NM 602 Module 4 Study Guide/UNIT C

Progesterone:
●Increases progressively though out pregnancy
●Is a respiratory stimulant
●Increases minute volume and enhances responses to increased CO2
-increases sensitivity to CO2 in respiratory center
-lowers the CO2 threshold of the respiratory center
-60% of CO2 sensitivity occurs by 20 weeks gestation
-increased CO2 sensitivity → dyspnea and hyperventilation while pushing during labor
Example:
-increase 1mmHg CO2 in non-pregnant women → increase 1.5L/min in ventilation
-increase 1mmHg CO2 in pregnant women → increase 6L/min
●Causes water retention in the lung → decreased diffusion capacity → can result in hyperventilation in an attempt to maintain normal O2 levels
●Relaxation of bronchial smooth muscles → decrease in airway resistance by up to 50% → decreased work of breathing and increased airflow

-cause is unclear, the following are things that may cause dyspnea of pregnancy
● increased respiratory drive & load, changes in oxygenation, or a combination of both
● in early pregnancy: increased sensitivity to CO2 and hypoxia may contribute
● in late pregnancy: mechanical factors may aggravate these changes (mechanical factors are discussed on pg. 315, and include:
-uterus enlargement → change in abdominal size and shape → diaphragm resting position 4cm higher than when not pregnant
-increased abdominal pressure → increased thoracic circumference by 6cm and transverse diameter by 2cm, and flaring of lower ribs
-subcostal angle increases from 68 to 103 degrees by late gestation
-relaxation of ligamentous rib attachments → increased elasticity of rib cage (mediated by Relaxin)
-increased movement of diaphragm (diaphragm does the major work of breathing in pregnancy)
● increased tidal volume and decreased CO2
● heightened maternal awareness of the normal hyperventilation with pregnancy

Upper respiratory tract- Capillary Engorgement: pg. 322
● hormonal changes:
-progesterone: inducing vascular smooth muscle relaxation and nasal vascular pooling
● increased blood volume (can also play a role in vascular pooling)
● these changes may be exacerbated in women with preeclampsia
-airways may be narrower due to soft tissue edema
-edema + other changes of pregnancy (weight gain, GI changes, increase in total body water) → increased risk during endotracheal intubation

Altered exercise tolerance: pg. 322-323
● the effect of exercise on the respiratory system is related to alveolar ventilation and is dependent on age, weight, body composition, and physical condition
● respiratory rates are higher in pregnant patients during mild exercise
● respiratory rates are no different in pregnant vs. non-pregnant patients with moderate exercise
● tidal volume and minute volume increase in all pregnant patients with exercise
● in pregnancy ventilation increases 38% and oxygen consumption increases 15%
● prolonged exercise leads to increased O2 and decreased CO2 levels (due to progesterone)
● O2 consumption increases with increasing gestational age (partly due to the increased work of carrying increased body weight)

Increased altitude → decreased O2 levels
• The maternal system attempts to maintain O2 levels under hypoxic conditions
• Maternal dyspnea and hyperventilation of pregnancy is more prominent
• Women that remain in high altitudes: results in morphological differences in the placental villi with increased capillary diameter
• Flying in an airplane is transient exposure to altitude
• Maternal heart rate and blood pressure increase, and aerobic capacity decreases during take off
• Fetal heart rate increases, but stays within normal limits during takeoff and landing
• Fetal hemoglobin and circulation prevent desaturation of O2 on commercial flights
• Airplane low cabin humidity → change in hemostasis and hemoconcentration → increased risk of thromboembolism

●Pre-pregnancy maternal risks: can interfere with the ability to conceive, increases perinatal morbidity and mortality
●Pregnant maternal risks: increase rate of spontaneous abortions, abruption placenta, placenta previa, early or late bleeding, premature ROM, and preterm labor
●Fetal risks: low birth weight, preterm delivery, fetal growth restriction (weigh an average of 200gm less)
-the number of cigarettes smoked per day is directly proportional to amount of decrease in birth weight
●Children of smokers risk: increased behavioral problems, attention-deficit disorders, altered lung function, SIDS, asthma, pneumonia, bronchitis, malformations (urinary tract anomalies, cleft lip and palate, absence of distal limb), non-Hodgkin’s lymphoma, acute lymphoblastic leukemia, Wilm’s tumor

Nicotine readily crosses the placenta
• Fetal levels are 90% of maternal levels
• Nicotine may compete with nutrients for placental nutrient carriers → decrease in nutrient transfer → decrease in fetal growth
• Nicotine can cause release of catecholamines from the adrenals.
-catecholamines increase maternal blood pressure and heart rate
-catecholamines cause peripheral vasoconstriction → decreased perfusion of the placenta and uterus
-chronic under-perfusion → fibrin deposits in arteries, inflammation and necrosis of tissue, lesions, and calcifications on the placenta
-the perimeter of the placenta is affected first because perfusion is lower in these areas
-decreased blood flow by these defects of chronic under-perfusion → placenta cannot sustain itself → increased incidence of placental abruption
-decreased placental blood flow → decreased available O2 to the fetus → hypoxia

●Smokers placentas are greater in weight (as related to fetal weight)
●Histological changes suggests hypoxia with a compensatory hypertrophy
●Smokers have: more areas of calcification, increased incidence of fibrin deposits, increased frequency of necrosis and inflammation in the margin, DNA changes, and increased risk of placental lesions.
●It is suggested that smoking causes direct damage to blood vessels of the placenta, resulting in placental under-perfusion.
●If placental under-perfusion is due to decreased uterine blood flow, it can lead to fetal acidosis and hypoxemia. Decreased blood flow → chronic hypoxia.

●Same level in maternal and fetal blood.
●Has a higher affinity for hemoglobin than does O2 → decreased oxygen carrying capacity
●Increases the affinity of oxygen for hemoglobin → oxygen is less readily unloaded to the fetal tissues → decrease in fetal oxygenation