- Respiratory Disease:

-Significant maternal changes in respiratory function and oxygenation can

result in fetal growth restrictions and fetal hypoxia.
- Astham medications (inhaled B-Blockers, inhaled corticosteroids and oral
corticosteriods) are usually safe for pregnancy.
- Women with good nutrition and well cotnrolled CF can concieve , however,
20% of mothers with CF will not see their chlds 10th birthdya and those with sever,
40% will have died.
- Fetal risks include prematurity, IUGR, and perinatal death, usually associated with
maternal hypoxemia and infection.
- Children born to mothers with CF will be heterozygous carriers

Maternal Behaviour:
Smoking
- Maternal smoking during pregnancy is a risk factor for stillbirth, IUGR,
placental abruption, placenta previa, PROM and preterm labour.
- Women with pregestational diabetes who smoke also have an increased risk
of congenital anomalies and preterm birth.
- Long-term effects include childhood obstructive airway diseas, SIDS,
neurodevelopmental abnomrlaities (ADHD, eating and movement disorders)
- Mechanism for fetal growth restrictions and healtj not compeltely
understood. Likely related to reduced uterine atery blood flow, reduced
placental blood flow, elevated nictone and carbon monoxide levels and
chronic fetal hypoxia.
- Fetal growth complications are the most common issues for infants of
smoking mothers.
- Neonates are at risk fro LBW (<2500g) and preterm birth.
- Some babies may undergo withdrawal-like symptoms which include jittery
movements and difficulty in settling.
Substance Use
- Perinatal morbidity related to the direct effects of the abused substance on
the developing fetus.
- Alcohol is the most commonly abused substance during pregnancy.
- Alcohol readily crosses the placenta, resulting in direct fetal exposure,
- Effects of alcohol include developmental and behavioral abnormalities,
spontaneous abortion, stillbirth, craniofacial malformations, growth
 restrictions, preterm birth, CNS dysfunction and organ or joint
abnormalities.
- The cause of these abnormalities are likely due to three main factors: a
teratogenic effect hypoxia as a result of increased oxygen consumption and a
diminished ability to use amino acids in protein synthesis.
- Expression of alcohol effects depend on time and exposure and secondary
factors such as maternal age, nutritional status, general health and use of
other substances.
- Fetal Alcohol Syndrome: severe effects, characterised by growth restrictions,
physical anomalies (small palpebral fissures, low nasal bridge, indistinct
philtrum, thin upper lip and shortened lower jaw) and neurological
dysfunction including mental retardation and neurodevelopmental disorders.
- Fetal Alcohol Spectrum Disorder is an umbrella term for noticeable
long-term effects of alcohol such as problems with suck, tremors, irritability,
hypertonus - related to withdrawal.
Chemical Dependency
- These women are also more likely to have medical and social issues such as
poor health, infectious diseases, UTI’s and hepatitis.
- Nutrition and prenatal care are often neglected - anemia is common.
- Opiates, barbiturates and sedative-hypnotic drugs cross the placenta and
affect the fetus.
- Fetal risks include” growth restrictions, malformations, intrauterine demise,
prematurity, asphyxia, CNS dysfunction and neurobehavioral abnormalities.
- Fetal dependency does occur and is associated with Neonatal Abstinence
Syndrome (NAS) which manifests as CNS irritability and vasomotor,
metabolic, respiratory and gastrointestinal dysfunction.
- Cannabis is the most commonly used illict drug in pregnancy. LBW and
preterm delivery are risks associated. Often tobacco use is linked which can
lead to altered neurobehaviour/sleep. Long-ter effects include altered
attention, academic achievement and behaviour.
- Cocaine - CNS stimulant causing vasoconstriction, tachycardia and
hypertension in both mother and fetus. Has ben linked to IUGR, small head
circumference, still birth, RDS, congenital infections, NAS and cerebra
infarcts. Urine or meconium samples can provide indiction of exposure.
Maternal Nutrition
- Nutritional problems that interfere with fetal cell division can have
permanent consequences.
- Excessive weight gain in obese women increases risk of emergency c-section
- Excessive gestational weight gain is an independent factor for fetal
macrosomia and birth <37 weeks.
- Protein, iron, vit A, and iodine requirements double during pregnancy.
- Malnourished and underweight mothers have more perinatal losses and
preterm births and newborns have lower APGAR scores and LBW.
- SGA (<10th %) have higher mortality rates in the perinatal periods and are at
risk for later problems such as insulin resistance and poor school
performance.
- Many fetuses grow well despite suboptimal maternal nutrition, part due to
the complexities of placental transport and the ability of the feus to be
preferentially supplied with some nutrients.
- Vitamin and mineral deficiencies have been linked to miscarriage, and
stillbirth, CHF, megaloblastic anemia (folic acid + b12), congenital anomalies
and skeletal abnormalities.
- Maternal Vitamin D deficiency is associated with poor pregnancy outcomes
such as preterm birth, preeclampsia, GDM, perinatal depression, SGA and
asthma symptoms.
- Obesity: Multitude of physiological complications such as cardiovascular
disease, GDM, infections, preeclampsia and other perinatal outcomes.
- BMI >30 are at risk for perinatal complications and BMI >40 are at risk for
chorioamnionitis, preeclampsia, stillbirth, cesarean section, instrumental
delivery, postpartum hemorrhage, perineal lacerations and prolonged stay.
- The infant can suffer macrosomia, shoulder dystocia, mec aspiration,
preterm birth, early neonatal death, abnormal labour, complications and
increased chance of admission to SCN.

