Effect of Passive Leg Raising on Systemic Hemodynamics of Pregnant Women: A Dynamic Assessment of Maternal Cardiovascular Function at 22–24 Weeks of Gestation

Abstract

ObjectiveTo investigate functional hemodynamic response to passive leg raising in healthy pregnant women and compare it with non-pregnant controls.Materials and MethodsThis was a prospective cross-sectional study with a case-control design. A total of 108 healthy pregnant women at 22–24 weeks of gestation and 54 non-pregnant women were included. Cardiac function and systemic hemodynamics were studied at baseline and 90 seconds after passive leg raising using non-invasive impedance cardiography.Main outcome measuresTrends and magnitudes of changes in impedance cardiography derived parameters of cardiac function and systemic hemodynamics caused by passive leg raising, and preload responsiveness defined as >10% increase in stroke volume or cardiac output after passive leg raising compared to baseline.ResultsThe hemodynamic parameters in both pregnant and non-pregnant women changed significantly during passive leg raising compared to baseline, but the magnitude and trend of change was similar in both groups. The stroke volume increased both in pregnant (p = 0.042) and non-pregnant (p = 0.018) women, whereas the blood pressure and systemic vascular resistance decreased (p<0.001) following passive leg raising in both groups. Only 14.8% of pregnant women and 18.5% of non-pregnant women were preload responsive and the difference between groups was not significant (p = 0.705).ConclusionStatic measures of cardiovascular status are different between healthy pregnant and non-pregnant women, but the physiological response to passive leg raising is similar and not modified by pregnancy at 22–24 weeks of gestation. Whether physiological response to passive leg raising is different in earlier and later stages of pregnancy merit further investigation.

Cardiac output and related haemodynamics during pregnancy: a series of meta-analyses

“…The non-pregnant data were collected from eligible studies that reported data for a non-pregnant control or preconception group 4 5 9 25 27–31. Details of the 39 included studies are reported in table 1.…”

Maternal cardiac function, uterine artery hemodynamics and natriuretic peptides at 22‐24 weeks of gestation and subsequent development of hypertensive disorders of pregnancy

“…6 Woman's age, present weight and height were input into the ICG machine, central venous pressure (CVP) was preset at 4 mmHg, and pulmonary artery occlusion pressure (PAOP) was preset at 8 mmHg. 6 Woman's age, present weight and height were input into the ICG machine, central venous pressure (CVP) was preset at 4 mmHg, and pulmonary artery occlusion pressure (PAOP) was preset at 8 mmHg.…”

“…Maternal cardiac function and systemic hemodynamics were investigated using impedance cardiography (ICG; Philips Medical Systems, Androver, MA, USA) as described previously. 6,7,23 ICG is a validated noninvasive technique 24 that allows continuous recording and onscreen display of measured parameters. A single investigator (Å.V.)…”

“…1,2 Passive leg raising (PLR), a maneuver of lifting the legs from the horizontal plane to 45° using a pivotable bed, provides a rapid reversible auto-fluid challenge by increasing venous return to the heart. 6,7 Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are the most important members of the natriuretic peptide family that are involved in maintaining volume homeostasis and endothelial function. 4,5 Using this method, we previously showed that pregnant women have a limited preload reserve.…”

“…4,5 Using this method, we previously showed that pregnant women have a limited preload reserve. 6,7 Atrial natriuretic peptide (ANP), brain natriuretic peptide(BNP) and C-type natriuretic peptide (CNP) are the most important members of the natriuretic peptide family that are involved in maintaining volume homeostasis and endothelial function. ANP and BNP are of myocardial origin 8 and are known to be produced in response to myocardial wall stress or pressure overload.…”