Monitoring the monitors--beyond risk management.
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Anesthesia↗
Biomedical subjects
R P Mahajan
Publications and source records attributed to R P Mahajan.
Effects of stellate ganglion block on cerebral haemodynamics as assessed by transcranial Doppler ultrasonography.
BACKGROUND: Stellate ganglion block (SGB) causes vasodilatation in the skin of the head and neck because of regional sympathetic block. Its effects on cerebral haemodynamics, in health or in disease, are not clear. We evaluated the effects of SGB on ipsilateral middle cerebral artery flow velocity (MCAFV), estimated cerebral perfusion pressure (eCPP), zero flow pressure (ZFP), carbon dioxide reactivity (CO2R) and cerebral autoregulation using transcranial Doppler ultrasonography (TCD). METHODS: Twenty male patients, with pre-existing brachial plexus injury, and undergoing SGB for the treatment of complex regional pain syndrome of the upper limb, were studied. For SGB, 10 ml of plain lidocaine 2% was used and the onset of block was confirmed by presence of ipsilateral Horner's syndrome. The MCAFV, eCPP, ZFP, CO2R, and cerebral autoregulation were assessed before and after SGB using established TCD methods. The changes in these variables were analysed using Wilcoxon's signed rank test. RESULTS: The block caused a significant decrease in MCAFV from median (inter-quartile range) value of 61 (53, 67) to 55 (46, 60) cm s(-1), a significant increase in eCPP from 59 (51, 67) to 70 (60, 78) mm Hg, and a significant decrease in ZFP from 32 (26, 39) to 25 (16, 30) mm Hg. There were no significant changes in CO2R or cerebral autoregulation. CONCLUSION: The increase in eCPP, decrease in ZFP, and no changes in CO2R or cerebral autoregulation suggest that the SGB decreases cerebral vascular tone without affecting the capacity of the vessels to autoregulate. These effects may be of therapeutic advantage in relieving cerebral vasospasm in certain clinical settings.
Adolescent↗
Effects of inhaled nitrous oxide 50% on estimated cerebral perfusion pressure and zero flow pressure in healthy volunteers.
The role of vascular tone in determining cerebral perfusion pressure is increasingly being appreciated. It has been suggested that zero flow pressure, the arterial pressure at which blood flow ceases, represents the effective downstream pressure of the cerebral circulation. Nitrous oxide is a cerebral vasodilator and may therefore decrease zero flow pressure and increase cerebral perfusion pressure. However, these effects may be opposed by the increase in intracranial blood volume produced by cerebral vasodilation. We studied eight healthy volunteers at normocapnia and studied the effects of the inhalation of nitrous oxide 50% on estimated cerebral perfusion pressure and zero flow pressure using transcranial Doppler ultrasonography. We found that nitrous oxide 50% significantly increased estimated cerebral perfusion pressure (p = 0.03), whilst decreasing zero flow pressure (p = 0.01). These results suggest that the vasomotor effects of nitrous oxide predominate in determining the effective downstream pressure of the cerebral circulation in healthy individuals.
Adolescent↗
Doppler estimation of zero flow pressure during changes in downstream pressure in a bench model of a circulation using pulsatile flow.
Zero flow pressure is the arterial pressure at which blood flow ceases in the cerebral circulation and may represent the effective downstream pressure of this system. We used a bench model of pulsatile fluid flow to determine whether simulated changes in downstream pressure may be detected by estimation of zero flow pressure. A Doppler probe was used to record flow velocity and a pressure transducer was used to measure driving pressure. Eight different configurations of the circuit were produced, and at each configuration the external pressure around a collapsible segment of the circuit was changed in order to simulate intracranial pressure. Perfusion pressure and zero flow pressure were estimated for each configuration and each level of external pressure. The sensitivity of the model in predicting the change in external pressure from the change in zero flow pressure was 94%. This indicates that estimation of zero flow pressure by this method is a sensitive way of monitoring trends in changes in downstream pressure.
Blood Flow Velocity↗
Transcranial Doppler ultrasonography in anaesthesia and intensive care.
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Anesthetics↗
Regional and temporal changes in cardiovascular responses to norepinephrine and vasopressin during continuous infusion of lipopolysaccharide in conscious rats.
