Dr. Zulkifli, SpAn-KIC.

,
MKes., MARS
 TWO TYPES

Type I Type II
Hypoxic Hypercapneic
respiratory failure respiratory failure
Type I Type II
When gas exchange is As a result of alveolar
inadequate at rest or hypoventilation, which
during exercise, leading can be due to a
to hypoxemia, and PaO2 pulmonary or
is less than 60 mmHg extrapulmonary cause
 HYPOXIA HYPERCAPNIA
Restlessness, anxiety Headache
Irritability, impaired intellectual Drowsiness, confusion
functioning, and consciousness
Cyanosis Warm extremities, flushing,
sweating
Tachycardia, hypertension Bounding pulse, tachycardia
Bradycardia, arrhythmia Tremors, myoclonic jerks,
asterixis
Shock, hypotension Seizures
Convulsion, coma, death Papilledema, coma
Type I Type II Type II acute resp failure
• Hypoxemia (PaO2 <60 • PaO2 <60 mmHg is • Low pH
mmHg) associated with PaCO2 • High PaCO2
• With or without >45 mmHg • Normal HCO3
widening of alveolar- • Respiratory acidosis
arterial oxygen gradient
• PaCO2 is either low or
normal

Type II acute on chronic Type II chronic resp failure

resp failure • Normal pH
• Low pH • High PaCO2
• High PaCO2 • High HCO3
• High HCO3
1. V/Q mismatch
Airways disease: COPD, Asthma, Cystic fibrosis, Bronchiolitis obliterans
Alveolar filling: cardiogenic pulmonary edema, mitral valve stenosis,
ARDS, Pneumonia, Alveolar hemorrhage, Partial atelectasis, Alveolar
hemorrhage, Partial atelectasis, Alveolar proteinosis, TRALI (Transfusion
related acute lung injury), Acute interstitiel pneumonia, Cryptogenic
organizing pneumonia, Aspiration, near-drowning, Pulmonary vascular
disease-thromboembolism, fat embolism
2 Shunt
Alveolar filling
Atelectasis
Intrapulmonary shunts-pulmonary AVM (Arterio Venous Malformation)
Intracardiac shunt-PFO, ASD, VSD
3 Hypoventilation-refer to type 2 respiratory failure for causes of
hypoventilation
4 Low inspired pressure of oxygen
1 CNS depression/decreased ventilatory drive
Respiratory center (medulla) dysfunction, Drug overdose,
Hypothyoidism, Sleep apnea, CNS causes (stroke, tumor)
2 Neuromuscular disease
GBS, Poliomyelitis, Myasthenia gravis, Amyotrophic lateral
sclerosis, Cervical cord lesions, Polyneuropathies, Muscle
diseases (muscular dystrophy, poliomyositis)
3 Chest wall/pleural diseases
Kyphoscoliosis, Morbid obesity, Pneumothorax
BRIEF PRECIPITATING EVENT followed by developing DYSPNEA

Markedly impaired respiratory system COMPLIANCE and REDUCED

AERATED LUNG VOLUME

HYPOXEMIA is refractory to low fraction of oxygen concentration and low

PEEP

MORTALITY is around 35-40%

Therapy is around UNDERLYING CAUSE, LUNG PROTECTIVE ventilatory

strategy, and appropriate FLUID MANAGEMENT
• Australia : ALI 34/100.000, ARDS 28/100.000
(Am J Respir Crit Care Med 2002;165;443-8)
• US : ALI 79/100.000, ARDS 59/100.000
(Chest 2007; 131: 554-62)

Mortality (influenced by the definitions used)

60% (ARDS):
Australia 32% (ALI) 34% (ARDS)
US 38.5% (ALI) 41% (ARDS)
Pulmonary (primary) Extrapulmonary (secondary)
Pneumonia Sepsis
Aspiration Pancreatitis
Smoke inhalation Blood transfusion
Lung contusion Fat emboli
Near-drowning Major burn
Venous air embolism Poly trauma
Amniotic fluid embolism
Neurogenic pulmonary edema
Cardiopulmonary bypass
Drug reactions (aspirin,
nitrafurantoin)
Acute onset

