Awad, Aymen A. MD; Ghobashy, M. Ashraf M. MD; Ouda, Wagih MD; Stout, Robert G. MD; Silverman, David G. MD; Shelley, Kirk H. MD, PhD
Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut
Presented in part at the American Society of Anesthesiologists Annual Meeting, San Francisco, CA, October 16, 2000.
February 14, 2001.
Address correspondence and reprint requests to Kirk H. Shelley, MD, PhD, Department of Anesthesiology, Yale University School of Medicine, 333 Cedar St., TMP-3, P.O. Box 208051, New Haven, CT 06520-8051. Address e-mail to email@example.com.
The cold pressor test is often used to assess vasoconstrictive responses because it simulates the vasoconstrictive challenges commonly encountered in the clinical setting. With IRB approval, 12 healthy volunteers, aged 25–50 yr, underwent baseline plethysmographic monitoring on the finger and ear. The contralateral hand was immersed in ice water for 30 s to elicit a systemic vasoconstrictive response while the recordings were continued. The changes in plethysmographic amplitude for the first 30 s of ice water immersion (period of maximum response) of the finger and ear were compared. The data indicate a significant disparity between the finger and the ear signals in response to the cold stimulus. The average finger plethysmographic amplitude measurement decreased by 48% ± 19%. In contrast, no significant change was seen in the ear plethysmographic amplitude measurement, which decreased by 2% ± 10%. We conclude that the ear is relatively immune to the vasoconstrictive effects. These findings suggest that the comparison of the ear and finger pulse oximeter wave forms might be used as a real-time monitor of sympathetic tone and that the ear plethysmography may be a suitable monitor of the systemic circulation.
The adrenergic responsiveness of the finger is more intense than that of other sites in the body (1). A technique such as plethysmography may therefore be more influenced by changes in adrenergic tone at the finger than at other sites. This has prompted anesthesiologists and other clinicians to explore the usefulness of plethysmographic signals at other sites as a means of minimizing the effect of local vasoconstriction on the measurements of oxygen saturation and assessments of wave form morphology (2). We compared the responses of the ear to those of the finger during the cold pressor test, a classic vasoconstrictive stimulus wherein a vasoconstrictive reflex is elicited by immersing a hand in ice water (4°C) (3–6).
With Human Investigation Committee approval, 12 healthy male volunteers, aged 25–50 yr, were instructed to abstain from caffeine and other known vasoconstrictive compounds for at least 24 h before reporting for this one-session study. Each subject lay recumbent in a temperature-regulated room (21°C ± 0.5°C). Electrodes were applied for electrocardiogram and respiratory monitoring, and a noninvasive blood pressure reading was taken before and after ice water immersion. Plethysmographic monitoring was obtained with fixed-gain pulse oximeters (Oxypleth; Novametrix Medical Systems, Inc., Wallingford, CT) on the finger and ear. The plethysmographic signals were recorded at 250 Hz with a microprocessor-based data acquisition system, with commercially available data acquisition software.
After 10 min of baseline monitoring, the contralateral hand was immersed in ice water for 30 s while the recordings were continued. The changes in plethysmographic amplitude of the finger and ear during ice water immersion (the period of maximum response) were analyzed with an Igor Pro program (Wave Metrics, Inc., Lake Oswego, OR). A procedure was used that calculated the beat-to-beat measurement of baseline, amplitude, area, and width of pulse oximeter wave (Tech Note 20—peak measurement and fitting). The amplitudes were compared with paired Student’s t-tests;P < 0.05 was considered to be significant. Data are reported as mean ± sd.
The plethysmographic signal at the finger precipitously declined immediately upon ice water immersion. In contrast, the ear signal displayed minimal changes in this subject (Fig. 1). Overall, there was a significant disparity between the changes in plethysmographic amplitude at the finger and ear (P < 0.0001), as shown in Figure 2. The average finger plethysmographic amplitude decreased by 48% ± 19% from baseline (P < 0.0001). In contrast, the average ear plethysmographic amplitude remained at near-baseline values and decreased by 2% ± 10% (P = 0.38), as shown in Table 1.
Although two subjects had a >10% decline in ear plethysmographic amplitude during ice water immersion, in each of these subjects there was a ≥70% decline in finger plethysmographic amplitude. There were no instances in which failure to record oxygen saturation was noted at either site. Systolic and diastolic blood pressure and respiratory rate increased with ice water immersion, whereas pulse rate decreased. Diastolic blood pressure and respiratory rate changes were statistically significant (P = 0.002 and P = 0.005, respectively); however, the systolic blood pressure and heart rate did not reach statistical significance (P = 0.08 and P = 0.5, respectively), as shown in Table 2.
A pulse oximeter is a noninvasive, accurate, continuous indicator of arterial oxygen saturation. The basic technology behind the pulse oximeter is photoelectric plethysmography, as reported by Hertzman in 1938 (1). The device works by using light at two wavelengths (660–940 nm). The light is transmitted through tissues and sensed by a photodetector; the emitted signal is then amplified and processed. During routine clinical monitoring, only the pulsatile component, or alternating current, portion is displayed. The static component, or direct current (created mostly by the absorption of light by surrounding tissue), is eliminated by an autocentering routine that is used to ensure that the wave form remains on the display screen. Clinicians typically apply the pulse oximeter to a finger because it is readily accessible and the finger probe is readily applied. Even though the tracing is affected by vasoconstriction, the accuracy of oxygen saturation measurement is generally maintained, as was the case in this study. Hence, especially in light of simplicity and availability, the finger is used. However, the sensitivity of the finger plethysmographic tracing to local vasoconstriction may significantly compromise its usefulness for monitoring systemic flow in many settings, and even as a measure of oxygen saturation in more extreme states (7).
