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

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.

scholarly journals Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Christian Stetter ◽  
Franziska Weidner ◽  
Nadine Lilla ◽  
Judith Weiland ◽  
Ekkehard Kunze ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Cardiac Output ◽  
Subarachnoid Hemorrhage ◽  
Partial Pressure ◽  
Rebound Effect ◽  
Target Range ◽  
Tissue Oxygen Saturation ◽  
Arterial Partial Pressure ◽  
Optimum Duration ◽  
Arterial Blood

AbstractTemporary hypercapnia has been shown to increase cerebral blood flow (CBF) and might be used as a therapeutical tool in patients with severe subarachnoid hemorrhage (SAH). It was the aim of this study was to investigate the optimum duration of hypercapnia. This point is assumed to be the time at which buffer systems become active, cause an adaptation to changes of the arterial partial pressure of carbon dioxide (PaCO2) and annihilate a possible therapeutic effect. In this prospective interventional study in a neurosurgical ICU the arterial partial pressure of carbon dioxide (PaCO2) was increased to a target range of 55 mmHg for 120 min 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 min. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary end points. Intracranial pressure (ICP) was controlled by an external ventricular drainage. Under continuous hypercapnia (PaCO2 of 53.17 ± 5.07), CBF was significantly elevated between 15 and 120 min 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 32% was noted at 45 min after the start of hypercapnia. Thereafter, the CBF enhancing slowly declined. No relevant adverse effects were observed. CBF and StiO2 reproducibly increased by controlled hypercapnia in all patients. After 45 min, the curve of CBF enhancement showed an inflection point when corrected by cardiac output. It is concluded that 45 min might be the optimum duration for a therapeutic use and may provide an optimal balance between the benefits of hypercapnia and risks of a negative rebound effect after return to normal ventilation parameters.Trial registration: The study was approved by the institutional ethics committee (AZ 230/14) and registered at ClinicalTrials.gov (Trial-ID: NCT01799525). Registered 01/01/2015.

Controlled transient hypercapnia: a novel approach for the treatment of delayed cerebral ischemia after subarachnoid hemorrhage?

2014 ◽  
Vol 121 (5) ◽  
pp. 1056-1062 ◽  
Author(s):  
Thomas Westermaier ◽  
Christian Stetter ◽  
Ekkehard Kunze ◽  
Nadine Willner ◽  
Judith Holzmeier ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Near Infrared ◽  
Therapeutic Potential ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rebound Effect ◽  
Delayed Cerebral Ischemia ◽  
Physiological Mechanism ◽  
Tissue Oxygen Saturation ◽  
Poor Grade ◽  
Continuous Drainage

Object The authors undertook this study to investigate whether the physiological mechanism of cerebral blood flow (CBF) regulation by alteration of the arterial partial pressure of carbon dioxide (PaCO2) can be used to increase CBF after aneurysmal subarachnoid hemorrhage (aSAH). Methods In 6 mechanically ventilated patients with poor-grade aSAH, the PaCO2 was first decreased to 30 mm Hg by modification of the respiratory rate, then gradually increased to 40, 50 and 60 mm Hg for 15 minutes each setting. Thereafter, the respirator settings were returned to baseline parameters. Intracerebral CBF measurement and brain tissue oxygen saturation (StiO2), measured by near-infrared spectroscopy (NIRS), were the primary and secondary end points. Intracranial pressure (ICP) was controlled by external ventricular drainage. Results A total of 60 interventions were performed in 6 patients. CBF decreased to 77% of baseline at a PaCO2 of 30 mm Hg and increased to 98%, 124%, and 143% at PaCO2 values of 40, 50, and 60 mm Hg, respectively. Simultaneously, StiO2 decreased to 94%, then increased to 99%, 105%, and 111% of baseline. A slightly elevated delivery rate of cerebrospinal fluid was noticed under continuous drainage. ICP remained constant. After returning to baseline respirator settings, both CBF and StiO2 remained elevated and only gradually returned to pre-hypercapnia values without a rebound effect. None of the patients developed secondary cerebral infarction. Conclusions Gradual hypercapnia was well tolerated by poor-grade SAH patients. Both CBF and StiO2 reacted with a sustained elevation upon hypercapnia; this elevation outlasted the period of hypercapnia and only slowly returned to normal without a rebound effect. Elevations of ICP were well compensated by continuous CSF drainage. Hypercapnia may yield a therapeutic potential in this state of critical brain perfusion. Clinical trial registration no.: NCT01799525 (ClinicalTrials.gov).

