APNEA

Dr Charanraj Hunnalli
DM PG (Neonatology)

Apnea
Cessation of airflow for at least 20
seconds or accompanied by
bradycardia or cyanosis.
Bradycardia and cyanosis are usually
present after 20 sec. of apnea.
After 30 to 45 sec., pallor and
hypotonia are seen, and infant may be
unresponsive to tactile stimulation.

Periodic
Breathing
Recurrent sequences of

pauses in respiration
lasting for 5-10
seconds and followed
by 10-15 seconds of
rapid respiration.

TYPES

CENTRAL
No respiratory effort, no nasal airflow
Developmental phenomenon

OBSTRUCTIVE

respiratory effort, no nasal airflow,

HR
Caused by aspiration,Obstruction,
laryngospasm or poor airway control

MIXED

Both obstructive and central

PERCENTAGE OF
APNEA:
Central 40-45%
Obstructive 10-

15%
Mixed 40-45%
More premature = more
mixed

INCIDENCE OF
APNEA:
25 % of infants under
1800 grams /<34 wks at
birth
50% of infants under
1200 grams /<32 wks at
birth
100% of infants <28 wks
at birth
25% of infants of all
gestational ages (Rigatto)

Reflex Effects of APNEA

sinus bradycardia
drop in blood pressure
change in cerebral blood flow

Apnea and periodic breathing are

common in premature infants after
the first 24 to 48 hours of life.
Premature infants sleep 80% of the
time, term infants 50%.
Apnea only occurs with active
sleep.

CNS
Immaturity
number of synaptic connections
and incomplete dendritic
arborization - cause sensitivity of
respiratory center to CO2
therefore in afferent traffic to
reticular formation and reduction and
fluctuation of respiratory center
output

Other factors contributing to

decreased inspiratory effort:
activity of protective respiratory

reflexes
minute ventilation
diaphragmatic fatigue
soft compliant chest

Therefore
mixed apnea occurs
frequently in premies.

PREMATURITY
Impaired
Inhibitory
Oxygenation
Reflexes
APNEA
Infection
pathology

CNS
Metabolic disorders
Specific causes of apnea

Neonatal
Apnea
Preterm infants respond
to a fall in inspired
oxygen with a transient
hyperventilation followed
by hypoventilation and
sometimes apnea.

The Respiratory
Pump
The neonatal

diaphragm
The ribcage and
chest wall muscles

The Neonatal Diaphragm

In the relaxed
state is located
higher in the
Thorax
Inc. insp. pressure

The Neonatal Diaphragm

Muscle fibers
Type I: Fast oxidative 20%

fatigue resistant
Type IIa: Fast oxidative
fatigue sensitive
Type IIb: Slow oxidative
fatigue resistant

The Neonatal Diaphragm

Is attached to a more pliable
chest wall
Distortion
Dec. tidal volume

The Newborn is Predisposed to

Fatigue of Resp. Muscles Because of:

The reduced number of fatigue

resistant fibers in the

diaphragm
A pliable chest wall
The rapid RR, which minimizes
relaxation time for perfusion of
the diaphragm

Consequences of
Apnea
Gas exchange is
compromised due to:
PA CO2, PAO2
Extrapulmonary
shunting
Muscle relaxation

 Proposed Pathogenic Mechanisms of Apnea

Primary central respiratory center depression

Decreased or inhibitory upper afferent input to the central respiratory

center
Abnormal or hyperactive reflexes

Hypoxemia

 Primary central respiratory center

depression
- likely to result in central apnea
Fewer neuronal synapses
Decreased carbon dioxide (CO2)
sensitivity
Decreased neurotransmitter levels
Metabolic disorders
Sepsis
Suppression by drugs

 Decreased or inhibitory upper afferent

input to the central respiratory center
- likely to result in obstructive, central,
or mixed apnea
Less cortical traffic
Sleep state, especially REM sleep
Seizures
Metabolic disorders
Sepsis

 Abnormal or hyperactive reflexes

- likely to result in central apnea
Head's paradoxical reflex (gasp and apnea following
lung inflation)
Laryngeal receptors (taste buds) acting through
superior laryngeal nerves
Posterior pharyngeal reflex (apnea induced by deep
repeated suctioning)
Vascular receptors (apnea induced by large vessel
distension)
Decreased or inhibitory lower afferent input to the
central respiratory center
- likely to result in central apnea
Sensory receptors (temperature receptors on face)
Chemoreceptor immaturity

 Hypoxemia
- likely to result in central or mixed
apnea
Immature ventilatory response to
hypoxemia
Presence of lung disease
Decreased lung volume
Patent ductus arteriosus
Anemia
Hypotension with decreased oxygen
delivery to the brain