Presence of predisposing condition

PaO2/FiO2 <200 mmHg for ARDS

PaO2/FiO2 <300 mmHg for ALI

Pulmonary artery occlusion pressure <18 mmHg or

no clinical evidence of left-sided heart failure
• Cardiogenic pulmonary • Goodpasture Syndrome
edema
• MOF of Sepsis
• Diffuse alveolar
hemorrhage • Pneumocystis Carinii
• Acute pulmonary embolism Pneumonia
• Acute eosinophilic • Transfusion related acute
pneumonia lung injury (TRALI)
• Acute hypersensitivity
pneumonitis • VAP
• Near drawning • Reperfusion Injury
• Fat embolism syndrome • Toxic shock syndrome
• Leukemic infiltration • Pneumonia aspiration
• Drug induced pulmonary
edema • Ventilation, Mechanical
Timing Within 1 week of a known clinical insult or new or
worsening respiratory symptoms
Chest imaging Bilateral opeacities– not fully explained by effusion,
lobar/lung/collapse, or nodules
Origin of edema Respiratory failure not fully explained by cardiac failure
or fluid overload
Need objentive assessment (eg. Echocardiography) to
exclude hydrostatic edema if no risk factor present
Oxygenation
Mild 200 mmHg <PaO2/FiO2 < 300 mmHg with PEEP or CPAP
>5 cmH2O
Moderate 100 mmHg <PaO2/FiO2 < 200 mmHg with PEEP >5
cmH2O
Severe PaO2/FiO2 < 100 mmHg with PEEP or CPAP >5 cmH2O
1.1. Exudative (acute) phase - 0- 4 days
2. Proliferative phase - 4- 8 days
3. Fibrotic phase - >8 days
4. Recovery
KatzensteinAA,AskinFB:Surgical Pathology of Non-Neoplastic Diseases. Phila.Saunders,1982
 Reproduced in Animal models by direct insult to the alveoli (
e.g intra tracheal instillation of endotoxin or live bacteria,
complement, TNF)
• Pulmonary epithelium injury 
activation of alveolar macrophages 
DIRECT
activate the inflammatory network 
pulmonary inflammation
• The prevalent damage is intra alveolar,
alveolar filling edema, fibrin, collagen,
neutrophilic aggregates , or blood (
pulmonary consolidation)
• Through extra pulmonary mediators released into
the blood, during peritonitis, pancreatitis, multiple
trauma etc.
• The target is pulmonary endothelial cell 
activation of the inflammatory network 
increase permeability of endothelial barrier and
recruitment of monocytes, PMN , platelets, and
other cells
• The prevalent damage is represented by micro
vessel congestion and interstitial edema.

INDIRECT
1. Pulmonary edema (damage alveolocapillary barrier)
epithelial pore 0.5 – 0.6 nm, endothelial pore 6.5 –
7.5 nm
2. A complex inflammatory infiltrate
3. Surfactant dysfunction

The sequence of events depends on precipitating

insult and host response
Acute phase: Lung edema Fibrosing alveolitis phase
( arrow= interlobar thickening ,Reticular and diffuse
septa),bilateral pleural effusion Opacities both lungs, a large
(common findings) bulla
 Histologic Findings
Hyaline Protein in air spaces

Cellular Congestion

Typical histological
findings in ARDS
www.burnsurgery.com/.../pulmonary/part3/sec4.htm
– alveolar inflammation,
thickened septal from
protein leak (pink),
congestion and decreased
alveolar volume

←Normal Lung Histology—large alveolar

volumes, septal spaces very thin, no cellular
congestion.
 ACUTE PHASE

HYALINE

Light Microscopy Electron Mycroscopy

C = Capillar
Lung Biopsy INJURY of LC = Leokocyte
Day 2 ARDS (Gastric Acid ENDOTHEL BM = Basal Membrane
Aspiration) and EPITHEL EN=Endothel
 FIBROSING ALVEOLITIS
PHASE

Type-II Cell
Microvilli
Lamelar bodies
(contain surfactant)

GRANULATION TISSUE
CHRONIC INFLAMMATORY-CELL
INFILTRATION

COLLAGEN DEPOSITION

RE EPITHELIALIZATION
ALVEOLAR TYPE –II CELL
Collagen
 Cardiogenic
• Patchy infiltrates appearing
in the lung bases first
• Effusions may be present
• Clinical signs and
symptoms lag behind
radiographic evidence (i.e.
CXR is more impressive
than the degree of
hypoxemia)
Non-Cardiogenic
• Infiltrates are more
homogeneous
• No pleural effusions
• Radiographic evidence lags
behind clinical signs and
symptoms (i.e. the CXR is
unimpressive given the
degree of hypoxemia)
 Cardiogenic Non-Cardiogenic
• Excess fluid in alveoli • Protein, inflammatory
• Due to high pulmonary cells, and fluid
capillary pressure accumulation in the
(estimated by alveoli
measuring pulmonary • Due to “other”
artery wedge pressure) systemic factors NOT
elevated pulmonary
capillary pressure
M 42yo, ARDS, Sepsis Gram –ve,
on Ventilator, PWCP 4mmHg,
diffuse bilateral alveolar opacities 
Pulmonary Edema (exudative phase)
M, 60yo ,ALI and ARDS
on ventilator day 7, reticular
opacities both lungs development
of fibrosing alveolitis (fibrosing -
alveolitis phase)
 Non-Cardiogenic
Cardiogenic