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

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.

scholarly journals Clinical condition of 120 patients alive at 3 years after poor-grade aneurysmal subarachnoid hemorrhage

2021 ◽  
Author(s):  
Anniina H. Autio ◽  
Juho Paavola ◽  
Joona Tervonen ◽  
Maarit Lång ◽  
Terhi J. Huuskonen ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Clinical Condition ◽  
Hospice Care ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Blood Clot ◽  
Neurointensive Care ◽  
Intracerebral Hematoma ◽  
Poor Grade ◽  
Final Study ◽  
Study Population

Abstract Background To study the clinical condition of poor-grade aneurysmal subarachnoid hemorrhage (aSAH) patients alive at 3 years after neurointensive care. Methods Of the 769 consecutive aSAH patients from a defined population (2005–2015), 269 (35%) were in poor condition on admission: 145 (54%) with H&H 4 and 124 (46%) with H&H 5. Their clinical lifelines were re-constructed from the Kuopio Intracranial Aneurysm Database and Finnish nationwide registries. Of the 269 patients, 155 (58%) were alive at 14 days, 125 (46%) at 12 months, and 120 (45%) at 3 years. Results The 120 H&H 4–5 patients alive at 3 years form the final study population. On admission, 73% had H&H 4 but only 27% H&H 5, 59% intracerebral hematoma (ICH; median 22 cm3), and 26% intraventricular blood clot (IVH). The outcome was favorable (mRS 0–1) in 45% (54 patients: ICH 44%; IVH clot 31%; shunt 46%), moderate (mRS 2–3) in 30% (36 patients: ICH 64%; IVH clot 19%; shunt 42%), and unfavorable (mRS 4–5) in 25% (30 patients: ICH 80%; IVH clot 23%; shunt 50%). A total of 46% carried a ventriculoperitoneal shunt. ICH volume was a significant predictor of mRS at 3 years. Conclusions Of poor-grade aSAH patients, 45% were alive at 3 years, even 27% of those extending to pain (H&H 5). Of the survivors, 75% were at least in moderate condition, while only 2.6% ended in hospice care. Consequently, we propose non-selected admission to neurointensive care (1) for a possibility of moderate outcome, and (2), in case of brain death, possibly improved organ donation rates.

scholarly journals The venous delay phenomenon in computed tomography angiography: a novel imaging outcome predictor for poor cerebral perfusion after severe aneurysmal subarachnoid hemorrhage

2018 ◽  
Vol 129 (4) ◽  
pp. 876-882 ◽  
Author(s):  
Po-Chuan Hsieh ◽  
Yi-Ming Wu ◽  
Alvin Yi-Chou Wang ◽  
Ching-Chang Chen ◽  
Chien-Hung Chang ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Multivariable Analysis ◽  
Outcome Predictor ◽  
Treatment Results ◽  
Tertiary Referral Center ◽  
Poor Grade ◽  
Poor Outcome ◽  
Delay Phenomenon

OBJECTIVEDiverse treatment results are observed in patients with poor-grade aneurysmal subarachnoid hemorrhage (aSAH). Significant initial perfusion compromise is thought to predict a worse treatment outcome, but this has scant support in the literature. In this cohort study, the authors correlate the treatment outcomes with a novel poor-outcome imaging predictor representing impaired cerebral perfusion on initial CT angiography (CTA).METHODSThe authors reviewed the treatment results of 148 patients with poor-grade aSAH treated at a single tertiary referral center between 2007 and 2016. Patients with the “venous delay” phenomenon on initial CTA were identified. The outcome assessments used the modified Rankin Scale (mRS) at the 3rd month after aSAH. Factors that may have had an impact on outcome were retrospectively analyzed.RESULTSCompared with previously identified outcome predictors, the venous delay phenomenon on initial CTA was found to have the strongest correlation with posttreatment outcomes on both univariable (p < 0.0001) and multivariable analysis (OR 4.480, 95% CI 1.565–12.826; p = 0.0052). Older age and a higher Hunt and Hess grade at presentation were other factors that were associated with poor outcome, defined as an mRS score of 3 to 6.CONCLUSIONSThe venous delay phenomenon on initial CTA can serve as an imaging predictor for worse functional outcome and may aid in decision making when treating patients with poor-grade aSAH.

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