scholarly journals Heat-stress-induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during heat stress

2011 ◽  
Vol 110 (5) ◽  
pp. 1283-1289 ◽  
Author(s):  
R. Matthew Brothers ◽  
David M. Keller ◽  
Jonathan E. Wingo ◽  
Matthew S. Ganio ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Central Venous Pressure ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Pressure Control ◽  
Stress Index ◽  
Central Venous ◽  
The Difference

The extent to which heat stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while heat stressed, while others are relatively tolerant. Heat stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to heat stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and heat-stress conditions. Tolerance to LBNP was quantified using a cumulative stress index (CSI), and the difference between normothermic CSI and heat-stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and heat-stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of heat stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the heat stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during heat stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the heat-stress-induced reductions in central venous pressure.

scholarly journals Effect of heat stress on cardiac output and systemic vascular conductance during simulated hemorrhage to presyncope in young men

2012 ◽  
Vol 302 (8) ◽  
pp. H1756-H1761 ◽  
Author(s):  
Matthew S. Ganio ◽  
Morten Overgaard ◽  
Thomas Seifert ◽  
Niels H. Secher ◽  
Pär I. Johansson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Heat Stress ◽  
Blood Pressure Control ◽  
Lower Body Negative Pressure ◽  
Pressure Control ◽  
Vascular Conductance ◽  
Low Cardiac Output ◽  
Primary Mechanism ◽  
Simulated Hemorrhage

During moderate actual or simulated hemorrhage, as cardiac output decreases, reductions in systemic vascular conductance (SVC) maintain mean arterial pressure (MAP). Heat stress, however, compromises the control of MAP during simulated hemorrhage, and it remains unknown whether this response is due to a persistently high SVC and/or a low cardiac output. This study tested the hypothesis that an inadequate decrease in SVC is the primary contributing mechanism by which heat stress compromises blood pressure control during simulated hemorrhage. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to presyncope in 11 passively heat-stressed subjects (increase core temperature: 1.2 ± 0.2°C; means ± SD). Cardiac output was measured via thermodilution, and SVC was calculated while subjects were normothermic, heat stressed, and throughout subsequent LBNP. MAP was not changed by heat stress but was reduced to 45 ± 12 mmHg at the termination of LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 to 11.7 ± 2.2 l/min ( P < 0.001) and increased SVC from 0.094 ± 0.018 to 0.163 ± 0.032 l·min−1·mmHg−1 ( P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 16% lower relative to pre-LBNP, presyncope cardiac output (7.3 ± 2.0 l/min) was not different than normothermic values ( P = 0.46). SVC did not change throughout LBNP ( P > 0.05) and at presyncope was 0.168 ± 0.044 l·min−1·mmHg−1. These data indicate that in humans a cardiac output adequate to maintain MAP while normothermic is no longer adequate during a heat-stressed-simulated hemorrhage. The absence of a decrease in SVC at a time of profound reductions in MAP suggests that inadequate control of vascular conductance is a primary mechanism compromising blood pressure control during these conditions.

Reflex control of the cutaneous circulation during passive body core heating in humans

2000 ◽  
Vol 88 (5) ◽  
pp. 1756-1764 ◽  
Author(s):  
Jochen K. Peters ◽  
Takeshi Nishiyasu ◽  
Gary W. Mack
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Laser Doppler ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Body Core ◽  
Doppler Techniques ◽  
The Impact

The impact of body core heating on the interaction between the cutaneous and central circulation during blood pressure challenges was examined in eight adults. Subjects were exposed to −10 to −90 mmHg lower body negative pressure (LBNP) in thermoneutral conditions and −10 to −60 mmHg LBNP during heat stress. We measured forearm vascular conductance (FVC; ml ⋅ min−1 ⋅ 100 ml−1 ⋅ mmHg−1) by plethysmography; cutaneous vascular conductance (CVC) by laser-Doppler techniques; and central venous pressure, arterial blood pressure, and cardiac output by impedance cardiography. Heat stress increased FVC from 5.7 ± 0.9 to 18.8 ± 1.3 conductance units (CU) and CVC from 0.21 ± 0.07 to 1.02 ± 0.20 CU. The FVC-CVP relationship was linear over the entire range of LBNP and was shifted upward during heat stress with a slope increase from 0.46 ± 0.10 to 1.57 ± 0.3 CU/mmHg CVP ( P < 0.05). Resting CVP was lower during heat stress (6.3 ± 0.6 vs. 7.7 ± 0.6 mmHg; P < 0.05) but fell to similar levels during LBNP as in normothermic conditions. Data analysis indicates an increased capacity, but not sensitivity, of peripheral baroreflex responses during heat stress. Laser-Doppler techniques detected thermoregulatory responses in the skin, but no significant change in CVC occurred during mild-to-moderate LBNP. Interestingly, very high levels of LBNP produced cutaneous vasodilation in some subjects.

