scholarly journals A Preliminary Evaluation of the Mean Arterial Pressure as Measured by Cuff Oscillometry

2008 ◽  
Vol 21 (2) ◽  
pp. 166-171 ◽  
Author(s):  
H. Smulyan ◽  
P. R. Sheehe ◽  
M. E. Safar
2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Muhammad Nadeem ◽  
Mansoor Abbas Qaisar ◽  
Ali Hassan Al Hakami ◽  
Fateh Sher Chattah ◽  
Muhammad Muzammil ◽  
...  

Background: The mean arterial pressure serves as an expression of blood pressure in patients on chronic hemodialysis. Serum calcium phosphorus product is considered as a risk factor of vascular calcification that is associated with hypertension in the patients of end stage renal disease. The literature regarding this relationship is inconsistent therefore this study is designed to determine the correlation between calcium phosphorus product and mean arterial pressure among hemodialysis patients with end stage renal disease. Methods: A total of 110 patients of end stage renal disease on hemodialysis for at least one year, 20 to 60 years of age were included. Patients with primary or tertiary hyperparathyroidism, peripheral vascular disease, malignancy, hypertension secondary to any cause other than kidney disease were excluded. Mean arterial pressure was calculated according to the standard protocol in lying position. Blood samples for estimation of serum calcium and phosphorous were taken and was sent immediately to the laboratory for serum analysis. Results: Mean age was 44.17 ± 10.94 years. Mean calcium phosphorous product was 46.71 ± 7.36 mg/dl and mean arterial pressure was 103.61 ± 12.77 mmHg. The values of Pearson correlation co-efficient (r) were 0.863 for age group 20 to 40 years and 0.589 for age group 41 to 60 years. This strong positive correlation means that high calcium phosphorous product goes with high mean arterial pressure (and vice versa) for both the age groups. Conclusion: A strong positive relationship exists between the mean arterial pressure and calcium phosphorous product and is independent of patients’ age.


2020 ◽  
Vol 5 (2) ◽  
pp. 138-145
Author(s):  
Ely Kurniati ◽  
Rusnawati

Preeclampsia complicates 4-7% of pregnancies and remains the leading cause of maternal and fetal morbidity and mortality worldwide. Despite improvements in health care over the last decade, preeclampsia remains the second most common cause of maternal mortality in Indonesia. This study aims to determine whether the mean arterial pressure (MAP) is related to the incidence of preeclampsia in pregnant women at the Bontobangun Puskesmas, Bulukumba district for the period 2018 to 2019. This research uses a descriptive-analytic approach with Historical Cohort Studies, namely by looking at the cohort book of the history of blood pressure measurement results for pregnant women at the Bontobangun Public Health Center, Bulukumba Regency for the period 2018 to 2019. Determining the sample using the sampling method taken by purposive sampling. 31 samples of pregnant women who experienced preeclampsia and 31 controls were pregnant women with normal conditions who had certain criteria (matching) with the sample. The results explained that from the paired T-test results, the value of α> 0.037 so that it is said that there is a relationship between mean artery pressure (MAP) and the incidence of preeclampsia in pregnant women at Bontobangun puskesmas for the period 2018-2019.


2018 ◽  
Vol 6 (3) ◽  
pp. 57
Author(s):  
Urjindelger Tserensambuu ◽  
Ariunbold Chuluun-Erdene ◽  
Munkhtsetseg Janlav ◽  
Erkhembaatar Tudevdorj

Preeclampsia (PE) is a major cause of maternal and perinatal morbidity and mortality, particularly in developing countries. In Mongolia, preeclampsia and eclampsia have occurred among pregnancy complications at a rate of 25% in recent years. Recent studies in the literature have screened for preeclampsia by combining maternal factors with biomarkers. This study was conducted using prospective cohort research including 393 singleton pregnancies at 11–13+6 weeks. Maternal plasmas pregnancy-associated plasma protein-A (PAPP-A) and maternal serum placental growth factor (PlGF) were measured using Perkin Elmer time-resolved fluoroimmunoassay (DELFIA) kits, and the measurement of mean arterial pressure (MAP) was performed by automated devices and the uterine artery pulsatility index was measured by Doppler ultrasound. In the study population, there were 16.7% showing complicated preeclampsia. The receiver-operating characteristics (ROC) curve analysis showed a sensitivity of 71.21%, and a specificity of 75.54% when the mean arterial pressure cut-off was 89.5 mm; while a sensitivity of 33.36% and specificity of 77.68% were observed when the uterine artery mean pulsatility index (mPI) cut-off was 2.34; a sensitivity of 79.66% and specificity of 44.04% were observed when the PAPP-A cut-off was 529.1 mU/L; and a sensitivity of 74.58% and specificity of 46.6% were observed when the PlGF cut-off was 39.87 pg/mL. The detection rates following the combination of markers with the maternal history were as follows: 62.7% with mean arterial pressure, 69.5–82.9% with two markers 86.5% with three markers and 91.4% with four markers. In conclusion, the mean arterial pressure was highly sensitive and demonstrated its easy usage and cost-effectiveness as a predictive marker for the early screening of preeclampsia from other biomarkers.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3185-3185
Author(s):  
David R. Archer ◽  
Shawn Elms ◽  
Joshua Boutwell ◽  
Jennifer Perry ◽  
Roy Sutliff

