Diagnosis and Management of

Acute Respiratory Failure (ARF)

Dr. Prabowo Wicaksono Y.P., SpAn

Department of Anesthesiology
UNISSULA Medical Faculty/ RSI Sultan Agung
Semarang
2007

I. DEFINITION/ CLASSIFICATION OF ARF

ARF : One of the most common disorders leading to ICU admission
Occurs when pulmonary systems is no longer able to meet the metabolic
demand of the body.
Pulmonary system : 2 metabolic roles:
- Oxygenation of arterial blood
- Elimination of CO2
Two basic types of RF:
TYPE I : Hypoxemic. Interference with the pulmonary systemss ability to
adequately oxygenate the blood as is circulates through the alveolar
capillaries. PaO2 (room air) < 60 mmHg. (Normal PaO2: 75-100 mmHg).
TYPE II : Hypercapnic. Failure to prevent CO2 retention (e.g., severe
airflow obstruction, central resp. failure, neuromuscular resp. failure)
PaCO2 > 50 mmHg. (Normal PaCO2: 35-45 mmHg)

II. CAUSES OF ARF

RF may results from primary pulmonary insults and from other systemic
nonpulmonary disorders (CNS, CV, neuromuscular systems, upper and lower
airways, pulmonary parenchyma). Often multifactorial.
CAUSES OF RESPIRATORY FAILURE
Disorders associated with Abnormal Oxygen Onloading (Hypoxemic RF)
Lower Airway and Parenchyma
NEOPLASM

TRAUMA (pulmo. contusion, laseration ARDS

INFECTION

OTHER (Broncospasm, CHF)

Interstitial lung disease

Pulmonary emboli
Atelectasis
Cystic fibrosis

Disorders associated with Inadequate CO2 Offloading (Hypercapneic RF)

BRAIN : Drugs (opioids, benzodiazepines, propofol, barbiturates, GA, poisons)
Metabolic (e.g.Hyperglycemia, hypocalcemia)
Neoplasma, Infection, Increased ICP.
NERVES AND MUSCLES: trauma, metabolic, drugs, poisons, neoplasm, infection

UPPER AIRWAY: Tissue enlargement, infenction, trauma.

CHEST BELLOWS: trauma (rib fractures, flail chest), other contributing factors (e.g.obesity,
ascites, spondylitis)

III. PATHOPHYSIOLOGY OF ACUTE RESPIRATORY FAILURE

A. HYPOXEMIA
The underlying physiologic abberation in hypoxemic RF is usually the results
of a mismatch of alveolar ventilation and pulmonary perfusion. Diseases
processes that cause progressive obstruction or atelectasis (e.g. pneumonia,
aspiration, edema) results in decrease in the amount of oxygen available in
distal airways for uptake.
This mismatch of ventilation (V) and perfusion (Q) wherein perfusion is
relatively greater than ventilation to a given lung unit is called shunt effect .
The venous blood entering pulmonary capillaries acts as if did not travel to
the lung at all because it remains relatively poorly oxygenated as it returns to
the left atrium, the physiologic effect of this type of V/Q mismatch is
hypoxemia.
Treatment should be directed toward removing obstruction, reopening
atelectasis zones, and preventing closure of the affected lung units.
The most likely reason for a patient to be hypoxemic is this type of V/Q
mismatch.

