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48 Cards in this Set
- Front
- Back
When does the most significant part of transition occur from fetal to extrauterine life |
24-72 hours. |
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Adaptive changes that occur |
Establish FRC Convert Circulation Recovery from Birth asphyxia Maintain core temperature |
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Fetal Respiration |
Gas exchange occurs in placenta O2 transport via Fetal Hgb Fetal Hgb shifts curve to the left Hgb of full term neonate 18-20g/dl |
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Fetal Lung devleopment |
4 weeks - primitive lung buds develop from foregut 16 weeks - breaching of bronchial tree complete to 28 divisions, no further formation of cartilaginous airways |
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Fetal lung development 24 weeks and 28-30 weeks |
24- primitive alveoli (saccules) and type 2 cells present, surfactant detectable. Survival possible with mechanical ventilation. 28-30 weeks - capillary network surround saccades; unsupported survival possible |
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Fetal lung development 36-40 weeks |
True alveoli present, roughly 20 million at birth |
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Birth to 3 months in fetal lung development then to 6 years |
birth to 3 monthsPaO2 rises as R to L mechanical shunts close 6 years- rapid increase in alveoli, 350 million at age 6 |
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Development of resp function -(air breathing) |
Fetus makes resp movements in utero. from 30 weeks gestation - present 30% of the time at a rate of 60 breaths/min Does respond to chemical stimuli Prenatal practice. |
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Adaptation of breathing |
Rhythmic breathing occurs with clamping of the umbilical cord and increasing O2 tensions from air breathing |
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Primary event of the respiratory system transition is |
Initiation of ventilation** changes the alveoli from fluid-filled to an air-filled state. |
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Pressure must infant generate to inflate lungs |
Infant must generate high negative pressure -70 cm H2O to inflate lung. |
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With onset of ventilation what happens |
PVR decreases dramatically and PBF increases allowing gas exchange to occur. Changes in PO2, PCO2, and pH are responsible for decrease in PVR |
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Resp System Transition |
FRC 25-30 ml/kg is established acts as a buffer against cyclical alterations in PO2 and PCO2 between breaths Neonates/infant lungs prone to collapse , weak elastic recoli, weak intercostal muscles, intrathoracic airways collapse during exhalation |
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Resp System Transition continued |
High closing volume encroaches upon FRC small airway closure beings at volumes at or above FRC leading to lung collapse and QV mismatch |
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Why doesn't infants have lung collapse all of the time? |
Infant terminate the exp phase of breathing before reaching their true FRC which results in intrinsic PEEP and a higher FRC. when anesthetized infants need 5 of PEEP helps maintain lung inflation/FRC |
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Control of ventilation in neonates
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system is normal by 3-4 weeks, but before resp control is poorly developed. Chemoreceptor control is present at birth |
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Newborns and Hypercarbia |
Newborns respond to hypercarbia by increasing ventilation, but the slope of the response curve is decreased Hypoxia depresses the neonate's response to CO2 |
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Response to Hypoxia in infants |
Biphasic - initial hyperpnea followed by depression of respiration in about 2 minutes. Initial hyperpneic response is abolished by hypothermia and low levels of anesthetic gases Apnea most common response in real danger. by 3 wks of age hypoxia produces sustained hyperventilation |
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Apnea of infancy |
Resp. pauses exceeding 20 sec or those accompanied by bradycardia or cyanosis
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Apnea of infancy factors |
increase work of breathing = fatigue** very compliant upper airway structures and ribcage which tend to collapse during inspiration 25% of muscle fibers in diaphragm are type 1 fatigue resistant compared to adults 55% |
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Apnea O2 consumption, FRC, closing volume |
O2 consumption 6ml/kg = twice adult decrease FRC= non functional increased closing volume apnea occurs much quicker due to these factors |
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CV system fetal vs newborn |
gas exchanges occur in placenta in fetal system Lungs require only nutrient flow (5-10% of CO) |
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Why do we have Shunts in CV system |