BACKGROUND: Reduced pressor responsiveness to norepinephrine (NE) in sepsis is well documented but the associated regional haemodynamic changes are less well characterized, and there are varying reports of changes in haemodynamic responses to arginine vasopressin (AVP). We compared changes in regional haemodynamic responsiveness to AVP and NE during a 24 h continuous infusion of lipopolysaccharide (LPS) in conscious rats. METHODS: Conscious, male Sprague-Dawley rats were infused with saline (0.4 ml h(-1)) or LPS (150 micro g kg(-1) h(-1)). Renal, mesenteric, and hindquarter haemodynamic responses to 3 min infusions of AVP (0.25, 0.625, and 1.25 ng kg(-1) min(-1)) or NE (75, 250, and 750 ng kg(-1) min(-1)) were assessed 2, 6, and 24 h after the onset of LPS or saline. RESULTS: Two and six hours after the onset of LPS, all haemodynamic effects of NE were markedly reduced, but by 24 h, there was some recovery in the vasoconstrictor actions of NE although the pressor and bradycardic effects were still depressed. Two hours after the onset of LPS, the cardiovascular effects of AVP were depressed but there was some recovery in vascular responsiveness at 6 h. By 24 h, only the mesenteric vasoconstrictor effect of AVP was consistently reduced. CONCLUSIONS: During low dose LPS infusion, there are differential changes in haemodynamic responsiveness to AVP and NE, which show different temporal and regional profiles of recovery with time. Furthermore, reduced pressor responsiveness to NE is not necessarily accompanied by a reduced capacity of vessels for vasoconstriction.
Animals↗
Effects of ephedrine, dobutamine and dopexamine on cerebral haemodynamics: transcranial Doppler studies in healthy volunteers.
BACKGROUND: Sympathomimetic drugs are assumed to have no direct effects on cerebral haemodynamics on the basis of animal experiments; there is little evidence of their direct effects in humans. This study aimed to address this issue. METHODS: The effects of ephedrine, dobutamine, and dopexamine on cerebral autoregulation, cerebral vascular reactivity to carbon dioxide, estimated cerebral perfusion pressure, and zero flow pressure (ZPF) were studied in 10 healthy volunteers using transcranial Doppler ultrasound. The strength of autoregulation was measured using the transient hyperaemic response test. The reactivity to carbon dioxide was measured as the change in middle cerebral artery flow velocity with a step change in end-tidal carbon dioxide. For the estimated cerebral perfusion pressure and the ZFP, established formulae were used which utilized instantaneous values of arterial pressure and middle cerebral artery flow velocity. Measurements were made at baseline and after i.v. infusion of the study drug to an endpoint of 25% increase in mean arterial pressure (MAP) (ephedrine, dobutamine) or cardiac index (dopexamine). RESULTS: There was no significant change in the strength of autoregulation (from (mean (SD)) 1.07 (0.16) to 1.07 (0.18); from 1.07 (0.16) to 1.03 (0.19); from 1.04 (0.12) to 1.04 (0.25)), reactivity to carbon dioxide (from 40% (8) to 36 (10); from 37 (12) to 37 (11); from 45 (12) to 43 (11)) with ephedrine, dobutamine, or dopexamine, respectively. Despite a clinically significant increase in MAP with ephedrine and dobutamine and a clinically significant increase in cardiac index with dopexamine, the estimated cerebral perfusion pressure did not change significantly (from 81 (38) to 60 (16) mm Hg with ephedrine; from 67 (22) to 63 (11) mm Hg with dobutamine; from 87 (27) to 79 (17) mm Hg with dopexamine). The ZFP increased significantly with ephedrine (from 29 (10) to 44 (11) mm Hg) and dobutamine (from 35 (14) to 43 (10) mm Hg) but not dopexamine (from 3 (23) to 11 (22) mm Hg). CONCLUSIONS: Sympathomimetic agents do not significantly change cerebrovascular homeostasis as assessed by the transient hyperaemic response test, reactivity to carbon dioxide and estimated cerebral perfusion pressure.
Adrenergic beta-Agonists↗
The effect of a mechanical glottis on peak expiratory flow rate and time to peak flow during a peak expiratory flow manoeuvre: a study in normal subjects and patients with motor neurone disease.
