Effects of cardiac output-guided hemodynamic management on fluid administration after aneurysmal subarachnoid hemorrhage

Introduction: Neurocardiac injury, a type of myocardial dysfunction associated with neurological insult to the brain, occurs in 31–48% of aneurysmal subarachnoid hemorrhage (aSAH) patients. Cardiac troponin I (cTnI) is commonly used to diagnose neurocardiac injury. Brain natriuretic peptide (BNP), another cardiac marker, is more often used to evaluate degree of heart failure. The purpose of this study was to examine the relationships between BNP and (a) neurocardiac injury severity according to cTnI, (b) noninvasive continuous cardiac output (NCCO), and (c) outcomes in aSAH patients. Method: This descriptive longitudinal study enrolled 30 adult aSAH patients. Data collected included BNP and cTnI levels and NCCO parameters for 14 days and outcomes (modified Rankin Scale [mRS] and mortality) at discharge and 3 months. Generalized estimating equations were used to evaluate associations between BNP and cTnI, NCCO, and outcomes. Results: BNP was significantly associated with cTnI. For every 1 unit increase in log BNP, cTnI increased by 0.05 ng/ml ( p = .001). Among NCCO parameters, BNP was significantly associated with thoracic fluid content ( p = .0003). On multivariable analyses, significant associations were found between BNP and poor mRS. For every 1 unit increase in log BNP, patients were 3.16 times more likely to have a poor mRS at discharge ( p = .021) and 5.40 times more likely at 3 months ( p < .0001). Conclusion: There were significant relationships between BNP and cTnI and poor outcomes after aSAH. BNP may have utility as a marker of neurocardiac injury and outcomes after aSAH.

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Bioreactance-Based Noninvasive Fluid Responsiveness and Cardiac Output Monitoring: A Pilot Study in Patients with Aneurysmal Subarachnoid Hemorrhage and Literature Review

Critical Care Research and Practice ◽

10.1155/2020/2748181 ◽

2020 ◽

Vol 2020 ◽

pp. 1-8

Author(s):

Sanjeev Sivakumar ◽

Christos Lazaridis

Keyword(s):

Blood Pressure ◽

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Pulmonary Edema ◽

Fluid Responsiveness ◽

Arterial Blood Pressure ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Cardiac Output Monitoring ◽

Arterial Blood ◽

Pulmonary Manifestations

Management of volume status, arterial blood pressure, and cardiac output are core elements in approaching the patients with aneurysmal subarachnoid hemorrhage (SAH). For the prevention and treatment of delayed cerebral ischemia (DCI), euvolemia is advocated and caution is made towards the avoidance of hypervolemia. Induced hypertension and cardiac output augmentation are the mainstays of medical management during active DCI, whereas the older triple-H paradigm has fallen out of favor due to lack of demonstrable physiological or clinical benefits and serious concern for adverse effects such as pulmonary edema and multiorgan system dysfunction. Furthermore, insight into clinical hemodynamics of patients with SAH becomes salient when one considers the frequently associated cardiac and pulmonary manifestations of the disease such as SAH-associated cardiomyopathy and neurogenic pulmonary edema. In terms of fluid and volume targets, less attention has been paid to dynamic markers of fluid responsiveness despite the well-established, in the general critical care literature, superiority of these as compared to traditionally used static markers such as central venous pressure (CVP). Based on this literature and sound pathophysiologic reasoning, reliance on static markers (such as CVP) is unjustified when one attempts to assess strategies augmenting stroke volume (SV), arterial blood pressure, and oxygen delivery. There are several options for continuous bedside cardiorespiratory monitoring and optimization of SAH patients. We, here, review a noninvasive monitoring technique based on thoracic bioreactance and focusing on continuous cardiac output and fluid responsiveness markers.

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Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic left ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.2003.98.3.0524 ◽

2003 ◽

Vol 98 (3) ◽

pp. 524-528 ◽

Cited By ~ 89

Author(s):

Ketan R. Bulsara ◽

Matthew J. McGirt ◽

Lawrence Liao ◽

Alan T. Villavicencio ◽

Cecil Borel ◽

...

Keyword(s):

Myocardial Infarction ◽

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Left Ventricular Dysfunction ◽

Ventricular Dysfunction ◽

Surgical Intervention ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Left Ventricular ◽

