Obtrusiveness and Quantification
As noted in the introduction, topics of special interest to psychophysiologists regarding the measurement of dependent variables are obtrusiveness and quantification. More specifically related to this paper are the questions, "Is carotid dP/dt relatively unobtrusive?" and "Is carotid dP/dt clearly, and preferably easily, quantifiable?"
In terms of obtrusiveness the present form of the dP/dt measure requires a piece of sensitive apparatus, i.e., a microphone over the carotid artery, which in turn contributes to a relatively heavy loss of data (see quantification discussion). The obtrusiveness of this microphone should not be underestimated since the subject is required to wear a neck collar to anchor the microphone over the carotid artery and is instructed "not to move, talk or swallow during critical measurement periods'' (Obrist, Gaebelein, & Langer, 1975, p. 279). These measurement periods have also been of substantial duration considering the various tasks imposed on the subject; for example, in one study Obrist et al. (1978) used a 90-sec cold pressor test and an 8-min pornographic movie.
From a quantification point of view, one desirable characteristic is minimal loss of data. Obrist et al. (1975) report approximately a 10-20% loss of data primarily due to movement artifact. This is a relatively high figure for modern psychophysiology, but the loss of data in the cited experiments actually seems to suggest that this approximation may even be conservative. In particular, it appears that the microphonic method of picking up the
carotid pulse wave is responsible for producing these serious artifact problems, problems which appear to be the main reason for Obrist and his colleagues' move to include the ascending slope following the dicrotic notch in their modified (Obrist et al., 1978) and questionable dP/dt measure. This move, as we have noted above, introduces more problems, and illustrates how problems of quantification and obtrusiveness can jointly exacerbate the difficulties.
The final and most essential characteristic of any measure is that the criteria used to define it be sufficiently objective as to be communicable. Obrist et al. 's recent specifications of their own criteria are inadequate in this respect. In particular, they justify their recent modification of the dP/dt measurement by using such vague and qualitative expressions like "reasonably constant" and "not usually accompanied by" (Obrist et al., 1978, p. 104). In addition, the reported scale of the dP/dt has also differed across experiments. Traditionally, dP/dt has usually been reported in terms of mmHg/sec, with the normal left ventricle averaging 1000 mmHg/sec (Mason, 1969); however, Obrist and his colleagues (e.g., Obrist et al., 1978) have quantified dP/dt in various ways including the percentage change from baseline, with baseline values unspecified across studies, and arbitrary ratio units. Moreover, since they perform their transformation to the dP/dt measure as the data are collected and do not have an untransformed pulse wave recording, it is therefore impossible for anyone to quantitatively assess the relationship between conventional dP/dt measures, the previous invasive dP/dt measure (Obrist et al., 1972), the noninvasive dP/dt measure (Obrist et al., 1974), and the recently modified dP/dt ratio measure (Obrist et al., 1978). The fact that carotid dP/dt cannot be calibrated is a serious quantification problem and one which has been recognized by Obrist and his associates (Obrist et al., 1978, p. 114; Obrist et al., 1979, p. 300).
Summary and Conclusions
In the context of the several attempts to devise maximally useful psychophysiological measures of beta-adrenergic myocardial effects (see Newlin & Levenson, 1979), this paper has examined and questioned the validity of the carotid dP/dt index, however specified. In Fig. 1 the various major points of inference were conceptualized and each step was examined in our consideration of the validity issue. The initial step involves inferring changes in sympathetic activity from changes in contractility. The validity of this inference is open to criticism inasmuch as the literature cited above indicates that parasympathetic activity can significantly alter contractility. The effect of parasympathetic activation
is usually to decrease contractile strength although it can also increase contractility (Higgins et al., 1973). It was shown that the magnitude of parasympathetic effects is usually markedly less than the effects of sympathetic activity, though the magnitude of the effect varies as a function of the background sympathetic tone. Therefore, contractility does not uniquely reflect sympathetic activity.
The next step in this inferential process involves the estimation of changes in contractility by intraventricular dP/dt. At this step it was noted that dP/dt is markedly influenced by preload and after-load as well as HR. Since these factors can alter intraventricular dP/dt independently of contractility changes if appropriate control procedures are not employed, the use of dP/dt alone is invalid. In particular, the inferential link between intraventricular dP/dt alone and contractility is questionable without appropriate corrective measures since it is unclear what source (either contractility, loading factors or HR changes) most contributes to changes in intraventricular dP/dt. In fact, it would appear that many of the results reported by Obrist and his colleagues can be alternatively interpreted as results of changes in loading factors rather than beta-adrenergic changes.
The final inferential step in the figure involves the estimation of intraventricular dP/dt from aortic, and finally from carotid, dP/dt. Since Obrist et al. have never utilized an intraventricular dP/dt measure as the critical comparison for aortic and carotid dP/dt, it cannot be assessed to what extent changes in aortic and carotid dP/dt provide an accurate estimate even of an uncorrected intraventricular dP/dt. It is certain, however, that there will be distortions in dP/dt with each further step from the intraventricular dP/dt, so that the correspondence between carotid dP/dt and an uncorrected intraventricular dP/dt will be less than perfect. Thus, from the validation considerations diagrammed in Fig. 1, it is clear that carotid dP/dt as currently defined has not received adequate validation to make it a useful psychophysiological index. In this regard, moreover, we indicated that Obrist et al. 's (1978) recent ratio redefinition of their measure increased rather than decreased the problems inherent in it (cf. also Furedy & Heslegrave, 1979).
This paper also examined the methodology of beta-adrenergic blockade as a more "empirical" technique for assessing beta-adrenergic influences. However, serious problems are associated with this approach. By removing sympathetic innervation to the myocardium, the normal interactive nature of the two branches of the ANS is disturbed. Since normal parasympathetic effects on the ventricle vary with background sympathetic tone, the removal of sympathetic innervation creates an unnatural situation. Compensatory parasympathetic adjustment must take place and the effects of the parasympathetic system on contractility are likely enhanced rather than depressed, as might be expected. Hence it is questionable whether any results using such a blockade methodology can be generalized to normal in vivo function. In addition, a critical examination of the actual results of those studies using the blockade methodology indicated that the results were not unequivocally supportive of the interpretation that carotid dP/dt reflects beta-adrenergic activity. The results, rather, seem to indicate an interpretation of changes in dP/dt reflecting alterations in non-neurogenic influences over dP/dt.
Our final section dealt with two issues of importance to psychophysiologists, namely obtrusiveness and quantification. The finding in that section was that carotid dP/dt was quite obtrusive for the subject, which has resulted in a considerable loss of data. In addition, carotid dP/dt cannot be calibrated, so its comparison across subjects and experiments is impossible, and the communicability to other investigators is restricted.
In summary, the objective of this paper was to critically examine the hypothesis put forward by Obrist and his associates that carotid dP/dt can be considered an index of sympathetic (myocardial) activity. The overall conclusion from our analysis of the data related to this hypothesis must perforce be negative. That conclusion, in brief, is that carotid dP/dt, offered by these workers as a psycho-physiological measure capable of unravelling neurogenic influences on the heart, cannot seriously be considered to reflect sympathetic, beta-adrenergic, or even ventricular functions.
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(Manuscript received July 31, 1979; accepted for publication March 5, 1980)
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