We have evaluated a mechanical glottis in healthy volunteers and in patients with bulbar motor neurone disease. In healthy volunteers, the mechanical glottis increased peak flow rate and decreased the time to peak flow during forced expiration, but cough produced even higher flow rates and shorter times to peak flow. In patients, the mechanical glottis increased peak flow rate and decreased the time to peak flow. The mechanical glottis also produced higher peak flow rates when compared to the cough manoeuvres, and the time to peak flow was also significantly shorter with the mechanical glottis. We have shown that the use of a mechanical glottis tends to convert the airflow profile of a peak expiratory flow manoeuvre into that of a cough in both healthy volunteers and patients with motor neurone disease. Its potential role as an aid to clearance of airway secretions in patients with impaired laryngeal function remains to be seen.
Adult↗
Cerebrovascular reactivity to carbon dioxide in sepsis syndrome.
Cerebral dysfunction in sepsis is common in critically ill adults. However, little is known of the effects of sepsis on cerebral haemodynamics. We studied 12 sedated and ventilated patients in whom sepsis had been established for > 24 h. Transcranial Doppler measurements of the middle cerebral artery flow velocity were made at normocapnia, then hypocapnia (-1 kPa) and hypercapnia (+1 kPa). From these data, cerebrovascular reactivity to carbon dioxide was calculated. Variables indicating disease severity, systemic cardiovascular status and outcome were also recorded. We found significant changes in cerebrovascular reactivity to carbon dioxide. Only three of 12 patients had a cerebrovascular reactivity to carbon dioxide in the normal range; seven patients had a reduced cerebrovascular reactivity to carbon dioxide, whereas in two patients it was raised. In this smaD sample, we could not find any trend of association between altered cerebrovascular reactivity to carbon dioxide and severity of illness, cardiovascular status or outcome. This study suggests that established sepsis profoundly affects the vascular tone and reactivity, not only of the systemic circulation, but also of the cerebral vasculature.
Adult↗
Transient hyperaemic response to assess vascular reactivity of skin: effect of locally iontophoresed acetylcholine, bradykinin, epinephrine and phenylephrine.
BACKGROUND: Recently, the transient hyperaemic response (THR) to brief compression (20 s) of the brachial artery has been described as a way to assess vascular reactivity of the forearm skin. We studied the effects of locally iontophoresed vasoactive agents on this response in 20 male volunteers. METHODS: An iontophoresis chamber attached to the anterior forearm permitted simultaneous administration of drugs by iontophoresis and measurement of skin blood flow-flux by laser Doppler probe. Three THR tests were performed before and after iontophoresis by compressing the brachial artery with digital pressure for 20 s and then releasing. The following were iontophoresed: saline 0.9% (iontophoresis vehicle control), acetylcholine, bradykinin, epinephrine and phenylephrine. The THR ratio (THRR) was calculated as F2/F1 where F1 was baseline blood flow-flux immediately before compression and F2 was peak blood flow-flux after release. RESULTS: When compared with saline 0.9%, acetylcholine and bradykinin increased median F1 from 9.2 (range 5.2-23.8) to 22.1 (8.7-61.5) and from 4.8 (3.0-23.2) to 15.0 (2.5-31.8), respectively, and reduced THRR from 1.26 (1.07-2.2) to 0.99 (0.93-1.04) and from 1.63 (1.06-2.58) to 1.09 (0.93-1.19), respectively. Epinephrine, but not phenylephrine, caused a significant reduction in F1 from 9.2 (5.2-23.8) to 4.0 (1.5-22.3). Neither epinephrine nor phenylephrine had significant effect on THRR. CONCLUSIONS: Iontophoresed acetylcholine and bradykinin significantly increase the flow-flux and impair THR in forearm skin, further validating the concept that THR represents true vasodilatation during arterial occlusion. In addition, iontophoresis of vasoconstrictors does not appear to have any consistent effect.
Acetylcholine↗
Effects of magnesium sulphate on cerebral haemodynamics in healthy volunteers: a transcranial Doppler study.
