Comparing the effect of arginine vasopressin on ear and finger photoplethysmography.

STUDY OBJECTIVE: To test whether the relative insensitivity of craniofacial vessels to catecholamines differs in response to arginine vasopressin. DESIGN: Prospective, observational human study. SETTING: University hospital. PATIENTS: 8 ASA physical status I and II women scheduled for elective myomectomy. INTERVENTIONS: Patients underwent elective myomectomy surgery with intrauterine injection of arginine vasopressin. MEASUREMENTS: Finger, ear, and forehead photoplethysmographs were monitored. Changes in the plethysmographic amplitudes were recorded before and after arginine vasopressin injection. MAIN RESULTS: In all subjects, ear photoplethysmographic amplitude (but not oxygen saturation) decreased precipitously (62% +/- 10%; P < 0.001) after arginine vasopressin injection. In contrast, there was no significant decline in the finger signal (4.5% +/- 27%; P = 0.19). The forehead plethysmograph decreased in amplitude, but this finding did not achieve significance (33% +/- 18%; P = 0.18). CONCLUSION: In contrast to prior observations during adrenergic activation, arginine vasopressin induced relatively greater vasoconstriction at the ear and forehead than at the finger. This finding has potential implications with respect to arginine vasopressin's effect on blood flow and indicates that monitoring the ear plethysmographic signal may provide useful information during arginine vasopressin administration.

The relationship between the photoplethysmographic waveform and systemic vascular resistance.

OBJECTIVE: The objective of this study was to determine the relationship between systemic vascular resistance (SVR), finger & ear photoplethysmographic measurements in 14 adult patients undergoing coronary artery bypass grafting (CABG). METHODS: Patients were monitored with photoplethysmographs of the finger and ear and continuous cardiac output (QT) via thermodilution catheter. The relationship between SVR, finger plethysmographic amplitude, width and ear plethysmographic amplitude, width was assessed with linear regression. RESULTS: The finger plethysmographic amplitude had a low correlation r value = -0.15, while finger plethysmographic width had a better correlation r value = 0.56. The correlation between SVR and ear plethysmographic amplitude and width were -0.24 and 0.62 respectively. Using receiver operating characteristic analysis the ear plethysmographic width had both better sensitivity and specificity than the finger plethysmographic width in identifying high and low SVR. Using a multiple regression analysis, SVR was estimated from the pulse oximeter waveforms: SVR calculated = 27.27 + (3978.53 x Ear pulse oximeter width) - (8.91 x Ear pulse oximeter area) + (1986.3 x Finger pulse oximeter width). Bland-Altman analysis was used the bias was 29.8 dynes s cm(-5), standard deviation was 587.3, upper and lower limit of agreement were 1204.45, and -1144.8 dynes s cm(-5) respectively. CONCLUSION: The data indicate that pulse width of finger and ear plethysmographic tracing are more sensitive to changes in SVR than the other indices. An appreciation of changes in pulse width may provide valuable evidence with respect to changes in peripheral vascular tone.

Impact of withdrawal of 450 ml of blood on respiration-induced oscillations of the ear plethysmographic waveform.

OBJECTIVE: It has been widely appreciated that ventilation-induced variations in systolic blood pressure during mechanical ventilation correlate with changes in intravascular volume. The present study assessed whether alterations in volume status likewise can be detected with noninvasive monitoring (ear plethysmograph) in non-intubated subjects (awake volunteers). METHODS: Eight healthy adults were monitored with EKG, noninvasive blood pressure, an unfiltered ear plethysmograph, and a respiratory force transduction belt before (PRE) and after (POST) withdrawal of 450 ml of blood from an antecubital vein. Spectral-domain analysis was used to determine the peak ventilatory frequency and the power of the associated variation in the ear plethysmographic tracing; Interphase differences in the respiration-induced plethysmographic variations were assessed by Wilcoxon signed rank test. In addition, the changes in the ear plethysmographic tracing were compared to changes in heart rate and blood pressure. RESULTS: There was a significant increase in respiratory-associated oscillations at the respiratory frequency between the PRE and POST phases (p = 0.012). These changes were detected despite lack of changes in heart rate or blood pressure. CONCLUSIONS: Respiration-induced changes of the ear plethysmographic waveform during spontaneous ventilation increase significantly as a consequence of withdrawal of approximately one unit of blood in healthy volunteers.

