Palpitations, Arrhythmias, and Awareness of Cardiac Activity

Somatic distress varies widely among healthy people and medical patients with similar levels of tissue pathology. After measuring and controlling statistically for the extent of demonstrable disease, investigators have shown wide interindividual variability in symptoms in coronary artery disease, asthma, chronic obstructive pulmonary disease, peptic ulcer, benign prostatic hypertrophy, rheumatoid arthritis, osteoarthritis, diabetes, and anemia (1). Obviously, many factors other than tissue damage and dysfunction contribute to somatic symptoms, perceived health, and bodily distress. These factors include personality characteristics (such as the general tendency to report psychological distress), physical or sexual trauma or abuse, stressful events and major life changes, and psychiatric disorders. We need to learn much more about the cognitive, behavioral, psychosocial, and psychiatric factors that can intensify or diminish symptoms. This requires a systematic, empirical exploration of the processes of symptom perception, processing, appraisal, and reporting. The neural pathways of symptom perception and formation are largely unexplored. We know little about the precise nature of the visceral events that result in conscious bodily sensations; the afferent sensory pathways involved; or the higher-order cognitive processing that filters, modulates, and amplifies visceral sensation and brings it to conscious attention. Such a science of symptom reporting requires investigations in which both the stimulus provoking the symptom and the patient's subjective experience of that stimulus are measured independently and simultaneously. The sensory stimulus could be administered experimentally, or, alternatively, a naturally occurring physiologic stimulus (such as respiration, cardiac activity, or peristalsis) could be measured. Precise patient symptom reports could be obtained concurrently. This would enable us to study the variability in symptom reporting among different persons who are subjected to similar somatic or visceral stimuli. One could also study intra-individual variability by assessing the same person's perception of the same stimulus under various circumstances and conditions (for example, during different moods or during and after stress). An exercise treadmill stress test could be used for such a study (2). In an attempt to develop this particular paradigm, my colleagues and I assessed four cardiopulmonary symptoms during a standardized, exercise tolerance test while simultaneously measuring the physiologic variables that induce the symptoms (for example, breathlessness and respiratory rate, racing heart and heart rate, and fatigue and total energy expended). Physiologic measures were obtained when a person first reported discomfort, and symptoms were recorded when the person reached 85% of age-adjusted, maximal exercise capacity. Compared with less anxious patients, patients who were more anxious at the start of the test became symptomatic at significantly lower levels of physiologic arousal and had significantly more intense cardiopulmonary symptoms at similar levels of arousal (2). Two recent advances in research methods seem to offer promise in advancing our understanding of symptom reporting. Functional magnetic resonance imaging may eventually let us identify the specific neural events underlying symptom reports. Numerous experiments suggest themselves: Patients with phantom limb pain or chronic idiopathic pain could be studied, as could patients with different symptoms but similar disease processes and patients with medically unexplained symptoms, such as those that occur in conversion disorder. Functional magnetic resonance imaging, positron emission tomography, and single-photon emission computed tomography may ultimately enable us to distinguish between nociception, which occurs in the somatosensory cortex, and the symptom modulation that occurs in the anterior cingulate cortex, where the nociceptive input is integrated with memory, association, and affect to create the total conscious experience of symptomatic discomfort and suffering. Functional imaging may thus enable us to locate the components of the total symptom experience in the brain and to see how they are combined in various activation patterns. A recent study was able to distinguish between the neurophysiologic correlates of pain unpleasantness and those of pain intensity by using positron emission tomography (3). Participants underwent an experimental pain test with and without a hypnotic suggestion of decreased pain unpleasantness. The hypnotic suggestion resulted in a modulation in pain-related brain activity in the anterior cingulate cortex; this modulation closely paralleled the reduction in perceived unpleasantness of the painful stimulus. However, hypnotic suggestion produced no change in the sensory component (intensity) of pain perception, and the activation of the primary and secondary