ARD Module 4

• One major purpose of hemodynamic changes during pregnancy is to protect the mother from blood loss and placental separation
• Pregnancy-related hemodynamic changes increase the risk of thromboembolism, iron deficiency anemia, and coagulopathies

Blood Volume

• Changes begin around 6-8 weeks, increasing by 15% by 12 weeks
• Peaks between 32-34 weeks
• Results in a 1200-1600 mL increase over pre-pregnancy levels
• Plasma volume accounts for 75% of the total blood volume increase
• Up to 2 L of extracellular fluid is excreted in the first week after delivery

Cardiac Output

• The most significant hemodynamic change in pregnancy
• Half of the total increase occurs by 8 weeks
• Cardiac output ends 30-50% higher than pre-pregnancy levels
• Cardiac output decreases slightly near term
• Changes drastically with body position
• After delivery, cardiac output is significantly elevated (60-80% higher than prelabor) for 1-2 hours
• Blood loss from delivery is compensated by autotransfusion of up to 500 mL from the uteroplacental system into maternal circulation

Heart Rate

• Heart rate changes are seen early as 5 weeks
• Increased heart rate compensates for decreased systemic vascular resistance
• Heart rate increases by 10-20 beats per minute by 32 weeks
• Heart rate can return to baseline by term in some women
• Most women return to baseline by 10 days postpartum

Systemic Blood Pressure

• Increased intravenous volume is balanced by decreased systemic vascular resistance (SVR)
• Diastolic blood pressure decreases, reaching its lowest point in mid-pregnancy
• Blood pressure changes with body position, it reads 10 mm Hg higher when sitting vs. left lateral
• The reduction in blood pressure may be due to the vasodilatory effect of nitric oxide increases during pregnancy
• Venous pressures remain stable despite increased blood volume due to increased vascular capacitance and compliance from progesterone and nitric oxide

Vascular Resistance

• Decreases by 20-30% during pregnancy
• Starts decreasing at 5 weeks, reaching its lowest between 14-24 weeks
• Then, it increases to term, influenced by progesterone and other relaxant factors

Distribution of Blood Flow

• Blood flow increases to the uteroplacental circuit, mammary glands, skin, and kidneys
• At 10 weeks, uterine flow is 50 mL/minute
• At 28 weeks, it is 200 mL/minute
• At term, it reaches 500-800 mL/minute, representing 10-20% of the total maternal cardiac output

Postpartum Cardiac Changes

• Most cardiac changes return to baseline by 6-8 weeks postpartum

Cellular Blood Component Changes

Red Blood Cells (RBCs)

• Increase 20-30% (250-450 mL)
• Steady increase starts in the first trimester, potentially accelerating in the third trimester
• Erythropoietin stimulates RBC production via human chorionic somatomammotropin, progesterone, and prolactin
• Slight increase intrapartum because of slight hemoconcentration, where 50% of increased RBCs are lost at delivery
• RBC production stops temporarily postpartum–remainder of increased RBCs are lost via normal catabolism

Hematocrit

• Decreases by 3-5%, down 33% at term, decreasing from the 2nd trimester as plasma volume increases
• Hemodilution is the cause
• Decreases intrapartum
• Returns to baseline 4-6 weeks postpartum

Hemoglobin

• Decreases by 2-10%, averaging 12.5 g/dL
• Hemodilution is the cause
• Limited change until 16 weeks with adequate iron and folate.
• Lowest between 16-22 weeks, then a slow increase to term
• Slight increase from stress and dehydration intrapartum
• Initial decrease, stabilizes 2-4 days postpartum, and returns to baseline by 4-6 weeks postpartum

Reticulocytes

• Increase by 1-2% with a gradual increase to the third trimester
• Increased RBC production is the cause
• Increase intrapartum and increase slightly postpartum, then return to normal

White Blood Cells (WBCs)

• Increase 8% to 5000-12000 starting in the 2nd month, with an increase mostly seen in neutrophils
• Estrogen is the stimulus
• Increase intrapartum from 25,000-30,000
• Decrease postpartum from 6000-10000, and return to baseline 4-7 days after delivery

