Name the three types of Apnea.

1) Central apnea

2) Obstructive apnea

3) Combination

What is the problem with the chemoreceptor responsiveness to hypoxia or hypercarbia?

It is immature at birth.

Name three miscellaneous causes of apnea.

1) Hypoglycemia

2) anemia

3) cold stress

What is central apnea due to?

-The immaturity of the respiratory system

-Poor organization or integration of the afferent input from the diaphragm

-intercostals and chemoreceptors

This apnea correlates with the degree of prematurity.

Central

Name two causes that will exacerbate central apnea.

1) Hypothermia

2) Hypoglycemia

3) Sepsis

4) Hypocalcemia

What is the treatment for central apnea?

Central acting xanthanines (caffeine or theophylline)

*If due to opioids-reverse w/ naloxalone

* if Hcts <27% tx w/ blood transfusion

This apnea is responsible for the majority of the apnea episodes in infants.

Obstructive apnea

What typically is the reason for obstructive apnea?

Poor muscle coordination with anatomical features of the infant airway.

What percentage of former premature infants may have post operative apnea?

20%

The incidence of apnea is inversely related to what?

Post conceptual age

Gestational age

I have a 32 weeker and and 37 weeker, who is more likely to have apnea?

The 32 weeker

Name three things that can lead to cyanosis or apnea in the infant.

-Edema

-choanal atresia

-stenosis

-presence of an NGT

Who's lungs are stiffer, a neonate or adult? So are they more or less compliant?

A neonates lungs are stiffer, so they are LESS compliant.

*The above, plus a smaller airway w/ more resistance leads to an increase in the work of breathing in an infant.

You start doing a peds case and realize that you forgot to change your circuit. DAMN IT-now what's going to happen? Why?

Your baby won't get their volumes because adult circuits are more compliant. You should have placed the appropriate circuit and run a compliance test.

Neonates have a relatively large abdomen which displaces the diaphragm cephalad. What's your concern with this?

-The neonates lung's closing capacity is placed within the expiratory reserve volume. If your over zealous w/ your masking, you can push your peak airway pressures high, & the closing capacity will impinge on the TV. 

*This may lead to atelectasis and intrapulmonary shunting requiring controlled ventilation w/ PEEP.

Your masking a baby and you begin having difficulty ventilating, you notice the abdomen is distended. What's your next step?

Quickly place an OG tube to decompress the belly to improve ventilation.

What facilitates oxygen delivery in the neonate?

Cardiac Output

*determined by preload, afterload, heart rate & contractility*

The major determinant of cardiac output in infants is what?

HEART RATE

*increased preload also improves it, but heart rate is the MAJOR determinant

RBC's have a 1/2 life of ______days.

Hgb A has a 1/2 life of _______days

RBCs 100 days

HgbA 120 days

Fetal Hgb has a higher/lower affinity for 2,3 DPG and thus a higher/lower affinity for oxygen?

Which way does the oxyhemoglobin curve shift?

It has a lower affinity for 2,3 DPG and thus a HIGHER affinity for oxygen.

The curve shifts LEFT!

Is parasympathetic activity fully developed in early gestation?

How about the sympathetic nervous system?

What does this mean to us?

PSN IS fully developed.

SNS is NOT.

This means neonates may not respond "normally" to hypovolemia (increasing his/her HR)

What is the first sign a child is hypovolemic? Why?

First sign is REDUCTION IN BLOOD PRESSURE!

Because the SNS is not fully developed.

Infants are prone to develop bradycardia or asystole as a response to succs, DVL, and opioids. How do we offset this?

Atropine (because it will increase HR faster than glyco)

What characterizes the fetal circulation? The have _______ pulmonary vascular resistance and a _____ systemic circulatory resistance.

-They have HIGH pulmonary vascular resistance (uninflated lungs and hypoxic vasoconstriction) and a LOW systemic circulatory resistance (high flow and low impedence of the placental vessels)

Describe the course of fetal circulation.

1) Oxygenated blood enters from placenta through umbilical vein (fyi-2 arteries 1 vein)

2) oxygenated blood bypasses liver through DUCTUS VENOSUS & combines w/ unoxygenated blood in IVC.

3) IVC blood combines w/ SVC blood & enters RA

4) Lung capillaries collapse producing high resistance (so RA pressure is higher than LA)

5) Blood is shunted from right to left through FORAMEN OVALE

6) Some blood transitions into pumonary arteries, but majority exits through DUCTUS ARTERIOSUS into aorta.

*Fetal circulation provides high concentration O2 for rapidly growing tissue.

When do aortic pressures increase in the fetal circulation?

With the cessation of placental blood flow.

What does clamping the umbilical vein do?

Doubles the systemic vascular resistance.

What drastically reduces pulmonary vascular resistance after birth?

Lung expansion 

&

An increase in PaO2 producing pulmonary vasodilation

Why does the foramen ovale close after birth?

Because the RA pressure decreases and the LA pressure increases.

When does the foramen ovale permanently close?

At any time can it be reopened?

What is the percent of adults w/ a patent FO?

At 2-3 months it permanently closes.

If there are sufficient increases in RA pressure (as w/ pulmonary HTN) the FO can be forced open.

25% of adults have a patent FO.