This document discusses factors to consider when removing a patient from mechanical ventilation (weaning). It outlines criteria to assess patient readiness, including respiratory function, oxygenation, hemodynamics, neurological status, secretions and comorbidities. Complications of failed weaning are also described. Key considerations involve addressing sedation, electrolyte imbalances, infection/inflammation and optimizing cardiac, nutritional and acid-base status.

1. By
Dr.Rajesh Sharma

2. Goal & Methods
 Removal from positive pressure
ventilation
 Extubation / decanulation

3. 1. Why the patient was intubated
2. For how long he remained on artificial
ventilation
3. How much sedation was given

4.  Nosocomial Pneumonia (VAP)
 Stretch injury and barotrauma
 Airway trauma
 Prolonged Sedation
 Obvious increase in associated cost
 Ventilator dependency

5.  Hypoxemia & hypercarbia
 Sympathetic discharge – cardiovascular
stress.
 Muscular fatigue and acidosis
 Loss of airway protection (aspiration).
 Reintubation into an edematous airway
(risk of hypoxic brain injury etc).

6.  Neurological : Central/ Peripheral
 Muscular
 Anatomical Problems

8.  Prolonged sedation, reduces
respiratory drive and prolongs
ventilation. Psychological dependence
on the ventilator follows prolonged
usage.
 A number of factors will reduce central
respiratory drive. As CO2 is the main
stimulus for ventilation, the pt’s PaCO2
must be returned to a normal level.
Metabolic or respiratory alkalosis
reduces hydrogen ion concentration in
the brainstem, and thus the stimulus to
breath.
 For weaning the patient must be awake
and co-operative and able to protect
his airway.

10.  It is essential to rule out the possibility
of a persistent neurological injury such
a phrenic nerve palsy, due to surgery.
 Some drugs such as aminoglycosides
can mimic NMBs.
 Prolonged critical illness may lead to
the development of a critical illness
polyneuropathy, due to axonal
degeneration.

11.  Muscular atrophy due to
malnutrition, prolonged muscle
relaxants or critical illness myopathy
may limit weaning.

13.  Chest Wall – flail chest: is the pain under
control?
 Does the patient have a compliant chest
wall?
 If the patient has to work hard just to lift
the chest wall - for example extensive
edema, large fat pads, tight
dressings, increased abdominal pressure -
due to bowel swelling, packs, blood
etc, then weaning will be very difficult.
 Pleural effusions – are they present, can
they be drained? Does the patient have a
chest drain in – is there much coming in.

14.  Airways – airway obstruction – mucus
plug, excessive secretions or
bronchospasm? Is there laryngeal edema
 Abdomen: does the patient have a
compliant abdominal surface. The
presence of ascites, distended
bowel, abdominal hypertension, packs or
tight surgical dressings may interfere with
ventilation.

15.  Avoid being drawn into the “minute volume
looks”
the ability to ventilate is related to
alveolar ventilation, not minute ventilation.

16. “Why A patient's PaCO2 so high when
he has a minute ventilation of 20 liters
per minute?"

17.  Clearance of carbon dioxide is determined
by the alveolar ventilation and the
physiologic dead space.
 This is a common trap to fall into:
confusing alveolar ventilation (difficult to
measure) with minute ventilation (always
measured). The difference between the
two is determined by the anatomical dead
space.
BEWARE OF TACHYPNEA WITH SMALL
TIDAL VOLUMES

18.  Patient A
taking 20 breaths of 500ml tidal
volume.
 Patient B
taking 50 breaths of 200ml tidal
volume.

19. Pt. A has a normal blood gas.
Pt. B has a significant respiratory
acidosis.
Vd/Vt ratio
Patient A Vd/Vt < 30%
Patient B Vd/Vt 75%.
????
In the case of patient B, 75% of his
respiratory effort is being
wasted, leading to severe muscular
fatigue and acidosis.

