Stroke Volume Optimization: The New Hemodynamic Algorithm

2015 ◽  
Vol 35 (1) ◽  
pp. 11-27 ◽  
Author(s):  
Alexander Johnson ◽  
Thomas Ahrens
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Optimization Strategy ◽  
Central Venous ◽  
Hemodynamic Optimization ◽  
Level Of Consciousness ◽  
Cardiac Output Monitor ◽  
Care Practices

Critical care practices have evolved to rely more on physical assessments for monitoring cardiac output and evaluating fluid volume status because these assessments are less invasive and more convenient to use than is a pulmonary artery catheter. Despite this trend, level of consciousness, central venous pressure, urine output, heart rate, and blood pressure remain assessments that are slow to be changed, potentially misleading, and often manifested as late indications of decreased cardiac output. The hemodynamic optimization strategy called stroke volume optimization might provide a proactive guide for clinicians to optimize a patient’s status before late indications of a worsening condition occur. The evidence supporting use of the stroke volume optimization algorithm to treat hypovolemia is increasing. Many of the cardiac output monitor technologies today measure stroke volume, as well as the parameters that comprise stroke volume: preload, afterload, and contractility.

Acute plasma expansion: left ventricular hemodynamics and endocrine function during exercise

1992 ◽  
Vol 73 (5) ◽  
pp. 1791-1796 ◽  
Author(s):  
I. L. Kanstrup ◽  
J. Marving ◽  
P. F. Hoilund-Carlsen
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Healthy Subjects ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Endocrine Function ◽  
Plasma Expansion ◽  
Central Venous ◽  
Mean Pressure ◽  
Dextran Solution

In 11 healthy subjects (8 males and 3 females, age 21–59 yr) left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volumes were measured in the supine position by isotope cardiography at rest and during two submaximal one-legged exercise loads before and 1 h after acute plasma expansion (PE) by use of a 6% dextran solution (500–750 ml). After PE, blood volume increased from 5.22 +/- 0.92 to 5.71 +/- 1.02 (SD) liters (P < 0.01). At rest, cardiac output increased 30% (5.3 +/- 1.0 to 6.9 +/- 1.6 l/min; P < 0.01), stroke volume increased from 90 +/- 20 to 100 +/- 28 ml (P < 0.05), and LVEDV increased from 134 +/- 29 to 142 +/- 40 ml (NS). LVESV was unchanged (44 +/- 11 and 42 +/- 14 ml). Heart rate rose from 60 +/- 7 to 71 +/- 10 beats/min (P < 0.01). The cardiac preload [central venous pressure (CVP)] was insignificantly elevated (4.9 +/- 2.1 and 5.3 +/- 3.0 mmHg); systemic vascular resistance and arterial pressures were significantly reduced (mean pressure fell from 91 +/- 11 to 85 +/- 11 mmHg, P < 0.01). Left ventricular peak filling and peak ejection rates both increased (19 and 14%, respectively; P < 0.05). During exercise, cardiac output remained elevated after PE compared with the control situation, predominantly due to a 10- to 14-ml rise in stroke volume caused by an increased LVEDV, whereas LVESV was unchanged. CVP increased after PE by 2.1 and 3.0 mmHg, respectively (P < 0.05).2+ remained unchanged during exercise compared with rest after PE in

scholarly journals A Comparison between Ketamine and Diazepam as Induction Agents for Pericardiectomy

1978 ◽  
Vol 6 (1) ◽  
pp. 66-70 ◽  
Author(s):  
H. G. G. Kingston ◽  
K. W. Bretherton ◽  
A. M. Holloway ◽  
and J. W. Downing
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Index ◽  
Central Venous Pressure ◽  
Systemic Vascular Resistance ◽  
Venous Pressure ◽  
Significant Rise ◽  
Central Venous ◽  
Induction Of Anaesthesia ◽  
Induction Agents

Ketamine 1 · 0 mg/kg and diazepam 0 · 3 mg/kg was used to induce anaesthesia in patients requiring pericardiectomy. A significant rise in blood pressure in patients receiving ketamine was noted. In contrast, a fall in blood pressure was seen when diazepam was administered. Changes in cardiac output, cardiac index, central venous pressure and systemic vascular resistance are discussed. Ketamine appears to be a more satisfactory agent for induction of anaesthesia in patients for pericardiectomy, whereas diazepam should be used with caution.

scholarly journals Studies on Australian Snake Venoms. Part 1: The Haemodynamic Effects of Brown Snake (Pseudonaja) Species in the Dog

1989 ◽  
Vol 17 (4) ◽  
pp. 466-469 ◽  
Author(s):  
J. Tibballs ◽  
S. Sutherland ◽  
S. Kerr
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Venous Pressure ◽  
Haemodynamic Effects ◽  
Peripheral Vascular ◽  
Snake Venoms ◽  
Central Venous ◽  
Induced Hypotension ◽  
Mechanically Ventilated