Obstetric Complications
Antepartum Bleeding:
- Umcompensated acute bleeding results in diminished blood flow,
decreased systolic pressure, decreased CO and decreased placental
perfusion.
 - Gestational bleeding in first o second trimester has been linked to
increased risk of preterm labour and birth, PROM and LBW.
- Most common causes include placental abruption (incidence in 1%, the
normally implanted placenta separates from the uterine wall before
the time of delivery, resulting in maternal bleeding and a functional
decrease in uteroplacental size) - can be related to HTN disorders,
cocaine use and tobacco use. Increased risk of 2-5% with PROM.
Separation can be partial or complete. Fetal compromise relates to the
extent of separation. When the abruption is small and bleeding
minimal, the pregnancy can continue without significant fetal
compromise, however the decrease in uteroplacental surface area is
irreversible and reduces the placental capability. Extensive abruptions
are poorly tolerated by both fetus and mother, resulting in hemorrhage
which led to decreased placental function causing fetal asphyxia and
without immediate treatment, intrauterine demise.
- Placetnal previa - placetal lies abnormally low in uterus and to some
extent covers or enroaches the cervix, so the baby cannot be born
vaginally. This can cause episodic, painless maternal bleeding and is
often accompanied by preterm labour. To avoid active labour, fetal
lung maturity is assessed at 36 to 37 weeks, and if mature a c-section
can be scheduled before the onset of labor. Multiparity, materna age,
previous >3 uterine operations and cigarette smoking are risk factors.
Fetal compromise relates to the extent of the previa, the haemorrhage,
fetal hypoxia, degrees of impaired fetal growth and gestation of
delivery.

