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Marek Czosnyka - One of the best experts on this subject based on the ideXlab platform.
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flow velocity pulsatility index autoregulation and critical Closing Pressure
2021Co-Authors: Marta Fedriga, Marek CzosnykaAbstract:Brain ultrasonography enables us to detect the flow velocity of the main arteries and veins of the brain other than the main brain structures, depending on the presence of an adequate insonation window and on the device we are using, whether transcranial Doppler (TCD) or transcranial colour-coded Doppler (TCCD). In this chapter, we describe basic and advance parameters that can be measured and calculated assessing the flow velocity of red blood cells flowing through the brain main arteries.
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transcranial doppler non invasive assessment of intracranial Pressure autoregulation of cerebral blood flow and critical Closing Pressure during orthotopic liver transplant
Ultrasound in Medicine and Biology, 2019Co-Authors: Marek Czosnyka, Joseph Donnelly, Danilo Cardim, Chiara Robba, Eric A Schmidt, Bernhard Schmidt, John KlinckAbstract:Abstract Transcranial Doppler (TCD) ultrasonography allows continuous non-invasive monitoring of cerebral blood flow velocity in a variety of clinical conditions. Recently, signal processing of TCD signals has provided several comprehensive parameters for the assessment of cerebral haemodynamics. In this work, we applied a TCD multimodal approach in patients with acute liver failure undergoing orthotopic liver transplant (OLT) to assess the clinical feasibility of using TCD for cerebral haemodynamics assessment in this setting. We retrospectively studied six patients undergoing OLT with continuous monitoring of arterial blood Pressure and blood flow velocity in the middle cerebral artery. The main cerebral haemodynamic parameters assessed were non-invasive intracranial Pressure, cerebral perfusion Pressure, cerebral autoregulation, pulsatility index, critical Closing Pressure and diastolic Closing margin. TCD monitoring revealed marked alterations of these parameters in the OLT setting, which could provide relevant clinical information when there is imminent risk of neurologic impairment.
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transcranial doppler a stethoscope for the brain neurocritical care use
Journal of Neuroscience Research, 2018Co-Authors: Danilo Cardim, Karol P Budohoski, Chiara Robba, Mypinder S Sekhon, Marek CzosnykaAbstract:Transcranial Doppler (TCD) ultrasonography is a noninvasive bedside monitoring technique that can evaluate cerebral blood flow hemodynamics in the intracranial arterial vasculature. TCD allows assessment of linear cerebral blood flow velocity, with a high temporal resolution and is inexpensive, reproducible, and portable. The aim of this review is to provide an overview of the most commonly used TCD derived signals and measurements used commonly in neurocritical care. We describe both basic (flow velocity, pulsatility index) and advanced concepts, including critical Closing Pressure, wall tension, autoregulation, noninvasive intracranial Pressure, brain compliance, and cerebrovascular time constant; we also describe the clinical applications of TCD to highlight their utility in the diagnosis and monitoring of cerebrovascular diseases as the “stethoscope for the brain.”
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effect of mild hypocapnia on critical Closing Pressure and other mechanoelastic parameters of the cerebrospinal system
Acta Neurochirurgica, 2018Co-Authors: Peter Smielewski, Georgios V Varsos, Karol P Budohoski, Luzius A Steiner, Corina Puppo, Marek CzosnykaAbstract:Objective: Brain arterial critical Closing Pressure (CrCP) has been studied in several diseases such as traumatic brain injury (TBI), subarachnoid haemorrhage, hydrocephalus, and in various physiological scenarios: intracranial hypertension, decreased cerebral perfusion Pressure, hypercapnia, etc. Little or nothing so far has been demonstrated to characterise change in CrCP during mild hypocapnia.
