Hypertension is defined as blood pressure equal to or more than 140mmgh systolic or equal to or more than 90mmhg diastolic.
Woman with hypertension of pregnancy may have mild elevation in blood pressure or severe hypertension with various organ dysfunction.
Common forms of pregnancy-related hypertension are:
1. chronic hypertension:
Present before the pregnancy or diagnosed before the 20 week’s gestation.
The complication: abruptio placenta, IUGR, IUFD.
The woman is monitored carefully throughout pregnancy to prevent serious complication, her prenatal visit scheduled every 2 weeks throughout entire pregnancy.
Chronic hypertension management:
• change life style may necessary, for example, limit sodium intake, limit exercise during pregnancy.
• teach woman how to measure BP.
– The time of birth is individualized, but woman at low risk can usually wait until her cervix is favorable for induction at 40 to 41 weeks of gestation.
– The woman at high risk should not continue her pregnancy past 40 weeks.
– In postpartum period, woman at high risk ,should be monitored for sign of complication such as renal failure, pulmonary edema, heart failure.
– All antihypertensive drugs are found in breast milk.
2. pregnancy-induced hypertension
– Gestational hypertension
The development of elevated blood pressure during pregnancy or during the first 24 hours postpartum, but without any sign or symptoms of preeclampsia, and with no preexisting hypertension.
gestational hypertension plus proteinuria “≥300 mg or more per 24 hrs, or ≥100 mg/ dl and edema.
Occur primary after the second trimester of pregnancy, representing a great danger to the fetus and neonate.
diagnosed when woman with pre eclampsia experiences convulsions or coma unrelated to other cerebral condition.
As a rule, maternal and perinatal morbidity and mortality are highest among cases in which eclampsia is seen in early in gestation “before 28 weeks”
If woman has not develop preclampsia and her blood pressure return to normal values by 12 weeks after delivery, the woman is said to have Transient Hypertension.
If blood pressure values remain elevated then ,the diagnosis of chronic hypertension is made.
– chronic hypertension affect 1 to 5% of pregnancies.
– gestational hypertension affect 5% to 10% of pregnancies
– It is more common in the first pregnancies “up to 25%”
– Preeclampsia occur in 6% to 8%
More common in nulliparous women( 4%_20% in primigravidas) (multipara 6%_7%)
– eclampsia occur in about one in 1000 pregnancies
– preeclampsia in previous pregnancy
– age younger than 18 years or older than 35 years
– family history of preeclampsia
– lower socioeconomic group
– increased placental mass due to multifetal gestation or molar pregnancy
– history of type I diabetes, hypertension, renal disease, or any condition in which circulation is impaired or vasoconstriction or vasospasm is present.
– antiphospholipid antibody syndrome
Physiologic changes with PIH
The cause of pregnancy-induced hypertension is not fully understood
In a normal pregnancy, there is a significant increase in vascular volume as well as increased cardiac output. Despite there factors ,blood pressure does not rise in a normal pregnancy
Normal physiologic adaptation
In hypertensive pregnant the following changes do occur:
There is thought to be a loss of resistance to the pressor effects of angiotensin II.
In a normal pregnancy, the ratio of thromboxane, vasoconstrictors , and prostacyclin, vasodilator is 1:1. women with preeclampsia produce much more thromboxane than prostacyclin resulting in vasoconstriction and platelet aggregation.
during pregnancy, fluid tends to shift to the extracellular compartment because of the normal hemodilation or pregnancy reduces colloid osmotic pressure in the intravascular compartment. In preeclampsia , there is further movement of fluid in that direction as the result of:
increased capillary permeability: increased capillary permeability in the kidneys allows albumin to escape in the urine, decreasing serum albumin levels. This further decreases plasma colloid osmotic pressure and moves even more fluid to extracellular spaces.
decreased renal perfusion: the reduced glomerular filtration rate results in decreased urine output and increased serum levels of creatinine, BUN, uric acids, and sodium. Sodium retention further increases extracellular fluid and edema, it also increases sensitivity to the pressor, angiotensin
decreased intravascular volume: causes increased blood viscosity and elevated HCT.
Pathophysiology of PIH
– Uterine vascular changes:
Endothelial injury, ranging from swelling to erosion in placental and non placental sites.
– Hemodynamic changes:
Myocardial contractility rarely impaired, ventricular function normal
Changes occur include elevation of afterload, decreased cardiac output, increased vascular resistance, reduced ventricular preload, reduced total blood volume.
– Hematologic changes:
The primary hematologic change is hemoconcentration, the plasma volume contract during decreased regional perfusion.
Other changes include
Thrombocytopenia, decreased clotting factors and red blood cell destruction characterized by hemolysis.
– Endocrine and metabolic changes:
– During pregnancy ,plasma level of renin, angiotensin II, and aldestrone increase.
– In preeclampsia , these levels often return toward prepregnancy range.