Abstract Clinically, pulmonary hypertension is a major risk factor for mortality in adults with sickle cell disease. Contributing factors probably include red cell hemolysis and vaso-occlusive injury with their associated oxidative and inflammatory stimuli. Previously, we have described RBC hemolysis and endothelial oxidative stress in the Berkeley sickle mouse model and extend those studies in this work to investigate cardiovascular and endothelial dysfunction. Eight to ten month old homozygous and hemizygous Berkeley sickle mice and C57BL/6 control mice were used for all aspects of these experiments. In vivo measurements of mean arterial pressure and right ventricular pressures were conducted in fully anesthetized mice using a pressure transducer inserted in the carotid and right ventricle respectively. Following in vivo readings hearts were excised for measurement of ventricular mass. The ascending aorta was removed and cut into 5 mm rings for in vitro studies of agonist- induced contractility and relaxation. The mean arterial pressure of the hemizygous sickle mice (70.6 ± 3.4) was significantly lower than the control mice (86.0 ± 3.1) and the mean arterial pressure of homozygous sickle mice (59.0 ± 2.2 mmHg) was significantly lower than the hemizygous and control mice (p≤0.05 and p≤0.001, respectively). The right ventricular pressure showed a trend that approached significance (p= 0.08) such that pressures in homozygous mice were ≥ than those in hemizygous which were ≥ than those in control mice. Increased basal cardiac output was suggested by significant left ventricular hypertrophy. In vitro examination of potassium chloride activation of voltage gated calcium channels showed no significant difference in sensitivity or maximal contraction. Similarly, there was no difference in sensitivity to the α1 agonist, phenylephrine. However, both hemi- and homozygous mice showed a significant reduction in maximal force of contraction (normalized to cross sectional area when compared to controls. Maximal acetylcholine induced relaxation of aortic rings was significantly reduced (p≤0.05) in homozygous sickle mice compared to controls. The same effect was not seen with sodium nitroprusside induced relaxation indicating that the acetylcholine effect was not due to effects on the smooth muscle but was endothelium-dependent. The Berkeley mouse model shows cardiac hypertrophy consistent with the increased cardiac output associated with chronic anemia and a reduced basal mean arterial blood pressure similar to that seen in humans. 8–10 month old mice have increased right ventricular pressure and RV mass indicative of pulmonary hypertension. Further endothelial dysfunction is characterized by a reduction in the maximal relaxation elicited by acetylcholine. Therefore, the Berkeley mouse is a good model for investigating sickle related endothelial dysfunction.


1969 ◽  
Vol 47 (7) ◽  
pp. 619-626 ◽  
Author(s):  
A. Gonda ◽  
N. Wong ◽  
J. F. Seely ◽  
J. H. Dirks

The effects of unilateral vasodilatation and alterations in the mean arterial pressure upon the renal handling of calcium and magnesium were studied by clearance methods in dogs. Unilateral vasodilatation was produced by infusion of acetylcholine or bradykinin into the left renal artery, while arterial pressure was altered by aortic constriction, carotid occlusion and vagotomy, or by systemic infusion of angiotensin. Urinary electrolyte excretion was increased markedly by the infusion of each vasodilator and also varied directly with the mean arterial pressure, despite the absence of any significant changes in the filtered load. The fractional excretion of both calcium and magnesium correlated significantly with that of sodium. These results indicate that acute changes in renal hemodynamics modify the tubular reabsorption of divalent cations as well as alter sodium reabsorption.


1984 ◽  
Vol 66 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Robert Fagard ◽  
Anne Cattaert ◽  
Paul Lijnen ◽  
Jan Staessen ◽  
Luc Vanhees ◽  
...  

1. The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin—angiotensin—aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. 2. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. 3. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position. 4. Exercise capacity as measured by peak oxygen uptake was similar during ketanserin (3.09 ± se 0.12 litres/min) and during placebo (3.11 ± 0.13). 5. The data suggest that 5-hydroxytryptamine can have only a small role, if any, in pressure homoeostasis in sodium replete man at rest in recumbency. At moderate and heavy levels of exercise, the results are compatible with a role for 5-hydroxytryptamine in pressure regulation. Activation of the sympathetic nervous system by ketanserin is suggested by increases of plasma catecholamines, heart rate, cardiac output and plasma renin. The suppression of plasma aldosterone suggests that 5-hydroxytryptamine may have a role in the regulation of aldosterone secretion which is independent of angiotensin II.


1992 ◽  
Vol 12 (3) ◽  
pp. 491-499 ◽  
Author(s):  
Antal G. Hudetz ◽  
Richard J. Roman ◽  
David R. Harder

The purpose of this study was to characterize spontaneous oscillations of blood flow in the cerebral cortex of anesthetized rats under control conditions and after mean arterial pressure was altered by various means. Blood flow was monitored using a laser–Doppler flowmeter through the closed cranium. Spontaneous flow oscillations with amplitudes of 14–30% of the mean flow and frequencies of 4–11 cycles/min were recorded when arterial pressures were less than 90 mm Hg. Stepwise hemorrhagic hypotension and unilateral carotid occlusion increased the amplitude of oscillations. The amplitude of oscillations was negatively correlated with the level of mean arterial pressure after manipulation with norepinephrine or sodium nitroprusside. The oscillations were reversibly abolished during dilation of the cerebral circulation by elevating the inspired carbon dioxide content to 5%. The frequency of flow oscillations was very stable during all of the above maneuvers except during the infusion of norepinephrine, which increased the oscillation frequency slightly. The results suggest that flow oscillations are determined primarily by cerebral arterial pressure.


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