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critical Closing Pressure during a controlled increase in intracranial Pressure
Acta Neurochirurgica, 2018Co-Authors: Katarzyna Kaczmarska, Peter Smielewski, Marek Czosnyka, Georgios V Varsos, Magdalena Kasprowicz, Antoni Grzanka, Wojciech M Zabolotny, Despina Afroditi Lalou, Zofia CzosnykaAbstract:Objectives: The objectives were to compare three methods of estimating critical Closing Pressure (CrCP) in a scenario of a controlled increase in intracranial Pressure (ICP) induced during an infusion test in patients with suspected normal Pressure hydrocephalus (NPH).
Danny J Eckert - One of the best experts on this subject based on the ideXlab platform.
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upper airway collapsibility measured using a simple wakefulness test closely relates to the pharyngeal critical Closing Pressure during sleep in obstructive sleep apnea
Sleep, 2019Co-Authors: Danny J Eckert, Amal M Osman, Jayne C Carberry, Peter G R Burke, Barbara Toson, Ronald R GrunsteinAbstract:STUDY OBJECTIVES A collapsible or crowded pharyngeal airway is the main cause of obstructive sleep apnea (OSA). However, quantification of airway collapsibility during sleep (Pcrit) is not clinically feasible. The primary aim of this study was to compare upper airway collapsibility using a simple wakefulness test with Pcrit during sleep. METHODS Participants with OSA were instrumented with a nasal mask, pneumotachograph and two Pressure sensors, one at the choanae (PCHO), the other just above the epiglottis (PEPI). Approximately 60 brief (250 ms) pulses of negative airway Pressure (~ -12 cmH2O at the mask) were delivered in early inspiration during wakefulness to measure the upper airway collapsibility index (UACI). Transient reductions in the continuous positive airway Pressure (CPAP) holding Pressure were then performed during sleep to determine Pcrit. In a subset of participants, the optimal number of replicate trials required to calculate the UACI was assessed. RESULTS The UACI (39 ± 24 mean ± SD; range = 0%-87%) and Pcrit (-0.11 ± 2.5; range: -4 to +5 cmH2O) were quantified in 34 middle-aged people (9 female) with varying OSA severity (apnea-hypopnea index range = 5-92 events/h). The UACI at a mask Pressure of approximately -12 cmH2O positively correlated with Pcrit (r = 0.8; p < 0.001) and could be quantified reliably with as few as 10 replicate trials. The UACI performed well at discriminating individuals with subatmospheric Pcrit values [receiver operating characteristic curve analysis area under the curve = 0.9 (0.8-1), p < 0.001]. CONCLUSIONS These findings indicate that a simple wakefulness test may be useful to estimate the extent of upper airway anatomical impairment during sleep in people with OSA to direct targeted non-CPAP therapies for OSA.
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role of common hypnotics on the phenotypic causes of obstructive sleep apnoea paradoxical effects of zolpidem
European Respiratory Journal, 2017Co-Authors: Jayne C Carberry, Ronald R Grunstein, Lauren P Fisher, Simon C Gandevia, David K Mckenzie, Jane E Butler, Danny J EckertAbstract:Hypnotics are contraindicated in obstructive sleep apnoea (OSA) because of concerns of pharyngeal muscle relaxation and delayed arousal worsening hypoxaemia. However, human data are lacking. This study aimed to determine the effects of three common hypnotics on the respiratory arousal threshold, genioglossus muscle responsiveness and upper airway collapsibility during sleep. 21 individuals with and without OSA (18–65 years) completed 84 detailed sleep studies after receiving temazepam (10 mg), zolpidem (10 mg), zopiclone (7.5 mg) and placebo on four occasions in a randomised, double-blind, placebo-controlled, crossover trial (ACTRN12612001004853). The arousal threshold increased with zolpidem and zopiclone versus placebo (mean±sd −18.3±10 and −19.1±9 versus −14.6±7 cmH 2 O; p=0.02 and p 2 O; p=0.17). Genioglossus muscle activity during stable non-REM sleep and responsiveness during airway narrowing was not different with temazepam and zopiclone versus placebo but, paradoxically, zolpidem increased median muscle responsiveness three-fold during airway narrowing (median −0.15 (interquartile range −1.01 to −0.04) versus −0.05 (−0.29 to −0.03)% maximum EMG per cmH 2 O epiglottic Pressure; p=0.03). The upper airway critical Closing Pressure did not change with any of the hypnotics. These doses of common hypnotics have differential effects on the respiratory arousal threshold but do not reduce upper airway muscle activity or alter airway collapsibility during sleep. Rather, muscle activity increases during airway narrowing with zolpidem.
