Arterial Blood Pressure Recordings Research Articles

The SLUScore: A Novel Method for Detecting Hazardous Hypotension in Adult Patients Undergoing Noncardiac Surgical Procedures.

It has been suggested that longer-term postsurgical outcome may be adversely affected by less than severe hypotension under anesthesia. However, evidence-based guidelines are unavailable. The present study was designed to develop a method for identifying patients at increased risk of death within 30 days in association with the severity and duration of intraoperative hypotension. Intraoperative mean arterial blood pressure recordings of 152,445 adult patients undergoing noncardiac surgery were analyzed for periods of time accumulated below each one of the 31 thresholds between 75 and 45 mm Hg (hypotensive exposure times). In a development cohort of 35,904 patients, the associations were sought between each of these 31 cumulative hypotensive exposure times and 30-day postsurgical mortality. On the basis of covariable-adjusted percentage increases in the odds of mortality per minute elapsed of hypotensive exposure time, certain sets of exposure time limits were calculated that portended certain percentage increases in the odds of mortality. A novel risk-scoring method was conceived by counting the number of exposure time limits that had been exceeded within each respective set, one of them being called the SLUScore. The validity of this new method in identifying patients at increased risk was tested in a multicenter validation cohort consisting of 116,541 patients from Cleveland Clinic, Vanderbilt and Saint Louis Universities. Data were expressed as 95% confidence interval, P < .05 considered significant. Progressively greater hypotensive exposures were associated with greater 30-day mortality. In the development cohort, covariable-adjusted (age, Charlson score, case duration, history of hypertension) exposure limits were identified for time accumulated below each of the thresholds that portended certain identical (5%-50%) percentage expected increases in the odds of mortality. These exposure time limit sets were shorter in patients with a history of hypertension. A novel risk score, the SLUScore (range 0-31), was conceived as the number of exposure limits exceeded for one of these sets (20% set). A SLUScore > 0 (average 13.8) was found in 40% of patients who had twice the mortality, adjusted odds increasing by 5% per limit exceeded. When tested in the validation cohort, a SLUScore > 0 (average 14.1) identified 35% of patients who had twice the mortality, each incremental limit exceeded portending a 5% compounding increase in adjusted odds of mortality, independent of age and Charlson score (C = 0.73, 0.72-0.74, P < .05). The SLUScore represents a novel method for identifying nearly 1 in every 3 patients experiencing greater 30-day mortality portended by more severe intraoperative hypotensive exposures.

Is 5 IU bolus of oxytocin as effective as 10 IU bolus for control of bleeding during cesarean section under spinal anesthesia?

Aim and Objectives: We sought to compare the hemodynamic effects of 5 international unit (IU) and 10 IU of intravenous (IV) boluses of oxytocin and their efficacy in reducing blood loss during cesarean section and also to determine the incidence of postoperative nausea and vomiting (PONV) and postdural puncture headache (PDPH). Patients and Methods: One hundred and ten parturients of American Society of Anesthesiologists' I and II scheduled for cesarean section under spinal anesthesia were randomized into two groups. Group A (n = 55) received 5 IU IV bolus of oxytocin and Group B (n = 55) received 10 IU IV bolus of oxytocin after delivery. Ten milliliters per kilogram of 0.9% saline was administered to both groups as volume preload. Subarachnoid block was performed with size 24G spinal needles at L2/L3 or L3/L4 intervertebral space with the patients in sitting position. Two milliliters of 0.5% heavy bupivacaine was administered slowly intrathecally. Following delivery of the baby, IV boluses of 5 IU (Group A) or 10 IU (Group B) of oxytocin were administered slowly, and recording of heart rate, systolic, diastolic, and mean arterial blood pressure was done every minute for 5 min after bolus injection. IV infusion of 30 IU of oxytocin in 500 ml of 0.9% saline (60 mU/ml) at a rate of 125 ml/h was continued in both groups till the end of surgery. Estimated blood loss (EBL) was assessed by visual estimation. Patients were monitored continuously until 24 h after surgery to evaluate PDPH and PONV. Results: There were no statistically significant differences in the EBL between the two groups. There was no significant rise in heart rate and no significant decrease in mean arterial blood pressure in Group A compared to Group B. The incidence of PDPH and PONV was also comparable in both groups. Conclusion: Five IU of IV bolus of oxytocin is as effective as 10 IU of IV bolus in reducing blood loss during cesarean section.