20.  Alveolar dead space:
A patient can be receiving tidal
volumes of 500ml and still have a dead
space / tidal volume ratio of 75%.
How???
Alveolar dead space is caused by
increased volume of zone 1 (zone 1 is
where alveolar pressure exceeds the
perfusion pressure to the lung unit:
alveoli are ventilated but not perfused):

21. Zone 1:
PA > Pa > Pv
Zone 2:
Pa > PA > Pv
Zone 3:
Pa > Pv > PA

23.  Hypoperfusion - low pulmonary
blood volume-pressure leads to
underperfusion of non dependent
lung segments.
 Overdistension of lung by
excessive PEEP
Vd/Vt = PaCO2 - PetCO2/PaCO2

24. V
Q
V/Q=1

25. VD V VA
Qc Q QS

26. PAO2
V/Q=
VD VA
Qc QS
V/Q=0
PaO2

27.  The patient is able to ventilate
 The patient is able to oxygenate
 The patient is able to protect his
airway

28.  Alveolar Ventilation keeps
PaCO2 < 50 mmHg
 Production of CO2 can be controlled by
 reducing the carbon load in the diet (high
fat),
 minimize agitation,
 pain,
 fever,
 shivering
 muscle workload.

29.  diffusion abnormalities,
 ventilation-perfusion mismatch,
 dead space and shunt
 persistent lower respiratory tract
infection,
 alveolar edema,
 airway/lobar collapse,
 lung fibrosis

31.  The commonest cause of airway collapse
is absorption atelectasis, distal to mucus
plugs
 Good quality of chest physiotherapy is
required to mobilize secretions
If the patient is requiring moderate to high
levels of PEEP to oxygenate , then
weaning is unlikely.

32.  A source of ventilation-perfusion
mismatch: this leads to hypoxemia and
hypercarbia.
 Tremendously difficult to reinflate:
leading to a huge increase in the work
of breathing & oxygen consumption.

36.  How much to give ?
Insufficient PEEP is of little benefit.
Excessive PEEP problems:-
barotrauma
wasted ventilation
Increased intrathoracic pressure
Ideal level of PEEP is that which prevents
derecruitment of the majority of
alveoli, while causing minimal over
distension

37.  Auto-PEEP is gas trapped in alveoli at
end expiration, due to inadequate time
for expiration, bronchoconstriction or
mucus plugging.
It increases the work of breathing.

38. Rapid Shallow Breathing Index
f/VT
RSBI OF < 105

39. Controlled Ventilation
Partial ventilator
support
 The objective of PVS is to allow the
patient to interact with the ventilator as
the neuro-mechanical cause of respiratory
failure resolves. The disease process and
ICU interventions (sedation), do not allow
for immediate movement from full support
to extubation.

40. Although partial support modes are
widely used, there is no evidence that
they are superior to multiple daily T-
piece trials. The most effective method
of PVS is targeted pressure support.
SIMV + PS
Pressure Assist control
PSV

41.  Ensure that patient is suitable for
weaning
 Communicate to the patient
 Conduct the trials early in the
morning, when the patient is fully
rested and there is a full supporting
staff available.
 During these trials the patient should
be awake and co-operative, afebrile and
on minimal pressor support

42.  Place the patient in the upright or semi-
upright position and explain what you
are attempting to do.
 Suction out the tube, airway and
oropharynx.

43. For How long
have to monitor the weaning process
with SBT

44. Criteria Description
Objective o Adequate oxygenation (eg, PaO2 >60 mm Hg on FIO2 > 0.4; PEEP <5cm
measurements H2O; PaO2/FIO2 >150–300);
o Stable cardiovascular system (HR <140; stable BP; (no or minimal
vasopressors)
o Afebrile (temperature < 38 C)
o No significant respiratory acidosis
o Adequate hemoglobin
o Adequate mental status (arousable, no continuous sedative Infusions)
o Stable metabolic status (acceptable electrolytes)
Subjective
clinical o Resolution of disease acute phase; physician believes discontinuation
assessment possible; adequate cough reflex

47. Two parts to weaning:
 weaning to partial ventilator support
 weaning to discontinuation.
There is little evidence that partial
modes are more effective than T-piece
trails.
Of these modes, pressure support is
the best.