Hypertension Disorders of Pregnancy

- Chronic HTN - HTN before pregnancy or 20 weeks.
- Related to IUGR, preterm birth, placental abruption and still birth.
- Gestational HTN - HTN after 20 weeks with the absence of proteinuria.
- Preeclampsia - type of pregnancy induced HTn which is accompanied by
proteinuria and edema. Develops in the second half of the pregnancy. Most
common in obese women, multiple gestation, family Hx and pregestational
diabetes. Pregnancy is associated with vasodilation and dcreassed PVR, HTN
causes vasoconstriction and increase PVR - reducing blood flow to kidney,
liver, brain and uterus, reduced maternal blood volume and maternal hepatic,
 cns and coagulation abnormalities. Associated fetal risks include IUGR,
prematurity, perinatal asphyxia and perinatal death.
- HELLP (Haemolysis, Elevated Liver enymes, Low Platelets) and renal
abnormalities. This is a severe type of pregnancy induced HTN. High risk for
maternal and fetal death regardless of gestation. Delivery recommended
despite gestation. Steriod help improve materal oliguria, mean arterial
pressure, increase platelet count and urinary output.
- Drugs used such as mag sulfate, hydralazine, labetalol, nifedipine.
- Mag sulfate most commonly used.
- Hypotonia and CNS depression have been reported as a neonatal side effect.
- HTN medications can also cause decreased BP due to reduced placental
perfusion and hypoglycemia.
- Infection: GBS - major cause of sepsis, meningitis, and death. 10-30% of
women are colonised with GBS. It is now recommended to get a vaginal or
rectal GBS swap at 35 to 37 weeks.
Preterm Labour:
- Prevention through identification of high-risk women to provide
intermvention is key.
- Fetal fibronectin - gylcoprotein secreted by fetal membranes. Its presence in
a cervical-vaginal swab between 22-35 weeks has been associated with
increased risk for preterm labor and delivery.
- Cervical length (~4cm at 26 weeks) - has been inversely correlated with risk
for preterm birth.
- Beta-sympathomimetic agents are sometimes used to prolong pregnancy in
women who are having contractions with no signs of infection. The fetus may
develop tachycardia and hyperglycemia.
- Newborns born after beta-sympathmimetic therapy may have rebound
hypoglycemia due to the in-utero overproduction on insulin. It can also
cause intracranial bleeding due to increased fetal cardiac output, systolic
pressure and cerebral blood flow.
- Magnesium sulfate can stop preterm labour by decrease muscle contractility,
inhibiting uterine activity and interupting labour.
- Magnesium sulfate can lead to decreased muscle tone and drowsiness and
decreased serum calcium in the newborn.
- Prostaglandin synthetase inhibitors such as indomethacin can inhibit
prostaglandin induced uterine contractions. They can cause in utero
 constriction or closure of the ductus arteriosus - causing fetal pulmonary
HTN and congestive hart failure. They can also lead to oligohydramnios,
neonatal decreased platelet activity and GIT irritation.
- Calcium Channel Blockers e.g Nifedipine - interferes with pre-term labour.
Uterine contractility directly related to free calcium.
- Coricosteroids: benefits with reduced severity of RDS and incidence of
patent ductus arteriosus. Little or no evidence to support reduction in
mortality, chronic lung disease, IVH, NEC or ROP. All pregnant women
between 24 and 34 weeks who are at risk of preterm delivery within 7 days
should be candidates for antenatal treatment (IM Bethamethasone x 2 within
24hrs). Also shown to reduce neonatal repsiraotry complication between 34
and 38 weeks.