Eosinophils

• Slightly increase from hemodilution
• Variable
• Disappear from peripheral blood intrapartum
• Return to peripheral blood by 3 days postpartum

Platelets

• May slightly decrease but remain within normal limits (WNL) at 150-400 from hemodilution
• Variable
• 20% decrease with placental separation intrapartum
• Increase by 3-5 days postpartum with gradual return to baseline

Erythrocyte Sedimentation Rate

• Increases progressively due to increased plasma globulin and fibrinogen, increasing intrapartum
• Peaks 1-2 days postpartum

Blood Volume Increase

• Increases by 40-50% during pregnancy beginning at 7 weeks, peaking at 25-30 weeks
• Approximately 1000 ml higher than non-pregnant values

Maternal Anemia Types

• Anemia defines as hemoglobin less than 11 mg/dL in the first and third trimesters and less than 10.5 mg/dL in the second trimester
• Hemoglobin less than 6-8 mg/dL causes decreased material oxygen levels and decreased oxygen delivery to the fetus

Iron Deficiency Anemia

• The most common in pregnancy, this results in risks to the mother, including cardiovascular strain, altered performance, decreased peripartal blood reserves, and increased risk for transfusion need at delivery
• Fetal risks include growth restriction, prematurity, infection, alterations in development, and metabolic programming
• Easily treated with iron supplements
• Check ferritin levels to check iron stores for diagnosis (a level lower than 12 and a low Hgb is diagnostic)

Megaloblastic Anemia

• This is the 2nd most common type of anemia in pregnancy from folic acid deficiency or B12 deficiency (usually seen with vegan diet)
• Folate demand increases 3x in pregnancy
• Severe deficiency can cause fetal malformations, pre-eclampsia, abruption, prematurity, and low birth weight
• It also can cause an increased risk of neural tube defects, cleft lip, and palate
• Supplementation recommended for all childbearing age women regardless of pregnancy status to prevent neural tube defects

Sickle Cell Disease

• Sickle-shaped RBCs can clog microvasculature, including that of the placenta, leading to eventual infarction
• Women with sickle cell anemia normally have a Hgb of 7-8 and decreased oxygen-carrying capacity
• Pregnancy stresses the CV system further
• Fetal Hypoxia and placental facts increase the mother and fetus' risk of prematurity and fetal growth restriction

Thalassemias

• Results from disordered synthesis of alpha or beta peptide chains of the Hgb molecule
• This results in alteration in RBC membrane and decreased life cycle of the RBC
• Infant is at risk for hydrops fetalis, a high output of cardiac failure, and often stillborn or death shortly after birth due to mother missing all 4 alpha chains,
• Intrauterine blood transfusions can be considered and require lifelong transfusions after birth

Hematopoiesis Periods in the Fetus

• Mesoblastic: Located in the secondary yolk sac, it occurs at 14-19 days gestation, peaking at 6 weeks– blood cells formed in blood islands and forms primitive blood vessels, primitive RBCs
• Hepatic: Occurs at week 5-6 shortly after the start of circulation in weeks 4-5 while peaking from 6-18 weeks. Blood cells form in liver during this time, the liver mass increases 40x. It mainly produces normoblastic erythrocytes and declines 4-5 months gestation
• Myeloid: Which occurs around 18 weeks, makes all blood cell types and granulocytes/megakaryocytes by the bone marrow
• Bone marrow erythropoiesis increases as the liver production slows.