Abstract 104: Dynamic Autoregulation of Glomerular Capillary Pressure

It is generally accepted that renal blood flow (RBF) autoregulation is mediated by myogenic and tubuloglomerular feedback responses acting on the pre-glomerular resistance. If this is so, then autoregulation of RBF and glomerular capillary pressure (PGC) should change in the same direction throughout an autoregulatory step response. We computed autoregulatory step responses from time series recordings of arterial blood pressure (BP) and RBF (Transonics) blood flow or tubular stop-flow pressure (micropuncture), which is a surrogate for PGC in Wistar-Froemter rats fed for one week on low or high salt diets (n=6-10 ). Autoregulatory step responses were generated from time series by an algorithm that treats BP as a leading indicator of RBF or PGC and uses the projection theorem to solve for the impulse response which is integrated to obtain the step response. Step responses shown in the figure represent the uncompensated changes in RBF and PGC (mean + SEM) following a 1 mmHg BP step. The data clearly reveal that the time courses of RBF and PGC differ such that changes in RBF cannot predict changes in PGC. This implies that the renal hemodynamic response to a blood pressure disturbance is not confined to the pre-glomerular resistance. Furthermore, the participation of post-glomerular resistance in the autoregulatory response is sensitive to dietary salt such that PGC is more sensitive to BP on low salt diet.

Chronic Treatment with Ivabradine Does Not Affect Cardiovascular Autonomic Control in Rats.

A low resting heart rate (HR) would be of great benefit in cardiovascular diseases. Ivabradine—a novel selective inhibitor of hyperpolarization-activated cyclic nucleotide gated (HCN) channels- has emerged as a promising HR lowering drug. Its effects on the autonomic HR control are little known. This study assessed the effects of chronic treatment with ivabradine on the modulatory, reflex and tonic cardiovascular autonomic control and on the renal sympathetic nerve activity (RSNA). Male Wistar rats were divided in 2 groups, receiving intraperitoneal injections of vehicle (VEH) or ivabradine (IVA) during 7 or 8 consecutive days. Rats were submitted to vessels cannulation to perform arterial blood pressure (AP) and HR recordings in freely moving rats. Time series of resting pulse interval and systolic AP were used to measure cardiovascular variability parameters. We also assessed the baroreflex, chemoreflex and the Bezold-Jarish reflex sensitivities. To better evaluate the effects of ivabradine on the autonomic control of the heart, we performed sympathetic and vagal autonomic blockade. As expected, ivabradine-treated rats showed a lower resting (VEH: 362 ± 16 bpm vs. IVA: 260 ± 14 bpm, p = 0.0005) and intrinsic HR (VEH: 369 ± 9 bpm vs. IVA: 326 ± 11 bpm, p = 0.0146). However, the chronic treatment with ivabradine did not change normalized HR spectral parameters LF (nu) (VEH: 24.2 ± 4.6 vs. IVA: 29.8 ± 6.4; p > 0.05); HF (nu) (VEH: 75.1 ± 3.7 vs. IVA: 69.2 ± 5.8; p > 0.05), any cardiovascular reflexes, neither the tonic autonomic control of the HR (tonic sympathovagal index; VEH: 0.91± 0.02 vs. IVA: 0.88 ± 0.03, p = 0.3494). We performed the AP, HR and RSNA recordings in urethane-anesthetized rats. The chronic treatment with ivabradine reduced the resting HR (VEH: 364 ± 12 bpm vs. IVA: 207 ± 11 bpm, p < 0.0001), without affecting RSNA (VEH: 117 ± 16 vs. IVA: 120 ± 9 spikes/s, p = 0.9100) and mean arterial pressure (VEH: 70 ± 4 vs. IVA: 77 ± 6 mmHg, p = 0.3293). Our results suggest that, in health rats, the long-term treatment with ivabradine directly reduces the HR without changing the RSNA modulation and the reflex and tonic autonomic control of the heart.

