Blackout

Author(s):  
Hugo Farne ◽  
Edward Norris-Cervetto ◽  
James Warbrick-Smith

Note that the terms ‘syncope’ and ‘loss of consciousness’ are not interchangeable as loss of consciousness can be due to either syncopal or non-syncopal causes. Syncope is a form of loss of consciousness in which hypoperfusion of the brain is the cause (from the Greek syn (together) and kopein (to cut), referring to the fact that the blood flow that joins the brain together with the rest of the body has been cut). Syncopal causes can be subdivided by mechanism as follows: • ‘Reflex’: this is believed to involve activation of a primitive reflex that leads mammals to ‘play dead’ when faced with danger. Their heart rate slows and their blood pressure drops temporarily, reducing cerebral perfusion and leading to syncope. Some people appear to have a low threshold for activating this reflex in specific situations—for example after standing still for a long time, after seeing something frightening (e.g. blood, needles), or when straining (micturition, defecation). • ‘Cardiac’: pathologies causing a reduction in cardiac output (such as arrhythmias or outlet obstruction) can also lead to syncope. • ‘Orthostatic’: orthostatic hypotension basically means low blood pressure on sitting or standing (as opposed to lying flat). When we stand up there is a sudden drop in blood pressure that we compensate for by vasoconstriction, particularly of the ‘capacitance’ veins in the legs. This reduces the intravascular space, enabling us to maintain the pressure. However, this vasoconstriction takes a few seconds, so to prevent a transient fall in blood pressure every time we stand, there is a temporary increase in heart rate. Patients with reduced intravascular volume (e.g. from dehydration) and/or in whom the normal autonomic response (transient tachycardia and peripheral vasoconstriction) to standing is blunted (e.g. due to drugs or autonomic neuropathy) are vulnerable to blackouts. • ‘Cerebrovascular’: these are non-cardiac structural causes of reduced cerebral perfusion, i.e. obstructions to the blood flow between the heart and the brain. They are relatively uncommon. The main causes of a transient loss of consciousness are summarized in Figure 3.1, with the most common in large font. You should also remember that patients may believe they have lost consciousness when in fact they haven’t.

2005 ◽  
Vol 289 (4) ◽  
pp. H1662-H1668 ◽  
Author(s):  
C. A. Wauschkuhn ◽  
K. Witte ◽  
S. Gorbey ◽  
B. Lemmer ◽  
L. Schilling

Cardiovascular parameters such as arterial blood pressure (ABP) and heart rate display pronounced circadian variation. The present study was performed to detect whether there is a circadian periodicity in the regulation of cerebral perfusion. Normotensive Sprague-Dawley rats (SDR, ∼15 wk old) and hypertensive (mREN2)27 transgenic rats (TGR, ∼12 wk old) were instrumented in the abdominal aorta with a blood pressure sensor coupled to a telemetry system for continuous recording of ABP, heart rate, and locomotor activity. After 5–12 days, a laser-Doppler flow (LDF) probe was attached to the skull by means of a guiding device to measure changes in brain cortical blood flow (CBF). After the animals recovered from anesthesia, measurements were taken for 3–4 days. The time series were analyzed with respect to the midline estimating statistic of rhythm (i.e., mean value of a periodic event after fit to a cosine function), amplitude, and acrophase (i.e., phase angle that corresponds to the peak of a given period) of the 24-h period. The LDF signal displayed a significant circadian rhythm, with the peak occurring at around midnight in SDR and TGR, despite inverse periodicity of ABP in TGR. This finding suggests independence of LDF periodicity from ABP regulation. Furthermore, the acrophase of the LDF was consistently found before the acrophase of the activity. From the present data, it is concluded that there is a circadian periodicity in the regulation of cerebral perfusion that is independent of circadian changes in ABP and probably is also independent of locomotor activity. The presence of a circadian periodicity in CBF may have implications for the occurrence of diurnal alterations in cerebrovascular events in humans.


