Oxygen saturation in the arterial blood (SaO2) provides information on the adequacy of respiratory function. SaO2 can be assessed noninvasively by pulse oximetry, which is based on photoplethysmographic pulses in two wavelengths, generally in the red and infrared regions. The calibration of the measured photoplethysmographic signals is performed empirically for each type of commercial pulse-oximeter sensor, utilizing in vitro measurement of SaO2 in extracted arterial blood by means of co-oximetry. Due to the discrepancy between the measurement of SaO2 by pulse oximetry and the invasive technique, the former is denoted as SpO2. Manufacturers of pulse oximeters generally claim an accuracy of 2%, evaluated by the standard deviation (SD) of the differences between SpO2 and SaO2, measured simultaneously in healthy subjects. However, an SD of 2% reflects an expected error of 4% (two SDs) or more in 5% of the examinations, which is in accordance with an error of 3%–4%, reported in clinical studies. This level of accuracy is sufficient for the detection of a significant decline in respiratory function in patients, and pulse oximetry has been accepted as a reliable technique for that purpose. The accuracy of SpO2 measurement is insufficient in several situations, such as critically ill patients receiving supplemental oxygen, and can be hazardous if it leads to elevated values of oxygen partial pressure in blood. In particular, preterm newborns are vulnerable to retinopathy of prematurity induced by high oxygen concentration in the blood. The low accuracy of SpO2 measurement in critically ill patients and newborns can be attributed to the empirical calibration process, which is performed on healthy volunteers. Other limitations of pulse oximetry include the presence of dyshemoglobins, which has been addressed by multiwavelength pulse oximetry, as well as low perfusion and motion artifacts that are partially rectified by sophisticated algorithms and also by reflection pulse oximetry.

Blood pressure pulse wave velocity (PWV) is a parameter which is related to arterial distensibility. Its direct assessment, by measuring the appearance time of a pressure pulse in two sites along an artery and the distance between the two sites, is complicated and inaccurate. In the current study, pulse transit time (PTT) to the toes and fingers of 44 normotensive male subjects was measured by photoplethysmography (PPG) and ECG. The arrival time of the pulses at the toe and finger was determined from the foot of the systolic rise of the PPG signal, i.e. at end-diastolic time. Two parameters, which are related to PWV, were tested: the time delay between the ECG R-wave and the arrival time of the pulses at the toe (E-T PTT), and the difference in the transit time of the blood pressure pulses between the toe and finger (T-F PTTD). E-T PTT and T-F PTTD decreased as functions of the subject's age and systolic blood pressure (SBP), but their dependence on the diastolic blood pressure (DBP) was not statistically significant. The decrease of the PTT parameters with age is attributed to the direct structural decrease of the arterial compliance with age and not to functional effects associated with the increase of the blood pressure with age, since the PTT parameters did not depend on DBP though the measurements were performed at end-diastole.

The heart rate variability is composed of low- and high-frequency fluctuations, which are mediated by the sympathetic and the parasympathetic nervous systems. The baseline and the amplitude of the photoplethysmographic (PPG) signal also show fluctuations in the same frequencies. In the current study, PPG examinations were performed on the fingers of normal subjects and diabetic patients, and three parameters were derived from each PPG pulse: the baseline of the pulse, its amplitude and its period (which is equal to the heart period). The level of the variability of each PPG pulse parameter was measured by the ratio of the standard deviation of the parameter to its mean value. The level of the low-frequency fluctuations for the PPG amplitude and for the heart cycle period did not differ between males and females, but was lower for diabetic patients, indicating lower activity of the autonomic nervous system. The curves of the baseline and the amplitude of the PPG signal for the non-diabetic subjects showed high correlation between the left and the right hands. For most of the diabetic patients the right-left correlation coefficients were significantly lower than those for the non-diabetic subjects. Our initial results have shown that the variability of the PPG parameters shows promise for the assessment of the function of the autonomic nervous system.

PI was an earlier, clearer and more sensitive indicator of the development of epidural-induced sympathectomy than either skin temperature or MAP.

Several lines of evidence support involvement of the parasympathetic system in migraine: (i) migraine-associated symptoms, such as exaggerated facial flushing, lacrimation and rhinorrhea; (ii) increased levels of cranial venous vasoactive intestinal peptide in migraineurs during attacks; and (iii) reports of migraine pain alleviation by intranasal instillation of lidocaine, which can block some of the parasympathetic outflow to the cranium. This study assessed cranial parasympathetic function in migraineurs in between attacks, assuming that abnormal function might imply involvement of the parasympathetics in migraine pathogenesis. We tested 39 female migraineurs outside attacks, of whom 11 had bilateral pain, 20 unilateral at a specific side and eight alternating unilateral head pain, and 16 controls. The trigemino-parasympathetic reflex was studied, using soapy and saline eye drops for stimulation of the afferent limb of the reflex arch, and cutaneous vascular response at the forehead for the efferent limb. The latter was recorded by photoplethysmography on both sides of the forehead. We found no difference in vasodilatation between migraineurs as a group and controls (83.7 +/- 6.5% and 80.8 +/- 7.6%, respectively, not significant). However, when analysing data by the site of pain, we found that those with bilateral pain had the largest vasodilatation response (141.6 +/- 16.2%, P < 0.05 versus controls, analysis of varance, post hoc Tukey-Kramer HSD), while those with unilateral pain had the least vasodilatation (45.5 +/- 3.3%, P < 0.05). The response of patients with alternating pain (97.2 +/- 12.6%) did not differ from controls. It is concluded that cranial parasympathetic function does differ among patients with various migraine types at rest. Based on the understanding of dysfunctional brainstem pain modulation in migraine, we suggest a model of within-brainstem interaction between the two locus coeruleus nuclei, which are involved in control of pain and cranial parasympathetic outflow. The model assumes various levels of inhibitory inter-relationships between these two nuclei; diminution or absence of the normal reciprocal inhibitory relationships between them may underlie the augmented cranial parasympathetic response in bilateral migraineurs, while an excess of reciprocal inhibitory relationship between them may underlie the diminished cranial parasympathetic response in unilateral migraineurs. These findings might help in clarifying inter-relationships between brainstem nuclei in the context of migraine pathogenesis.