What is the best site for measuring the effect of ventilation on the pulse oximeter waveform?

The cardiac pulse is the predominant feature of the pulse oximeter (plethysmographic) waveform. Less obvious is the effect of ventilation on the waveform. There have been efforts to measure the effect of ventilation on the waveform to determine respiratory rate, tidal volume, and blood volume. We measured the relative strength of the effect of ventilation on the reflective plethysmographic waveform at three different sites: the finger, ear, and forehead. The plethysmographic waveforms from 18 patients undergoing positive pressure ventilation during surgery and 10 patients spontaneously breathing during renal dialysis were collected. The respiratory signal was isolated from the waveform using spectral analysis. It was found that the respiratory signal in the pulse oximeter waveform was more than 10 times stronger in the region of the head when compared with the finger. This was true with both controlled positive pressure ventilation and spontaneous breathing. A significant correlation was demonstrated between the estimated blood loss from surgical procedures and the impact of ventilation on ear plethysmographic data (r(s) = 0.624, P = 0.006).

The use of joint time frequency analysis to quantify the effect of ventilation on the pulse oximeter waveform.

OBJECTIVE: In the process of determining oxygen saturation, the pulse oximeter functions as a photoelectric plethysmograph. By analyzing how the frequency spectrum of the pulse oximeter waveform changes over time, new clinically relevant features can be extracted. METHODS: Thirty patients undergoing general anesthesia for abdominal surgery had their pulse oximeter, airway pressure and CO(2) waveforms collected (50 Hz). The pulse oximeter waveform was analyzed with a short-time Fourier transform using a moving 4096 point Hann window of 82 seconds duration. The frequency signal created by positive pressure ventilation was extracted using a peak detection algorithm in the frequency range of ventilation (0.08-0.4 Hz = 5-24 breaths/minute). The respiratory rate derived in this manner was compared to the respiratory rate as determined by CO(2) detection. RESULTS: In total, 52 hours of telemetry data were analyzed. The respiratory rate measured from the pulse oximeter waveform was found to have a 0.89 linear correlation when compared to CO(2) detection and airway pressure change. the bias was 0.03 breath/min, SD was 0.557 breath/min and the upper and lower limits of agreement were 1.145 and -1.083 breath/min respectively. The presence of motion artifact proved to be the primary cause of failure of this technique. CONCLUSION: Joint time frequency analysis of the pulse oximeter waveform can be used to determine the respiratory rate of ventilated patients and to quantify the impact of ventilation on the waveform. In addition, when applied to the pulse oximeter waveform new clinically relevant features were observed.

Analysis of the ear pulse oximeter waveform.

OBJECTIVE: For years researchers have been attempting to understand the relationship between central hemodynamics and the resulting peripheral waveforms. This study is designed to further understanding of the relationship between ear pulse oximeter waveforms, finger pulse oximeter waveforms and cardiac output (CO). It is hoped that with appropriate analysis of the peripheral waveforms, clues can be gained to help to optimize cardiac performance. METHODS: Part 1: Studying the effect of cold immersion test on plethysmographic waveforms. Part 2: Studying the correlation between ear and finger plethysmographic waveforms and (CO) during CABG surgery. The ear and finger plethysmographic waveforms were analyzed to determine amplitude, width, area, upstroke and downslope. The CO was measured using continuous PA catheter. Using multi-linear regression, ear plethysmographic waveforms, together with heart rate (HR), were used to determine the CO Agreement between the two methods of CO determination was assessed. RESULTS: Part 1: On contralateral hand immersion, all finger plethysmographic waveforms were reduced, there was no significant change seen in ear plethysmographic waveforms, except an increase in ear plethysmographic width. Part 2: Phase 1: Significant correlation detected between the ear plethysmographic width and other ear and finger plethysmographic waveforms. Phase 2: The ear plethysmographic width had a significant correlation with the HR and CO. The correlation of the other ear plethysmographic waveforms with CO and HR are summarized (Table 5). Multi-linear regression analysis was done and the best fit equation was found to be: CO=8.084 - 14.248 x Ear width + 0.03 x HR+ 92.322 x Ear down slope+0.027 x Ear Area Using Bland & Altman, the bias was (0.05 L) but the precision (2.46) is large to be clinically accepted. CONCLUSION: The ear is relatively immune to vasoconstrictive challenges which make ear plethysmographic waveforms a suitable monitor for central hemodynamic changes. The ear plethysmographic width has a good correlation with CO.

