Prospective Evaluation of a Multibeat Analysis Cardiac Index Estimation in Patients With Cardiogenic Shock.

OBJECTIVES: The decision algorithm for managing patients in cardiogenic shock depends on cardiac index (CI) estimates. Cardiac index estimation via thermodilution (CI-TD) using a pulmonary artery catheter is used commonly for obtaining CI in these patients. Minimally invasive methods of estimating CI, such as multibeat analysis (CI-MBA), may be an alternative in this population. DESIGN: A prospective, observational study. SETTING: Cardiac intensive care unit. PARTICIPANTS: Twenty-two subjects in cardiogenic shock provided 101 paired CI measurements. INTERVENTIONS: Measurements were obtained concomitantly by intermittent CI-TD and CI-MBA (Argos Cardiac Output Monitor; Retia Medical, Valhalla, NY). For each CI-TD, CI-MBA estimates were averaged over 1 minute to provide paired values. Bland-Altman and 4-quadrant analyses were performed by plotting changes between successive CI measurements (ΔCI) from each of the 2 methods. Concordance was calculated as a percentage using ΔCI data points from the 2 methods, outside an exclusion zone of 15%. MEASUREMENTS AND MAIN RESULTS: The correlation coefficient between CI-MBA and CI-TD was 0.78 across patients. Mean CI-TD was 2.19 ± 0.46 L/min/m2 and mean CI-MBA was 2.38 ± 0.59 L/min/m2. The mean difference between CI-MBA and CI-TD (bias ± SD) was 0.20 ± 0.47 L/min/m2, and the limits of agreement were -0.72 to 1.11 L/min/m2. The percentage error was 40.0%. The concordance rate was 94%. A secondary analysis of a subgroup of patients during periods of arrhythmia demonstrated a similar accuracy of performance of CI-MBA. CONCLUSIONS: Cardiac index-MBA is not interchangeable with CI-TD. However, CI-MBA provides reasonable correlation and clinically acceptable trending ability compared with CI-TD. Cardiac output-MBA may be useful in trending changes in CI in patients with cardiogenic shock, especially in those whose pulmonary artery catheterization placement carries a high risk or is unobtainable.

Chemosensitivity of Phox2b-expressing retrotrapezoid neurons is mediated in part by input from 5-HT neurons.

KEY POINTS: Neurons of the retrotrapezoid nucleus (RTN) and medullary serotonin (5-HT) neurons are both candidates for central CO2 /pH chemoreceptors, but it is not known how interactions between them influence their responses to pH. We found that RTN neurons in brain slices were stimulated by exogenous 5-HT and by heteroexchange release of endogenous 5-HT, and these responses were blocked by antagonists of 5-HT7 receptors. The pH response of RTN neurons in brain slices was markedly reduced by the same antagonists of 5-HT7 receptors. Similar results were obtained in dissociated, primary cell cultures prepared from the ventral medulla, where it was also found that the pH response of RTN neurons was blocked by preventing 5-HT synthesis and enhanced by blocking 5-HT reuptake. Exogenous 5-HT did not enable latent intrinsic RTN chemosensitivity. RTN neurons may play more of a role as relays from other central and peripheral chemoreceptors than as CO2 sensors. ABSTRACT: Phox2b-expressing neurons in the retrotrapezoid nucleus (RTN) and serotonin (5-HT) neurons in the medullary raphe have both been proposed to be central respiratory chemoreceptors. How interactions between these two sets of neurons influence their responses to acidosis is not known. Here we recorded from mouse Phox2b+ RTN neurons in brain slices, and found that their response to moderate hypercapnic acidosis (pH 7.4 to ∼7.2) was markedly reduced by antagonists of 5-HT7 receptors. RTN neurons were stimulated in response to heteroexchange release of 5-HT, indicating that RTN neurons are sensitive to endogenous 5-HT. This electrophysiological behaviour was replicated in primary, dissociated cell cultures containing 5-HT and RTN neurons grown together. In addition, pharmacological inhibition of 5-HT synthesis in culture reduced RTN neuron chemosensitivity, and blocking 5-HT reuptake enhanced chemosensitivity. The effect of 5-HT on RTN neuron chemosensitivity was not explained by a mechanism whereby activation of 5-HT7 receptors enables or potentiates intrinsic chemosensitivity of RTN neurons, as exogenous 5-HT did not enhance the pH response. The ventilatory response to inhaled CO2 of mice was markedly decreased in vivo after systemic treatment with ketanserin, an antagonist of 5-HT2 and 5-HT7 receptors. These data indicate that 5-HT and RTN neurons may interact synergistically in a way that enhances the respiratory chemoreceptor response. The primary role of RTN neurons may be as relays and amplifiers of the pH response from 5-HT neurons and other chemoreceptors rather than as pH sensors themselves.