The effect of Trendelenburg and modified trendelenburg positions on cardiac output, blood pressure, and oxygenation: a preliminary study

1994 ◽  
Vol 3 (5) ◽  
pp. 382-386 ◽  
Author(s):  
CL Ostrow ◽  
E Hupp ◽  
D Topjian

BACKGROUND: Although we have insufficient knowledge about the effects of Trendelenburg positions on various hemodynamic parameters, these positions are frequently used to influence cardiac output and blood pressure in critically ill patients. OBJECTIVES: To determine the effect of Trendelenburg and modified Trendelenburg positions on five dependent variables: cardiac output, cardiac index, mean arterial pressure, systemic vascular resistance, and oxygenation in critically ill patients. METHODS: In this preliminary study subjects were 23 cardiac surgery patients (mean age, 55; SD, 8.09) who had a pulmonary artery catheter for cardiac output determination and who were clinically stable, normovolemic and normotensive. Baseline measurements of the dependent variables were taken in the supine position. Patients were then placed in 10 degrees Trendelenburg or 30 degrees modified Trendelenburg position. The dependent variables were measured after 10 minutes in each position. A 2-period, 2-treatment crossover design with a preliminary baseline measurement was used. RESULTS: Five subjects were unable to tolerate Trendelenburg position because of nausea or pain in the sternal incision. In the 18 who were able to tolerate both position changes, no statistically significant changes were found in the five dependent variables. Changes in systemic vascular resistance over time approached statistical significance and warrant further study. CONCLUSIONS: This preliminary study does not provide support for Trendelenburg positions as a means to influence hemodynamic parameters such as cardiac output and blood pressure in normovolemic and normotensive patients.

2019 ◽  
Vol 126 (2) ◽  
pp. 444-453 ◽  
Author(s):  
Silvana Roberto ◽  
Raffaele Milia ◽  
Azzurra Doneddu ◽  
Virginia Pinna ◽  
Girolamo Palazzolo ◽  
...  

Metaboreflex is a reflex triggered during exercise or postexercise muscle ischemia (PEMI) by metaboreceptor stimulation. Typical features of metaboreflex are increased cardiac output (CO) and blood pressure. Patients suffering from metabolic syndrome display hemodynamic abnormalities, with an exaggerated systemic vascular resistance (SVR) and reduced CO response during PEMI-induced metaboreflex. Whether patients with type 2 diabetes mellitus (DM2) have similar hemodynamic abnormalities is unknown. Here we contrast the hemodynamic response to PEMI in 14 patients suffering from DM2 (age 62.7 ± 8.3 yr) and in 15 age-matched controls (CTLs). All participants underwent a control exercise recovery reference test and a PEMI test to obtain the metaboreflex response. Central hemodynamics were evaluated by unbiased operator-independent impedance cardiography. Although the blood pressure response to PEMI was not significantly different between the groups, we found that the SVR and CO responses were reversed in patients with DM2 as compared with the CTLs (SVR: 392.5 ± 549.6 and −14.8 ± 258.9 dyn·s−1·cm−5; CO: −0.25 ± 0.63 and 0.46 ± 0.50 l/m, respectively, in DM2 and in CTL groups, respectively; P < 0.05 for both). Of note, stroke volume (SV) increased during PEMI in the CTL group only. Failure to increase SV and CO was the consequence of reduced venous return, impaired cardiac performance, and augmented afterload in patients with DM2. We conclude that patients with DM2 have an exaggerated vasoconstriction in response to metaboreflex activation not accompanied by a concomitant increase in heart performance. Therefore, in these patients, blood pressure response to the metaboreflex relies more on SVR increases rather than on increases in SV and CO. NEW & NOTEWORTHY The main new finding of the present investigation is that subjects with type 2 diabetes mellitus have an exaggerated vasoconstriction in response to metaboreflex activation. In these patients, blood pressure response to the metaboreflex relies more on systemic vascular resistance than on cardiac output increments.


1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.


