PRE-GESTATIONAL

CARDIOVASCULAR
CONDITIONS IN
PREGNANCY

INCIDENCE
Hypertension Complicates 1% of
Pregnancy (Cunningham, 2008)
CVD causes 5% of Maternal Deaths
(Crombesholme, 2009)

MOST COMMON CVDS

Valve Damage caused by Rheumatic
Heart Disease (RHD)
Kawasaki Disease (Mucocutaneous
Lymph Node Syndrome- aff ecting young
children <5, leads to Myocarditis and
Aneurysm

DANGERS
Pregnancy taxes the circulatory system of
every woman even without heart disease
because both the blood volume and cardiac
output increases approx. 30%-50% by midpregnancy.
Peaks 28-32 weeks- Heart can be
overwhelmed that her cardiac output falls
thus leads to decreased perfusion ( Oxygen
and Nutritional Requirements)
Estimation of whether a woman can complete
pregnancy is based on extent and type of the
disease

SIBANDA , 2007
Women with Pacemakers, Artifi cial but wellfunctioning heart valves or women who have had
heart transplants can be expected to complete
pregnancy without diffi culty provided with consistent
prenatal/postpartum care
To predict pregnancy outcomes, heart disease is
divided into 4 categories by New York State Heart
Association (1994)

RHEUMATIC HEART
DISEASE

RHD
Chronic Infl ammation and scarring of
the heart and the valves leading to
heart failure, murmurs and damage to
valves
Arises as a delayed complication of
infection of the URT with hemolytic
streptococci (GAS Pharyngitis)
ETIOLOGIC AGENT: Group A Hemolytic
Streptococcus

ASSESSMENT
S/Sx:
Fever
Arthritis
Reddish circular patches on the skin
Small painless nodules
Sydenhams Chorea- abnormal involuntary
movements of the limbs and head
Myocarditis
Valvulitis
Endocarditis
pericarditis

TREATMENT
Penicillin G (Benzylpenicillin)- BetaLactam Antibiotic
Aspirin to relieve joint pain
Corticosteroids
ACE Inhibitors
Digoxin
Diuretics

DIAGNOSTIC TESTS

Elevated WBC count

Elevated ESR
Throat culture (+) GAS
CXR- Cardiomegaly/
Pericardial Effusion

TREATMENT
Following acute attack, long term prophylaxis is
recommended to prevent relapse
Monthly injections of PenG (Benzathine Penicillin)
Treatment lasts for 5 years or until age 21 which ever
is longer
SURGICAL MANAGEMENT
Valvuloplasty
Commissurotomy (Separation of adhered valves and
surrounding tissues
Prophylactic Antibiotics for dental work and other
invasive surgical procedures to prevent endocarditis

COMPLICATIONS

Destruction of Mitral Valves

Pancarditis
Heart Failure

NURSING CONSIDERATIONS
Teach the patient about the disease
and the need for prolonged antibiotic
therapy to promote compliance
Check for allergies before drug
administration
Instuct patient to report signs of heart
failure such as dyspnea, hacking and
non productive cough
Stress the need for bedrest during the
acute phase and suggest appropriate,
physically undemanding diversions

DIABETES MELLITUS
IN PREGNANCY

DIABETES MELLITUS
An endocrine disorder in which the pancreas cannot
produce adequate insulin to regulate the bodys
glucose levels.
Aff ects 3-5% of all pregnancies
TYPES:
1. TYPE 1 (IDDM) Insulin Dependent- Juvenile DM.
Children died before childbearing age, or had
spontaneous miscarriages or infertile
2. TYPE 2 (NIDDM)- more frequent in young adults.

GESTATIONAL DIABETES MELLITUS

Abnormal carbohydrate, fat and protein metabolism
that is fi rst diagnosed during pregnancy. 50-60%
develops to DM2
TYPES:
1. GDM with Abnormal GTT without S/Sx, Normal FBSControlled by diet
2. GDM with Abnormal GTT, Elevated FBS with S/SxControlled by Insulin

ETIOLOGY
GDM is a disorder caused by pancreatic stimulation
associated with pregnancy
RISK FACTORS
1. Obesity
2. Age >25
3. History of Large babies (10lbs or more)
4. History of Unexplained fetal or perinatal loss
5. History of Congenital anomalies in previous
pregnancy
6. History of Polycystic Ovarian Syndrome
7. Family History of DM
8. Race: Native American, Hispanic, Asian