Effects of Labour on the Fetus

Contractions:
- Strong contractions are characterised by decreased blood flow through the
intervilluous spaces in the placenta. As blood flow decreases, there is a ecline
in placental gas exchange and the fetus must rely on existing reserves to
maintain oxygenation until blood flow is re-established.
Fetal Reserve:
- Two factors that influence fetal reserves are those that diminish reserves and
those that exhaust reserves.
- When oxygen reserves are diminished the fetus has less than optimal
oxygenation at the onset of the contraction. This can occur as a consequenc
of any condition that decreases placetnal exchange including reduced
placental surface area caused by abruption, placenta previa, maternal
hypotension or hypertension or hypoxia.
- A fetal reserve that is adequate at the onsent of labor can be exhaused by
factors that place unusual demands on the fetus.
- Exhaustion of reserves occurs with contractions that last for a prolonged
period of time, that are of an extremely high intensity, or occur with
increased frequency without periods of rest. Often this is the consequence of
the use of oxytocic agents to induce or augment labor
- Cord gases at delivery can give evidence of fetal metabolic state at the time
of birth.
- Base excess can indicate threshold of hypoxic injury.
Fetal Response to contraction-Induced hypoxia
- Fetus is limited in ability to compensate for hypoxemia related to uterine
contractions.
- The fetus responds by redistributing cardiac output in order to maintain
critical function. Blood flow to the brain and heart is prioritised.
- Acute hypoxemia leads to the development of hypoxia and causes a reflex
bradycardia as a result of vagal stimulation.
- Myocardial hypoxia has a direct bradycardic effect. They give signs of fetal
distress - late decelerations - where the peak of uterine contraction is
followed by a decline in fetal heart rate. Late decelerations help identify the
fetus who cannot tolerate labor due to inadequate oxygen reserves.
- Late decelerations are ominous and when accompanied by loss of fetal heart
rate and/or fetal tachycardia, are indicative of fetal acidosis
- In preterm infants the findings of decreased variability and tachycardia with
or without late decelerations correlate highly with acidosis, depression and
low APGARS.
Head Compression
- Pushing on the head during labor, especially in the second stage produces a
vagal response and a reflect which slows the fetal HR.
- This in general does not indicate hypoxia or fetal compromise.
- The deceleration that accompanies head compression, called early
compromise - the HR begins to fall as a contraction builds and as the
contraction subsides the HR returns of baseline.
Cord Compression:
- Occurs when the cord is looped around the fetal body parts, when it is
knotted or prolapses or with oligohydramnios.
- Can be exacerbated by contractions
- Partial venous occlusion can be manifested by fetal heart rate acceleration,
whereas significant occlusion is a rapid drop in HR.
- Variable decelerations can be spontaneous - often identified by a decline in
HR pre contraction peak but does not mirror the contraction shape.

Maternal pain medication

- Risk is increase if pre-term or compromised.
- Narcotics can cause CNS depression, fetal bradycardia, decreased resp effort,
decreased muscle tone and reflexes
 - Paracervical block: fetal bradycardia and asphyzia related to decreased
uterine blood flow and direct fetal myocardial depression.
- Epidural and spinal block: fetal bradycardia and asphyxia related to maternal
hypotension, fetal and neonatal toxicity, neonatal resp depression after an
epidural with fentanyl.
- General inahled anesthesia: Effects related to duration but can include CNS
depression, resp depression and decreased responsiveness.

Care at Birth
Fetal Lung Fluid
- Canalicular stage (16-26weeks) - fetal lung fluid secreted.
- The fluid is the product of distal lung epithelium
- Abscense or reduction in amniotic fluid results in abnormal development of
the lung parachemyma and pulmonary vascularity.
- Certain conditions which reduce lung expansion include oligiohydraminous,
CDH, space-occupying leisos and musculoskeletal defomities - which in turn
leads to pulmonary hypoplasia.
- Fetal lung fluid moves into upper airway, with some being swallowed and
some moving out into the amniotic fluid.
- Upper airway leisons obstructing the flow leads to increased fetal lung fluid
volume.
- In cases such as Congenital Diaphragmatic Hernias - fetal interventions such
as a ‘FETO - Fetoscopic Endoluminal Tracheal Occulusion’ is done -
procedure involves placing a balloon in your unborn baby's airway for
several weeks, which allows the lungs to grow.
- The volume of lung fluid per kg of body weigh increases as gestation
progresses at 2-4mls/kg/hr or 20-30mls/kg for the average neonate
and roughly equals functional residual capacity.

