Effect of Mean Arterial Pressure Change by Norepinephrine on Peripheral Perfusion Index in Septic Shock Patients After Early Resuscitation

Effect of Mean Arterial Pressure Change by Norepinephrine on Peripheral Perfusion Index in Septic Shock Patients After Early Resuscitation

Mean arterial pressure (MAP) plays a critical role in tissue perfusion, serving as the primary driving pressure that pushes blood through organs. However, determining the optimal target MAP for hemodynamic management in septic shock remains a subject of debate. While a MAP cutoff of 65 mmHg is recommended during the early resuscitation stage to maintain vital organ perfusion, the optimal MAP should be individualized based on each patient’s specific circumstances after early resuscitation. Blood pressure levels recorded in a patient’s medical history are often used as a reference for defining optimal blood pressure during the optimization stage of septic shock resuscitation. Some studies suggest that a higher MAP may protect against acute kidney injury and improve microcirculation, particularly in patients with a history of hypertension. Despite these findings, the effects of MAP on tissue perfusion in septic shock patients are highly variable due to the complex pathophysiological status of these patients. Therefore, a tissue perfusion-based approach may be necessary to determine a precise blood pressure target.

The peripheral perfusion index (PI), defined as the ratio of the pulsatile to non-pulsatile component of the pulse oximetry plethysmograph, has emerged as a simple and accurate indicator of peripheral arteriole pulsation intensity. PI has been shown to reflect tissue perfusion and hypovolemia, identify the success of regional blocks, and predict organ failure and outcomes in critically ill patients. Importantly, PI provides real-time, bedside information on peripheral tissue perfusion, making it a potentially valuable tool for optimizing MAP titration with norepinephrine (NE) in septic shock patients. However, no studies have investigated changes in PI during MAP titration using NE based on a patient’s usual blood pressure levels from medical records. This study aimed to explore the effect of MAP on PI by titrating MAP to different levels around the patient’s usual blood pressure using NE and to investigate the relationship between changes in PI and global circulation during blood pressure titration.

The study enrolled 20 septic shock patients who required pulse-induced contour cardiac output (PiCCO) monitoring for resuscitation. Patients were included if they had a usual MAP under NE infusion after early resuscitation. Exclusion criteria included pregnancy, arrhythmia, cardiac output (CO) less than 2.5 L/min, ice cooling blanket therapy, peripheral artery stenosis, extracorporeal membrane oxygenation (ECMO) therapy, and intra-aortic balloon pump therapy. The study protocol involved titrating NE to achieve three MAP levels: the patient’s usual MAP minus 10 mmHg, the patient’s usual MAP, and the patient’s usual MAP plus 10 mmHg. Global hemodynamic parameters and PI were recorded at each MAP level. The general linear model with repeated measures was used to analyze the variance of related parameters at the three MAP levels.

The results showed that increasing NE infusion led to significant changes in MAP and central venous pressure (CVP). However, there were no significant or consistent changes in continuous cardiac output (CO) and PI at different MAP levels. Among the 20 patients, seven reached the maximum PI value at the usual MAP minus 10 mmHg, three at the usual MAP, and ten at the usual MAP plus 10 mmHg. The change in PI was not significantly correlated with the change in CO from the usual MAP minus 10 mmHg to the usual MAP or from the usual MAP to the usual MAP plus 10 mmHg. These findings suggest that differing MAP levels induced by NE infusion result in diverse PI responses in septic shock patients, and these responses may be independent of changes in CO.

The study’s clinical characteristics revealed that the average age of the patients was 58 years, with 11 females and 9 males. The primary infection sites included lung infection (25%), abdomen infection (30%), brain infection (5%), soft tissue infection (15%), bloodstream infection (15%), and an unknown source of infection (10%). All patients received mechanical ventilation and sedation. The average dose of NE increased significantly from 0.58 to 0.71 mg/kg/min and then to 0.89 mg/kg/min to achieve the different MAP levels. No adverse effects were associated with the increased NE doses. The changes in hemodynamic variables showed significant increases in CVP, MAP, and systemic vascular resistance (SVR) with increasing NE infusion. However, there were no significant changes in CO and PI.

The individual PI values of the 20 patients at the three MAP levels demonstrated broad variability. Seven patients had the maximum PI value at the usual MAP minus 10 mmHg, three at the usual MAP, and ten at the usual MAP plus 10 mmHg. This variability underscores the need for precise titration based on tissue perfusion when MAP is set to the patient’s usual level. The study also found no significant relationship between the change in CO and the change in PI or between the change in MAP minus CVP and the change in PI. These results suggest that the change in PI may be independent of changes in macrocirculation during MAP titration with NE after early resuscitation in septic shock patients.

The discussion highlights the ongoing debate over how to titrate an optimal perfusion pressure with NE during resuscitation after septic shock. Previous studies have shown inconsistent results regarding the effect of NE-induced increases in MAP on tissue perfusion. Some studies suggest that higher MAP improves cutaneous microvascular flow and tissue oxygenation, while others report no improvement in microcirculatory blood flow. The study’s findings reinforce the need for precise titration based on tissue perfusion, as the optimal MAP determined by the patient’s usual level may not always improve peripheral perfusion. Monitoring PI could be helpful in setting an optimal perfusion pressure target, as it provides non-invasive, real-time, and continuous information on peripheral perfusion.

The study also acknowledges several limitations. The sample size was small, and the study was conducted in a single center, which may introduce selection bias. The study period may not have been long enough to evaluate other relevant clinical outcomes, such as lactate clearance, organ function, and mortality. Additionally, finger perfusion may not reflect perfusion of other organ tissues, and other factors such as room temperature and peripheral artery stenosis can impact PI values. Despite these limitations, the study provides valuable insights into the potential use of PI for optimizing MAP titration with NE in septic shock patients.

In conclusion, differing MAP levels induced by NE infusion result in diverse PI responses in septic shock patients, and these responses may be independent of changes in CO. PI may have potential applications for MAP optimization based on changes in peripheral tissue perfusion. Further investigations are required to determine whether using the maximum PI value to guide the setting of the MAP target can improve the outcomes of septic shock patients after early resuscitation.

doi.org/10.1097/CM9.0000000000001017

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