DIABETES MELLITUS PATHOGENESIS

PATHOPHYSIOLOGY
GDM is due to increased pancreatic stimulation
brought about by pregnancy. In GDM, insulin
antagonism by placental hormones, Human Placental
Lactogen, Progesterone, Cortisol, and Prolactin leads
to increased blood glucose level. The eff ect of these
hormones peaks at about 26 week AOG. This is called
the DIABETOGENIC EFFECT OF PREGNANCY

PATHOPHYSIOLOGY
hPL affects the metabolic system of the maternal organism
in the follow ing manners:
Metabolic
maternal insulin sensitivity leading to an increase in
maternal blood glucose levels.
maternal glucose utilization, w hich helps ensure adequate
fetal nutrition (the mother responds by increasing beta
cells). Chronic hypoglycemia leads to a rise in hPL.
lipolysis w ith the release of free fatty acids. With fasting
and release of hPL, free fatty acids become available for the
maternal organism as fuel, so that relatively more glucose
can be utilized by the fetus. Also, ketones formed from free
fatty acids can cross the placenta and be used by the fetus.
These functions help support fetal nutrition even in the case
of maternal malnutrition.

PATHOPHYSIOLOGY
The Pancreatic Beta Cell functions are impaired in
response to the increased pancreatic stimulation and
induced insulin resistance.
Pregnancy complicated by Diabetes puts the mother
at risk for the development of complications such as
spontaneous abortion, hypertensive disorders,
preterm labor and birth complications

EFFECTS OF GDM ON FETUS

HYPOGLYCEMIA
KETOACIDOSIS
HYPERGLYCEMIA
a. Congenital Defects
b. Macrosomia
c. Intrauterine growth restriction
d. Intrauterine fetal death
e. Delayed lung maturity
f. Neonatal hypoglycemia
g. Neonatal Hyperbilirubinemia

ASSESSMENT
Normal Parameters:
CBG- 80-120mg/dL
FBS- 70-80mg/dL, Pregnant 65mg/dL
Post Prandial- 60-110mgdL, Pregnant 140mg/dL after
a 100g carbohydrate is considered normal
HbA1c- Glycosylated Hemoglobin
Normal (no diabetes): Less than 5.7%
Pre-diabetes: 5.7% to 6.4%
Diabetes: 6% or 6.5% or higher

ASSESSMENT
Screening- done between 24-28 t h week AOG
Diagnosis- 126 mg/dL Fasting or 200mg/dL non-fasting
needs to be confi rmed with 50g glucose load via OGTT
the subsequent day
ORAL Glucose Tolerance Test (OGTT)/ Oral Glucose
Challenge Test:
Prep. 50g glucose load is ingested
A venous blood sample is taken for glucose
determination 60 minutes later
If serum glucose level at 1 hr is .140mg/dL, the woman is
scheduled for 100g, 3-Hr fasting glucose tolerance test
If two of four blood samples collected are abnormal or
FBS is >95mg/dL- GDM is confi rmed

ORAL GLUCOSE CHALLENGE TEST

VALUES
(FAST IN G P L ASM A GLUC OS E VALU E S F OR P RE GN AN CY
Test TYPE

Glucose Level (mg/dL)

Fasting
1 hr (50g)
2 hrs (100)
3 hrs

95
180
155
140

*following a 100g glucose load

rate is abnormal if two values are
exceeded

SIGNS AND SYMPTOMS OF

HYPOGLYCEMIA VS HYPERGLYCEMIA
Hypoglycemia

Hyperglycemia

Shakiness, dizziness
Sweating
Pallor, cold, clammy skin
Disorientation, Irritability
Headache
Hunger
Blurred Vision
Nervousness
Weakness, fatigue
Shallow respirations but normal
pulse rate
Urine negative for glucose and
acetone
CBG <60mg/dL

Fatigue
Flushed, hot skin
Dry mouth, excessive thirst
Frequent Urination
Rapid, deep respirations, fruity
odor
Deepressed reflexes
Drowsiness, headachee

NURSING MANAGEMENT
Monitor Blood glucose level
Teach and demonstrate self-blood glucose monitoring and
insulin self-injection as necessary
Discuss potential complications and management:
DKA- multisystem disorder resulting from hyperglycemia
in which plasma glucose levels exceed 350mg/dL in non
pregnant state 200mg/dL or more during pregnancy
HYPOGLYCEMIA- a disorder caused by too much insulin,
insuffi cient food, excess exercise, diarrhea or vomiting
Discuss mgt of hypo and hyperglycemia ( administer 12
fl uid o orange juice or 20 g of carbohydrates and waiting
20 minutes before repeating the procedure)
Report any episode to the health care provider asap
Explain the need for continued evaluation during the
postpartum period until blood glucose levels are within
normal limits