Preeclampsia is a disorder unique to human pregnancy. Its basic pathophysiology is arteriolar vasoconstriction characterized by increased systemic vascular resistance that is inappropriate for the high level of cardiac output in pregnancy.1–3 The hemodynamics of preeclampsia have been reported to be a continuum ranging from relatively normal high cardiac output and low systemic vascular resistance to more dysfunctional low cardiac output and high systemic vascular resistance.4
At its most severe, preeclampsia can be life-threatening to women and their fetuses. Life-threatening complications include malignant hypertension, stroke, renal failure, and placental abruption. Elevated hydrostatic forces with reduced colloidal oncotic pressure can create a filtration imbalance, displacing intravascular fluid into the surrounding interstitium and potentially causing pulmonary edema.
Pulmonary edema associated with severe preeclampsia is one indication for invasive hemodynamic monitoring by pulmonary artery catheterization.5 Invasive hemodynamic monitoring is not used routinely in uncomplicated severe preeclampsia. Noninvasive techniques, such as thoracic electrical bioimpedance, have been investigated as alternatives in critically ill, non-pregnant women, particularly for measuring cardiac output.6–8 Thoracic electrical bioimpedance has also been used to measure hemodynamic performance in obstetric situations from normal pregnancies at term to severe preeclampsia.9,10 Thoracic electrical bioimpedance can also indirectly measure thoracic fluids.
In the present study we measured the level of thoracic-fluid conductivity associated with pulmonary edema in peripartum women by noninvasive thoracic electrical bioimpedance.
Materials and Methods
One hundred thirty-four pregnant women were recruited between March 1994 and August 1996 as a convenience sample in an observational study of thoracic electrical bioimpedance monitoring of hemodynamic performance. Twelve subjects had pulmonary edema, 33 had severe preeclampsia, 17 had mild preeclampsia, and 72 were in uncomplicated early labor. A convenience sample was chosen because this study was observational, and there was a lack of published normative values for thoracic-fluid conductivity in peripartum women.
Mild and severe preeclampsia were diagnosed on the basis of ACOG clinical criteria.11 Pulmonary edema was diagnosed by clinical and radiologic criteria in ten cases of severe preeclampsia, one case of urosepsis, and one case of volume overload secondary to postoperative transfusion. Clinical and radiologic criteria included maternal shortness of breath, tachycardia (over 100 beats per minute), tachypnea (over 24 respirations per minute), rales and rhonchi on lung auscultation, reduced partial pressure of arterial oxygen (typically under 80 mm Hg with room air), reduced pulse oximetry (typically under 95% with room air), and chest radiographic findings consistent with pulmonary edema. Demographic and clinical characteristics of the women are given in Table 1.
Thoracic electrical bioimpedance (Model NCC0M3-R7S; BoMed, Irvine, CA) is a noninvasive, operator-independent technique of hemodynamic monitoring. All biologic tissues have unique electrical properties. Except for nerve tissue, blood is the most electrically conductive. Thoracic electrical bioimpedance takes advantage of detectable changes in resistance of the thoracic cavity to constant, low-voltage, high-frequency, alternating current applied to the thorax by electrodes. Thoracic-fluid conductivity is calculated as 1/thoracic impedance (Z) to an alternating transthoracic electrical current (2.5 mA at 70 KHz) × 100.
Women identified as good candidates for the study were approached and informed consent was obtained according to institutional review board-approved protocol. All subjects were at least 18 years old and at least 24 weeks' gestation. Subjects were recruited before initiation of magnesium sulfate therapy, antihypertensive therapy, or placement of epidural catheters for labor anesthesia. One hundred thirty-seven women who met inclusion criteria were approached and 134 consented.