fetal intracardiac and extracardiac shunts exist to minimize blood flow to the lungs while maximizing the blood flow/O2 delivery to organ systems Ductus venosus(extra), Foramen ovale, and Ductus Arteriosus |
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Fetal Circulation is what |
Parallel Deoxygenated blood travels the descending aorta to the umbilical arteries to the placenta (very low resistance) oxygenated blood returns via the umbilical vein (PO2 35) |
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Ductus Venosus |
Diverts approx 50% of blood away from the liver into the IVC then to the RA |
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Preferential streaming? |
Causes O2 rich blood to be directed across the Foramen oval which connects the right and left atrium O2 rich blood fed to the LV and ejected into the aorta, thereby feeding the coronary and cerebral circulations |
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SVC and hepatic venous flow delivered to the |
RV.. pulmonary vascular resistance is high |
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RV output is delivered across the what? |
Ductus Ateriosus - which connects the PA to the descending aorta. Blood entering the descending aorta returns to the placenta and feeds lower body (PO2 22) |
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Transitional Circulation series |
At birth placental vessels are clamped, SVR increases dramatically initiation of ventilation increase arterial and alveolar Po2 which dilates pulm vasculature - which decreases PVR dramatically and increased PBF by 450%. |
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Ductus arteriosus closure |
constricts within several minutes due to increase PO2 and decrease in circulating prostaglandins. Physiologic closure in 10-15 hours, anatomic closure 2-3 weeks. Ductus venosus closes |
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What is Persistent pulmonary HTN of the newborn |
fetal shunting beyond the normal transition period. |
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Cause of Persistent Pulmonary Hypertension of the newborn |
Hypoxia and Acidosis |
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Consequences of PPHN |
increase PVR, pulm htn, decrease PBF, RAP>LAP, and increase in ductal flow |
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PPHN signs and symptoms |
Marked cyanosis, tachypnea, acidosis, and right to left shunt across FO and DA |
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What can cause transient right to left shunting in normal neonates |
Coughing, bucking, or straining during anesthetic induction or emergence can cause shunting prior to anatomic close of fetal shunts |
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PPHN treatment |
Adequate ventilation and oxygenation is key* hyperventilate (maintain alkalosis) Prostagladin, minimal handling, avoid stress |
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Renal systen |
Major function - passive production of urine which contributes to the formation of amniotic fluid Amniotic fluid important for normal development of the fetal lung and acts as a shock absorber for the fetus. |
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Characteristics of the fetal kidney |
Low renal blood flow and glomerular filtration rate |
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Transitional changes in the newborn renal system |
increase in arterial pressure decrease in vascular resistance increase in size and function occur through maturity |
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Renal system depends on what age |
Post-conceptual age, by 34 weeks all nephrons are developed, so a premature baby has incomplete renal development |
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Renal system at birth |
first several day in full term infant - diminished ability to concentrate urine from low GFR at birth. urine osmo 700-800 and Cr 0.8-1.2 |
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Renal system and Na at birth |
Neonates have a normal renin-angiotension aldosterone system. they have immature neonatal tubules do not completely resorb Na under the stimulus of aldosterone. |
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Neonate and Na |
The neonate will continue to excrete Na even in the presence of a severe Na deficit The neonate is therefore considered an obligate sodium loser *** |
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Na filter 1week, 2week, adult |
1week =70% 2 week = 84% adult = 99.5% urine Na 5-10 adult and 20-25 in neonate |
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IV fluid neonate |
must contain Na because they can't conserve it. |
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Increased RBF and decreased RVR result in what |
rapid improvement of renal function within the first 3-4 days of life. |
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Best way to conserve heat |
Warming the room. heat lamps are helpful. |
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Thermal regulation - major component in the neonate is what |
Nonshivering thermogenesis. metabolism of brown fat. develops between 26-30weeks. |