Alteration in heart rate response to hemorrhage in conscious dogs with volume overload

1978 ◽  
Vol 235 (4) ◽  
pp. H422-H428
Author(s):  
M. M. LeWinter ◽  
J. S. Karliner ◽  
J. W. Covell
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Pulse Pressure ◽  
Pressure Pulse ◽  
Heart Rate Response ◽  
Parasympathetic Nervous System ◽  
Venous Pressure ◽  
Volume Overload ◽  
Conscious Dogs ◽  
Central Venous

The heart rate response to hemorrhage was studied in conscious dogs before and up to 2 mo after the establishment of volume overload due to systemic arteriovenous (a-v) fistulas. Before a-v fistula, heart rate increased markedly during hemorrhage. When hemorrhage was preceded by dextran infusion, bleeding resulted in a gradual reduction in heart rate. The a-v fistula caused marked increases in resting heart rate, central venous pressure, pulse pressure, and blood volume. During hemorrhage, heart rate initially remained constant, but then declined abruptly from the resting value of 121 +/- 3.7 beats/min to a nadir of 89 +/- 6.5 beats/min (P less than 0.01). Although mean arterial pressure decreased markedly, there was no significant change in pulse pressure, and central venous pressure tended to stabilize with the heart rate decline. The abrupt heart rate decline was prevented by atropine but unaltered by propranolol. The response was observed as early as 5 days after a-v fistula. We conclude that an alteration in the heart rate response to hemorrhage appears early during volume overload. This alteration appears to be reflex in nature and to be mediated by the parasympathetic nervous system.

Effects of the First (Ether) Extract of Ginseng on the Cardiovascular Dynamics of Dogs During Halothane Anesthesia

1978 ◽  
Vol 06 (02) ◽  
pp. 115-121 ◽  
Author(s):  
MYUNG O. LEE ◽  
DONALD H. CLIFFORD ◽  
CHONG YUL KIM ◽  
DO CHIL LEE
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Pressure Pulse ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Ether Extract ◽  
Halothane Anesthesia ◽  
Central Venous ◽  
Cardiovascular Variables

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in ten dogs. Subsequently, these animals were maintained under halothane (0.75%) anesthesia during the intravenous administration of an ether extract (40 mg/kg) of ginseng. Five other dogs were anesthesized without injecting ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO, PaO and base deficit were compared during tthe ensuing 120 minutes. The heart rate was significantly decreased and central venous pressure increased significantly following ginseng. There were no other meaningful changes in either group.

scholarly journals Should we stop using the determination of central venous pressure as a way to estimate cardiac preload?

2012 ◽  
pp. 181-184 ◽  
Author(s):  
Johann Smith Ceron Arias ◽  
Manuel Felipe Muñoz Nañez
Keyword(s):  
Central Venous Pressure ◽  
Blood Volume ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Pressure Change ◽  
Cardiac Preload ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Dynamic Variables

The determination of the values of central venous pressure has long been used as a guideline for volumetric therapy in the resuscitation of the critical patient, but the performance of such parameter is currently being questioned as an effective measurement of cardiac preload. This has aroused great interest in the search for more accurate parameters to determine cardiac preload and a patient’s blood volume. Goals and Methodology: Based on literature currently available, we aim to discuss the performance of central venous pressure as an effective parameter to determine cardiac preload. Results and Conclusion: Estimating variables such as end-diastolic ventricular area and global end-diastolic volume have a better performance than central venous pressure in determining cardiac preload. Despite the best performance of these devices, central venous pressure is still considered in our setting as the most practical and most commonly available way to assess the patient’s preload. Only dynamic variables such as pulse pressure change are superior in determining an individual’s blood volume.

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise

2004 ◽  
Vol 96 (2) ◽  
pp. 668-673 ◽  
Author(s):  
Thad E. Wilson ◽  
Robert Carter ◽  
Michael J. Cutler ◽  
Jian Cui ◽  
Michael L. Smith ◽  
...  
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Sweat Rate ◽  
Venous Pressure ◽  
Thoracic Impedance ◽  
Active Recovery ◽  
Central Venous ◽  
Cycle Exercise ◽  
Vascular Conductance ◽  
Cutaneous Vascular Conductance

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (Tcore), mean skin temperature (Tsk), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure ( n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, Tcore, and Tsk. Baroreceptor loading and thermal status were similar during trials because MAP (90 ± 4, 88 ± 4 mmHg), thoracic impedance (29 ± 1, 28 ± 2 Ω), central venous pressure (5 ± 1, 4 ± 1 mmHg), Tcore (37.5 ± 0.1, 37.5 ± 0.1°C), and Tsk (34.1 ± 0.3, 34.2 ± 0.2°C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 ± 6% of maximum) and inactive (28 ± 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 ± 0.16 mg·cm-2·min-1) compared with inactive (0.34 ± 0.19 mg·cm-2·min-1; P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.

