Module 2: Vinod Flashcards
Transition: Cardiovascular changes
Review Cardiovascular system in utero and post utero
- constriction of the ductus arteriosus is a gradual process permitting bidirectional shunting of the blood
- PVR may be higher than the SVR, allowing right to left shunting until SVR rises above the PVR and blood flow is directed left to right.
- Most neonates have a patent ductus arteriosus in the first 8 hrs of life
- spontaneous closure occurs about 42% in the 1st 24 hrs
- 90 % and 48 hrs-96 hours
- Permanent anatomic closure of the ductus arteriosus occurs 3wks to 3 months after birth
Transition: Respiratory changes
- at birth clamping of cord signals end of oxygenated blood flow to fetus
- for respirations to be established, fetus must clear lungs of fluid, establish regular pattern of breathing and match pulmonary perfusion to ventilation
- other factors: pulmonary flow, surfactant production, and respiratory musculature also influence respiratory adaptation.
- Catecholamine surge experienced prior to birth helps to remove fluid from fetal lungs
- infants that do not experience labor and are born via c-section are more likely to have residual fluid in the lungs and develop TTN (Transient Tachypnea of the Newborn) because of the lower levels of catecholamine.
Transition: Thermal and metabolic adaptation
-Newborns are predisposed to heatless because: a large surface area in relation to body weight, limited body fat, and a decreased ability to shiver. Newborns attempt to stay warm by increasing muscle activity and by burning brown fat (non-shivering thermogenesis), which increases metabolic rate. Peripheral vasoconstriction also decreases heat loss to the skin surface. The production of heat requires oxygen and glucose and produces lactic acid; therefore persistent hypothermia may result in metabolic acidosis, hypoglycemia, decreased surfactant production, and over the longer term, poor growth.19
Maternal glucose readily crosses the placenta and, under normal circumstances, supplies the fetus with enough energy to grow appropriately and to store glycogen in the liver for use after birth. The release of catecholamines occurring during labor and birth mobilizes glycogen; however, blood glucose levels decline after birth, reaching their lowest point at one hour of age.
Normal Transitional findings of the Newborn
-most of the transition occurs 4-6 hours after birth while cardiovascular changes may take up to 6 weeks.
During the initial hours after birth, the majority of fetal lung uid is reabsorbed, a normal functional residual capacity is estab- lished in the lungs, and the cardiovascular system redistrib- utes blood ow to the lungs and tissues. The infant moves through a fairly predictable series of events, mediated by the sympathetic nervous system, that results in changes in heart rate, respirations, gastrointestinal function, and body tem- perature. In a classic description still used today, Desmond and colleagues organized these changes into three stages:21 • The rst period of reactivity (0–30 minutes) is character-
ized by an increase in heart rate, irregular respirations, and
ne crackles in the chest with grunting and nasal aring
• A period of decreased responsiveness (30 minutes to 3 hours) with rapid shallow respirations, lower heart rate, and decreased muscle activity interspersed with jerks and
twitches and sleep
• A second period of reactivity (2–8 hours) in which exagger-
ated responsiveness, tachycardia, labile heart rate, abruptchanges in tone and color, and gagging and vomiting are commonly seen
Residual symptoms of transition such as crackles in the lungs, a soft cardiac murmur, and acrocyanosis may persist for periods up to 24 hrs in otherwise healthy infants.
Red flags in Transition
-Symptoms of greater than 2 hours duration
• Worsening distress
• Congenital anomalies
• Abnormal muscle tone
• Central cyanosis
• Apnea in a near-term or term infant
• Moderate-to-severe respiratory distress:
grunting
nasal flaring
marked retractions
need for supplemental oxygen beyond two hours of age
What is PPHN
persistent pulmonary hypertension of the newborn
PPHN is a special case of a cardiopulmonary disorder occurring in term or near-term infants that is triggered by an insult such as hypoxia, hypotension, or hypercarbia. PPHN develops when the expected drop in pulmonary vascular resistance does not occur after birth. Pressure within the pul- monary vasculature remains elevated, leading to continued shunting of blood away from the lungs and across the foramen ovale and ductus arteriosus.
Risk factors for problems in Transition: Maternal
Diabetes Hypertension Cardiac or respiratory disease Severe anemia Shock Infection or febrile illness
Risk factors for problems in Transition: Antepartum
Intrauterine growth restriction Placenta previa, Abruptio placenta Fetal-maternal hemorrhage Malpresentation, Multiple gestation Pregnancy-induced hypertension Illicit or prescription drug exposure
Risk factors for problems in Transition: Intrapartum
Chorioamnionitis
Fetal distress
Prolapsed cord
Premature or prolonged rupture of membranes Narcotic or magnesium sulfate administration Malpresentation
Shoulder dystocia
Vacuum forceps or cesarean delivery
Presence of meconium-stained amniotic fluid
Risk factors for problems in Transition: Neonatal Complications
Prematurity
Congenital malformations
Postmaturity
Birth trauma
TTN
Transient tachypnea of the newborn
Retained fetal lung fluid
due to
Late preterm infant Delivery by cesarean section, especially with no labor
Infants of diabetic mothers
Respiratory distress syndrome (RDS)
Surfactant deficiency and anatomic immaturity
Due to:
Prematurity
Meconium aspiration
Chemical pneumonitis secondary to meconium
Surfactant deactivation
Ball and valve obstruction leading to air trapping
Due to:
Term or postterm
History of meconium-stained amniotic fluid
May accompany signs of fetal intolerance of labor
Pneumonia
Initiation of inflammatory cascade
Secondary surfactant deficiency
Systemic illness
Due to:
Preterm
Prolonged rupture of membranes
Maternal Group B Streptococcus colonization
Maternal urinary tract infection or febrile illness
Persistent pulmonary hypertension
of the newborn (PPHN)
Failure of pulmonary vascular resistance to lower after birth, leading to continued right-to-left shunting, severe hypoxemia, and acidosis
Due to:
Late preterm/term infant
History of meconium aspiration, sepsis, RDS, congenital diaphragmatic hernia, and congenital heart disease
What is the PO2 of the fetus (intrauterine) compared to the newborn (extrauterine)?
fetus: 30
Newborn: 60-80
What is the organ of gas exchange for the fetus compared to the newborn?
fetus: placenta
newborn: lungs
What is the % of CO to the lungs in fetus compared to newborn?
fetus: 10%
newborn: 50%
What is the pulmonary vascular resistance in fetus compared to the newborn?
fetus: high
newborn: low
What is the systemic vascular resistance in fetus compared to newborn?
fetus: low
newborn: high
What is the pressure gradient in fetus compared to the newborn?
fetus : right > left
newborn: left > right
How is the foramen ovale presented in fetus compared to newborn?
fetus: patent
newborn: closed
How is the ductus arteriosus presented in fetus compared to newborn?
fetus: patent
newborn: closed
What is the direction of shunting in fetus compared to a newborn?
fetus: right to left
newborn: none or left to right