BACKGROUND: Magnesium is increasingly being considered as a neuroprotective agent. We aimed to study its effects on middle cerebral artery blood flow velocity (V(mca)), cerebral autoregulation and cerebral vascular reactivity to carbon dioxide (CRCO(2)) in healthy volunteers. METHODS: Fifteen healthy volunteers were recruited. Using transcranial Doppler ultrasonography, V(mca) was recorded continuously. The strength of autoregulation was assessed by the transient hyperaemic response test, and the CRCO(2) was measured by assessing changes in V(mca) to the induced changes in end-tidal carbon dioxide. I.V. infusion of magnesium sulphate was then started (loading dose of 16 mmol followed by an infusion at the rate of 2.7 mmol h(-1)) for 45 min. The cerebral haemodynamic variables were measured again near the end of the infusion of magnesium sulphate. RESULTS: Total serum magnesium levels were doubled by the infusion regimen. However, there were no significant changes in V(mca), strength of autoregulation, or CRCO(2). Five of the volunteers reported marked nausea and two developed significant hypotension during the loading dose. CONCLUSIONS: Infusion of magnesium sulphate, in a dose that doubles its concentration in plasma, does not affect V(mca), strength of autoregulation or CRCO(2) in healthy volunteers. However, it can be associated with nausea and hypotension.
Adolescent↗
Non-selective and cyclo-oxygenase-2-specific non-steroidal anti-inflammatory drugs impair the hyperaemic response of skin to brief axillary artery occlusion.
BACKGROUND: Cyclo-oxygenase-2 (COX-2)-specific inhibitors are marketed as safer analgesics than non-selective non-steroidal anti-inflammatory drugs. However, there has been conflicting evidence concerning endothelial function and cardiovascular risk after COX-2 inhibitor use. We investigated forearm skin vascular reactivity to brief axillary artery occlusion in healthy volunteers after a single dose of the non-steroidal anti-inflammatory drugs ibuprofen (non-selective) and rofecoxib (COX-2 specific). METHODS: Ten healthy male volunteers were studied. Forearm skin blood flow was measured using laser Doppler flowmetry. Two non-invasive probes were placed on the volar surface of the forearm. The magnitude of hyperaemic response to brief (20 s) and prolonged (5 min) occlusion of the axillary artery was measured before and 2-3 h after administration of ibuprofen 800 mg or rofecoxib 25 mg. The transient hyperaemic response ratio (THRR), defined as the net peak hyperaemic flow-flux divided by the net baseline flow-flux, was calculated. Each volunteer received both drugs in random order at least 1 week apart. RESULTS: Ibuprofen and rofecoxib increased net baseline blood flow (median (range): ibuprofen, from 23.3 (12.1-40.8) to 31.5 (17.4-77.3); rofecoxib, from 22.0 (14.6-41.0) to 29.9 (19.5-112.0); P<0.01). The net hyperaemic peak flow-flux after brief and prolonged occlusion was unchanged after both drugs. THRR was reduced by both drugs (ibuprofen, from 2.92 (2.38-3.86) to 2.09 (1.45-3.54); rofecoxib, from 3.36 (2.06-5.16) to 2.67 (1.15 -3.84); P<0.01). CONCLUSIONS: Both COX-2 and non-selective non-steroidal anti-inflammatory drugs, when given to healthy volunteers as single therapeutic doses, decrease skin microvascular tone but do not impair maximal vasodilatory ability.
Adult↗
Preliminary findings in the neurophysiological assessment of intercostal nerve injury during thoracotomy.
OBJECTIVE: Previous work has suggested that intercostal nerve injury is a major factor in the aetiology of chronic post-thoracotomy pain. The aim of this study was to establish if there was identifiable intercostal nerve injury during thoracotomy. METHODS: Intercostal nerves were stimulated and motor evoked potentials were recorded from intercostal muscles in 13 patients undergoing thoracotomy. Measurements were taken before and after entering the pleural space, after removal of the rib retractor and after intercostal space closure. RESULTS: Intercostal nerves functioned normally before and after entering the pleural space. After the rib retractor was removed, there was a total conduction block in the nerve immediately above the incision in every patient. In the nerves above this, six had a total block, one a partial block and three had normal conduction. There was a total conduction block in the nerve immediately below the incision in all but one patient. Of the nerves below this, four had a total block, two a partial block and three had normal conduction. In the cases of total conduction block, there was either a discrete block at the level of the distal end of the rib retractor or impairment throughout the whole nerve. Intercostal space closure did not injure any previously uninjured nerve. In a solitary patient where rib retraction was not employed, there was no impairment of the intercostal nerves throughout the operation. CONCLUSIONS: This study demonstrates for the first time that intercostal nerve injury occurs routinely due to rib retraction during thoracotomy. We believe that it may be an important step toward understanding the cause of post-thoracotomy neuralgia.
