High-normal versus low-normal mean arterial pressure thresholds in critically ill patients: A systematic review and meta-analysis of randomized trials

Abstract

Targeted blood pressure thresholds remain unclear in critically ill patients. Two prior systematic reviews have not demonstrated differences in mortality with a high mean arterial pressure (MAP) threshold but they only included patients with septic shock. Thus, we conducted an updated systematic review and meta-analysis of randomized controlled trials (RCTs) that compared the effect of a high-normal versus low-normal MAP on mortality in all pertinent disease states for critically ill patients. We searched six databases from inception until September 5th 2021 for RCTs of critically ill patients targeted to either a high-normal (≥ 65 mm Hg) versus a low-normal (≥ 60 mm Hg) MAP threshold for at least 24-hours. We assessed study quality using the RoB-2 tool and the risk ratio (RR) was used as the summary measure of association. We included 7 RCTs with 3772 patients. Three trials were conducted in patients following out-of-hospital cardiac arrest, two in distributive shock, one in septic shock, and one in hepatorenal syndrome. The pooled RR for mortality was 1.06 (95%CI 0.98 to 1.17). There was no significant between-study heterogeneity (I2 = 0%, 95%CI: 0 to 47%). Furthermore, there was no difference in the rates of favourable neurologic outcome or renal replacement therapy between the high-normal versus low-normal MAP groups. This systematic review and meta-analysis demonstrates that there is no difference in mortality amongst critically ill patients targeted to a high-normal versus low-normal MAP target.

Clinical targeting of the cerebral oxygen cascade to improve brain oxygenation in patients with hypoxic–ischaemic brain injury after cardiac arrest

“…Authors have previously suggested that MAP augmentation may be an effective treatment strategy in the post-resuscitation setting [ 38 , 40 ]. However, the neutral results of randomised control trials investigating MAP augmentation [ 7 – 9 , 14 ], and lack of influence of MAP augmentation on neurologic outcome demonstrated in a recent meta-analysis [ 41 ], have led investigators to call into question the effectiveness of such an approach. Such discordance between the perceived importance of augmenting MAP and the lack of benefit for neurologic outcome demonstrated in clinical trials may be explained by dysfunction in the latter stages of the oxygen cascade (see Stage 2: oxygen diffusion & Stage 3: oxygen utilisation ) and by individualised perfusion thresholds that may reflect patient-specific cerebrovascular physiology [ 42 ].…”