Transcript PREGNANCY INDUCED HYPERTENSION

Structural Disorders
Fetal Demise / Intrauterine Fetal Death
DEFINITION:
Death of a fetus after the age of viability
Interventions and Nursing Care
• Allow patient to decide when she wants to deliver
• Most women go into labor on their own in 2 weeks, so may
wait for labor to begin spontaneously
• Induce labor
• Prostaglandin (Prostin E) causes smooth muscles to
contract: Side effects - nausea, vomiting, diarrhea
• Cytogel
• Provide with Emotional Support, allow to hold baby
Assessment:
1. First indication is usually NO fetal
movement
2. NO fetal heart tones
Confirmed by ultrasound
3. Decrease in the signs and symptoms of
pregnancy
PREGNANCY INDUCED
HYPERTENSION
A hypertensive disease of pregnancy. Known
as pre-eclampsia and eclampsia.
Pre-eclampsia = hypertension, proteinuria,
edema
Eclampsia = other signs plus convulsions
It develops between the 20th and 24th week of
gestation and disappears after the tenth day
postpartum
PRIMIGRAVIDA
UNDER 17 AND OVER 35
MULTIPLE PREGNANCY
HYDATIFORM MOLE
PREDISPOSING FACTORS
FAMILY HISTORY
VASCULAR DISEASE
Diabetes, renal
LOWER SOCIOECONOMIC STATUS
Severe malnutrition, decrease Protein intake
Inadequate or late prenatal care
PATHOLOGICAL CHANGES
PIH is due to:
GENERALIZED
ARTERIOLAR
CYCLIC
VASOSPASMS
(decrease in diameter
of blood vessel)
INCREASED PERIPHERAL
RESISTANCE;
IMPEDED BLOOD FLOW
(
in blood pressure)
Endothelial
CELL DAMAGE
Intravascular
Fluid Redistribution
Decreased Organ
Perfusion
Multi-system failure Disease
Clinical Manifestations
Clinical Manifestation
HYPERTENSION
Earliest and The Most
Dependable Indicator
of PIH
Hypertension
B/P = 140 / 90 if have no baseline.
1. 30 mm. Hg. systolic increase or
a 15 mm. Hg. diastolic increase
(two occasions four to six hours apart)
2. Increase in MAP > 20 mm.Hg
over baseline or >105 mm. Hg.
with no baseline
Positive Roll Over Test
Rationale for HYPERTENSION
The blood pressure rises due to:
ARTERIOLAR VASOSPASMS AND
VASOCONSTRICTION causing
(Narrowing of the blood vessels)
an increase in peripheral resistance
fluid forced out of vessels
HEMOCONCENTRATION
Increase blood viscosity = Increased hematocrit
Key Point to Remember !
HEMOCONCENTRATION develops because:
Vessels became narrowed forcing fluid to
shift
Fluid leaves the intracellular spaces
and moves to extracellular spaces
Now the blood viscosity is increased
(Hemocrit is increased)
**Very difficult to circulate thick blood
Test Yourself !
Which of these readings indicates
hypertension in the patient whose
blood pressure normally is 100 / 60
and MAP of 77?
a. 120 / 76;
b. 110 / 70;
c. 130 / 80;
d. 125 / 70;
MAP 96
MAP 83
MAP 98
MAP 88
Proteinuria
With Renal vasospasms, narrowing of
glomular capillaries which leads to decreased
renal perfusion and decreased glomerular
filtration rate (damage to glomeruli)
PROTEINURIA
Protein leaks across the membrane, tubules cannot reabsorb
The degree of PROTEINURIA reflects the severity
of the disease
Spilling of 1+ of protein is significant to begin treatment
Oliguria and tubular necrosis may precipitate
acute renal failure
Significant Lab Work
Changes in Serum Chemistry
• Decreased urine creatinine clearance (80-130 mL/ min)
• Increased BUN (12-30 mg./dl.)
• Increased serum creatinine (0.5 - 1.5 mg./dl)
• Increased serum uric acid (3.5 - 6 mg./dl.)
Weight Gain and Edema
• Clinical Manifestation:
– Edema may appear rapidly
– Begins in lower extremities and moves
upward
– Pitting edema and facial edema are late
signs
– Weight gain is directly related to
accumulation of fluid
WEIGHT GAIN AND EDEMA
Rationale:
• Decreased blood flow to the kidneys causes a
loss of plasma proteins and albumin
• This leads to a decreased colloid osmotic
pressure.
• A  in COP allows fluid to shift from from
intravascular to extravascular.
• Now there is an accumulation of fluid in the
tissues.
• Increased angiotensin and aldostersone
triggers retention of sodium and water.
The Nurse Must Know
The difference between
dependent edema and
generalized edema is important.
The patient with PIH has
generalized edema because
fluid is in all tissues.
Placenta
With Vasospasms and Vasoconstriction of the
the vessels in the placenta.