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Please send correspondence to:
2016Co-Authors: Danny J Eckert, Nancy L Chamberlin, Amy S Jordan, Phd^ Sebastian Zaremba, Matthias EikermannAbstract:Question of the study: We hypothesized that pentobarbital would improve upper airway mechanics based on an increase in: a) latency to arousal, b) amplitude of the phasic genioglossus electromyogram, and decrease in: c) the active upper-airway critical Closing Pressure (Pcrit). Materials and methods: Twelve healthy subjects received pentobarbital 100 mg or placebo in a double-blind, cross-over protocol. During wakefulness, we measured the genioglossus reflex response to negative-Pressure pulses. During sleep, carbon dioxide was insufflated into the inspired air. Airway Pressure was then decreased in a stepwise fashion until arousal from sleep. Results: With basal breathing during sleep, flow-rate was lower in volunteers given pentobarbital, end-tidal carbon dioxide concentration and upper airway resistance wer
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upper airway collapsibility and patterns of flow limitation at constant end expiratory lung volume
Journal of Applied Physiology, 2012Co-Authors: Robert L Owens, Danny J Eckert, Atul Malhotra, Bradley A Edwards, Scott A Sands, James P Butler, David P White, Andrew WellmanAbstract:The passive pharyngeal critical Closing Pressure (Pcrit) is measured using a series of Pressure drops. However, Pressure drops also lower end-expiratory lung volume (EELV), which independently affe...
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critical Closing Pressure during midazolam induced sleep
Journal of Applied Physiology, 2011Co-Authors: Pedro R Genta, Danny J Eckert, Atul Malhotra, Marcelo Gervilla Gregorio, Naury J Danzi, Henrique Takachi Moriya, Geraldo LorenzifilhoAbstract:The critical Closing Pressure (Pcrit) is the airway Pressure at which the airway collapses and reflects the anatomical contribution to the genesis of obstructive sleep apnea. Pcrit is usually deter...
Atul Malhotra - One of the best experts on this subject based on the ideXlab platform.
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Running Head: Determinants of UAW calibre.. Address for Correspondence:
2016Co-Authors: Robert Pierce, Atul Malhotra, David White, Jill K Edwards, Lyle Palmer, John Trinder, Prof Rob PierceAbstract:The calibre of the upper airway is thought dependant upon its passive anatomy/collapsibility and the activation of pharyngeal dilator muscles. Awake, the more collapsible upper airway in obstructive sleep apnea (OSA) increases dilator muscle activity through a negative Pressure reflex (NPR). We hypothesised a direct correlation between the Closing Pressure of the passive upper airway (Pcrit) as a measure of anatomy/collapsability and EMG activity of genioglossus (GGEMG) and tensor palatini (TPEMG). We also set out to determine the relationship between these indices and pharyngeal resistance (Rphar). We studied 8 males with OSA aged 48 (46,52) years, [median (IQR)], AHI 75 (65, 101) / hr on two nights- breathing normally and on nCPAP. Pcrit was measured during NREM sleep on nCPAP using brief, incremental reductions in Pmask. GGEMG and TPEMG were measured breath-by-breath, awake, during sleep onset and on nCPAP. Rphar was measured from airway Pressures and flow. Wakeful GGEMG, early sleep TPEMG and the sleep decrement in TPEMG were directly related to Pcrit. Muscle activation was negatively correlated with Rphar for TPEMG awake an
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upper airway collapsibility and patterns of flow limitation at constant end expiratory lung volume
Journal of Applied Physiology, 2012Co-Authors: Robert L Owens, Danny J Eckert, Atul Malhotra, Bradley A Edwards, Scott A Sands, James P Butler, David P White, Andrew WellmanAbstract:The passive pharyngeal critical Closing Pressure (Pcrit) is measured using a series of Pressure drops. However, Pressure drops also lower end-expiratory lung volume (EELV), which independently affe...