somatosensory cortices did not change (3). The tendency to report more symptom distress, or to report symptoms that are disproportionate to demonstrable medical disease, may result from either a heightened perceptual sensitivity to somatic and visceral stimuli or a difference in labeling, describing, and reporting these stimuli (that is, a greater tendency to describe the stimuli as unpleasant or noxious). In traditional studies of pain sensitivity, pain threshold and tolerance are measured by administering stimuli of increasing intensity. Such a procedure confounds true sensitivity with reporting style, and it is not possible to disentangle them. Signal detection analysis is a strategy for measuring pain sensitivity that allows sensitivity and reporting style to be distinguished (4). By measuring the patient's ability to distinguish between two stimuli of similar intensity, rather than assessing his or her threshold and tolerance, it is possible to derive separate measures of perceptual acuity or discriminative ability on the one hand and a consistent tendency to report all stimuli as more intense or more unpleasant on the other (4). A study of pain responses among Nepalese porters furnishes a striking example of the potential power of this strategy (5). Nepalese porters used to high altitudes reported less pain and discomfort than did western visitors during a Himalayan trek. Signal detection analysis of an experimental pain task (electrical stimulation) administered to the two groups showed that the Nepalese did not differ from the westerners in their discriminative ability to detect pain but that they did have a higher threshold for acknowledging and reporting the pain: That is, the Nepalese were as able to perceive pain as the westerners but were more reluctant to complain about it (5). The difference between discriminative ability and the general tendency to report discomfort is particularly salient when the problem of somatization and medically unexplained complaints is considered. The symptoms of somatizing patients could result from two distinct mechanisms: 1) The somatizing patients might be especially astute perceivers who can detect and focus on subtle, mild, or ambiguous bodily sensations that nonsomatizers do not perceive or 2) the somatizing patients' perceptual experience may not differ from that of the nonsomatizers, and their symptoms may result from a lower threshold for describing and labeling sensations as painful, noxious, or disturbing. For years, my colleagues and I have been interested in studying these alternative mechanisms in ambulatory medical patients. We have chosen to study the symptom of palpitations for several reasons. First, cardiac activity can be measured precisely and reliably with noninvasive methods, making it possible to determine the cardiac stimulus occurring at the precise moment when the patient reports a symptom. Second, palpitations are a relatively precise symptom that are sharply demarcated in time and are either present or absent, unlike more diffuse and ambiguous symptoms, such as weakness or nausea. Palpitations and Cardiac Activity The subjective symptom of palpitations does not stand in a fixed, one-to-one relationship with demonstrable changes in cardiac rhythm or rate (6). Ambulatory electrocardiographic (Holter) monitoring of both cardiac patients and healthy volunteers has shown that the relationship between palpitations and cardiac irregularities is weak: Many people with palpitations have no arrhythmias, and most arrhythmias do not generate a symptom report (7-11). Some of the variability in this relationship may arise because patients and physicians both use the term palpitations to refer variously to changes in rate, rhythm, or force of contraction and to numerous different sensations, including acceleration, irregularity of rhythm, increased force of contraction, or pause. Several important clinical questions emerge from this variable relationship between subjective palpitations and objective arrhythmias. In treating patients with palpitation, are there characteristic symptom descriptors or clinical histories that are more likely to indicate the presence of an arrhythmia? Do particular symptom descriptors correspond to particular types of arrhythmias? (For example, does the complaint of racing indicate tachycardia, or does the sensation of one's heart stopping follow a pause? ) Do patients themselves have characteristics that suggest whose symptom reports are more likely to reflect underlying arrhythmic activity and whose are more likely to be medically unexplained? More basic questions arise about the sensory pathways that underlie the perception of cardiac activity: What are the peripheral afferent pathways for perceiving cardiac activity, and what are the ascending pathways in the central nervous system that modulate peripheral sensations? To investigate some of these questions, my colleagues and I have conducted several studies of medical outpatients who reported palpitations