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)

Ventricular receptors stimulate vasopressin release during hemorrhage

1988 ◽  
Vol 254 (2) ◽  
pp. R204-R211 ◽  
Author(s):  
B. C. Wang ◽  
G. Flora-Ginter ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Left Atrial ◽  
Heart Rate Response ◽  
Venous Pressure ◽  
Control Level ◽  
Conscious Dogs ◽  
Central Venous ◽  
Vasopressin Release ◽  
Cardiac Denervation ◽  
Plasma Vasopressin ◽  
Vasopressin Secretion

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Microcirculatory Perfusion during Volume Therapy

1995 ◽  
Vol 82 (4) ◽  
pp. 975-982. ◽  
Author(s):  
Wolfgang Funk ◽  
Verena Baldinger
Keyword(s):  
Heart Rate ◽  
Oxygen Partial Pressure ◽  
Partial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Tissue Perfusion ◽  
Volume Replacement ◽  
Surface Oxygen ◽  
Tissue Oxygen ◽  
Central Venous

Background Because of the passage of water and salt molecules into the interstitial space, volume replacement with crystalloid solutions requires an amount at least four times that of lost blood. The resulting tissue edema may interfere with nutritive capillary perfusion and oxygen delivery. To prove this hypothesis, the effects of isovolemic hemodilution (hematocrit 30%) with Ringer's lactate solution or dextran 60 on tissue perfusion and oxygenation were investigated in awake Syrian golden hamsters. Methods Experiments were performed by using a chronic dorsal skinfold window giving access to skeletal muscle tissue (musculus cutaneus) with in vivo microscopy, quantitative video image analysis, and surface oxygen partial pressure electrodes. Central venous and arterial pressures were measured by means of chronically implanted jugular venous and carotid catheters. Results Isovolemic exchange of blood with dextran caused no significant changes in arterial or central venous pressure, heart rate, capillary flow velocity, functional capillary density, or surface oxygen partial pressure during the 1-h observation period. A volume of Ringer's solution equal to four times of the amount of blood lost maintained arterial pressure and heart rate when central venous pressure was kept at predilution control values. However, tissue perfusion determined by counting perfused capillaries per terminal arteriole was reduced by 62%, and mean tissue oxygen partial pressure decreased from 19 to 8 mmHg. Conclusions In this model, volume replacement with artificial colloids yielded hemodynamic stability and adequate tissue oxygen supply, whereas administration of crystalloids alone jeopardized tissue perfusion and oxygenation.

Pulse Pressure Variation Is Comparable With Central Venous Pressure to Guide Fluid Resuscitation in Experimental Hemorrhagic Shock With Endotoxemia

Shock ◽  
2013 ◽  
Vol 40 (4) ◽  
pp. 303-311 ◽  
Author(s):  
Jessica Noel-Morgan ◽  
Denise Aya Otsuki ◽  
José Otávio Costa Auler ◽  
Júlia Tizue Fukushima ◽  
Denise Tabacchi Fantoni
Keyword(s):  
Central Venous Pressure ◽  
Hemorrhagic Shock ◽  
Fluid Resuscitation ◽  
Pulse Pressure ◽  
Pulse Pressure Variation ◽  
Venous Pressure ◽  
Pressure Variation ◽  
Central Venous ◽  
Experimental Hemorrhagic Shock

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Central venous pressure in humans during short periods of weightlessness

1987 ◽  
Vol 63 (6) ◽  
pp. 2433-2437 ◽  
Author(s):  
P. Norsk ◽  
N. Foldager ◽  
F. Bonde-Petersen ◽  
B. Elmann-Larsen ◽  
T. S. Johansen
Keyword(s):  
Heart Rate ◽  
Central Venous Pressure ◽  
Supine Position ◽  
Parabolic Flight ◽  
Venous Pressure ◽  
Central Venous Catheters ◽  
Sitting Position ◽  
Central Venous ◽  
Pressure Transducers ◽  
Gauge Pressure

Central venous pressure (CVP) was measured in 14 males during 23.3 +/- 0.6 s (mean +/- SE) of weightlessness (0.00 +/- 0.05 G) achieved in a Gulfstream-3 jet aircraft performing parabolic flight maneuvers and during either 60 or 120 s of +2 Gz (2.0 +/- 0.1 Gz). CVP was obtained using central venous catheters and strain-gauge pressure transducers. Heart rate (HR) was measured simultaneously in seven of the subjects. Measurements were compared with values obtained inflight at 1 G with the subjects in the supine (+1 Gx) and upright sitting (+1 Gz) positions, respectively. CVP was 2.6 +/- 1.5 mmHg during upright sitting and 5.0 +/- 0.7 mmHg in the supine position. During weightlessness, CVP increased significantly to 6.8 +/- 0.8 mmHg (P less than 0.005 compared with both upright sitting and supine inflight). During +2 Gz, CVP was 2.8 +/- 1.4 mmHg and only significantly lower than CVP during weightlessness (P less than 0.05). HR increased from 65 +/- 7 beats/min at supine and 70 +/- 5 beats/min during upright sitting to 79 +/- 7 beats/min (P less than 0.01 compared with supine) during weightlessness and to 80 +/- 6 beats/min (P less than 0.01 compared with upright sitting and P less than 0.001 compared with supine) during +2 Gz. We conclude that the immediate onset of weightlessness induces a significant increase in CVP, not only compared with the upright sitting position but also compared with the supine position at 1 G.

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