PEDIATRIC

EMERGENCY
Silvia Triratna
Divisi Pediatri Gawat Darurat
Bagian Ilmu Kesehatan Anak FK UNSRI
Palembang

RESPIRATORY EMERGENCY
CIRCULATORY EMERGENCY
NEUROGY EMERGENCY
ENDOCRINE EMERGENCY
TRAUMA
POISONING/ INTOXICATION
.......

 A fundamental concept in
pediatric emergency care is
that children are not simply
scaled-down adults and
cannot be treated as such.

Pediatric consideration
A childs physiologic response to a
critical illness or injury is different
from an adults..
Children are also developing
mentally and behaviorally.
Infants and young children cannot
tell you what the problem is or where
it hurts.

KOMINIKASI SULIT
CENDRUNG
KETAKUTAN
PEMERIKSAAN
SULIT DILAKUKAN
PENILAIAN KEGAWATAN
SULIT DILAKUKAN

CHILD IS NOT SMALL ADULT

The key differences to consider
in children are:
1. Weight
2. Anatomical size and shape
3. Physiological
cardiovascular, respiratory,
immune function
4. Psychological intellectual
ability and emotional response

Infant is nasal breather

Nose is responsible for 50% of total
airway resistance at all ages
Infant: blockage of nose =
respiratory distress or failure
So
Sometimes, oral and nasal
suctioning is all that is
needed!!

Tongue
Large in proportion to rest of oral cavity
Loss of tone with sleep, sedation, CNS
dysfunction
Frequent cause of upper airway obstruction

Positioning with or without

oral airway can be enough.

Pediatric Cardiopulmonary Arrest

100%

75 90 %

10%

75%

10
%

Survival
rate
7 11 %
Henti
Napas

80%

Henti
Kardiopulmonal

Almost all pediatric codes are of respiratory origin

9

Internal Data. B.C. Childrens Hospital, Vancouver. 1989.

PediatricCPR

Penyebab Kegawatan Kardiopulmonal

KEHILANGAN
CAIRAN

MALDISTRIBUSI
CAIRAN

DISTRES
PERNAPASAN

DEPRESI
PERNAPASAN

PERDARAHAN
GE
LUKA BAKAR

SYOK SEPTIK
PENY.JANTUNG
ANAFILAKSIS

ASPIRASI
ASMA
BP

KEJANG
TIK
KERACUNAN

GAGAL SIRKULASI

GAGAL NAPAS

GAGAL KARDIOPULMONAL

HENTI JANTUNG
10

ESPIRATORY

EMERGENC

The Need for Oxygen

0 1 minute: cardiac irritability

0 4 minutes: brain damage not likely
4 6 minutes: brain damage possible
6 10 minutes: brain damage very likely
> 10 minutes: irreversible brain damage

Respiratory Emergencies
In children, illness and injury
frequently result in respiratory
compromise, a leading cause of
pediatric morbidity and mortality;
Management of the airway and
breathing should be your first
concern in all pediatric patients

Respiratory Emergencies
Respiratory distress is one of the most
common chief complaints for which
children seek medical care.
nearly 10 % of pediatric emergency
department visits and 20 % of
hospitalizations

 Respiratory distress in children,

particularly neonates and infants,
must be promptly recognized and
aggressively treated because they
may decompensate quickly.

15

 Respiratory arrest is the most

common cause of cardiac arrest in
children and outcomes are poor for
patients who develop
cardiopulmonary arrest as the result
of respiratory deterioration

16

PediatricCPR

Manifestasi klinis
Oksigen/Glukos
a
Peningkata
n
penggunaa
n Substrat

SSP

Kardiovaskul
er

Organ
Abdomen

Irritabl
e

Takikard
i

Dysmotili
ty

Mottle
d

Gelisah

Resistens
i kapiler

Ileus

Pulses

Respon
(voice,
pain)

Gagal
jantung

Third
spacing
fluids

CRT

Kejang

Bradikar
di

Bowel
slough

Koma

Asystol
e

Kulit

Dingin
Pucat

17

Ginjal

Urine
output
Oliguri
a
Anuria

18

Pediatric considerations
The frequency of acute respiratory
failure is higher in infants and young
children than in adults, for several
reasons.