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critical Closing Pressure during midazolam induced sleep
Journal of Applied Physiology, 2011Co-Authors: Pedro R Genta, Danny J Eckert, Atul Malhotra, Marcelo Gervilla Gregorio, Naury J Danzi, Henrique Takachi Moriya, Geraldo LorenzifilhoAbstract:The critical Closing Pressure (Pcrit) is the airway Pressure at which the airway collapses and reflects the anatomical contribution to the genesis of obstructive sleep apnea. Pcrit is usually deter...
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effects of pentobarbital on upper airway patency during sleep
European Respiratory Journal, 2010Co-Authors: Matthias Eikermann, Danny J Eckert, Nancy L Chamberlin, Amy S Jordan, Carl E Rosow, Scott Smith, Sam Zaremba, Atul MalhotraAbstract:We hypothesised that pentobarbital would improve upper airway mechanics based on an increase in latency to arousal and amplitude of the phasic genioglossus electromyogram (EMG), and a decrease in the active upper airway critical Closing Pressure ( P crit ). 12 healthy subjects received pentobarbital (100 mg) or placebo in a double-blind, crossover protocol. During wakefulness, we measured the genioglossus reflex response to negative Pressure pulses. During sleep, carbon dioxide was insufflated into the inspired air. Airway Pressure was then decreased in a stepwise fashion until arousal from sleep. With basal breathing during sleep: flow rate was lower in volunteers given pentobarbital; end-tidal CO 2 concentration and upper airway resistance were greater; and P crit was unaffected (pentobarbital mean±sd -11.7±4.5 versus placebo -10.25±3.6 cmH 2 O; p = 0.11). Pentobarbital increased the time to arousal (297±63s versus 232±67 s; p versus 3.1±3%; p 2 levels. The increase in genioglossus EMG after CO 2 administration was greater after pentobarbital versus placebo. Pentobarbital did not affect the genioglossus negative-Pressure reflex. Pentobarbital increases the time to arousal and stimulates genioglossus muscle activity, but it also increases upper airway resistance during sleep.
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upper airway collapsibility dilator muscle activation and resistance in sleep apnoea
European Respiratory Journal, 2007Co-Authors: Robert J Pierce, Atul Malhotra, David P White, Jill K Edwards, Darci Kleverlaan, Lyle J Palmer, John TrinderAbstract:The calibre of the upper airway is thought to be dependant upon its passive anatomy/collapsibility and the activation of pharyngeal dilator muscles. During awake periods, the more collapsible upper airway in obstructive sleep apnoea (OSA) increases the dilator muscle activity through a negative-Pressure reflex. A direct correlation between the critical Closing Pressure (P(crit)), as a measure of anatomy/collapsability and electromyogram (EMG) activity of genioglossus EMG (GG-EMG) and tensor palatini EMG (TP-EMG), was hypothesised. The relationship between these indices and pharyngeal resistance (R(phar)) was also examined. The study involved eight males with a mean age of 48 (interquartile range 46-52) yrs with OSA, and an apnoea/hypopnoea index of 75 (65-101).hr(-1) on two nights breathing normally and on nasal continuous positive airway Pressure (nCPAP). The P(crit )was measured during nonrapid eye movement sleep on nCPAP using brief, incremental reductions in mask Pressure. GG-EMG and TP-EMG were measured breath-by-breath, awake, during sleep onset and on nCPAP. R(phar) was measured using airway Pressures and flow. Wakeful GG-EMG, early sleep TP-EMG and the sleep decrement in TP-EMG were directly related to P(crit). Muscle activation was negatively correlated with R(phar) for TP-EMG awake and GG-EMG early in sleep. In conclusion these results confirm that dilator muscle activation is directly related to airway narrowing and reduces resistance across patients with obstructive sleep apnoea.
