Definition

Respiratory failure is said to exist when the lung

cannot fulfill its primary function of adequate gas
exchange.
Essentially this means a fall in PaO2 with or
without a rise in PaCO2.
In practice
PaO2 less than 8kpa(60mmHg) while breathing room
air
Or a PaCO2 greater than 6.5kpa(49mmHg)

Classification
According to Duration
Acute occurring over minutes or hours
Chronic occurring over days or months
Pathophysiology
Hypoxaemic respiratory failure (Type 1) Characterized
by a PaO2 of less than 60mmHg with a normal or low
PaCO2(< or = to 40mmHg)
Hypercapnic respiratory failure (Type11) Characterized
by a PaCO2 of more than 49mmHg. Also Hypoxaemia
Respiration
Respiration involves 3 processes
Transfer of O2 across the alveolus
Transport of O2 to the tissues
Removal of carbon dioxide from the alveolus and then
into the environment.
Respiratory failure can arise from the abnormality of
any components
Airways, alveoli, CNS, peripheral nervous system,
respiratory muscles and chest wall
Physiology
Respiration occurs at the alveolar capillary units of the
lung
Exchange of O2 and CO2 b/w alveolar gas and blood takes
place.
Each molecule of HB combines with a maximum of
1.36ml of oxygen level depends on PaO2.
O2 dissociation curve sigmoid in shape.
Oxygen dissociation curve
Physiology
The CO2 is transported in 3 ways
In simple solution carbonic acid
As bicarbonate
Combined with HB as carbamino compd
In steady state
CO2 production equals CO2 elimination
PaCO2=K(VCO2/VA) VA (Alveolar ventilation) VCO2 is
CO2 production
K is a constant (0.863).
VE=VA+ VD VA= VE- VD
Hypercapnia occurs with
Decreased minute ventilation or Increased dead space
Usually only slight A to a PaO2 diff.
An increase above 15-20mmHg indicates pulmonary disease
In Ideal Gas exchange
Ventilation and perfusion are matched
High V/Q Low V/Q

Pathophysiologic causes of Acute RF
Hypoventilation

V/Q mismatch

Shunt

Diffusion
abnormality



Pathophysiology
Acute respiratory failure
Hypoventilation Type 11 Resp. Failure
Occurs when ventilation is <4-6l/min
Depression of CNS drugs
Neuromuscular disease
Relationship b/w PaCO2 and alveolar ventilation is inverse
Alveolar arterial gradient normal
Increased PaCO2 decreased PaO2

Pathophysiology
V/Q mismatch most common cause of Type 1
Hypoxaemic Respiratory failure
Low V/Q ratio may occur
Decrease in ventilation secondary to
Airway or interstitial disease
Overperfusion in the presence of normal ventilation
Pulmonary embolism
100% oxygen very effective


Diffusion deficit
Less common
Due
to abnormality of alveolar membrane
Decrease in number of alveoli
Cardiogenic and non cardiogenic pulmonary oedema
Fibrotic lung disease

Pathophysiology
Shunt
Admixture of oxygenated and deoxygenated blood
Hypoxia persistent with 100% oxygen#
Hypercapnia when shunt >60%
Disease processes
Intrapulmonary, intracardiac, Pneumonia atelactasis
collapse, haemorrhage, cardiogenic and non cardiogenic
pulmonary oedema A/V malformation



Aetiology
Aetiology
Affecting the brain Depression of neural drive
Drugs narcotics poisons trauma tumors infection myxoedema,
Affecting the nerves and muscles
Guillain Barre Myasthenia Gravis Poliomyelitis Muscular
dystrophy
Affecting upper airways
Tumours oedema foreign body trauma
Affecting the chest wall
Crushed chest, Kyphoscoliosis, morbid obesity
Affecting the lower airways and lung parenchyma
COPD, ARDS, Trauma, infection neoplasm
Causes
Type 1
Associated with conditions affecting the interstitium
alveolar wall
Acute causes
Severe Asthma, cardiogenic and non cardiogenic pulmonary
oedema pulmonary embolus ARDS Pneumonia
Chronic causes
COPD, Lymphangitis carcinomatosis fibrosing alveolitis
pneumoconiosis
Type 11
Associated with alveolar hypoventilation
Acute causes
Drug overdose with hypnotics opiates narcotics tranquilizers
poisoning Myasthenia gravis Guillain Barre syndrome
Crushed chest poliomyelitis
Chronic causes
COPD Primary alveolar hypoventilation Kyphoscoliosis
Clinical Features
This reflects the underlying disease condition
examples such as pneumonia, asthma, pulmonary
oedema COPD are readily apparent
Also symptoms and signs of Hypoxia with or without
Hypercapnia