A practical algorithm to reduce false critical ECG alarms using arterial blood pressure and/or photoplethysmogram waveforms

There has been a high rate of false alarms for the critical electrocardiogram (ECG) arrhythmia events in intensive care units (ICUs), from which the ‘crying-wolf’ syndrome may be resulted and patient safety may be jeopardized. This article presents an algorithm to reduce false critical arrhythmia alarms using arterial blood pressure (ABP) and/or photoplethysmogram (PPG) waveform features. We established long duration reference alarm datasets which consist of 573 ICU waveform-alarm records (283 for development set and 290 for test set) with total length of 551 patent days. Each record has continuous recordings of ECGs, ABP and/or PPG signals and contains one or multiple critical ECG alarms. The average length of a record is 23 h. There are totally 2408 critical ECG alarms (1414 in the development set and 994 in the test set), each of which was manually annotated by experts. The algorithm extracts ABP/PPG pulse features on a beat-by-beat basis. For each pulse, five event feature indicators (EFIs), which correspond to the five critical ECG alarms, are generated. At the time of a critical ECG alarm, the corresponding EFI values of those ABP/PPG pulses around the alarm time are checked for adjudicating (accept/reject) this alarm. The algorithm retains all (100%) the true alarms and significantly reduces the false alarms. Our results suggest that the algorithm is effective and practical on account of its real-time dynamic processing mechanism and computational efficiency.

Testosterone improves erectile function through inhibition of reactive oxygen species generation in castrated rats.

Testosterone is overwhelmingly important in regulating erectile physiology. However, the associated molecular mechanisms are poorly understood. The purpose of this study was to explore the effects and mechanisms of testosterone in erectile dysfunction (ED) in castrated rats. Forty male Sprague-Dawley rats were randomized to four groups (control, sham-operated, castration and castration-with-testosterone-replacement). Reactive oxygen species (ROS) production was measured by dihydroethidium (DHE) staining. Erectile function was assessed by the recording of intracavernous pressure (ICP) and mean arterial blood pressure (MAP). Protein expression levels were examined by western blotting. We found that castration reduced erectile function and that testosterone restored it. Nitric oxide synthase (NOS) activity was decrease in the castrated rats, and testosterone administration attenuated this decrease (each p < 0.05). The testosterone, dihydrotestosterone, cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) concentrations were lower in the castrated rats, and testosterone restored these levels (each p < 0.05). Furthermore, the cyclooxygenase-2 (COX-2) and prostacyclin synthase (PTGIS) expression levels and phospho-endothelial nitric oxide synthase (p-eNOS, Ser1177)/endothelial nitric oxide synthase (eNOS) ratio were reduced in the castrated rats compared with the controls (each p < 0.05). In addition, the p40phox and p67phox expression levels were increased in the castrated rats, and testosterone reversed these changes (each p < 0.05). Overall, our results demonstrate that testosterone ameliorates ED after castration by reducing ROS production and increasing the activity of the eNOS/cGMP and COX-2/PTGIS/cAMP signaling pathways.

Baroreceptor reflex during forced expiratory maneuvers in individuals with chronic spinal cord injury