48.  If it is possible to wean a patient to
extubation, but the patient cannot
protect his airway.
It is best to perform tracheotomy.

49. It may be difficult to wean a patient if
ongoing inflammatory processes
persist in the lungs:
 consolidation
 fibrosis
 auto-PEEP
 diffusion defects

50.  A 77 year old male F/c Lapratomy.
Complicated by perioperative
MI, systemic sepsis required insertion of a
pulmonary artery catheter, volume loading
and vasopressors, and moderate renal
dysfunction, with s.creatinine 3.3.
 He is now at 14 days postop on ventilator
 Currently he is difficult to arouse, on a
sedation of fentanyl 50μg/hr & medazolam
 His temperature is 37.8.
 Pulse is 76 and regular, B.P. is 130/70 and
CVP is 12.

51.  lungs are clear on auscultation, CXR reveals
some patchy infiltrates, atelectasis and a left
sided pleural effusion. On SIMV rate
8, pressure support 16 and PEEP 5
cmH2O, FIO2 35% . ABG :- pH 7.52, PaO2
72, PaCO2 44, BE +8, SaO2 94%.
 Abdomen is tense, with a wound closed with
tension sutures and two drains, currently
draining very little.
 LFT: normal except for an albumin of 1.6 . He
has edema of lower limb, sacral and scrotal
area.
 His fluid balance is even over the past five
days.
 Hb 8.1, WBC 18.5, Plat 1.2 Lac, Na 148, K
3.1, Urea37,Creat 1.2, MgSO4 3.2, PO4 1.5, Ca
2.0.
 The patient is completing a 14 day course of
ampi., genta. & metronidazole.

52.  CNS – he remains sedated with
medazolam and fentanyl. These will both
reduce level of consciousness and impair
central respiratory drive. These agents
must be aggressively weaned.
 PNS – although he has only been
ventilated for two weeks, he is doing little
work himself, and may have some
muscular atrophy. In addition, the
combination of a low serum
potassium, magnesium and phosphate
need to be supplemented for muscular
function.

53.  CVS – the patchy infiltrates on CXR and
the history of MI are worrisome, this
indicates that this patient will not easily
tolerate the autotransfusion associated
with moving from positive to negative
pressure ventilation. It is essential to do
an echocardiogram, assess cardiac
performance and consider the use of an
agent that remodels the ventricle and
reduced preload and afterload – an ACE
inhibitor. We must be cautious in this
circumstance with the history of renal
failure. Alternative therapies would be the
introduction of either nitrates or
dobutamine in the hours peri-extubation.

54.  Renal – renal function is reasonably good now,
metabolic alkalosis indicate sodium
bicarbonate use – seen in the high serum
sodium. This alkalosis can be corrected with
judicious use of sodium chloride (the chloride
will correct the alkalosis by returning to
electro-neutrality) or increasing enteral free
water delivery.
 Gastrointestinal/Abdomen – a tense tight
abdomen will interfere with diaphragmatic
excursion, and thus respiratory mechanics.
We have little control over this. It is worth
asking, nonetheless, with a tense abdomen
and nothing draining, if the drains are
blocked. Does the patient have ascites? If so,
it may be worth draining this to reduce intra-
abdominal pressure.

55.  Extremities – peripheral edema and a low
serum albumin, as the patient probably also
has soggy lungs, from sepsis induced
capillary leak (low oncotic pressure and fluid
extravascation). There is little that can be
done about this edema, the fact that it is
resistant to diuretics is interesting. Has the
patient been given adequate prophylaxis
against deep venous thrombosis and
pulmonary embolism?
 Pulmonary function – the x-ray findings
indicate patchy consolidation (difficult to
oxygenate) and a pleural effusion (difficult to
ventilate). The effusion can be drained if
necessary. Think for a possible nosocomial
pneumonia – because of persistent
leucocytosis, lung infiltrates and a low grade
temperature.

