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
What is perinatal asphyxia?
Perinatal asphyxia occurs during the perinatal period. It is a life-threatening disorder that occurs when a fetus or newborn doesn’t adequately exchange gases. Asphyxia, as it is characterized by hypoxia, threatens successful transition.
What are the results of impaired gas exchange?
impaired gas exchange –> decreased blood oxygen levels–> increased CO2 levels –> Multisystem organ effects (MSOE)
Asphyxia can happen for a variety of reasons. About ninety percent of asphyxia occurs prenatally when gas exchange through the placenta decreases as a result of problems such as:
- pregnancy induced hypertension (PIH)
- abruptio placenta
- cord compression
Fetal monitoring will often reveal an infant’s response to antenatal asphyxia:
- fetal heart rate decelerations suggest asphyxia
- passage of meconium is also a clue to the presence of asphyxia
Post-natally gas exchange can also be interrupted and this accounts for approximately 10% of asphyxia. Some disorders that affect gas exchange in a newborn are:
congenital diaphragmatic hernia
sepsis
meconium aspiration
some congenital heart defects
Alteration of blood flow is an attempt to provide those organs necessary for immediate survival. Where is the blood shunted to?
the brain and the heart — with as much oxygen as possible. In order to do this, blood is shunted away from non-vital organs such as the lungs, intestines, kidneys, and peripheral vessels. The longer those organs receive less blood, the more damage they sustain. Unless the cause of the asphyxia is remedied, the heart and brain eventually also succumb to hypoxia and are damaged
Why is tachycardia present during times of hypoxia?
Reflects the heart’s effort to increase cardiac output to respond to the decrease in blood oxygen levels
How does hypoxia and asphyxia alter glucose production?
Hypoxia and asphyxia alter glucose production and utilization by requiring an increase in glycogeolysis to meet the increased metabolic and energy demands. Because oxygen availability is compromised, the infant switches from aerobic to anaerobic metabolism. Anaerobic metabolism is less efficient than aerobic metabolism and requires significantly more glucose to create energy. This rapidly depletes the glucose reserves; this decreased energy production is often inadequate to maintain normal cell processes and leads to the accumulation of lactic acid which causes metabolic acidosis. Hypoxia will also lead to hypercapnia (CO2) due to the body’s attempt to bring in more oxygen and will result in respiratory acidosis. Left uncorrected, these problems (hypoxia, hypercapnia, and acidosis) worsen. The result can be tissue and cell damage in all organ systems, and if enough cells in an organ are damaged organ failure will result. In addition if enough organs fail, death may ensue.
There are 4 criteria for asphyxia:
- Arterial cord blood sample < 7
- Apgar score of 0-3 for more than 5 minutes
- Seizures, hypotonia, coma, or hypoxic-ischemic encephalopathy in the early postnatal period
- Multiple organ dysfunction in the early postnatal period
Conditions Contributing to Asphyxia: Antepartum
- Placental insufficiency
- Maternal pulmonary disease
- Maternal cardiac disease
- Congenital fetal abnormalities
- Prematurity
Conditions Contributing to Asphyxia: Intrapartum
- Rotational maneuvers
- birth trauma
- abnormal presentation
- placental abruption
- prolapsed umbilical cord
- maternal hypotension
- infection
Conditions Contributing to Asphyxia: Postnatal
- severe lung disease
- severe apnea
- congenital heart disease
- persistent fetal circulation
- sepsis
- shock
Adjusting to extrauterine life, the newly born infant experiences a complex series of…
biologic, physiologic, and metabolic changes