Pulmonary and cardiovascular dysfunctions are leading causes of morbidity and mortality in patients with chronic Spinal Cord Injury (SCI). Impaired respiratory motor function and decreased Baroreflex Sensitivity (BS) are predictors for the development of cardiopulmonary disease. This observational case-controlled clinical study was undertaken to investigate if respiratory motor control deficits in individuals with SCI affect their ability to perform the Valsalva maneuver, and to determine if a sustained Maximum Expiratory Pressure (MEP) effort can serve as an acceptable maneuver for determination of the BS in the event that the Valsalva maneuver cannot be performed. The BS outcomes (ms/mmHg) were obtained using continuous beat-to-beat arterial blood pressure (BP) and heart rate (HR) recordings during Valsalva or MEP maneuvers in thirty nine individuals with chronic C3–T12 SCI. Twenty one participants (54%) reported signs of intolerance during the Valsalva maneuver and only 15 individuals (39%) were able to complete this task. Cervical level of injury was a significant risk factor (p=0.001) for failing to complete the Valsalva maneuver, and motor-complete injury was a significant risk factor for symptoms of intolerance (p=0.04). Twenty eight participants (72%) were able to perform the MEP maneuver; the other 11 participants failed to exceed the standard airway pressure threshold of 27cm H2O. Neither level nor completeness of injury were significant risk factors for failure of MEP maneuver. When the required airway pressure was sustained, there were no significant differences between BS outcomes obtained during Valsalva and MEP maneuvers. The results of this study indicate that individuals with high-level and motor-complete SCI are at increased risk of not completing the Valsalva maneuver and that baroreflex-mediated responses can be evaluated by using sustained MEP maneuver when the Valsalva maneuver cannot be performed.

Elevated Diastolic Closing Margin Is Associated with Intraventricular Hemorrhage in Premature Infants

To determine whether the diastolic closing margin (DCM), defined as diastolic blood pressure minus critical closing pressure, is associated with the development of early severe intraventricular hemorrhage (IVH). A reanalysis of prospectively collected data was conducted. Premature infants (gestational age 23-31weeks) receiving mechanical ventilation (n=185) had ∼1-hour continuous recordings of umbilical arterial blood pressure, middle cerebral artery cerebral blood flow velocity, and PaCO2 during the first week of life. Models using multivariate generalized linear regression and purposeful selection were used to determine associations with severe IVH. Severe IVH (grades 3-4) was observed in 14.6% of the infants. Irrespective of the model used, Apgar score at 5minutes and DCM were significantly associated with severe IVH. A clinically relevant 5-mm Hg increase in DCM was associated with a 1.83- to 1.89-fold increased odds of developing severe IVH. Elevated DCM was associated with severe IVH, consistent with previous animal data showing that IVH is associated with hyperperfusion. Measurement of DCM may be more useful than blood pressure in defining cerebral perfusion in premature infants.

Do the carotid body chemoreceptors mediate cardiovascular and sympathetic adjustments induced by sodium overload in rats?

Acute plasma hypernatremia induces several cardiovascular and sympathetic responses. It is conceivable that these responses contribute to rapid sodium excretion and restoration of normal conditions. Afferent pathways mediating these responses are not entirely understood. The present study analyses the effects of acute carotid chemoreceptor inactivation on cardiovascular and sympathetic responses induced by infusion of hypertonic saline (HS). All experiments were performed on anesthetized male Wistar rats instrumented for recording of arterial blood pressure (ABP), renal blood flow (RBF) and renal sympathetic nerve activity (RSNA). Animals were subjected to sham surgery or carotid chemoreceptor inactivation by bilateral ligation of the carotid body artery (CBA). In sham rats (n=8), intravenous infusion of HS (3 M NaCl, 1.8 ml/kg b.wt.) elicited a transient increase (9±2mmHg) in ABP, and long lasting (30 min) increases in RBF (138±5%) and renal vascular conductance (RVC) (128±5%) with concurrent decrease in RSNA (-19±4%). In rats submitted to CBA ligation (n=8), the pressor response to HS was higher (24±2mmHg; p<0.05). However, RBF and RVC responses to HS infusion were significantly reduced (113±5% and 93±4%, respectively) while RSNA was increased (13±2%). When HS (3M NaCl, 200μl) was administrated into internal carotid artery (ICA), distinct sympathetic and cardiovascular responses were observed. In sham-group, HS infusion (3M NaCl, 200μl) into ICA promoted an increase in ABP (26±8mmHg) and RSNA (29±13%). In CBA rats, ABP (-3±5.6mmHg) remained unaltered despite sympathoinhibition (-37.6±5.4%). These results demonstrate that carotid body chemoreceptors play a role in the development of hemodynamic and sympathetic responses to acute HS infusion.

