Assessment Final - Apgar Scoring

Front 1

1st breath TV (and pressures needed)

Back 1

TV - 12-67 ml; pressure 20-60 cm/H20

Front 2

1st breath stimulates which receptors

Back 2

carotid chemo-receptors & aortic baro-receptors

Front 3

Near normal FRC established within...

Back 3

15 minutes

Front 4

Increased blood flow to lungs affects pge in what way

Back 4

Prostaglandins metabolized in lungs; therefore increase blood flow in lungs = increased metabolism (+ increased O2) = closure of PDA

Front 5

Closure of: Ductus arteriosus, ductus venosus, foramen ovale

Back 5

DA - fx @ 15-24 hrs; structural @ 3-4 weeks

DV - structurally @ 1-2 weeks

FO - fx @ min-hours; structural @ month

Front 6

If transition doesn't occur you get hypoxia with.... (4)

Back 6

- Increased PVR

-PDA with patent FO

-R to L shunting

-PPHN

(Increased CO2, decreased O2 & pH)

Front 7

Flow of umbilical arteries versus vein without cutting of cord.

% of blood in cord vs baby at 3 min versus 15 seconds

Back 7

Umbilical arteries - flow rapidly decreases in 1st 20-25 seconds, negligible by 40-45 seconds

Umbilical vein - allows flow up to 3 minutes

By 3 min of age 87% of blood in baby, 13% left in placenta versus 73% in baby @ 15-30 seconds

Front 8

What happens if cord is clamped BEFORE effective respirations begin?

Back 8

PVR remains high:

-blood flow to lungs is decreased

-volume of blood returning to L atrium is decreased

-preload for L ventricle is decreased

COMPENSATION FOR LOSS OF PRELOAD FROM PLACENTA DOES NOT OCCUR

-Results in insufficient L ventricular preload * DECREASED CO

Front 9

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

Back 9

preload

Front 10

Benefits of delayed cord clamping for term vs preterm

Back 10

Term --> extra blood may = 40-50 mg/kg of Fe and may prevent Fe deficiency anemia in 1st year of life

Preterm --> Increased BP & Hgb, Decreased transfusions & IVH

Front 11

Concerns with delayed cord clamping (& why they're NBD): 6

Back 11

1. Hypothermia (cord blood warm)

2. Polycythemia (no symptomatic increase)

3. Hyperbili (mixed; higher but not significant)

4. Difficulty obtaining cord gas (obtain immediately to reflect fetal status)

5. Ability to obtain cord blood for banking (not enough after DD (20+/- 10 ml)) --> individual must decide best use of cord blood

6. Delayed resuscitation (try to resuscitate while waiting for cord to stop pulsing)

Front 12

APGAR - what does each letter represent

Back 12

A-Appearance (color)

P-Pulse (heart rate)

G-Grimace (reflex irritability)

A-Activity (muscle tone)

R-Respirations

Front 13

If scores less than 7 @ 5 min, repeat ____

Back 13

Every 5 min until 20 min pass or 2 consecutive scores of 7 or greater

Front 14

3 things to focus on with new NRP

Back 14

Focus on: respirations, HR, & oxygenation

**No longer relying on baby's color for need of O2

Front 15

Normal O2 saturations at 1 min / 5 min

& term c/s @ 7 min

& preterm at 6.5 min

Back 15

1 min - 60%

5 min - 90%

Term c/s @ 7 min - 90%

Preterm @ 6.5 min - 90%

** most research says takes 5-10 min for healthy late-preterm and term nbn to "look pink"

Front 16

Too much O2 during resuscitation may cause ____

Back 16

Oxidative damage & damage tissues unnecessarily

Front 17

Targeted preductal SPO2 after birth @ 1-5 & 10 min

Back 17

1 - 60-65%

2-65-70%

3-70-75%

4-75-80%

5-80-85%

10-85-90%

Front 18

Which scores are predictive of neurologic status?

Back 18

1 min score NOT predictive of survival and long term neurological status

5 min score & alter more predictive of survival & neurological status

**Risk for CP increases with severely depressed APGAR scores -- Most CP comes from nbn nursery so a good APGAR score does not guarantee there will be no CP

Front 19

Causes of asphyxia (maternal / placental / fetal)

Back 19

Asphyxia - Failure to establish normal respirations

Maternal - infection, asthma

Placental - severe PIH, abruption

Fetal - anemia, cord compression

Front 20

Physiologic changes with asphyxia (pH, O2, CO2, PVR vs SVR, DA/FO)

Back 20

-Metabolic acidosis

-Hypoxemia (low O2)

-Hypercapnea (high CO2)

-PVR High

-DA (R-->L shunt d/t high PVR)

-FO (R-->L shunt d/t high PVR)

Front 21

If asphyxia is not quickly reversed what occurs?

Back 21

-Severe hypoxemia

-Ischemia

-Acidosis

-Irreversible organ damage

**Babies should respond to ventilation/resuscitation (NRP) if asphyxia occurred just prior to birth. Poor response? Likely d/t prolonged severe acidosis

Front 22

Vigorous baby at birth and then apnea, cyanosis, bradycardia develop. What are 2 things you're thinking?

Back 22

1. YOU are doing something wrong with resuscitation

2. Baby has airway/lung disorder/anomaly

Front 23

**Differential diagnosis of asphyxia (important)

Back 23

Rapid assessment of conditions that might be causing OBSTRUCTION of the airway

Front 24

Causes of airway obstruction (4)

Back 24

1. MAS/severe pneumonia

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

3. Congenital anomalies of airway (laryngeal web, vascular ring)

4. Pneumothorax

Front 25

Markers of birth asphyxia (3) Which is the BEST marker?

