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We utilized a data-driven, unsupervised machine learning approach to examine patterns of peripheral physiological responses during a motivated performance context across two large, independent data sets, each with multiple peripheral physiological measures. Results revealed that patterns of cardiovascular response commonly associated with ‘challenge’ and ‘threat’ states emerged as two of the predominant patterns of peripheral physiological responding within both samples, with these two patterns best differentiated by reactivity in cardiac output (CO), pre-ejection period (PEP), interbeat interval (IBI), and total peripheral resistance (TPR). However, we also identified a third, relatively large group of apparent physiological “non-responders” who exhibited minimal reactivity across all physiological measures in the motivated performance context. This group of “non-responders” was best differentiated from the others by minimal increases in electrodermal activity. We discuss implications for identifying and characterizing this third group of individuals in future research on physiological patterns of challenge and threat.

Drowsiness is one of the leading causes of traffic accidents. A technique for fast and easy measurement of the level of drowsiness is desirable. The objective of the present paper is to evaluate the dynamics of forehead skin temperature (FHT) under induced drowsiness. With a precursory change associated with drowsiness from the FHT, which is a noninvasive measurement, drowsiness can be detected at an early stage and, possibly, traffic accidents can be prevented. In this study, the measured FHTs were categorized into five drowsiness levels according to facial expressions (Level 1 is awake and Level 5 is extremely drowsy). In an experiment, the thermoregulation process of drowsiness was represented by a decrease in the total peripheral resistance, elevation of the nasal skin temperature, and decline in the tympanum temperature. The experimental results showed a significant decrease in FHT for drowsiness Levels 3–5 compared to the rest state (Mann–Whitney U-test, p < 0.01). Because FHT did not increase in accordance with the process for nasal skin temperature, FHT could represent both skin and core temperatures. The results suggest that FHT can be an indicator for predicting drowsiness. © 2017 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc.

Mental stress can trigger myocardial infarction, with poor vascular responses to stress implicated as a pathway. Vascular stress reactivity can be assessed by different methods, such as total peripheral resistance (TPR) and forearm blood flow (FBF). Little is known about how these vascular assessments are linked. This was examined in two separate studies. Healthy men (Study 1: N = 29, Study 2: N = 23) completed rest and mental arithmetic (Study 1: 8 min, Study 2: 16 min). In both studies, heart rate, mean arterial pressure, and FBF increased in response to stress. In Study 1, no changes in TPR were seen, but Study 2 found stress-induced increases in TPR. FBF was not linked to TPR at any time (all ps > .05). It appears that limb vasculature and TPR responses to stress do not give the same information about impairments of the vasculature. These findings are relevant to the interpretation of prior research findings and the design of future studies on stress and vascular responses.

This study examined how the outcomes of joint decision making relate to cardiovascular reactions when group members disagree about the decision to be taken. A conflict was experimentally induced during a joint decision-making task, while cardiovascular markers of challenge/threat motivational states were assessed following the biopsychosocial model of challenge and threat (BPSM; J. Blascovich, 2008). Results show that individuals were less likely to adjust their initially preferred decision alternative the more they exhibited a cardiovascular pattern indicative of threat (i.e., relatively high total peripheral resistance and low cardiac output) compared to challenge. This finding extends the BPSM by showing a link between threat and rigidity, and emphasizes the importance of psychophysiological processes for studying intragroup conflict and decision making.

Echocardiography was performed at every six months in hypertensives well controlled on metoprolol, 100 mg twice a day. After six months' treatment blood pressure was reduced from 177/110 mm Hg to 147/88 (p less than 0.02). LV wall thickness (septum + posterior wall) was unchanged 2.10 cm (2.14), and a significant drop in cardiac output (CO) to 5.0 l/min (6.1, p less than 0.02) was recorded (pretreatment values in brackets). After 24 months' treatment LV wall thickness was reduced to 1.94 cm (p less than 0.02), total peripheral resistance (TPR) to 17.3 mm Hg/l/min (23.4, p less than 0.02) and CO increased to 6.7 l/min (6.1, n.s.). After six months' treatment, there was thus a drop in BP with a significant drop in CO and unchanged TPR. After 24 months' treatment, however, CO was back to the pretreatment level and the drop in BP was entirely caused by a drop in TPR which was probably secondary to a reduction in the wall thickness of the arterial resistance vessels as judged by the relationship between the reduction in wall thickness in the LV and the reduction in TPR during the treatment.

