Assessment Final - Transition, Cord Clamping, Apgar, Asphyxia

Front 1

SVR vs PVR

Back 1

SVR - resistance offered by the vasculature of the peripheral circulation

PVR - resistance offered by vasculature of the lungs

Front 2

What causes resistance for the R ventricle and L ventricle?

Back 2

R ventricle - into lungs

L ventricle - into body / placenta

Front 3

What is the main risk with PIH related specifically to FLOW?

Back 3

increased vascular resistance may = reverse diastolic flow (bad) bc resistance so high and blood can't get into the placenta. Eventually leads to CHF

Front 4

What is the main function of the placenta?

Back 4

Exchange organ for O2, CO2, nutrients, waste

Front 5

What is the main function of the ductus venosus?

Back 5

blood from placenta bypasses lier to enter IVC

Front 6

What is the main function of the foramen ovale?

Back 6

blood from IVC bypasses lungs to LA

Front 7

What is the main function of the ductus arteriosus?

Back 7

Blood from PA bypasses lungs to aorta

Front 8

What does R --> L shunting mean? Name 2 examples

Back 8

BYPASSING LUNGS

-FO (R to L atrium)

-DA (PA to aorta)

Front 9

Where is the highest O2 content (and what is it?)

Back 9

umbilical vein; 35 mmHg or 70% SpO2

Front 10

Where is the lowest O2 content (and what is it?)

Back 10

R atrium from SVC; 15 mmHg or 40% SpO2

Front 11

Normal time to transition

Back 11

6-12 hrs; physiologic changes occur simultaneously (pulmonary and systemic changes)

Front 12

What causes elimination of fetal lung fluid?

Back 12

Catecholamine surge just before or during labor changes NA channel transport in the lung from secretion to absorption

> 75% of fetal lung fluid absorbed prior to normal term birth

Front 13

What does the first breath do --> what volumes/pressures are needed? what receptors are simtulated?

Back 13

Replaces fluid with air

12-67 mL TV needed, 20-60 cm H2O pressure needed (sometimes baby needs help with 1st breath)

Stimulates carotid chemo-receptors (sense O2/CO2 in blood) & aortic baro-receptors (sense stretch of blood through vessel)

Front 14

What does the expansion of the lungs with air cause to happen? (3)

Back 14

-Release of surfactant

-Decreased alveolar tension

-Stable FRC (~30 mL/kg)

Front 15

Near normal FRC is established within _____ minutes

Back 15

15 minutes

Front 16

What does an increase in blood flow to lungs cause to happen? (6)

Back 16

Increased O2, Increased pH, Decreased CO2

-decreased PVR

-decreased pressure in R side of heart (RV doesn't have to pump as hard)

-Increase blood return to L side of heart

-Pressure in L side > R side

-Functional closure of FO (dt increased pressure in L side of heart)

Front 17

What stimulates the ductus arteriosus to be closed?

Back 17

1. Increased metabolism of prostaglandins (in lungs! that are now oxygenated!)

2. Increased O2 stimulates closure of DA

*placenta makes the MOST pge. It's metabolized in lungs so during fetal life, it's metabolized slowly keeping DA open.

Front 18

No blood flow FROM placenta causes what to happen to the pressure in the R atrium?

Back 18

DECREASED pressure

Front 19

PVR decreases due to ___ O2, ____ pH, ____ CO2

Back 19

Increased O2

Increased pH

Decreased CO2

Front 20

No blood flow TO the placenta causes (5)

Back 20

- increased SVR

-increased aortic pressure

-increased pressure in L atrium

-pressure in L side > R side of heart

-functional closure of FO

Front 21

Loss of placenta causes (2)

Back 21

-Loss of large source of pge

-closure of ductus arteriosus

Front 22

Functional vs structural closure of DA

Back 22

functional - 15-24 hrs

structural - 3-4 weeks

Front 23

Structural closure of DV

Back 23

1-2 weeks (may get UVC for ~ 1 week)

Front 24

If transition doesn't occur, and you have hypoxia with low O2, low pH, and high CO2.... (4)

Back 24

-Increased PVR

-PDA and PFO

-R --> L shunting

-PPHN

Front 25

What happens if you don't clamp the cord at all?

Back 25

Flow of umbilical arteries rapidly decreases in 1st 20-25 seconds (negligible by 40-45 seconds)

Flow of umbilical vein (allows flow up to 3 minutes)

physiologic closure of vessels occurs WITHOUT intervention of clamping cord

Front 26

blood distribution at 15 sec vs 3 min (placenta vs baby blood)

Back 26

15-30 seconds: 73% in baby, 27% in placenta

3 min: 87% in baby, 13% in placenta

Front 27

What happens if cord clamped BEFORE effective respirations begin?

Back 27

Preload is from placenta... No preload = reason for decreased HR before baby takes 1st breath = decreased CO.

PVR remains high, volume of blood to lungs decreased, volume of blood returning to L atrium decreased, preload for L ventricle decreased -> compensation for loss of preload from placenta does NOT occur

= insufficient L ventricular preload and decreased CO

Front 28

Breathing triggers a large increase in pulmonary blood flow, replacing umbilical blood as source of ________ for L ventricle

Back 28

preload

Front 29

Key factors affecting transfusion of placental volume (4)

Back 29

-Time

-Gravity (affects SPEED of transfusion but not overall amount, ~ 10 cm above/below (ie moms belly perfect)

-Uterine contractions - pumps blood into baby

-Onset of respirations - negative intrathoracic pressure pulls blood into baby

Front 30

Extra blood from delayed cord clamping (term) may = ________ of Fe

Back 30

40-50 mg/kg of Fe

May prevent iron deficiency anemia in 1st year of life (iron deficiency anemia could lead to mental retardation)

Front 31

How does delayed cord clamping help preterm infants? (4)

Back 31

-Increased Hgb

-decreased transfusions

-Increased BP

-Decreased IVH

Front 32

What are the concerns with delayed cord clamping?

