Calcium channel blockers may cause periferal edema. Does it contribute further pathological fluid retension?
In my opinion, it depends on the type of preeclampsia. In late-onset type vessels are relaxed, therefore nifedipine is not the best choice.
Yes, you are right, howerever, when the clinical features are characteristic (obesity, serious edema, mild hypertension with just significant proteinuria appearing after the 34th week, and normal weight's or large fetus) one can be sure that this is not a true (early-onset) PE. In such ceses we use alfa-methydopa, urapidil and frequently diuretics (when hemoconcentration is not serious).
In cases with doubt we do hemodynamic examination with impedance cardiograph.
The overly aggressive control of the BP may compromise maternal perfusion of the intervillous space and adversely impact fetal oxygenation.
You are right again, but it is true only in the hypoperfusion (early-onset) PE. In this type the hypertension must have a compensatoric nature (simply: perfusion = pressure / resistance). In the true PE microcirculation is diminished and basically responsible for increased resistance. Therefore, decrease of pressure will decrease the blood supply of the placenta and other organs as well. In late-onset or hyperpefusion (I like this) type PE (this is PE at all?) placental circulation is good (markers of placental function are mostly normal). Easterlin suggested beta-blockers.
So, the goal is to distinguesh PE type and use dilators carefully is early-onset cases (Prof. Wallenburg applied parallel 200-300 ml infusion) and avoid it in late-onset type.
I think, PE definition requires a new classification.
The fetus increases angiotensin( A-II )and vasopressin( AVP) in preeclampsia(both early onset and late onast) , suggesting that fetus makes an effort to increase blood presure (BP) in the feto-placental unit.Fetal BP is much lower than mother, in addition BP of placental peripheral circulation is further lower than mother. When nifedipine is administered to preeclamsia patients, it easily move to the feto-placental unit and then it block the fetal action to hypoxia, namely an effort to increase BP.
Agents administered to mother, more or less, enters fetal circulation. Antihypertensives are known to decrease fetal weight (probably through lowering maternal and fetal BP). This effect could be the consenquence you discussed above.
I do not know any data about fetal hemodynamics. I woud appreciate if you let me know the source of your information.
Theoretically we could evaluate fetal hemodynamical response to hypotensive drugs using spectral analysis of fetal HRV. Typically regulatory fetal reactions are similar to deep suppression of autonomous nervous system tone with activation of metabolic and humoral branch (VLF).
It is known that mean fetal systolic blood pressure(BP) is around 40-60mmHg and BP of placental peripheral circulation is estimated to be 20mmHg or less.
The doses of the antihypertensive agents are determined according to the mean body weight of the adult. Therefore the doses of the antihypertensive drug might be enormously much for the fetus. In addition fetal growth restriction is common in severe preeclampsia. Please consider about fetal hemodynamics,when calcium antagonist to preeclampsia patients in any stage of preeclampsia.
I've been involved in the activity on the first ukrainian noninvasive fetal ECG monitor creation (CardioLab Baby Card). This device provides information on both fetal and maternal HRV. The similar abilities on expert level gives british Monica. It's rather difficult to distinguish between the influence of preeclampsia and hypotensive drug itself on fetal autonomous regulation. The current experience is not sufficient.
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