Introduction: Vascular pathophysiology is a hallmark of hypertension (HTN)-linked cardiovascular disease, as increased peripheral resistance leads to vascular remodeling. Consistent with this is th...

A quantitative scale for identifying cardiac versus vascular reactor, balance of blood pressure equivalents (BE), was newly advocated and compared with a very recently advocated one, hemodynamic profile (HP), by Gregg, Matyas and James (2002). BE was defined as “(ΔQ/Q0)P0′ − (ΔR/R0)P0.” Here, P0, Q0, and R0 were mean blood pressure (P), cardiac output (Q), and total peripheral resistance (R) during baseline, and ΔQ and ΔR were the difference scores of Q and R from baseline to stress, respectively. This was named as BE because the two terms in the formula indicated changes in Q and R in their blood pressure equivalents. Comparisons of the BE and HP scales were carried out, theoretically, in a newly introduced pressor space, on orthogonality with the extent of elevation of P (ΔP); and then, practically, by using hypothetical data. In summary, it was shown that data points in the neighborhood in the pressor space can be judged as having not so different hemodynamic balance whether the BE or HP scale was used. As a merit, the BE scale seemed helpful to an intuitive understanding of the hemodynamics during stress. As a demerit, it cannot maintain the quasi-orthogonal relationship with ΔP when Q or R changes profoundly in the face of stress.

Background During the physiological course of pregnancy maternal peripheral vascular resistance decreases. Using the Doppler technique, the decreasing resistance and disappearance of the early diastolic notch in the arterial uterine perfusion can be observed. These changes in the Doppler flow velocity wave form are caused by the trophoblast invasion in which the spiral arteries loose their musculoelastic structure of the arterial wall. The aim of this study was to investigate whether maternal systemic alteration in the Doppler flow velocity waveform and Pulsatility Index (PI) could be monitored at the cubital artery during normal pregnancy. Methods and results Forty-five patients were investigated in a prospective study in 4–6-week intervals for Dopplersonographic evaluation of the two uterine arteries and the right cubital artery; 20 of the patients were also investigated after delivery. The presence or absence of the early diastolic reverse flow of the cubital artery was analyzed. Furthermore, the PI was calculated for all vessels. With increasing duration of gestation, the reverse flow of the cubital artery disappeared. During the course of gestation a significant decrease in the PI of the cubital artery was observed in addition to a significantly decreased PI of the uterine arteries. The PI of the placental and nonplacental uterine arteries showed a significant correlation to the PI of the cubital artery. Conclusions This study demonstrates systemical changes in arterial resistance correlating to those of the uterine arteries during the course of physiological pregnancy.

A quantitative, theory-driven model of hemodynamics was developed, relating reactivity in blood pressure to orthogonal dimensions of hemodynamic profile and compensation deficit, which were derived from the (multiplicative) interaction of cardiac output and total peripheral resistance. A Finapres 2300e was used to estimate blood pressure, cardiac output, and total peripheral resistance in 100 healthy men and women during mental arithmetic and cold pressor tasks on two occasions. Results were consistent with model predictions. As predicted, cardiac output and peripheral resistance reactions were curvilinearly related, and blood pressure reactivity was strongly related to compensation deficit (r = .76-.89). Conversely, the orthogonally defined hemodynamic profile remained independent of blood pressure reactivity (r = .11 or less). The data show that the present model overcomes several difficulties and inconsistencies in previous attempts to obtain an independent measure of hemodynamic profile. The new model could help to elucidate sources of cardiovascular pathogenesis not suggested from the study of blood pressure reactivity alone.

In early essential hypertension, an increase in cardiac output (CO) is seen in about two-thirds of the patients. In established essential hypertension, CO is usually normal or subnormal, while total peripheral resistance (TPR) is increased. Treatment with beta-adrenergic blocking agents accentuates these haemodynamic changes; in particular CO is further decreased. Comparison of the effects of beta-blockers with and without beta 1-selectivity and intrinsic activity reveals slight differences in the haemodynamic responses. Although none of the beta-blockers normalizes the haemodynamics, satisfactory blood-pressure reduction may be achieved at rest and during exercise with minimal side effects.