Content Type ◽

Fine Print

Object. Differentiating myocardial infarction (MI) from reversible neurogenic left ventricular dysfunction (stunned myocardium [SM]) associated with aneurysmal subarachnoid hemorrhage (SAH) is critical for early surgical intervention. The authors hypothesized that the cardiac troponin (cTn) trend and/or echocardiogram could be used to differentiate between the two entities. Methods. A retrospective study was conducted for the period between 1995 and 2000. All patients included in the study met the following criteria: 1) no history of cardiac problems; 2) new onset of abnormal cardiac function (ejection fraction [EF] < 40% on echocardiograms); 3) serial cardiac markers (cTn and creatine kinase MB isoform [CK-MB]); 4) surgical intervention for their aneurysm; and 5) cardiac output monitoring either by repeated echocardiograms or invasive hemodynamic monitoring during the first 4 days post-SAH when the patients were euvolemic. Of the 350 patients with SAH, 10 (2.9%) had severe cardiac dysfunction. Of those 10, six were women and four were men. The patients' mean age was 53.5 years (range 29–75 years) and their SAH was classified as Hunt and Hess Grade III or IV. Aneurysm distribution was as follows: basilar artery tip (four); anterior communicating artery (two); middle cerebral artery (one); posterior communicating artery (two); and posterior inferior cerebellar artery (one). The mean EF at onset was 33%. The changes on echocardiograms in these patients did not match the findings on electrocardiograms (EKGs). Within 4.5 days, dramatic improvement was seen in cardiac output (from 4.93 ± 1.16 L/minute to 7.74 ± 0.88 L/minute). Compared with historical controls in whom there were similar levels of left ventricular dysfunction after MI, there was no difference in peak CK-MB. A 10-fold difference, however, was noted in cTn values (0.22 ± 0.25 ng/ml; control 2.8 ng/ml; p < 0.001). Conclusions. The authors determined the following: 1) that the CK-MB trend does not allow differentiation between SM and MI; 2) that echocardiograms revealing significant inconsistencies with EKGs are indicative of SM; and 3) that cTn values less than 2.8 ng/ml in patients with EFs less than 40% are consistent with SM.

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High Early Fluid Input After Aneurysmal Subarachnoid Hemorrhage: Combined Report of Association With Delayed Cerebral Ischemia and Feasibility of Cardiac Output–Guided Fluid Restriction

Journal of Intensive Care Medicine ◽

10.1177/0885066617732747 ◽

2017 ◽

Vol 35 (2) ◽

pp. 161-169 ◽

Cited By ~ 5

Author(s):

Leonie J. M. Vergouw ◽

Mohamud Egal ◽

Bas Bergmans ◽

Diederik W. J. Dippel ◽

Hester F. Lingsma ◽

...

Keyword(s):

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Cerebral Ischemia ◽

Fluid Balance ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Delayed Cerebral Ischemia ◽

Fluid Restriction ◽

Invasive Hemodynamic Monitoring ◽

Risk Patients ◽

Early Fluid

Background: Guidelines on the management of aneurysmal subarachnoid hemorrhage (aSAH) recommend euvolemia, whereas hypervolemia may cause harm. We investigated whether high early fluid input is associated with delayed cerebral ischemia (DCI), and if fluid input can be safely decreased using transpulmonary thermodilution (TPT). Methods: We retrospectively included aSAH patients treated at an academic intensive care unit (2007-2011; cohort 1) or managed with TPT (2011-2013; cohort 2). Local guidelines recommended fluid input of 3 L daily. More fluids were administered when daily fluid balance fell below +500 mL. In cohort 2, fluid input in high-risk patients was guided by cardiac output measured by TPT per a strict protocol. Associations of fluid input and balance with DCI were analyzed with multivariable logistic regression (cohort 1), and changes in hemodynamic indices after institution of TPT assessed with linear mixed models (cohort 2). Results: Cumulative fluid input 0 to 72 hours after admission was associated with DCI in cohort 1 (n=223; odds ratio [OR] 1.19/L; 95% confidence interval 1.07-1.32), whereas cumulative fluid balance was not. In cohort 2 (23 patients), using TPT fluid input could be decreased from 6.0 ± 1.0 L before to 3.4 ± 0.3 L; P = .012), while preload parameters and consciousness remained stable. Conclusion: High early fluid input was associated with DCI. Invasive hemodynamic monitoring was feasible to reduce fluid input while maintaining preload. These results indicate that fluid loading beyond a normal preload occurs, may increase DCI risk, and can be minimized with TPT.

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Transpulmonary thermodilution monitoring–guided hemodynamic management improves cognitive function in patients with aneurysmal subarachnoid hemorrhage: a prospective cohort comparison

Acta Neurochirurgica ◽

10.1007/s00701-019-03922-4 ◽

2019 ◽

Vol 161 (7) ◽

pp. 1317-1324 ◽

Cited By ~ 1

Author(s):

Achmet Ali ◽

Taner Abdullah ◽

Mukadder Orhan-Sungur ◽

Gunseli Orhun ◽

Elif Aygun ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Cognitive Function ◽

Prospective Cohort ◽

Transpulmonary Thermodilution ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Hemodynamic Management ◽

Cohort Comparison

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Dose Optimization Study of Therapeutic Hypercapnia for Prevention of Secondary Ischemia After Severe Subarachnoid Hemorrhage

10.21203/rs.3.rs-138551/v1 ◽

2021 ◽

Author(s):

Christian Stetter ◽

Franziska Weidner ◽

Nadine Lilla ◽

Judith Weiland ◽

Ekkehard Kunze ◽

...

