What causes pregnancy-induced hypertension?

How is pregnancy-induced hypertension caused? Women who are pregnant are more vulnerable in all aspects and need our special care. We should pay more attention to the seemingly small things in their daily food, clothing, housing and transportation, because details are very important. Preeclampsia is a high blood pressure disease during pregnancy, which is a common obstetric disease. It is a major cause of death in pregnant women and a very serious disease. When the disease occurs, it must be treated in time. Let us understand what this disease is caused by.

Causes:

It may involve multiple factors such as the mother, placenta and fetus, including abnormal trophoblast invasion, abnormal immune regulation function, endothelial cell damage, genetic factors and nutritional factors. However, no single factor can explain all the causes and mechanisms of preeclampsia.

1. Abnormal trophoblast invasion

It may be an important factor in the development of preeclampsia. The patient's trophoblast invasion into the spiral arterioles was incomplete, the spiral arterioles in the uterine myometrium did not undergo recasting, and the abnormally narrow spiral arteries led to reduced placental perfusion and hypoxia, ultimately leading to the occurrence of preeclampsia.

2. Abnormal immune regulation function

The lack or disorder of maternal immune tolerance to paternal placental and fetal antigens is an important component of the etiology of preeclampsia.

3. Vascular endothelial damage

Oxidative stress, anti-angiogenic and metabolic factors, and other inflammatory mediators can lead to endothelial damage and induce preeclampsia.

4. Genetic factors

Preeclampsia is a multifactorial, multigenic disease with a familial tendency: the incidence of preeclampsia in daughters of mothers with preeclampsia is 20-40%; the incidence of preeclampsia in sisters of women with preeclampsia is 11-37%; and the incidence of preeclampsia in sisters of twins with preeclampsia is 22-47%. But until now, its inheritance pattern is unclear.

5. Nutritional factors

Vitamin C deficiency may increase the risk of preeclampsia-eclampsia.

Pathogenesis:

Important mechanisms associated with the pathogenesis of preeclampsia include vasospasm, endothelial cell activation, increased pressor response, prostaglandins, nitric oxide, endothelins, and angiogenic and antiangiogenic proteins.

1. Vasospasm

Vasospasm and contraction of the blood vessels lead to increased vascular resistance and hypertension, reduced blood flow, and eventually tissue ischemia, necrosis, hemorrhage, and other manifestations of organ damage.

2. Endothelial cell activation

It is the core mechanism of the pathogenesis of preeclampsia. Activated or damaged vascular endothelial cells produce less nitric oxide, secrete procoagulant substances, and increase sensitivity to vasopressor factors, ultimately leading to preeclampsia.

3. Increased pressor response

Patients with preeclampsia have increased vascular reactivity to infusion of norepinephrine and angiotensin II before the onset of the disease.

4. Prostaglandins

It is the central link in the pathophysiological changes of preeclampsia. The production of prostacyclin (PGI2) by endothelial cells in preeclampsia is lower than that in normal pregnancy, the secretion of thromboxane A2 by platelets is increased, and the ratio of prostacyclin/thromboxane A2 is reduced, ultimately leading to vasospasm and contraction.

5. Nitric Oxide

Preeclampsia is associated with increased nitric oxide inactivation resulting from decreased expression of endothelial nitric oxide synthase. May lead to an increase in mean arterial pressure and increased responsiveness to vasopressor factors.

6. Endothelin (ET)

Abnormally elevated ET-1 levels in pregnant women with preeclampsia can lead to vasospasm and constriction.

7. Angiogenesis and anti-angiogenesis substances

Pregnant women with preeclampsia overproduce antiangiogenic substances, such as soluble fms-like tyrosine kinase 1 (sFlt-1) and soluble endoglin (sEng), which can lead to endothelial dysfunction and reduced nitric oxide-dependent vasodilation of endothelial cells.

Disease Treatment:

General treatment

You should rest and lie on your side. Make sure you get enough protein and calories. Restricting salt intake is not recommended. To ensure adequate sleep, if necessary, take 2.5 to 5 mg of diazepam (Valium) orally before bedtime.

Antihypertensive therapy

Pregnant women with severe hypertension whose blood pressure is ≥160/110 mmHg should receive antihypertensive treatment; patients with non-severe hypertension whose blood pressure is ≥140/90 mmHg can use antihypertensive treatment. Blood pressure should drop steadily and should not be lower than 130/80 mmHg to ensure uterine placental blood perfusion.

Commonly used oral antihypertensive drugs include: labetalol, nifedipine short-acting or sustained-release tablets. If oral medications do not control blood pressure well, intravenous medications can be used, commonly used ones include: labetalol, nicardipine, and phentolamine. Diuretics are generally not used to lower blood pressure during pregnancy to prevent hemoconcentration, decreased effective circulating blood volume and hypercoagulability. The use of atenolol and prazosin is also not recommended. The use of angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) is prohibited. Magnesium sulfate should not be used as an antihypertensive drug.

Magnesium sulfate for preventing and treating eclampsia

Magnesium sulfate is the first-line drug for the treatment of eclampsia and is also a preventive drug for preventing eclamptic attacks in severe preeclampsia. Magnesium sulfate may also be considered for patients with non-severe preeclampsia.

1. Usage:

(1) Control of eclampsia: a loading dose of 2.5-5 g of magnesium sulfate dissolved in 20 ml of 10% GS and administered intravenously (15-20 minutes), or 100 ml of 5% GS administered by rapid intravenous drip, followed by maintenance drip of 1-2 g/hour. The total amount of magnesium sulfate in 24 hours is 25 to 30 g, and the treatment course is 24 to 48 hours.

(2) Prevention of eclampsia (applicable to pre-eclampsia and post-eclampsia): loading and maintenance doses are the same as those for controlling eclampsia. The dosage and time of medication depend on the condition of the patient. Generally, it is given by intravenous drip for 6 to 12 hours a day, and the total amount in 24 hours should not exceed 25g.

2. Notes:

Necessary conditions for the use of magnesium sulfate: ① existence of knee tendon reflex; ② breathing ≥ 16 times/min; ③ urine volume ≥ 25ml/hour or ≥ 600ml/day; ④ availability of 10% calcium gluconate. In case of magnesium ion poisoning, discontinue magnesium sulfate and slowly push (5 to 10 minutes) 10% calcium gluconate 10 ml intravenously. If the patient also has renal insufficiency, cardiomyopathy, myasthenia gravis, etc., magnesium sulfate should be used with caution or in reduced dosage.

Volume expansion therapy

Volume expansion therapy may lead to serious complications such as pulmonary edema and cerebral edema. Therefore, volume expansion therapy is generally not recommended unless there is severe fluid loss (such as vomiting, diarrhea, and blood loss during childbirth).