Although there is a good correlation between the amplitude of the finger photoplethysmographic signal and the blood flow in the finger (8), it should be noted that the changes at the finger are not necessarily representative of changes at other sites. The amplitude of the photoplethysmographic signal, just like the blood volume pulsations (ΔV), depends not only on the systemic intravascular pulse pressure (ΔP), but also on the distensibility of the vascular wall (D), and hence on the autonomic nervous system (9). The relationship is given by Burton (10) as ΔV = ΔP × D.
In the finger, where the walls of the cutaneous vessels are innervated by α-adrenoceptors (11), during cold immersion there is an increase in the sympathetic tone. This causes the amplitude of the finger plethysmographic wave form to be decreased (12–15). Although the sensitivity of plethysmography at the finger may give misleading information about stroke volume and systemic flow, it can provide valuable information about change in sympathetic tone. It thus may be used to detect a vasoconstrictive state and to guide vasodilator therapy. During surgery, the plethysmograph may be viewed as a semiquantitative assessment of the degree of analgesia (16).
It might be used to determine the dose of anesthetic required to block adrenergic response in 50% of individuals who have a surgical skin incision (17). Photoplethysmographic signals reflect a combination of volume and flow change in skin microcirculation (18). In normal subjects, the plethysmographic and blood pressure fluctuations are similar and highly correlated, with a generalized synchronization of the low-frequency oscillations in different areas of the body, such as finger and ear (19).
The degree of sympathetic responsiveness a patient retains during anesthesia may have important clinical implications. This may be particularly true in patients with compromised coronary circulation (limited cardiac reserve), in whom dramatic shifts in the hemodynamic status should be avoided. These findings suggest that the ear is relatively immune to the vasoconstrictive effects of the sympathetic system, and the vasoconstrictor responses were much less pronounced; therefore, the amplitude of the ear plethysmography will respond mainly to changes in pulse pressure. Earlobe plethysmography thus may be a more suitable monitor of the systemic circulation and, perhaps, even of stroke volume (9). The aforementioned findings suggest that the comparison of the ear and finger pulse oximeter wave form might be used as a real-time monitor of sympathetic tone.
We are grateful to Stacey Shelley, BSN, BA, for her valuable editorial advice, and we thank Novametrix Medical System, Inc., for providing the pulse oximeter device.
1. Hertzman AB. The blood supply of various skin areas as estimated by the photoelectric plethysmograph. Am J Physiol 1938; 124: 328–40.
2. Nijboer JA, Dorlas JC. Comparison of plethysmograms taken from finger and pinna during anaesthesia. Br J Anaesth 1985; 57: 531–4.
3. Brigges JF, Oerting H. Vasomotor response of normal and hypertensive individuals to thermal stimulus (cold). Minn Med 1933; 16: 481–6.
4. Hines EA Jr, Brown GE. The cold pressor test for measuring reactibility of blood pressure. Am Heart J 1936; 11: 1–9.
5. Schwab EH, Curb DL. A note on the diagnosis of hypertensive cardiovascular disease without hypertension. J Lab Clin Med 1938; 24: 125–7.
6. Hines EA Jr. The significance of vascular hyperreaction as mea-sured by the cold pressor test. Am Heart J 1940; 19: 408–16.
7. Alexander CM, Teller LE, Gross JB. Principle of pulse oximetry: theoretical and practical considerations. Anesth Analg 1989; 68: 367–76.
8. Hertzman AB. Vasomotor regulation of cutaneous circulation. Physiol Rev 1959; 39: 280–306.
9. Burton AC. Relation of structure to function of the tissues of the wall of blood vessels. Physiol Rev 1954; 34: 619–42.
10. Burton AC. Physiology and biophysics of the circulation: an introductory text. 2nd ed. Chicago: Year Book Medical Publishers, 1972: 160–2.
11. Lefkowitz RJ, Hoffman BB, Taylor P. Neurotransmission. In: Hardman JG, Limbird LE, Molinoff PB, et al., eds. Goodman & Gillman’s The pharmacological basis of therapeutics. 9th ed. New York: McGraw-Hill, 1996: 106–10.
12. Foster AD, Neuman C, Rovenstein EA. Peripheral circulation during anesthesia, shock and hemorrhage: the digital plethysmograph as a clinical guide. Anesthesiology 1945; 6: 246–57.
13. Hertzman AB, Roth LW. The vasomotor components in the vascular reactions in the finger to cold. Am J Physiol 1942; 136: 669–79.
14. Hertzman AB, Roth LW. The reaction of the digital artery and minute pad arteries to local cold. Am J Physiol 1942; 136: 680–91.
15. Hertzman AB, Roth LW. The absence of vasoconstrictor reflexes in the forehead circulation: effects of cold. Am J Physiol 1942; 136: 692–7.
16. Ezri T, Steinmetz A, Geva D, Szmuk P. Skin vasomotor reflex as a measure of depth of anesthesia. Anesthesiology 1998; 89: 1281–2.
17. Roizen MF, Horrigan RW, Frazer BM. Anesthetic doses blocking adrenergic (stress) and cardiovascular responses to incision: MAC BAR. Anesthesiology 1981; 54: 390–8.
18. Challoner AVJ. Photoelectric plethysmography for estimating cutaneous blood flow. In: Rolfe P, ed. Noninvasive physiologic measurements. London: Academic Press, 1979: 125–51.
19. Bernardi L, Radaelli A, Solda PL, et al. Autonomic control of skin microvessels: assessment by power spectrum of photoplethysmographic waves. Clin Sci 1996; 90: 345–55.