56.  The patient has not been covered for
pseudomonas or MRSA pneumonia, and it
is essential to rule out this possibility by
performing a broncho-alveolar lavage at
this time. How long have the pt’s lines
been in – is that the source?
 This patient will probably tolerate a
pressure support mode of ventilation fairly
well, although his electrolytes and acid
base status require correction. If there is
no movement towards minimal ventilator
settings within 48 hours, a prolonged
wean is probably likely (due to low
physiological reserve) and the patient will
require a tracheostomy.

58.  Cardiovascular – pulmonary edema due to left
ventricular failure or volume overload decreases
lung compliance and will make weaning more
difficult. When mechanical ventilation is
discontinued, significant physiological changes
occur which will influence cardiovascular
performance: change from positive pressure to
negative pressure ventilation, reduced mean
intrathoracic pressure, increased preload and
afterload. This may lead to critical loading of
myocardial fibers and provoke ischemia – failure
and edema.
 Gastroinestinal – recurrent aspiration
pneumonitis, ascites or abdominal wounds leading
to diaphgramatic splinting. Abdominal distension
or hypertension, for any reason (massive fluid
resuscitation, surgical packs etc), will reduce
chest wall compliance and lead to failure to
ventilate.

59.  Nutrition -protein malnutrition leading to
muscular atrophy, which affects the
diaphragm and intercostals.
 Acid base – metabolic alkalosis, particularly
due to use of diuretics reduces respiratory
drive. Conversely, muscles perform poorly in
an acidic environment. Metabolic acidosis is
caused by excessive amounts of measured
anions (chloride) or unmeasured anions
(lactate - from hypoperfusion), ketones and
renal acids.
 Electrolytes–
hypophosphatemia, hypomagnesemia, hypokal
emia, hypocalcemia: these all affect muscular
function and protein metabolism.

60.  Endocrine – muscle weakness due to
hypothyroidism or steroid induced
myopathy.
 Oxygen delivery capacity – the
circulating hemoglobin concentration:
anemia increases respiratory drive and
cardiac output in order to maintain
oxygen delivery.
 Pain control – it is very difficult to wean
patients who are in pain, particularly
from upper abdominal or thoracic
surgery or injuries. If a patient has a
flail chest, it may be necessary to
insert a thoracic epidural prior to
extubation

61. Indicators of deterioration are:
1. respiratory rate >35/mt.
2. falling tidal volume <5ml/kg
3. PaO2 <55mm Hg; Rising PaCO2
4. fall in blood pressure
5. tachycardia, cardiac arrythmias,
sweating -increased sympathetic
activity
6. altered mental status - restlessness,
anxiety, confusion

62.  The Cuff leak test:
The ventilator is used in Assist Control mode
with a tidal volume of 10-12ml/kg. The expired
tidal volume is measured with the cuff inflated.
The cuff is then deflated and after elimination of
artefacts due to cough, four to six consecutive
breaths are used to compute the average value
for the expiratory tidal volume. The difference in
the tidal volumes with the cuff inflated and
deflated is the leak. A value of 130ml (12% of
inspiratory tidal volume) gave a sensitivity of
85% and a specificity of 95% to identify patients
with an increased risk of post extubation stridor.

63. Cough / Leak test: In spontaneously
breathing patients
The tracheal cuff is deflated and monitored
for the first 30 seconds for cough. Only
cough associated with respiratory
gurgling (heard without a stethoscope and
related to secretions) is taken into
account.
The tube is then obstructed with a finger
while the patient continues to breath. The
ability to breathe around the tube is
assessed by the auscultation of a
respiratory flow.