Decreased Placental Perfusion and Placental Aging
Positive OCT / Late Decelerations
With Prolonged decreased Placental Perfusion:
Fetal Growth is retarded - IUGR, SGA
Condition
is
Worsening
• Oliguria – 100ml./4 hrs or less than 30
cc. / hour
• Edema moves upward and becomes
generalized (face, periorbital, sacral)
• Excessive weight gain – greater than 2
pounds per week
Central Nervous System
Changes
• Cerebral edema -- forcing of fluids to
extracellular
–Headaches -- severe, continuous
–Hyperreflexia
–Level of Consciousness changes –
changes in affect
–Convulsions / seizures
Visual Changes
Retinal Edema and spasms leads to:
• Blurred vision
• Double vision
• Retinal detachment
• Scotoma (areas of absent or depressed
vision)
• Nausea and Vomiting
• Epigastric pain –often sign of
impending coma
Pre-Eclampsia
Mild
Severe
B/P
Protein
Edema
Weight
140/90
1+ 2+
1+, lower legs
<1 lb. / week
Reflexes
1+ 2+ brisk
160/110
3+ 4+
3+ 4+
>2lb. / week
3+ 4+ (Hyperreflexia)
Clonus present
Retina
0
GI, Hepatic
0
CNS
0
Fetus
0
Blurred vision, Scotoma
Retinal detachment
N & V, Epigastric pain,
changes in liver enzymes
Headache, LOC changes
Premature aging of placenta
IUGR; late decelerations
Interventions and Nursing Care
• Home Management
– Decrease activities and promote bed rest
» Sedative drugs
» Lie in left lateral position
» Remain quiet and calm – restrict visitors
and phone calls
– Dietary modifications
» increase protein intake to 70 - 80 g/day
» maintain sodium intake
» Caffeine avoidance
– Weigh daily at the same time
– Keep record of fetal movement - kick counts
– Check urine for Protein
Hospitalization
• If symptoms do not get better then the patient
needs to be hospitalized in order to further
evaluate her condition.
• Common lab studies:
– CBC, platelets; type and cross match
– Renal blood studies -- BUN, creatitine, uric
acid
– Liver studies -- AST, LDH, Bilirubin
– DIC profile -- platelets, fibrinogen, FSP, DDimer
Hospital Management
Nursing Care Goal
1. Decrease CNS Irritability
2. Control Blood Pressure
3. Promote Diuresis
4. Monitor Fetal Well-Being
5. Deliver the Infant
Decrease CNS Irritability
 Provide for a Quiet Environment and Rest
 1. MONITOR EXTERNAL STIMULI
 Explain plans and provide Emotional Support
 Administer Medications
 1. Anticonvulsant -- Magnesium Sulfate
 2. Sedative -- Diazepam (Valium)
 3. Apresoline
 Assess Reflexes
 Assess Subjective Symptoms
 Keep Emergency Supplies Available
Magnesium Sulfate
ACTION
CNS Depressant, reduces CNS irritability
Calcium channel blocker- inhibits cerebral
neurotransmitter release
ROUTE
IV effect is immediate and lasts 30 min.
IM onset in 1 hour and lasts 3-4 hours
• Prior to administration:
– Insert a foley catheter with urimeter for
assessment of hourly output
Magnesium Sulfate
 NURSING IMPLICATIONS
1. Monitor respirations > 14-16; < 12 is critical
2. Assess reflexes for hyporeflexia -- D/C for
hyporeflexia
3. Measure Urinary Output >100cc in 4 hrs.
4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl
Therapeutic is 4-8mg/dl. Toxicity - >9mg/dl; Absence of reflexes
is >10 mg/dl; Respiratory arrest is 12-15 mg/dl; cardiac arrest is
> 15 mg/dl.
• Have Calcium Gluconate available as antagonist
Test Yourself !
A Woman taking Magnesium Sulfate has a
respiratory rate of 10. In addition to
discontinuing the medication, the nurse
should:
a. Vigorously stimulate the woman
b. Administer Calcium gluconate
c. Instruct her to take deep breaths
d. Increase her IV fluids
Nursing Care
Hospital Management
1. Decrease CNS Irritability
2. Control Blood Pressure
3. Promote Diuresis
4. Monitor Fetal Well-Being
5. Deliver the Infant
Control Blood Pressure
• Check B / P frequently.
• Give Antihypertensive Drugs
– Hydralzine ( apresoline)
– Labetalol
– Aldomet
– Procardia
• Check Hemocrit
* Do NOT want to decrease the B/P too low or
too rapidly. Best to keep diastolic ~90.
Need to maintain uteroplacental perfusion!
Nursing Care
Hospital Management
1. Decrease CNS Irritability
2. Control Blood Pressure
3. Promote Diuresis
4. Monitor Fetal Well-Being
5. Deliver the Infant
Promote Diuresis
**Don’t give Diuretic, masks the
symptoms of PIH
• Bed rest in left or right lateral position
• Check hourly output -- foley cath with urimeter
• Dipstick for Protein
• Weigh daily --
same time, same scale
Nursing Care
Hospital Management
1. Decrease CNS Irritability
2. Control Blood Pressure
3. Promote Diuresis
4. Monitor Fetal Well-Being
5. Deliver the Infant
Monitor Fetal Well-Being
FETAL MONITORING-- assessing for late
decelerations.
