Pulse wave analysis (PWA) allows estimation of cardiac output (CO) based on continuous analysis of the arterial blood pressure (AP) waveform. We describe the physiology of the AP waveform, basic principles of PWA algorithms for CO estimation, and PWA technologies available for clinical practice. The AP waveform is a complex physiological signal that is determined by interplay of left ventricular stroke volume, systemic vascular resistance, and vascular compliance. Numerous PWA algorithms are available to estimate CO, including Windkessel models, long time interval or multi-beat analysis, pulse power analysis, or the pressure recording analytical method. Invasive, minimally-invasive, and noninvasive PWA monitoring systems can be classified according to the method they use to calibrate estimated CO values in externally calibrated systems, internally calibrated systems, and uncalibrated systems.

It remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm−5*m2 (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility.

Pulse wave analysis enables stroke volume to be estimated from an arterial blood pressure waveform. Multi-beat analysis is a novel pulse wave analysis method. We aimed to investigate cardiac output (CO) estimations using multi-beat analysis of the radial arterial blood pressure waveform in patients undergoing off-pump coronary artery bypass surgery (OPCAB) using intermittent pulmonary artery thermodilution (PATD) as the reference method. This was a prospective clinical method comparison study. In 58 patients, we measured CO using PATD (PATD-CO; reference method) and simultaneously recorded the radial arterial blood pressure waveform that we used for off-line estimation of CO based on multi-beat analysis (MBA-CO; test method) using the Argos CO monitor (Retia Medical; Valhalla, NY, USA). The final analysis was performed using 572 paired CO measurements. We performed Bland-Altman analysis accounting for multiple observations per patient. To describe the ability of the test method to track changes in CO over time we computed four-quadrant plots using a central exclusion zone of 15% and calculated the concordance rate. Mean PATD-CO was 4.13 ± 1.26 L/min and mean MBA-CO was 4.31 ± 1.25 L/min. The mean of the differences between PATD-CO and MBA-CO was − 0.20 L/min with a standard deviation of ± 1.14 L/min and 95% limits of agreement of − 2.48 to + 2.08 L/min. The concordance rate for CO changes between PATD-CO and MBA-CO was 89%. CO estimations using multi-beat analysis (Argos monitor) show reasonable agreement and trending ability compared with PATD-CO as the reference method in adult patients during OPCAB.

This study identifies sSDC1 as potential biomarker for sepsis and survival after abdominal surgery.

Cardiac output (CO) is a key hemodynamic variable that can be minimally invasively estimated by pulse wave analysis. Multi-beat analysis is a novel pulse wave analysis method. In this prospective observational clinical method comparison study, we compared CO estimations by multi-beat analysis with CO measured by intermittent pulmonary artery thermodilution (PATD) in adult patients treated in the intensive care unit (ICU) after off-pump coronary artery bypass surgery (OPCAB). We included patients after planned admission to the ICU after elective OPCAB who were monitored with a radial arterial catheter and a pulmonary artery catheter. At seven time points, we determined CO using intermittent PATD (PATD-CO; reference method) and simultaneously recorded the radial arterial blood pressure waveform that we later used to estimate CO using multi-beat analysis (MBA-CO; test method) with the Argos monitor (Retia Medical; Valhalla, NY, USA). Blood pressure waveforms impaired by inappropriate damping properties or artifacts were excluded. We compared PATD-CO and MBA-CO using Bland-Altman analysis accounting for repeated measurements, the percentage error, and the concordance rate derived from four-quadrant plot analysis (15% exclusion zone). We analyzed 167 CO values of 31 patients. Mean PATD-CO was 5.30 ± 1.22 L/min and mean MBA-CO was 5.55 ± 1.82 L/min. The mean of the differences between PATD-CO and MBA-CO was 0.08 ± 1.10 L/min (95% limits of agreement: − 2.13 L/min to + 2.29 L/min). The percentage error was 40.7%. The four-quadrant plot-derived concordance rate was 88%. CO estimation by multi-beat analysis of the radial arterial blood pressure waveform (Argos monitor) shows reasonable agreement compared with CO measured by intermittent PATD in adult patients treated in the ICU after OPCAB.