VENTILATION
VENTILATION (V)
(V) and
and PERFUSION
PERFUSION (Q)
(Q)
ANATOMICAL
DEAD SPACE

TRAKEA

PHYSIOLOGICAL
DEAD SPACE
V/Q =
PULMONARY
CAPILLARY

ALVEOLAR
DEAD SPACE
V/Q > 1

MECHANICAL
DEAD SPACE:
TUBE

V/Q = 1

NORMAL

ET CO2
BREATHING
CIRCUIT

V/Q < 1
VENOUS ADMIXTURE
(SHUNT)
V/Q = 0

CONNECTOR

FREE AIR:
PiO2

: 20.9 % x 760 = 159 mmHg

PiCO2 : 0.04 % x 760 = 0.3 mmHg

PiN2

ALVEOLUS

: 78.6 % x 760 = 597mmHg

PiH2O : 0.46 % x 760 = 3.5 mmHg

N2
PAN2:
573 mmHg

DIFUSSION
PROCESS

PAO2:
104 mmHg

O2

O2
PaO2:
40 mmHg

H2O

PULMONARY
CAPILLARY

PAH2O:
47 mmHg
PACO2:
40 mmHg

O2

CO2
CO2

CO2
PaCO2:
45 mmHg

PaCO2:
40 mmHg

PaO2:
104 mmHg

B. HYPERCAPNIA
Hypercapnia RF is caused by one or more factors describes in equation fo
alveolar minute ventilation:
VA= (VT-VD) . f
VA : minute alveolar ventilation
VT : tidal volume
VD : physiologic dead space (alveolus is well ventilted but poorly perfused)
f : respiration frequency
Hypercapnia may results from decreased VT or f as occurs with drug ingestion,
anestesia, change in medullary center for respiration, fatigue. An elevated PaCO2
normally increases ventilatory drive. Therefore, hypercapnic respiratory failure
may also imply that the patient is:
- Unable to sense the elevated PaCO2 due to drug, alkalemia, COPD, etc
- Unable to neurologically signal the effector mechanism of ventilation because
of spinal cord injury, neuromuscular blockade, Guillan-Barre synd, Myastenia
Gravis.
- Unable to effect a response from the muscle of respiration because of fatigue,
malnutrition etc.

Tratment of decrease VT or respiration rate may require special medications

(e.g. for Myastenia), reversal of sedation or other drugs, intubation/ mechanical
ventilation to rest fatigued muscles, nutrition, resp. stimulant and as always
treatment of other possible primary cause.
Increased physiologic dead space (VD) may also produce hypercapnia and
represents the other type of V/Q mismatch. When gas flow to and from airways
remain adequate but blood flow is absolutely or relatively diminished, CO2 does
not have the opportunity to diffuse from the pulmonary artery blood, and CO2
rich blood is returned to the left atrium. This condition may occur in hypovolemia,
pulmonary embolus, poor cardiac output.

IV. MANIFESTATIONS OF ARF

Clinical manifestations of respiratory distress commonly reflect signs and
symptoms of hypoxemia, hypercapnia, or both. These include:
-Altered mental status, ranging from agitation to somnolence.
-Evidence of increased work of breathing (i.e., nasal flaring, use of accessory
muscles, intercostal/suprasternal/supraclavicular retraction, tachypnea,
hyperpnea, or a paradoxical breathing pattern)
- Bradypnea

- Cyanosis of mucosal membranes (e.g., tongue, mouth) or nail beds.

- Diaphoresis, tachycardia, hypertension, and other sign of catecolamine release.
Laboratory test :
- A key test is the arterial blood gas (PaO2 and PaCO2, to differentiate between
ARF type I and II )
- Additional test: electrolytes, drug level : clue to underlying etiology of ARF
- A chest radiograph: pumonary infiltrates: a hypoxemic component for ARF, a
clear lung fields suggest possible hypercapnic RF, although considerable overlap
exists.

MANAGEMENT
1.

Clear the airway

2.

Oxygen supplementation

3.

Noninvasive positive pressure ventilation

4.

Tracheal intubation and mechanical ventilation

5.

Pharmacologic adjuncts

1. CLEAR THE AIRWAY

PRIMARY SURVEY
Airway :

Open the airway

Breathing :

Provide positive-pressure
ventilation
Circulation :

Give chest compressions

Defibrillation :

Shock VF / pulseless VT

SECONDARY SURVEY
Airway :

Establish advanced airway

control

Perform endotracheal intubation

Breathing :

Assess the adequacy of

ventilation via endotracheal tube

Provide positive-pressure
ventilations
Circulation :

Obtain iv access

Continue CPR

Provide rhythm cv
Differential Diagnosis

AIRWAY OBSTRUCTION
Airway obstruction caused
inadequate ventilation although the
patient breathing sontaneously. The
caused of obstruction:

Tongue, epiglottis
Foreign object

OBSTRUKSI AIRWAY
LIDAH

PRIMARY PRIORITY: CLEAR

THE AIRWAY
Manual: Triple airway maneuver: - Head Tilt
- Chin lift
- Jaw Thrust
Airways : - Oropharyngeal airways (Guedel)
- Nasopharyngeal airways
- Laryngeal mask airway
Endotracheal Intubation

HEAD TILT CHIN LIFT

CAUTIONS !!! CERVICAL
TRAUMA ??

JAW THRUST

Oropharyngeal Airway

To prevent obstruction of
hypofaring by the tongue
To facilitate suction
To prevent tongue or ETT
bite
Unconscious patient
without gag reflect.