The haemodynanic effects of Brown Snake (Pseudonaja) species (textilis, nuchalis, affinis) were investigated in anaesthetised, mechanically ventilated dogs. Blood pressure decreased to minimal levels five minutes after intravenous envenomation. Hypotension was accompanied by significant decrements in cardiac output and stroke volume and a rise in peripheral vascular resistance. Heart rate increased transiently during 0.5-2.0 minutes after envenomation but had declined below resting levels five minutes after envenomation. No statistically significant change was recorded in central venous pressure. Depression of myocardial contractility is postulated as the mechanism of venom induced hypotension.

scholarly journals Central venous pressure and cardiac function during spaceflight

1998 ◽  
Vol 85 (2) ◽  
pp. 738-746 ◽  
Author(s):  
Ronald J. White ◽  
C. Gunnar Blomqvist
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Shape Change ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Reference Measurements

Early in spaceflight, an apparently paradoxical condition occurs in which, despite an externally visible headward fluid shift, measured central venous pressure is lower but stroke volume and cardiac output are higher, and heart rate is unchanged from reference measurements made before flight. This paper presents a set of studies in which a simple three-compartment, steady-state model of cardiovascular function is used, providing insight into the contributions made by the major mechanisms that could be responsible for these events. On the basis of these studies, we conclude that, during weightless spaceflight, the chest relaxes with a concomitant shape change that increases the volume of the closed chest cavity. This leads to a decrease in intrapleural pressure, ultimately causing a shift of blood into the vessels of the chest, increasing the transmural filling pressure of the heart, and decreasing the central venous pressure. The increase in the transmural filling pressure of the heart is responsible, through a Starling-type mechanism, for the observed increases in heart size, left ventricular end-diastolic volume, stroke volume, and cardiac output.

scholarly journals Understanding basic vein physiology and venous blood pressure through simple physical assessments

2019 ◽  
Vol 43 (3) ◽  
pp. 423-429 ◽  
Author(s):  
Etain A. Tansey ◽  
Laura E. A. Montgomery ◽  
Joe G. Quinn ◽  
Sean M. Roe ◽  
Christopher D. Johnson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Central Venous Pressure ◽  
Venous Return ◽  
Venous Pressure ◽  
Venous Blood ◽  
Venous System ◽  
Arterial System ◽  
Right Atrial ◽  
Central Venous

An understanding of the complexity of the cardiovascular system is incomplete without a knowledge of the venous system. It is important for students to understand that, in a closed system, like the circulatory system, changes to the venous side of the circulation have a knock-on effect on heart function and the arterial system and vice versa. Veins are capacitance vessels feeding blood to the right side of the heart. Changes in venous compliance have large effects on the volume of blood entering the heart and hence cardiac output by the Frank-Starling Law. In healthy steady-state conditions, venous return has to equal cardiac output, i.e., the heart cannot pump more blood than is delivered to it. A sound understanding of the venous system is essential in understanding how changes in cardiac output occur with changes in right atrial pressure or central venous pressure, and the effect these changes have on arterial blood pressure regulation. The aim of this paper is to detail simple hands-on physiological assessments that can be easily undertaken in the practical laboratory setting and that illustrate some key functions of veins. Specifically, we illustrate that venous valves prevent the backflow of blood, that venous blood pressure increases from the heart to the feet, that the skeletal muscle pump facilitates venous return, and we investigate the physiological and clinical significance of central venous pressure and how it may be assessed.

Effects of the Third (Aqueous) Extract of Ginseng on the Cardiovascular Dynamics of Dogs During Halothane Anesthesia

1978 ◽  
Vol 06 (03) ◽  
pp. 253-259
Author(s):  
DONALD H. CLIFFORD ◽  
DO CHIL LEE ◽  
CHONG YUL KIM ◽  
MYUNG O. LEE
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Aqueous Extract ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Central Venous ◽  
Cardiovascular Variables

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in a group of dogs. Subsequently, ten dogs were lightly anesthetized with halothane (0.75%), and a third (aqueous) extract of ginseng (40 mg/kg) was administered intravenously. Five dogs were anesthesized without the administration of ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2, and base deficit were compared. The cardiac output, stroke volume, and central venous pressure were decreased significantly, while total peripheral resistance was increased significantly following ginseng.