Matthias Eikermann - One of the best experts on this subject based on the ideXlab platform.
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Please send correspondence to:
2016Co-Authors: Danny J Eckert, Nancy L Chamberlin, Amy S Jordan, Phd^ Sebastian Zaremba, Matthias EikermannAbstract:Question of the study: We hypothesized that pentobarbital would improve upper airway mechanics based on an increase in: a) latency to arousal, b) amplitude of the phasic genioglossus electromyogram, and decrease in: c) the active upper-airway critical Closing Pressure (Pcrit). Materials and methods: Twelve healthy subjects received pentobarbital 100 mg or placebo in a double-blind, cross-over protocol. During wakefulness, we measured the genioglossus reflex response to negative-Pressure pulses. During sleep, carbon dioxide was insufflated into the inspired air. Airway Pressure was then decreased in a stepwise fashion until arousal from sleep. Results: With basal breathing during sleep, flow-rate was lower in volunteers given pentobarbital, end-tidal carbon dioxide concentration and upper airway resistance wer
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effects of depth of propofol and sevoflurane anesthesia on upper airway collapsibility respiratory genioglossus activation and breathing in healthy volunteers
Anesthesiology, 2016Co-Authors: Jeroen C P Simons, Carl E Rosow, Eric T Pierce, Daniel Diazgil, Sanjana A Malviya, Matthew J Meyer, Fanny P Timm, Janne B Stokholm, Robert M Kacmarek, Matthias EikermannAbstract:BACKGROUND Volatile anesthetics and propofol impair upper airway stability and possibly respiratory upper airway dilator muscle activity. The magnitudes of these effects have not been compared at equivalent anesthetic doses. We hypothesized that upper airway Closing Pressure is less negative and genioglossus activity is lower during deep compared with shallow anesthesia. METHODS In a randomized controlled crossover study of 12 volunteers, anesthesia with propofol or sevoflurane was titrated using a pain stimulus to identify the threshold for suppression of motor response to electrical stimulation. Measurements included bispectral index, genioglossus electromyography, ventilation, hypopharyngeal Pressure, upper airway Closing Pressure, and change in end-expiratory lung volume during mask Pressure drops. RESULTS A total of 393 attempted breaths during occlusion maneuvers were analyzed. Upper airway Closing Pressure was significantly less negative at deep versus shallow anesthesia (-10.8 ± 4.5 vs. -11.3 ± 4.4 cm H2O, respectively [mean ± SD]) and correlated with the bispectral index (P < 0.001), indicating a more collapsible airway at deep anesthesia. Respiratory genioglossus activity during airway occlusion was significantly lower at deep compared with light anesthesia (26 ± 21 vs. 35 ± 24% of maximal genioglossus activation, respectively; P < 0.001) and correlated with bispectral index (P < 0.001). Upper airway Closing Pressure and genioglossus activity during airway occlusion did not differ between sevoflurane and propofol anesthesia. CONCLUSIONS Propofol and sevoflurane anesthesia increased upper airway collapsibility in a dose-dependent fashion with no difference at equivalent anesthetic concentrations. These effects can in part be explained by a dose-dependent inhibiting effect of anesthetics on respiratory genioglossus activity.
