Psychophysiology, a discipline that traces its roots back to ancient Greek society, is one of several scientific disciplines that examine relations between mind and body. Psychophysiology has traditionally been defined as any research in which the dependent variable is a physiological measure and the independent (or predictor) variable is a behavioral one. Studies examining how different stimuli (e.g., nude photos and accident victims) affect physiological parameters (e.g., heart rate and palmar sweating) accurately reflect the discipline of psychophysiology. Psychophysiology differs from related disciplines such as physiological psychology mainly in that psychophysiological research tends to be conducted on humans and is noninvasive, whereas physiological psychology tends to be conducted on animals and is more likely to use invasive procedures.
Recent decades have witnessed a dramatic increase in psychophysiological research. New technology, user-friendly equipment, and increasing expertise of researchers have aided this trend. More importantly, however, psychophysiological measures have allowed researchers to assess theoretical constructs that hitherto had remained hypothetical. In doing so, psychophysiological methods have facilitated theoretical advances. Classic areas of psychophysiology include study of orienting, attentional activity, and defensive reflexes; cognitive processing; anxiety, stress, and, emotion; and personality.
Although all are interested in central nervous system processing, most psychophysiologists are either “neck up” or “neck down,” a distinction that reflects the measures they use and more specifically the placement of their sensors. Neck-up psychophysiologists tend to study brain electrical activity and potentials, whereas neck-down psychophysiologists tend to study the endpoints of autonomic nervous system activity (e.g., heart rate and blood pressure) or musculoskeletal activity.
Perhaps no area exemplifies psychophysiology better than the study of stress, a phenomenon uniquely suited to psychophysiological investigation because of its familiar association with bodily responses. Rare is the individual who has never felt his or her heart leap with excitement or his or her blood boil with anger. For good and bad, stress is part of being alive. Moreover, stress has been related to a host of diseases including hypertension, cardiovascular disease, and stroke. As such, stress-related psychophysiology has a long and distinguished history, as well as a bright future.
Stress-related psychophysiology has focused on the activity of the autonomic nervous system (ANS) in general and the cardiovascular system in particular. Indeed this area is often called the study of cardiovascular reactivity to stress (CVR). Researchers in this area typically assess ongoing cardiovascular activity during a rest or baseline period and then during a stress period in which where participants are required to perform mental arithmetic, solve complicated problems, present a short speech, or similar task. Cardiovascular reactivity refers to the change in physiological activity from resting levels to task levels. The general hypothesis guiding this research is that exaggerated, repeated, or prolonged cardiovascular reactivity to stress indicates enhanced risk for cardiovascular diseases and/or hypertension. The autonomic reaction responsible for cardiovascular changes is also responsible for other physiological sequella, including changes in neuroendocrine and immune system activity. The health-damaging effects of stress have been attributed to the activity of the sympathetic nervous system (SNS), the system historically associated with the fight-or-flight response.
The simplest and most widely used measures of CVR are heart rate and blood pressure (i.e., systolic and diastolic). Researchers can assess these measures with minimal equipment and training. Unfortunately, measures such as heart rate and blood pressure lack sufficient specificity in terms of their autonomic origin because they have multiple ANS determinants. Take heart rate, for example, which is dually controlled by the SNS and parasympathetic (PNS) branches of the ANS. Because of tonic PNS suppression of heart rate under normal circumstances, increases in heart rate from baseline to stress may be caused by (1) release of normal parasympathetic restraint, (2) increased sympathetic activation, or (3) some combination of the two. As such, increased heart rate does not necessarily indicate SNS activity. Moreover, what may appear to be no change in heart rate may reflect countervailing parasympathetic and sympathetic influences, which effectively cancel each other out. A similar conundrum exists for blood pressure changes, which may reflect (1) increased cardiac output, (2) increased peripheral resistance, (3) a synergistic combination of the two, or (4) a countervailing combination of the two.
The inability of these measures to provide unambiguous information about SNS activity has prompted the search for measures that can provide such information. One notable development in this regard is a technique called impedance cardiography.
Impedance cardiography (ZCG) is a noninvasive technique that allows researchers to assess cardiac stroke volume on an ongoing, beat-by-beat, basis. In addition, the waveform resultant from ZCG can be used in combination with other waveforms, such as the electrocardiogram (ECG), to derive a wealth of information about ongoing cardiac performance and to better specify the ANS origins of such activity.