19

Factors that contribute to rapid

respiratory compromise in children

smaller airways,
increased metabolic demands,
decreased respiratory reserves,
inadequate compensatory
mechanisms as compared to adults.

20

Extrathoracic airway differences

The area extending from the nose
through the nasopharynx,
oropharynx, and larynx to the
subglottic region of the trachea
constitutes the extrathoracic airway.
This area differs in pediatric versus
adult patients
21

Extrathoracic airway differences

Neonates and infants are obligate
nasal breathers until the age of 2-6
months because of the proximity of
the epiglottis to the nasopharynx.
Nasal congestion can lead to
clinically significant distress in this
age group.
22

Extrathoracic airway differences

The airway is small; this is one of the
primary differences in infants and
children younger than 8 years compared
with older patients.
Infants and young children have a large
tongue that fills a small oropharynx.
Infants and young children have a
cephalic larynx. The larynx is opposite
vertebrae C3-4 in children versus C6-7
23
in adults.

Extrathoracic airway differences

The epiglottis is larger and more
horizontal to the pharyngeal wall in
children than in adults.
The cephalic larynx and large epiglottis
can make laryngoscopy challenging.

24

Extrathoracic airway differences

Infants and young children have a narrow
subglottic area.
In children, the subglottic area is cone
shaped, with the narrowest area at the
cricoid ring.
A small amount of subglottic edema can
lead to clinically significant narrowing,
increased airway resistance, and
increased work of breathing.
25

Extrathoracic airway differences

Adolescents and adults have a cylindrical
airway that is narrowest at the glottic
opening.

26

Extrathoracic airway differences

In slightly older children, adenoidal and
tonsillar lymphoid tissue is prominent and
can contribute to airway obstruction.
Uncorrected congenital anatomic
abnormalities (eg, cleft palate, Pierre
Robin sequence) or acquired
abnormalities (eg, subglottic stenosis,
laryngomalacia/tracheomalacia) may
cause inspiratory obstruction
27

Intrathoracic airway differences

The intrathoracic airways and lung

include the conducting airways and
alveoli, the interstitia, the pleura, the
lung lymphatics, and the pulmonary
circulation.

28

Intrathoracic airway differences

The intrathoracic airways and lung

include the conducting airways and
alveoli, the interstitia, the pleura, the
lung lymphatics, and the pulmonary
circulation.

29

Intrathoracic airway differences

Infants and young children have fewer
alveoli than do adults. The number
dramatically increases during childhood,
from approximately 20 million at birth to
300 million by 8 years of age.
The alveolus is small. Alveolar size
increases from 150-180 to 250-300 m
during childhood.

Therefore, infants and young

children have a relatively small
area for gas exchange
30

Intrathoracic airway differences

Collateral ventilation is not fully
developed;
therefore, atelectasis is more common
in children than in adults.
Smaller intrathoracic airways are more
easily obstructed than larger ones
Infants and young children have
relatively little cartilaginous support of
the airways
31

Respiratory pump differences

The respiratory pump includes
the nervous system with central control
(ie, cerebrum, brainstem, spinal cord,
peripheral nerves),
respiratory muscles, and
chest wall.