2012 ◽  
Vol 67 (10) ◽  
pp. 38-43
Author(s):  
V. F. Fokin ◽  
N. V. Ponomareva ◽  
M. V. Krotenkova ◽  
R. N. Konovalov ◽  
M. M. Tanashyan ◽  
...  

In patients with discirculatory encephalopathy the influence of verbal fluency test on the characteristics of cerebral perfusion, DC-potentials of the brain, as well as on blood pressure and heart rate was investigated. Two patterns of responses to the verbal fluency test were observed. The first one is the process of generalized activation, manifested by the reduction of the TTP (time to peak) parameters of brain perfusion, the rise of the DC-potentials in all areas of brain and the modulation of blood pressure and heart rate. The second process, directly connected with cognitive processing, was manifested by the shifts of local characteristics of brain perfusion and DC-potentials in the frontal, temporal and central cortex, especially in the left hemisphere. Correlations were found between the characteristics of cerebral perfusion and DC-potentials on the one hand and the number of words during the verbal fluency test performance on the other hand. 


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Nephtali Marina ◽  
Isabel N. Christie ◽  
Alla Korsak ◽  
Maxim Doronin ◽  
Alexey Brazhe ◽  
...  

AbstractAstrocytes provide neurons with essential metabolic and structural support, modulate neuronal circuit activity and may also function as versatile surveyors of brain milieu, tuned to sense conditions of potential metabolic insufficiency. Here we show that astrocytes detect falling cerebral perfusion pressure and activate CNS autonomic sympathetic control circuits to increase systemic arterial blood pressure and heart rate with the purpose of maintaining brain blood flow and oxygen delivery. Studies conducted in experimental animals (laboratory rats) show that astrocytes respond to acute decreases in brain perfusion with elevations in intracellular [Ca2+]. Blockade of Ca2+-dependent signaling mechanisms in populations of astrocytes that reside alongside CNS sympathetic control circuits prevents compensatory increases in sympathetic nerve activity, heart rate and arterial blood pressure induced by reductions in cerebral perfusion. These data suggest that astrocytes function as intracranial baroreceptors and play an important role in homeostatic control of arterial blood pressure and brain blood flow.


1982 ◽  
Vol 100 (1) ◽  
pp. 223-244
Author(s):  
J H Coote

A survey of the literature on a large number of vertebrate animals shows that sleep is associated with profound cardiovascular and respiratory adjustments which are very similar in each species. A hypothesis is advanced that these adjustments are 'goal directed' by neural structures in the brainstem, to ensure an adequate O2 and CO2 transport to and from the brain whilst at the same time reducing energy cost. During synchronised sleep there is a vagal bradycardia leading to reduced cardiac output and a fall in blood pressure; despite this cerebral blood flow increases. During desynchronized sleep there is a tonic fall in blood pressure and heart rate resulting from a unique repatterning of sympathetic discharge, that to heart, kidney, splanchnic and pelvic vascular beds decreasing whilst that to skeletal muscle increasing; cerebral blood flow shows a further increase. This differential pattern is probably initiated by neurones located in the caudal raphe nucleus obscurus. Phasic increases in blood pressure and heart rate also occur during desynchronized sleep mainly as a consequence of increases in sympathetic activity. Ventilation decreases during synchronized sleep accompanied by an increase in partial pressure of arterial CO2, which vasodilates cerebral blood vessels, indicating that the influence of CO2 on the level of ventilation has changed. During desynchronized sleep ventilation increases and becomes very irregular but the partial pressure of O2 and CO2 in arterial blood is little changed from wakefulness. Control of respiration is shifted to a central generator which apparently is different to the automatic/metabolic one which is normally dominant during wakefulness. Reflex control of the circulation and respiration is mainly governed by peripheral chemoreceptors, the threshold of most other afferent inputs being significantly raised during sleep.


