Weaning overview

1. Overview on Weaning from
Mechanical Ventilation
Prof. Mohamed Mostafa Metwally,
MD, FCCP
Assiut University, Egypt

2. Contents
1- Preliminary concerns during MV
2- Readiness criteria for weaning
3- The spontaneous breathing trial (SBT)
4- Highlights on some weaning problems
5- Extubation.

3. Introduction
Discontinuing mechanical ventilation
(weaning) is a rapid and uneventful affair
for most patients,
In one of every four or five patients, the
transition from MV to unassisted breathing
is a prolonged process that can consume
almost half of the time spent on a
ventilator

4. PRELIMINARY CONCERNS
I- Ventilatory Support Strategies:
These measures can contribute to shorter stays on
the ventilator by facilitating the attempts to
discontinue MV when the time arises.
1- Patient-Triggered Ventilation
Ventilator-induced diaphragm dysfunction is
prominent when contractions of the diaphragm are
suppressed (e.g., during controlled MV), and is
attenuated when the diaphragm is allowed to
contract and initiate a ventilator breath (i.e., during
patient-triggered ventilation).

5. CMV (but not AMV) was associated with a significant
reduction in the power output of the diaphragm.

6. 2- Physical Rehabilitation
Prolonged bed rest and physical inactivity during
MV often leads to generalized muscle
weakness. Therefore, early regular physical
rehabilitation and ambulation in patients who are
awake and hemodynamically stable is
encouraged in selected patients to facilitate the
transition to spontaneous breathing.

7. ATS/ACCP guidelines 2017

8. 3- Sedation Practices
Deep sedation and sustained use of
benzodiazepines are associated with delays in
weaning from mechanical ventilation.
Recent studies include the following
recommendations:
1. Maintain a light level of sedation, where
patients are easily aroused.
2. Avoid or minimize the use of benzodiazepines
for sedation. Non-benzodiazepine sedatives
include propofol and dexmedetomidine.

9. ATS/ACCP guidelines 2017

10. Readiness Criteria

12. THE SPONTANEOUS BREATHING
TRIAL
The traditional approach to discontinuing
mechanical ventilation by gradual reduction in
ventilatory support (over hours to days)
creates unnecessary delays in weaning.
This delayed approach is still evident in the
practice of placing patients back on a
ventilator at night to “rest them”.
In contrast, spontaneous breathing trials
(SBTs) are conducted either with or with
without ventilatory support, so that patients
capable of breathing can be identified quickly.

13. ATS/ACCP guidelines 2017

14. I- Using the Ventilator Circuit
advantage of this method is the ability to
monitor the tidal volume (VT) and
respiratory rate (RR), since rapid, shallow
breathing is a common breathing pattern
in patients who fail the SBT.
The drawback of this method is the
resistance of the ventilator circuit, which
can increase the work of breathing.

15. Pressure Support
To counteract the resistance of the ventilator
circuit, low levels of pressure support (8 cm
H2O) are routinely used.
The use of PS results in a small decrease in
the WOB.

16. II-Disconnecting the Ventilator
T-piece circuit:
The WOB is considered to be lower when
breathing through a T-piece circuit
compared to a ventilator circuit.
The major disadvantage of the T-piece
circuit is the inability to monitor the
respiratory rate and tidal volume.

17. T-piece circuit

18. Which Method Is Preferred?
The ATS/ACCP recommends inspiratory
pressure augmentation (5-8 CmH2O) than
T-Piece in initial SBT. However, the T-
piece method has the following theoretical
advantages:
(a) it is better suited for patients with
increased ventilatory demands
(b) it is a closer approximation of the
normal conditions.

19. ATS/ACCP guidelines 2017

20. Success vs. Failure
1. Signs of respiratory distress; e.g.,
agitation, diaphoresis, rapid breathing, and
use of accessory muscles of respiration.
2. Signs of respiratory muscle weakness;
e.g., paradoxical inward movement of the
abdominal wall during inspiration.
3. Adequacy of gas exchange in the lungs;
e.g., arterial O2 saturation, PaO2/FIO2 ratio
and arterial PCO2.