NST -- Non-stress test
OCT --oxytocin challenge test
If all else fails ---- Deliver the baby
Key Point to Remember !
SEVERE COMPLICATIONS OF PIH:
 PLACENTAL SEPARATION - ABRUPTIO PLACENTA; DIC
 PULMONARY EDEMA
 RENAL FAILURE
 CARDIOVASCULAR ACCIDENT
 IUGR; FETAL DEATH
 HELLP SYNDROME
HELLP Syndrome
• A multisystem condition that is a
form of severe preeclampsia eclampsia
• H = hemolysis of RBC
• EL = elevated liver enzymes
• LP = low platelets <100,000mm
(thrombocytopenia)
Etiology of HELLP
Hemolysis occurs from destruction of RBC’s
Release of bilirubin
Elevated liver enzymes occur from blood flow that is
obstructed in the liver due to fibrin deposits
Vascular vasoconstriction  endothelial damage 
platelet aggregation at the sites of damage  low
platelets.
HELLP
Assessment:
1.
2.
3.
4.
5.
Right upper quadrant pain and tenderness
Nausea and vomiting
Edema
Flu like symptoms
Lab work reveals –
a. anemia – low Hemoglobin
b. thrombocytopenia – low platelets. < 100,000.
c. elevated liver enzymes:
-AST asparatate aminotransferase (formerly SGOT)
exists within the liver cells and with damage to liver
cells, the AST levels rise > 20 u/L.
- LDH – when cells of the liver are lysed, they spill into
the bloodstream and there is an increase in serum.
> 90 u/L/
HELLP
• Intervention:
• 1. Bedrest – any trauma or increase in intraabdominal pressure could lead to rupture
of the liver capsule hematoma.
• 2. Volume expanders
• 3. Antithrombic medications
Heart Disease in
Pregnancy
Cardiac Response in All
Pregnancies
Every Pregnancy affects the cardiovascular
system
 Increase in Cardiac Output 30% - 50%
 Expanded Plasma Volume
 Increase in Blood (Intravascular) Volume
A woman with a healthy heart can tolerate the stress
of pregnancy, but a woman with a compromised
heart is challenged Hemodynamically and will have
complications
Effects of Heart Disease on
Pregnancy
 Growth Retarded Fetus
 Spontaneous Abortion
 Premature Labor and Delivery
Effects of Pregnancy on
Heart Disease
The Stress of Pregnancy on an already
weakened heart may lead to cardiac
decompensation (failure).
The effect may be varied depending upon the
classification of the disease
Classification of Heart Disease
 Class 1
 Uncompromised
 No alteration in activity
 No anginal pain, no symptoms with activity
 Class 2
 Slight limitation of physical activity
 Dyspnea, fatigue, palpitations on ordinary exertion
 comfortable at rest
p. 669
 Class 3
 Marked limitation of physical activity
 Excessive fatigue and dyspnea on minimal exertion
 Anginal pain with less than ordinary exertion
 Class 4




Symptoms of cardiac insufficiency even at rest
Inability to perform any activity without discomfort
Anginal pain
Maternal and fetal risks are high
p. 669
 Nursing Care
- Antepartum
 Decrease Stress
– Teach the importance of REST!
– watch weight
– assess for infections - stay away from
crowds
– assess for anemia
– assess home responsibilities
 Teach signs of cardiac decompenstion
Key Point to Remember
Signs of Congestive Heart Failure
 Cough (frequent, productive, hemoptysis)
 Dyspnea, Shortness of breath, orthopnea
 Palpitations of the heart
 Generalized edema, pitting edema of legs and feet
 Moist rales in lower lobes, indicating pulmonary
edema
Teach about diet
high in iron, protein
low in sodium and calories ( fat )
Watch weight gain
Teach how to take their medicine
– Supplemental iron
– Heparin, not coumarin – monitor lab work
– Diuretics – very careful monitoring
– Antiarrhythmics –Digoxin, quinidine,
procainamide. *Beta-blockers are
associated with fetal defects.
Reinforce physicians care
Key point to remember !
Never eat foods high in Vitamin K while on
an anticoagulant!
( raw green leafy vegetables)
Nursing Care
Intrapartum
 Labor in an upright or side lying position
 Restrict fluids
 On O2 per mask throughout labor and cardiac
monitoring.
 Sedation / epidural given early
Report fetal distress or cardiac failure
 Stage 2 - gentle pushing, high forceps
delivery
Nursing Care Postpartum
 The immediate post delivery period is the MOST
significant and dangerous for the mom with cardiac
problems
 Following delivery, fluid shifts from extravascular
spaces into the blood stream for excretion
 Cardiac output increases, blood volume increases
 Strain on the heart!
Watch for cardiac failure
Test Yourself !
• Mrs. B. has mitral valve prolapse. During the
second trimester of pregnancy, she reports
fatigue and palpitations during routine
housework. As a cardiac patient, what would
her functional classification be at this time?
a. Class I
b. Class II
c. Class III
d. Class IV
The End
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