module 4

Hemoglobin

Decreases 2 %-10% to 12.1-12.5 g/dl (range, 11-13 g/dl) at term If iron and folate are adequate, little change to 16 weeks, lowest values at 16-22 weeks; slowly increases to term Hemodilution: total body hemoglobin increases by 65-150 g Slight increase as a result of stress and dehydration Initial decrease stabilizes at 2-4 days' non-pregnant values by 4-6 weeks

Hematocrit

Decreases 3%-5% to 33.8% at term (range, 33%-39%) Decreases from second trimester as plasma volume peaks hemodilution Returns to non-pregnant levels by 4-6 weeks as a result of RBC catabolism

• Gestational hypertension:

Development of hypertension without other signs of preeclampsia" (Blackburn et al., p 267).

Red blood cells (RBCs)

Increases 20%-30% (250-450 ml) Slow, continuous increase beginning in first trimester, may accelerate slightly in third trimester Erythropoietin stimulates by human placental lactogen, progesterone, and prolactin Slight increase due to slight hemoconcentration, 50 % of increased RBCs lost at delivery RBC production ceases temporarily, remainder of increased RBCs lost via normal catabolism

Eosinophils Basophils

Increases slightly, decreases slightly variable Hemodilution Disappear form peripheral blood By 3 days return to peripheral blood

Hemolysis:

Infants with hemolytic disorders due to isoimmunization may experience a slate and often severe anemia that is not physiologic but the result of continued hemolysis. Infants with severe hemolysis who never required an exchange transfusion are at greatest risk for this form of late anemia because of the presence in the infant's blood of maternal antibodies that continue to hemolyze the infant's RBCs. Maternal antibodies are normally removed during an exchange transfusion, reducing the risk of late anemia (Blackburn, 2013, p.243).

Myeloid period

begins at about 18 weeks, with eventual production of all types of blood cells. The bone marrow is the major site for blood productions after 30 weeks' gestation. Centers for blood formation arise in mesenchymal tissues and invade cavities produced during bone formation" (Blackburn, 2013, p. 230).

"Hepatic Period

begins during the fifth to sixth week, shortly after the onset of circulation during weeks 4-5. This period peaks from 6 to 18 weeks. Thus from 3 to 5 months the liver is a major source of fetal blood cells, although some blood formation continues in this site through the first week after birth. Liver mass increases 40 fold after liver hematopoiesis begins, and at 11 to 12 weeks' gestation, hematopoietic cells make up 60 % of the liver" (Blackburn, 2013, p. 230).

thicker alevoli wall

decreased alveolar surface area- Less efficient gas transport and exchange (Blackburn, 2013).

immature alveoli

decreased size and number of alveoli- Risk of Respiratory insufficiency and pulmonary problems

• Preeclampsia superimposed on chronic hypertension

"Highly likely in women who develop new proteinuria or with preexisting hypertension and proteinuria who develop sudden increases in blood pressure or proteinuria, thrombocytopenia, or increases in hepatocellular enzymes" (Blackburn et al., p 267).

Which infants are at risk for physiologic jaundice?

"Physiologic jaundice in the newborn is seen in 50 to 60% of term infants and up to 80% of preterm infants during the first days after birth" (Blackburn, 2013). It is a normal process in the first days after birth and is due to normal physiologic adaptations. Blackburn (2013) describes that there are numerous factors that contribute to the development of physiologic jaundice. Infants who have increased red blood cell production with decreased RBC lifespan are at increased risk, as well as infants who have a delayed first meconium. There is also a delay in bilirubin clearance in the first weeks of life, that gradually resolves. (Blackburn, 2013).

Tetralogy of fallot(TOF):

"This defect is the most common cause of right to left shunting. TOF includes a combination of VSD, pulmonary valve stenosis, RV hypertrophy, and rightward displacement of the aortic root. PVR is normal. Surgical correction usually occurs in infancy, although there may be some residual shunting following correction. Pregnancy outcome is relatively good for those individuals who have undergone surgical correction who have good ventricular function and no significant right ventricular outflow tract obstruction. In pregnant women with uncorrected VSDs, the decrease in systemic vascular resistance (SVR) leads to increases in right to left shunting and cyanosis. This can be complicated by intrapartum blood loss, leading to systemic hypotension. Therefore, careful monitoring is warranted" (Blackburn, 2013, p. 266)

the timeline in normal fetal cardiac development

18 days: Horseshoe-shaped cardiac primordium 20 days: bilateral cardia primordia fuse, cardiac jelly, and arotic arch is forming. 22 days: heart looping into S shape, heart begins to beat, aortic arches 1 and 2 are forming, dorsal mesocardium breaking down. 24 days: atria are beginning to bulge, righ and left ventricles act like two pumps in series, outflow tract is distinguished from right ventricle. Late Week 4: Sinus venosus is incorporated into right atrium, endocardial cushions appear, septum primum appears between right and left atria, muscular interventricular septum is forming, truncononal ridges are forming, Aortic arch 1 is regressing, aortic arch III forming and aortic arch IV is forming. Early Week 5: Endocardial cushions are coming together and forming right and left AV canals, continued growth of interatrial septum primum and muscular interventricular septum, truncus arteriosus dividing into aorta and pulmonary artery, AV bundle is forming (possible neurogenic control of heart beat), pulmonary veins into atrium, aortic arches I and III regressed, aortic arches III and IV formed and aortic arch VI is forming. Late Week 5-Early Week 6 : Fusion endocardia cushions, interatrial septum primum is almost contracting endocardial cushions, membranous part of interventricular septum starts to form, semilunar valves begin to form. Late in Week 6: Interatrial foramen secundum is large, interatrial septum secundum starts to form, interventricular septum is almost complete, coronary circulation is becoming established. 8-9 Weeks: Membranous part of interventricular septum complete. (Blackburn et al., p 270).

Blood pressure:

: Although there are subsequent increases in both blood volume and cardiac output during pregnancy, these changes are not associate with increases in either venous or arterial pressure since the increase in intravenous volume is balanced by decreased SVR. Blood pressure, especially diastolic pressure, is generally reported to decrease, reaching a nadir by mid pregnancy. The initial decrease is thought to be due to a lag in compensation for changes in peripheral vascular resistance. The diastolic blood pressure decrease reaches nadir at 24 to 32 weeks and then gradually returns to nonpregnant baseline values by term. The magnitude of BP changes varies from the position of the women during measurement. Systolic BP remains either stable or decreased slightly, whereas diastolic pressure decreases 10 to 15 mmHg. The reduction in blood pressure may be secondary to vasodilatory effects of nitric oxide, which increases in pregnancy, as well as hormonal and other factors such as prostacyclin and relaxin that mediate a decrease in peripheral vascular resistance.

Red blood cell volume

: RBC production and thus volume increase throughout pregnancy to a level 20% to 30% higher than nonpregnant values. Intravascular expansion is mainly due to an increase in plasma volume; therefore, hemodilution occurs.

TTN - Transient Tachypnea of the Newborn

A disorder characterized by inadequate or delayed clearance of lung fluid leading to a transient pulmonary edema" (Blackburn, 2013). Most often see in cesearean before labor onset or infants who have experienced a perinatal hypoxic stress event. Manifestations include respiratory rates of 120-140 breaths per minute. Mild to moderate retractions and grunting may be present. Typically lungs sound moist but clear quickly. Treatment is supportive and lungs are cleared within 48-72 hours, sepsis must be ruled out. (Blackburn, 2013).

Thalassemia

A disorder in the synthesis of either the a or B peptide chains of the hemoglobin molecule. This leads to alterations in the RBC membrane and decreased RBC lifespan. Most pregnant women with a-thelessemia have one or two genes affected and have either a silent presentation or mild anemia. If all four a-chain genes are missing, the fetus cannot synthesize either normal fetal hemoglobin nor adult hemoglobin. Infants develop high output, cadiac failure, fetal hydrops, and are often stillborn or die shortly after birth. Intrauterine transfusion is associated with decreased perinatal mortality and morbidity" (Blackburn, 2013, p. 227).

Physiologic anemia of infancy:

A tolerable decline without any clinical difficulties in hemoglobin experienced by term infants during the first few months of life as a result of postnatal suppression of hematopoiesis. In the term infant, the lowest hemoglobin level (11.4 +/- 0.9 g/dL) is reached at 6-12 weeks, then slowly increases by 4-6 months with the resumption of Epo production and erythropoiesis. This process may be delayed in infants who have had an exchange transfusion or multiple blood transfusions. (Blackburn, 2013, p.242).