32

Respiratory pump differences

The respiratory center is immature in
infants and young children
leads to irregular respirations and an
increased risk of apnea.
The ribs are horizontally oriented.
During inspiration, a decreased
volume is displaced,
the capacity to increase tidal volume
is limited compared with that in
older individuals.
33

Respiratory pump differences

The small surface area for the
interaction between the diaphragm
and thorax limits displacing volume in
the vertical direction.
The musculature is not fully
developed. The slow-twitch fatigueresistant muscle fibers in the infant
are underdeveloped.
34

Respiratory pump differences

The soft compliant chest wall provides
little opposition to the deflating
tendency of the lungs.
This leads to a lower functional
residual capacity in pediatric
patients than in adults, a volume
that approaches the pediatric
alveolus critical closing volume.
35

36

Causes of acute respiratory

compromise in children

Respiratory tract
Cardiovascular
Nervous system
Gastointestinal
Metabolic and endocrine diseases
Hematology
Poisoning
INFECTION, etc
37

Causes of acute respiratory

compromise in children
Decrease muscle tone
Infection

Respiratory tract
Asthma
Anaphylaxis
Foreign body (upper airway, lower airway, esophagus)
Airway anomalies (eg, laryngomalacia, laryngospasm,
tracheoesophageal fistula, tracheal stenosis, tracheal ring)
Biologic or chemical weapons (eg, anthrax, nerve agents, ricin)
Chest wall abnormalities (eg, flail chest, open pneumothorax)
Thoracic cavity conditions (eg, pneumothorax, hemothorax, pleural
effusion, empyema, mediastinal mass)
Pulmonary contusion
Pulmonary embolism
Smoke inhalation
Submersion injury (near-drowning)

38

Causes of acute respiratory

compromise in children
Respiratory tract
INFECTION
Uvulitis,
Epiglottitis
Retropharyngeal abscess, Peritonsillar
abscess
Croup
Bacterial tracheitis;Bronchiolitis,
Pneumonia
39

Causes of acute respiratory

compromise in children
Cardiovascular
Congenital heart disease
Acute decompensated heart failure
Myocarditis
Pericarditis
Shock
Cardiac tamponade
Smoke inhalation
Submersion injury (near-drowning)

40

Causes of acute respiratory

compromise in children
Nervous system
Depressed ventilation (eg, ingestion, CNS
trauma, seizures, or CNS infection)
Hypotonia (variety of etiologies causing poor
airway or respiratory tone and ineffective
respiratory effort)
Pulmonary aspiration due to loss of airway
protective reflexes
41

Causes of acute respiratory

compromise in children
Gastrointestinal system
Splinting from abdominal pain
(intraabdominal trauma)
Abdominal distention (eg, small bowel
obstruction, bowel perforation)
Gastroesophageal reflux with pulmonary
aspiration
42

Causes of acute respiratory

compromise in children
Metabolic and endocrine diseases
Metabolic acidosis (eg, diabetic ketoacidosis, severe
dehydration, sepsis, toxic ingestions)
Hyperthyroidism
Hypothyroidism
Hyperammonemia

Hematologic
Decreased O2 carrying capacity (eg, acute severe anemia from
hemolysis, methemoglobinemia, carbon monoxide poisoning)
Acute chest syndrome (patients with sickle cell disease)
43

Causes of upper and lower

airway problems in children
Upper
Aiway

Lower
Airway

Both

Trauma
Croup
Bacterial
Tracheitis
Abscess
Epiglotitis
Neck Imjury

Asthma
Bronchiolitis
Pneumonia
Bruising of
the Lung
Collapse
Lung
Submersion
Injury

Foreign Body
Smoke
Inhalation
Allergic
Reaction

44

Respiratory problems have

3 levels of severity
Respiratory distress,
Respiratory failure, and
Respiratory arrest.

45

Respiratory Emergencies
Respiratory distress is a state where a
child is able to maintain adequate
oxygenation of the blood, but only by
increasing his or her work of breathing.
Respiratory failure occurs when a child
cannot compensate for inadequate
oxygenation and the circulatory and
respiratory systems begin to collapse.