Hypoxia
Cyanosis easy to detect in polycythaemia diff in
anaemia
Restlessness agitation irritability clouding of
consciousness convulsions tachypnoea tachycardia
coma death. Cardiac arrhythmias
Pulmonary hypertension with or without cor
pulmonale
Polycythaemia
CYANOSIS
Hypercapnia
Dyspnoea
Dilatation of cerebral blood vessels with increases
intracranial pressure cerebral oedema papilloedema
headache
Flapping tremor (asterexis) stupor Coma
Hypoxaemia hypercapnia acidosis cause
Increased gastric acid production
In severe cases gastric dilatation and paralytic ileus.
Haemorrhage stress ulcers

Acute respiratory failure
life-threatening derangements in arterial blood gases
and acid-base status PH low less than 7.3
Chronic respiratory failure
Symptoms less dramatic
Usually PH only slightly decreased due to renal
compensation
Polycythaemia
Investigations
Arterial blood gases
FBC Anemia, polycythaemia
Chemistry- EUC K Mg Ph cardiac enzymes
CXR
ECG- arrhythmias may show CVS cause
Echocardiography Rt heart catheterization
Lung Function tests

Distinction between Noncardiogenic (ARDS) and
Cardiogenic pulmonary edema
ARDS Pulmonary edema
Diagnosis
Depends on demonstration of abnormal Blood Gas
tensions
Laboratory diagnosis
Clinical features may be non specific and very
significant respiratory failure may be present without
dramatic symptoms
Management
Priorities depend on aetiology.
Generally
Admit intensive care unit
Maintain adequate airway Vital
Correction of Hypoxaemia most important
Threat to organ function
Address Hypercapnia and respiratory acidosis
Ventilator management
Type 1
Treatment with Oxygen using nasal cannulae oxygen
masks
Treatment of underlying cause
Asthma
Pneumonia
Antibiotics
Pulmonary embolism
If hypoxaemia persists assisted ventilation




















Type11
Commonest cause is COPD
Patent airways- remove secretions Phsio
pharyngeal suction
Hypoxaemia Controlled O2 therapy
Bronchodilatation
Antibiotics
Diuretics
Respiratory stimulants
If above efforts fail to improve respiratory function
consider assisted ventilation.

Rx for other causes of type two
Respiratory depression sec to drugs give antagonists or
enhance drug removal by dialysis
Myasthenia gravis treated with specific drugs
Guillian Barre respiratory support required for
duration of disorder
Case 1
A 36 yo man who has had a recent viral illness now is
admitted to the ICU with rapidly progressive ascending
paralysis (diagnosed as Guillain-Barre Syndrome). He is
breathing shallowly at 36/min and complains of shortness
of breath. His lungs are clear on exam. CXR shows small
lung volumes without infiltrates. With the patient
breathing room air, ABG are obtained.
pH 7.18
PaCO2 68 mm Hg
PaO2 49 mm Hg
Why is he hypoxemic?
A-a O2 gradient
PAO2 = FIO2 PaCO2/0.8
PAO2 = 150 68/0.8 = 150 85= 65
A-aO2 gradient = PAO2 PaO2
= 65 49 = 16
His A-aO2 gradient is minimally increased, although
his PaO2 is significantly reduced.
His hypoxemia is due to alveolar hypoventilation.
Case 2
A 65 yo man has smoked cigarettes for 50 yrs. He
has chronic cough with sputum production and
chronic dyspnea on exertion (stops once when
climbing 1 flight of stairs). He is now admitted
with several days of increased cough productive of
green sputum and is short of breath even at rest.
On exam his breathing is labored (32/min) and his
breath sounds are quite distant. The expiratory
phase is greatly prolonged and there are soft
wheezes in expiration.
Case 2 ABG analysis
pH=7.38
PCO2=48
PO2=48
O2 sat=78%
How would you describe his ABG?
He is hypoxemic with a respiratory acidosis.
What is the likely mechanism of hypoxemia?
Is his hypercarbia acute or chronic?
Why is he hypoxemic?
What is his A-a O2 gradient?
PAO2 = (149-48/0.8) = 149-60 = 89
A-a O2 gradient = 90 48 = 41
His hypoxemia is predominantly due to V/Q mismatch.
An enormous number of conditions cause hypoxemia
due to V/Q mismatch
disorders effecting pulmonary vascular, airways, or
alveolar space
Mechanical Ventilation
Increase PaO
2