Stroke volumes measured by impedance were compared with values obtained by dye dilution and an electromagnetic flowmeter (EMF) on 14 dogs during drug-induced changes in cardiac contraction strength and peripheral resistance changes. Grouping all data for a total of 305 points showed correlations between dye and EMF, dye and impedance, and EMF and impedance of 0.89, 0.68, and 0.72, respectively. Correlations for individual dogs between dye and EMF, dye and impedance, and EMF and impedance ranged from 0.60 to 0.99, −0.39 to 0.96, and −0.26 to 0.89, respectively. These data suggest that the use of impedance cardiac output measurements to make treatment decisions about individual patients could result in serious error.

Elevated central pressures and arterial stiffness are associated with increased peripheral resistance and higher sympathetic nervous system activity. Additionally, consumption of a meal is known to be sympathoexcitatory. However, the acute effects of a meal on aortic wave reflection and stiffness are unknown. Therefore, we tested the hypothesis that aortic wave reflection and stiffness would increase after a meal.We examined these effects using high-fidelity radial arterial pressure waveforms and carotid-femoral pulse wave velocity measured noninvasively by applanation tonometry before and 60 and 180 minutes after ingestion of a liquid mixed meal (Ensure; 40% of daily energy expenditure) in 17 healthy adults (9 men/8 women; aged 29 ± 2 years). Additionally, we measured sympathetic activity by microneurography at baseline and up to 60 minutes after the meal.Although sympathetic activity increased after the meal, both peripheral and central pressures were reduced at 180 minutes from baseline (all P0.05). Contrary to our hypothesis, augmentation index (14% ± 3% vs. 2% ± 3% vs. 8% ± 3%), augmentation index normalized for heart rate (8% ± 3% vs. -3% ± 3% vs. 3% ± 3%), augmented pressure (5 ± 1 mm Hg vs. 1 ± 1 mm Hg vs. 3 ± 1 mm Hg), and pulse wave velocity (7.1 ± 0.2 m/s vs. 6.7 ± 0.2 m/s vs. 6.7 ± 0.1 m/s) were substantially reduced at 60 and 180 minutes after the meal (all P0.05).Taken together, our results suggest that a liquid mixed meal acutely decreases central hemodynamics and arterial stiffness in healthy adults, which may be a result of meal-related increases in insulin and/or visceral vasodilation.

Intravenous anaesthetic (iv) agents act as antagonists of L-type calcium (Ca2+) channels to elicit changes in peripheral resistance. We propose that L-type Ca2+ channel dysfunction during hypertens...

This paper reports experiments to determine the relative roles of changes in cardiac output and systemic vascular resistance in determining the blood pressure response to intermittent step-changes and continuous sinusoidal changes in carotid sinus transmural pressure. Conscious rabbits with a variable-pressure capsule implanted around an innervated carotid sinus were used. After step-change in capsule pressure the approximate proportions of the changes in blood pressure attributable to changes in cardiac output were, during the pressor response, 7% after 2.5 s, 22% after 10 s and 27% at plateau, and during the depressor response 100%, 8% and 17%, respectively. During sinusoidal change in capsule pressure a mean 7% of the change in blood pressure over the full cycle was attributable to change in cardiac output.

SUMMARY 1. The haemodynamic effects of short-term prostacyclin infusions (0.05-0 50 /μg/kg per min) were investigated in conscious adult sheep. 2. Haemodynamic dose-response curves to prostacyclin were performed before, during and after production of ACTH-induced hypertension. 3. Prior to ACTH administration prostacyclin produced dose-dependent reductions in mean arterial pressure, total peripheral resistance and stroke volume and these were accompanied by increases in heart rate and cardiac output. 4. After 5 days of ACTH-induced hypertension prostacyclin produced similar effects on mean arterial pressure to those seen prior to ACTH but the effects on heart rate, cardiac output, stroke volume and total peripheral resistance were markedly increased. 5. These studies demonstrate that the responsiveness of the circulation to prostacyclin is altered in ACTH-induced hypertension.

Summary The haemodynamic changes following induction of anaesthesia with equipotent doses of propofol and thiopentone have been compared. Propofol caused a significant fall in arterial blood pressure and total peripheral resistance, with a slight fall in cardiac output. There were no changes in heart rate. Apart from an initial, but statistically insignificant increase in heart rate, similar changes were produced by thiopentone, but to a lesser degree. It is concluded that induction of anaesthesia with propofol results in acceptable haemodynamic changes, but that the agent is more depressant to the cardiovascular system than thiopentone.

