Lecture of acute pregnancy failure in labor

2021-03-21 12:00 AM

The blood flow in the hematoma depends on the blood pressure associated with maternal hemodynamic status and on the resistance of the vessel wall.

Acute pregnancy failure is a condition that threatens the fetal life, health and future mental and motor development. Acute pregnancy failure is the cause of one-third of perinatal deaths. The consequences of acute pregnancy failure are difficult to evaluate because some of these effects manifest only after many years of school age. Treatment for acute pregnancy failure is based on two factors:

The degree of pregnancy failure.

Resistance of the fetus.

The first factor is quite well known, but the latter is still very difficult to evaluate.

Pathophysiology

Acute fetal failure is the result of a disorder of the gas exchange between mother and baby during labor, making the fetus lack of oxygen. This exchange is largely dependent on circulating blood vessels and spikes. When the oxygen supply to the fetus is reduced, the fetus will start up metabolic and hemodynamic mechanisms to adapt to exist.

Hemoglobin circulation (maternal side)

The mother's blood follows the spiral artery and its ends poured into the pool of blood. The helical arteries work independently of each other, not at the same time. The average pressure of the blood reaching the blood vessel is 25mm Hg. The pressure in the vein that carries the blood away from the blood vessel is 3 to 8 mm Hg. This is the hemodynamic system with low pressure, but also enough to circulate and mix the blood flow in the blood vessels. The resistance of the blood vessels in the vegetable cake is low.

The volume of the hematoma is from 150ml to 250ml. During pregnancy in the third trimester, maternal blood flow to the blood vessel is 135 ± 47ml / min / 100g vegetables.

Factors that alter circulating blood vessel flow

The blood flow in the hematoma depends on the blood pressure associated with maternal hemodynamic status and on the resistance of the vessel wall. During labor, many factors can decrease blood flow. The effect on the fetus depends not only on the degree of decreased flow, but also on the previous hemodialysis flow. If the flow is decreased during pregnancy then the fetus is very susceptible to hypoxia during labor.

The muscle of the uterus causes blood flow to the blood vessel to be significantly reduced, sometimes with a complete delay. Initially increased pressure in the uterine muscle disrupts venous circulation, while arterial circulation continues to function. As a result, the blood is accumulating in the blood pool. When the pressure in the uterine muscle reaches 30 to 50mm Hg, the arterial circulation is stopped, this green blood exchange in the blood is done with oxygen-poor blood. Usually uterine circulation - vegetables are stopped in the uterine contraction muscle from 10 seconds to 20 seconds and the fetus is well tolerated. In uterine contractions (too quickly, too strong) will reduce circulation in the blood vessel.

Change in blood pressure: Decreased blood pressure is not proportional to the degree of drop in blood pressure. A moderate drop in blood pressure only slightly reduces flow. Towards a certain threshold of blood pressure, the hemothorax is a sudden drop due to an increase in peripheral vascular resistance. The threshold in animals is 40mm Hg, but not known in women.

Change positions: When lying on your back, a contraction of the uterus corrects the right rotation of the uterus, which can cause the uterus to press on the right main and right pelvic artery, reducing blood flow (Poseiro effect). The uterus also compresses the lower aorta, especially when lying on your back. The consequences of this compression vary widely among women, depending on the degree of collateral circulation developed next to the spine, allowing blood from the lower limbs and pelvis to return to the heart. If collateral circulation is satisfactory, no changes in blood pressure are caused. If collateral circulation is inadequate, a supine hypotension syndrome may develop. The blood returning to the heart must drop suddenly, causing the cardiac output to decrease, the blood pressure to drop and reducing the circulation in the blood vessel. In some cases, hypotension does not occur as it is compensated for by peripheral vasoconstriction.

Bleeding in the mother: There is no specific data in humans. On experimental animals it is found:

A 15% rapid flow would result in a 10% reduction in arterial pressure and a 20% decrease in hemothorax.

30% volume flow of blood reduces blood flow by 65%.

Mother work, too much physical activity. Physical activity reduces blood flow in the organs and blood vessels because it partially increases blood volume to the muscles and skin.

Changes in blood gas: A mother is deprived of oxygen will lead to constriction of the uterine arteries, reducing blood flow to the blood vessel.

Circulation in vegetable spines (fetal side)

Fetal blood flow through the vegetable cake is estimated at 500ml / min. The blood flow in the umbilical cord is about 180 to 200 ml / kg body in the fetus. Blood flow through the umbilical cord accounts for about 40% of the fetal cardiac output in late pregnancy.

Factors affecting circulation in vegetable thorns

Physiological Changes: Umbilical cord blood flow varies mainly with fetal arterial pressure and fetal heart rate. The relationship between these discharges and these factors is calculated by the relationship. An increase of 1mm Hg in mean arterial pressure leads to an increase in umbilical cord flow by 6 ml / min / 1 kg of fetal body weight. Increasing heart rate 1 time / minute increases flow by 1 ml / min / kg body weight.