– Increase in levels of antidiuretic hormone.
– Fluid and electrolytes changes:
– Extracellular volume increase as a result of increased capillary permeability.
– In eclampsia , bicarbonate level decrease owning to lactic acid and compensatory respiratory alkalosis.
– Renal changes:
– During pregnancy, renal blood flow and glomerular filtration rate (GFR) increase. In preeclampsia, these factors are reduced toward non pregnant levels.
– Other changes include sodium retention, increased plasma creatinine, increased uric acid. Decreased urinary exertion of calcium, increased permeability to large-molecular-weight proteins leading to proteinuria, and endothelial damage to renal vasculature.
– Hepatic changes:
◊ HLLP occur in 10% of women with severe preeclampsia.
◊ Serum transaminase level increase.
◊ Hepatic rupture is possible but rare, require surgical intervention.
– Uteroplacental perfusion:
◊ Vasospasm causes compromised placental perfusion and can result in poor fetal growth or even death.
– Central nervous system:
◊ Headaches and visual disturbances (blurred vision) occur because of retinal artery spasm, retinal detachment occur rarely.
◊ Reflexes can become hyperactive.
◊ CNS sign and symptoms may indicate a high risk of seizure.
Sign and symptoms
Syndrome of pregnancy- induced hypertension accompanied by proteinuria, edema and frequently other organ dysfunction.
Mild preeclampsia Is characterized by:
– hypertension: arise of 30 mmHg systolic and 15 mmHg diastolic, blood pressure:140/90 mmHg.
– proteinuria:+2 or 1 g/l.
– edema: generalized, facial, hands and fingers reflecting weight gain of over 0.7 kg/ week.
– it is essential of prenatal assessment of all women is to establish a baseline blood pressure.
– in each prenatal visit blood pressure and other signs of hypertension are assessed.
– assessment includes urine testing for proteinuria.
– weighing on the same scale.
– assessing for edema, headache, epigastric pain.
– assessment of fetal movement, non stress test.
– initial management consists of rest and observation if patient is not a candidate for delivery. Bed rest maximizes uteroplacental flow.
– delivery should be accomplished by 38 th week or sooner if the fetus is mature.
– diet: increase protein diet with moderate sodium intake.
– rest and activity: resting on the left lateral recumbent position is beneficial by increasing renal blood flow glomerular filtration rate and placental perfusion. Complete bed rest may not necessary , reduced activity is beneficial.
– medical supervision: office visit are scheduled every 2 weeks or less depending on the symptoms for assessment of signs of preeclampsia.
– danger sign: mother are instructed to report any sudden change in their condition such as generalized edema, headache, fever, muscle tremors, or seizures and sudden increase of body weight.
– blood pressure: consistently>(160 mmHg systolic) or >(110 mmHg diastolic)
– new onset of proteinuria >2 g in 24 hours urine collection or >3 g in a randomly collected specimen.
– edema : generalized, weight gain of 0.9 kg over a period of one week or less.
– platelets count: less than 100,000 ,hemolytic anemia and increase in lactic acid dehydrogenase (LDH) and direct bilirubin level.
– headache, visual disturbances or other cerebral sign.
– epigastric or right upper quadrant pain.67
– cardiac decompensation, pulmonary edema or cyanosis.
– fetal growth retardation: due to reduction of intervillous perfusion.
– hospitalization is necessary.
– the goal of care is prevent seizure, lowering blood pressure, establishing adequate renal function and to continue the pregnancy until fetal maturity.
– if the pregnancy is at the 36 th week or more labor is induced or cesarean birth is performed.
– serial examination recommended for preeclampsia hospitalized patients include:
– Blood pressure four times daily.
– assessment for proteinuria, edema, weight, hyperreflexia, headache, visual disturbances, epigastric pain (daily)
– hematocrit, platelets count (every 2 day)
– serum uric acid and creatinine level, 24- hours urine for total protein and creatinine clearance( twice daily)
– liver function test (weekly)
– urinary output( at each voiding or by catheterization, should be more than 700 ml/ 24 hours or 30 ml/ hour).
– Fetal heart rate ( every 4 hours or continuously)
– Placental separation (hourly in case of severe preeclampsia)
– Ultrasound for fetal growth (every 2 weeks)
– Non stress test (twice weekly)
– delivery is always the appropriate maternal therapy.
– fetal risk must be balanced against maternal risk.
– consider conservative management between 25_30 weeks.
– delivery indicated for severe preeclampsia, IUGR or fetal distress.
– treating hypertension
– treat for greater than 160/110 mmHg.
– goal is to lower diastolic to 90 to 100 mmHg.
– drug therapy: hydralazine
– carefully monitor urinary output.
– preventing convulsion
– drug of choice is magnesium sulfate
– treat all preeclamptic patient during labor and 24 hours postpartum.