21. A majority of patients (∼80%) who tolerate
SBTs for 2 hours can be permanently
removed from the ventilator.
For patients with prolonged periods of
ventilator dependence (e.g., 3 or more
weeks), longer trials of spontaneous
breathing may be necessary before
claiming success.

23. Highlights on
1- Rapid Breathing
Rapid breathing during SBTs may be the result of
dyspnea provoked by anxiety rather than ventilatory
failure. Monitoring the tidal volume can be useful in
distinguishing anxiety from ventilatory failure.
Adverse Effects
1. In patients with asthma and COPD, rapid
breathing promotes hyperinflation and intrinsic PEEP,
which can:
(a) decrease the cardiac output,
(b) increase dead space ventilation,
(c) decrease lung compliance, and
(d) produce diaphragm dysfunction by flattening the
diaphragm.

24. 2. For patients with ARDS, rapid breathing
reduces ventilation in diseased lung regions
(where time constants for alveolar ventilation
are prolonged), and this promotes alveolar
collapse and hypoxemia.
3. For all patients with acute respiratory
failure, rapid breathing can increase whole-
body O2 consumption, which places an
added burden on systemic O2 transport.

25. Management
If ventilatory failure is suspected as the cause
of rapid breathing, the patient should be placed
back on the ventilator.
If anxiety is suspected as the culprit,
administration of a sedative drug should be
considered.
A failed trial is usually a sign that the
pathologic condition requiring ventilatory
support needs further improvement.

26. A highlight on
2- Cardiac Dysfunction
Cardiac dysfunction can develop during a trial
of spontaneous breathing in 40% of failed
weaning trials.
Potential sources of cardiac dysfunction
include: (a) negative intrathoracic pressures,
which increase left ventricular afterload
(b) hyperinflation and intrinsic PEEP, which
impair venous return and restrict ventricular
distensibility, and
(c) silent myocardial ischemia.

27. The adverse effects of cardiac dysfunction
include
1- Pulmonary congestion,
2- Decrease in the contractile strength of
the diaphragm. This latter effect is
explained by the fact that the diaphragm
(like the heart) maximally extracts O2
under normal conditions, and thus is highly
dependent on the cardiac output for its O2
supply.

28. Monitoring
1- CARDIAC ULTRASOUND is the most
useful tool for detecting changes in
systolic and diastolic function during failed
trials of unassisted breathing.
2- B-TYPE NATRIURETIC PEPTIDE:
plasma levels of B type natriuretic peptides
are significantly increased when cardiac
dysfunction develops during a trial of
spontaneous breathing.

29. Management
Patients who develop systolic dysfunction
should benefit from continuous positive
airway pressure (CPAP), which promotes
cardiac output by cancelling the afterload-
increasing effect of negative intrathoracic
pressure.

30. A highlight on
Respiratory Muscle Weakness
Respiratory muscle weakness is on the top
of the list for causes of difficulty in weaning.
Potential Sources of weakness
1- MECHANICAL VENTILATION:
when patients are not allowed to trigger a
ventilator breath.

31. 2- CRITICAL ILLNESS
NEUROMYOPATHY:
These are inflammatory conditions
involving peripheral nerves and skeletal
muscle that typically appear in patients
with severe sepsis and multiorgan failure,
and are recognized only when patients fail
to wean from mechanical ventilation.
There is no specific treatment for these
conditions, and the weakness can persist
for months.

32. 3- ELECTROLYTE DEPLETION:
Magnesium and phosphorous depletion
can promote respiratory muscle weakness
but the clinical relevance of this effect is
unproven.
deficiencies in these electrolytes should be
corrected in patients who fail repeated
attempts to discontinue mechanical
ventilation.