. One major purpose for the hemodynamic changes in pregnancy is protection for the

maternal tolerance of blood loss and placental separation at delivery.

Platelets

Decrease slightly but in normal adult range (150,000- 400,000/mm) variable 20 % decrease with placental separation Increase by 3-5 days with gradual return to non-pregnant levels

Decreased lung elastic and recoil

Decreased lung compliance requiring higher pressures and more work to expand, increased risk of atelectasis (Blackburn, 2013).

Chemical factors

All chemical drive factors for breathing are regulated by chemoreceptors within the neonate's lungs and body to give information about the metabolic needs of the infant. These are a few of the many ways in which chemical factor influence respiration. 1. Response to hypoxemia or decreases in O2 concentration. This causes an increased tidal volume, but if hypoxia continues or gets worse the respiratory depth and rate will decrease again, followed by a failure of arousal. This is dependent on environmental factors in the first few weeks, (keeping baby warm). (Blackburn, 2013). 2. Response to Hypercapnia or increased CO2 concentration. Increased ventilation is directly proportional to inspired CO2 concentration. (Blackburn, 2013). 3. Response to hyperoxia or increase in FIO2 concentration causes a transient respiratory depression (Blackburn, 2013)

evaluation of fetal lung maturity

Amniotic fluid can be assessed for the presence of surfactant phospholipids (Blackburn, 2013, p. 318). This is possible because the surfactant phospholipid concentration changes with the maturity of the surfactant system and lung (Blackburn, 2013, p. 318). The ratio between sphingomyelin and lecithin is used to predict RDS if born within 2 days of testing (via amniocentesis) (Blackburn, 2013, p. 318). Sphingomyelin, a membrane lipid, remains relatively stable, where lecithin has a dramatic increase at approximately the 34-35 week of pregnancy (Blackburn, 2013, p. 318). The L/S ratio aids in prediction of lung maturity (Blackburn, 2013, p. 318). The higher ratio the more mature the lungs (Blackburn, 2013, p. 318). Lungs with a ratio of >2:1 are mature and not at risk for RDS, 1.5:1 -2:1 are considered immature, and <1:1 is a great risk for RDS (Blackburn, 2013, p. 318).

Atrial Septal Defect (ASD):

An uncorrected ASD is usually asymptomatic but may become symptomatic for the first time in pregnancy. The most common complications include arrhythmias, pulmonary HTN, and heart failure. If additional load of left to right shunting is not tolerated, RV failure occurs, leading to marked peripheral edema, atrial arrhythmias, pulmonary hypertension, and paradoxical systemic emboli across the septal defect.

Canalicular (16-26 weeks gestation)-

Around 16 weeks. The epithelial cells of the distal air spaces (future alveolar lining) begin to flatten (becoming more cuboidal) and increase in glycogen (which serves as a substrate for surfactant synthesis), signaling the beginning of the canalicular stage" (p.311). The vascular capillaries are multiplying in the interstitial space during this time (Blackburn, 2013, p. 311). During week 19 the alveolar capillary membranes are formed by changes to the mesenchymal and bringing capillaries closer airway epithelium (Blackburn, 2013, p. 311). This stage also mark the beginning of surfactant production (Blackburn, 2013, p. 311).

Embryonic (3-6 weeks gestation)-

As early as day 24 ventricular diverticulum can be seen forming from the foregut (Blackburn, 2013, p. 309). This structure continues to expand down (Blackburn, 2013, p. 309). The esophagus is separated from that structure by a septum (Blackburn, 2013, p. 309). Dichotomous branches are visible at day 26-28 (Blackburn, 2013, p. 309). By the end of the 6th week of gestations the 2 lungs with and there divisions are visible (3 lobes on the right, 2 left) (Blackburn, 2013, p. 309). There are 10 rudimentary bronchopulmonary segments on the right and 8-9 on the left (Blackburn, 2013, p. 309).

Maturity of CNS

Blackburn (2013) discusses that the first neurological control over neonate respiration is the maturity of the CNS. How much of the CNS is myelinated influences how quickly impulses can travel between chemoreceptors and the brain to stimulate ventilation. This is also influenced by the degree of "dendritic interconnections (synapses)" in the CNS, which set the response level in relationship to neuronal depolarization.

• Chronic Hypertension

Blood pressure 140/90 mmHg or greater before the twentieth week of gestation or, if only diagnosed during pregnancy, persisting 6 weeks after pregnancy" (Blackburn et al., p 267).

Cardiac output and stroke volume

Cardiac output, which is a product of heart rate times stroke volume, is one of the most significant hemodynamic changes encountered during pregnancy. 50% of the increase occurs by 8 weeks gestation, mediated by changes n SVR. Cardiac output continues to rise more slowly until the 3rd trimester. A slight decline in cardiac output may be seen in late pregnancy due to the decrease in stroke volume near term. The increase in cardiac output is associated with an increase in venous return and greater right ventricular output, especially in the left lateral position. The increase in cardiac output is due to changes in both stoke volume and heart rate. Changes in heart rate and stroke volume are reported by 5 weeks and 8 weeks gestation. The rise in cardiac output early in pregnancy is due primarily to an increase in stroke volume. Stroke volume increases progressively during the first and second trimesters, to a peak value of approx 25% to 30% above nonpregnant values, peaking at 16 t 24 weeks. Stroke volume declines during the latter stages of pregnancy and returns to values that are with the prepregnant rage by term. During pregnancy (especially the third trimester) the resting cardiac output fluctuates markedly with changes in body position.

MAS- Meconium Aspiration Syndrome

Cause of respiratory failure in term and postterm infants. There are a variety of factors that play into respiratory failure after meconium, and it is not clear whether meconium is aspirated or found in the lungs by coincidence. What is known is that meconium will partially obstruct the lower airways causing atelectasis as well as air trapping and over inflation distal to the obstruction (V/Q mismatch). Meconium also deactivates type II alveolar cells, or the cells responsible for surfactant. This also leads to atelectasis in the lung. Meconium activates cytokines causing inflammation within the lung. Vasoconstriction along with possible fetal hypoxia can lead to Persistent Pulmonary Hypertension, leading to respiratory failure. Manifestations include meconium staining at birth, increased respiratory rate, increased work of breathing. Treatment options for depressed infants as told by Cunningham et. al, (2010) "the trachea is intubated and meconium suctioned from beneath the glottis. If the newborn is vigorous, then tracheal suction is not necessary and may injure the vocal chords".

Eisenmenger Syndrome:

Combines the presence of congenital communication between systemic and pulmonary circulations with progressive pulmonary hypertension that leads to shunt reversal or bidirectional flow. It is often associated with VSD or PDA. The fetal and maternal mortality rate for pregnant women with Eisenmenger syndrome can be 50% when pulmonary hypertension is associated with a VSD. Because of the high mortality rate, women are usually discouraged from becoming pregnant and pregnancy termination is usually recommended.

Air travel

Commercial flights expose a person to altitude, as the aircraft pressurizes between 6000 and 8000 ft. above sea level (Blackburn, 2013, p. 305). Increased heart rate, increased blood pressure, and decreased aerobic capacity are all pregnancy compensation mechanisms that may occur during takeoff (Blackburn, 2013, p. 305). The higher altitude may also cause the pregnant women to feel dyspnea and an elevated respiratory rate (Blackburn, 2013, p. 305).

RDS

Developmental deficiency in surfactant synthesis accompanied by lung immaturity and hypoperfusion". Most common source of respiratory failure in the preterm infant. Alterations in surface tension lead to overdistention of normal alveoli. These alveoli reach their elastic limit, causing the infant to require more pressure to inspire the same volume. Smaller alveoli progressively collapse reducing lung compliance. Uneven V/Q ratios, decreased FRC, and increased closing capacity. Manifestations- The infant will initially attempt to compensate by increasing respiratory rates and depths. These symptoms will increase in severity over 72 hours. Pitting edema, cyanosis, and diminished breath sounds may also be present. Retractions in RDS can be marked, with substernal retractions severe. Interventions are supportive and active. Hydration is important at the correct rate and amount, as to not increase risk for congestive heart failure. Administration of exogenous surfactant and CPAP with PEEP can sometimes avoid mechanical ventilation, but intubation is sometimes necessary. (Blackburn, 2013).