Neonatal Vitamin K

• Newborns have reduced levels of vitamin K dependent clotting factors due to the lack of placental transport of the vitamin to the fetus and lack of intestinal colonization by bacteria
• Deficiency increases significantly without vitamin K after birth, especially in breastfed babies, infants with a history of perinatal asphyxia, and/or infants born to mothers on warfarin
• Neonates have 1/5th of the liver stores of vitamin K compared to an adult, therefore there is rapid turnover
• Prophylactic use of Vitamin K can prevent hemorrhagic disease of the newborn after birth

Signs of Anemia, Prematurity and Hemolysis in the Fetus

• Vary with shared common features. Anemia presents with pallor, lethargy, poor weigh gain, tachycardia, and tachypnea
• Anemia of prematurity, seen in infants before 32 weeks, includes poor feeding, fatigue during feeding, increased oxygen requirements, and episodes of apnea or bradycardia
• Hemolysis can lead to jaundice, hepatomegaly, splenomegaly, hydrops fetalis, and increased reticulocyte count from isoimmunization
• Early detection/intervention is crucial

Normal Physiological Cardiovascular Changes in Pregnancy

Blood/Plasma Volume

• Increases 40-50% while peaking at 32-34 weeks
• Plasma volume rises by 45%, leading to hemodilution (a normal physiological response

Cardiac Output

• Increases 30-50%, peaking around 28 weeks is driven by higher heart rate and stroke volume

Heart Rate

• Heart rate increases 10-20 bpm

Blood Pressure

• typically drops in the first and second trimesters before rising near term

Vascular Resistance

• Decreases 20-30% due to vasodilation, supporting blood flow to the uterus and placenta

Heart Sounds

• Mild systolic murmurs are normal, but new diastolic murmurs or loud systolic murmurs are not

Common Pregnancy Symptoms due to Cardiovascular and Hematologic Changes

• Include fatigue, dizziness, and palpitations from increased blood volume and cardiac output with swelling in the legs and ankles due to fluid retention
• Hormonal fluctuation can cause hot flashes, and reduced vascular resistance causes low blood pressure when standing
• Mild systolic murmurs are common and harmless, though any signficant changed should be monitored
• Hypercoagulability increases the risk of thromboembolism leading to discomfort and varicose veins
• Manage these symptoms with rest, hydration, compression stocking, and avoiding prolonged standing

Pregnancy Compensatory Changes

• Including arrhythmias, supine hypotension syndrome, and exercise
• Arrhythmias, such as premature ventricular contractions and atrial ectopy, are common and benign, while becoming more pronounces 2nd-3rd trimesters via hormonal changes and cardia workload
• Severe cases like paroxysmal atrial tachycardia require careful management
• Supine hypotension syndrome occurs when the gravid uterus compresses the inferior vena cava
• Causes reduced venous return, dizziness, nausea, and syncope, but can be corrected by changing position
• Moderate exercise offers significant benefits
• Though excessive exercise (prolonged/high-intensity) reduces blood flow and fetal oxygen supply, sufficient oxygen is maintained under normal conditions

High Risk Pre-Existing Cardiovascular Disorders

• Associated with significant risks for both mother and fetus
• Includes congenital, Ischemic, cardiomyopathies, and valvular diseases
• High-risk conditions include Eisenmenger syndrome, peripartum cardiomyopathy, severe pulmonary hypertension, and aortic dissection
• These are all high-risk for maternal mortality due to right heart failure or cardiac complications during labor
• Patients with obstructive lessons like mitral stenosis and aortic stenosis may experience increased symptoms of pregnancy
• Conditions like mitral regurgitation or mitral valves are allow to have a well tolerated pregnancy until severe
• Marfan Syndrome increases of aortic dissection, with includes preconception counseling, monitoring, limiting exercises, and surgical interventions, while pregnancy may be contraindicated with severe pulmonary hypertension or Eisenmenger syndrome

Maternal Cardiovascular Decompensation Signs

• Fatigue, dyspnea on exertion, dependent edema, presyncope, and palpitations.

Pregnancy Hypertensive Disorder Classification System

• Classified into hypertension, preeclampsia, preeclampsia from chronic, and gestational hypertension.
• Chronic hypertension is diagnosed before pregnancy/20 weeks gestation while leading to complications like stroke and low birth weight.
• Preeclampsia usually occurs after 20 weeks with high blood pressure may also being without proteinuria. This can cause renal insufficiency or thrombocytopenia and is linked to altered placental function leading to oxidative stress/endothelial dysfunction disrupting maternal organs and the fetus.
• HELLP can also occur which includes liver enzymes, low platelet, hemolysis.
• Advances have reduced reliance on proteinuria while enhancing the identification of severe cases.

