Leg vasoconstriction during dynamic exercise with reduced cardiac output

Hanel, Birgitte; Pawelczyk, James A.; Warberg, Jørgen; Secher, Niels H.

doi:10.1152/jappl.1992.73.5.1838

Cited by 100 publications

(120 citation statements)

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“…Whether aortic compression by a gravid uterus enhances cerebral blood flow at the expense of lower extremity blood flow remains unknown. Through their experiments on healthy controls Ide et al showed that an impaired ability to increase cardiac output during exercise with a large muscle mass appears to limit blood flow distribution not only to active muscle 15 but also to such a vital organ as the brain, and that this flow restriction was by way of the sympathetic nervous system 16 . During central blood volume depletion, the increase in sympathetic nerve activity shifts the cerebral autoregulation curve to the right 17 and the vasoconstrictor sympathetic nerve activity overrides vasodilatation 18 .…”

Section: Discussionmentioning

confidence: 99%

Maintained consciousness during witnessed asystole after spinal anesthesia for Cesarean section

2013

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Despite its low incidence, cardiac arrest after spinal anesthesia carries a high mortality. Counterintuitively, young and healthy patients with low resting pulse are at increased risk. We report the case of a healthy 24 yr G P0 at term scheduled for elective Cesarean section whose heart rate decreased to 30 bpm, followed by more than 30 seconds of asystole 3 minutes after spinal anesthesia with a T4 level block. Following atropine and epinephrine administration, the patient had several single heart beats when startled by the anesthesiologist's loud voice and when touching her chest to prepare for chest compressions. Eventually, regular sinus rhythm returned with a heart rate of up to 160 bpm. The patient was rapidly prepped, and within 5 minutes, the fetus was delivered surgically with Apgar scores of 8 and 9. Most unusually, the patient remained responsive during the entire event and denied having lost consciousness. Supine position and volume loading may have contributed to venous pooling within the cerebral vasculature, so even in the absence of cerebral blood flow during asystole venous blood may still have been present and delayed cerebral hypoxia. Therefore, loss of consciousness in the supine position may occur considerably after the onset of asystole which may reduce the time available for treatment and contribute to its high mortality. Inspiration during the two startle reactions may have decreased vagal tone and permitted enough spontaneous cardiac activity to circulate the resuscitative drugs without CPR.

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Section: Discussionmentioning

confidence: 99%

Maintained consciousness during witnessed asystole after spinal anesthesia for Cesarean section

2013

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“…Third, with respect to the limitations of the model used to evoke the metaboreflex, both static and dynamic contractions followed by local circulatory occlusion increase HR, SV, and CO in humans (3,24,32) and in dogs (29), but the effects on the heart appear to be intensity-dependent (7,8,40). However, the local circulatory occlusion used to trap metabolites that activate metaboreflex prevents venous dilation, which is a major component of metaboreflex activation (10,25).…”