Apnea is Associated with Many

Clinical Conditions:
Intraventricular bleed
May see hypoventilation, apnea or respiratory
arrest

Subtle seizures
Along with fluttering eyelids, drooling or
sucking, tonic posturing

Sepsis

Bacterial (GBS, staph. Proteus, Listeria,

Coliforms
Viral (RSV, , herpes, CMV
Chlamydial)
NEC

Congestive Heart Failure

PDA and CHD
Due to decreased lung compliance
Respiratory muscle fatigue
Chest wall distortion
Hypoxemia

Respiratory Distress Syndrome

Due to atelectasis, work of breathing,
fatigue
May lead to chronic lung disease
Anemia

oxygen carrying capacity of blood

Arterial pressure perfusing CNS

Polycythemia

blood viscosity and blood flow to

CNS
begins at 2-4 hours of age

 High temperature of environment

Feeding problems

overdistention of stomach

aspiration

GER (gastroesphogeal reflux) with or without

aspirations
due to laryngospasm
stimulation of irritant receptors in lower
esophagus causing reflux apnea
Metabolic conditions

Hypoglycemia

Hypocalcemia

Hypernatremia

Alkalosis
Others

Myelomeningocele

Meningitis

Careful Evaluation of Episode

Obtain accurate report including feeding

and sleeping history

Physical exam, vital signs
Temperature
Calcium ,Glucose,Magnesium
CBC, lytes, ABGs, pulse ox
Septic screen
Chest xray
Cranial ultrasound
Echocardiogram
Placement of feeding tubes (OG/NG)

Monitoring
All preterm infants below 35

WG must be monitored for

at least the first week after
birth. Monitoring should
continue until no significant
apneic episode has been
detected for at least 5 days.

Monitoring
Because impedance apnea

monitors may not

distinguish respiratory
efforts during airway
obstruction from normal
breaths, heart rate should
be monitored in addition to,
or instead of, respiration.

Monitoring
BP should be measured

frequently and
hypotension with
oliguria< 1 mL/kg/h should
be treated accordingly
Hct should be> 45% ???

Care of The
Infant
1. Prevent hyperflexion of the

neck
2. Nurse the baby in prone
position
3. Set the thermal
environment to obtain a
central temperature of
36.5-37 C

Care of The
Infant
5. Place the orogastric tube
carefully
6. Avoid sudden gastric
distension
7. Continuous gastric
feeding if apnea occurs
with gavage
8. Warm air and oxygen to

Nursing Management During

Apneic Episode

1.Check infant at once

2.Cancel alarm
3.Stimulate if there is no

obvious vomit
4.Suction
contd

Nursing Management
During Apneic Episode
5. Give O2 via face mask in
same concentration as infant
had been receiving
6.Inform Doctor
7. Summon help
8. Document and report

Apnea
Diagnosis and treatment of specific

causes
Nursing care
Nasal CPAP (4-6 cm H2O)
Methylxanthine therapy
Increased environmental O2 only as
necessary to maintain adequate
baseline O2 saturation. Often
associated with treatment of anemia
Assisted ventilation if all else fails

When apneic spells are repeated and

prolonged, (i.e., more than 2 to 3

Management of Idiopathic
Apnea
A. General measures
1. Diagnosis and treatment of
specific causes
2. SO2 : 85-95%
3. Avoid reflexes that may
trigger apnea. Suctioning of
the pharynx should be done
carefully, and oral feeding
should be avoided.

Management of Idiopathic
Apnea

4.

Position of extreme flexion or

extension of the neck should be avoided,
to reduce the likelihood of airway
obstruction.
5. Avoid swings in environmental
6.

temperature.
Consider a transfusions of PRBCs if the
Hct is <25% and the infant has
episodes of apnea and bradycardia
that are frequent or severe while
methylxanthine levels are therapeutic

Management of Idiopathic
Apnea
B. Nasal CPAP (4-6 cm H2O) can
reduce the number of mixed and
obstructive apneic spells.
C. Methylxanthine (caffeine of
theophylline) therapy, commencing
with a loading dose followed by
maintenance therapy, and serum
level monitoring, especially for
theophylline.
D. Assisted ventilation if all else fails

CPAP
Effects

PaO2 with increased lung

volume & C
Work of breathing
Splitting of the upper
airways
Elimination of the intercostal
inspiratory- inhibitory reflex