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effects of pentobarbital on upper airway patency during sleep
European Respiratory Journal, 2010Co-Authors: Matthias Eikermann, Danny J Eckert, Nancy L Chamberlin, Amy S Jordan, Carl E Rosow, Scott Smith, Sam Zaremba, Atul MalhotraAbstract:We hypothesised that pentobarbital would improve upper airway mechanics based on an increase in latency to arousal and amplitude of the phasic genioglossus electromyogram (EMG), and a decrease in the active upper airway critical Closing Pressure ( P crit ). 12 healthy subjects received pentobarbital (100 mg) or placebo in a double-blind, crossover protocol. During wakefulness, we measured the genioglossus reflex response to negative Pressure pulses. During sleep, carbon dioxide was insufflated into the inspired air. Airway Pressure was then decreased in a stepwise fashion until arousal from sleep. With basal breathing during sleep: flow rate was lower in volunteers given pentobarbital; end-tidal CO 2 concentration and upper airway resistance were greater; and P crit was unaffected (pentobarbital mean±sd -11.7±4.5 versus placebo -10.25±3.6 cmH 2 O; p = 0.11). Pentobarbital increased the time to arousal (297±63s versus 232±67 s; p versus 3.1±3%; p 2 levels. The increase in genioglossus EMG after CO 2 administration was greater after pentobarbital versus placebo. Pentobarbital did not affect the genioglossus negative-Pressure reflex. Pentobarbital increases the time to arousal and stimulates genioglossus muscle activity, but it also increases upper airway resistance during sleep.
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impaired upper airway integrity by residual neuromuscular blockade increased airway collapsibility and blunted genioglossus muscle activity in response to negative pharyngeal Pressure
Anesthesiology, 2009Co-Authors: Frank Herbstreit, Jurgen Peters, Matthias EikermannAbstract:BACKGROUND Residual neuromuscular blockade increases the risk to develop postoperative complications. The authors hypothesized that minimal neuromuscular blockade (train-of-four [TOF] ratio 0.5-1) increases upper airway collapsibility and impairs upper airway dilator muscle compensatory responses to negative pharyngeal Pressure challenges. METHODS Epiglottic and nasal mask Pressures, genioglossus electromyogram, respiratory timing, and changes in lung volume were measured in awake healthy volunteers (n = 15) before, during (TOF = 0.5 and 0.8 [steady state]), and after recovery of TOF to unity from rocuronium-induced partial neuromuscular blockade. Passive upper airway Closing Pressure (negative Pressure drops, random order, range +2 to -30 cm H2O) and Pressure threshold for flow limitation were determined. RESULTS Upper airway Closing Pressure increased (was less negative) significantly from baseline by 54 +/- 4.4% (means +/- SEM), 37 +/- 4.2%, and 16 +/- 4.1% at TOF ratios of 0.5, 0.8, and 1.0, respectively (P < 0.01 vs. baseline for any level). Phasic genioglossus activity almost quadrupled in response to negative (-20 cm H2O) pharyngeal Pressure at baseline, and this increase was significantly impaired by 57 +/- 44% and 32 +/- 6% at TOF ratios of 0.5 and 0.8, respectively (P < 0.01 vs. baseline). End-expiratory lung volume, respiratory rate, and tidal volume did not change. CONCLUSION Minimal neuromuscular blockade markedly increases upper airway Closing Pressure, partly by impairing the genioglossus muscle compensatory response. Increased airway collapsibility despite unaffected values for resting ventilation may predispose patients to postoperative respiratory complications, particularly during airway challenges.
Georgios V Varsos - One of the best experts on this subject based on the ideXlab platform.
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critical Closing Pressure during experimental intracranial hypertension comparison of three calculation methods
Neurological Research, 2020Co-Authors: Katarzyna Kaczmarska, Georgios V Varsos, Magdalena Kasprowicz, Zofia Czosnyka, Agnieszka Uryga, Michal M Placek, Leanne Calviello, Ewa Koźniewska, Tomasz Sierzputowski, Waldemar KoszewskiAbstract:Objectives: The critical Closing Pressure (CrCP) defines arterial blood Pressure below which cerebral arteries collapse. It represents a clinically relevant parameter for the estimation of cerebrov...
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critical Closing Pressure during a controlled increase in intracranial Pressure
Acta Neurochirurgica, 2018Co-Authors: Katarzyna Kaczmarska, Peter Smielewski, Marek Czosnyka, Georgios V Varsos, Magdalena Kasprowicz, Antoni Grzanka, Wojciech M Zabolotny, Despina Afroditi Lalou, Zofia CzosnykaAbstract:Objectives: The objectives were to compare three methods of estimating critical Closing Pressure (CrCP) in a scenario of a controlled increase in intracranial Pressure (ICP) induced during an infusion test in patients with suspected normal Pressure hydrocephalus (NPH).