Respiratory Emergencies
Respiratory arrest
are unresponsive and limp, with cyanosis
around the lips.
Respiratory rate and work of breathing
may be very slow or absent, or you may
note agonal respiration
infrequent, gasping breaths with no
chest rise
a pattern that is seen in dying

 Respiratory arrest
Children are unresponsive and
limp, with cyanosis around the lips.
Respiratory rate and work of
breathing may be very slow or
absent, or you may note agonal
respirationinfrequent, gasping
breaths with no chest rise
48

 Respiratory arrest is the most

common cause of cardiac arrest in
children and outcomes are poor for
patients who develop
cardiopulmonary arrest as the result
of respiratory deterioration

49

Clinical evaluation of
Respiratory Emergency
How do you initially assess a
patient in respiratory distress?
should be rapid and quickly determine
if patient needs emergent interventions
and rule out life threatening conditions

50

LA

Suara nafas
abnormal
Posisi abnormal
Retraksi
Napas cuping
hidung

AS

PE

AF

NA

PI

AY

T = Tonus
I =
Interactiveness
C = Consolability
L = Look/Gaze
S = Speech/Cry

UP

S E G I T I G A P E N I L A I A N P E D I AT R I K
( PEDIATRIC ASSESSMENT TRIANGLE = PAT)

SIRKULASI KULIT
Pucat

Mottled

Sianosi
s
51

 After completing the Triangle,

begin a more complete
pediatric primary survey.
DISABILITY
CIRCULATION
BREATHING

AIRWAY

Tachypnea: World Health

Organization
Age
Less than 2 months
2 to 12 months
1 to 5 years
More than 5 years

Breaths per minute

>60 breaths/min
>50 breaths/min
>40 breaths/min
>20 breaths/min

Reproduced with permission from: World Health Organization. The management of acute respiratory infections in
children. In: Practical guidelines for outpatient care. World Health Organization, Geneva, 1995. Copyright 1995 World
Health Organization.

Diagnostic studies for evaluation

of acute respiratory distress
Bedside testing: Pulse oximetry
INDICATION:
All patients with respiratory distress

54

Diagnostic studies for evaluation

of acute respiratory distress
Bedside testing: Pulse oximetry
Normal values despite hypoxia seen in patients with severe
anemia, carboxyhemoglobin, or sickle cell disease
Falsely low values obtained in patients with pulse oximeter
not correlating with pulse, poor peripheral perfusion, venous
congestion, methemoglobinemia, certain nail polish colors,
and in patients receiving vital dyes (eg, methylene blue)
during surgical procedures
55

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Bedside testing
End-tidal
CO2
(ETCO2)
measurem
ent

Confirmation of
succesful endotracheal
intubation
Noninvasive monitoring
of ventilation in
intubated patients
Noninvasive monitoring
for sedation in children

Measurable in non-intubated and

intubated, patients

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Bedside testing
Electrocar
diogram

Clinical suspicion of
cardiac disease
(eg, cardiac
murmur, gallop,
differential pulses
or blood pressure
between upper and
lower extremities)

Typically combined with chest

radiograph to assess heart size and
pulmonary vasculature in order to
determine need for echocardiography

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Laboratory testing
Determine PaO2 for
calculation of
physiologic measures
of oxygenation (eg, Aa gradient, PaO2/FiO2
Arterial blood ratio)
gas
Correlate pCO2 with
end-tidal CO2
measurments
Measure pH and
correlate with venous
pH

End-tidal CO2, pulse oximetry,

and venous blood gases may be
used as less invasive methods
for ongoing monitoring of
oxygenation, ventilation, and
acid-base status if they
correlate with arterial blood gas
measurements

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Laboratory testing
Electrolytes
, blood urea Patients with
nitrogen,
metabolic acidosis
creatinine
Glucose

Altered mental
status

Ammonia

Altered mental
status and other
findings suggestive
of urea cycle
defects

Assesses for the presence of

an anion gap and renal
dysfunction

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Laboratory testing
Carboxyhem
oglobin

Smoke inhalation
Altered mental status,
headache, vomiting and
possible exposure to
carbon monoxide (eg,
blocked furnace flue)

Cyanosis in the presence

of a normal PaO2 on
arterial blood gas
Methemoglob Exposure to agents
in
known to cause
methemoglobinemia (eg,
nitrites, benzocaine,
aniline dyes)

