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48 Cards in this Set

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When does the most significant part of transition occur from fetal to extrauterine life

24-72 hours.

Adaptive changes that occur

Establish FRC


Convert Circulation


Recovery from Birth asphyxia


Maintain core temperature

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

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

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

Fetal lung development 36-40 weeks

True alveoli present, roughly 20 million at birth

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

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.

Adaptation of breathing

Rhythmic breathing occurs with clamping of the umbilical cord and increasing O2 tensions from air breathing

Primary event of the respiratory system transition is

Initiation of ventilation**




changes the alveoli from fluid-filled to an air-filled state.

Pressure must infant generate to inflate lungs

Infant must generate high negative pressure -70 cm H2O to inflate lung.

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

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

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

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

Control of ventilation in neonates

system is normal by 3-4 weeks, but before resp control is poorly developed.




Chemoreceptor control is present at birth

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

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

Apnea of infancy

Resp. pauses exceeding 20 sec or those accompanied by bradycardia or cyanosis


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%

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

CV system fetal vs newborn

gas exchanges occur in placenta in fetal system




Lungs require only nutrient flow (5-10% of CO)

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

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)

Ductus Venosus

Diverts approx 50% of blood away from the liver into the IVC then to the RA

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

SVC and hepatic venous flow delivered to the

RV.. pulmonary vascular resistance is high

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)

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%.

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

What is Persistent pulmonary HTN of the newborn

fetal shunting beyond the normal transition period.

Cause of Persistent Pulmonary Hypertension of the newborn

Hypoxia and Acidosis

Consequences of PPHN

increase PVR, pulm htn, decrease PBF, RAP>LAP, and increase in ductal flow

PPHN signs and symptoms

Marked cyanosis, tachypnea, acidosis, and right to left shunt across FO and DA

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

PPHN treatment

Adequate ventilation and oxygenation is key*


hyperventilate (maintain alkalosis)


Prostagladin, minimal handling, avoid stress

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.

Characteristics of the fetal kidney

Low renal blood flow and glomerular filtration rate

Transitional changes in the newborn renal system

increase in arterial pressure


decrease in vascular resistance


increase in size and function occur through maturity

Renal system depends on what age

Post-conceptual age, by 34 weeks all nephrons are developed, so a premature baby has incomplete renal development

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

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.

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 ***

Na filter 1week, 2week, adult

1week =70%


2 week = 84%


adult = 99.5%




urine Na 5-10 adult and 20-25 in neonate

IV fluid neonate

must contain Na because they can't conserve it.

Increased RBF and decreased RVR result in what

rapid improvement of renal function within the first 3-4 days of life.

Best way to conserve heat

Warming the room.




heat lamps are helpful.

Thermal regulation - major component in the neonate is what

Nonshivering thermogenesis.




metabolism of brown fat. develops between 26-30weeks.