T-wave amplitude utility revisited: some physiological and psychophysiological considerations

This study addresses the hypothesis that electrocardiographic T-wave amplitude is influenced by beta-adrenergic stimulation of the heart. Beta-adrenergic activity was manipulated both pharmacologically and through behavioral challenge. Under resting conditions, 12 healthy men underwent infusion of placebo and then the beta-agonist, isoproterenol, and the beta-blocker, propranolol, in a counterbalanced, crossover design. During infusion of placebo, subjects also underwent two behavioral challenges, a structured interview and mental arithmetic. Analysis of the resting data indicated that propranolol produced a significant increase in T-wave amplitude, and isoproterenol produced significant T-wave amplitude attenuation. As previously reported, drug effects were also in evidence for heart rate. Behaviorally-induced reduction of T-wave amplitude was observed for mental arithmetic but not structured interview, which again paralleled heart rate data. Both pharmacological and behavioral data reported in this study support the hypothesis that the T-wave is significantly affected by beta-sympathetic influence on the heart. However, a nonspecific effect of heart rate change on T-wave amplitude would also account for these results. The findings are discussed in terms of their implications for the utility of T-wave amplitude in psychophysiological research.

Pre-ejection period (PEP) and T-wave amplitude (TWA) have been used to assess sympathetic nervous system (SNS) activity. Here we report two single-blinded, placebo-controlled intravenous (IV) drug application studies in which we pharmacologically modified SNS activity with epinephrine (study 1) as well as dexmedetomidine (alpha2-agonist) and yohimbine (alpha2-antagonist) (study 2). Restricted heart rate (HR) intervals were analyzed to avoid confounding effects of HR changes. Study 1 served to replicate previous findings and to validate our approach, whereas study 2 aimed to investigate how modulation of central SNS activity affects PEP and TWA. Forty healthy volunteers (58% females) participated in study 1 (between-subject design). Twelve healthy men participated in study 2 (within-subject design). TWA and PEP were derived from ECG and impedance cardiography, respectively. Epinephrine shortened PEP and induced statistically significant biphasic TWA changes. However, although the two alpha2-drugs significantly affected PEP as expected, no effects on TWA could be detected. PEP is better suited to reflect SNS activity changes than TWA.

The paper begins with an argument for going “beyond” heart rate for greater specificity in the measurement of mental effort. The added measure must reflect sympathetic nervous system (SNS) influences more clearly than does heart rate, which is predominantly influenced by parasympathetic factors. In considering what the human factors practitioner is seeking in the SNS measure, I discuss three requirements, the issue of convenience, and two marginally relevant considerations. The characteristics of T-wave amplitude (TWA) are then examined in this light. Recent evidence for the utility of TWA used jointly with heart rate as a psychophysiological index is then reviewed in terms of reactive sensitivity, specific sensitivity, complementary utility, and physiological utility. There follows a section that considers difficulties and confounding possibilities concerning TWA. The paper concludes that, although controversial, TWA appears to provide a promising psychophysiological path for using cardiac performance measures to aid in the measurement and understanding of the psychological process of mental effort.

24 An integrative model of the brain functions and its application for hypothesis building in psychophysiology research

The purpose of the present study was to determine whether cardiovascular reactivity to mental stress may be comparable in sitting and standing postures. Fifteen healthy males performed two 1-min mental arithmetic tasks, either while sitting or while standing, in counterbalanced order. Heart rate, pulse transit time, and T-wave amplitude were recorded in the last 10 s of the minute before, during, and after the mental arithmetic. Reactivity scores for each of the dependent measures were computed by calculating the percentage change from baseline values. Data were analyzed with multivariate and univariate repeated measures analysis of variance. Heart rate reactivity to the combination of orthostatic and mental stress was greater than to either stressor alone. Cardiac-sympathetic reactivity was greater in response to orthostatic than to mental stress as revealed by greater changes in T-wave amplitude and pulse transit time in response to the former. No additional decreases in T-wave amplitude, in response to mental stress, were observed during standing, but pulse transit time decreased in the same situation. However, no changes in pulse transit time in response to mental stress were observed in the sitting position. These results demonstrate that cardiovascular reactivity to mental stress depends on the body position in which the stressor is encountered.

