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Cold Intravenous Fluids Shown to Significantly Boost Blood Pressure in Healthy Volunteers

• A randomized controlled trial reveals that administering cold (15°C) Ringer's lactate intravenously leads to a greater and more prolonged increase in mean arterial pressure (MAP) compared to fluids at body temperature. • The study indicates that cold fluids induce the release of noradrenaline, resulting in peripheral vasoconstriction and increased systemic vascular resistance, which contributes to the observed blood pressure elevation. • Researchers found that fluid temperature, rather than volume alone, significantly impacts blood pressure during fluid bolus therapy, suggesting that approximately 90% of the blood pressure increase is temperature-dependent. • The findings challenge current understanding of fluid bolus therapy's effects on blood pressure and suggest cold fluids may be a cost-effective option for short-term management of hypotension.

A recent study published in Scientific Reports indicates that administering intravenous fluids at a cooler temperature (15°C) results in a more significant and sustained increase in blood pressure compared to fluids administered at body temperature (37°C). The randomized controlled crossover trial, conducted on healthy volunteers, challenges the conventional understanding of fluid bolus therapy and its impact on blood pressure regulation.
The research team, led by investigators, hypothesized that altering the temperature of intravenous fluid boluses could significantly affect blood pressure response. The study involved administering Ringer's lactate at both 15°C and 37°C to participants, while continuously monitoring hemodynamic parameters. Results showed that after 45 minutes, the cold fluid infusion led to a statistically significant increase in mean arterial pressure (MAP), whereas the body-temperature fluids had minimal effect. Furthermore, the effect of cold fluids on MAP was more prolonged.

Physiological Mechanisms

The study revealed that the increase in MAP following cold fluid administration was accompanied by a strong increase in systemic vascular resistance and intrinsic noradrenaline levels. Interestingly, the renin–angiotensin–aldosterone system was not activated. These findings suggest that the cold-induced increase in blood pressure is primarily mediated by the release of noradrenaline, leading to peripheral vasoconstriction.
"Our study suggests that fluid temperature, rather than volume only, contributes to MAP increase in fluid bolus therapy," the authors stated. They estimated that temperature might account for approximately 90% of the blood pressure increase observed when administering 30 ml/kg of isotonic crystalloid in healthy, normovolemic individuals.

Comparison with Previous Research

While previous studies have explored the hemodynamic effects of fluid boluses at different temperatures, this trial provides a more comprehensive examination of the physiological responses involved. The researchers noted that their findings align with earlier research indicating that cold fluid administration can increase MAP. However, this study uniquely elucidates the role of noradrenaline release and vasoconstriction in mediating this effect.

Implications and Limitations

The study's findings have potential clinical implications for the treatment of hypotensive patients. Given the negligible costs associated with cooling fluids, cold intravenous fluids could represent a cost-effective short-term strategy for managing low blood pressure. However, the authors caution that their study was conducted on healthy volunteers and that further research is needed to assess the safety and efficacy of cold fluids in clinical settings.
"Future studies should also investigate the effects of cold fluid bolus on coagulation, to ensure safe applicability in both medical and surgical patients," the researchers noted. They also highlighted potential risks associated with hypothermia, such as increased oxygen consumption and impaired wound healing, particularly in surgical patients.
The study's limitations include the use of healthy volunteers, the specific fluid bolus volume and infusion rate, and the lack of invasive hemodynamic measurements. Despite these limitations, the findings provide valuable insights into the physiological mechanisms underlying the blood pressure response to fluid bolus therapy and warrant further investigation in clinical populations.
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