Functional Interaction between Angiotensin and Sympathetic Reflexes in Cats

1982 ◽  
Vol 62 (1) ◽  
pp. 51-56 ◽  
Author(s):  
R. Hatton ◽  
D. P. Clough ◽  
S. A. Adigun ◽  
J. Conway
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Partial Recovery ◽  
Ang Ii ◽  
Central Venous ◽  
Efferent Nerve ◽  
Arterial Blood ◽  
Sympathetic Reflexes

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

scholarly journals Reflex-Mediated Reduction in Human Cerebral Blood Volume

2005 ◽  
Vol 25 (1) ◽  
pp. 136-143 ◽  
Author(s):  
Timothy D Wilson ◽  
J Kevin Shoemaker ◽  
R Kozak ◽  
T-Y Lee ◽  
Adrian W Gelb
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Lower Body Negative Pressure ◽  
Mean Transit Time ◽  
Venous Pressure ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Lower Body ◽  
Central Venous

Adrenergic nerves innervate the human cerebrovasculature, yet the functional role of neurogenic influences on cerebral hemodynamics remains speculative. In the current study, regional cerebrovascular responses to sympathoexcitatory reflexes were evaluated. In eight volunteers, contrast-enhanced computed tomography was performed at baseline, –40 mmHg lower body negative pressure (LBNP), and a cold pressor test (CPT). Cerebral blood volume (CBV), mean transit time (MTT), and cerebral blood flow (CBF) were evaluated in cortical gray matter (GM), white matter (WM), and basal ganglia/thalamus (BGT) regions. Lower body negative pressure resulted in tachycardia and decreased central venous pressure while mean arterial pressure was maintained. Cold pressor test resulted in increased mean arterial pressure concomitant with tachycardia but no change in central venous pressure. Neither reflex altered end-tidal carbon dioxide. Cerebral blood volume was reduced in GM during both LBNP and CPT ( P<0.05) but was unchanged in WM and BGT. Mean transit time was reduced in WM and GM during CPT ( P<0.05). Cerebral blood flow was only modestly affected with either reflex ( P<0.07). The combined reductions in GM CBV (˜ –25%) and MTT, both with and without any change in central venous pressure, with small CBF changes (˜ –11%), suggest that active venoconstriction contributed to the volume changes. These data demonstrate that CBV is reduced during engagement of sympathoexcitatory reflexes and that these cerebrovascular changes are heterogeneously distributed.

ANP-mediated volume depletion attenuates renal responses in humans

1992 ◽  
Vol 263 (6) ◽  
pp. R1303-R1308 ◽  
Author(s):  
T. J. Ebert ◽  
L. Groban ◽  
M. Muzi ◽  
M. Hanson ◽  
A. W. Cowley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Central Venous Pressure ◽  
Sodium Excretion ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Urine Volume ◽  
Positive Pressure ◽  
Plasma Norepinephrine ◽  
Central Venous

Brief low-dose infusions of atrial natriuretic peptide (ANP) that emulate physiological plasma concentrations in humans have little if any effect on renal excretory function. This study explored the possibility that ANP-mediated reductions in cardiac filling pressures (through ANP's rapid effect on capillary dynamics) could attenuate its purported renal effects. Protocol A consisted of 16 healthy subjects (ages 19-27 yr old) who underwent three consecutive 45-min experimental sequences: 1) placebo, 2) ANP (10 ng.kg-1 x min-1), and 3) ANP alone (n = 8) or ANP with simultaneous lower body positive pressure (LBPP, n = 8). Electrocardiogram and direct measures of arterial and central venous pressures were continuously monitored. Blood was sampled at the end of each 45-min sequence before subjects stood to void. Compared with control (placebo), ANP produced a hemoconcentration and increased plasma norepinephrine, but did not change heart rate, blood pressure, plasma levels of renin, aldosterone, or vasopressin, or renal excretion of volume or sodium. In subjects receiving LBPP to maintain central venous pressure during the last 45 min of ANP infusion, norepinephrine did not increase and urine volume and sodium excretion increased (P < 0.05). In a second study (protocol B), five healthy subjects received a placebo infusion for 45 min followed by two consecutive 45-min infusions of ANP (10 ng.kg-1 x min-1). Central venous pressure was maintained (LBPP) at placebo baseline throughout the two ANP infusion periods. Urine volume and sodium excretion rates increased progressively and significantly during both ANP infusion periods (P < 0.05) without significant changes in creatinine clearance, blood pressure, or heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Prospective Study of Central Venous Pressure Trends during Major Neurosurgical Procedures in an Elective Operation Theatre Setting of a Tertiary Care Centre

2021 ◽  
Vol 8 (07) ◽  
pp. 369-373
Author(s):  
Rajeev Damodaran Sarojini ◽  
Sanjay Sahadevan ◽  
Jayakumar Christhudas
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Prospective Study ◽  
Central Venous Pressure ◽  
Inferior Vena ◽  
Venous Pressure ◽  
Ultra Sound ◽  
Neurosurgical Procedures ◽  
Central Venous ◽  
Intraoperative Period

BACKGROUND There are extensive variations in central venous pressure during intraoperative period of a major neurosurgical patients. Monitoring of central venous pressure is vital for guiding the administration of fluids, blood and blood products. Central venous pressure (CVP) also measures the intracranial pressure indirectly. Increased intracranial pressure thereby reduces the cerebral blood flow, leading to cerebral ischemia. METHODS This is a prospective study where 25 major neurosurgical cases posted for elective major neurosurgery were selected. Right subclavian vein was selected for cannulation, by blind technique in all these cases. CVP was recorded every 15 minutes. Central venous catheter was connected to a pressure transducer linked to a multichannel monitor; zeroing was done and the CVP reading obtained. RESULTS Central venous pressure reading was done serially and showed the trends in haemodynamics in various stages of surgery. Initial intraoperative periods showed lower values due to intravenous (I / V) induction of anaesthesia, use of mannitol and diuretics. Later on, the trends changed to higher side subsequent to administration of fluids and blood as required. CONCLUSIONS Monitoring of CVP is an important component of haemodynamic monitoring along with non-invasive blood pressure (NIBP), intra-arterial blood pressure (IABP), and urine output. Central venous pressure can be used to aspirate an air embolism occurring during the intraoperative period after employing Durant’s position. KEYWORDS CVP, NIBP , USS – Ultra Sound Scan, IVC – Inferior Vena Cava, IVCCI – Inferior Vena Cave Collapsibility Index, PEEP – Positive End Expiratory Pressure, C / L – Central Line, IABP.

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