Biochemical factors of respiration

During pregnancy hormones and biochemical factors foster changes in respiratory system (Blackburn, 2013, p. 297). There are 2 ways for this to occur either centrally on the system or targeting the smooth muscle of the lung (Blackburn, 2013, p. 297). Progesterone, estradiol, and prostaglandins crucial for these modifications on the respiratory system (Blackburn, 2013, p. 297). Progesterone, a respiratory stimulant, has many functions including: lowering CO2 threshold in respiratory system, decreases work breathing, lowers airway resistance and increases airflow (Blackburn, 2013, p. 298). PGs have effects on smooth muscles of the bronchial airway (Blackburn, 2013, p. 298).

Discuss symptoms women may experience with these normal changes, and how to counsel them

During pregnancy, healthy women experience some increased shortness of breath and rapid heart rate on exertion and increased fatigue. They may experience dizziness and lightheadedness upon abrupt position changes related to supine hypotension syndrome. They may also experience edema in their hands and feet, nasal stuffiness, varicose veins, and anemia. You would want to counsel the patient on the fact that these are all normal changes during pregnancy. If they are experiencing shortness of breath or rapid heart rate on exertion and fatigue it is a sign that your body needs to rest. When going from laying to sitting or standing it should not be done abruptly, the patient needs to be sure they are consuming a gallon of water a day and if syncope occurs they should receive medical attention right away. Edema in the lower extremities is common in late pregnancy as is varicosities. Thigh high support hose may help decrease the swelling and discomfort from varicose veins by increasing systemic vascular resistance (SVR). Elevating feet when able will also help. A pregnant woman may wish to sleep with head elevated (use a second pillow) to help with the nasal stuffiness. If notice redness, local heat, or bleeding is noted, consult care provider. To prevent anemia, eat iron rich foods such as green vegetables, nuts, egg yolks, red meat, turkey, and whole grains. One may also take iron tablets supplements if anemia persists.

Alveolar (36-2-3years post birth)-

During this time primitive alveoli form. Primitive alveoli are present and are smooth walled transitional ducts and saccules with primitive septa with double capillary loops (Blackburn, 2013, p. 311). Postnatally the true alveoli form, via the saccules increase and deepen, as only20% are present at term (Blackburn, 2013, p.311). The stage also marks the formation of a single capillary network (Blackburn, 2013, p. 311).

Exercise in pregnancy

Exercise has significant benefit for the mother and fetus. Regular aerobic exercise done two to three times per week maintains or improves maternal fitness during pregnancy. Fit women have been shown to have shorter labors and few're perinatal complications. Concerns regarding exercise during pregnancy include the effects on the fetus and mother, including risks of hyperthermia and increased cardiac workload" (Blackburn,2013, p. 261). One thing to consider is that both pregnancy and exercise increase oxygen consumption. With exercise the blood flow is redistributed to the skin and bones and away from internal organs including the uterus. This decreased blood supply could be harmful to the fetus but in order for fetal hypoxia to occur the blood flow reduction has to be more than 50%. In a healthy pregnant woman this is not likely and would require prolonged strenuous exercise. The fetal heart rate has been noted to increase 5-25 beats per minute with maternal exercise. This can be related to the decrease in oxygen, the increase of maternal vasoactive hormones, or, contraction caused by exercise. The FHR may not return to baseline for up to 30 minutes. Although there are many benefits to exercise in pregnancy including fitness, cardiovascular health, control of BP, decreased backaches and fatigue, shorter labors, and circulation support, at no time should exercise continue if pain or contractions are present. The provider should be called if the woman experiences bleeding, dizziness, shortness of breath, palpitations, faintness, tachycardia, back pain, pubic pain or difficulty walking (Blackburn, 2013, p.261-263).

White blood Cells

Increase 8% to 5000-12,000/mm (up to 15,000/mm seen) Begins in second month, increase involves primarily neutrophils Estrogen Increase to 25,000-30,000/mm Decrease to 6000-10,000/mm, normal values by 4-7 days

Increased oxygen consumption

Increased respiratory rate and work of breathing, risk of hypoxia (Blackburn, 2013).

Megaloblastic Anemia

Folic acid deficiency is the most common cause of megaloblastic anemia encountered during pregnancy. Folate demands increase threefold during pregnancy. Because folic acid is essential for DNA synthesis and cell duplication, folate is needed for growth of the fetus and placenta as well as for maternal RBC production. Maternal serum folate levels fall during pregnancy, and women with inadequate dietary intake need supplements. Severe folic acid deficiency has been associated with fetal malformations, preeclampsia, placenta abruption, prematurity and low birth weight. Maternal folate deficiency increases the risk of neural tube defects and has been associated with an increased risk for cleft lip and palate and preterm birth" Blackburn, 2013, p. 227).

Heart Rate

Heart rate is determinant of cardiac output that has the widest range of values. The maternal heart rate increases progressively during pregnancy, averaging 10 to 20 bpm higher by 32 weeks. At term the heart rate may return to near baseline levels in some women. Twin pregnancies have an earlier acceleration in heart rate, with the maximum increase 40% above the nonpregnant level near term. The increased heart rate results in elevated myocardial oxygen requirements, which is probably not important in women without cardiac disease but may become significant with underlying cardiovascular pathology.

Iron Deficiency Anemia

Hematologic changes in pregnancy can make diagnosis of iron deficiency difficult. Total iron binding capacity and serum iron often fall during pregnancy, as well as with iron deficiency. A useful test for iron deficiency in the pregnant woman is measurement of serum ferritin levels, which correlate well with iron stores during pregnancy. Serum ferritin levels lower than 12 mcg/L with a low hemoglobin indicate iron deficiency, which can be treated with ferrous sulfate until the hemoglobin returns to levels normal for the stage of gestation. If untreated is associated with an increased risk of low birth rate, preterm birth, and perinatal mortality" (Blackburn, 2013, p. 226-227).

URI

Hormonal changes (especially the increase in estrogen) alone with increased blood volume, hyperemia, edema, glandular hypersecretion, and increase phagocyte activity alter the mucosa of the oro- and nasopharynx with capillary engorgement through the respiratory tract" (p. 304). Some experience inflammation and redness to the nasopharynx, larynx, trachea, and bronchi (Blackburn, 2013, p. 304). These usually more annoying than worrisome (Blackburn, 2013, p. 304). Symptoms are worse with URI and preeclampsia (Blackburn, 2013, p. 304). Inflammation can cause hoarseness, difficulty breathing, and nosebleeds (Blackburn, 2013, p. 304).

Which infants are at risk for hyperbilirubinemia

Hyperbilirubinemia can be caused from a combination of pathologic and physiologic factors. "Risk is increased in breastfed, late preterm, and preterm infants" (Blackburn, 2013). Major risk factors within late preterm and preterm babies includes: "Total serum bilirubin (TSB) level in the high-risk zone on the bilirubin nomogram, jaundice in the first 24 hours postbirth, blood group incompatibility with positive direct Coombs test, other known hemolytic disease, gestational age of 35 to 36 weeks, previous sibling having received phototherapy, cephalohematoma or significant bruising, East Asian ethnicity, and exclusive breastfeeding, particularly in infants with difficulties nursing and excessive infant weight loss" (Blackburn, 2013).

• Preeclampsia:

Hypertension with proteinuria. Hypertension: blood pressure >140mmHg systolic or 90mmHg diastolic after 20 weeks' gestation in a woman normotensive before 20 weeks' gestation. Proteinuria: 300mg/L (30mg/dL) protein in a random specimen and excretion of 300mg/24 hours. Hypertension with other systemic symptoms of preeclampsia in the absence of proteinuria is highly suspicious of preeclampsia

Reticulocytes

Increases 1%-2 % Gradual increase to third trimester Increased RBC production Increases slightly, non-pregnant values 4-6 weeks

Hypoxia

Involves a decreased oxygen level of the tissues, whereas hypoxemia involves a decreased oxygen content of the blood" (Blackburn, 2013). Hypoxia indicates impaired aerobic metabolism, and a subsequent depletion of ATP. Brief hypoxic events are quickly reversed, but prolonged hypoxia results in cell death. Manifestations include abnormal organ function, muscles weakness and fatigue, tachypnea, tachycardia and increased amounts of immature red blood cells (anemia). Treatment includes treating the cause of the hypoxia- if it is due to decreased blood flow, or some histology that prevents O2 uptake, or chemical and hormonal imbalances. (Blackburn, 2013).