Evoked Potentials, Motor↗
Effects of propofol and nitrous oxide on middle cerebral artery flow velocity and cerebral autoregulation.
We studied the effects of adding 50% nitrous oxide to propofol anaesthesia administered by target-controlled infusion on middle cerebral artery flow velocity and autoregulatory indices derived from transient hyperaemic response tests. Nine healthy (ASA 1) adult patients scheduled to undergo elective surgery were recruited. A standardised anaesthetic comprising alfentanil 10 microg x kg(-1), propofol via a target-controlled infusion pump and vecuronium 0.1 mg x kg(-1) was used. Transcranial Doppler ultrasonography was used to measure middle cerebral artery (MCA) blood flow velocity and the transient hyperaemic response test was used to assess cerebral autoregulation. These measurements were performed while awake and then at an induction target concentration of propofol (the target at which consciousness was lost, mean 6.2 (SD 1.1) microg x ml(-1)). The measurements were repeated after the addition of 50% nitrous oxide to the breathing gas mixture. Propofol caused a significant decrease in MCA flow velocity and a significant increase in the strength of autoregulation. The addition of nitrous oxide had no significant effect on MCA flow velocity or cerebral autoregulation. These results suggest that addition of 50% nitrous oxide does not influence propofol-induced changes in cerebral haemodynamics.
Adolescent↗
Transient hyperaemic response to assess vascular reactivity of skin; effect of locally iontophoresed sodium nitroprusside.
BACKGROUND: We aimed to study if brief compression (20 s) of the brachial artery could provoke a hyperaemic response in forearm skin. In addition, we studied the effect of pre-dilating the skin vessels with locally iontophoresed sodium nitroprusside on the hyperaemic response. METHODS: Ten healthy male volunteers were studied. A custom-made perspex iontophoresis chamber was attached to the anterior aspect of the distal forearm; this chamber allowed simultaneous administration of drugs by iontophoresis and measurement of skin blood flow flux by the laser Doppler probe. The flow flux signal, measured in volts, was continuously recorded onto a paper chart recorder. Three control transient hyperaemic response (THR) tests were performed by releasing the manual occlusion of the brachial artery maintained for 20 s. Thereafter, 2% sodium nitroprusside was iontophoresed using a current of 100 mAmp for 240 s. The THR tests were repeated three more times. From the recordings, baseline blood flow flux immediately before the onset of compression (or F1) and maximum blood flow flux immediately after the release of compression (or F2) were taken for analysis. The THR ratio (THRR) was calculated as: THRR = F2/F1. Average values of F1 and THRR were taken from the tests before and after iontophoresis and a paired t-test was used for analysing the changes. RESULTS: Nine of the 10 subjects showed a hyperaemic response at the release of compression. Iontophoresis of sodium nitroprusside significantly increased the baseline flow flux from 0.77 (range 0.29-1.61) to 1.88 V (0.73-2.91). It also completely abolished the THR in all subjects; THRR decreased from 1.65 (1.00-2.78) to 1.00 (0.98-1.03). CONCLUSION: A brief compression of the brachial artery results in a significant hyperaemic response in the forearm skin; this response is abolished by pre-dilatation of skin vessels. These findings support the hypothesis that the THR test assesses true vasodilatation occurring during arterial compression.
Adult↗
Cerebral haemodynamics in pregnancy and pre-eclampsia as assessed by transcranial Doppler ultrasonography.