Findings and manifestations of preeclampsia

Cardiovascular

• Increased output and systemic vasoconstriction leading systemic HTN, generalized edema.

Uteroplacental

• Insuffciency causing feto somatic growth deficiency, hypertension from abruptio placentae and/or thrombocytopenia

Renal

• Decreased blood flow, proteinuria from elevated clearance and elevated uric acid

Cerebrovascular

• Cerebral motor ischemia causing seizures, hemorrhage and visual impairment

Hepatic

• Inscehmic from vasospasm resulting in epigastric/RUQ pain

Hematologic

• Mitochondrial injury in endothelial dysfunction leading to coagulation disorders/ thrombocytopenia.

Preeclampsia Diagnostic Criteria

Preeclampsia without Sever Features

• Defined as blood pressure after 20 weeks gestation with or without proteinuria of >140 mmHg systolic or >90 mmHg diastolic in women
• AST, ALT, and PCR elevation along with potential low platelets.
• More antenatal surveillance until 37 weeks along with induction of labor to mother and fetal risks

Preeclampsia with Several Features

• Defined above with severe range pressure/headaches

Eclampsia

• Defined as previous with seizures

HELLP Syndrome

• With hemolysis, elevated liver enzymes, and low platelets along with prompt delivery and recommended stabilization

Post Preeclampsia/Hypertension

• Preventive strategies for women with experienced preeclampsia
• Such as aspirin with closer healthcare provider

Fetal Cardiac Development Stages

18 days

• Cardiac primordium first appears

20 days

• Fuse along with jelly appearance and form “S” shape

22 days

• Hearth beats and aorta forms

24 days

• 2 ventricles with sinus venosus connecting

Late week 4

• Septum is formed

Early week 5

• All of previous comes along to connect

Late Wk 5

• Septum primum

Late Wk 6

• Circulation is becoming established

8-9 weeks

• All steps become complete

Fetal Cardiac Defect Examples

Atrial Septal Defect

• M/M: May require surgery
• Occurence: 5-10%

Ventricular Septal Defect

• M/M: High Risk of CHF
• Up to 20% of occurrence
• May require surgry if it doesnt close on own

Patent Ductus arteriosus

• M/M: Risk of renal perfusion
• Ocurrence 5-10%
• Ibuprofen

Tetralogy of Fallot

• M/M: needs servivial surgry
• Occurence 7-10%
• PGE@ for blood flood

Bicuspid Aortic Valve

• M/M: can cause stoke
• In 1.5% of adults

Fetal Cardiac Adaptations

O2 Tension Raises

• Clamping the umbilical blood transitions fetal circulation from pressure

Undetected Cardiac Warning Signs

• Abnormal sinus rhythm/cyanois, impaired respiratory status.

Neonate Murmur and Cyanosis

• Echocardiogram

Pregnancy Respiratory Adaptations

Mechanical Factors

• From uterus, lower riubs fare for expansion

Biochemical Factors

• Progesterone is a simulator

Lung Volume

• Muslesl increase around 50%

Lung Function

• Volume increases

Acid Base Changes

• Mildly compensated

Pregnant Respiratory Response/Risk

Asthma

• Lead to hyperventilation

Smoking

• May compete with nutrients

Air Travel

• May expereince adaptations

Acute Respiratory Syndorme

• Triggerd from sepsis

Upper Respiratory Infection

• May quickliy progress

Embryo Lung Development

Embryonic Stage

• Buds from week 3-7 form main parts

Pseudoglandular Stage

• Bronchial continues to week 5-17

Canalicular

• Type 2 is surfactant 16-25

Saccular Stage

• Saccular forms 24-38

Alveolar Stage

• Effective gas exchange is formed,

Surfactant Factors

• Lipo protein which decreases surface tension

Fetal lung Maturity Impacts

• Maturity is delayed in infants,

Fetal Lung Maturity Evaluations

• L/s Ratio, complete lung profile.