Acid / Base changes

The normal pregnant woman is in a state of compensated respiratory alkalosis, which is thought to be the result of the effects of progesterone on the respiratory system and lung volume changes, especially increased minute volume" (p.300). These changes lead to the increase of PaO2, lowering of arterial and alveolar CO2 (Blackburn, 2013, p. 300). Respiratory alkalosis is thought to enables the transfer CO2 from fetus to mother (Blackburn, 2013, p. 300).

Arrhythmias

Many women experience rhythm disruptions that become more intense during the second and third trimester. Most of these arrhythmias are benign and are not indicative of heart disease. The most common, seen in 50-60%, are simple ventricular or atrial ectopy. The woman might experience skipped beats, momentary pressure in the neck or chest, or extra beats. These are usually premature ventricular beats and require no further treatment. Extra systoles or supraventricular tachycardia may also occur. The reason for the increase in arrhythmias may be related to the electrophysiological effects of hormones, increased sympathetic nervous system activity, hemodynamic alterations, increased potassium, or in some cases, underlying cardiac disease. In addition, atrial stretching and estrogen may lower the threshold for arrhythmias. Most arrhythmias are neither life-threatening nor due to structural defects. Occasionally cardiac problems may present during pregnancy, so arrhythmias should be evaluated and managed in a manner similar to that in nonpregnant women. Awareness of the increased heart rate can be uncomfortable for some women. True tachycardia, such as paroxysmal atrial tachycardia or paroxysmal atrial fibrillation, may be evident for the first time during pregnancy". The woman may try taking a deep breath, coughing, or the Valsalva maneuver which could slow the heart rate to a more normal pattern (Blackburn, 2013. p. 260).

Marfan syndrome:

Marfan syndrome is an autosomal dominant disorder of connective tissue whose clinical manifestations include skeletal, ocular, and cardiovascular abnormalities. Aortic dilation is one of the manifestations. Complications that can result include aneurysm formation and rupture, aortic dissection, and aortic regurgitation. Structural changes in the aortic wall due to high estrogen levels predispose pregnant women to aortic dissections. Rupture is more likely to occur in the third trimester or in the first stage of labor. Counseling regarding the risk of inheritance and the potential maternal complications should be given before conception if possible. If pregnancy occurs, the use of long-acting Beta blockers to decrease pulsatile pressure on the aortic wall in indicated, along with limitations on physical activity and preventing hypertensive complications (Blackburn, 2013, p. 266).

Mitral Regurgitation

May be due to rheumatic disease, however there are numerous conditions that can lead to its development, including congenital heart disease, HTN, ischemia, and idiopathic myocardial disease. Fatigue is main symptom. Women with mild regurgitation are usually able to tolerate pregnancy well and development of CHF is rare.

Sleep State

Neonates engaged in quiet or non-REM sleep have more regular respirations with "directly proportional relationship between PCO2 and degree of ventilation" (Blackburn, 2013). During REM sleep, the neonate has more irregular respirations, and paradoxical

Supine hypotension syndrome

Orthostatic stress generated by changes in position (from recumbent to sitting to standing) is associated with acute hemodynamic changes. Blood pools in dependent vessels, which reduces venous return and decreases cardiac output and blood pressure with increasing orthostatic stress. Heart rate and systemic vascular resistance (SVR) increase; mean arterial pressure changes, however, are not significant. In addition, decreased baroreflex sensitivity during pregnancy leads to blunted reflex activation of the sympathetic nervous system and inadequate peripheral vasoconstriction. The gravid uterus is associated with significant amount of caval blood flow obstruction in the supine position. Approximately 90% of gravid women experience obstruction of the inferior vena cava in the supine position late in pregnancy, but rarely does this lead to hypotension or other symptoms. Late in pregnancy, but before the the fetal presenting part becomes engaged, the uterus is mobile enough to fall back against the inferior vena cava in the supine position. This results in vena caval tamponade. Vascular compression may also be applied to the aorta and its branches. In most women, paravertebral collateral circulation develops during pregnancy. This, along with the dilated utero-ovarian circulation, permits blood flow from the legs and pelvis to bypass the vena cava. These changes are reversed in the left lateral position which displaces the uterus to the left and off the vena cava. In the supine position the aorta may also be compressed, which can also alter arterial blood pressure. Usually the fall in cardiac output due to posture change is compensated for by an increase in peripheral resistance. This allows systemic blood pressure and heart rate to remain unchanged. However, up to 8% of pregnant women in the supine position may experience a significant decrease in heart rate and blood pressure leading to symptoms of weakness, lightheadedness, nausea, dizziness, or syncope. This is referred to as supine hypotensive syndrome of pregnancy and is usually corrected when position is changed

need for neonatal Vitamin K at birth

Newborns have reduced level of all of the vitamin K-dependent clotting factors (II, VII, IX, X) at birth, leading to a physiologic hypothrombinemia. The reduction in these factors is the consequence of poor placental transport of vitamin K to the fetus as well as lack of intestinal colonization by bacteria that normally synthesize vitamin K. Low vitamin K levels may occur due to the need to regulate the levels of other (noncoagulation-related) vitamin K-dependent proteins that regulate growth in the fetus. Unless the infant is given vitamin K at birth, the deficiency intensifies in the first few days after birth as maternally acquired vitamin K is catabolized (half-life is about 24 hours). The decline is more marked in infants who are breastfed, have a history of perinatal asphyxia, or are born to mothers on coumarin derivative anticoagulants. Neonatal liver stores are one fifth those of adults because placental transport of K is low. Vitamin K stores gradually increase in the first month more rapidly in formula fed babies in comparison to breastfed babies due to higher levels of vitamin K in formula and differences in intestinal colonization. Vitamin K is given after birth to prevent hemorrhagic disease of the newborn (HDN) also known as vitamin K deficiency bleeding (VKDB). Three forms of VKDB include early, classic and late. The early form of VKDB is seen in infants of women on certain medications including antiepileptic drugs, barbiturates, and phenytoin. The classic from of VKDB is seen at 24 hours to 7 days as the vitamin K deficiency intensifies. Late VKDB is rare and is seen at 2-12 weeks and is seen in infants that did not receive Vitamin K at birth or an inadequate oral dose and were breastfed or with hepatobiliary problems. VKDB involves bleeding from gastrointestinal tract, umbilical cord, or circumcision site; oozing from puncture sites; and generalized ecchymosis. Although it is likely that many newborns do not need vitamin K at birth, VKDB usually occurs in infants without specific risk factors. In countries where routine use of vitamin K was eliminated the incidence of VKDB is increased, thus prophylaxis at birth is recommended. Term neonates respond to prophylactic vitamin K administration at birth by achieving normal or near normal PTs, although actual values for several weeks or more. The response in preterm infants is less predictable, with minimal response to vitamin K seen in some VLBW infants due to an inability of the immature liver to synthesize adequate amounts of the precursor proteins (Blackburn, 2013, p.239-240).