Changes in blood gas: Mild hypoxia causes systemic vasoconstriction, increased arterial pressure, increased blood flow through the umbilical cord. Although the heart rate was moderately slow, an increase in flow was observed. But when severe hypoxia leads to a very slow fetal heart rate and decreased blood flow in the umbilical cord.

Effects of some drugs: The umbilical cord has no dominant nerve, drugs that affect blood flow in the umbilical cord are not through the systemic effect of the drug (changes blood pressure, heart rate ..).

Fetal adaptation to hypoxia

Metabolic adaptation

Reduced oxygen supply will change the catabolism of glucose, the cell's main energy source. Normally, having enough O2, catabolizing one molecule of glucose will provide 38 ATP molecules and 6 molecules of CO2, achieving maximum energy efficiency (aerobic metabolism). In the absence of O2, catabolism of one molecule of glucose gives only 2 molecules of ATP and 2 molecules of lactic acid (anaerobic metabolism). Therefore, to have enough energy to operate it is necessary to mobilize a very large amount of glucose. Provide glucose mainly through vegetable cakes. When fetal failure, glucose supply decreases, because the mother-child exchange in the vegetable cake decreases, the demand increases, so the fetus has to rely on stored glucose in the form of glycogen, which is abundant in the liver, myocardium. , kidney. The fetal tolerance to O2 deficiency depends on this reserve. This reserve is more abundant in preterm than in term, normal development in fetuses compared with malnourished pregnancies. The tendency of anaerobic metabolism will cause metabolic acidosis because lactic acid stagnation in the organization, especially the vasoconstrictor organization. Thus, metabolic acidosis has contributed to the previous respiratory acidosis due to the stagnation of CO2 (reducing CO2 exchange between mother and child in vegetable cakes).

To combat acidification, the fetus cannot remove CO2 and the acid-mediated metabolite through the vegetable cake, the fetus must use its own buffer system, which is hemoglobin. Acidification makes O2 - hemoglobin more looser technique, O2 is easier to release (Bohr effect); the other hemoglobin combines with H + to maintain pH balance. When the hemoglobin count system is saturated, the pH drops suddenly. So buffering capacity depends on the hemoglobin concentration of fetal blood.

Adaptation of the heart

In terms of metabolism, the heart has an enzyme system that performs anaerobic metabolism of glucose and is a storage site for glycogen. The heart therefore adapts well to the O2 deficiency. The heart has made changes to try to secure blood supply to certain priority organs. Heart rate slows down (contrary to adults), diastolic time is longer, left ventricular blood is more. However, there are also cases where the fetal heart rate has accelerated, making it difficult to explain this different response. There is a phenomenon of cyclic redistribution. Acidosis causes pulmonary artery and ductus arteriosus to constrict. These changes allow the blood to be focused on and nourish vital organs. Blood flow to organs such as lungs, kidneys, intestines, canal, muscle, skin is decreased, while in the organs of the brain, heart, adrenals, and kidneys, blood flow is increased. There are many factors involved in this regulation, There are many unknown things. By weight, the fetal brain consumes O2 more than half of the adult brain. During pregnancy failure, blood flow to the brain increases. The blood flow to the brain increases a lot as the O2 saturation in the blood decreases. In the brain, the brain stem takes precedence.

Other consequences

The consequences of O2 deficiency in fetal failure can last until after delivery, even worse if the neonatal resuscitation is not performed quickly.

Less perfusion of the kidneys reduces urinary excretion. In particular, severe fetal failure can cause anemia damage to the kidney parenchyma. In the intestine, nourishing anemia increases bowel motility, relaxes the anal sphincter muscles and pushes the stool into the amniotic chamber. Bowel anemia is one of the factors that causes necrotizing enterocolitis after delivery. Sometimes there is liver function damage that causes premature jaundice with continued elevation of bilirubin and possibly disturbance of the coagulation factors. Contraction of pulmonary blood vessels can cause circulatory survival syndrome in the newborn. Poor fetal skin nourishment makes the skin flaky.

In the organization, the lack of O2 causes the release of certain enzymes in the cell. Theoretically, the quantification of these enzymes could allow for an assessment of O2 deficiency in the organization. Changes in some enzymes are closely related to brain damage.

Reason

There are many causes of fetal failure, so systematization can be divided into the following 3 groups:

Abnormal uterine contractions.

Labor is abnormally long.

The remaining causes.

Abnormal uterine contractions

Hyperstimulation of the uterus can be primary, may be secondary due to fetal mismatch (common), possibly due to incorrect use of oxytocin. An intense uterine contraction can be:

Increased frequency of contractions (rapid contractions).

Increase the intensity of the contractions (strong contractions).

Increases both frequency and intensity (strong contractions).

Intense uterine contractions reduce circulatory flow in the blood vessels, prolong the time of blood stasis in the blood vessels to lack of O2 and CO2 deposition in the fetus.

Labor is abnormally long

In some cases, the uterine contraction is normal, there is no fetal mismatch - the pelvis but the cervix opens very slowly, not even opening. Commonly seen in the cusp of the posterior style, the head is not bowed well. If this situation is left, the patient will be tired, anxious, the uterine contraction will be disturbed and fetal failure.

