Inappropriate Heart Rate Response to Hypotension in Critically Ill COVID-19-Associated Acute Kidney Injury

Abstract

Angiotensin-converting enzyme 2 (ACE2) receptor of severe acute respiratory syndrome coronavirus 2 is involved in baroreflex control mechanisms. We hypothesize that severe coronavirus infectious disease 2019 (COVID-19) patients may show an alteration in baroreflex-mediated heart rate changes in response to arterial hypotension. A pilot study was conducted to assess the response to hypotension in relation to continuous venovenous hemodiafiltration (CVVHDF) in critically ill patients with PCR-confirmed COVID-19 (from February to April 2020) and in critically ill non-COVID-19 patients with sepsis (from February 2018 to February 2020). The endpoint was a change in the heart rate in response to CVVHDF-induced hypotension. The association between COVID-19 status and heart rate change was estimated using linear regression. The study population included 6 COVID-19 patients (67% men; age 58 (53–64) years) and 12 critically ill non-COVID-19 patients (58% men; age 67 (51–71) years). Baseline characteristics, laboratory findings, hemodynamic parameters, and management before CVVHDF-induced hypotension were similar between the two groups, with the exception of a higher positive end-expiratory pressure and doses of propofol and midazolam administered in COVID-19 patients. Changes in the heart rate were significantly lower in COVID-19 patients as compared to critically ill non-COVID-19 patients (−7 (−9; −2) vs. 2 (2;5) bpm, p = 0.003), while the decrease in mean arterial blood pressure was similar between groups. The COVID-19 status was independently associated with a lower change in the heart rate (−11 (−20; −2) bpm; p = 0.03). Our findings suggest an inappropriate heart rate response to hypotension in severe COVID-19 patients compared to critically ill non-COVID-19 patients.

Naringina, Trimetazidina e Barorreflexo na Lesão de Isquemia e Reperfusão Renal

“…7 Attenuation of the baroreflex in acute kidney injury can make it difficult to respond to hemodynamic instability during an episode of acute kidney injury. 8,9 Acute kidney injury also shows an increase in oxidative stress. 2 Free radicals and reactive oxygen species are produced in abundance in kidney damage due to ischemia/reperfusion and flood the circulatory system causing undesirable effects on various organs, including the solitary tract, which, as we have seen, is an important integrator of the baroreflex activity.…”

“…These results have pathophysiological implications, insofar as they demonstrate the participation of oxidative stress in the dysfunction of the solitary tract nucleus and consequently of the baroreflex in acute kidney injury, as well as therapeutic implications, since it encourages work with these drugs in order to mitigate the complications of acute kidney injury in humans, [9][10][11] a clinical situation that denotes an ominous prognosis. 12 Therefore, this line of research may help understand the treatment in humans with this nosological entity.…”