A review of methods for the signal quality assessment to improve reliability of heart rate and blood pressures derived parameters.

The assessment of signal quality has been a research topic since the late 1970s, as it is mainly related to the problem of false alarms in bedside monitors in the intensive care unit (ICU), the incidence of which can be as high as 90%, leading to alarm fatigue and a drop in the overall level of nurses and clinicians attention. The development of efficient algorithms for the quality control of long diagnostic electrocardiographic (ECG) recordings, both single- and multi-lead, and of the arterial blood pressure (ABP) signal is therefore essential for the enhancement of care quality. The ECG signal is often corrupted by noise, which can be within the frequency band of interest and can manifest similar morphologies as the ECG itself. Similarly to ECG, also the ABP signal is often corrupted by non-Gaussian, nonlinear and non-stationary noise and artifacts, especially in ICU recordings. Moreover, the reliability of several important parameters derived from ABP such as systolic blood pressure or pulse pressure is strongly affected by the quality of the ABP waveform. In this work, several up-to-date algorithms for the quality scoring of a single- or multi-lead ECG recording, based on time-domain approaches, frequency-domain approaches or a combination of the two will be reviewed, as well as methods for the quality assessment of ABP. Additionally, algorithms exploiting the relationship between ECG and pulsatile signals, such as ABP and photoplethysmographic recordings, for the reduction in the false alarm rate will be presented. Finally, some considerations will be drawn taking into account the large heterogeneity of clinical settings, applications and goals that the reviewed algorithms have to deal with.

Spectral analysis of intracranial pressure: Is it helpful in the assessment of shunt functioning in-vivo?

ObjectiveShunt failure is common in hydrocephalic patients. The cerebrospinal fluid (CSF) infusion test enables the assessment of CSF absorption capacity, which is represented by the resistance to CSF outflow (ROUT) However, shunt failure may not only affect the CSF absorption capacity but also the intracranial compliance or compensatory properties. Spectral analysis of the ICP signal obtained during the infusion test may enable the comprehensive assessment of the overall deterioration caused by shunt failure. Material and methodsA total of 121 hydrocephalic shunted patients underwent the infusion test with continuous intracranial pressure (ICP) and arterial blood pressure (ABP) recording. The maximum amplitudes of three major frequency bandwidths (0.2–2.6, 2.6–4.0 and 4.0–15Hz, respectively) were calculated from the ICP. Statistical analyses were conducted to identify factors significantly associated with shunt failure, to construct an index (i.e., the shunt response parameter, SRP) for detecting shunt failure, and to define thresholds for ROUT and SRP. ResultsThe ROUT threshold for detecting shunt failure was 7.59mmHg/ml/min, and this threshold showed an accuracy of 82.64%. All spectral parameters were found to be significantly associated with shunt patency (p<0.05). The SRP exhibited significantly better accuracy than ROUT in detecting shunt failure (91.74%). ConclusionThe hydrodynamic assessment of shunted patients enhanced by spectral analysis during the infusion test detected shunt failure with high accuracy. Although further validation is needed, the SRP exhibited promising results.

Morphological Feature Extraction From a Continuous Intracranial Pressure Pulse via a Peak Clustering Algorithm.

An increase in intracranial pressure (ICP) is frequently observed in patients with severe traumatic brain injury (TBI). The information derived from the observation of temporal changes in the mean ICP is insufficient for assessment of the compensatory reserve of the injured brain. This assessment can be achieved via continuous morphological analysis of the pulse waveform of the ICP. Continuous arterial blood pressure (ABP) and ICP recordings from 292 TBI patients were analyzed. The algorithm extracted morphological landmarks (peaks, troughs, and flats) from the ICP. Among the extracted peaks, P1, P2, and P3 were assigned through peak clustering. The performance of the proposed method was validated through a comparison of the algorithm-defined peaks and those manually identified by experienced observers. The proposed algorithm successfully identified the three distinguishing peaks of the ICP with satisfactory accuracy (95.3%, 87.8%, and 87.5% for P1, P2, and P3, respectively), even from minimally filtered raw signals. The algorithm extracted the morphological features from both ABP and ICP recordings with high accuracy. The ABP and ICP pulse waveforms can be simultaneously analyzed in real time using the proposed algorithm. The morphological features from these signals may aid the continuous care of patients with TBI.