The remaining causes

Completely normal uterine contractions can cause fetal failure due to mother-to-child exchange disorders caused by other medical conditions.

The cause of the mother

Insufficient blood supply to the hematoma:

Chronic: Pregnancy poisoning, old pregnancy, pre-existing high blood pressure ... these diseases often make the fetus malnourished, easily at risk of acute fetal failure in labor.

Acute: Dizziness (vegetable striker, young vegetables ...).

Hypotension caused by lying on the back, overdosing on antihypertensive drugs, dizziness due to pain relief methods (epidural anesthesia can drop blood due to vascular paralysis)

O2 saturation of maternal blood is not enough: mother has anemia, severe heart disease, lung disease (bronchial asthma).

Cause of the appendage

Vegetable cake: Reduced exchange area (young peeling vegetables, gliomas ...).

Umbilical cord: Sa umbilical cord before the throne, in the throne, umbilical cord knotted, umbilical cord tightly necked, abnormal anatomy of the umbilical cord.

Causes of pregnancy

Some cases are already weakened, always threatened with acute fetal failure in labor. These include preterm pregnancy, old pregnancy, malnutrition, twins, anemia, infection.

Symptom

Acute pregnancy failure can occur at any time during labor. Weak, high-risk pregnancies may emerge as soon as labor begins because uterine contraction is an attacking factor that aggravates the already disturbed placenta.

Amniotic fluid mixed with meconium

Usually occurs when the amniotic fluid ruptures. It is necessary to proactively detect amniotic fluid mixed with meconium immediately at the beginning of labor, the amniotic fluid has not yet patted by amniocentesis. Amniotic fluid is a witness to past or present pregnancy failure. The poop has long been in the amniotic fluid and will dissolve evenly. The risk of pregnancy failure is very high when the amniotic fluid is mixed with gum.

The amniotic fluid mixed with chayote paves the way for infection, causing severe prognosis for children to inhale the stool. Gut and amniotic fluid alone is not enough to diagnose fetal failure. There are authors that only 1/3 of the cases of fetal acidosis have amniotic fluid mixed with meconium and only 20% of cases of amniotic fluid and meconium have acidosis in pregnancy.

Changes in fetal heart rate

Hear the fetal heartbeat with an obstetric stethoscope at the position of the fetal shoulder. The fetal heart rate normally ranges from 120 times / minute to 160 times / minute. In addition to the uterine muscle attack, the sound of the fetal heart is clear. If there is fetal failure can see: tachycardia (over 160 times / minute); fetal slow heart rate (less than 120 times / minute), fetal heart rate is irregular. Classic see the sound of fetal heart weak, blurry, far away.

Since there are electronic labor monitoring (monitor), the method of listening to the fetal heart has many disadvantages. The fetal heart rate cannot be continuously monitored, the fetal heartbeat cannot be heard during uterine contractions, so the fetal heart rate changes associated with uterine contractions cannot be seen. So detecting pregnancy failure by stethoscope is usually slow and inaccurate. American authors believe that the time spent hearing cardiac and fetus only accounts for about 5% of labor time.

Symptoms on monitoring

Monitoring is a method of using a continuous monitor with both uterine contractions and fetal heart rate simultaneously. The uterine contraction and fetal heart rate recorded on paper are the basis for the analysis of the results.

The uterine contraction line shows: the intensity of the contraction, the base force field of the uterus and the frequency of the contraction (the number of contractions over a 10-minute period). The contractional muscle strength and the uterine basal force field are only of real value if the probe is placed in the uterine cavity (internal method). The fetal heart rate track showed baseline fetal heart rate, fetal heart rate fluctuation and fetal heart rate variation associated with uterine contraction.

Basic fetal heart rate analysis

Normal fetal heart rate ranges from 120 to 160 beats/minute.

Tachycardia can be seen when the mother has a fever, the mother takes drugs (atronpin, betamimetic), and the fetus is infected. Gestational tachycardia can also originate from fetal failure.

Tachycardia is from 160 times/min or more.

The fetal heart rate is slow from less than 120 times/minute.

Usually slow fetal heart rate is a sign of fetal failure. If the fetal heart rate is slow, lasting more than 3 minutes, it is necessary to think about pregnancy failure. However, it is necessary to exclude the cause of hyperstimulation contractions that cause delayed fetal heartbeat.

Analysis of fetal heart fluctuation

The fetal heart fluctuation is divided into levels:

Oscillation degree 0 (flat beat): less than 5 times/minute.

Oscillation degree I: from 6 to 10 times/minute.

Degree II oscillation: from 11 to 25 times/minute.

Vibration degree III (bouncing rhythm): over 25 times/minute.

Flat rhythm occurs only when the fetus is very severely impaired, sometimes even when the fetus is in sleep state.

In the case of sleep, if the fetus is stimulated (palpation; vaginal visit, uterine contractions ...), the flat rhythm will lose room for other types of oscillation rhythms. There is also a flat rhythm can also be seen in the case of an infarction, very preterm fetus, in some cases of heart malformations.