Pulse oximetry is falsely

elevated in the presence of
carboxyhemoglobin

Oxygen saturation by
cooximetry identifies the
presence of an abnormal
hemoglobin if specific
measure of methemoglobin
is not available

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Laboratory testing

D-dimer

Clinical findings
suggestive of
pulmonary embolus
(eg, low oxygenation,
pleuritic chest pain,
wedge-shaped
infiltrate on chest
radiograph, and
predisposing condition
[eg, sickle cell
disease, thrombotic
condition])

Pulmonary embolus is a rare

cause of respiratory distress in
children
Imaging options in patients with
moderate to high clinical
probability and elevated Ddimer include
ventilation/perfusion scan,
ultrasound of extremity veins
and deep veins, CT pulmonary
angiography, and pulmonary
angiography

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Imaging
Clinical findings
suggestive of
Croup can usually be
Lateral neck epiglottitism
diagnosed clinically
radiograph retropharyngeal
without a radiograph
abscess or ingested
foreign body
Chest
radiograph

All children with

significant
respiratory distress
and those with focal
lung findings

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Imaging
Forced
expiratory or
bilateral
decubitus
chest
radiograph

Suspected foreign body

aspiration

Hyperaeration noted on the

side with the bronchial
foreign body

Unilateral
decubitus
chest
radiograph

Assess whether lung opacity

is due to parenchymal
disease or effusion

Loculated effusions and

very large effusions may
not show evidence of
layering

Diagnostic studies for evaluation

of acute respiratory distress
Test

Indications

Comments

Imaging
Abdominal
radiographs
(supine and
upright, or
cross-table
lateral)

Other testing (eg,

ultrasound, upper
Significant abdominal
gastrointestinal contrast
tenderness and/or distension
study, abdominal CT) may
with concern for intestinal
also be indicated depending
obstruction or perforation
upon clinical findings and
likely etiologies

Computed
tomography
(CT) of the
head

Clinical findings suggestive

of increased intracranial
pressure or intracranial mass
lesion

Steeple sign

The AP view demonstrates tapering of the upper trachea, known as the "steeple sign" of croup. Note
that the finding can be simulated by differing phases of respiration even in normal children.
Courtesy of the Department of Diagnostic Imaging, Texas Children's Hospital.
65

Croup lateral neck radiograph

Lateral neck radiograph showing subglottic narrowing66and

distended hypopharynx consistent with acute laryngotracheitis.

Bacterial tracheitis

Lateral neck radiograph showing intraluminal membranes and tracheal wall

irregularity consistent with bacterial tracheitis.
67
Courtesy of R. Paul Guillerman, MD, Department of Radiology,
Baylor College of
Medicine.

Retropharyngeal
abscess

Lateral neck radiograph demonstrating widening of the retropharyngeal space and reversal of the
normal cervical spine curvature. The retropharyngeal space is considered widened if it is greater than
7 mm at C2 or 14 mm at C6. The epiglottis and subglottic area in this radiograph
68are normal.
Courtesy of Joe Black, Department of Diagnostic Imaging, Texas Children's Hospital.

GENERAL ASSESSMENT OF PEDIATRIC

RESPIRATORY EMERGENCIES

69

70

AIRWAY ASSESSMENT AND

MANAGEMENT

71

Airway and Breathing

Management
Positioning is the first step in airway
management.
Infants : should be placed in the
"sniffing position" by a head tilt-Chin
lift or jaw-thrust maneuver that
brings the angle of the chin up 90
degrees from the bed

72

Airway Obstruction
Croup
A viral infection of the airway below
the level of the vocal cords

Epiglottitis
Infection of the soft tissue in the
area above the vocal cords

Foreign body airway obstructions

Croup
is a common viral infection that usually
affects children 2 to 4 years old.
affects the larynx and trachea, although
this illness may also extend to the
bronchi.
85% of children to have mild croup,
less than 1% with severe croup.