Physiology:
- Key is drying, warming and stimulating, with clearing of the airway only as
needed.
- Effective respirations within 1 minute. Cool ambient temp and tactile
estimation help initiating respirations.
- Changes a PaO2 and PaCO2 affect
chemoreceptors and air in the
reflexive initiation of respirations.
- Initial breath generates 20 to
70cm H20 of negative
intrathoracic pressure to replace
lung liquid with air in alveoli.
- A rapid decrease in pulmonary
vascular resistance and increase
in pulmonary blood flow occur
post inflating the lungs with air
and filling of the pulmonary
circuit.
- Resorption of fetal lung liquid
across the respiratory epithelium
accelerates during labor, resulting
in net clearance from potential air spaces.
- Colloid osmotic pressure and the lower postnatal hydrostatic pressure of
blood assists in absorbing alveolar fluid after delivery. During this process
fetal R = L shunts through the ductus arteriosus and foramen ovale gradually
close.
- ⅔ of total clearance of lung fluid is cleared during labor.
- Neonates born via SVD and C-Section had less lung fluid than those born via
C-section without labor.
 - Increase in fetal adrenaline in response to labor and birth is thought to
initiate a chemical switch from lung fluid secretion to absorption.
- Small amount of lung fluid cleared via mouth, with most dispersed across the
pulmonary epithelium into the interstitial spaces by ventilation.
- Lymphatic uptake and increased pulmonary circulation helps remove fluid
from the interstitial spaces and completes the transition to the postnatal
state.

Pulmonary Vascular Resistance

- Pulmonary vascular resistance is high - tightly coiled and constricted blood
vessels - limiting blood flow to lungs.
- High pulmonary pressures and low systemic vascular resistance - most blood
enters the pulmonary artery to be shunted through the ductus arteriosus to
the descending aorta (R=L blood flow).
- Blood flowing through the ductus arteriosus has low oxygen content and
supplies the lower fetal body before going through the umbilical arteries to
the placenta to reoxygenate and gas exchange.
- Despite only 10% of pulmonary blood flow going to the lungs, they still
stimulate breathing pattern, secrete surfactant and fetal lung fluid in
preparation for the extrauterine life.
Fetal Breathing Movements
- Detected on US at 11 weeks
- Fetal breathing movements essential for growth.
- Some lung fluid moves into amniotic fluid and assists in lung fluid volume
regulation.
- It is with this flow that surfactant components and organelles - Lecithin and
lamellar bodies - in the amniotic fluid form the basis of fetal lung maturity
tests such as lecithin-sphingomyelin ratio and lamellar body counts.
- The lecithin to sphingomyelin ratio of 2:1 or greater is characteristic of
mature fetal lungs. Fetuses delivered prior to this gestational age are at
increased risk of neonatal respiratory distress syndrome.
- Amniotic fluid lamellar body counts (LBC) above 50,000/mcL are predictive
of fetal lung maturity. Amniotic fluid LBC below 15,000/mcL are suggestive
of fetal lung immaturity and increased risk of neonatal respiratory distress
syndrome (RDS).
Adaptation to Extrauterine life
- Fetus lives in a relatively hypoxic environment
- Healthy fetus uses reserves to maintain PaO2 during labor as blood flow
decreases.
- Compromised fetus has less reserves with limited ability to compensate.
- Impaired or interruption to the normal processes can result in difficulty
adapting to the extrauterine life and environment, through signs such as mild
to moderate tachypnea to intractable or fatal persistent pulmonary
hypertension.
- PaO2 of fetus is 25-30mmHg.
- Fetal Hb has a higher affinity to bind to oxygen.
- Once the lungs expand, alveolar fluid must be cleared to close intracardiac
and extracardiac shunts.
- Breathing triggers increased pulmonary blood flow and alveolar oxygen
pressures causing vasodilation in pulmonary blood vessels.
- Within minutes to hours the ductus arteriosus constricts and become
ligamentum arteriosum. Can take months for this to anatomically close.
- Increased pressure in the left atrium due to increased pressure in systemic
circulation and decreased pressure in pulmonary circulation causes the
foramen ovale to close and become fossa ovalis.
- The ductus venosus contracts and becomes ligamentum venosum.
- Preterm infants or neonates who suffer sever hypoxia at birth - the ductus
arteriosus can remain patent for minutes to days post birth.
- In labour, increase in catecholamines (adrenaline and vasopressin) cause
reversal of production of lung fluid.
- The icreased transpulmonary pressure generated by inspiration or lung
inflation increases hydrostatic pressure gradient, causing liquid to move from
airway into surrounding tissue, which is absorbed by lymphatic and
pulmonary circulation over next few hours.
- The thoracic squeeze during a vaginal birth helps remove ⅓ of fetal lung
fluid, therefore, infants born via a C-section have an increased risk of
needing breathing resus at birth.