Pharmacologic Mechanisms for

Methylxanthine

Sensitivity of respiratory center to CO2

Afferent nerve traffic to brain st
Central stimulation (inspiratory drive)
Improved skeletal muscle contraction
Improved metabolic homeostasis
Improved oxygenation via increased
cardiac output and decreased hypoxic
episodes

Signs of Toxicity in Infants

Receiving Theophylline

Failure to gain weight 10-20 g/mL

Sleeplessness
Irritability
Tachycardia
Hyperglycemia
Vomiting
20 g/mL
Diuresis/dehydration
Jitteriness
> 20 g/mL
Hyperreflexia
Cardiac arrhythmias
> 40 g/mL
Seizures

METHYLXANTHINES
CAFFEINE
2.5 - 5 mg /kg / day once per day
(therapeutic range 8-15 mcg/ml)
THEOPHYLLINE
3-6 mg/kg/day divided in 2 doses
per day
(therapeutic range 6-12 mcg/ml)

METHYLYXANTHINES
Caffeine is often preferable:
More centrally active
Not metabolized by the liver

GOAL: HOME DRUG FREE

Goal is to discharge without

methylxanthines
No apneic events for 5 days
If discharge on methylxanthines, standard in

this community is also discharge with monitor

May discharge with monitor only and no
medications (rare)

HOME MONITORS
At Risk Group:
Infants less than 1000 grams
Infants who continue to have apnea and

bradycardia
Infants requiring methylxanthines to
control apnea
Infants with severe reflux
Less risk but for familys peace of mind
Infants with severe BPD requiring oxygen
SIDS sibling or twin of SIDS

CRITERIA FOR SUCCESS

OF HOME MONITORING
Training is crucial!
Apnea class including CPR
Caregivers have adequate time

to use equipment prior to

discharge

Support is imperative!
Support system includes:

medical, technical, psychosocial,

community support

Choose the right monitor!

TERMINATION OF MONITOR USE

Usually by 4-6 months of age

No significant apnea for 2 months
If on methylxanthines, 1-2 weeks

after discontinuation of
medications and not significant
apnea
Resolution of primary problem

MONITORING
CANNOT GUARANTEE

 Persistent apnea
Apneic episodes may persist beyond 37-40 weeks in some infants,

especially those born before 28 weeks of gestation.

Methylxanthine therapy should be continued if apneic episodes
continue to occur beyond 34 weeks of corrected gestational age.
The neonate should be re-evaluated for secondary causes of apnea
especially neurological problems and gastro-esophageal reflux.
Home monitoring is not possible in our country and these infants
would require NICU care until drugs can be weaned and stopped.
16. Sudden Infant Death Syndrome (SIDS) and Apnea

AOP is not found to be an independent risk factor for SIDS. Only 24% of patients with SIDS have a history of AOP.
Neurodevelopment outcome

Most reports have found little evidence of any neurodevelopment

risk directly attributed to a history of AOP. Precisely measured
predischarge apnea related to AOP, however, has been reported to
be predictive of lower developmental indices at two years

Thank You

SUDDEN INFANT DEATH

SYNDROME (SIDS)
Sudden death of any infant or
young child which is
unexplained by history and in
which a thorough post mortem
fails to demonstrate and
adequate cause of death.*
*Definition taken from the NIH Consensus
Development Conference on Infantile Apnea
and Home Monitoring

SIDS STATISTICS
1-2 deaths per 1000 live births per

year

with Back to Sleep campaign in the US

- by 40%
leading cause of death in infants older
than one month

Most common age for SIDS is 2-4

months

99% of deaths before 6 months

1 % of deaths 6-12 months
extremely rare in the 1st month of life
infants have change in response to
hypoxia around 6 months of age

SIDS FACTS
SIDS risk for an infant with AOP or who

has had an ALTE is at no greater risk than

the general population
Premature infants have a slightly greater
risk which increases as their gestational
age decreases
Home monitoring of infants has NOT
decreased the incidence of SIDS
The SIDS sibling is not at greater risk of
SIDS than the general population

SIDS PREVENTION
Research indicates that
SIDS is more complex than
a single abnormality in a
single system.
Failure of arousal mechanism
Ethnicity is a factor
Back to Sleep campaign
AAP discourages the use of
monitors

SIDS RESEARCH
Research indicates that SIDS is more
complex than a single abnormality in a
single system.

Research findings:

Supine sleeping position most protective, side

lying better than prone but not protective as

supine
Overheating contributory
Smoking contributory
Any breastfeeding is protective
Research indicates SIDS is a malfunction in arousal
CHIME study indicates that normal infants have
apnea, bradycardia and desaturations into the 70s
- question why they can recover and the infant
who dies of SIDS does not
Tachycardia then bradycardia prior to fatal event -