74

Croup
Typical signs include a low-grade fever
of 38C to 39C,
a seal-bark cough, and stridor,
particularly if the child is agitated.
onset is gradual.
Breathing problems worsen at night, and
may appear severe and extremely
upsetting to caregivers.
75

Severity level of croup

Mild severity - Occasional barking cough, no audible stridor at

rest, and either no or mild suprasternal and/or intercostal
retractions
Moderate severity - Frequent barking cough, easily audible
stridor at rest, and suprasternal and sternal wall retractions at
rest, with no or minimal agitation
Severe severity - Frequent barking cough, prominent inspiratory
(and occasionally expiratory) stridor, marked sternal wall
retractions, significant agitation and distress
Impending respiratory failure - Barking cough (often not
prominent), audible stridor at rest, sternal wall retractions may
not be marked, lethargy or decreased consciousness, and often
dusky appearance without supplemental oxygen support
76

Severe Croup Management

ABC
Nebulized Racemic Epinephrine (2.25%)
observe for at least 3 hours post last treatment because of
concerns for a rebound phenomenon of bronchospasm

Dose: 0.05 ml/kg (maximum 0.5 ml in children)

Child under 6 months: 0.25 ml
Child: 0.5 ml
Adolescent: 0.75 ml

L Epinephrine 1:1000
Dose: 0.5 ml/kg (maximum 5 ml)
77

Severe Croup Management

CORTICOSTEROIDS
decreasing edema in the laryngeal
mucosa,
usually effective within six hours of
treatment.
decreases the need for additional
medical care, hospital stays, and
intubation rates and duration.
78

Epiglottitis
A bacterial infection that usually affects
children 4 to 6 years old
usually presents with a higher fever ranging
from 39C to 40C.
Difficulty swallowing may cause the child to
drool.
Stridor will be present even if the child is
resting.
Children with epiglottitis often assume a tripod
position to maximize breathing comfort.
As with most upper airway problems, onset is
rapid..
79

Bacterial tracheitis
This bacterial infection causes the
trachea to swell,
resulting in partial airway obstruction.
High fever,
low-pitched stridor (a snoring sound)
a productive cough are usually
present

80

Questions ?

82

83

84

Congenital anomalies associated with stridor

Nose

Malformation

Characteristics

Nasal deformities

Choanal atresia or agenesis, septum deformities, turbinate

hypertrophy, vestibular atresia or stenosis.

Craniofacial
Pharyn anomalies
x
Tongue

Larynx

Trache
a

Anomalies causing facial retrusion are associated with upper

airway obstruction, including Crouzon's, Pierre Robin, and Apert's
Syndrome.
Macroglossia and glossoptosis

Laryngomalacia

Most common cause of chronic stridor in infants. Almost all

patients present by 6 weeks of age. Symptoms are more
pronounced after upper respiratory infections.

Laryngeal webs

75 percent located in the glottic area. Complete webs cause

respiratory distress at birth, partial webs produce stridor, weak
cry and different degrees of respiratory distress.

Laryngeal cysts

Located in supraglottic area may cause respiratory distress and

stridor.

Subglottic
hemangioma

Presents as progressive loud stridor with increased respiratory

distress. Associated with hemangiomas in other parts of the
body.

Subglottic stenosis

May be congenital but more often acquired secondary to

intubation. Usually located 2- 3 mm below the glottis.

Tracheal stenosis

Usually present with stridor or both stridor and wheezing. If

stenosis is significant, respiratory distress occurs.

Vascular rings or
slings

74 percent of vascular rings are symptomatic.

Associated with other congenital anomalies. May be secondary
to a vascular ring or cysts. Worsens with upper respiratory

Definitions
Acute respiratory failure
inability of the lung to meet the
metabolic demands of the body.
This can be from failure of tissue
oxygenation and/or failure of CO2
homeostasis
86

Definitions
hypoxaemic respiratory failure:
PaO2 50 mm Hg when
breathing room air
hypercapnic respiratory failure:
PaCO2 50 mm Hg.