Lower PaCO
2
.
Also rests Respiratory muscles

Controlled
Patient assisted
Mechanical ventilation
Negative pressure vs positive pressure
Pressure targeted or volume targeted
8-10L/kg at 10-12 breaths per min
Flow triggered or pressure triggered
Use lowest F1O2 that produces SAO2>90%
Or PO2>60mmHg to avoid O2 toxicity

Negative pressure ventilation
Assisted Ventilation
Non invasive
IPPV PSV CPAP has been used in COPD
Use face mask or nasal mask
Invasive with ETT/ tracheostomy
The most common indication for endotracheal
intubation (ETT) is respiratory failure
Several methods PSV IMV SIMV HFPPV
Patient monitored closely


Weaning
Patients have to be weaned off ventilator
Should be stable and considerably improved
Depends on length of time on ventilator
PaO2 >= to 65mmHg
Techniques
SIMV CPAP PSV
Allow Pt to breath spontaneously for small intervals
gradually increasing the length of time and reducing
length of spontaneous respiration


Dangers
Wrong position of tube
Obstruction
Mucosal oedema
Pneumothorax Barotrauma
Haemothorax
Infection VAP
Ventilator dependence
Other Modes of Management
Extracorporeal gas exchange
Extracorporeal membrane exchange
Extracorporeal carbon dioxide removal
Lung transplantation
Employed in patients with end stage respiratory disease
Prevention
Influenzae and Pneumococcal vaccines
Smoking cessation
Mortality
Varies according to aetiology usually high
30% in COPD
40% in ARDS
Worse in Patients with Type11
FIO2
Ventilation
without
perfusion
(deadspace
ventilation)
Diffusion
abnormali
ty
Perfusio
n
without
ventilati
on
(shuntin
g)
Hypoventilati
on
Normal
ARDS
Also called non cardiogenic pulmonary oedema
Adult respiratory distress syndrome
Increased permeability pulmonary oedema
Often accompanied by MODS MOF
Renal
Hepatic
cardiac
CAUSES
Sepsis, pneumonia
Trauma Multiplefractures,pulmonarycontusion
Aspiration, Near drowning, toxic inhalation
Acute Pancreatitis
Multiple Blood transfusions
Drug toxicity, methadone overdose

ARDS
Insult direct or indirect
Activation of inflammatory cells
Damage to alveolar capillary membrane
Increased permeability
Influx of protein rich exudate and inflammatory cells dysfunction of
surfactant
Pathophysiology
DAD Lung capillary endothelial damage
Early phase exudative
Secondary stage fibroproliferative
Two types of Alveolar cells
Type 1 easily injured 99%
Type 11 resistant
Surfactant production Differentiates into type1
Alveolar collapse defect in repair
Neutrophils
Cytokines
Leukotrienes
TNF
Macrophage Inhibitory factor

Clinical features
Acute onset
Tachypnoea Dyspnoea
Wide spread Crepitations some rhonchi
Refractory hypoxaemia
Bilateral infiltrates in the lung fields
Normal pulmonary capillary wedge pressure

ARDS
PaO2/FiO2 < 200
ALI
PaO2/FiO2 <300
Management
Respiratory support CPAP with40-60% O2

Management
Treatment of underlying cause oxygen
Anti inflammatory Steroids
Vasodilators Nitric Acid
Surfactant
Prone position
Antibiotics for sepsis
Diuretics fluid restriction
Assisted ventilation