Peri-partum cardiomyopathy:

Peripartum cardiomyopathy is a form of dilated cardiomyopathy seen in women without a previous history of heart disease, which develops during the last month of pregnancy or up to 5 months postpartum. In dilated cardiomyopathy the cardiac chambers become significantly dilated with a hypokinetic LV and progressive decrease in LV function. Peripartum cardiomyopathy has a frequency of 1/3000 to 1/4000 live births with recurrence risk in subsequent pregnancies of up to 50%. This disorder has a variable and unpredictable clinical course. Generally, 30% to 50% of women demonstrate partial recovery with persistence of some cardiac dysfunction; needing a heart transplant. In women with partial recovery, cardiac function may improve over time. The cause of pregnancy/postpartum state causes the disorder or aggravates an underlying cardiomyopathic process. The risk of developing peripartum cardiomyopathy is higher with increased maternal age, chronic hypertension, multiple gestation, multiparity, and preeclampsia

the evaluation process for a neonate with a murmur and cyanosis

Physical Exam: specific attention to abnormal precordia activity, abnormal heart sounds (gallop, click, or single S2), pathologic murmurs (loud, harsh, pansystolic etc), hepatomegaly, diminished or absent lower exremity pulses, abnormal four extremity blood pressure. Pulse Oximetry: Pre-and Post-ductal oxygen saturation assessing for cyanosis and differential cyanosis Chest Radiograph: Helpful in differentiating between pulmonary and careidac disorders. Should be obtained in neonates exhibiting cyanosis or respiratory symptoms. EEG: Hyperoxia Test: Useful in distinguishing from cardiac and non-cardiac causes of cyanosis. Echocardiography: Provides a definitive diagnosis of CHD giving information on the structural anatomy of the heart (Altman, 2016)

Mechanical factors of respiration

Several changes occur as the uterus enlarges including abdominal size, abdominal shape, and upward shift of the diaphragm (Blackburn, 2013, p. 297). The expanding uterus causes the diaphragm to move upward 4cm. During pregnancy, the diaphragm has increased movement of about 2cm and completes most the exertion for respiration, the costal muscles are not as active as the diaphragm (Blackburn, 2013, p. 297). Increased intraabdominal pressures causes the thoracic circumference to increase by 5-7cm, transverse diameter expands by 2cm (Blackburn, 2013, p. 297). There is also flaring of the lower ribs (Blackburn, 2013, p. 297). Late in pregnancy there is an increase in the subcostal angle, from 68 to 103 degrees (Blackburn, 2013, p. 297). The ribs cage is also more flexible due to ligamentous rib attachment relaxation (Blackburn, 2013, p. 297). Some of these changes mentioned aren't related to intraabdominal pressure, as the subcostal angel has increased prior to abdominal pressure (Blackburn, 2013, p. 297).

• Cardiovascular

Preeclampsia can cause an increase in CO and systemic vasoconstriction, increase in hydrostasis and hypertension causing systemic HTN, generalized edema and increased hemolysis (Blackburn et al., p 268).

• Cerebrovascular

Preeclampsia can cause cerebral motor ischemia, increase cerebral perfusion pressure with edema, cerebral edema, regional ischemia that can lead to grand mal seizures (eclampsia), cerebral hemorrhage, coma and central blindness and loss of speech (Blackburn et al., p 268).

• Renal

Preeclampsia can cause decreased renal blood flow and GFR, endothelial damage, hyperesponsivenesss of Angiotensin II in the tubular vasculature leading to possibility of proteinuria, increase creatinine and decreased creatinine clearance, oligura, increase in uric acid (Blackburn et al., p 268).

• Hepatic

Preeclampsia can cause ischemia and hepatic cellular injury, mitochondrial injury increasing risk for increase liver enzymes and intracellular fatty deposition (Blackburn et al., p 268).

• Uteroplacental:

Preeclampsia can cause uteroplacental insufficiency, decidual ischemia, decidual thrombosis causing increase risk for fetal somatic growth deficiency, hypoxemia and distress of the fetus, abruptio placentae, placental infarcts, thrombocytopenia (Blackburn et al., p 268).

• Hematologic:

Preeclampsia can lead to intravascular hemolysis and decidual thrombosis, release of fibrin degradation productions increasing risk of Schistocyte burr cells, elevated free hgb and iron decreased haptoglobin levels, thrombocytopenia and antiplatelet antibodies (Blackburn et al., p 268).

Lung volume-

Pregnancy has an impact on lung volume. These changes start in the middle of the second trimester and continue until term (Blackburn, 2013, p. 298). Per Blackburn (2013), "The most significant change is 30% to 40% (from 500 to 700mL) increase in Vt3 with a progressive 15% to 20% decreased expiratory reserve volume (ERV), 20% to 25% decrease in residual volume (RV), and 20% to 30% decrease in FRC" (p. 298). The supine position is even more compromised in supine position (Blackburn, 2013, p. 298).

Anemia of Prematurity

Preterm infants also experience a decline in Hgb during the first few months after birth secondary to postnatal suppression of hematopoiesis. However, preterm infants experience a greater decline in hemoglobin, and their hgb levels remain low for a longer period of time. This is a normocytic, normochromic anemia characterized by low Epo levels. Seen most often in infants less than 32 weeks' gestation with the lowest hemoglobin levels seen in the most immature infants. These levels may be as low as 7-10 g/dL even without significant loss from blood draws. The hemoglobin nadir is reached by 3-12 (usually 4-6) weeks and hemoglobin levels remain low for 3-6 months. The level of the nadir is inversely related to gestational age. These infants may be symptomatic or asymptomatic. Clinical findings may include tachycardia, tachypnea, lethargy, poor feeding, fatigue with feeding, poor weight gain (less than 25 g/day), pallor increased serum lactate, increased oxygen requirements, and episodes of apnea or bradycardia (Blackburn, 2013, p.243-244).

Discuss management of jaundice while breastfeeding.

Prevention is the focus of jaundice while breastfeeding. Encouraging feeding in the first 1-3 hours after birth helps to stimulate gut flora, intestinal motility, and meconium passage (as colostrum acts as a laxative). "This removes conjugated bilirubin from the small intestine, thus reducing the likelihood that this bilirubin will be recirculated by the enterohepatic shunt" (Blackburn, 2013). Frequent feedings help to enhance breast milk intake which has an inverse relationship with bilirubin levels. As feedings fall, bilirubin tends to rise. "Supplements should be avoided as they can interfere with establishment of breastfeeding" (Blackburn, 2013). Supplementation for medical reasons should always be done with formula or expressed milk rather than water or dextrose. "An inverse relationship between the number of feedings per day and bilirubin levels have been reported" (Blackburn, 2013). AAP recommends breastfeeding 8-10 times in a 24 hours period initially, to ensure adequate intake. "Initial and continuing support of the mother and other family members is essential to enhance breastfeeding success" (Blackburn, 2013). Managing jaundice while breastfeeding weighs many issues and concerns including maternal-infant interaction, stress, desire to breastfeed and advantages of breastfeeding. "AAP guidelines recommend that breastfeeding be continued whenever possible, but the supplementation with expressed breast milk of formula be considered if the infant's intake is inadequate, weight loss is excessive, or the infant seems dehydrated" (Blackburn, 2013). "Maisels recommends that any interruption of breastfeeing be avoided, unless the infant develops bilirubin levels above 25 mg/DL, and rather to continue frequent breastfeeding (every 2 to 3 hours) while using intensive phototherapy, unless the infant's weight loss from birth is greater than 12% or there is clinical evidence of dehydration" (Blackburn, 2013).

Pulmonary Artery Hypertension:

Severe pulmonary hypertension associated with pregnancy carries a 50% maternal mortality rate and a 40% fetal mortality rate if the mother survies, although a recent study found a lower maternal mortality rate of 25%. Significant pulmonary hypertension is a contraindication to pregnancy and pregnancy should be prevented or termination recommended if it occurs.

Mitral Stenosis

This lesion is caused almost exclusively by rheumatic heart disease. The stenotic valve restricts CO, resulting in fatigue, which is most common symptom. Risk of death is greatest in third trimester and after delivery. Management includes avoidance of supine position and prophylaxis against rheumatic disease during pregnancy and against endocarditis during labor and delivery. If severe, mitral commissurotomy prior to conception is advised. If symptomatic during pregnancy, activity and sodium restrictions, diuretics, and dig may be used.

Small compliant airway passages with higher airway resistance and immature reflexes

Risk of airway obstruction and apnea (Blackburn, 2013).

Systemic vascular resistance

SVR (mean arterial pressure divided by cardiac output) is decreased 20% to 30% during pregnancy and parallels the decrease in BP. SVR decreases by 5 weeks and usually reaches its lowest level by 16 to 34 weeks, then progressively increases to term. The decrease in vascular resistance is due to softening of collagen fibers and hypertrophy of smooth muscle, systemic vasodilation due to the vasodilatory effects of progesterone and prostaglandins, remodeling the maternal spiral arteries, fluid retention, and the addition of the low-resistance uteroplacental circulation, which receives a large proportion of cardiac output (Blackburn, 2013, p. 252-256).