Characterization of Disopyramide derivative ADD424042 as a non-cardiotoxic neuronal sodium channel blocker with broad-spectrum anticonvulsant activity in rodent seizure models

It was reported that antiarrhythmic drugs (AADs) can be useful in controlling refractory seizures in humans or in enhancing the action of antiepileptic drugs (AEDs) in animal models.Disopyramide phosphate (DISO) is an AAD that blocks sodium channels in cardiac myocytes. We evaluated a DISO derivative, 2-(2-chlorophenyl)-2-(pyridin-2-yl)acetamide (ADD424042) for its anticonvulsant activity in a battery of rodent models of epileptic seizures. The compound displayed a broad spectrum of activity in the ‘classical’ models as well as in the models of pharmacoresistant seizures. Furthermore, ADD424042 showed good therapeutic indices between the anticonvulsant activity and the motor impairment. On the contrary, no anticonvulsant effects but severe lethality were observed in the primary anticonvulsant testing of the parent DISO. By performing the whole-cell voltage-clamp experiments in dispersed cortical neurons we demonstrated that ADD424042 decreased the maximal amplitude of voltage-gated sodium channels with an IC50 value in nM range. Moreover, the compound enhanced use-dependent block and decreased excitability in pyramidal neurons in the current-clamp experiments in cortical slices. Importantly, we found that ADD424042 possessed either no, or very small cardiotoxic effect. In contrast to DISO, ADD424042 did not produce any apparent changes in electrocardiogram (ECG) and arterial blood pressure recordings. ADD424042 had no effect on QT and corrected QT intervals, at a dose which was 15 times higher than ED50 for the anticonvulsant effect in the MES model. Taken together, these data suggest that ADD424042 has the potential to become a lead structure for novel broadly acting AEDs with wide margin of cardiac safety.

Abstract P191: Increases in Cerebrospinal Fluid NaCl Concentration Excites Neurons of the Organum Vasculosum of the Lamina Terminalis to Elevate Sympathetic Outflow and Blood Pressure

Accumulating evidence suggests salt-sensitive hypertension is mediated partly by an increase in cerebrospinal fluid (CSF) NaCl concentration and elevation in sympathetic nerve activity (SNA). Increased NaCl concentration or osmolality is sensed by specialized neurons in the organum vasculosum of the lamina terminalis (OVLT). The present study investigated the contribution of these neurons to the SNA and arterial blood pressure (ABP) responses during acute increases in CSF NaCl concentrations. Male Sprague-Dawley rats were anesthetized with Inactin (120mg/kg, IV) and prepared for SNA and ABP recordings. Lateral ventricle infusion of 1M NaCl (5uL over 10 min) increased CSF [Na+] by 5±1 mM and elevated mean ABP (9±1 mmHg), lumbar SNA (125±3%) and adrenal SNA (121±5%) but decreased renal SNA (-9±1%, n=8) and did not alter splanchnic SNA (102±3%). Inhibition of the OVLT with injection of the GABAA agonist muscimol (2.5mM per 20nL, n=5) significantly attenuated the NaCl-induced increase in ABP (2±1 mmHg), lumbar SNA (102±1%), adrenal SNA (103±2%) and decrease in renal SNA (-3±1%). In vivo single-unit recordings demonstrate that lateral ventricular infusion of 1M NaCl (5uL per 10 min) significantly increased the firing rate in 75% (3/4) of OVLT neurons from 1.2±0.4Hz to 5.1±1.2Hz (P&lt;0.05). Furthermore, direct injection of NaCl (100nL over 20s, n=3) into the OVLT produced dose-dependent increases in mean ABP (0.15M: 0±1mmHg; 0.5M: 2±1mmHg; 1.0M: 4±1mmHg; 2.0M: 7±1mmHg) and lumbar SNA (0.15M: 101±2%; 0.5M: 107±1%; 1.0M: 112±3%; 2.0M: 118±4%). Altogether, these findings suggest that increases in CSF NaCl concentrations excite OVLT neurons to elevate lumbar and adrenal SNA and ABP.

