Respiratory part 2

Respiratory Failure -
Algorithmic Approach –
Diagnosis and Management
Dr.DoHA RASHEEDY ALY

Definition:
• Respiratory failure is a syndrome in which the
respiratory system fails to maintain an adequate gas
exchange at rest or during exercise resulting in
hypoxemia with or without concomitant hypercarbia.
• Clinically respiratory failure is diagnosed when Pao2
is less than 6omm of Hg with or without elevated Co2
level, while breathing room air.
•

Classification
 Type 1 (hypoxaemic) respiratory failure is most often associated with
those conditions that affect the interstitium and alveolar walls of the
lungs e.g. fibrosing alveolitis and pulmonary edema, but is also seen in
other conditions such as pulmonary embolism and pneumonia. It may
also be seen in obstructive lung disease, such as CoPD and asthma. It is
often associated with marked VA/Q mismatching and oxygen is the
critical therapy in the management of these patients.
 Alveolar hypoventilation leads to type 2 (hypercapnic) respiratory
failure, the most common cause of which is acute exacerbation of CoPD.
1. Acute hypercarbic respiratory failure is characterized by a patient with no, or
minor, evidence of pre-existing respiratory disease and arterial blood gas tensions
will show high PaCo2, low pH, and normal bicarbonate.
2. Acute on chronic hypercarbic respiratory failure is characterized by an acute
deterioration in an individual with significant pre-existing hypercarbic respiratory
failure, high PaCo2, low pH, and high bicarbonate.
3. Chronic hypercarbic respiratory failure is characterized by the evidence of chronic
respiratory disease, high PaCo2, normal pH and high bicarbonate.

Hypoxemia results from one of six basic
pathophysiologic mechanisms.
1. Decreased inspired oxygen pressure
2. Hypoventilation
3. Impaired diffusion
4. Ventilation/perfusion mismatch
5. Shunt
6. Low mixed venous oxygen content

Causes:
• It occurs due to dysfunction of one or more essential
components of the respiratory system: essential
components of the respiratory system:
1. Chest wall (including pleura and diaphragm)
2. Airways
3. Alveolar – capillary unit
4. Pulmonary circulation
5. Nerves
6. CNS (brain stem)

Common causes of type 1 (hypoxaemic)
respiratory failure
Common causes of type 2 respiratory
failure
1. Chronic bronchitis and emphysema
2. Pneumonia
3. Pulmonary edema
4. Pulmonary fibrosis
5. Asthma
6. Pneumothorax
7. Pulmonary embolism
8. Thromboembolic pulmonary
hypertension
9. Lymphatic carcinomatosis
10.Pneumoconiosis
11.Granulomatous lung disease
12.Cyanotic congenital heart disease
13.Acute respiratory distress syndrome
14.Fat embolism
15.Pulmonary arteriovenous fistulae
1. Chronic bronchitis and emphysema
2. Asthma
3. Drug overdose
4. Poisoning
5. Myasthenia gravis
6. Polyneuropathy
7. Poliomyelitis
8. Primary muscle disorders
9. Porphyria
10.Cervical cord disorders
11.Primary alveolar hypoventilation
12.Sleep apnea syndrome
13.Pulmonary oedema
14.Acute respiratory distress syndrome
15.Laryngeal oedema
16.Foreign body

Clinical features of hypoxemia:
1. Central cyanosis
2. Hypoxemia affects the central nervous system (CNS), causing
irritability, impaired intellectual function and clouding of
consciousness, which may progress to convulsions, coma and death.
3. Hypoxemia stimulates ventilation via the carotid chemoreceptor,
increases heart rate and cardiac output and dilates peripheral vessels.
Cardiac dysrhythmias may occur.
4. Persistent hypoxia results in secondary polycythaemia due to
increased production of erythropoietin.
5. The pulmonary arteries respond to hypoxia by vasoconstricting,
producing increased vascular resistance and pulmonary
hypertension, with the later development of right ventricular
enlargement or cor pulmonale

Clinical features of hypercarbia:
1. The central nervous system (CNS) manifestation of
hypercarbia is irritability, confusion, somnolence and
coma.
2. Hypercarbia also produces tremor, myoclonic jerks,
asterixis, and even seizures.
3. The vasodilator properties of Co2 may results in
increased cerebral blood flow and an increase in
intracranial pressure, producing headache and
papilloedema.
4. Hypercarbia tends to dilate the vessels of the peripheral
circulation result in a warm flushed skin with a
bounding pulse.
5. Sympathetic stimulation is responsible for tachycardia
and sweating.
6. Marked hypercarbia, producing generalized
vasodilation, may be associated with hypotension.
7. other features occasionally encountered in severe and
well established respiratory failure are gastric dilation