Oropharyngeal Airway/Guedel

Measure the right size of

Oropharyngeal airway/Guedel
Complication :
Total obstruction
Laringospasm
Vomit

Oropharyngeal airway
How to insert correctly

Nasopharyngeal Airway
Indication:
- Spontaneous breathing, unconscious patient.
- Better tolerated than OPA

Nasopharyngeal Airway
Complication
Nasal mocous damaged
Laryngospasme

How to insert Nasophryngeal Airway

1.

2.

3.

LARYNGEAL MASK AIRWAY

Very useful in difficult intubation situation

Tracheal Intubation
- Gold standart in airway management.
- Not easy to perform, complication can be serious
- Skill, experience and training are essential to minimaze complication

Advantages of Tracheal Intubation

Clear and secure airway

Reduced aspiration risk
To fasicilitate intra tracheal suction
To fasicilitate high concentration oxygen
support

Complication of tracheal intubation

Hipoxia
Trauma
Vomiting, aspiration
Hipertension, dysritmia
One lung intubation
Oesophageal intubation
Bradycardia, vagal reflex
Cardiac arrest

TRACHEAL INTUBATION EQUIPMENT

Oral intubation
technique
1

VISUALIZATION OF THE CORD

VOCAL CORD: MUST SEE THIS WHEN INTUBATE !!!
TRAKEA

BURP MANUEVER

To aid visualization of the cord

Push the cricoid cartilage back, up and right (BURP)

ADAMS APPLE

BURP

THYROID
CRICOID

3
4

Nasal Intubation technique

TRAINING IS ESSENTIAL

Measures to prevent complication of tracheal

intubation

Skilled trained personnel

Complete intubation equipment
Performed less than 30 seconds
Perform BURP Manuever
Use high volume low pressure cuff ETT

MANUAL POSITIVE PRESSURE VENTILATION WITH

ETT

2. Oxygen supplementation
Most patient with ARF require supplemental oxygen. Oxygen transfer from
alveolar gas to capillary blood occurs by diffusion through alveolar-capillary
membrane, which driven by te oxygen partial pressure gradient between the
PAO2 (alveolus) and the PaO2 (arterial blood) of the pulmonary capillary
blood. In most cases, the PAO2 can be substantially increased by use of
supplemental oxygen, thus increasing the gradient across the membrane and
improving PaO2. This should be considered a temporizing intervention while
the primary etiology of hypoxemia is diagnosed and treated.
The effectiveness of each oxygen supplement devices is determined by the
capacity of the device to deliver sufficient oxygen at high enough flow rate to
match the patients spontaneous inspiratory flow rate.
Any entrained room air (FiO2 = 0.21) will dilute (decrease) the FiO2 of the
delivered gas in such a way that the tracheal FiO2, and hence PAO2 may be
considerably lower than the FiO2 delivered from the oxygen source.

Oxygen supplement systyem are classified as :

1. Low oxygen, low flow devices e.g. nasal cannula
2. Controlled oxygen, high flow devices e.g. venturi mask
3. Variable oxygen, moderate flow devices e.g. aerosol face mask
4. High oxygen, high flow devices e.g. reservoir face mask, Resuscitation Bag
Mask-Valve Unit.

1. Nasal Cannula
Short prongs of the nasal cannula are inserted into
the nares. Oxygen (100%) is delivered through
cannula, but at low flow rates (0.5-5 L/min).
The maximal tracheal FiO2 is 0.40 - 0.50 (40-50%).
Higher flow rates do not result in much higher FIO2
levels and have drying and irritating effect on nasal
mucosa. Comfortable and well tolerated by many
ARF patient in whom precise control of FiO2 is not
necessary.

NASAL CANNULA
Flow (L/men)

Desired FiO2

Measured FiO2
Gibson et al

Schachter et al

0.24

0.22

0.23

0.28

0.21 0.22

0.24

0.32

0.22 0.24

0.25

0.36

0.40

0.24 0.25

10

0.52

0.30 0.46

15

0.56

0.35 0.61

0.26

2. Air-Entrainment Face Mask (Venturi Mask)

Deliver 100% oxygen through a jet-mixing device that
increase the velocity of oxygen and caused a
controlled entrainment of air. The FiO2 can be rather
precisely controlled from 0.24 0.50 (24-50%) at high
flow rate.
Most useful in COPD patient known to require a
degree to hypoxemia to sustain the respiratory drive.