Back 32

1. hypothermia (cord blood warm)

2. polycythemia (no increase in symptomatic polycy)

3. hyperbilirubinemia (mixed results, use lights as needed)

4. Difficulty getting cord gas (get IMMEDIATELY if needed to reflect fetal status)

5. Ability to obtain cord blood for banking (individual decision what's best - not enough blood once it stops pumping to bank)

6. Delayed resuscitation (allowing asphyxiated baby to get placental blood probably beneficial... resuscitate next to mom?)

Front 33

Cord milking as alternative to DCC?

Back 33

~ 15-20 ml of blood in cord (better than nothing?)

-Increased BP, UOP, Hgb

-Decreased transfusions

-Stabilizes cerebral oxygenation and perfusion

Front 34

What does APGAR stand for?

Back 34

A-appearance (color)

P-pulse (heart rate)

G-grimace (reflex irritability)

A-activity (muscle tone)

R-respirations

Front 35

IF score < 7 at 5 min, repeat q5 min until _____

Back 35

20 min pass OR 2 consecutive scores of 7 or greater

Front 36

1 min score reflects ____ and 5 min score reflects ____

Back 36

L&D - how baby did during labor

resuscitation - how well have you done

Front 37

Things that influence APGAR score (6)

Back 37

-GA

-maternal meds (narcotics, gen anesthesia)

-infection (TORCH, chorio, GBS)

-congenital disorder (CDH, CHD)

-cardiopulmonary conditions (PPHN)

-neurologic conditions

Front 38

True or False: An APGAR score assigned during resuscitation is NOT equivalent to a score assigned to a spontaneously breathing infant

Back 38

TRUE - AAP recommends using an expanded apgar score reporting form

Front 39

Are low apgar scores predictive of later neurological dysfunction?

Back 39

-1 min score NOT predictive of survival/long term neuro status

-5 min score and later more predictive of survival and neuro status than 1 min score

persistent low apgar scores have fair relationship to long term outcomes - 10 min score may provide useful prognostic data

Risk for CP increases with severely depressed apgar score. 75% of children who develop CP have normal apgar scores at birth --> most CP comes from term nursery

Front 40

Define asphyxia

Back 40

failure to establish normal respirations

- can be prior to birth, during L&D, after birth

Front 41

Causes of asphyxia (3)

Back 41

1. maternal - infection, asthma

2. placental - severe PI, abruption

3. Fetal - anemia, cord compression (vein compresses so no blood TO baby, but arteries keep sending blood OUT of baby... bad!)

*Duration is critical to outcome

Front 42

What do you see with asphyxia (in terms of inhaled gases / resistance / FO / DA)

Back 42

Low O2, high CO2, low pH

PVR remains high

DA remains open (R--> L)

FO remains open (R --> L)

.... So no blood to lungs

Front 43

Asphyxia just prior to brith should / should not respond to NRP

Back 43

SHOULD respond well to NRP - if response is poor, likely due to prolonged severe acidemia

Front 44

If process of asphyxia is not quickly reversed, it is self-perpetuating and may result in....

Back 44

severe hypoxemia

ischemia

acidosis

and irreversible organ damage

Front 45

If baby vigorous at birth, then apnea/cyanosis/bradycardia develop what are you thinking....

Back 45

YOU are either doing something wrong in resuscitation OR baby has airway/lung disorder/anomaly

*Differential diagnosis of asphyxia requires rapid assessment of conditions that might be causing obstruction of the airway

Front 46

Causes of airway obstruction (4)

Back 46

1. meconium aspiration or severe pneumonia

2. intrathoracic malformations that interfere with ventilation (CDH, CAM)

3. congenital anomalies of airway - laryngeal web, vascular ring

4. Pneumothorax

Front 47

Markers of birth asphyxia (4)

Back 47

1. meconium in amniotic fluid (10-15% of normal term deliveries)

2. fetal heart rate (< 60 bpm)

3. APGAR score (cannot be used ALONE as evidence of perinatal asphyxia)

4. pH & other acid/base measures (low pH is the BEST MARKER to identify asphyxia during L&D)

Front 48

The only clinical predictor of later neurological outcome is _______

Back 48

neonatal encephalopathy with early seizures (HIE)

H-hypoxemia (low O2 to brain)

I-ischemia (low blood perfusing brain)

E-encephalopathy (any dysfunction of brain)

Front 49

What four factors are needed to make a diagnosis of HIE?

Back 49

1. Low APGAR score (-0-3 for > 5 min)

2. Cord gas pH < 7

3. Evidence of neuro manifestations in 1st 24 hrs (hypotonia, coma, seizures)

4. Evidence of other organ damage (bc baby shunts blood to brain. motor cortex affected 1st so mental retardation without CP NOT from birth)

START COOLING IN 6 HRS

Front 50

What happens following HIE insult?

Back 50

A cascade of deleterious events result in cell death (necrosis & apoptosis)

Front 51

What 2 major areas of brain affected with HIE?

Back 51

basal ganglia and thalamus

-hearing loss

-learning disability

-mild motor dysfunction

-cerebral palsy

-severe motor dysfunction

-death