Transcript Slide 1

ALOK SINHA
Department of Medicine
Manipal College of Medical Sciences
Pokhara, Nepal
Inability of the lungs to perform the function
of gas exchange- the transfer of oxygen
from inhaled air into the blood and the
transfer of carbon dioxide from the blood
into exhaled air
•
•
Defined as a
PaO2 value of less than 60 mm Hg while
breathing air
or a PaCO2 of more than 50 mm Hg
Classification
 Type 1
hypoxemic respiratory failure
Acute

Type 2
hypercapnic respiratory failure
Chronic
Respiratory failure is caused by:
1. failure to oxygenate
 characterized
by decreased PaO2
2. failure to ventilate
 characterized
by increased PCO2
1. Failure to oxygenate:
1. due to
1. decreased inspired O2 tension
2. increased CO2 tension
2. ventilation perfusion mismatch



Pneumonia
Oedema
PE
3. reduced O2 diffusion capacity
1. due to interstitial edema
2. fibrosis
3. thickened alveolar wall
Deoxygenated blood from
pulmonary artery
V – Q Mismatch

V/Q incresed =
physiological dead
space
• Pulmonary
embolism
• Obliteration of
blood vessels
 emphysema

V/Q reduced = physiological
shunt
• Collapse of alveoli –
atelectasis
 Loss
of surfactant
 Airway obst. - COPD
•
•
Fluid filling
Anatomical shunt
increased – anastomosis
between pulmonary & systemic
vessels
2. Failure to ventilate
Respiratory centers
Causes:
•Airway
•Chest wall
•Respiratory muscles
Hypoxemic (type I)
Hypercapnic (type II)
PaO2 <60 mm Hg
 PaCO2 of >50 mm Hg
 CO2 level may be normal
pH depends on the level of
or low
bicarbonate, dependent on the
 associated with virtually all duration of hypercapnia
acute diseases of lung with caused byV/Q mismatch
Alveolar hypoventilation
Common causes
 C.O.P.D.
C.O.P.D.
 Pneumonia
 Pulmonary edema
 Pulmonary fibrosis
 Asthma

severe obstruction with a FEV1 of
less than 1 L or 35% of normal

Neuromuscular disorders
 Guillain-Barré
syndrome
 Diaphragm paralysis



Amyotrophic lateral sclerosis
Muscular dystrophy
Myasthenia gravis
Pulmonary embolism
 Pulmonary arterial
hypertension
 Pneumoconiosis
 Granulomatous lung
diseases
 Cyanotic congenital
heart disease
 Bronchiectasis
 Adult respiratory
distress syndrome
 Fat embolism
syndrome



Chest wall deformities
 Kyphoscoliosis
 Ankylosing spondylitis
Central respiratory drive
depression
 Drugs
- Narcotics,
benzodiazepines,
barbiturates
 Neurologic
disorders -
Encephalitis, brainstem
disease, trauma
 Primary
alveolar
hypoventilation

Obesity hypoventilation
syndrome (Pickwickian Syn)
Carol Yager (1960 – 1994)
730 KG
BMI 252
Acute and chronic respiratory failure
Acute respiratory failure Chronic respiratory failure
develops over minutes to
Hours
• No time for renal compen.
• pH is less than 7.3.
• clinical markers of chronic
Hypoxemia polycythemia
 cor pulmonale
•
Are absent
• develops over several days
allowing time for renal
compensation
• an increase in bicarbonat conc.
• pH -only slightly decreased.
• clinical markers of chronic
hypoxemia
 polycythemia
 cor pulmonale
Are present
Alveolar-to-arterial PaO2 difference (A-a Gradient
Determines the efficiency of lungs at carrying
out of respiration

Aa Gradient = (150 - 5/4(PCO2)) - PaO2
Normal < 10mm
• increase in alveolar-to-arterial PO2 above 1520 mm Hg indicates pulmonary disease as the
cause of hypoxemia
• Normal in Hypoventilation
Underlying disease process
(pneumonia, pulmonary edema, asthma, COPD)
associated hypoxemia
hypercapnia
Hypoxemia
Symptoms
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shortness of breath
confusion & restlessness
Seizures
coma
Signs
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Cyanosis
variety of arrhythmias from hypoxemia &
acidosis
Polycythemia – in long-standing hypoxemia
Hypercapnia
Vasodilation leading to
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
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Morning headache
flushed skin & warm moist palms
full & bounding pulse
Extrasystoles & other arrythmias
muscle twitches
flapping tremors - asterixis
drowsiness
Asterix
Now answer this questionIf you are forced to choose one of these, which one you
will like to have ?
Hypoxia
Hypercapnia
A.B.G. (arterial blood gases)
complete blood count
.
•
anemia
 contribute
•
to tissue hypoxia
polycythemia
 indicate
chronic hypoxemic respiratory failure
Associated organ involvement
 R.F.T.