Effects of the prolonged administration of isoflurane on haemodynamics were studied in 17 healthy volunteen under normocarbic conditions. The anaesthetic was administered for 90 min at a constant alveolar concentration. Cardiac index was unchanged in the presence of decreased stroke volume index and increased heart rate. The mean arterial pressure decreased with parallel reductions in total peripheral resistance. 1, eft ventricular work decreased. The left ventricular ejection time index increased marginally but significantly. Isoflurane caused no change in the pump performance of the heart but depressed the muscle performance.

Hypertension, a disease that affects about 23 million Americans, is unique in that i t is a disease of degree with no clearly defined division of normal and abnormal and with symptomatology quantitatively related to the elevation of arterial diastolic pressure. High blood pressure usually begins as a functional disorder superimposed upon a normal cardiovascular tree. In response to this, a functional vasoconstriction occurs which results in an increased peripheral resistance and cardiac output. The heart as a pump is burdened as well as the blood vessels of the kidney and brains. The etiology of initial functional disorder resulting in hypertension may be hereditary, related to renal

Several extracardiac age changes may affect cardiovascular efficiency. Extracellular fluid and blood volume are relatively increased with age. The loss of aortic elasticity results in a rise in systolic pressure when work produces increases in cardiac output. The vascular rigidity further consumes energy by loss of the propulsive effect of elastic recoil. Finally, peripheral resistance increases due to arteriolar constriction; this appears to be under reversible physiologic control. The sum of these normal changes contributes to the functional decrement of aging; it is more universal and more important than atherosclerosis, yet has commanded inadequate attention.

1. A steroid-like compound has been isolated from cat heart muscle by thin-layer chromatography. 2. This compound has been characterized by measurement of its RF values in two solvent systems. 3. No similar substance could be detected in the 1 hr venous outputs of cat adrenals. 4. It could not be detected in heart-lung circuit blood when the heart had been perfusing for 1¼-1½ hr at constant venous input and peripheral resistance. The compound was however extractable from the circuit blood 10-15 min after reduction in venous input. 5. The actions of this compound on the isolated kidney resemble those of aldosterone but are of much shorter latency. 6. The heart substance differs from aldosterone in RF values and has more than 10 times the renal activity of aldosterone when the two substances are equated (visually) for ability to reduce blue tetrazolium.

Summary (1) The evidence, in brief, of the sequence of events leading to the development of the glandular nodule in benign glandular enlargement of the prostate is:- (a) At any one time during the growth of the prostate there are present groups of tubules (though, maybe, unrecognisable) arising from the terminations of its primary and subsidiary tubules; they may be collective as in the prespermatic region, or individual. (b) With further increase of the glandular tissue in general, a circumscribed resistance to the growing groups is, in due course, created by the tissues in which they are situated and it is caused indirectly by a passive force applied to those tissues from the periphery of the prostate as a whole and also from that of the prespermatic region. (c) Growth of the groups against that resisting tissue is accompanied by and causes the formation of circumscribed capsules of fibrous and/or compressed glandular tissue about them; the groups are thus isolated and so form the glandular nodules associated with the benign enlargement of the prostate. (d) Within the limiting capsules growth of the groups may continue: acinous forrdation and intra-acinous epithelial proliferation are followed by acinous dilatation and rupture. (2) The direct cause of benign glandular enlargement of the prostate is continuity of active glandular growth against a passive and due circumscribed resistance derived from the periphery of the prostate as a whole and also from that of the prespermatic region. (3) The glandular nodule in the benign enlarged prostate is evidence of an attempt to limit the size of the gland. (4) Peripheral resistance to the glandular growth becomes duly effective in the upper parts of the prostate first and in the lower parts last, because of the disproportionate increase of growth in the two regions, and glandular nodules are, in point of time and place, likewise formed. (5) The absence of benign enlargement from the upper part of the posterior lobe of the prostate is due to the destruction of its groups of tubules by pressure from the enlarging lobes in front of it; absence from the lower part is caused by lack of adequate peripheral resistance to its growing groups of tubules. (6) Benign glandular enlargement of the terminal parts of the lateral lobes of the prostate is equally as rare as that of the same condition in the posterior lobe and is due to lack of adequate peripheral resistance to the growth of the tubules in those parts.

Summary A death following epidural anaesthesia for Caesarean section in a patient with aortic incompetence and pre-eclampsia is described. Possible hazards of epidural anaesthesia in aortic incompetence are described and it is suggested that reduction of total peripheral resistance is contraindicated in such patients.

COMPARISON OF THE REFLEX EFFECTS OF CAROTID SINUS AND AORTIC ARCH BARORECEPTOR STIMULATION ON PERIPHERAL RESISTANCE