Reduced nocturnal cardiac output associated with preeclampsia is minimized with the use of nocturnal nasal CPAP.

STUDY OBJECTIVES Recent studies suggest a specific association between intrauterine growth restriction that commonly occurs in preeclampsia and decreased maternal cardiac output. Sleep is associated with marked hypertension in preeclampsia. We therefore aimed to determine how sleep influences other hemodynamic parameters in preeclampsia, specifically to determine if sleep-induced exacerbation of hypertension was associated with reductions in cardiac output. STUDY DESIGN Randomized controlled trial of nasal continuous positive airway pressure. SETTING King George V, Royal Prince Alfred Hospital. PATIENTS Twenty-four women with severe preeclampsia and 15 control nulliparous subjects. INTERVENTION Full polysomnography including beat-to-beat blood-pressure recording. Stroke volume, heart rate, cardiac output, total peripheral resistance, and ejection duration were derived from the blood pressure waveform. Half of the 24 preeclamptic subjects were randomly assigned to receive treatment with nasal continuous positive airway pressure and the other half to receive no treatment. MEASUREMENTS AND RESULTS Heart rate, stroke volume, and cardiac output were similar in controls and patients with preeclampsia during wakefulness, while total peripheral resistance was significantly elevated. Sleep induced marked decrements in heart rate, stroke volume, and cardiac output in preeclamptic subjects and resulted in further increments in total peripheral resistance. Cardiac output during sleep was correlated with fetal birth weight (r2 = 0.64, P < .001). When preeclamptic subjects were treated with continuous positive airway pressure, reductions in cardiac output were minimized, while increments in total peripheral resistance were also reduced. CONCLUSIONS These data indicate that sleep is associated with adverse hemodynamic changes in women with preeclampsia. These changes are minimized with the use of continuous positive airway pressure. Reduced cardiac output during sleep may have an adverse effect on fetal development.

[1]  S. Boschi,et al.  Relationship of systemic hemodynamics, left ventricular structure and function, and plasma natriuretic peptide concentrations during pregnancy complicated by preeclampsia. , 2000, American journal of obstetrics and gynecology.

[2]  C. Sullivan,et al.  Nasal continuous positive airway pressure reduces sleep-induced blood pressure increments in preeclampsia. , 2000, American journal of respiratory and critical care medicine.

[3]  E. van Cauter,et al.  Interrelations between sleep and the somatotropic axis. , 1998, Sleep.

[4]  P. Beeby,et al.  New South Wales population‐based birthweight percentile charts , 1996, Journal of paediatrics and child health.

[5]  Yuh‐Cheng Yang,et al.  Central and peripheral hemodynamics in severe preeclampsia , 1996, Acta obstetricia et gynecologica Scandinavica.

[6]  B. Sibai,et al.  A longitudinal study of cardiac output in normal human pregnancy. , 1994, American journal of obstetrics and gynecology.

[7]  Lippincott Williams Wilkins,et al.  National High Blood Pressure Education Program Working Group Report on Hypertension in Diabetes , 1994, Hypertension.

[8]  J. Dripps,et al.  A transducer for detecting foetal breathing movements using PVDF film. , 1993, Physiological measurement.

[9]  J R Jansen,et al.  Computation of aortic flow from pressure in humans using a nonlinear, three-element model. , 1993, Journal of applied physiology.

[10]  P. Rubin,et al.  Comparative study of pressor and heart rate responses to angiotensin II and noradrenaline in pregnant and non-pregnant women. , 1992, Clinical science.

[11]  T. Benedetti,et al.  The effect of maternal hemodynamics on fetal growth in hypertensive pregnancies. , 1991, American journal of obstetrics and gynecology.

[12]  J. Pivarnik,et al.  Central hemodynamic assessment of normal term pregnancy , 1989 .

[13]  R. Boys,et al.  Serial study of factors influencing changes in cardiac output during human pregnancy. , 1989, The American journal of physiology.

[14]  A. Murray,et al.  Reproducibility of cardiac output measurement by cross sectional and Doppler echocardiography. , 1988, British heart journal.

[15]  H. Nisell,et al.  Maternal Hemodynamics and Impaired Fetal Growth in Pregnancy-Induced Hypertension , 1988, Obstetrics and gynecology.

[16]  S. Hunter,et al.  Haemodynamic changes during the puerperium: a Doppler and M‐mode echocardiographic study , 1987, British journal of obstetrics and gynaecology.

[17]  A. Abdulla,et al.  Serial noninvasive evaluation of cardiovascular hemodynamics during pregnancy. , 1987, American journal of obstetrics and gynecology.

[18]  K. Sagar,et al.  Echocardiographic left ventricular mass to differentiate chronic hypertension from preeclampsia during pregnancy. , 1986, American journal of obstetrics and gynecology.

[19]  A. Piela,et al.  Left ventricular function in preeclamptic patients: an echocardiographic study. , 1983, American journal of obstetrics and gynecology.

[20]  R. Resnik,et al.  Effects of a Natural Volume Overload State (Pregnancy) on Left Ventricular Performance in Normal Human Subjects , 1978, Circulation.

[21]  W. Walters,et al.  Cardiac output at rest during pregnancy and the puerperium. , 1966, Clinical science.

[22]  P. Rosso,et al.  Maternal hemodynamic adjustments in idiopathic fetal growth retardation. , 1993, Gynecologic and obstetric investigation.

[23]  N. T. Smith,et al.  A simple device for the continuous measurement of cardiac output. Its model basis and experimental verification , 1983 .

[24]  A. Rechtschaffen A manual of standardized terminology, techniques and scoring system for sleep of human subjects , 1968 .

[25]  A. Rechtschaffen,et al.  A manual of standardized terminology, technique and scoring system for sleep stages of human subjects , 1968 .