2021 ◽  
pp. 187-215
Author(s):  
Graham Mitchell

As discussed in this chapter, giraffes have, compared with any other mammal, a very high mean blood pressure of ~250 mmHg. Human blood pressure is ~90 mmHg. Its size is determined by the length of the neck, the height of the head above the heart, by hydrostatic pressure generated by gravity acting on the column of blood in the carotid artery, and contractions of the heart muscles: blood pressure must be high enough to ensure that blood reaches the brain. Uniquely in giraffes blood pressure is regulated by receptors that are located in both the carotid and occipital arteries. Once thought to be ~2.5% of body mass the heart is smaller (~0.5% of body mass) but its muscle walls, especially of the interventricular wall and left ventricle wall, are exceptionally thick (up to 8 cm). The relative cardiac output is the same as in other mammals (~5 L 100 kg–1 of body mass) through a combination of a higher than predicted heart rate (70 b min–1 vs 50 b min–1) and smaller than predicted stroke volume (~0.7 ml kg–1 body mass vs 1.2 ml kg–1). Stroke volume is small because the left ventricle muscle wall is thick. The origin of high blood pressure is the resistance to blood flow, which is about twice what it is in other mammals. The higher resistance results from a combination of the thick muscular walls and narrow lumens of a giraffe’s blood vessels and unique mechanisms that regulate blood flow to the brain.


1992 ◽  
Vol 73 (5) ◽  
pp. 1756-1761 ◽  
Author(s):  
H. M. Frankel ◽  
E. Garcia ◽  
F. Malik ◽  
J. K. Weiss ◽  
H. R. Weiss

This study investigated the effects 2 h after administration of acetazolamide on cerebral blood flow and the pattern of cerebral capillary perfusion. Arterial blood pressure, heart rate, arterial blood gases, and pH were recorded in two groups of rats along with either regional cerebral blood flow or the percentage of capillary volume per cubic millimeter and number per square millimeter perfused as determined in cortical, thalamic, pontine, and medullary regions of the brain. Blood pressure, heart rate, and arterial PCO2 were not significantly different between the rats receiving acetazolamide (100 mg/kg) and the controls. Arterial blood pH was significantly lower in the acetazolamide rats. Blood flow increased significantly in the cortical (+ 102%), thalamic (+ 89%), and pontine (+ 88%) regions receiving acetazolamide. In control rats, approximately 60% of the capillaries were perfused in all of the examined regions. The percentage of capillaries per square millimeter perfused was significantly greater in the cortical (+ 52%), thalamic (+ 49%), and pontine (+ 47%) regions of acetazolamide rats compared with controls. In the medulla the increases in blood flow and percentage of capillaries perfused were not significant. Thus in the regions that acetazolamide increased cerebral blood flow, it also increased the percentage of capillaries perfused.


2014 ◽  
Vol 19 (5) ◽  
pp. 3-12
Author(s):  
Lorne Direnfeld ◽  
David B. Torrey ◽  
Jim Black ◽  
LuAnn Haley ◽  
Christopher R. Brigham

Abstract When an individual falls due to a nonwork-related episode of dizziness, hits their head and sustains injury, do workers’ compensation laws consider such injuries to be compensable? Bearing in mind that each state makes its own laws, the answer depends on what caused the loss of consciousness, and the second asks specifically what happened in the fall that caused the injury? The first question speaks to medical causation, which applies scientific analysis to determine the cause of the problem. The second question addresses legal causation: Under what factual circumstances are injuries of this type potentially covered under the law? Much nuance attends this analysis. The authors discuss idiopathic falls, which in this context means “unique to the individual” as opposed to “of unknown cause,” which is the familiar medical terminology. The article presents three detailed case studies that describe falls that had their genesis in episodes of loss of consciousness, followed by analyses by lawyer or judge authors who address the issue of compensability, including three scenarios from Arizona, California, and Pennsylvania. A medical (scientific) analysis must be thorough and must determine the facts regarding the fall and what occurred: Was the fall due to a fit (eg, a seizure with loss of consciousness attributable to anormal brain electrical activity) or a faint (eg, loss of consciousness attributable to a decrease in blood flow to the brain? The evaluator should be able to fully explain the basis for the conclusions, including references to current science.


1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.


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