PubMed · 16648080
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Werner Irnich. 2006-03-03. Bioelectricity.. https://doi.org/10.1016/j.hrthm.2006.02.1027
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Transthoracic and whole-body bioimpedance monitoring has been commercially available for years; however, attention to its use as a diagnostic and event-monitoring modality has not been routinely applied in patients with heart failure (HF). In 2005, intrathoracic bioimpedance monitoring via an implantable cardioverter defibrillator brought new awareness of bioimpedance technology. In addition, new knowledge about congestion in HF, including length of time a patient is congested before seeking emergency care, lack of sensitivity of common signs and symptoms used to monitor congestion and diagnose HF exacerbation, and poor clinical outcomes when hypervolemia is present, heightened the need for more aggressive assessment and management. Bioimpedance device monitoring provides data needed to make treatment decisions that promote euvolemia and optimal cardiac performance. This review summarizes three options for measurement of bioimpedance hemodynamic data, discusses its use in preventing HF hospitalization, and describes issues that need to be overcome before bioimpedance monitoring can be routinely used in HF management.
OBJECTIVE: The purpose of this study was to determine whether fetuses with a congenital heart defect demonstrate changes in cerebrovascular impedance. STUDY DESIGN: Fetal echocardiograms from January 2001 to May 2005 were reviewed. Cases had sonographically diagnosed congenital heart defects; control subjects were gestational age-matched fetuses with normal echocardiograms. The pulsatility index in the middle cerebral artery was used to measure impedance to cerebral blood flow. Abnormal middle cerebral artery pulsatility index was defined as less than the 5th percentile. Cases were subgrouped into mixing versus nonmixing lesions. RESULTS: Of 142 total fetuses, there were significantly more abnormal middle cerebral artery pulsatility indices in the cases (5/71) than in the control subjects (0/71; P = .023); all abnormal middle cerebral artery pulsatility indices occurred in the fetuses with admixing cardiac lesions. CONCLUSION: Fetuses with congenital heart defect are significantly more likely to have decreased cerebrovascular impedance. This may represent a marker of cerebral hypoxemia that is due to intracardiac mixing of oxygenated and deoxygenated blood. Theoretically, this hypoxemia may contribute to the cause of abnormal neurologic development in these infants.
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