L.F.T.
Chest radiograph
frequently reveals the cause of respiratory failure
distinguishes between


cardiogenic
noncardiogenic pulmonary edema
Echocardiography
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when cardiac cause of acute respiratory failure is
suspected
left ventricular dilatation
regional or global wall motion abnormalities
severe mitral regurgitation
provides an estimate of right ventricular function
and pulmonary artery pressure in patients with
chronic hypercapnic respiratory failure
Other Tests
PFT
 in the evaluation of chronic respiratory failure
ECG
 to evaluate the possibility of a cardiovascular
cause of respiratory failure
 dysrhythmias resulting from severe
hypoxemia and/or acidosis
Hypoxemia
major immediate threat to organ function
oxygen supplementation and/or ventilatory
assist devices

The goal is to assure adequate oxygen
delivery to tissues, generally achieved with a
PaO2 of 60 mm Hg or more
SaO2 of greater than 92%
Supplemental oxygen administered via
nasal prongs
face mask
in severe hypoxemia, intubation and
mechanical ventilation often are required
Airway management


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Adequate airway vital in a patient with acute
respiratory distress
The most common indication for
endotracheal intubation (ETT) is respiratory
failure
What is the role of tracheostomy??
Hypercapnia without hypoxemia
generally well tolerated
not a threat to organ function
hypercapnia should be tolerated until the
arterial blood pH falls below 7.2
hypercapnia and respiratory acidosis managed
by
correcting the underlying cause
providing ventilatory assistance
Treatment of coexisting condition with
approptiate drugs
 Mechanical
ventilation is a method to
 mechanically
assist
or
 replace
spontaneous breathing
Mechanical Ventilatior What is it?

Machine that generates a controlled flow of gas into a
patient’s airways

Oxygen and air are received from cylinders or wall
outlets blended according to the prescribed inspired
oxygen tension (FiO2)

Delivered to the patient using one of many available
modes of ventilation.The magnitude of rate and
duration of flow are determined by the operator
INDICATIONS FOR TRACHEAL INTUBATION AND
MECHANICAL VENTILATION
•Protection of airway
•Removal of secretions
•Hypoxaemia
•PaO2 < 60 mmHg
Body_ID: B008019
•SpO2 < 90% despite CPAP with FIO2 > 0.6
•Hypercapnia if conscious level impaired or risk of raised
intracranial pressure
•Increased Alveolar-arterial gradient of oxygen tension
(A-a DO2) with 100% oxygenation
•Vital capacity falling below 1.2 litres in patients with
neuromuscular disease
•Removing the work of breathing in exhausted patients

Ventilatory workload is increased by loss
of lung compliance

inspiration/ventilation is usually supported to
reduce O2 requirements and increase patient
comfort
Respiratory failure is caused by
1. Failure to ventilate
 characterized
by increased PCO2
2. Failure to oxygenate
 characterized
by decreased PaO2
Failure to ventilate
 Increase
the patient’s alveolar ventilation
rate
depth
of breathing
by using mechanical ventilation
Failure to oxygenate

Restoration and maintenance of lung volumes
by using recruitment maneuvers
 Recruitment
maneuvers are used to reinflate
collapsed alveoli: due to pressure generated by
ventilator during inspiration alveoli are inflated
 PEEP
is used to prevent derecruitment
What do we mean by PEEP ?
Girl’s changing
room
PEEP

amount of pressure above atmospheric
pressure present in the airway at the end of the
expiratory cycle

PEEP improves gas exchange by
preventing alveolar collapse
 recruiting more lung units
 increasing functional residual capacity
 redistributing fluid in the alveoli

Dangers of PEEP
1. Overdistension of lungs – Barotrauma
2. Will increase intracranial tension
3. Reduce venous return to right side of heart leading
to


reduced cardiac out put & hypotension
The ideal level of PEEP is that which prevents
derecruitment of the majority of alveoli, while
causing minimal overdistension
Modes of ventilation:
 Air flow continues until
a
predetermined volume has been delivered
– volume controlled
 airway
pressure generated
– pressure controlled

Flow reverses, when the machine cycles into
the expiratory phase, the message to do this is
either at a preset time
 preset tidal volume
 preset percentage of peak flow

 Mechanical
breaths may be
 Controlled (Controlled mandatory ventilation -CMV)
 ventilator
is active
 patient passive
 assisted (Synchronised intermittent mandatory ventilation - SIMV)
 patient
initiates and may or may not participate in
the breath
Controlled mandatory ventilation (CMV)
Most basic classic form of ventilation
Pre-set rate and tidal volume
Does not allow spontaneous breaths