ABSTRACTThis study examines the interrelationship of five noninvasive measures of cardiac performance: T‐wave amplitude (TWA), the P‐Q interval of the EKG (PQI), Pulse Transit Time (PTT), Carotid dP/dt, and heart rate or interbeat interval (IBI). These measures were manually derived from high‐speed recordings of EKG and carotid displacement pulse made as subjects performed a demanding mental arithmetic task. Within‐subject correlations between the measures were determined from 18 cardiac cycles sampled from baseline and task periods. Five of the median correlations were significant in the overall sample (N=19), most notably that between IBI and PQI. When subjects were partitioned into high and low PTT reactors, a larger number of significant correlations were observed in the more reactive group. PTT reactivity significantly enhanced the magnitude of three correlations: PTT vs IBI, PTT vs PQI, and PQI vs TWA.Comparing the two electrocardiographic indices, PQI displayed larger correlations with both IBI and PTT than did TWA. The pattern of correlations suggests that PQI measurement provides little information beyond that provided by HR alone and that TWA, although strongly related to PTT in a few subjects, is not consistently related to any measure except PQI. The results are discussed in light of reports suggesting that these indices might be used to assess beta‐adrenergic influences on the myocardium.

Ambulatory recording of the preejection period (PEP) can be used to measure changes in cardiac sympathetic nervous system (SNS) activity under naturalistic conditions. Here, we test the ECG T-wave amplitude (TWA) as an alternative measure, using 24-h ambulatory monitoring of PEP and TWA in a sample of 564 healthy adults. The TWA showed a decrease in response to mental stress and a monotonic decrease from nighttime sleep to daytime sitting and more physically active behaviors. Within-participant changes in TWA were correlated with changes in the PEP across the standardized stressors (r = .42) and the unstandardized naturalistic conditions (mean r = .35). Partialling out changes in heart rate and vagal effects attenuated these correlations, but they remained significant. Ambulatory TWA cannot replace PEP, but simultaneous recording of TWA and PEP provides a more comprehensive picture of changes in cardiac SNS activity in real-life settings.

Effects of psychological and physiological challenges on heart rate, T-wave amplitude, and pulse-transit time

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The T-wave amplitude of ECG is thought to reflect the sympathetic tone of the heart but anaesthesia studies on this topic are rare. Haemodynamic and ECG T-wave amplitude changes were studied during induction of anaesthesia in 24 ASA I-II patients. Twelve patients were given alfentanil 30 micrograms kg-1 at induction while physiologic saline was given to the rest (control). Thiopentone was then administered at the rate of 5 mg s-1 until eyelash reflex disappeared. Vecuronium 0.1 mg kg-1 was given thereafter. No anticholinergics were used. The lungs were ventilated with 40% oxygen in air. Haemodynamic parameters and T-wave amplitude were measured before induction, before intubation, 30 s, 3 min and 5 min after intubation. A significantly higher amount of thiopentone was needed to abolish the eyelash reflex in the control group than in the alfentanil group (P < 0.001). There were no changes in heart rate (HR) in the alfentanil group during the trial. Systolic and diastolic arterial pressures (SAP and DAP) were continuously below the preinduction levels in the alfentanil group. After baseline HR, SAP and DAP were significantly higher in the control group than in the alfentanil group at each data point. T-wave amplitude flattened significantly (P < 0.001) after intubation in the control group while no significant changes were seen in the alfentanil group. T-wave flattening correlated to the increases in HR (P < 0.01) and SAP (P < 0.01). Three control patients with flattened T-wave had a transient bigeminia period after intubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic pulse wave velocity, calculated from pulse transit time (PTT), is often used as an indicator of arterial stiffness and suggested to be standardized for heart rate (HR). This study aimed to determine whether PTT obtained directly from radial arterial waveforms could be used to assess arterial stiffness and the effect of HR on it. Measurements of anthropometric parameters, blood pressure (BP) and radial PTT were taken in 266 apparently healthy adults (113 men and 153 women; age 18-78 years). BP and radial PTT were measured in a subgroup of 11 young subjects (seven men and four women, age 24-35 years) in a 3-month follow-up study, which aimed to investigate the effect of HR changes. Radial PTT was significantly higher in men compared with women (0.116 ± 0.022 s compared with 0.103 ± 0.031 s, P < 0.001). It was inversely related to age in men and women (r=-0.838 and r=-0.804, respectively, P < 0.01 for both). Multiple regression analysis showed that HR was a potent predictor of radial PTT in addition to age, sex and systolic BP. There was no significant change in radial PTT when HR ranged from 60 to 75 b.p.m. A significant decrease was found in radial PTT when HR was up to 80 b.p.m. (P < 0.01). These findings indicate that the simple and easily obtainable radial PTT could be a useful index of arterial stiffness, and HR changes should be considered when it is up to 80 b.p.m.