Neonatal Resus
 - Neonates exposed to cold stress at birth are more likely to experience
morbidity or death due to immature skin, increases SA to weigh ratio and
reduced stores of subcutaneous fat.
- ANCOR recommends delaying cord clamping to a minimum of 1 minute, or
until it stops pulsating for infants >34weeks gestation.
- Clamping for at least 30 secs if <34weeks who do not need immediate resus
- If the infant requires resuscitation, the cord shold be clamped and severed
immediately to provide appropriate resuscitation.
- Cord milking is an alternative to DCC but not recommended in <28weeks as
there is a risk of IVH.
- Having placental ciruclation during onset of spontaneous respirations and
inflation of lungs smooths the cardiovascular transition.
- 30ml to 150ml can be transferred during 30 to 120 secs before cord clamping.
- Immediate clamping can block normal transfer of blood, resulting in a deficit
of about 25% of normal blood volume.
- Preterm infants <34weeks may require FiO2 30%
- Mec Stained Liqour: Suction only if the neonate is not vigourous, has poor
tone, minimal resp effort or HR <100. Care to be taken with excess and
vigorous stimulation due to inhalation. In other cases, an ETT may need to be
used to suction the trachea using and meconium aspirator
- Pneumothorax: air or gas in pleural space. Can occur most commonly in
preterms, or neonates who had PPV, or infants who generated large negative
pressure during the first few breaths. Signs incl: decreased breathing sounds,
resp distress, poor response to resus.
- Choanal atresia: unilateral or bilateral blockage between nasal cavity and
nasopharynx.
- Rapid assessment post birth: Are they term? Are they breathing or crying
Good muscle tone?

Respiratory Assessment
- Lung develops from 28 days’ gestation until childhood.
- 5 stages: embryonic, pseudoglandular, canalicular, saccular and alveolar.
- Lung epithelium is derived from the gut.
- At 5 weeks gestation, tracheal bud divides into lateral growths (bronchial
buds) which are the R and L bronchi
 - From 6 weeks the pseudoglandular phase begins (because the lung resembles
a gland) - during this phase type 2 alveolar begin to appear (pneumocytes).
- By 16 weeks the whole respiratory tree has formed and the canalicular stage
begins.
- The canalicular stage is when the terminal bronchioles, the alveolar ducts
and terminal sacs. The sacs are smooth walled and coated with type 1 and 2
pneumocytes. Alveoli are primitive at this point and life cannot be sustained
pre 22weeks.
- Saccular stage from 25 weeks where terminal sacs are abundant, lung
epithelium thins and type 1 and 2 pneumocytes develop.
- Alveolar stage 36weeks to 3 years - secondary septation and true alveoli
develop.

Assessing status and function:

- Symptoms can arise due to an immature respiratory system, congenital
anomalies, cardiac disease, sepsis, CNS disorders, hematological disorders,
metabolic disorders and asphyxia.
- Auscultation over areas of pneumothorax or atelectasis may still be present.
- Localisation of sounds can be difficult due to small chest size and wide
transmission of sound.
- Auscultation of the point of maximum impulse (PMI) of the neonatal heart is
lateral to midclavicular line at 3rd to 4th ICS. A shift may indicate tension
pneumothorax, dextrocardia or diaphragmatic hernia.
- Fine crackles at end of respiration can indicate inflammation, RDS or BPD.
- Medium crackles - pneumonia, pulmonary congestion or TTn