Intraspinal pressure and spinal cord perfusion pressure after spinal cord injury: an observational study.

In contrast to intracranial pressure (ICP) in traumatic brain injury (TBI), intraspinal pressure (ISP) after traumatic spinal cord injury (TSCI) has not received the same attention in terms of waveform analysis. Based on a recently introduced technique for continuous monitoring of ISP, here the morphological characteristics of ISP are observationally described. It was hypothesized that the waveform analysis method used to assess ICP could be similarly applied to ISP. Data included continuous recordings of ISP and arterial blood pressure (ABP) in 18 patients with severe TSCI. The morphology of the ISP pulse waveform resembled the ICP waveform shape and was composed of 3 peaks representing percussion, tidal, and dicrotic waves. Spectral analysis demonstrated the presence of slow, respiratory, and pulse waves at different frequencies. The pulse amplitude of ISP was proportional to the mean ISP, suggesting a similar exponential pressure-volume relationship as in the intracerebral space. The interaction between the slow waves of ISP and ABP is capable of characterizing the spinal autoregulatory capacity. This preliminary observational study confirms morphological and spectral similarities between ISP in TSCI and ICP. Therefore, the known methods used for ICP waveform analysis could be transferred to ISP analysis and, upon verification, potentially used for monitoring TSCI patients.

Ontogeny of cerebrovascular critical closing pressure.

Premature infants are at risk of vascular neurologic insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to determine the ontogeny of CrCP. Premature infants (n = 179) with gestational age (GA) from 23-31 wk had recordings of ABP and middle cerebral artery flow velocity twice daily for 3 d and then daily for the duration of the first week of life. All infants received mechanical ventilation. CrCP was calculated using an impedance-model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. The association between GA and CrCP was determined in a multivariate analysis. The median (interquartile range) CrCP for the cohort was 22 mm Hg (19-25 mm Hg). CrCP increased significantly with GA (r = 0.6; slope = 1.4 mm Hg/wk gestation), an association that persisted with multivariate analysis (P < 0.0001). CrCP increased significantly from 23 to 31 wk gestation. The low CrCP observed in very premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage.

Assessment of dynamic cerebral autoregulation and cerebral carbon dioxide reactivity during normothermic cardiopulmonary bypass.

Despite increased risk of neurological complications after cardiac surgery, monitoring of cerebral hemodynamics during cardiopulmonary bypass (CPB) is still not a common practice. Therefore, a technique to evaluate dynamic cerebral autoregulation and cerebral carbon dioxide reactivity (CO2R) during normothermic nonpulsatile CPB is presented. The technique uses continuous recording of invasive arterial blood pressure, middle cerebral artery blood flow velocity, absolute cerebral tissue oxygenation, in-line arterial carbon dioxide levels, and pump flow measurement in 37 adult male patients undergoing elective CPB. Cerebral autoregulation is estimated by transfer function analysis and the autoregulation index, based on the response to blood pressure variation induced by cyclic 6/min changes of indexed pump flow from 2.0 to 2.4 up to 2.8 L/min/m(2). CO2R was calculated from recordings of both cerebral blood flow velocity and cerebral tissue oxygenation. Cerebral autoregulation and CO2R were estimated at hypocapnia, normocapnia, and hypercapnia. CO2R was preserved during CPB, but significantly lower for hypocapnia compared with hypercapnia (p < 0.01). Conversely, cerebral autoregulation parameters such as gain, phase, and autoregulation index were significantly higher (p < 0.01) during hypocapnia compared with both normocapnia and hypercapnia. Assessing cerebral autoregulation and CO2R during CPB, by cyclic alteration of pump flow, showed an impaired cerebral autoregulation during hypercapnia.

The mixing rate of the arterial blood pressure waveform Markov chain is correlated with shock index during hemorrhage in anesthetized swine.