Thoracic electrical bioimpedance electrodes were affixed at appropriate sites with self-adhering tape. After placement of thoracic electrical bioimpedance electrodes, women were stabilized in the left-lateral, recumbent position and monitored for at least 15 minutes, and the highest measured thoracic-fluid conductivity value was recorded. The highest value, rather than the mean, was chosen because we wanted to identify a thoracic-fluid conductivity threshold value associated with pulmonary edema. The highest thoracic-fluid conductivity value was correlated with each patient's clinical presentation. Kruskal-Wallis one-way analysis of variance by ranks (nonparametric analysis) was used to compare the mean thoracic-fluid conductivity values for each group. Pairwise comparisons between groups were done with the Mann-Whitney test. A receiver operating characteristic (ROC) curve was used to identify thoracic-fluid conductivity values associated with pulmonary edema. Results were expressed as mean ± standard deviation (SD) and significance was established at P < .05.
Thoracic-fluid conductivity values for the 12 women with pulmonary edema were compared with the values of women with severe preeclampsia (n = 33), mild preeclampsia (n = 17), or uncomplicated early labor (n = 72). Thoracic-fluid conductivity values were significantly higher for women with pulmonary edema compared with the other groups (Table 2). The mean thoracic-fluid conductivity value increased in a stepwise manner. The lowest values were in women with uncomplicated early labor. Values were successively higher for women with mild preeclampsia, severe preeclampsia, and pulmonary edema.
The ROC curve identified thoracic-fluid conductivity of 65 kohm−1 as a threshold value strongly associated with peripartum pulmonary edema (Figure 1), with a sensitivity of 83.3%, specificity of 86.9%, positive predictive value of 38.5%, and negative predictive value of 98.1%. In women with a thoracic-fluid conductivity of at least 65 kohm−1 (ten of 29; 34.5%), the relative risk (RR) of pulmonary edema was 18.2 (95% confidence interval [CI] 4.2, 78.8; P < .001) compared with women whose thoracic-fluid conductivity values were less than 65 kohm−1 (two of 105; 1.9%).
It was not surprising that thoracic-fluid conductivity values could be stratified by severity of preeclampsia. Because clinicians lack noninvasive means to assess hemodynamic status or pulmonary fluid, obstetricians have only been able to intervene reactively to the clinical progression of preeclampsia. Interventions are usually delayed until women present with overt complications associated with preeclampsia. Thoracic electrical bioimpedance might allow clinicians to proactively treat preeclamptic women to prevent those complications.
The clinical heterogenicity and progressive nature of preeclampsia are well known. Thoracic electrical bioimpedance provides a safe, easy, and economic assessment of hemodynamic performance and thoracic-fluid conductivity. Women with pulmonary edema had higher thoracic-fluid conductivity values than women who had preeclampsia or were in early labor. Ten of 12 pregnant women with pulmonary edema also had severe preeclampsia.11
Women with thoracic-fluid conductivity values at or near 65 kohm−1, but without symptoms of pulmonary edema, might be candidates for alternative laboratory (colloid oncotic pressure) or hemodynamic (echocardiography) evaluation and medical intervention to reduce the risk of pulmonary edema. Possible interventions include reduction of intravenous infusion rates, preload or afterload reduction, or even delivery. Women with progressively increasing thoracic-fluid conductivity values might also be candidates for proactive intervention. Thoracic electrical bioimpedance might enable us to assess the efficacy of interventions such as antihypertensives to decrease afterload, diuretics to decrease preload, or inotropic drugs to increase cardiac output, by allowing clinicians to observe the effect of those interventions on thoracic-fluid conductivity and other indicators of hemodynamic performance.
Limitations of this study include the use of a convenience sample. We believe that all eligible subjects with pulmonary edema were recruited during the study period, but the women in other groups were recruited based on availability of the investigator and the monitor. As a result, the severe preeclampsia, mild preeclampsia, and normal early labor groups were of varying sizes. The small size of the pulmonary edema and mild preeclampsia groups and their unequal variances required that nonparametric statistical analyses be done.
Although not addressed in this study, thoracic electrical bioimpedance monitoring might also allow researchers to differentiate cardiogenic from noncardiogenic pulmonary edema by evaluating other hemodynamic factors. Cardiogenic pulmonary edema is typically associated with low measures of cardiac index. In preeclampsia, altered cardiac performance measures have been linked with very high systemic vascular resistance.12,13 The relationship between extremes in these parameters of cardiac performance and the occurrence of pulmonary edema should continue to be a fruitful avenue for future investigation.
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