Bilateral infiltrates predominately in

Diffuse Bilateral patchy infiltrates
lung bases. Cardiomegaly.
homogenously distributed throughout the
lungs. Positive tube sign.
 Cardiogenic
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http://rad.usuhs.edu/medpix/medpix_image.html?mode=quiz&imid

Non-Cardiogenic

No septal thickening. Diffuse

alveolar infiltrates. Atelectasis of
Septal thickening. More severe in lung dependent lobes usually seen (not
bases. well shown here)
• Initial resuscitation (A, B, C)
• Take history
• Perform quick physical examination
• Initiate basic investigation such as ABG and
chest X-ray to arrive a propable cause for
deterioration in respiratory status
• NIV/CPAP has a very limited role in a patient developing
ARDS
• May be used in selected patients who are
immunosuppresed, with close monitoring to help
improve oxygenation and decrease the work of
breathing
• Minority of patients show a marked improvement and
may be taken off this cautiously after days of
stabilization
• Most of patients show very little or transient
improvement and not to persist with NIV and instead
proceed to tracheal intubation before major
deterioration occures
• Mechanical ventilation should be initiated
electively
• To avoid complications of emergent intubation, it
is improper to wait till patient deteriorates
further:
– Persistent hypoxemia (SpO2 <90%) on non-breathing
facemask oxygen or NIV
– Excessive WOB and high minute ventilation, which is
often a subjective assessment
– Hemodynamic instability
• Major principle: keep patients stable and cause
minimal iatrogenic damage till such time the
underlying disease resolves
• Mechanical ventilation is primarily used to reverse
hypoxemia and decrease the WOB
• Positive-pressure ventilation is unphysiologycal, and
adverse effects must be prevented or rapidly reversed
• High volumes, high airway pressures, and repeated
opening and closing of collapsed alveoli may further
damage the lung, worsen the ARDS, and contribute to
systemic inflammation
• Patients are prone to VAP due to prolonged ventilation
required and occasionally due to the use of corticosteroid
• Mechanical ventilation protocol is based on the concept
that the lung is largely consolidated, and may be viewed as
a “baby lung” with only about a third of the alveoli
remaining open
• Consolidation primarily results from the alveolar wall
becoming stiff and shutting down, rather than being fluid-
filled
• Sponge lung implies the gravitational effect of lung injury
and the appropriate ventilatory strategy can open up or
recruit shut alveoli
• Open up the lung and keep it open
• Mode-volume control ventilation (ARDS network
protocol) or pressure control as starting mode
– Tidal volume (TV) (in volume control mode)
• Male IBW: 50 + 2,3 [height (inches) – 60]
• Female IBW: 45,5 + 2,3 [height (inches) – 60]
• Set initial TV: 8 ml/kgIBW
• Reduce TV by 1 ml/kg intervals every 2 hr until 6 ml/kgIBW
– Inspiratory pressure (in pressure control)
• <30 cmH2O
– FiO2 and PEEP
• Initial FiO2 should be kept high and PEEP 5-10 cmH2O to keep SpO2
>90%
• FiO2 should be titrated down if SpO2 >90%. Titrate PEEP as per
ARDSnet table
• Mode-volume control ventilation (ARDS network
protocol) or pressure control as starting mode
– Minute Ventilation
• Adjust respiratory rate (maximum up to 35/min) to
achieve a minute ventilation commensurate with patients’
demand
– Inspiratory flow or inspiratory time or I:E ratio
(depending on ventilator type)
• Set inspiratory flow rate above patients’ demand (usually
>80 L/min); adjust flow rate to achieve goal of inspiratory-
expiratory ratio of 1:1,0-1,3
• Monitor for safety and efficacy of ventilator
settings and an attempt should be made to
ventilate within certain goals
• Oxygenation goal: PaO2 55-80 mmHg or SpO2
88-95%
• Plateau pressure (Pplat) goal 30 cmH2O
• pH goal: 7,3-7,45
FiO2 0,3 0,4 0,4 0,5 0,5 0,6 0,7 0,7
PEEP 5 5 8 8 10 10 10 12