Oxygen Therapy
- Higher in neonates due to increased respiratory rate and metabolic rate.
- Oxygen needed to produce ATP, without this, anaerobic metabolism occurs,
which produces lactic acid which leads to metabolic acidosis
- O2 is transported to tissue cells bound by Hb and dissolve in plasma.
- Oxygen Fetal Hb helps transfer oxygen from maternal to fetal circulation and
has a higher affinity to O2 than adults = higher capacity to carry oxygen.
- Events or stimuli can alter the Hb affinity to bind to O2 and then alter the
delivery of oxygen to tissue. This can cause a shift in the oxyhaemoglobin
dissociation curve.
 - Affinity to bind is affected by pH, temperature, pCO2 and 2,3 DPG (promotes
hemoglobin transition from a high-oxygen-affinity state to a
low-oxygen-affinity state)
- The curse represents relationship between SpO2 and PaO2 (partial pressure
of oxygen dissolved in plasma)
- The oxygen cascade is a process where O2 is transported from the
mitochondria. The distribution to systemic tissues is based on the passive
movement of gas along a descending partial pressure gradient.
- Oxygen required for normal cellular function ad the rate and degree of fas
transfer are determined by partial pressure.
- Gases move from area of high concentration to low concentration.
- O2 moves along a gradient from a high level of air in the respiratory ract, to
the arterial blood, capillaries and cells. The partial pressure is at its lowest in
the mitochondria.
- The change in PO2 from air to mitcochondria is cakked the oxygen cascade,
any change i oxygenation can result in hypoxia.

V/Q Mismatch
- In healthy lungs there is an equal exchange in alveolar ventilation , and the
pulmonary capillaries on the aveloi would receive an equal distribution of
cardiac output = V/Q match
- Neonatal lungs there is a mismatch usually due to prematurity, and/or lung
disease due to: limited alveoli, shunting due to PPHN or open ducts.

Transport:
- O2 carried in blood depends on Hb concentration and also percentage of
how saturated the Hb is.
- E.g Anemia = inadequate Hb to carry O2 reaching cells.
- The affinity that O2 has for Hb is demonstrated on a O2/Hb dissociation
curve, showing the percentage saturation of Hb at various partial pressure of
O2
- The curve represents relationship between PaO2 (partial pressure of oxygen
dissolved in arterial plasma) and oxygen saturations (percental of oxygen
bound to Hb)
- High fetal Hb = high fetal haematocrit = higher potential oxygen content per
liter of blood.
 - Hematocrit is the percentage by volume of
red cells in your blood.
- When you shift right the SaO2 will
decrease - meaning there is less oxygen on
the Hb, meaning the oxygen is in the blood.
- Left shift, SaO2 increases, more O2 on Hb,
oxygen away from tissue.
- Things that will shift right and promote O2
to tissue include low pH, increase Co2,
increase temp, increase DPG
- Left shift: low CO2, temp, DPG, low fetal
Hb and Met Hb, PaO2 of >60mmhg will
equate to a plateau SaO2% of 90-100%
(therefore, there is no use providing
further oxygen as it makes little difference
to the SaO2 nor improve tissue
oxygenation), Increasing the PaO2 too high
can lead to oxidative stress on the preterm
neonate
- Oxygen therapy when PaO2 is low can have a dramatic difference for saO2
- PaO2 highest in lungs and systemic arterial blood
- tissues PaO2 ~40mmHg = ~75% SaO2 - in systemic venous blood
- O2 unloading = amount of oxygen delivered to tissues
- Increased metabolism = increased O2 absorption and increased Co2 production
- Right shift: More oxygen unloaded due to situation such as increase CO2, increase
DPG, increase temp, decreased affinity, increase O2 dissociation
- Left shift: less O2 unloaded, higher affiinity

Pulse Oximetry
-