Keyword(s):

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Rebound Effect ◽

Comparative Trial ◽

Target Range ◽

Tissue Oxygen Saturation ◽

Enhancing Effect ◽

Poor Grade ◽

Arterial Blood

Abstract BackgroundAim of this study was to investigate the time point at which the cerebral blood flow (CBF) enhancing effect of controlled hypercapnia in patients with severe aneurysmal subarachnoid hemorrhage (SAH) starts to extenuate. This point is assumed to be the time at which buffer systems become active and annihilate a possible therapeutic effect. MethodsIn this prospective interventional study in a neurosurgical ICU the arterial partial pressure of carbon dioxide (PaCO2) was increased to a target range of 50 - 55 mmHg for 120 minutes by modification of the respiratory minute volume (RMV) one time a day between day 4 and 14 in 12 mechanically ventilated poor-grade SAH-patients. Arterial blood gases were measured every 15 minutes. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary end points. Intracranial pressure (ICP) was controlled by an external ventricular drainage. ResultsUnder continuous hypercapnia (PaCO2 of 53.17 ± 5.07), CBF was significantly elevated between 15 and 120 minutes after the start of hypercapnia. During the course of the trial intervention, cardiac output also increased significantly. To assess the direct effect of hypercapnia on brain perfusion, the increase of CBF was corrected by the parallel increase of cardiac output. The maximum direct CBF enhancing effect of hypercapnia of 31% was noted at 45 minutes after the start of hypercapnia. Thereafter, the CBF enhancing slowly declined. No relevant adverse effects were observed. Conclusion CBF and StiO2 reproducibly increased by controlled hypercapnia in all patients. After 45 minutes, the curve of CBF enhancement showed an inflection point when corrected by cardiac output. Temporary hypercapnia of 45 minutes is, thus, likely to be the optimum duration for a therapeutic use and for a controlled comparative trial. Longer intervals bear the risk of a negative rebound effect after return to normal ventilation parameters and may be counterproductive inducing ischemia in a state of critical perfusion after SAH. Trial registrationThe study was approved by the institutional ethics committee (AZ 230/14) and registered at ClinicalTrials.gov (Trial-ID: NCT01799525). Registered 01 January 2015. Retrospectively registered.

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The effect of the volemic and cardiac status on brain oxygenation in patients with subarachnoid hemorrhage: a bi-center cohort study

Annals of Intensive Care ◽

10.1186/s13613-021-00960-z ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Verena Rass ◽

Elisa Gouvea Bogossian ◽

Bogdan-Andrei Ianosi ◽

Lorenzo Peluso ◽

Mario Kofler ◽

...

Keyword(s):

Cardiac Output ◽

Subarachnoid Hemorrhage ◽

Brain Tissue ◽

Fluid Management ◽

Repeated Measurements ◽

Brain Oxygenation ◽

Brain Tissue Oxygenation ◽

Hemodynamic Management ◽

Poor Grade ◽

Normal Ranges

Abstract Background Fluid management in patients after subarachnoid hemorrhage (SAH) aims at the optimization of cerebral blood flow and brain oxygenation. In this study, we investigated the effects of hemodynamic management on brain oxygenation by integrating advanced hemodynamic and invasive neuromonitoring. Methods This observational cohort bi-center study included data of consecutive poor-grade SAH patients who underwent pulse contour cardiac output (PiCCO) monitoring and invasive neuromonitoring. Fluid management was guided by the transpulmonary thermodilution system and aimed at euvolemia (cardiac index, CI ≥ 3.0 L/min/m2; global end-diastolic index, GEDI 680–800 mL/m2; stroke volume variation, SVV < 10%). Patients were managed using a brain tissue oxygenation (PbtO2) targeted protocol to prevent brain tissue hypoxia (BTH, PbtO2 < 20 mmHg). To assess the association between CI and PbtO2 and the effect of fluid challenges on CI and PbtO2, we used generalized estimating equations to account for repeated measurements. Results Among a total of 60 included patients (median age 56 [IQRs 47–65] years), BTH occurred in 23% of the monitoring time during the first 10 days since admission. Overall, mean CI was within normal ranges (ranging from 3.1 ± 1.3 on day 0 to 4.1 ± 1.1 L/min/m2 on day 4). Higher CI levels were associated with higher PbtO2 levels (Wald = 14.2; p < 0.001). Neither daily fluid input nor fluid balance was associated with absolute PbtO2 levels (p = 0.94 and p = 0.85, respectively) or the occurrence of BTH (p = 0.68 and p = 0.71, respectively). PbtO2 levels were not significantly different in preload dependent patients compared to episodes of euvolemia. PbtO2 increased as a response to fluid boluses only if BTH was present at baseline (from 13 ± 6 to 16 ± 11 mmHg, OR = 13.3 [95% CI 2.6–67.4], p = 0.002), but not when all boluses were considered (p = 0.154). Conclusions In this study a moderate association between increased cardiac output and brain oxygenation was observed. Fluid challenges may improve PbtO2 only in the presence of baseline BTH. Individualized hemodynamic management requires advanced cardiac and brain monitoring in critically ill SAH patients.

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