Briefly, impedance cardiography works by sending a high-frequency (alternating current or radio) current across the thoracic cavity and assessing the electrical impedance of the thorax. Small variations in this activity, magnified mathematically and electronically, indicate discrete cardiac events including the onset of left ventricular ejection, the peak ejection velocity, and the closing of the aortic valve, the latter signaling the end of systole. Using specialized equations, one can score the ZCG waveform to estimate cardiac stroke volume (SV). Stroke volume estimates, in turn, can be combined with heart rate estimates to derive cardiac output (CO = HR x SV).
In addition to stroke volume and cardiac output, the ZCG and ECG waveforms can be used to assess several systolic time intervals (STIs), expressed in milliseconds. STIs describe various aspects of the heart’s performance during the contraction process. Systole consists of two phases, the preejection period (PEP) and the left ventricular ejection time (LVET). PEP reflects the time from depolarization of the ventricular nerve fibers and muscle tissue to the onset of ventricular ejection and reflects how long it takes the contracting heart to generate sufficient force to eject blood into the atrial system. A heart that is beating hard (i.e., with great contractile force) will have a relatively short PEP, whereas a heart that is beating less hard will have a relatively long PEP. As such, PEP directly reflects changes in cardiac contractile force. Because anatomic studies have shown that cardiac contractile force is almost exclusively under control of the SNS, with little or no countervailing PNS influence, PEP provides a relatively unambiguous measure of sympathetic influence on the heart. PEP’s counterpart, LVET, reflects the time in milliseconds from onset of ventricular ejection to closing of the aortic valve. Although important in the calculation of SV, LVET alone does not convey unique information on ANS function.
Impedance cardiography also allows derivation of other useful measures, most notably, total peripheral resistance (TPR), which reflects the overall state of arterial vasoconstriction and/or vasodilation. TPR is estimated by taking mean arterial pressure (MAP) and factoring out changes in cardiac output (TPR = MAP/CO * 80). Theoretically, after factoring out the effect of cardiac output on blood pressure change, what remains must reflect changes in total peripheral resistance.
Total peripheral resistance is important to psychophysiologists because they can use it along with CO to explore the underlying hemodynamics of blood pressure. For example, increases in systolic blood pressure and diastolic blood pressure might reflect a change in cardiac output, a change in peripheral vascular resistance, or both. Perhaps more importantly, what appears as no change in blood pressure might reflect increasing CO combined with decreasing TPR, influences that can cancel each other out in terms of overall blood pressure.
Measures derived from impedance cardiography can shed considerable light on this issue. Moreover, disorders such as cardiac arrest and hypertension may differentially relate to cardiac versus vascular reactions.
Total peripheral resistance is also important as an indicator of sympathetic nervous system activity. This is because processes of vasoconstriction and vasodilation—the origins of TPR—are controlled exclusively by the SNS, with no countervailing PNS influence. Therefore, an increase in TPR can indicate increased SNS activity in terms of vasoconstriction. Unfortunately, the global assessment of TPR, as is done in most psychophysiological research, can reflect countervailing vasoconstrictive and vasodilatory influences, the former caused by SNS neural stimulation, the latter by circulating epinephrine primarily at the heart, lungs, and large muscles. Thus, no change in TPR may reflect no measurable autonomic activity, or may reflect countervailing vasoconstriction and vasodilatory effects.
How does stress affect these parameters? There is no straightforward answer to this question, primarily because the construct of stress is not singular. Despite prevailing belief to the contrary, psychophysiologists have known for some time that there is no single form of stress, but that stress takes several forms. These forms are distinguished by different combinations of parasympathetic and sympathetic activity and patterns of activity within the SNS (e.g., vasoconstriction vs. vasodilation, increased cardiac output vs. increased peripheral resistance, presence or absence of epinephrine and Cortisol). Complicating matters, researchers do not agree regarding the form or utility of specific types of stress, nor do they agree regarding the psychological significance of each. Nonetheless, several good candidates exist in this regard. For example, although they use different nomenclature, researchers have identified an energy mobilization response that consists of large increases in cardiac performance, increased vasodilation and receptivity of the arteries to blood flow, and the release of epinephrine. Moreover, this cardiovascular pattern has been associated with both appetitive (e.g., challenge) and aversive affective reactions (e.g., fear, anger). A second good candidate reflects a more restrained form of stress, and consists of strong increases in peripheral vascular resistance and low or reduced cardiac output. This form has been associated more uniformly with negative affective states such as threat and vigilance.
Although more work is needed to delineate the various types of stress reaction, the important lesson here is that no single physiological measure can suffice as an indicator of “stress.” Instead, researchers taking a psychophysiological approach should employ as many measures of autonomic function as they can, and use these measures to look for patterns of physiological response. In addition, researchers should also take care to supplement their physiological measures with measures of behavioral activity or performance and affective reaction to further delineate the type or types of stress being evidenced by participants in their studies.
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