Section: Limitationsmentioning

confidence: 99%

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

Delliaux

Ichinose

Watanabe

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Ten healthy males participated under three experimental conditions: 1) hypercapnia (HCA, PET CO 2 : ϩ10 mmHg, by inhalation of a CO 2-enriched gas mixture); 2) muscle metaboreflex activation (MMA, by 5 min of local circulatory occlusion after 1 min of 50% maximum voluntary contraction isometric handgrip under normocapnia); and 3) HCAϩMMA. We measured mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO); calculated stroke volume (SV), and total peripheral resistance (TPR); and evaluated myocardial oxygen consumption (MV O2) and cardiac work (CW) noninvasively. MAP increased in the three experimental conditions but HCAϩMMA led to the highest MAP, CO, and HR. Moreover, HCAϩMMA increased SV and was associated with the highest MV O2 and CW. HCA and MMA exhibited inhibitory interactions with MAP, HR, TPR, MV O2, and CW, increases of which were smaller during HCAϩMMA than the sum of the increases during HCA and MMA alone (MAP: ϩ28 Ϯ 2 vs. ϩ34 Ϯ 2 mmHg, P Ͻ 0.001; HR: ϩ15 Ϯ 2 vs. ϩ22 Ϯ 3 bpm, P Ͻ 0.01; TPR: ϩ1.1 Ϯ 1.4 vs. ϩ3.0 Ϯ 1.5 mmHg·l·min Ϫ1 , P Ͻ 0.05; MV O2: ϩ50.25 Ϯ 4.74 vs. ϩ59.48 Ϯ 5.37 mmHg·min Ϫ1 ·10 Ϫ2 , P Ͻ 0.01; CW: ϩ59.10 Ϯ 7.52 vs. ϩ63.67 Ϯ 7.71 ml mmHg·min Ϫ1 ·10 Ϫ4 , P Ͻ 0.05). Oppositely, HCA and MMA interactions were linearly additive for CO (ϩ2.3 Ϯ 0.4 l/min) and SV (ϩ13 Ϯ 4 ml). We showed that muscle metaboreflex and hypercapnia interact in healthy humans, reducing vasoconstriction but enhancing SV.hypercapnia; muscle metaboreflex; hypertension; stroke volume; myocardial oxygen consumption REGULATION OF ARTERIAL BLOOD pressure involves the integration of humoral, hormonal, and neurogenic components. For example, whereas hypercapnia has direct humoral vasodilatory effects (19,20), the neurally mediated central chemoreflex increases cardiovascular sympathetic nervous system activity, leading heart rate (HR), stroke volume (SV), cardiac output (CO), vascular resistance, and then blood pressure all to increase (31). During exercise, blood pressure is also regulated by muscle reflexes (2, 17). The muscle metaboreflex forms a second direct excitatory input for the neural control of cardiovascular function (21, 29, 42) that also stimulates sympathetic pathways (29,30,33) leading to increases in HR, SV, CO, vascular resistance, and then blood pressure.It is known that central chemoreflex and muscle metaboreflex signals converge to common areas in the brain (43) and exert similar excitatory effects through the cardiovascular autonomic nervous system. On the other hand, little is known about the hemodynamic effects of muscle metaboreflex activation during hypercapnia. Ponikowski (35) showed that muscle ergoreflex activation was an independent predictor of ventilation sensitivity to hypercapnia in chronic heart failure and argued for the existence of interactions between the muscle metaboreflex and hypercapnic chemoreflex. Despite the likelihood that these two reflexes interact during exercise, this topic received little direct attention before the pioneering work of Lykidis et al. (22,23),...

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“…Fig. 3 compares the percentage changes in heart rate (HR), cardiac output (CO), mean systemic arterial pressure (MAP), systemic vascular conductance (SVC), and blood flow in active muscles (Q am ) computed with the model at four different exercise levels, with analogous data in humans [2]. As it is clear from the figure, the agreement between simulation and in vivo results is satisfactory.…”

Section: Resultsmentioning

confidence: 74%

“…In order to reproduce muscle exercise hyperemia, we assumed that peripheral resistance in the active muscle compartment (R amp ) depends not only on neural influences, but also on local metabolic control mechanisms. The latter comprise the effect of increased oxygen consumption rate and of metabolic production of vasodilator substances [2,12], each described as a function of exercise intensity through a static characteristic and a firstorder low-pass dynamics. Both an increase of O 2 consumption over the basal level and the release of vasodilator substances produce a decrease in R amp .…”

Section: B Control Mechanismsmentioning

confidence: 99%

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A mathematical model of cardiovascular response to dynamic exercise

Magosso

Felicani

Ursino

2001 Conference Proceedings of the 23rd Annual International Conference of the IEEE Engineering in Medicine and Biology Society

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Abstract-A mathematical model of cardiovascular response to dynamic exercise is presented. The model includes the pulsating heart, the systemic and pulmonary circulation, a functional description of muscle exercise hyperemia, the mechanical effects of muscle contractions on hemodynamics, and various neural regulatory mechanisms working on systemic resistance, venous unstressed volume, heart rate and ventricle contractility. These mechanisms comprehend the direct effect of motor command signals on cardiovascular and respiratory control centers (the so called central command), arterial baroreflex and the lungstretch receptor reflex. The model is used to simulate the steady state response of the main cardiovascular hemodynamic quantities (systemic arterial pressure, heart rate, cardiac output, systemic vascular conductance, and blood flow in working muscle) to various intensity levels of two-legs dynamic exercise. A good agreement with physiological data in the literature has been obtained. The model sustains the hypothesis that motor command signals emanating from cerebral cortex provide the primary drive for changes of circulation and respiration during exercise. The model may represent an important tool to improve understanding of exercise physiology.

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Leg vasoconstriction during dynamic exercise with reduced cardiac output

Cited by 100 publications

References 0 publications

Maintained consciousness during witnessed asystole after spinal anesthesia for Cesarean section

Maintained consciousness during witnessed asystole after spinal anesthesia for Cesarean section

Cardiovascular responses to forearm muscle metaboreflex activation during hypercapnia in humans

A mathematical model of cardiovascular response to dynamic exercise

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