Heart rate (HR) and arterial blood pressure (BP) changes have been reported during conscious sedation with propofol and midazolam. One potential mechanism to explain these changes is that propofol and midazolam affect HR and BP via changes in the cardiac autonomic nervous system. Two specific hypotheses were tested by HR variability analysis: 1) propofol induces predominance of parasympathetic activity, leading to decreased HR and BP, and 2) midazolam induces predominance of sympathetic activity, leading to increased HR and decreased BP. Thirty dental patients were included in a prospective, randomized study. HR, BP, low frequency (LF), high frequency (HF), and entropy were monitored during the awake, sedation, and recovery periods and depth of sedation was assessed using the Observer's Assessment of Alertness/Sedation score. Propofol induced a significant decrease in total power (503 +/- 209 ms(2)/Hz versus 162 +/- 92 ms(2)/Hz) and LF/HF ratio (2.5 +/- 1.2 versus 1.0 +/- 0.4), despite the absence of any change in HR during the sedation period compared with baseline. Midazolam decreased normalized HF (34 +/- 10% versus 10 +/- 4%) but did not significantly change LF/HF ratio (2.3 +/- 1.1 versus 2.2 +/- 1.4) and increased HR in the sedation period. Compared with baseline, propofol was associated with a significant increase in normalized HF in the recovery period (34 +/- 11% versus 44 +/- 12%) and a significant decrease in HR, whereas midazolam was associated with an increase in LF/HF ratio (2.3 +/- 1.1 versus 3.7 +/- 1.8) with no change in HR. These results indicated a dominant parasympathetic effect of propofol and a dominant sympathetic effect of midazolam in both periods. These results should be considered during conscious sedation, especially in patients at risk of cardiovascular complications.
The aims were to investigate (1) if temporomandibular disorders (TMD) patients with temporomandibular joint (TMJ) pain had different conditioned pain modulation (CPM) compared with healthy subjects and, (2) if clinical pain characteristics influenced CPM. Sixteen TMD pain patients and 16 age-matched healthy subjects were participated. A mechanical conditioning stimulus (CS) was applied to pericranial muscles provoking a pain intensity of 5/10 on a visual analogue scale. Pressure pain thresholds (PPT) and pressure pain tolerance thresholds (PPTol) were assessed at masseter, forearm and painful TMJ (only PPT) before, during, and 20 min after CS. Data were analyzed with ANOVAs. The correlations between CPM effect and ratings of TMD pain intensity on a numerical rating scale (NRS) or the pain duration were calculated (correlation coefficient; R). The relative PPT and PPTol increases (mean for the three assessment sites) during CS were significantly higher than baseline in healthy subjects (43.0 ± 3.6, 33.0 ± 4.0 %; P < 0.001, P < 0.001) but not in the TMD pain patients (4.9 ± 2.7, -1.4 ± 4.1 %; P = 0.492, P = 1.000) with significant differences between groups (P < 0.001). In the patients, the relative PPT changes during CS were not significantly higher than baseline at TMJ (5.3 ± 3.8 %, P = 0.981) and masseter (-2.8 ± 4.8 %, P = 1.000) but significantly higher at forearm (12.3 ± 4.7 %, P = 0.039). No correlation was detected between TMD pain intensity and CPM effect (R = -0.261; P = 0.337) or between pain duration and CPM effect (R = -0.423; P = 0.103) at painful TMJ. These findings indicate that CPM is impaired in TMD pain patients especially at sites with chronic pain but not at pain-free sites and that the clinical pain characteristics do not influence CPM.
The present study shows that systemic administration of an α(2) -adrenoceptor agonist (DEX), less than the clinical dose, inhibited CPM in humans. These results may provide some mechanistic insight into why many chronic pain patients show impaired CPM.
SummaryIn a prospective, blind, randomised study, we examined the effects of midazolam-propofol co-induction on haemodynamic (blood pressure, heart rate and stroke volume) and heart rate variability. The latter was measured by spectral analysis using the maximum-entropy method to calculate the following: the low frequency component (LF), which reflects both the cardiac sympathetic and parasympathetic activity, the high frequency component (HF) and entropy, which reflects the cardiac parasympathetic activity, the total power (TP), calculated by the addition of LF and HF, and the LF ⁄ HF ratio, which reflects the balance between the cardiac sympathetic and parasympathetic nervous activity. Forty patients were randomly allocated to the propofol group and the midazolam-propofol group, and the parameters described above were calculated at baseline (T1), post induction (T2), after tracheal intubation (T3), and 3 min (T4) and 5 min after intubation (T5). Propofol was administered at 2.5 mg.kg )1 in the propofol group and midazolam at 0.1 mg.kg )1 followed by propofol at 1.5 mg.kg )1 in the midazolam-propofol group for anaesthesia induction. Then, propofol was administered at 4-6 mg.kg )1 propofol for maintenance in both groups. The midazolam-propofol group showed compensated haemodynamic changes, which were related to significant increases in the LF ⁄ HF ratio at T2, T4 and T5 (p = 0.011, 0.038 and 0.034). These results suggest that the midazolam-propofol combination yielded compensated modulatory effects on the cardiovascular system, including preserved baroreflex activity. Combined induction (co-induction) refers to the administration of a small dose of a sedative or anaesthetic agent prior to the induction of anaesthesia, with the aim of achieving more specific 'target' responses, while minimising side-effects. Co-induction with midazolam and propofol has been mainly studied in relation to the drugs' synergistic hypnotic actions of the drugs and haemodynamic changes [1-4] during induction of anaesthesia, but there are no reports to date of the haemodynamic changes occurring during tracheal intubation. Propofol decreases the arterial blood pressure, associated with a decrease of the cardiac output ⁄ index, stroke volume index, and systemic vascular resistance [5]; on the other hand, the cardiac output ⁄ index and ventricular filling pressures are maintained after the administration of midazolam [5,6]. The autonomic nervous system exerts important neural control on the heart for maintaining cardiovascular stability. Previous studies have evaluated the effects of propofol [7][8][9][10] and midazolam [11][12][13] on the cardiac autonomic nervous system by means of heart rate variability (HRV) analysis, a non-invasive technique [14][15][16]. There are, however, no reports on simultaneous analysis of the changes of the stroke volume and HRV during midazolam-propofol co-induction. The aim of this study was to investigate the haemodynamic changes and heart rate variability during midazolam co-induction with propofol as comp...
The authors controlled trigeminal neuralgia pain by blocking the mandibular nerve with local anesthetics administered through an indwelling catheter. Because the continuous nerve block with local anesthetics is reversible and only mildly toxic, this method is beneficial for pain control in patients with trigeminal neuralgia scheduled to undergo microvascular decompression.
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