Topical non-iontophoretic application of acetylcholine and nitroglycerin via a translucent patch: a new means for assessing microvascular reactivity.

OBJECTIVE: Assessments of endothelial cell function with acetylcholine have typically used systemic, regional intra-arterial, or iontophoretic delivery of drug. Each of these techniques induces systemic and/or local changes that compromise their safety or effectiveness. Using translucent drug preparations applied under laser Doppler flowmetry (LDF) probes, we tested whether local vasodilation can be induced with non-iontophoretic transdermal delivery of acetylcholine and how such dilation would compare to the dilation achieved with topical nitroglycerin in healthy volunteers. METHODS: Ten subjects without known vascular disease were recruited for LDF monitoring at sites of drug application for this preliminary investigation. Topical acetylcholine chloride, nitroglycerin, and placebo were applied via translucent patches to the forehead directly below LDF probes. RESULTS: LDF readings increased by 406 percent (245 percent to 566 percent) and 36 percent (26 percent to 46 percent), respectively, at the acetylcholine and placebo sites (p = .005 by Wilcoxon Signed Rank Test (WSRT) for acetylcholine vs. placebo); and they increased by 365 percent (179 percent to 550 percent) at the nitroglycerin site (p = .005 by WSRT for nitroglycerin vs. placebo; p = .6 vs. acetylcholine). CONCLUSION: Transdermal delivery of acetylcholine can induce significant local vasodilatory responses comparable to those achieved with nitroglycerin without requiring iontophoresis. The means of transdermal delivery and monitoring described herein may constitute a new minimally invasive way to interrogate the microvasculature and thereby assess the microcirculatory changes induced by various disorders and therapeutic interventions.

The effect of venous pulsation on the forehead pulse oximeter wave form as a possible source of error in Spo2 calculation.

Reflective forehead pulse oximeter sensors have recently been introduced into clinical practice. They reportedly have the advantage of faster response times and immunity to the effects of vasoconstriction. Of concern are reports of signal instability and erroneously low Spo(2) values with some of these new sensors. During a study of the plethysmographic wave forms from various sites (finger, ear, and forehead) it was noted that in some cases the forehead wave form became unexpectedly complex in configuration. The plethysmographic signals from 25 general anesthetic cases were obtained, which revealed the complex forehead wave form during 5 cases. We hypothesized that the complex wave form was attributable to an underlying venous signal. It was determined that the use of a pressure dressing over the sensor resulted in a return of a normal plethysmographic wave form. Further examination of the complex forehead wave form reveal a morphology consistent with a central venous trace with atrial, cuspidal, and venous waves. It is speculated that the presence of the venous signal is the source of the problems reported with the forehead sensors. It is believed that the venous wave form is a result of the method of attachment rather than the use of reflective plethysmographic sensors.

Recovery of neuromuscular function after a combination of mivacurium and rocuronium.

PURPOSE: The present study was undertaken to evaluate onset, and early and late recovery of neuromuscular block after a combination of mivacurium (M) and rocuronium (R). METHODS: In this controlled, randomized study, 45 consenting ASA I-II patients were assigned to one of three treatment groups: 2.ED95 R alone (2R); 2.ED95 R plus 1.ED95 M (2R1M). or 2.ED95 R plus 2.ED95 M (2R2M). Neuromuscular monitoring of the ulnar nerve consisted of surface electrode stimulation and force transduction of the adductor pollicis muscle. Stable baseline stimulation (1 Hz, square-wave, supramaximal current) was established prior to relaxant administration and continued until 95 percent twitch height depression (onset). Thereafter, train-of-four stimulation every 10 seconds was used to record recovery data until 95 percent recovery (T(95%)). Data were analyzed using grouped t-tests, ANOVA, and Newman-Keuls multiple comparison tests. Significance was defined at the p < 0.05 level. RESULTS: The addition of mivacurium to rocuronium did not accelerate onset of block. The combination prolonged the clinical duration (time to 5 percent recovery, T(5%)), but did not affect subsequent recovery parameters: T(5%) in the 2R1M and 2R2M groups were 100 percent and 118 percent longer than in the 2R group, respectively (p < 0.05) the T(5-25%) (early recovery) and T(25-75%) (linear recovery) indexes were similar in all three groups. CONCLUSIONS: The present study did not note an acceleration of block onset when mivacurium was added to rocuronium. The findings suggest that the addition of mivacurium (1-2.ED95) to rocuronium (2.ED95) prolongs the clinical duration of the longer-acting agent, rocuronium, but has no effect on the early or linear recovery indexes of rocuronium. Thus, although clinical duration is prolonged, recovery from the combination regimens proceeds as if no mivacurium had been added to rocuronium.