Smoking

Smoking during pregnancy is among the leading preventable causes of adverse maternal and fetal outcome" (p.307). The cause of these complications is still not entirely understood, however, there are direct and indirect adverse effects (Blackburn, 2013, p.307). Smoking leads to decreased blood flow to the uterus and is considered an indirect effect (Blackburn, 2013, p. 307). Nicotine and other toxins that cross the placenta during smoking are direct adverse effects (Blackburn, 2013, p. 307). Nicotine may inhibit fetal growth as it reduces the number of nutrients available to the fetus, as it competes with the nutrients for placental nutrient carriers (Blackburn, 2013, p. 307). There are also changes to the placenta and its ability to function (Blackburn, 2013, p. 307). Placental changes of smokers suggest hypoxia and a compensatory hypertrophy (Blackburn, 2013, p. 307). The changes mimic the other conditions of chronic intrauterine hypoxia, such as anemia or living in high altitude (Blackburn, 2013, p. 308). Per Blackburn (2013), "The placentas of smokers also have more area of calcifications, an increased incidence of fibrin deposits, an increased frequency of necrosis and inflammation in the margin, and evidence of deoxyribonucleic acid (DNA) changes" (p. 308). These adverse effects to the placenta are due to decreased blood flow and can lead to acidosis and hypoxemia in the fetus (Blackburn, 2013, p. 308).

Fetal lung maturity

Surfactant synthesis is maintained through the collaboration of hormones, growth factor, and other substances (Blackburn, 2013, p. 317). Per Blackburn (2013), "Normal lung function is dependent on the presence of surfactant, which permits a decrease in surface tension at end-expiration (to prevent atelectasis) and an increase in surface tension during lung expansion (to facilitate elastic recoil on inspiration)" (p. 317). These actions are responsible for lessening the workload of breathing and maintaining blood gas pressures (Blackburn, 2013, p. 317). Hormones also play a role in the development of fetal lungs. Glucocorticoids, thyroid hormones, estradiol, vascular epithelial growth factor, fibroblast growth factor, prolactin, thyrotropin-releasing hormone, catecholamine, TGF-a, and epidermal growth factor all positively influence lung maturation (Blackburn, 2013, p. 317). Preparation for the decreased pulmonary vascular resistance after birth is prepared by stimulation of the phospholipid synthesis this is mediated by estradiol (Blackburn, 2013, p. 317). T3 and T4 are also thought to accelerate the synthesis of phospholipids (Blackburn, 2013, p. 317). Glucocorticoids have an important role in fetal lung development, as they are involved in surfactant synthesis and lung maturity (Blackburn, 2013, p. 318). Antenatal corticosteroids have the ability speed up lung maturity (Blackburn, 2013, p. 319). ACS is noted to improve maturity morphologically and functionally (Blackburn, 2013, p. 319).

PPHN- Persistent Pulmonary Hypertension of the Newborn

Syndrome of actue respiratory distress with hypoxemia and academia caused by decreased pulmonary blood flow due to elevated pulmonary resistance" (Blackburn, 2013). These infants have central cyanosis as associated with right to left shunting. Treatment with inhaled Nitrous Oxide can reverse changes of inflammation and endothelial dysfunction. (Blackburn, 2013).

Total blood volume

TBV is a combination of plasma volume and RBC volume, each of which is increased during pregnancy. Circulation blood volume increases by 30% to 40% (approx 1 ½ L). TBV increases rapidly until mid-pregnancy and then more slowly during the latter half, peaking at 28 to 34 weeks, then plateaus or decreases slightly to term. Changes in blood volume are due to the increase steroid hormones, plasma renin activity, aldosterone, human placental lactogen, atrial natriuretic factor, and other mediators.

Asthma

The modifications pregnancy induces on the respiratory system has a mixed impact on asthma (Blackburn, 2013, p. 306). Hyperventilation, that occurs in pregnancy, may be more noticeable in an asthmatic patient (Blackburn, 2013, p. 306). Factors that may improve asthma during pregnancy include: "increased progesterone-mediated bronchodilation, B-Adrenergic-stimulated bronchodilation, decreased plasma histamine level, increase free cortisol levels, increased glucocorticoid-mediated bronchodilation, PGI2-mediated bronchial stabilization, increased half-life of bronchodilators, decreased protein-binding of bronchodilators (Blackburn, 2013, p. 307, table 10-2). Pregnancy can worsen asthma via pulmonary refractoriness to cortisol effects, Increased PCF2A-mediated bronchoconstriction, decreased functional residual capacity, causing airway closure, and altered ventilation perfusion ratios, increased major basic protein in lung, increased incidence of viral or bacterial respiratory infection, increased gastroesophageal reflux, increased stress" (Blackburn, 2013, p. 307, table 10-2)

Surfactant

The lipoprotein, made up of 70-80% phospholipids, is respiratory surfactant (Blackburn, 2013, p. 314). Surfactant has many roles such as, suitable lung function, dropping surface tension in alveoli at that the air-liquid boundary, modification of lung mechanics, and innate host defense (Blackburn, 2013, p. 314). Per Blackburn (2013), "The majority (80%) of the lipid is saturated phosphatidylcholine (DPPC) is the most abundant. The latter is the component responsible for decreasing the surface tension to almost zero when compressed at the surface during inspiration" (p. 314). Another component of surfactant is phosphatidylglycerol (PG), making up 5-10% of the phospholipid (Blackburn, 2013, p. 314). PG is a good indication of surfactant, as it is special to lung cells, bronchoalveolar fluid, and amniotic fluid (Blackburn, 2013, p. 314). Underdeveloped lungs have more phosphatidylinositol PI than PG (Blackburn, 2013, p. 314). The two have an inverse relationship, as PG increases PI decrease (Blackburn, 2013, p. 314). The PG increase marks maturing lungs (Blackburn, 2013, p. 314). Surfactant is also composed of four proteins (Blackburn, 2013, p. 314). The proteins are labelled SP-A, SP-B, SP-C, and SP-D. SP-A is involved in innate host defense, modifies inflammatory response, promotes phagocytosis, surfactant turnover, formation of tubular myelin, and aids in the removal of pathogens per macrophages (Blackburn, 2013, p. 314-315). SP-B is hydrophobic, aides in manufacturing of lamellar bodies, reproduction of surfactant, and maintains surface tension-lowering effect that promotes the monolayer, lipid adhesion, and surface film development (Blackburn, 2013, p. 314-315). SP-C is also hydrophobic (Blackburn, 2013, p. 314). SP-B and SP-C work together to enable spreading surface absorption and lipid uptake (Blackburn, 2013, p. 315-316). SP-D is hydrophilic, pertinent in surfactant structure, and controls alveolar surfactant pool and uptake (Blackburn, 2013, p.316). SP-D encourages phagocytosis and macrophage opsonization as it attaches to bacteria, fungi and viruses (Blackburn, 2013, p. 316). Alterations in surfactant proteins can lead to adverse effects to fetus. Mutations in SP-A, SP-B, SP-C and transport proteins can cause acute or chronic respiratory issues after birth, due to surfactant production problems (Blackburn, 2013, p. 316). SP-B deficiency causes low surfactant, respiratory failure, risk air leak, and risk pulmonary hypertension (Blackburn, p. 2013, p. 316). Absence of SP-B leads to RDS, has a poor prognosis (3-6 months of life), and only treatment for infant is lung transplant (Blackburn, 2013, p. 316). The alterations to SP-C has a wide array of symptoms including: tachypnea, cyanosis, failure to thrive, and interstitial lung disease (Blackburn, 2013, p. 316).