Critical Care 2017, 21(Suppl 1):P349 Introduction Imbalance in cellular energetics has been suggested to be an important mechanism for organ failure in sepsis and septic shock. We hypothesized that such energy imbalance would either be caused by metabolic changes leading to decreased energy production or by increased energy consumption. Thus, we set out to investigate if mitochondrial dysfunction or decreased energy consumption alters cellular metabolism in muscle tissue in experimental sepsis. Methods We submitted anesthetized piglets to sepsis (n = 12) or placebo (n = 4) and monitored them for 3 hours. Plasma lactate and markers of organ failure were measured hourly, as was muscle metabolism by microdialysis. Energy consumption was intervened locally by infusing ouabain through one microdialysis catheter to block major energy expenditure of the cells, by inhibiting the major energy consuming enzyme, N+/K + -ATPase. Similarly, energy production was blocked infusing sodium cyanide (NaCN), in a different region, to block the cytochrome oxidase in muscle tissue mitochondria. Results All animals submitted to sepsis fulfilled sepsis criteria as defined in Sepsis-3, whereas no animals in the placebo group did. Muscle glucose decreased during sepsis independently of N+/K + -ATPase or cytochrome oxidase blockade. Muscle lactate did not increase during sepsis in naïve metabolism. However, during cytochrome oxidase blockade, there was an increase in muscle lactate that was further accentuated during sepsis. Muscle pyruvate did not decrease during sepsis in naïve metabolism. During cytochrome oxidase blockade, there was a decrease in muscle pyruvate, independently of sepsis. Lactate to pyruvate ratio increased during sepsis and was further accentuated during cytochrome oxidase blockade. Muscle glycerol increased during sepsis and decreased slightly without sepsis regardless of N+/K + -ATPase or cytochrome oxidase blocking. There were no significant changes in muscle glutamate or urea during sepsis in absence/presence of N+/K + -ATPase or cytochrome oxidase blockade. ConclusionsThese results indicate increased metabolism of energy substrates in muscle tissue in experimental sepsis. Our results do not indicate presence of energy depletion or mitochondrial dysfunction in muscle and should similar physiologic situation be present in other tissues, other mechanisms of organ failure must be considered. , and long-term follow up has shown increased fracture risk [2]. It is unclear if these changes are a consequence of acute critical illness, or reduced activity afterwards. Bone health assessment during critical illness is challenging, and direct bone strength measurement is not possible. We used a rodent sepsis model to test the hypothesis that critical illness causes early reduction in bone strength and changes in bone architecture. Methods 20 Sprague-Dawley rats (350 ± 15.8g) were anesthetised and randomised to receive cecal ligation and puncture (CLP) (50% cecum length, 18G needle single pass through anterior and posterior wa...

Sepsis is an acute life-threatening multiple organ failure caused by a dysregulated host response to infection. Endothelial dysfunction, particularly barrier disruption leading to increased vascular permeability, edema, and insufficient tissue oxygenation, is critical to sepsis pathogenesis. Sphingosine-1-phosphate (S1P) is a signaling lipid that regulates important pathophysiological processes including vascular endothelial cell permeability, inflammation, and coagulation. It is present at high concentrations in blood and lymph and at very low concentrations in tissues due to the activity of the S1P-degrading enzyme S1P-lyase in tissue cells. Recently, four preclinical observational studies determined S1P levels in serum or plasma of sepsis patients, and all found reduced S1P levels associated with the disease. Based on these findings, this review summarizes S1P-regulated processes pertaining to endothelial functions, discusses the possible use of S1P as a marker and possibilities how to manipulate S1P levels and S1P receptor activation to restore endothelial integrity, dampens the inflammatory host response, and improves organ function in sepsis.

The aim of this study was to evaluate the accuracy and precision of non-invasive continuous blood pressure measurement by applanation tonometry (AT) in awake or anaesthetised cardiological intensive care patients. Patients suffering from highly impaired left ventricular function atrial fibrillation or severe aortic valve stenosis were included into the study. Arterial blood pressure was recorded by applanation tonometry (T-Line 400, Tensys Medical, USA) and an arterial line in awake or anaesthetised patients. Discrepancies in mean (MAP), systolic (SAP), and diastolic (DAP) arterial pressure between the two methods were assessed as bias, limits of agreement and percentage error respectively. In 31 patients a total of 27,900 measurements were analyzed. The concordance correlation coefficient was 0.23, 0.45 and 0.06 for MAP, SAP and DAP, respectively. For all patients bias for MAP compared to MAP was 14.96 mmHg (SAP 4.51 mmHg; DAP 19.12 mmHg) with limits of agreement for MAP of 46.25 and - 16.33 mm Hg (SAP 48.00 and - 38.98 mmHg; DAP 50.12 and - 11.89 mmHg). Percentage error for MAP was 56.8% (42.7% for SAP; 75.2% for DAP). We conclude that the AT method is not reliable in ICU patients with severe cardiac comorbidities.