can antihypertension medicines harm the baby inside?

Answer 1

Once again.... DOCTOR!! but, my guess is, uhh, YES.

Answer 2

1

Answer 3

Hypertensive disease in pregnancy is a major cause of maternal and fetal morbidity and mortality. Pregnancy-related hypertension is divided into 4 categories.

The first category consists of normotensive, pregnant patients who have sustained hypertension, proteinuria, and edema after the 20th week of gestation, with preeclampsia or pregnancy-induced hypertension. Preeclampsia causes 50-70% of cases of hypertension in pregnancy. Mild preeclampsia is characterized by an increase in systolic BP of 30 mm Hg, an increase in diastolic BP of 15 mm Hg, or an absolute reading of 140 mm Hg/90 mm Hg in a pregnant patient with minimal proteinuria and pathologic edema. A systolic BP greater than 160 mm Hg or a diastolic BP greater than 110 mm Hg with significant proteinuria (>5.0 g/d) and evidence of end-organ damage indicate severe preeclampsia.

In the second category, chronic hypertension begins prior to pregnancy. A BP greater than 140 mm Hg/90 mm Hg occurs prior to the 20th week of gestation, is not associated with significant proteinuria or end-organ damage, and continues well after delivery.

The third category consists of patients with chronic hypertension with superimposed preeclampsia; this condition is responsible for 15-30% of cases of pregnancy-related hypertensive disease. Pregnant patients with documented hypertension before pregnancy may have preeclampsia.

In the fourth category, transient hypertension results in a BP greater than 140 mm Hg/90 mm Hg without proteinuria or end-organ damage. Initially normotensive women may become hypertensive late in pregnancy, during labor, or within 24 hours postpartum, and their BPs return to normal within 10 days postpartum.


Pathophysiology: The cause of preeclampsia remains unknown; however, placental dysfunction may initiate the systemic vasospasm, ischemia, and thrombosis that eventually damages maternal organs.

Females with pregnancy-induced hypertension have been noted to have an increased responsiveness to a variety of endogenous substances (prostaglandins, thromboxane) that can cause vasospasm and platelet aggregation. Thrombus formation or hemorrhage causes the central nervous system findings of headache, local neurological deficits, and seizure. Renal necrosis leads to a decreased glomerular filtration rate and proteinuria. Liver injury from hepatocellular necrosis causes right upper quadrant pain and elevated liver function tests. Cardiovascular manifestations include a lower than normal intravascular volume, increased cardiac output, and an abnormally elevated peripheral vascular resistance. Microangiopathic hemolysis leads to anemia and thrombocytopenia. Placental infarction and abruptio placentae lead to intrauterine growth retardation and fetal death.

Preeclampsia typically develops after the 20th week of gestation and involves a wide spectrum of clinical signs and symptoms. Mild preeclampsia is characterized by mild hypertension with no evidence of end-organ pathology aside from minimal proteinuria (<2.0 g/d). Severe preeclampsia is at the other end of the spectrum and is characterized by significant hypertension, more pronounced proteinuria (>5.0 g/d), and evidence of end-organ damage due to systemic vasoconstriction. The following signs and symptoms can indicate severe preeclampsia: (1) headache, (2) visual disturbances, (3) confusion, (4) abdominal pain, (5) impaired liver function with hyperbilirubinemia, (6) proteinuria, (7) oliguria, (8) pulmonary edema, (9) microangiopathic hemolytic anemia, (10) thrombocytopenia, and (11) fetal growth retardation.

Risk factors for preeclampsia include extremes of maternal age, primigravida, multiple gestations, molar pregnancy, preexisting HTN, diabetes mellitus (DM), renal disease, preexisting connective tissue disease, vascular disease, prior history of preeclampsia or eclampsia, and family history of preeclampsia or eclampsia.

Answer 4

surely your doctor knows you are on them