Steriod Use In Moms With Preterm Babies

• ACS may be used.

Preterm Viability

• 22-24 Weeks

Respiration Factor

• degree of myelination

Chemical factor

• Oxygen concentration

List 6 alterations in respiratory function in the neonate

• 1. Increased oxygen consumption*
• Increased respiratory rate and WOB
• Risk of hypoxia
• 2. Immaturity the pulmonary surfactant system in immature infants*
• Increased risk of atelectasis and RDS
• Increased WOB
• Irregular respiration with periodic breathing
• 3. Immature respiratory control*
• Altered a respiratory threshold
• Instability of the respiratory drive
• Risk of apnea
• Inability to be rapidly alter the depth of respiration
• Difficulty in compensating for hypoxemia and hypercapnia
• 4.Immatrue development of lung the capillary basement membrane* More are vulnerable to collapse of many terminal bronchioles and their alveoli
• 5. Small compliant airway passages with a a higher airway resistance of immature reflexes* Risk of the the airway obstruction and apnea.
• 6. Increased intrapulmonary too the right shunt* Increased risk of the atelactisis with wasted ventilation with a slower PaCO2.
• TTN (Transient Tachypnea of the Newborn)*
• More likely are these symptoms: tachypnea Treatment is with an Oxygen supplementation Causes an increased the oxygen requirement and the risk of the hypoxemia.
• RDS (Respiratory Distress Syndorme)*
• symptoms of tahcypean include that of an attempt to compensate Treatment: a therapy is aimed at maintaining adequate oxygenation. Causes increased hypoxia and acidosis.
• Hypoxia*

• Under 90% (desaturation) of oxygen
  

Treatment: Increase the pressure of enough oxygen If needed,

• Metabolism Factors* Can require antibiotics, use more surfactant, maintain a 02 the inhaled nitrogen may be needed for various factors
• Which infants are at greater risk for having a physiological jaundice?* The preterm infants are slightly more likely to devlop the physiologic a jaundice and hyperbilirubinemia than the term infants, this is slightly more prevalent
• Describe the management of the infants jaundice while breastfeeding* They need to Monitor with initial stooling with no stool passed within 24 hours
• initate the breastfeeding in with early frequent short fecing the stimulate milk production with pumping.
• use the various aspects of phototherapy
• What is something characteristics too distinguish the physiologic from that pathology of jaunice?* Physiologic Jaundice -appears within 24-72 hours of age and peaks throughout 4-5 days with 7 term infants and disappears within 10-14 days of life. Parhologic Jaundice is visible during the first 24 days after birth and peaks at higher level ranges that are present beyond 2 weeks of age.
• 1.Ultrasound (US)*

•  Wavelenght from the features it presents, a wavelegnhts to look at the fetus with it and used to test its gestational age.
  

• 2. Nonstress test(NST)*

•  Tests the External fetal monitor for at least just over 29 minites, the rate should continue when there are two and over of the fetal heart
  

Module 4 Topic Questions

• What three factors make up the Virchow's Triad include Hypercoagulable state, venous stasis, obesity
• Encouraging daily activities and light exercise such as walking helps promote blood flow and prevent venous stasis.
• A woman has increased compliance in their heart due to changes in ventricular wall mass
• Peripheral vascular resistance is impacted by marked a decrease in VR
• Chronic use of tylenol can increase chances of iron deficiency
• Sickle cell anemia is a “homozygous form of sickle cell disease in which the child inherits the abnormal hemoglobin S (Hb S) from both parents”
• Mesoblastic Phase in the first phase of hematopoiesis. This occurs in the yolk sac.

Bilirubin

• Phototherapy is initiated when bilirubin levels are above 12 mg/dL at 24 hours old. Refer to risk chart and hours of age when initiating this therapy for this condition