Back 25

1. Meconium in amniotic fluid (10-15% normal deliveries)

2. Fetal HR (< 60 bpm)

3. pH & other acid/base measurements (low pH is the BEST marker to identify asphyxia during L&D... although research not conclusive that pH correlates to neuro outcome)

Front 26

The only clinical predictor of later neurological outcomes....

Back 26

Neonatal encephalopathy with early seizures (HIE - hypoxic ischemic encephalopathy)

1. Hypoxemia (low O2 to brain)

2. Ischemia (low blood perfusing brain)

3. Encephalopathy (any dysfunction of the brain)

Front 27

Four factors necessary to diagnose HIE

Back 27

1. Low APGAR scores (0-3 for > 5 minutes)

2. Cord gas pH < 7

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

4. Evidence of other organ damage

*** START COOLING WITHIN 6 HRS ***

Front 28

Following termination of insult, a cascade of deleterious events = cell death (2)

Back 28

Necrosis & apoptosis

Front 29

2 major areas of brain affected (and what they affect)

Back 29

Basal ganglia & thalamus

- hearing loss

-learning disability

-mild motor dysfunction

-CP

-severe motor dysfunction

death

Front 30

Clinical presentation of hypothermia (10)

Back 30

- Pale

- Cool to touch

- Acrocyanosis

- Central cyanosis

- Apnea

- Bradycardia

- Respiratory distress

- Irritability ---> lethargy

-Feeding intolerance

Front 31

Defenses against heat loss (4)

Back 31

1. Flexed position of healthy term infant (flaccid position of sick/preterm baby promotes heat loss)

2. Peripheral vasoconstriction

3. Shivering thermogenesis

4. Nonshivering thermogenesis

Front 32

How does shivering thermogenesis work

Back 32

*Poorly developed in NBN

Cold --> brain stem --> spinal cord -->anterior motor neurons --> increased muscle tone --> increased muscle metabolism --> heat production

Front 33

How does non shivering thermogenesis work

Back 33

**Main method of heat production for NBN

Cold stress --> hypothalamus --> epinephrine

--> brown fat metabolism

Front 34

Brown fat purpose / development

Back 34

ONLY function is for heat production

Development:

- 26 weeks through 3-5 weeks post delivery

- Accounts for 1/10th adipose tissue in full term

- Appearance: Smaller vacuoles than white fat (increased glucose, increased mitochondria, increased sympathetic nerves, increased blood supply)

**Brown fat lipolysis releases heat into circulation & transfers to other parts of the body; Needs increased O2 & glucose

Front 35

Location of brown fat metabolism

Back 35

mid scapula

back of neck

under clavicles

abdominal aorta

esophagus

mediastinum

trachea

heart

liver

kidneys

adrenal glands

Front 36

Classifications of hypothermia (mild-severe)

Back 36

Mild - 36.0 - 36.4

Moderate - 32-35.9

Severe - < 32

Front 37

Thermal stress effects (mild vs severe)

Back 37

Mild - helps establish respirations, thyroid & catecholamine surge

Severe - acidosis, hypoxia, hypoglycemia, DIC, IVH, shock, death

Front 38

DR for babies less than 1500 gm (what are your interventions)

Back 38

- Place in bowel bag/plastic wrap

- Place on blanket covered thermal mattress

- Double hat

(Goal DR tem pis 77-79)

Front 39

Conduction & ways to minimize conductive heat loss

Back 39

Direct contact with scales, blankets, etc (skin touches surface = heat loss)

Minimize:

-Prewarm radiant warmer/incubator

-Cover scales & xray plates

-Prewarm hands, stethoscopes, blankets, and other equipment

Front 40

Convective heat loss & ways to minimize

Back 40

Skin --> air (depends on air flow, air temp, humidity, clothes, hat).

Minimize:

- Increase environmental temp

-Eliminate drafts

-Cover baby's head (21% of SA; produces 44% of heat)

-Dress baby

-Heat O2

Front 41

Evaporative loss & ways to minimize

Back 41

BIGGEST SOURCE OF HEAT LOSS. When water evaporates from skin and respiratory tract (depends on air flow & humidity). 58 kcal burned for each gram of H20 evaporated

Minimize:

-Dry & remove wet blankets in DR/plastic wrap

-Increase temperature & humidity

-Eliminate drafts

-Heat & humidify O2

-Warm solutions before contact with baby

-Delay 1st bath until temp stable

Front 42

Radiant loss & ways to minimize

Back 42

Radiation to walls, windows, objects NOT in direct contact

Minimize:

-Keep baby away from outside walls and windows

-Dress baby

-Use double walled incubator or plexiglass heat shield in incubator

-Mylar blankets for transport

Front 43

Considerations for re-warming a cold infant

Back 43

BP may drop as baby rewarms (sudden vasoconstriction to vasodilation)

Re-warm ~ 1 degree C/hr

*IF < 1200 gm or < 28 weeks OR temp < 32, rewarm at 0.5 degree C/hr

You can set control temp 1-1.5 degrees C higher than current skin temperature

Front 44

Clinical presentation of hyperthermia (6)

Back 44

-Hypotension

-Apnea

-Tachypnea

-Dehydration

-Seizures

-Sweating