1992 ◽  
Vol 263 (5) ◽  
pp. R1147-R1155 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals

Our purpose was to test the hypothesis that human aging alters sympathoadrenal-circulatory control of arterial blood pressure during orthostasis. Plasma catecholamine and hemodynamic adjustments to two different forms of orthostatic stress, lower body suction (-10 to -50 mmHg) and standing, were determined in 14 young (26 +/- 1 yr) and 13 older (64 +/- 1) healthy, normally active men. During quiet supine rest, cardiac output tended to be lower and systemic vascular resistance higher in the older men, but no other differences were observed. On average, arterial blood pressure was well maintained during both forms of orthostasis in the two groups; the older men actually demonstrated better maintenance of pressure (P < 0.05) and a lesser incidence of orthostatic hypotension than the young men during lower body suction. Despite a blunted reflex tachycardia during orthostatic stress (P < 0.05), cardiac output tended to decrease less in the older men because of a smaller decline in stroke volume (P < 0.05, suction only), whereas the reflex increases in systemic vascular resistance were not different in the two groups. The whole forearm vasoconstrictor response tended to be attenuated in the older men during lower body suction, but was identical in the two groups with standing. Forearm skin vascular resistance was unaltered during lower body suction in both groups. Orthostasis-evoked increases in antecubital venous plasma norepinephrine concentrations were similar in the young and older men, whereas little or no increases in plasma epinephrine concentrations were observed in either group.(ABSTRACT TRUNCATED AT 250 WORDS)


Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 373-380 ◽  
Author(s):  
Lizzy M. Brewster ◽  
Yentl C. Haan ◽  
Aeilko H. Zwinderman ◽  
Bert Jan van den Born ◽  
Gert A. van Montfrans

The ATP-regenerating enzyme CK (creatine kinase) is strongly associated with blood pressure, which lowers upon experimental CK inhibition. The enzyme is thought to affect cardiovascular hemodynamics through enhanced systemic vascular resistance, stroke volume, and cardiac contractility, but data on these parameters are lacking. We hereby report hemodynamics by CK levels in the multiethnic, cross-sectional HELIUS study (Healthy Life in an Urban Setting). Physical examination included sitting brachial blood pressure and noninvasively assessed supine systemic vascular resistance, stroke volume, cardiac output, and cardiac contractility, which we associated with resting plasma CK. Data from 14 937 men and women (mean age, 43.3; SD, 12.9) indicated that per log CK increase, blood pressure increased with 20.2 (18.9–21.4) mm Hg systolic/13.0 (12.2–13.7) diastolic, an odds ratio for hypertension of 6.1 (5.1–7.2). Outcomes were similar by sex, body mass index, and ancestry, although higher blood pressures in men, with overweight/obesity, and West-African ancestry were partially explained by higher CK, with an adjusted increase in systolic/diastolic pressure of 10.5 (10.0–10.9)/6.4 (6.0–6.7) mm Hg per log CK increase. Systemic vascular resistance, stroke volume, cardiac output, and cardiac contractility (n=7876), increased by respectively 20%, 39%, 14%, and 23% SD per log CK increase. This study indicates that the association of CK with blood pressure likely results from an increase in systemic vascular resistance and stroke volume. These data expand the knowledge on the nature of hypertension associated with CK and may inform further experiments on CK inhibition as a means to lower blood pressure.


1998 ◽  
Vol 94 (4) ◽  
pp. 347-352 ◽  
Author(s):  
W. Wieling ◽  
J. J. Van Lieshout ◽  
A. D. J. Ten Harkel

1. The initial circulatory adjustments induced by head-up tilt and tilt-back were investigated in six healthy subjects (aged 30–58 years) and six patients with orthostatic hypotension due to pure autonomic failure (aged 33–65 years). 2. Continuous responses of finger arterial pressure and heart rate were recorded by Finapres. A pulse contour algorithm applied to the arterial pressure waveform was used to compute stroke volume responses. 3. In the healthy subjects, head-up tilt induced gradual circulatory adjustments. After 1 min upright stroke volume and cardiac output had decreased by 39 ± 9% and 26 ± 10% respectively. Little change in mean blood pressure at heart level (+1 ± 7 mmHg) indicated that systemic vascular resistance had increased by 39 ± 24%. The gradual responses to head-up tilt contrasted with the pronounced and rapid circulatory responses upon tilt-back. After 2–3 s a rapid increase in stroke volume (from 62 ± 8% to 106 ± 10%) and cardiac output (from 81 ± 11% to 118 ± 20%) was observed with an overshoot of mean arterial pressure above supine control values of 16 ± 3 mmHg at 7 s. In the patients a progressive fall in blood pressure on head-up tilt was observed. After 1 min upright mean blood pressure had decreased by 59 ± 8 mmHg. No change in systemic vascular resistance and a larger decrease in stroke volume (60 ± 7%) and cardiac output (53 ± 8%) were found. On tilt-back a gradual recovery of blood pressure was observed. 4. In healthy humans upon head-up tilt neural compensatory mechanisms are very effective in maintaining arterial pressure at heart level. The gradual circulatory adjustments to head-up tilt in healthy subjects contrast with the pronounced and abrupt circulatory changes on tilt-back. In patients with a lack of neural circulatory reflex adjustments, gradual blood pressure decreases to head-up tilt and gradual increases to tilt-back are observed.