What are signs of maternal CV decompensation

The profound alterations in the cardiorespiratory system and hemodynamics during pregnancy can result in death or disability to women with underlying heart disease. Many early symptoms of cardiac disease, such as fatigue, dyspnea on exertion, dependent edema, presyncope (due to pressure on the inferior vena cava), and palpitations are normal findings in pregnancy. Thus the diagnosis of cardiac disease may be delayed in women who present with symptoms of cardiac disorders for the first time during pregnancy. Some women may actually benefit somewhat from the increase in cardiac output decrease in SVR, and increased heart rate. On the other hand, cardiac diseases associated with fixed lesions do not tolerate the volume increase because the stenotic area cannot accommodate the increased flow. When blood volume reaches its peak, the potential for congestive heart failure increases. The increased heart rate shortens the diastolic filling time, thereby preventing adequate filling of the heart. This combined with the decrease in SVR may result in a drop in blood pressure, increased fatigue, dizziness, and reduced uterine blood flow. At delivery the risk for CHF is further increased by the increase in blood volume. Acute pulmonary edema may occur. The increased cardiac load with the marked increase in cardiac output immediately after delivery may significantly increase ventricular filling pressures and stroke volume increasing the risk of clinical deterioration. (Blackburn, 2013, p. 263-264)

Truncus Arteriosis:

This occurs when there is failure of the aorta and pulmonary artery to separate. The type of Truncus is dependent on how the arteries remain connected. Typically, there is also a VSD. There is only one truncus valve instead of a pulmonic and artic valve. This valve is quite commonly ill functioning. Oxygen poor blood is and oxygen rich blood are mixed as the blood flows to the lungs the body (Parker, 2016). • Morbidity: 300 cases a year in the US (Parker, 2016). • Interventions: Surgical intervention done in the first few months. The goal of repair is to create a separate flow of oxygen poor blood to the lunch from the oxygen rich blood to the body. The VSD will be closed using a patch, the original truncus will be make into the aorta to carry oxygen rich blood to the body and an artificial conduit with an artificial valve will be connected to the RV to the arteries going to lungs. Most babies survive but will require additional surgery. Medications may be prescribed to help strengthen the heart muscle and decrease blood pressure and to rid body of extra fluid. Nutrition is important and infants may not feed well due to poor oxygenation (Parker, 2016).

Transposition of the Great Arteries

Transposition occurs when there is an abnormal septation that occurs in the truncus arteriosus allowing the aorta to arise from the RV and the pulmonary artery to arise from the LV. There are two separate circulating systems. One system is pumping deoxygenation blood into RA to RV and out the aorta then back out to the circulatory system (never to the lung to be oxygenated). The other circulation, blood is pumping oxygenated blood (from the lungs) to the LA then to the LV and back to the pulmonary artery and then on to the lungs. Typically, these infants have other heart defects such as septal defects in the ventricle or the atrium, thus allowing for mixing of unoxygenated blood with oxygenated blood (Blackburn, 2013, p. 289) • Morbidity/Mortality: 1 in 3,300 babies will have Transposition of the Great Arteries • Interventions: Arterial Switch Operation: Most common procedure and typically done in the first month of life. Enables BF to the heart and rest of body. The pulmonary arteria will be switched to arise from RV and the aorta to the LV. Coronary arteries are also reattached to the aorta. Atrial Switch Operation: Less common procedure. There is a tunnel made between top atria of heart allowing poorly oxygenation blood to move from the right atrium to the left ventricle and to the pulmonary artery to the lungs. Oxygenated blood then through the tunnel of the left atrium to the right ventricle and out the aorta to the body (Parker S.E, 2016)

fetal cardiac adaption to extrauterine life

Two major events trigger extrauterine neonatal circulation, they are the placenta being removed from baby and the other is oxygenation of the lungs. Upon birth, there is change as PVR will decrease (by 80%) and SVR will increase. As the infant breaths and there is lung expansion, there is alveolar oxygenation that will trigger dilation of the pulmonary vascular bed. After delivery 90% of the CO will go to the pulmonary arteries, then to the LV to be pumped out to the periphery. This is a big change for the LV, as 80% of the CO went through ductal shunting in utero. The foramen ovale will close due to increase left sided pressure within the first few minutes after birth, thus separating the atria. The ductus venosus will close due constriction of umbilical vessels secondary to increase of PO2. Closure of the DA begin immediately but will remain patent for several hours to days. Immediately after delivery, the PVR will remain higher than systemic and allow for small right to left shunt. This will allow mixture of oxygenated blood with deoxygenated blood. If this does not resolve, then persistent pulmonary hypertension will develop. By 10-15 hours, in most term infant, the DA will close, this is because of oxygen and prostaglandins (Blackburn, 2013, pp. 281-282)

Plasma volume

about 75% of the TBV increases in the plasma volume. Plasma volume increases progressively from 6 to 8 weeks by approximately 45% to 50% or about 1200 to 1600 mL above nonpregnant values. This change begins at 6 to 8 weeks and increases rapidly during the second trimester, followed by a slower but progressive increase that reaches its maximum of 4700 to 5200 mL at about 32 weeks. Alterations in blood and plasma volume are influence by hormonal effects, nitric oxide mediated vasodilation, mechanical factors (blood flow in uteroplacetal vessels) and changes in the renal system and in fluid and electrolyte homeostasis.

ARD

acute lung injury involving diffuse interstitial infiltrates, decreased lung compliance, and hypoxia" (p. 305). There are several causes to ARDs including: sepsis, DIC, preeclampsia, amniotic fluid embolism, abruptio placenta, or fetal demise (Blackburn, 2013, p. 305). Pregnancy increases the risk of ARDS after an insult to the lung, much of this is due to colloid osmotic pressure change caused by the physiologic changes of pregnancy (Blackburn, 2013, p. 305).

tendency to nose breath

altered position of larynx and epiglottis- Risk of airway obstruction, more difficult intubation, enhanced ability to synchronize breathing and swallowing (Blackburn, 2013).

Thrombophilias

being increasingly regarded as having potential roles in the pathophysiology of preeclampsia, fetal growth restriction, and miscarriage due to the effects of thrombotic changes in the placental bed. Pregnancy is characterized by increases in fibrinolytic activity, plasminogen and plasminogen activators in the uterus, and ongoing low-grade activation of the coagulation system within the uteroplacental circulation. As a result, events such as extravasation of blood into the myometrium or rupture of blood vessels in the area can activate the fibrinolytic system and lead to a consumptive coagulopathy. The risk of coagulopathies such as disseminated intravascular coagulation (DIC) is higher during pregnancy, particularly in association with placental abruption, severe preeclampsia, eclampsia, intrauterine fetal death, amniotic fluid embolism, or septic abortion" (Blackburn, 2013, p. 229).

Ventricular Septal Defect (VSD):

can occur either as an isolated lesion or in conjunction with other cardiac anomalies (such as tetralogy of Fallot, transposition of the great vessels, or coarctation of the aorta). Large VSDs can lead to CHF, arrhythmias, or development of pulmonary hypertension or Eisenmenger syndrome. A large VSD is often associated with some degree of aortic regurgitation, which contributes to the risk of CHF during pregnancy.

Pseudoglandular (6-16 weeks gestation)-

during this stage there is formation of a narrow tree of tubules (Blackburn, 2013, p. 309). The tubules are composed of thick epithelial wall that are formed from columnar or cuboidal cells (Blackburn, 2013, p. 309). This stage also is when the principal pulmonary arteries form, this occurs by week 14 (Blackburn, 2013, p. 309). The tracheobronchial tree is also established by the end of this stage (Blackburn, 2013, p. 309). No longer able to increase in number, these preacinar airways continue to grow in length and width (Blackburn, 2013, p. 309). Terminal bronchioles make up the peripheral lung structure during this period (Blackburn, 2013, p. 309). There is also the development of 15-20 generations of airways (Blackburn, 2013, p. 309).d

"Mesoblastic Period

from 14 to 19 days to a peak at 6 weeks getation), blood cells are formed in blood island in the secondary yolk sac. The secondary yolk sac arises at 12-15 days and is a site of early protein synthesis, nutrient transfer, and hematopoiesis" (Blackburn, 2013, p. 230).

Lung function-

here are 3 major function changes in pregnancy ventilation, airflow, and diffusing capacity (Blackburn, 2013, p. 299). Minute ventilation increases by the 8th week of gestation (Blackburn, 2013, p. 299). Pregnancy induces hyperventilation, the resting ventilation surpasses oxygen consumption and it thought to be cause by progesterone (Blackburn, 2013, p. 299). The work of breathing does not change much during pregnancy (Blackburn, 2013 p. 300). The amount of airflow is reliant on the resistance meet in the bronchial tree (Blackburn, 2013, p. 300). Congestion in bronchial wall capillaries and smooth muscle tone in bronchi impact resistance. Resistance does not change due to balance between bronchoconstriction and bronchodilation factors (Blackburn, 2013, p. 300). The diffusing capacity or is the effort it takes for gas to cross the pulmonary membrane (Blackburn, 2013, p. 300). CO2 shows a slight to no change in diffusion capacity in early pregnancy that is resolved by second half (Blackburn, 2013, p. 300).