A recent study demonstrated that changes in both heart rate (HR; positive if ≥10 bpm increase) and T-wave amplitude (positive if ≥25% increase) reliably detect accidental intravascular injection when a full test dose containing epinephrine 0.5 μg/kg is injected intravascularly. We designed this study to prospectively determine whether a smaller dose of epinephrine would produce reliable HR and T-wave changes in sevoflurane-anesthetized children. We studied 80 ASA physical status I infants and children (6–72 mo) undergoing elective surgeries during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen. After the administration of IV atropine 0.01 mg/kg, the patients were randomly assigned to receive either IV saline (n = 20), an IV test dose (0.1 mL/kg) consisting of 1% lidocaine with 1:200,000 epinephrine (epinephrine 0.5 μg/kg group, n = 20), an IV test dose (0.05 mL/kg) (epinephrine 0.25 μg/kg group, n = 20), or an IV test dose (0.025 mL/kg) (epinephrine 0.125 μg/kg group, n = 20) via a peripheral vein to simulate the intravascular injection of the test dose. HR and systolic blood pressure were recorded every 20 and 30 s, respectively, and T-wave amplitude of lead II was continuously recorded for subsequent analysis. After the IV injection of the test dose, all children in the epinephrine 0.5 and 0.25 μg/kg groups developed positive responses based on the peak T-wave amplitude, whereas all children in the epinephrine 0.5 μg/kg group and 17 children (85%) in the epinephrine 0.25 μg/kg group elicited a positive response according to the peak HR criterion. No false-positive responses were observed with saline injections. Children in the epinephrine 0.125 μg/kg group showed clinically unacceptable efficacy based on either criterion. We conclude that the efficacies of detecting an intravascular injection of the test dose based on the hemodynamic and T-wave criteria are reduced with smaller doses of epinephrine and that HR and T-wave changes are still useful indicators in most patients if epinephrine 0.25 μg/kg is accidentally injected intravascularly. Implications To determine whether an epidurally administered local anesthetic has been unintentionally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that an increase in T-wave amplitude ≥25% in lead II and a heart rate increase ≥10 bpm are useful indicators for detecting the accidental intravascular injection of a small dose of epinephrine in sevoflurane-anesthetized children.