2008 ◽  
Vol 109 (5) ◽  
pp. 856-863 ◽  
Author(s):  
Eldrid Langesæter ◽  
Leiv Arne Rosseland ◽  
Audun Stubhaug

Background Prevention of hemodynamic instability during cesarean delivery during spinal anesthesia has been the aim of several studies. Noninvasive monitoring has been used in all previous studies. This is the first study in healthy pregnant women with continuous invasive recording of arterial blood pressure, cardiac output, and systemic vascular resistance. The aim of this randomized trial was to compare the effects of two different intrathecal doses of bupivacaine, with or without intravenous phenylephrine infusion, on cardiac output and systolic blood pressure. Methods In this double-blinded study, 80 healthy women scheduled to undergo elective cesarean delivery were randomly assigned to one of four different groups receiving 7 mg spinal bupivacaine with or without a concomitant low-dose infusion of phenylephrine (0.25 microg . kg(-1) . min(-1)) or 10 mg spinal bupivacaine with or without phenylephrine infusion. All patients had 4 microg sufentanil added to the spinal solution and had cohydration with 750 ml saline, 0.9%. Results The low-dose spinal bupivacaine group with intravenous phenylephrine infusion was the most stable group regarding all hemodynamic variables. The authors found significant differences between this group and the group that was given the high dose of bupivacaine with intravenous placebo infusion regarding cardiac output (P = 0.005), systemic vascular resistance (P &lt; 0.0001), and systolic blood pressure (P = 0.012). Conclusions This study shows that low-dose bupivacaine (with sufentanil), combined with a low-dose infusion of phenylephrine and moderate cohydration, gives the best hemodynamic stability during spinal anesthesia for cesarean delivery.


2000 ◽  
Vol 279 (2) ◽  
pp. R484-R491 ◽  
Author(s):  
Nagi Mimassi ◽  
Fatemeh Shahbazi ◽  
Jörgen Jensen ◽  
Dominique Mabin ◽  
J. Michael Conlon ◽  
...  

The cardiovascular effects of centrally and peripherally administered synthetic trout urotensin (U)-I, a member of the corticotropin-releasing hormone family of neuroendocrine peptides, were investigated in unanesthetized rainbow trout Oncorhynchus mykiss. Intracerebroventricular injections of U-I (5.0 and 12.5 pmol) produced a sustained increase in mean dorsal aortic blood pressure (PDA) without significant change in heart rate (HR). This elevation in PDA was associated with an increase in cardiac output, but systemic vascular resistance did not change. Intra-arterial injection of U-I (12.5–500 pmol) evoked a dose-dependent increase in PDA, but in contrast to the hemodynamic effects of centrally administered U-I, the hypertensive effect was associated with an increase in systemic vascular resistance and an initial fall in cardiac output. HR did not change or underwent a delayed increase. Pretreatment of trout with prazosin, an α-adrenoreceptor antagonist, completely abolished the rise in arterial blood pressure after intra-arterial administration of U-I, which was replaced by a sustained hypotension and tachycardia. Trout U-I produced a dose-dependent (pD2 = 7.74 ± 0.08) relaxation of preconstricted rings of isolated trout arterial vascular smooth muscle, suggesting that the primary action of the peptide in the periphery is vasorelaxation that is rapidly reversed by release of catecholamines. Our results suggest that U-I may regulate blood pressure in trout by acting centrally as a neurotransmitter and/or neuromodulator and peripherally as a neurohormone functioning either as a locally acting vasodilator or as a potent secretagogue of catecholamines.


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