG (Fig. 2) [13, 15]. Fig.…”
PurposeAcute kidney injury (AKI) frequently occurs after heart transplantation (HTx), but its relation to preoperative right heart hemodynamic (RHH) parameters remains unknown. Therefore, we aimed to determine their predictive properties for postoperative AKI severity within 30 days after HTx.MethodsFrom 1984 to 2016, all consecutive HTx recipients (n = 595) in our tertiary referral center were included and analyzed for the occurrence of postoperative AKI staged by the kidney disease improving global outcome criteria. The effects of preoperative RHH parameters on postoperative AKI were calculated using logistic regression, and predictive accuracy was assessed using integrated discrimination improvement (IDI), net reclassification improvement (NRI), and area under the receiver operating characteristic curves (AUC).ResultsPostoperative AKI occurred in 430 (72%) patients including 278 (47%) stage 1, 66 (11%) stage 2, and 86 (14%) stage 3 cases. Renal replacement therapy (RRT) was administered in 41 (7%) patients. Patients with higher AKI stages had also higher baseline right atrial pressure (RAP; median 7, 7, 8, and in RRT 11 mmHg, p trend = 0.021), RAP-to-pulmonary capillary wedge pressure ratio (median 0.37, 0.36, 0.40, 0.47, p trend = 0.009), and lower pulmonary artery pulsatility index (PAPi) values (median 2.83, 3.17, 2.54, 2.31, p trend = 0.012). Higher RAP and lower PAPi values independently predicted AKI severity [adjusted odds ratio (OR) per doubling of RAP 1.16 (1.02–1.32), p = 0.029; of PAPi 0.85 (0.75–0.96), p = 0.008]. Based on IDI, NRI, and delta AUC, inclusion of these parameters improved the models’ predictive accuracy.ConclusionsPreoperative PAPi and RAP strongly predict the development of AKI early after HTx and can be used as early AKI predictors.Electronic supplementary materialThe online version of this article (10.1007/s00134-018-5159-z) contains supplementary material, which is available to authorized users.
“…99 Additional published clinical, imaging, and hemodynamic variables associated with in-hospital mortality in the CS population include anoxic brain damage, end-organ hypoperfusion, elevated lactate, prior CABG, ACS pathogenesis, LV ejection fraction, RV function, pulmonary artery pulsatility index (defined as the ratio of pulmonary artery pulse pressure to right atrial pressure), mitral regurgitation, LV stroke work, cardiac power output, SBP, number of vasopressors, systemic inflammatory response syndrome, and TIMI (Thrombolysis in Myocardial Infarction) flow. 39,48,[100][101][102][103][104][105] Limitations of available models included the lack of a CS-specific derivation population, external validation, dynamic application (ie, single point in time only), applicability to all CS types, and capture of all potentially prognostic clinical, laboratory, hemodynamic, imaging, and biomarker data.…”
Section: Prognostic Models and Variablesmentioning
Cardiogenic shock is a high-acuity, potentially complex, and hemodynamically diverse state of end-organ hypoperfusion that is frequently associated with multisystem organ failure. Despite improving survival in recent years, patient morbidity and mortality remain high, and there are few evidence-based therapeutic interventions known to clearly improve patient outcomes. This scientific statement on cardiogenic shock summarizes the epidemiology, pathophysiology, causes, and outcomes of cardiogenic shock; reviews contemporary best medical, surgical, mechanical circulatory support, and palliative care practices; advocates for the development of regionalized systems of care; and outlines future research priorities.
Cardiogenic shock (CS) is a low-cardiac-output state resulting in life-threatening end-organ hypoperfusion and hypoxia.1,2 Acute myocardial infarction (MI) with left ventricular (LV) dysfunction remains the most frequent cause of CS. 1,3 Advances in reperfusion therapy have been associated with improvements in survival, but significant regional disparities in evidence-based care have been reported, and in-hospital mortality remains high (27%-51%).1,4-9 Management recommendations are distributed between disease-specific statements and guidelines, and a dedicated and comprehensive clinical resource in this area is lacking. Thus, consolidating the evidence to define contemporary best medical and surgical CS practices for both MI-associated CS and other types of CS may be an important step in knowledge translation to help attenuate disparities in evidence-based care.Regional systems of care coupled with treatment algorithms have improved survival in high-acuity time-sensitive conditions such as MI, out-of-hospital cardiac arrest (OHCA), and trauma.10-12 Applying a similar framework to CS management may lead to similar improvements in survival, and CS systems of care are emerging within existing regional cardiovascular emergency care networks; however, guidance from a national expert group on structure and systems of care has not been available. 13,14 Accordingly, the purposes of this American Heart Association (AHA) scientific statement on CS are to summarize our contemporary understanding of the epidemiology, pathophysiology, and in-hospital best care practices into a single clinical resource document; to suggest a stepwise management algorithm that integrates medical, surgical, and mechanical circulatory support (MCS) therapies; and to propose a Mission: Lifelinesupported pathway for the development of integrated regionalized CS systems of care.
DEFINITION OF CSAcute cardiac hemodynamic instability may result from disorders that impair function of the myocardium, valves, conduction system, or pericardium, either in isolation
HISTORICAL PERSPECTIVESBefore the routine use of early revascularization, MIassociated CS had an in-hospital mortality exceeding 80%. A registry trial of 250 patients with acute MI described the association between bedside physical examination (Killip classification) for the as...
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