The Effect of PEEP on Pulmonary Vascular Resistance Depends on Lung Recruitability in ARDS Patients.

Rationale. A U-shape relationship should exist between lung volume and pulmonary vascular resistance (PVR), with minimal PVR at functional residual capacity. Thus, positive end-expiratory pressure (PEEP) in patients with acute respiratory distress syndrome (ARDS) should increase PVR if it induces significant lung distension compared to recruitment. However, this has never been proven in patients. Objectives. To study the effects of PEEP on PVR according to lung recruitability, evaluated by the recruitment-to-inflation (R/I) ratio. Methods. In patients with ARDS, we measured hemodynamic (pulmonary artery catheter), echocardiographic and ventilatory variables (including esophageal pressure), at both low PEEP and higher PEEP by 10 cmH2O. Preload responsiveness was assessed by the passive leg raising test at high PEEP. Measurements and Main Results. We enrolled 23 patients, including 10 low recruiters (R/I <0.5) and 13 high recruiters (R/I ≥0.5). Raising PEEP from 4 (2-5) to 14 (12-15) cmH2O increased PVR in low recruiters (from 160 (120-297) to 243 (166-380) dyn.s/cm5, p<0.01), while PVR was unchanged in high recruiters (from 224 (185-289) to 235 (168-300) dyn.s/cm5, p=0.55). Right-to-left ventricular end-diastolic areas ratio simultaneously increased in low recruiters (from 0.54 (0.50-0.59) to 0.64 (0.56-0.70), p<0.01), while remaining stable in high recruiters (from 0.70 (0.65-0.79) to 0.68 (0.58-0.80), p=0.48). Raising PEEP decreased cardiac index only in preload responsive patients. Conclusions. PEEP increases PVR only when it induces significant lung distension compared to recruitment according to the recruitment-to-inflation ratio. Tailoring PEEP on this recruitability index should mitigate its hemodynamic effects.

Peripheral tissue hypoperfusion predicts post intubation hemodynamic instability.

BACKGROUND: Tracheal intubation and invasive mechanical ventilation initiation is a procedure at high risk for arterial hypotension in intensive care unit. However, little is known about the relationship between pre-existing peripheral microvascular alteration and post-intubation hemodynamic instability (PIHI). METHODS: Prospective observational monocenter study conducted in an 18-bed medical ICU. Consecutive patients requiring tracheal intubation were eligible for the study. Global hemodynamic parameters (blood pressure, heart rate, cardiac function) and tissue perfusion parameters (arterial lactate, mottling score, capillary refill time [CRT], toe-to-room gradient temperature) were recorded before, 5 min and 2 h after tracheal intubation (TI). Post intubation hemodynamic instability (PIHI) was defined as any hemodynamic event requiring therapeutic intervention. RESULTS: During 1 year, 120 patients were included, mainly male (59%) with a median age of 68 [57-77]. The median SOFA score and SAPS II were 6 [4-9] and 47 [37-63], respectively. The main indications for tracheal intubation were hypoxemia (51%), hypercapnia (13%), and coma (29%). In addition, 48% of patients had sepsis and 16% septic shock. Fifty-one (42%) patients develop PIHI. Univariate analysis identified several baseline factors associated with PIHI, including norepinephrine prior to TI, sepsis, tachycardia, fever, higher SOFA and high SAPSII score, mottling score ≥ 3, high lactate level and prolonged knee CRT. By contrast, mean arterial pressure, baseline cardiac index, and ejection fraction were not different between PIHI and No-PIHI groups. After adjustment on potential confounders, the mottling score was associated with a higher risk for PIHI (adjusted OR: 1.84 [1.21-2.82] per 1 point increased; p = 0.005). Among both global haemodynamics and tissue perfusion parameters, baseline mottling score was the best predictor of PIHI (AUC: 0.72 (CI 95% [0.62-0.81]). CONCLUSIONS: In non-selected critically ill patients requiring invasive mechanical ventilation, tissue hypoperfusion parameters, especially the mottling score, could be helpful to predict PIHI.