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effect of mild hypocapnia on critical Closing Pressure and other mechanoelastic parameters of the cerebrospinal system
Acta Neurochirurgica, 2018Co-Authors: Peter Smielewski, Georgios V Varsos, Karol P Budohoski, Luzius A Steiner, Corina Puppo, Marek CzosnykaAbstract:Objective: Brain arterial critical Closing Pressure (CrCP) has been studied in several diseases such as traumatic brain injury (TBI), subarachnoid haemorrhage, hydrocephalus, and in various physiological scenarios: intracranial hypertension, decreased cerebral perfusion Pressure, hypercapnia, etc. Little or nothing so far has been demonstrated to characterise change in CrCP during mild hypocapnia.
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cerebral critical Closing Pressure is the multiparameter model better suited to estimate physiology of cerebral hemodynamics
Neurocritical Care, 2016Co-Authors: Corinna Puppo, Georgios V Varsos, J Camacho, Bernardo Yelicich, Leandro Moraes, Alberto Biestro, H Gomez, Marek CzosnykaAbstract:Cerebral critical Closing Pressure (CrCP) is the level of arterial blood Pressure (ABP) at which small brain vessels close and blood flow stops. This value is always greater than intracranial Pressure (ICP). The difference between CrCP and ICP is explained by the tone of the small cerebral vessels (wall tension). CrCP value is used in several dynamic cerebral autoregulation models. However, the different methods for calculation of CrCP show frequent negative values. These findings are viewed as a methodological limitation. We intended to evaluate CrCP in patients with severe traumatic brain injury (TBI) with a new multiparameter impedance-based model and compare it with results found earlier using a transcranial Doppler (TCD)–ABP pulse waveform-based method. Twelve severe TBI patients hospitalized during September 2005–May 2007. Ten men, mean age 32 years (16–61). Four had decompressive craniectomies (DC); three presented anisocoria. Patients were monitored with TCD cerebral blood flow velocity (FV), invasive ABP, and ICP. Data were acquired at 50 Hz with an in-house developed data acquisition system. We compared the earlier studied “first harmonic” method (M1) results with results from a new recently developed (M2) “multiparameter method.” M1: In seven patients CrCP values were negative, reaching −150 mmHg. M2: All positive values; only one lower than ICP (ICP 60 mmHg/ CrCP 57 mmHg). There was a significant difference between M1 and M2 values (M1 ICP). M2 results in positive values of CrCP, higher than ICP, and are physiologically interpretable.
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the ontogeny of cerebrovascular critical Closing Pressure
Acta Neurochirurgica, 2016Co-Authors: Christopher J Rhee, Peter Smielewski, Marek Czosnyka, Georgios V Varsos, Charles D Fraser, Kathleen K Kibler, Ronald B Easley, Dean B Andropoulos, Craig G Rusin, Kenneth Martin BradyAbstract:Premature infants are at risk of vascular neurological insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Critical Closing Pressure (CrCP) is the arterial blood Pressure (ABP) at which cerebral blood flow ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to quantify CrCP as a function of gestational age (GA). One hundred eighty-six premature infants with a GA range of 23-33 weeks, were monitored with umbilical artery catheters and transcranial Doppler insonation of middle cerebral artery flow velocity (FV) for 1-h sessions over the first week of life. CrCP was calculated using an impedance model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. CrCP increased significantly with GA (r = 0.47; slope = 1.4 mmHg/week gestation), an association that persisted with multivariate analysis (p < 0.001). Higher diastolic ABP and higher GA were associated with increased CrCP (p <0.001 for both). CrCP increases significantly at the end of the second and beginning of the third trimester. The low CrCP observed in premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.