Blood volume

increases during pregnancy. This begins at 6-8 weeks, peaks at 28-34 weeks, and is 1200 to 1600 ml higher than non-pregnant values. (Blackburn, 2013, p. 216)

Erythrocyte sedimentation rate

increases progressive Increased plasma globulin and fibrinogen increases Initially 55-80 mm/hr, peaks 1-2 days postpartum

Sickle Cell Disease

is a group of disorders that involve mutations in the genes that determine hemoglobin B-chain structure. A woman with sickle cell anemia normally has a lower hemoglobin level and oxygen carrying capacities, to which her system has adjusted. Pregnancy places both the woman and her infant at greater risk for complications due to in part to the effects of hematologic, cardiovascular, renal and respiratory changes during pregnancy. As plasma volume increases during pregnancy, the woman may become slightly more anemic. In addition, she may experience increased sickling attacks. Fetal and neonatal complications such as prematurity and fetal growth restriction may arise due to placental infarction and fetal hypoxia" (Blackburn, 2013, p. 227).

Mitral Valve Prolapse (MVP)

is one of the most common congenital heart diseases. Most women with MVP are asymptomatic and tolerate pregnancy well. The woman may experience an increase in palpitations, lightheadedness, dizziness, fainting with prolonged standing, arrhythmias, or chest pains that may require medical intervention with the use of Beta Blockers.

Patent Ductus Arteriosus (PDA):

is usually identified during infancy and surgically corrected at the time. Therefore, it is uncommon to find this type of defect in childbearing women. However, if it does exist, it is usually well tolerated during gestation, labor, and delivery, although closure before pregnancy is usually recommended. If PDA is complicated by pulmonary hypertension, the prognosis is poorer.

Iron deficiency anemia

most typical cause of anemia in pregnancy. It can be preventable and easily treated with supplements. Iron requirements increase during pregnancy by about 1 gram above the typical body iron stores of 2-2.5 g in women. Typically, even with significant maternal iron deficiency, the fetus is usually protected and receives adequate iron stores, however this can affect the mother. If the mother is severely anemic and iron deficient, the fetus can display decreased RBC volume, hemoglobin, iron stores, and cord ferritin levels and has an increased risk for iron deficiency throughout infancy. Iron deficiency anemia before midpregnancy is associated with and increased risk of low birth weight, preterm birth, and perinatal mortality. (Blackburn, 2013, p. 225-226)

hypercoagulable state

the hypercoagulable state is also a disadvantage because it significantly increases the risk of thromboembolic disorders during pregnancy and postpartum. Venous Thromboembolism (VTE) is a leading cause of maternal mortality in the U.S. The risk of VTE increases up to sixfold during pregnancy. The risk increases with parity and age, and is 9 times higher among women with cesarean deliveries than among women with vaginal deliveries. The three factors (Virchow triad) that predispose to thromboembolic disorders (stasis, altered coagulation, and vascular damage) are all present or potentially present during pregnancy" (Blackburn, 2013, p. 228)

Saccular (26-36 weeks gestation)-

this stage is marked by the formation of the "terminal air sacs begin to appear as outpouchings of the terminal bronchioles" (Blackburn, 2013, p. 311). The amount of terminal sac are increasing during this time this is the future alveolar duct (Blackburn, 2013, p. 311). Week 30 marks the increase of lung surface area and volume (Blackburn, 2013, p. 311). The number of air spaces, that will be alveoli dramatically increase from 65,000 at 18weeks to 50-150 million at term (Blackburn, 2013, p. 311).

These hemodynamic changes also increase the risk for

thromboembolism, iron deficiency anemia, and coagulopathies in pregnant women.

Reflex Responses

• Hering-Breuer reflex- inspiratory time is limited based on stretch receptors located within the lungs. • Head's Reflex- inspiratory effort goes up due to rapid lung inflation. This is "thought to produce the frequently observed biphasic signs of newborns that may be crucial for promoting and maintaining lung inflation after birth" (Blackburn, 2013). • Intercostal-phrenic Reflex- Inspiration is inhibited in response to proprioception receptors located in the intercostal muscles. • Trigeminal-cutaneous Reflex- "Tidal volume increases and respiratory rate decreases in response to facial stimulation" (Blackburn, 2013). • Glottic Closure Reflex-" Glottis is narrowed through reflec constriction of the laryngeal adductor muscles during respiration" (Blackburn, 2013).

Left-Sided Obstructive Lesions

• Hypoplastic Left Heart Syndrome: The left side of the fetal heart does not develop correctly and normal blood flow through the heart is impacted. Structural anomalies associated with HLHS are underdeveloped left ventricle, poorly developed mitral valves and aortic valve and there is often and ASD. With the left ventricle being hypoplastic creates a barrier for effective pumping of oxygenated blood to the body. During the first days of life the PDA and FO allow for the right heart to pump blood into lungs but when these close the left ventricle will not be able to perform this duty (Parker, 2016). Morbidity: 1 in 4,344 babies born in the US will have HLHS (Parker, 2016). Intervention: These babies may not have trouble for a few days while to PDA and FO are open but symptoms quickly appear after closing. Medications will be prescribed to strengthen heart, lower blood pressure and diurese. Nutrition is important due poorly oxygenated blood and poor feeds. Surgery will occur soon after delivery and will include multiple surgeries. The surgeries will restore function of the left ventricle in three separate steps (Parker, 2016)They are as follows: 1. Norwood Procedure: Within the first two weeks of life. Creation of new aorta and connect to the right ventricle. A tube is placed form the aorta or the RV to the pulmonary arteries. This allows the RV to pump blood to both the lungs body (Parker, 2016). 2. Bi-directional Glenn Shunt Procedure: Occurs about 4-6 months. This connects the pulmonary artery and the SVC that is returning deoxygenated blood. This allows for less work for the RV by allowing blood that is returning from the body to flow directly to lungs (Parker, 2016). 3. Fontan Procedure: This procedure occurs between 18 months and 3 years. The pulmonary artery and the IVC are connected and then to lungs. At this point, oxygenated blood will no longer be mixed (Parker SE, 2016). Melissa Picard The heart may become weak after so many surgeries and a transplant may be required. (Parker SE, 2016). Coarctation of the Aorta: This defect involves constriction of the aorta that is distal to the left subclavian artery. Most of these infants will also have a VSD. Fetal growth is typically no affected due the fact that very little blood flow occurs across the isthmus in utero and blood is shunted across the DA. Following birth the aortic constriction increases the LV afterload because blood is backed as it is unable to descend the descending aorta. This will cause an increase in afterload and create CHF leading to lactic acidosis, hypoxia and eventual death (Blackburn, 2013, p. 290). • Morbidity: Coarctation of the Aorta occurs in about 4 out of 10,000 babies (Parker, 2016) • Interventions: Once symptoms manifest there needs to be corrective intervention, angioplasty, to expand the aorta. A stent will often be placed to keep the vessel open. Sometimes the coarctation is removed and the aorta is reconstructed or patched to allow for normal blood flow. Often, these children will have increase in blood pressure that requires medication management (Parker, 2016). Melissa Picard Ventricular Septal Defect: This is the most common CHD. VSD may be an isolated defect or associated with another HD (Blackburn, 2013, p. 290). The four types of VSD are as follows: Conoventricular Ventricular Septal Defect, Perimembranous Ventricular Septal Defect, Inlet Ventricular Septal Defect, Muscular Ventricular Septal Defect (Parker, 2016). The hemodynamic instability after birth is dependent on the size of the VSD and PVR. If the VSD is large there is little resistance to blood flow. Systemic and PV resistance will determine the amount of intracardiac shunting. As PVR decreases there is an increase in amount of blood in LV, thus increasing the amount that is ejected through the VSD and out the pulmonary artery. This will create increase in pulmonary blood flow and lead to CHF. By 4-6 weeks moderate to large VSD will become hemodynamically significant as the PVR decreases and the pulmonary blood flow increases (Blackburn, 2013, p. 290). • Morbidity: VSD affects 1 in 250 live births and up to half of isolated VSD's will close spontaneously in infancy or childhood (Blackburn, 2013). • Interventions: Intervention is dependent on the size of the VSD. If the VSD is small and infant is not symptomatic cardiac surveillance will be initiated. If the VSD is large a cardiac catheterization or open heart surgery will be performed to close the VSD and restore normal blood flow. Medications may be used to strengthen heart muscle, lower blood pressure or assist with diuresis (Parker, 2016). Melissa Picard