Synchronous rhythmical vasomotion in the human cutaneous microvasculature during nonpulsatile cardiopulmonary bypass.

BACKGROUND: The origin, control mechanisms, and functional significance of oscillations in microvascular flow are incompletely understood. Although the traditional belief has been that only low-frequency oscillations (0.04-0.10 Hz) can originate at the microvascular level, recent evidence in healthy volunteers has suggested that high-frequency oscillations (> 0.10 Hz) also may have a microvascular origin (as opposed to being mechanically transmitted respiratory-induced variations in stroke volume). The current study determined if such oscillations would emerge in the absence of cardiac and respiratory activity during nonpulsatile cardiopulmonary bypass (NP-CPB). METHODS: Forehead and finger laser Doppler flow, arterial pressure, and core temperature were simultaneously recorded in eight patients during NP-CPB. Analyses included time- domain indices, frequency-domain indices (auto power spectral density), and a measure of regularity (approximate entropy) for standardized time segments. RESULTS: Nonpulsatile cardiopulmonary bypass was associated with the emergence of rhythmical oscillations in laser Doppler flow, with characteristic frequencies for the forehead (0.13 +/- 0.03 Hz) and finger (0.07 +/- 0.02 Hz). Forehead vasomotion became progressively synchronized, with a gain in high-frequency spectral power from 17.5 (minute 1) to 89.1 (minute 40) normalized units, and a decrease in approximate entropy from 1.2 (before NP-CPB) to less than 0.5 (minute 40). CONCLUSIONS: The emergence of forehead microvascular oscillations at greater than 0.10 Hz (characteristic of parasympathetic frequency response), in the absence of cardiac and respiratory variability, demonstrates their peripheral origin and provides insights into parasympathetic vasoregulatory mechanisms. The progressive synchronization of forehead vasomotion during NP-CPB, suggestive of increased coupling among microvascular biologic oscillators, may represent a microcirculatory homeostatic response to systemic depulsation, with potential implications for end-organ perfusion.

Distinction between atropine-sensitive control of microvascular and cardiac oscillatory activity.

This study tested whether "high frequency" oscillations (HF; >0.12 cycles/s) in microvascular flow during a vasoconstrictive challenge constitute a homeostatic cholinergic response at the level of the microvasculature or simply represent oscillations that originate at the heart and are transmitted to passive microvascular beds. Heart rate, blood pressure, respiratory rate, and laser Doppler flowmetry of the forehead and finger were monitored in healthy volunteers at baseline, during systemic infusion of phenylephrine (0.4-0.6 microg/kg/min), and during subsequent addition of intravenous atropine (< or = 2.0 mg/70 kg). Spectral-domain analysis documented that atropine-sensitive oscillatory power of the R-wave to R-wave intervals of the electrocardiogram was predominant at the respiratory frequency (0.20 Hz) at baseline and during phenylephrine infusion. In contrast, arteriolar-capillary networks of the forehead developed a prominent atropine-sensitive oscillatory peak at 0.14 +/- 0.02 Hz during phenylephrine infusion (P < 0.05 for differences in oscillatory magnitude and frequency between forehead flow and R-R intervals). The cross-power spectral density confirmed the lack of common power between forehead flow and R-R oscillations. Post hoc assessments showed that---similar to heart rate---systemic pressure and systemic flow also had persistent power at 0.20 Hz and did not develop a peak at the forehead oscillatory frequency; phenylephrine likewise did not induce atropine-sensitive oscillations in the finger, a finding attributable to adrenergic predominance in this region. We conclude that atropine-sensitive oscillatory activity in the forehead microvasculature in response to a vasoconstrictive challenge constitutes a local response that is not due to, nor associated with, mechanical transmission from the heart and proximal vasculature.