Basic respiratory physiology

88

The major function of the lung is to get oxygen into the

body and carbon dioxide out

CO2

O2

90

Oxygen in
Depends on
PAO2
Diffusing capacity
Perfusion
Ventilation-perfusion matching

Oxygen

A
lv
e
o
la
rp
e
s
u
re

P
A
O
2

P
A
C
O
2

P
A
H
2
O

P
A
N
2
Carbon
dioxide

Water
vapour

Nitrogen

Oxygen in

Depends on
PAO2

FIO2
PACO2
Alveolar pressure
Ventilation

Diffusing capacity
Oksigen terus-menerus berdifusi dari udara dalam alveoli ke dalam aliran darah
dan karbon dioksida (CO2) terus berdifusi dari darah ke dalam alveoli. Difusi
adalah pergerakan molekul dari area dengan konsentrasi tinggi ke area
konsentrasi rendah. Difusi udara respirasi terjadi antara alveolus dengan
membrane kapiler.

Perfusion:
Perfusi paru adalah gerakan darah melewati sirkulasi paru untuk dioksigenasi,
dimana pada sirkulasi paru adalah darah deoksigenasi yang mengalir dalam
arteri pulmonaris dari ventrikel kanan jantung.

Ventilation-perfusion matching:
Ventilasi adalah proses keluar masuknya udara dari dan paru-paru, jumlahnya
sekitar 500 ml

A
lv
e
o
la
rv
e
n
tila
o
n
R
x
(V
-V
)

Carbon dioxide out

Largely dependent on alveolar

ventilation

TD

Anatomical deadspace constant but

physiological deadspace depends on
ventilation-perfusion matching

Carbon dioxide out

Respiratory rate
Tidal volume
Ventilation-perfusion matching

Pathophysiology

 Hypoxemia, defined as a decreased

level of oxygen in the blood
hypoxia, defined as a decreased level
of oxygen in the tissues.
.

These 2 conditions may be

closely related and may or may
not coexist, but they are not
synonymous
97

Causes of Hypoxemia
Mismatch between alveolar ventilation (V) and
pulmonary perfusion (Q)
Intrapulmonary shunt
Hypoventilation
Abnormal diffusion of gases at the alveolarcapillary interface
Reduction in inspired oxygen concentration
Increased venous desaturation with cardiac
dysfunction plus one or more of the above 5
factors
98

The 3 most important abnormalities in

gas exchange that lead to respiratory
failure are
V/Q mismatch,
intrapulmonary shunt, and
hypoventilation

99

FIO2

Ventilation
without
perfusion
(deadspace
ventilation)

Hypoventilatio
n

Diffusion
abnormality
Normal
Perfusion
without
ventilatio
n
(shunting

Perfusi jalan darah menuju pembuluh darah paru

Difusi pergerakan oksigen dan karbon dioksida melintasi
membran kapiler alveoli
Ventilasi pertukaran udara dari rongga alveoli dan
atmosfer

101

75%

75%
100%

87.5%

75%

Perfusion without ventilation

(Shunting)
Intra-cardiac
Any cause of right to left shunt
eg Fallots, Eisenmenger

Intra-pulmonary

Pneumonia
Pulmonary oedema
Atelectasis
Collapse
Pulmonary haemorrhage or contusion

Perfusion without ventilation

(shunting)
Intra-pulmonary
Small airways occluded ( e.g asthma, chronic
bronchitis)
Alveoli are filled with fluid ( e.g pulm edema,
pneumonia)
Alveolar collapse ( e.g atelectasis)

V/Q mismatch:
Dead space ventilation
Alveoli that are normally ventilated but
poorly perfused

Anatomic dead space

Gas in the large conducting airways that does
not come in contact with the capillaries e.g
pharynx

V/Q mismatch:
Dead space ventilation
Physiologic dead space
Alveolar gas that does not equilibrate fully with
capillary blood