Intravascular application of a small dose of local anesthetics (LA) with epinephrine as well as larger doses of LA under sevoflurane anesthesia results in increase in T-wave amplitude in the electrocardiogram (ECG). The aim of this study was to elucidate whether propofol anesthesia affects these ECG alterations or not. Thirty neonatal pigs were randomized into two groups. Group 1 was anesthetized with sevoflurane, group 2 with sevoflurane plus continuous propofol infusion (10 mg·kg(-1)·h(-1)). A test dose of 0.2 ml·kg(-1) bupivacaine 0.125% + epinephrine 1 : 200,000 was injected intravenously. Arterial pressure was monitored. ECG was analyzed for changes in T-wave amplitude (positive if ≥25% baseline) and heart rate. In another setting, bupivacaine 0.125% was intravenous infused at a rate of 4 mg·kg(-1)·min(-1). ECG was analyzed for alteration in T-wave amplitude and heart rate at 1.25, 2.5, and 5 mg·kg(-1) bupivacaine infused. T-wave elevation after the administration of an epinephrine containing LA test dose was similar between the two groups. Increase in heart rate caused by the test dose were significantly higher in group 2 (P = 0.008). During continuous bupivacaine administration, T-wave elevation occurred in 40% and 71% (group 1 and 2) at 1.25 mg·kg(-1), in 80% and 100% at 2.5 mg·kg(-1), and in 93% and 86% at 5 mg·kg(-1) bupivacaine infused. Continuous propofol infusion does not suppress the ECG signs of a systemically administered epinephrine containing LA test dose nor does it suppress the ECG signs caused by high doses of intravenous applied bupivacaine.

A recent study demonstrated that changes in both heart rate (HR; positive if > or = 10bpm increase) and T-wave amplitude (positive if > or = 25% increase) reliably detect accidental intravascular injection when a full test dose containing epinephrine 0.5 microg/kg is injected intravascularly. We designed this study to prospectively determine whether a smaller dose of epinephrine would produce reliable HR and T-wave changes in sevoflurane-anesthetized children. We studied 80 ASA physical status I infants and children (6-72 mo) undergoing elective surgeries during 1.0 minimum alveolar anesthetic concentration sevoflurane and 67% nitrous oxide in oxygen. After the administration of i.v. atropine 0.01 mg/kg, the patients were randomly assigned to receive either i.v. saline (n = 20), an i.v. test dose (0.1 mL/kg) consisting of 1% lidocaine with 1:200,000 epinephrine (epinephrine 0.5 microg/kg group, n = 20), an i.v. test dose (0.05 mL/kg) (epinephrine 0.25 microg/kg group, n = 20), or an i.v. test dose (0.025 mL/kg) (epinephrine 0.125 microg/kg group, n = 20) via a peripheral vein to simulate the intravascular injection of the test dose. HR and systolic blood pressure were recorded every 20 and 30 s, respectively, and T-wave amplitude of lead II was continuously recorded for subsequent analysis. After the i.v. injection of the test dose, all children in the epinephrine 0.5 and 0.25 microg/kg groups developed positive responses based on the peak T-wave amplitude, whereas all children in the epinephrine 0.5 microg/kg group and 17 children (85%) in the epinephrine 0.25 microg/kg group elicited a positive response according to the peak HR criterion. No false-positive responses were observed with saline injections. Children in the epinephrine 0.125 microg/kg group showed clinically unacceptable efficacy based on either criterion. We conclude that the efficacies of detecting an intravascular injection of the test dose based on the hemodynamic and T-wave criteria are reduced with smaller doses of epinephrine and that HR and T-wave changes are still useful indicators in most patients if epinephrine 0.25 microg/kg is accidentally injected intravascularly. To determine whether an epidurally administered local anesthetic has been unintentionally injected into a blood vessel, a small dose of epinephrine is often added to a local anesthetic. We found that an increase in T-wave amplitude > or = 25% in lead II and a heart rate increase > or = 10 bpm are useful indicators for detecting the accidental intravascular injection of a small dose of epinephrine in sevoflurane-anesthetized children.

Phasic changes in heart rate (HR) and electrocardiographic T-wave amplitude (TWA) were monitored in healthy Type A (coronary-prone) and Type B (non-coronary-prone) men during the performance of a difficult arithmetic task. Type As showed significantly greater reductions in TWA as compared to Type Bs, though no group differences were present in HR change. This pattern of results, wherein a significant Type A-B difference was observed in a phasic measure of ventricular performance (TWA), but not in one of supraventricular performance (HR), suggests that Type As experience excessive neurally mediated sympathetic stimulation of the myocardium during mental work.