Changes in cardiac output, stroke volume, and central venous pressure induced by atropine in man

1959 ◽  
Vol 58 (2) ◽  
pp. 204-213 ◽  
Author(s):  
J.Norman Berry ◽  
Howard K. Thompson ◽  
D.Edmond Miller ◽  
Henry D. McIntosh
Keyword(s):  
Cardiac Output ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Central Venous

The control of blood pressure during external hypercapnia in the rainbow trout (Oncorhynchus mykiss)

1999 ◽  
Vol 202 (16) ◽  
pp. 2177-2190 ◽  
Author(s):  
S.F. Perry ◽  
R. Fritsche ◽  
T.M. Hoagland ◽  
D.W. Duff ◽  
K.R. Olson
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Blood Pressures

Adult freshwater rainbow trout (Oncorhynchus mykiss) were exposed acutely (approximately 20 min) in a stepwise manner to increasing levels of environmental carbon dioxide ranging between 1.7 and 9.0 mmHg (0.23-1.2 kPa). Experiments were performed to examine, for the first time, the influence of hypercapnic acidosis on aspects of cardiovascular physiology including blood pressure, cardiac output and vascular resistance. Fish displayed dose (water CO(2) partial pressure) -dependent increases in ventral aortic (13–39 %) and dorsal aortic (17–54 %) blood pressures that reflected marked increases in systemic vascular resistance (16–78 %); branchial vascular resistance was unaffected by hypercapnia. At the highest level of hypercapnia (9.0 mmHg), central venous pressure was significantly elevated by 54 %. Although cardiac output remained constant, heart rate was significantly lowered by 4–7 beats min(−)(1) at the two highest levels of hypercapnia. To determine whether the cardiovascular responses to hypercapnia were being blunted by the stepwise increase in external P(CO2), a separate group of fish was exposed directly to a single step of hypercapnia (water P(CO2) 8.0 mmHg). The cardiovascular responses were similar to those exhibited by the more gradually exposed fish except that central venous pressure did not increase and the extent of the bradycardia was greater (13 beats min(−)(1)). After confirming the effectiveness of yohimbine in blocking the vasoconstrictory (α)-adrenoreceptors of the systemic vasculature, this antagonist was used as a tool to assess the importance of (α)-adrenoreceptor stimulation in promoting the cardiovascular responses during hypercapnia. Prior treatment of fish with yohimbine prevented the increased blood pressures and systemic vascular resistance during hypercapnia but did not influence the CO(2)-induced bradycardia. Plasma levels of catecholamines did not change during hypercapnia, and therefore the stimulation of the systemic (α)-adrenoreceptors presumably reflected increased sympathetic nerve activity. To determine whether the cardiovascular changes elicited by hypercapnia were related to acidosis-induced hypoxaemia, fish were exposed to hypoxia in a stepwise manner (water P(O2) 65–151 mmHg). The cardiovascular responses to hypoxia were markedly different from those to hypercapnia and consisted of pronounced increases in systemic and branchial vascular resistance, but only at the most severe level of hypoxia; ventral and dorsal aortic pressures were unaffected. The differences between the responses to hypercapnia and hypoxia, coupled with the smaller reductions in blood oxygen content during hypercapnia, support the hypothesis that the cardiovascular responses to CO(2) are direct and are unrelated to hypoxaemia.

Cardiac remodeling and increased central venous pressure underlie elevated stroke volume and cardiac output of seawater-acclimated rainbow trout

2017 ◽  
Vol 312 (1) ◽  
pp. R31-R39 ◽  
Author(s):  
Jeroen Brijs ◽  
Erik Sandblom ◽  
Esmée Dekens ◽  
Joacim Näslund ◽  
Andreas Ekström ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Rainbow Trout ◽  
Stroke Volume ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Central Venous ◽  
End Diastolic Volume ◽  
Gastrointestinal Blood Flow ◽  
Cardiac Filling

Substantial increases in cardiac output (CO), stroke volume (SV), and gastrointestinal blood flow are essential for euryhaline rainbow trout ( Oncorhyncus mykiss) osmoregulation in seawater. However, the underlying hemodynamic mechanisms responsible for these changes are unknown. By examining a range of circulatory and cardiac morphological variables of seawater- and freshwater-acclimated rainbow trout, the present study revealed a significantly higher central venous pressure (CVP) in seawater-acclimated trout (~0.09 vs. −0.02 kPa). This serves to increase cardiac end-diastolic volume in seawater and explains the elevations in SV (~0.41 vs. 0.27 ml/kg) and CO (~21.5 vs. 14.2 ml·min−1·kg−1) when compared with trout in freshwater. Furthermore, these hemodynamic modifications coincided with a significant increase in the proportion of compact myocardium, which may be necessary to compensate for the increased wall tension associated with a larger stroke volume. Following a temperature increase from 10 to 16.5°C, both acclimation groups exhibited similar increases in heart rate (Q10 of ~2), but SV tended to decrease in seawater-acclimated trout despite the fact that CVP was maintained in both groups. This resulted in CO of seawater- and freshwater-acclimated trout stabilizing at a similar level after warming (~26 ml·min−1·kg−1). The consistently higher CVP of seawater-acclimated trout suggests that factors other than compromised cardiac filling constrained the SV and CO of these individuals at high temperatures. The present study highlights, for the first time, the complex interacting effects of temperature and water salinity on cardiovascular responses in a euryhaline fish species.

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