Identifying the need for interventions during hemorrhage is complicated due to physiological compensation mechanisms that can stabilize vital signs until a significant amount of blood loss. Physiological systems providing compensation during hemorrhage affect the arterial blood pressure waveform through changes in dynamics and waveform morphology. We investigated the use of Markov chain analysis of the arterial blood pressure waveform to monitor physiological systems changes during hemorrhage. Continuous arterial blood pressure recordings were made on anesthetized swine (N=7) during a 5 min baseline period and during a slow hemorrhage (10 ml/kg over 30 min). Markov chain analysis was applied to 20 sec arterial blood pressure waveform segments with a sliding window. 20 ranges of arterial blood pressure were defined as states and empirical transition probability matrices were determined for each 20 sec segment. The mixing rate (2(nd) largest eigenvalue of the transition probability matrix) was determined for all segments. A change in the mixing rate from baseline estimates was identified during hemorrhage for each animal (median time of 13 min, ~10% estimated blood volume, with minimum and maximum times of 2 and 33 min, respectively). The mixing rate was found to have an inverse correlation with shock index for all 7 animals (median correlation coefficient of -0.95 with minimum and maximum of -0.98 and -0.58, respectively). The Markov chain mixing rate of arterial blood pressure recordings is a novel potential biomarker for monitoring and understanding physiological systems during hemorrhage.

Signal quality quantification and waveform reconstruction of arterial blood pressure recordings.

Arterial blood pressure (ABP) is an important vital sign of the cardiovascular system. As with other physiological signals, its measurement can be corrupted by different sources of noise, interference, and artifact. Here, we present an algorithm for the quantification of signal quality and for the reconstruction of the ABP waveform in noise-corrupted segments of the measurement. The algorithm quantifies the quality of the ABP signal on a beat-by-beat basis by computing the normalized mean of successive differences of the ABP amplitude over each beat. In segments of poor signal quality, the ABP wavelets are then reconstructed on the basis of the expected cycle duration and envelope information derived from neighboring ABP wavelet segments. The algorithm was tested on two datasets of ABP waveform signals containing both invasive radial artery ABP and noninvasive ABP waveforms. Our results show that the approach is efficient in identifying the noisy segments (accuracy, sensitivity and specificity over 95%) and reliable in reconstructing beats that were artificially corrupted.

A continuous correlation between intracranial pressure and cerebral blood flow velocity reflects cerebral autoregulation impairment during intracranial pressure plateau waves.

In the healthy brain, small oscillations in intracranial pressure (ICP) occur synchronously with those in cerebral blood volume (CBV), cerebrovascular resistance, and consequently cerebral blood flow velocity (CBFV). Previous work has shown that the usual synchrony between ICP and CBFV is lost during intracranial hypertension. Moreover, a continuously computed measure of the ICP/CBFV association (Fix index) was a more sensitive predictor of outcome after traumatic brain injury (TBI) than a measure of autoregulation (Mx index). In the current study we computed Fix during ICP plateau waves, to observe its behavior during a defined period of cerebrovascular vasodilatation. Twenty-nine recordings of arterial blood pressure (ABP), ICP, and CBFV taken during ICP plateau waves were obtained from the Addenbrooke's hospital TBI database. Raw data was filtered prior to computing Mx and Fix according to previously published methods. Analyzed data was segmented into three phases (pre, peak, and post), and a median value of each parameter was stored for analysis. ICP increased from a median of 22-44mmHg before falling to 19mmHg. Both Mx and Fix responded to the increase in ICP, with Mx trending toward +1, while Fix trended toward -1. Mx and Fix correlated significantly (Spearman's R=-0.89, p<0.000001), however, Fix spanned a greater range than Mx. A plot of Mx and Fix against CPP showed a plateau (Mx) or trough (Fix) consistent with a zone of "optimal CPP". The Fix index can identify complete loss of cerebral autoregulation as the point at which the normally positive CBF/CBV correlation is reversed. Both CBF and CBV can be monitored noninvasively using near-infrared spectroscopy (NIRS), suggesting that a noninvasive method of monitoring autoregulation using only NIRS may be possible.