Dead space vantilation

DSV increase:
Alveolar-capillary interface destroyed
e.g emphysema
Blood flow is reduced e.g CHF, PE
Overdistended alveoli e.g positivepressure ventilation

Diffusion abnormality:
Less common
Abnormality of the alveolar membrane or a
reduction in the number of capillaries
resulting in a reduction in alveolar surface
area
Causes include:
Acute Respiratory Distress Syndrome
Fibrotic lung disease

Hypoventilation
can be caused by
disease at any of the anatomical sites
involved in ventilation.
Brainstem injury or disease may
result in impaired functioning of the
respiratory centre,
impaired functioning of the
respiratory centre which suppressed
by depressant drugs
109

Brainstem
Airway

Lung

Spinal
cord root
Nerve

Nerve

Pleura

Chest
wall

Neuromuscular
junction
Respiratory
muscle

tes at which disease may cause ventilatory disturbanc

 The nerve roots may be damaged by trauma or tumour

nerve injuries and neuropathies such as Guillain Barre or
critical illness neuropathy may affect motor neurons
supplying respiratory muscles
Neuromuscular blockers or disease of the neuromuscular
junction (eg myasthenia gravis) may impair transmission of
nerve impulses to respiratory muscles
Or the problem may be in the muscle itself. Respiratory
muscle fatigue, disuse atrophy and malnutrition are
important causes of respiratory muscle failure in the ICU
Alternatively the problem may be a problem of increased
resistance to airflow. For example due to obstruction of the
upper airway or bronchospasm
Or the problem may be decreased compliance of the lung
itself, the pleura or the chest wall.
111

Respiratory Failure
Symptoms
CNS:

Headache
Visual Disturbances
Anxiety
Confusion
Memory Loss
Weakness
Decreased Functional Performance

Respiratory Failure
Symptoms
Pulmonary:

Cough
Chest pains
Sputum production
Stridor
Dyspnea

Respiratory Failure
Symptoms
Cardiac:
Orthopnea
Peripheral edema
Chest pain

Other:
Fever, Abdominal pain, Anemia, Bleeding

Clinical

Respiratory compensation
Sympathetic stimulation
Tissue hypoxia
Haemoglobin desaturation

Clinical
Respiratory compensation

Tachypnoea
Accessory muscles
Recesssion
Nasal flaring

Sympathetic stimulation
Tissue hypoxia
Haemoglobin desaturation

Clinical
Respiratory compensation
Sympathetic stimulation
HR
BP
sweating

Tissue hypoxia
Haemoglobin desaturation

Clinical
Respiratory compensation
Sympathetic stimulation
Tissue hypoxia
Altered mental state
HR and BP (late)

Haemoglobin desaturation

Clinical
Altered mental state
PaO2 +PaCO2 acidosis
dilatation of cerebral resistance
vesseles ICP
Disorientation Headache
coma
asterixis
personality changes

Clinical
Respiratory
compensation
Sympathetic
stimulation
Tissue hypoxia
Haemoglobin
desaturation
cyanosis

Respiratory Failure
Laboratory Testing
Arterial blood gas
PaO2
PaCO2
PH

Chest imaging
Chest x-ray
CT sacn
Ultrasound

Respiratory Failure
Laboratory Testing
Other tests
Hemoglobin
Electrolytes, blood urea nitrogen, creatinine
Creatinine phosphokinase, aldolase
EKG, echocardiogram
Electromyography (EMG)

Pulse oximetry

Hb saturation (%)

90

PaO2 (kPa)

Sources of error

Poor peripheral perfusion

Dark skin
False nails or nail varnish
Lipaemia
Bright ambient light
Poorly adherent probe
Excessive motion
Carboxyhaemoglobin or methaemoglobin

 EACH MINUTE
IS CRITICAL TO
ACHIEVING
BOTH SURVIVAL AND
A FAVORABLE
NEUROLOGIC
OUTCOME.
127