VENTURI MASK

Gas flow (L/men)

FiO2

48

0.24 / 0.28 / 0.35 / 0.40 /

0.50 / 0.60

3. Aerosol Face Mask

The mask with large side holes is attached by largebore tubing to a nebulizer, which blends 100%
oxygen and room air to deliver gas at a preset FiO2
level. Flow matching can be evaluated by observing
the patient during spontaneous breathing. If the
entire aerosol mist dissappears from mask during
inhalation, the patients inspiratory flow demands are
probably exceeding the capacity of nebulizer.

4. Reservoir Face Mask

Incorporates a reservoir bag with the face mask from
which the patients breathes. The reservoir bag is
filled from the 100% oxygen supply source. The flow
rate of oxygen is adjusted so that bag remains
completely or partially distended throughout the
respiratory cycle. FiO2: 0.6-0.9 (60-90%).

SIMPLE FACE MASK

Flow (L/men)

Desired FiO2

5 -6
67
78

0.4
0.5
0.6

RESERVOIR FACE MASK

Flow (L/men)

Desired FiO2

6
7
8
9 -10

0.6
0.7
0.8
0.9 0.99

Oxygen Masks (see pg. 493)

5. Resuscitation Bag-Mask-Valve Unit

Part of emergency equipment, readily
accessible. When the mask is held firmly
over the face, room air entrainment is
largely excluded. If the oxygen flow to the
bag is kept high (>15L/min), a high oxygen
supply is provided at sufficient flow.

3. NONINVASIVE POSITIVE PRESSURE

VENTILATION
NPPV provides ventilatory assistance,
controlled FiO2 and positive airway
pressure without invasive artificial
airway, thus avoids meany of the
complication associated with intubation
and mechanical ventilation.
Two form of NPPV: CPAP (Continuous
Positive Airway Pressure) and BIPAP
(Bilevel Positive Airway Pressure).

CPAP: functionally equivalent to PEEP which delireved by a mechanical

ventilator through face mask instead of ETT.
BIPAP: Combination of PSV (Pressure Support Ventilation) and CPAP
Best utilized in the alert, cooperative patient whose respiratory condition is
expected to improve in 48-72 hours, e.g. acute exacerbations of COPD.

4. TRACHEAL INTUBATION AND

MECHANICAL VENTILATION
TUJUAN KLINIS / INDIKASI PEMAKAIAN
VENTILASI MEKANIK
GAGAL NAFAS HIPOKSEMIK:
Reverse hypoxemia dgn pemberian PEEP dan konsentrasi O2
tinggi (ARDS,edema paru atau pneumonia akut)
GAGAL NAFAS VENTILASI:
Reverse acute respiratory acidosis
- Kom a : trauma kepala, encefalitis, overdosis, CPR
- Trauma med spinalis, polio, motor neuron disease
- Polineuropati, miastenia gravis
- Anesthesia (relaksan u/operasi, tetanus, epilepsi)
STABILISASI DINDING DADA:
Flail chest
MENCEGAH ATAU M ENGOBATI ATELEKTASIS

5. PHARMACOLOGIC ADJUNCTS
Many disease causing ARF produce similar anatomic and physiologic
derangements, incluiding bronchial inflammation, mucosal edema, smooth
muscle contraction, and increased mucos production and viscosity. Each of
these processes may contribute to obstruction of airway gas flow, increased
airway resistance, V/Q mismatch, and elevated VD. Some pharmacologic
agents have proven helpful in the care of such patients and may directly alter
the shunt or dead space effect.
1. 2 Agonists
Inhaled 2 agonists (e.g. Albuterol, Terbutaline, Metoproterenol sulfate)
stimulate 2-adrenergic receptor causes bronchial and vascular smooth
muscle relaxation.
2. Anticholinergic agents
Ipratropium bromide competes with acetylcholine at bronchial receptor site,
causing an increase in intracellular cGMP, signaling bronchial smooth muscle
relaxation.

3. Corticosteroids
The central role of inflammation in obstructive airway disease is established, and
the benefit from aggressiv corticosteroid use in ashmatic patient with ARF is well
documented.
4. Antibiotics
Bacterial infection (bronchitis/ pneumonia) frequently precipitates ARF. Antibiotics
shoud be used when there is clinical suspicion that bacterial pulmonary infection
is present (e.g., change in sputum characteristics, pulmonary infiltrates on chst
radiograph, fever, leukocytosis)