BACKGROUND: Altered cerebral circulation, as reported during normal pregnancy, and in patients with pre-eclampsia, can be associated with changes in cerebral vascular reactivity and/or cerebral autoregulation. The aim of our study was to perform a comparative assessment of cerebral haemodynamics, including vascular reactivity and autoregulation, in pre-eclamptic patients, healthy pregnant women, and healthy non-pregnant women. METHODS: Thirty patients with pre-eclampsia were recruited. Age- and height-matched healthy pregnant (n=30) and non-pregnant control (n=30) groups were also recruited. Monitoring included transcranial Doppler ultrasonography, end-tidal carbon dioxide and non-invasive arterial pressure measurement. Cerebral autoregulation was assessed by performing the transient hyperaemic response (THR) test. The cerebrovascular reactivity to carbon dioxide (CRCO(2)) was assessed by measuring middle cerebral artery blood flow velocity (MCAFV) after induced changes in end-tidal carbon dioxide. Estimated cerebral perfusion pressure (eCPP) and critical closing pressure (CrCP) were calculated using established formulae. Statistical analysis included ANOVA with Tukey's pairwise comparisons. RESULTS: Mean arterial pressure (MAP) was increased in pre-eclampsia (P<0.05). Mean MCAFV was lower in healthy pregnancy (P<0.05), but in pre-eclampsia it was similar to the non- pregnant group. When compared with the non-pregnant group, mean eCPP was higher in the healthy pregnant and pre-eclamptic groups (P<0.05). There were no meaningful differences in cerebral autoregulation or CRCO(2). CONCLUSIONS: Healthy pregnancy increases eCPP, presumably by decreasing CrCP. In pre-eclampsia, eCPP is maintained at the same level as in healthy pregnancy despite an increased MAP. Pre-eclampsia has no significant effect on cerebral autoregulation or CRCO(2).
Adolescent↗
Effects of desflurane on cerebral autoregulation.
The aim of this study was to determine the effects of desflurane, at 1 and 1.5 MAC, on cerebral autoregulation. Data were analysed from eight patients undergoing non-neurosurgical procedure. The blood flow velocity in the middle cerebral artery was measured by transcranial Doppler ultrasound and cerebral autoregulation was assessed by the transient hyperaemic response test. Partial pressure of the end-tidal carbon dioxide (PE'(CO(2))) and mean arterial pressure were measured throughout the study. Anaesthesia was induced with propofol and was maintained with desflurane at end-tidal concentrations of 7.4% (1 MAC) or 10.8% (1.5 MAC). The order of administration of the desflurane concentrations was determined randomly and a period of 15 min was allowed for equilibration at each concentration. The transient hyperaemic response tests were performed before induction of anaesthesia and after equilibration with each concentration of desflurane. An infusion of phenylephrine was used to maintain pre-induction mean arterial pressure and ventilation was adjusted to maintain the pre-induction value of PE'(CO(2)) throughout the study. Two indices derived from the transient hyperaemic response test (the transient hyperaemic response ratio and the strength of autoregulation) were used to assess cerebral autoregulation. Desflurane resulted in a marked and significant impairment in cerebral autoregulation; at concentrations of 1.5 MAC, autoregulation was almost abolished.
Adolescent↗
Video imaging to assess neuromuscular blockade at the larynx.
UNLABELLED: We describe video imaging as a technique for assessing neuromuscular blockade at the larynx. We sought to determine the stability and reproducibility of this technique and to compare the effect of succinylcholine at the adductor pollicis and the larynx. Ten patients were studied. Anesthesia was induced and maintained with propofol. The recurrent laryngeal nerve was stimulated superficially and movements of the vocal cords were recorded on videotape by using a fiberoptic bronchoscope passed via a laryngeal mask airway. Neuromuscular function was recorded at the adductor pollicis by using a mechanomyograph. Twenty images of the vocal cords were examined repeatedly by one investigator and by ten independent observers. The mean difference between the two sets of observations was 0.86 degrees with a correlation coefficient (r) of 0.997. For 3 min before the administration of relaxant the coefficient of variation in the cord movement during supramaximal stimulation ranged from 1%-4% (median 2.7%). After the administration of succinylcholine 1 mg. kg(-1) the times to loss of T1 at the larynx and hand were 63 +/- 15 s and 63 +/- 12 s respectively. Times to 25% recovery were 215 +/- 36 s at the larynx and 436 +/- 74 s at the hand and times to 75% recovery were 285 +/- 55 s and 525 +/- 85 s respectively. These results indicate that video imaging may be a useful research technique for estimating neuromuscular blockade at the larynx and that the time to onset of succinylcholine at the larynx is similar to that at the hand, whereas the duration of blockade is significantly shorter at the larynx. IMPLICATIONS: Assessment of neuromuscular blockade at the larynx is possible by using a video imaging technique. By using this technique, the time to onset of neuromuscular blockade at the larynx is similar to that at the hand after the administration of succinylcholine; this finding is different from previously published data obtained by using a cuff pressure measurement technique.
Adult↗