• Initial diagnostic testing will likely include pulse oximetry, CXR, and
arterial blood gas (ABG).
• Further diagnostic testing will depend on the differential diagnosis.
• A standard complete blood count (CBC) should be obtained as
changes in hemoglobin can alter oxygen delivery.
• A drug screen (serum or urine) can assist in some cases of
hypoventilation.
• If that patient is believed to have acute respiratory distress syndrome
(ARDS), it is prudent to obtain more specific labs to diagnose the
cause.
• Cultures (blood, sputum, and urine) should always be obtained if the
possibility of infection is entertained.
• If diffuse alveolar hemorrhage is suspected, a vasculitis work-up
would consist of antineutrophil cytoplasmic antibody (ANCA),
antinuclear antibody (ANA), antiglomerular basement membrane
(anti-GBM), rheumatoid factor (RF), complement levels,
cryoglobulins, creatine phosphokinase (CPK), and other pertinent
testing.
• CT chest: depending on the clinical situation

Arterial blood gas analysis:
1. It is important to measure the arterial pH or to
determine the primary acid-base disturbance.
2. The chronicity of respiratory failure should be
assessed by evaluating the pH and the degree to
which this is compensated by an increase in the serum
bicarbonate.
a. An acute increase in PaCo2 of 1ommHg is roughly
associated with a decrease in pH of o.o8 units and an
increase in serum bicarbonate of 1 mEq/L.
b. Chronic increase in PaCo2 of 1ommHg is associated with a
decrease in pH of o.o3 units and an increase in bicarbonate

Management:
• Urgent resuscitation of the patient requires
airway control, ventilator management, and
stabilization of the circulation.
• At the same time patient should be evaluated for
the cause of respiratory failure and therapeutic
plan should be derived from an informed clinical
and laboratory examination.

Type 1 respiratory failure:
• This condition usually presents little difficulty and apart from the use of
oxygen, treatment of the primary causes (e.g. antibiotics for lobar pneumonia),
may be all that it required.
• The goal should be to increase hemoglobin o2 saturation to at least 85- 9o%
without risking significant oxygen toxicity.
• Prolonged exposure to high concentration of oxygen (Fio2>5o%) should be
avoided because pulmonary toxicity depends on both the duration of treatment
and Fio2.
• The use of positive end-expiratory pressure (PEEP), changes in position,
sedation and paralysis may be helpful in lowering Fio2.
• Fever, agitation, overfeeding, vigorous respiratory activity and sepsis
can all markedly increase Vo2. Measures to eliminate these factors
should be undertaken.
• Failure of high Fio2, to improve Pao2 implies a significant
intrapulmonary shunt, as occurs in ARDS.
• ARDS is the most severe form of acute lung injury and is characterized
by bilateral, widespread radiographic pulmonary infiltrate, normal
pulmonary capillary wedge pressure (≤18 mm Hg) and a Pao2/FIo2
ratio ≤ 2oo regardless of level of positive end-expiratory pressure
(PEEP).
• Acute lung injury (ALI) is a mild form of ARDS, and differs from ARDS

Type 2 respiratory failure
• The general principles of management are : (i) to correct
life threatening hypoxaemia; (ii) to correct life
threatening acidosis; (iii) to treat the underlying cause;
and (iv) to prevent complications.
 The first priority in treatment of acute-on-chronic
respiratory failure that occurs during exacerbations of
CoPD is the relief of hypoxia by the cautious
administration of oxygen. Supplemental oxygen should be
administered by nasal prongs with flow of 1-3L/min or by
a Venturi mask with flow set to deliver 24-28% oxygen.
 The goal of supplemental oxygen therapy should be to
achieve a Pao2 of greater than 6ommHg.

oxygen Delivery Devices
Two classes:
1. Low-flow devices, for example, nasal cannulas
and face masks
2. High-flow devices, for example, Venturi masks
and high-flow nasal cannulas.(provide a
constant Fio2 by delivering either a higher-flow
rate of oxygen than the patient’s peak
inspiratory flow rate, and/or by providing an
oxygen flow admixed with a fixed proportion
of room air.