Appropriate for initial control of patients with
little respiratory drive
severe lung injury
circulatory instability
Synchronized Intermittent Mandatory
Ventilation (SIMV)

method of partial ventilatory support to facilitate
liberation from mechanical ventilation

patient could breathe spontaneously while also
receiving mandatory breaths

As the patient’s respiratory function improved,
the number of assisted is decreased, until the
patient breaths unassisted
Iron Lung
CONDITIONS REQUIRING MECHANICAL
VENTILATION
Post-operative
• After major abdominal or cardiac surgery
Respiratory failure
ARDS
Pneumonia
COPD
Acute severe asthma
Aspiration
Smoke inhalation, burns
Circulatory failure
Following cardiac arrest
Pulmonary oedema
•Low cardiac output-cardiogenic shock
Neurological disease
Coma of any cause
Status epilepticus
Drug overdose
Respiratory muscle failure (e.g. Guillain-Barré, poliomyelitis, myasthenia gravis)
Head injury-to avoid hypoxaemia and hypercapnia, and to reduce intracranial pressure
Bulbar abnormalities causing risk of aspiration (CVA, myasthenia gravis)
Multiple trauma
TERMS USED IN MECHANICAL VENTILATORY SUPPORT
Controlled mandatory ventilation (CMV)
Most basic classic form of ventilation
Pre-set rate and tidal volume
Does not allow spontaneous breaths
Appropriate for initial control of patients with little respiratory drive, severe lung injury or circulatory
instability
Synchronised intermittent mandatory ventilation (SIMV)
Pre-set rate of mandatory breaths with pre-set tidal volume
Allows spontaneous breaths between mandatory breaths
Spontaneous breaths may be pressure-supported (PS)
Allows patient to settle on ventilator with less sedation
Pressure controlled ventilation (PCV)
Pre-set rate; pre-set inspiratory pressure
Tidal volume depends on pre-set pressure, lung compliance and airways resistance
Used in management of severe acute respiratory failure to avoid high airway pressure, often with
prolonged inspiratory to expiratory ratio (pressure controlled inverse ratio ventilation, PCIRV)
Pressure support ventilation (PSV)
Breaths are triggered by patient
Provides positive pressure to augment patient's breaths
Useful for weaning
Usually combined with CPAP; may be combined with SIMV
Pressure support is titrated against tidal volume and respiratory rate
Continuous positive airways pressure (CPAP)
Positive airway pressure applied throughout the respiratory cycle, via either an
endotracheal tube or a tight-fitting facemask
 Improves oxygenation by recruitment of atelectatic or oedematous lung
 Mask CPAP discourages coughing and clearance of lung secretions; may increase
the risk of aspiration
Bi-level positive airway pressure (BiPAP/BIPAP)
Describes situation of two levels of positive airway pressure (higher level in inspiration)
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
In fully ventilated patients, BiPAP is essentially the same as PCV with PEEP
In partially ventilated patients, and especially if used non-invasively, BiPAP is essentially PSV with CPAP
Non-invasive intermittent positive pressure ventilation (NIPPV)
Most modes of ventilation may be applied via a facemask or nasal mask
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
Usually PSV/BiPAP (typically 15-20 cmH2O) often with back-up mandatory rate
Indications include acute exacerbations of COPD
Of mechanical ventilation
The science of mechanical
ventilation is to optimize
pulmonary gas exchange
The art is to achieve this
without damaging the lungs
.

There is no ideal mode of ventilation for any
particular patient
Major immediate complication
1. Hypotension
 due
to vasodilatory effects of hypnotic drugs
 Treated
with vasoconstrictors
 have
an ampule of phenylephrine (a selective alpha
adrenoceptor agonist) at hand to reverse vasodilatory
hypotension
 Increase
 Treated
in intrathoracic pressure
with fluid boluses
 Always
have an intravenous fluid drip running and be
prepared to run in a liter or more of fluid quickly
Late complications
2. Barotrauma
Pneumothorax
 subcut emphysema

3. VALI (Ventilator Associated Lung Injury)
4. O2 toxicity
5. From prolonged immobility and inability to
eat normally
venous thromboembolic disease
 skin breakdown
 atelectasis

6. From endotracheal intubation
ventilator-associated pneumonia (VAP)
 tracheal stenosis
 vocal cord injury
 tracheal-esophageal or tracheal-vascular
fistula

Measures to reduce complications
Elevating the head of the bed to > 30°
decreases risk of ventilator-associated
pneumonia
 routine turning of patient every 2 h decreases
the risk of skin breakdown
 Keep the PEEP & TV in optimal range
 All patients receiving mechanical ventilation
should receive deep venous thrombosis
prophylaxis

Some special techniques
1. Inhaled nitric oxide

very short-acting pulmonary vasodilator
 Delivered
to the airway in concentrations of between 1
and 20 parts per million

Improves blood flow to ventilated alveoli, thus
improving V/Q mismatch, Oxygenation can be
improved markedly
 benefit
only lasts for 48 hours and outcome is not
improved
2. techniques to reduce the high inflation
pressures resulting from the stiff lungs (low
compliance)
1. Low tidal volumes to reduce inflation
pressures

(6 ml/kg ideal body weight compared to
12 ml/kg) reduces mortality
Minute ventilation reduced
PaCO2 rises – permissive hypercapnia
3. Inverse ratio ventilation :
• may improve oxygenation
• PCO2 may rise further
4. Prone positioning:
• improves oxygenation in ~70% of patients
with ARDS