FiO2 0,7 0,8 0,9 0,9 0,9 1,0 1,0 1,0

PEEP 14 14 14 16 18 20 22 24
• Keep insp pressure in pressure control <30 cmH2O
• In volume assist control, check Pplat (use 0,5 s
inspiratory pause), SpO2, total RR, TV, and ABG
• If Pplat >30 cmH2O: decrease TV 1 ml/kg (minimum 4
ml/kg)
• If Pplat <30 cmH2O and breath stacking occurs,
increase TV in 1 ml/kgIBW increments (to maximum of
8 ml/kg) as long as Pplat <30 cmH2O
• In patients with obesity and stiff chest wall or high
intrabdominal pressure: higher Pplat may be tolerated
• Acidosis management
– If pH 7,15-7,30: increase RR until pH >7,3 or PaCo2
<25 mmHg (maximum RR 35); If RR is 35 and
PaCO2 <25 mmHg, NaHCO3 may be given
– If pH <7,15 and NaHCO3 is considered or infused,
TV may be increased in 1 ml/kg steps until pH is
more than 7,15 (Pplat goal may be exceeded).
• Alkalosis management
– If pH is more than 7,45, decrease RR if possible
• Recruitment maneuver
• Airway pressure release ventilation
(APRV)/inverse ratio ventilation (IRV)
• Prone positioning
• High-frequency ventilation
• Extracorporeal membrane oxygenation
• Inhaled nitric oxide
 Static lung compliance = VT
Pplat – (PEEP + AutoPEEP)

• Normal static compliance is 100 ml/cmH2O

• Significant improvement: continue therapy
• No significant improvement: next intervention
• Weigh the risk and benefits for individual patients
• Should be avoid in active infection
• Used only when paralytic agents are discontinued
• Responses is seen within 5 days. If no response the
discontinued
• Dose should be methylprednisolone 1 mg/kg bolus
followed by 1 mg/kg/day infusion
• If response is favorable, continue for 14 days or until
extubation. Thereafter half dose for 7 days followed by one-
fourth for next 7 days and then stop
• Safety profile is proven including no added risk of infection
• Monitoring fluid status with central line is
• Pulmonary artery catheter is not
recommended
• Conservative fluid management but not at the
risk of organ perfusion
• Hemodynamic is maintained with fluids,
vassopressors, and dobutamine for low
cardiac index
• Present guidelines recommend to initiate
immunonutrition with formulation containing
antiinflammatory lipid profile:
– Eicosapentenoic acid
– Gamalinoleic acid (GLA) (omega-3 fish oil, borage
oil)
– Antioxidants
• Recent study: doubt on enteral immune
nutrition
• Tracheostomy should be performed when:
– Off high FiO2 and PEEP support
– Still needs continuing ventilator support due to
high minute ventilation
• Started when:
– FiO2 and PEEP support decrease
– Minute ventilation comes down
• To prevent long-term neuromuscular disability
• Started from initial days
OXYGEN THERAPY
 Definitions
• Oxygen therapy is given gas stream more than
20% at pressure 1 atmosphere so that
concentration of oxygen increases in blood.

• Hyperbaric oxygen Therapy if stream of 100%

O2 at pressure above 1 atmosphere
 Goals

• Prevent and improve

– hypoxemia
– tissue hypoxia
 Indications
• Hypoxemia
• Increased work of breathing
• Increased myocardial work
• Pulmonary hypertension
• Transport of patients
• Cardiac or respiratory Arrest
• Respiratory failure
• Heart-Failure or infarct myocard
• Shock
• Metabolic increases
• Post surgery
• Carbon monoxide Poisoning
 Contraindications

• No absolute contraindications
• Relative contraindications
– relate to the dangers of hyperoxemia
 Precautions/Hazards/Complications
• Induced hypoventilation and CO2 narcosis
• Oxygen Toxicity
• Absorption atelectasis
• Retrolental fibroplasia
• Barotrauma
• Fire hazzard
• Hyperbaric oxygen Toxicity
• Drying of the nasal and pharyngeal mucosa
• Potentially inadequate flow
• Skin irritation
• Nasal obstruction
• Aspiration of vomitus
 Adverse Reactions and Interventions
• signs of hypoventilation
• Hyperoxemia

EQUIPMENT

• Oxygen Delivery devices

• Humidifier
• oxygen flowmeter
 Oxygen Delivery devices

• Nasal cannula
• Simple mask
• Venturi mask
• Partial rebreather
• Nonrebreather
• Mechanical ventilation

Monitoring
 Stopping oxygen treatment
• arterial oxygenation is adequate with the
patient breathing room air

Summary

• Oxygen is a life saving treatment

• required flow rate and the method of delivery
• Careful monitoring