Nasal Cannulas
• These low-flow systems provide insufficient gas to replace an entire
inspired tidal volume (Vt). As a result, a large part of each inhaled
breath is composed of ambient (room air) gas.
• Nasal cannulas are appropriate in patients with minimal or no
respiratory distress, or those who are unable to tolerate a facemask.
• The benefits include allowing the patient to eat, drink, and speak.
• Their main disadvantage is that the exact Fio2 is unknown. This is
because the oxygen flow rate, the patient’s inspiratory flow rate, and
the inhaled Vt all influence the final Fio2.
• As a general rule, for every liter per minute delivered, the oxygen
concentration increases by ∼3%. Therefore, with a normal Vt, the
commonly utilized nasal cannula flow rates of 1–6 L/min provide an
Fio2 of 24–4o%.
• Routine humidification of oxygen may provide little or no benefit in
reducing the drying effects of nasal cannula oxygen on the nose and
throat, especially with flow rates >5 L/min.
• At rates >6 L/min, flows become turbulent and the oxygen being
delivered is no more effective than that delivered at 6 L/min.

Reservoir Nasal Cannulas (oxymizers)
• The reservoirs facilitate conservation of oxygen
by storing oxygen from exhalation for delivery
during subsequent inhalation.
• The reservoirs trap the initial portion of expired
gas from the large conducting airways that
contain a high percentage of oxygen (i.e., dead-
space gas that did not participate in gas exchange
in the alveoli).
• The reservoirs also receive a continuous flow of
oxygen from the oxygen source

Simple Facemasks
• delivering a higher Fio2 than can be achieved via
nasal cannula.
• Two types of facemask exist: those with and
those without an oxygen reservoir.
• To avoid accumulation of expired air within the
mask, and subsequent retention of Co2, the
oxygen flow rates should be >5–6 L/min.
• Simple facemasks generally provide a Fio2 of 35–
6o%.

High-Flow Nasal Cannulas
• allow oxygen to be delivered at rates that exceed
a patient’s inspiratory flow rate.
• Using special tubing, along with warming and
humidification, allows for nasal delivery of oxygen
flows of >6o L/min.
• This allows for the elimination of room air during
inspiration so that a patient can breathe high
fractions of oxygen without dilution by ambient
air. Fractions of oxygen of up to 1oo% can be
effectively delivered.
• In addition, the high flows used result in positive
airway pressures of between 3 and 7 cm H2o that

Venturi Masks
• oxygen passes through a narrow orifice under
pressure into a larger tube, creating a sub
atmospheric pressure. This drop in pressure
results in a shearing force that draws room air into
the delivery system through a number of openings
(entrainment ports) in the tube.
• oxygen concentration is adjusted by changing both
the size of the entrainment ports and the oxygen
flow.
• The maximum Fio2 achievable is 5o%.
• This type of mask provides a constant Fio2
independent of changes in inspiratory flow rate.

other pathophysiologic types of
respiratory failure
• Type 3: postoperative or atelectatic respiratory
failure.
• Type 4: circulatory shock-associated respiratory
failure associated with hypoperfusion of
respiratory muscles.

There are four basic classes of hypoxia
• Hypoxemic hypoxia: low arterial oxygen content
with impaired oxygen delivery.
• Anemic hypoxia: low circulating hemoglobin
concentration with impaired oxygen delivery.
• Circulatory hypoxia: low cardiac output with
impaired oxygen delivery.
• Cytotoxic hypoxia: poisoning with cyanide where
oxygen is delivered to the tissues but cannot be
used.

Airway management

Assessment
• Assessment of airway patency and spontaneous
breathing effort is the crucial first step. The clinician
must look, listen, and feel for diminished or absent air
movement.
1. Assess the patient’s level of consciousness.
2. determine if apnea is present.
3. Identify injury to the airway or other conditions (eg, cervical
spine injury) that will affect assessment and manipulation of
the airway
4. observe chest expansion, abdominal movement.
5. observe for suprasternal, supraclavicular, or intercostal
retractions; laryngeal displacement toward the chest during
inspiration (a tracheal tug); or nasal flaring
6. fogging of the oxygen mask
7. Auscultate over the neck and chest for breath sounds.

Establish an airway manual support of
the airway
• Airway obstruction occur with tongue, FB,
secretions, laryngeospasm
• Signs of airway obstruction (no air exchange,
stridor,gurgle)
• Triple airway maneuver If
1. spontaneously breathing
2. no possible injury to the cervical spine
• Steps:
1. Slight neck extension
2. Elevation of the mandible (jaw thrust maneuver)
3. opening of the mouth
• If a cervical spine injury is suspected, neck extension is eliminated. After
the cervical spine is immobilized, manual elevation of the mandible and
opening of the mouth are performed.
• Adjunctive devices such as properly sized oropharyngeal or

The operator extends the neck and maintains extension with his/her hands on both
sides of the mandible. The mandible is elevated with the fingers of both hands to lift
the base of the tongue, and the thumbs or forefingers are used to open the mouth.