Severe form of preeclampsia with seizure or coma. The occurrence of one or more convulsion not attributable to other cerebral disorders such as epilepsy or cerebral hemorrhage in a patient with preeclampsia.
Convulsion usually preceded by headache, epigastric pain, hyperreflexia and hemoconcentration .it occur before labor in 50 %, during labor in 25% and early postpartum in 25%.
– turn the woman on her side.
– establish airway and administer oxygen.
– administer 4 _6 g of magnesium sulfate I.V. over 10-15 minutes.
Follow by a 2 g/hour maintenance dose, adjust dose later based on patellar reflexes, urine output and serum magnesium level.
– obtain arterial blood gases measurement and chest X ray.
– if convulsion are controlled and maternal condition is stable, initiate induction or delivery within 3-6 hours.
– continue to administer magnesium sulfate for at least 24 hours after delivery or last convulsion.
– obtain computed tomographic scan or magnetic resonance imaging if seizure are typical or coma is prolonged.
Nursing intervention during the tonic phase of convulsion:
– turn the woman to her side to allow saliva to drain from her mouth.
– inserting a padded tongue blade may prevent injury to the mouth, it can be done without force.
– side rails should be padded or a pillow placed between them and woman.
When clonic phase begin:
– remain nearby and assist as an oral airway is inserted.
– administer oxygen
– monitor maternal vital sign and FHR.
– magnesium sulfate, diazepam, lasix and other drugs as prescribed.
– keep the woman on her left side
– a decision about delivery is made based on maternal condition and fetal maturity.
– signs and symptoms usually decrease rapidly after delivery, however, dangers of seizures don’t pass until 48 hours following delivery.
– follow up care is necessary.
– pregnant women with chronic hypertension are at increased risk of preeclampsia and placental abruption, health problem for the mother, such as heart attack, slow fetal growth and low birthweight.
signs and symptoms:
The etiologic factors of HELLP syndrome:
Unclear, clinical and pathologic manifestation result from an insult that leads to intravascular platelet activation and microvascular endothelial injury.
Nursing Care Plan
Excess fluid volume related to pathophysiologic changes of gestational hypertension and increased fluid overload.
– monitor vital sign every hour
– monitor intake and output strictly, notify health care provider if urine output is less than 30 ml/hr
– An indwelling urinary catheter may be inserted to allow accurate recording of output.
– control I.V fluid intake using continuous infusion pump.
– assess edema status and report pitting edema of ≥ ±2.
– monitor hematocrit level to evaluate Intravascular fluid status
– auscultate breath sound every 2 hrs and report sign of pulmonary edema “wheezing, crackles, shortness of breath, increase pulse rate, increased respiratory rate”
Ineffective tissue perfusion related to altered placental blood flow caused by vasoconstriction of blood vessels.
– promote bed rest
– When the body is in a recumbent position, sodium tend to be excreted at a faster than during activity. Bed rest, therefore, is the best method of aiding increased evacuation of sodium and encouraging diuresis. Rest should always be in a lateral recumbent position to avoid uterine pressure on the vena cava and prevent supine hypotension syndrome.
– monitor fetal activity
– evaluate NST to determine fetal status.
– increased protein intake to replace protein lost through kidney.
Risk for injury related to seizure or to prolonged bed rest or other therapeutic regimens.
– instruct on the importance of reporting headaches, visual changes, dizziness and epigastric pain.
– instruct to lie down on the left side if symptoms are present.
– keep the environment quiet and as calm as possible.
– if patient is hospitalized, side rails should be padded and remain up to prevent injury if seizures occurs.
– if patient is hospitalized, have oxygen and suction setup along with a tongue blade and emergency medications, immediately available for treatment of seizures.
– assess DTRs and clonus every 2 hrs. increase frequency of assessment as indicated by patient’s condition.
Alteration in pattern of urinary elimination related to hypertension, proteinuria and edema.
– check urinary output every hour.
– report urinary output of less than 100 ml/4hour.
– check intake every 8 hours.
– check urine for protein every 8 hours
Anxiety related to diagnosis and concern for self and fetus
– explain the disease process and treatment plan including signs and symptoms of the disease process.
– explain that preeclampsia does’nt lead to chronic hypertension.
– discuss the effects of all medications on the mother and fetus
– allow time to ask questions and discuss feelings regarding the diagnosis and treatment plan.
– Hypertensive disorders during pregnancy are a leading cause of worldwide infant and maternal morbidity and mortality.
– The cause of PIN is not fully understood, but there are some factors that lead to.
– Historic risk factors: primigravida or history of vascular disease and multiple gestation.
– The pathologic changes of preclampsia, involving every organ system in the body, are present long before clinical manifestation are evident.
– HELLP syndrome can occur in women with severe preeclampsia and is considered life threatening.
– The intent of emergency intervention for eclampsia is to prevent self injury ,ensure adequate oxygenation, reduce aspiration risk, establish seizure control with magnesium sulfate.