33. Monitoring
1- MAXIMUM INSPIRATORY
PRESSURE: (PImax), which is the
negative pressure that is generated by a
maximum inspiratory effort against a closed
airway.
The normal values of Pimax are a mean of
-120 cm H2O for men and -84 cm H2O for
women
Ventilation at rest is threatened when the
PImax drops to -15 to -30 cm H2O.

34. 2- ULTRASOUND: to assessing
diaphragm strength by measuring the
thickness of the diaphragm, and the length
of excursion during inspiration.

35. Management
When respiratory muscle weakness is
strongly suspected, trials of spontaneous
breathing should continue, but should be
terminated before patients show evidence
of respiratory distress (to avoid
aggravating the weakness).
Strategies designed to promote muscle
strength, such as patient-triggered
ventilation and physical rehabilitation are
encouraged.

36. EXTUBATION
Extubation should never be performed to
reduce the WOB as it can actually increase
after extubation.
Before extubation, we should consider:
(a) the patient’s ability to clear secretions and
(b) the risk of symptomatic laryngeal edema
following extubation.

37. a) Airway Protective Reflexes
The ability to protect the airway from
aspirated secretions is determined by the
strength of the gag and cough reflexes.
Cough strength can be assessed by
holding a piece of paper 1–2 cm from the
end of the endotracheal tube and asking
the patient to cough. If wetness appears
on the paper, the cough strength is
considered adequate.

38. b) Laryngeal Edema
Upper airway obstruction from laryngeal
edema is the major cause of failed
extubations, and is reported in 5–22% of
patients who have been intubated for
longer than 36 hours.
Contributing factors include difficult and
prolonged intubation, endotracheal tube
diameter, and self-extubation.

39. 1- The Cuff-Leak Test
The cuff-leak test measures the volume of
inhaled gas that escapes through the larynx
when the cuff on the endotracheal tube is
deflated.
the absence of an air leak indicates a high
risk of upper airway obstruction following
extubation, but the presence of an air leak
does not indicate a low risk of upper airway
obstruction following extubation.

40. ATS/ACCP guidelines 2017

41. Risk factors for postextubation
stridor
1- Traumatic intubation
2- Intubation more than 6 days
3- Large endotracheal tube
4- Female sex
5- Reintubation after unplanned extubation.

42. 2- Pretreatment with Steroids?
Pretreatment with intravenous methyl-
prednisolone, 20–40 mg every 4–6 hrs for
12 to 24 hours prior to extubation results in
fewer cases of laryngeal edema and upper
airway obstruction and fewer
reintubations.
A single dose of methylprednisolone (40
mg IV) given one hour prior to extubation
did not reduce the incidence of post-
extubation laryngeal edema.

43. ATS/ACCP guidelines 2017

44. Postextubation Stridor
The first sign of a significant laryngeal
obstruction may be inspiratory stridor as
narrowing of the extrathoracic larynx
during inspiration occur.

45. Post-extubation stridor is apparent within
30 minutes of extubation in a large
majority (∼80%) of cases but delays in
appearance of up to 2 hours can occur.
Reintubation is not always required.
Inhalation of an epinephrine aerosol (2.5
mL of 1% epinephrine) is a popular
practice for post-extubation stridor.
However, while effective in children, this
practice is unproven in adults.

46. Noninvasive Ventilation
Noninvasive ventilation is effective in
reducing the rate of reintubation when
used immediately after extubation in
patients with a high risk of laryngeal
edema.
Thus, the benefit of noninvasive ventilation
occurs when it is used as a preventive
measure early after extubation.

47. ATS/ACCP guidelines 2017

48. Summary
Be Vigilant
Vigilance involves early recognition of
candidates for trials of unassisted breathing
(with daily assessments using the readiness
criteria), and early recognition that the
candidates can sustain spontaneous
ventilation (with trials of spontaneous
breathing).