• Placement of a pillow or
folded blanket beneath
their head, together with
a chin-lift manoeuvre.
The pillow effectively
flexes the neck in relation
to the torso; the chin-lift
manoeuvre extends the
head in relation to the
neck. The so called
sniffing position is
achieved.
• Beware application of a
chin-lift manoeuvre
without raising the
occiput. This may lead to
hyperextension of the
The chin-lift manoeuvre

• In obese patients,
especially those with
short necks, the pillow
may compromise the
airway further by
causing flexion of the
head in relation to the
neck. As a result, their
chin is brought into
closer proximity to their
chest. This will also make
subsequent intubation
more difficult, if this is
planned.
• The solution is to place a
pillow under the patients
shoulders and a number
of pillows under their
The chin-lift manoeuvre obese
patients

• The oropharyngeal airway is intended to hold the base of the tongue forward toward
the teeth and away from the glottic opening. The plastic flange should rest against
the outer surface of the teeth while the distal end curves around the base of the
tongue.
• small oropharyngeal airway → may push the tongue back over the glottic opening;
• too large oropharyngeal airway→ may stimulate gagging and emesis.
• oropharyngeal airways should not be inserted if airway reflexes are intact, as gagging, laryngospasm,
and emesis will be provoked.
• The diameter of a nasopharyngeal airway should be the largest that will easily pass
through the nostril into the nasopharynx (A 6mm size for women and 7mm for
men is recommended).. Its length should extend to the nasopharynx
• if so long as to obstruct gas flow through the mouth or touch the epiglottis.
• A nasopharyngeal airway is contraindicated in patients with suspected basilar skull
fracture or coagulopathy.
1. The correct length for each airway may be estimated by placing the device against
the face in the correct anatomic position.
2. During manual support of the airway, supplemental oxygen should be supplied with
a device providing a high concentration of oxygen (1oo%) at a high flow rate. Such
devices include a face mask or a bag-mask resuscitation unit, possibly with a positive
end-expiratory pressure (PEEP) valve.

MANUAL MASK VENTILATIoN
• Indications:
1. if the patient is apneic.
2. if spontaneous tidal volumes are determined to be
inadequate based on physical examination or
arterial blood gas analysis.
3. to reduce the work of breathing by assisting
spontaneous inspiration.
4. if hypoxemia is associated with poor spontaneous
ventilation.
• Successful manual mask ventilation depends
upon:
(1) maintaining an open airway,
(2) establishing a seal between the patient’s face and the mask,
and Dr.DoHA RASHEEDY ALY

• The total gas volume within most adult resuscitation bags is 1 to 1.5
liters.
• If the patient is apneic but has a pulse, one-handed bag compressions
should be delivered 1o to 12 times per minute.
• If spontaneous breathing is present, bag compression should be
synchronized with the patient’s inspiratory efforts.
• If the patient is breathing easily and inhaling adequate tidal volumes
frequently enough to produce sufficient minute ventilation, the bag
need not be compressed at all.

Sellick maneuver "cricoid pressure“
• The Sellick maneuver describes pressure placed
on the patient's cricoid cartilage in an effort to
occlude the esophagus. Cricoid pressure should
be instituted in patients who have full stomachs
(e.g., from recent food ingestion, pregnancy, or
bowel obstruction) and who have a history of
gastroesophageal reflux.
• If the patient lacks protective airway reflexes,
cricoid pressure should be applied during mask
ventilation and during attempts at tracheal
intubation; it should be discontinued only after
tracheal intubation has been confirmed. Proper
application of cricoid pressure may improve

Airway adjuncts
• laryngeal mask airway
• esophageal-tracheal double-lumen airway device

tracheal intubation
• orotracheal(direct laryngeoscopy, flexible
fiberoptic intubation)
• Nasotracheal(blind)

KEY PoINTS: WARNING SIGNS oF A
PoSSIBLY DIFFICULT INTUBATIoN
• 1. Short mandible
• 2. Small mouth opening
• 3. Prominent incisors or overbite
• 4. Cervical spine immobility or instability
• 5. History of a difficult intubation

Indications for Tracheal Intubation
• Airway protection
• Relief of obstruction
• Provision of mechanical ventilation and oxygen
therapy
• Respiratory failure
• Shock
• Hyperventilation for intracranial hypertension
• Reduction of the work of breathing
• Facilitation of suctioning/pulmonary toilet

Surgical airway
• Needle cricothyrotomy
• Surgical cricothyrotomy/tracheostomy
• Percutaneous tracheostomy

• Intracranial pressure may rise during
laryngoscopy and intubation, and this may be
harmful in patients with preexisting intracranial
hypertension. Intravenous lidocaine (1-1.5
mg/kg) has been shown to blunt this response
and should be administered prior to
laryngoscopy when intracranial pathology is
suspected

Respiratory part 2

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Respiratory part 2