case scenario

1. Mechanical ventilation in patients
with AECOPD
AHMED HAWASH
ASSOCIATE LECTURER OF CRITICAL CARE MEDICINE
FACULTY OF MEDICINE ALEXANDRIA UNIVERSITY

2. A 58-year-old man comes to see you because of shortness of breath. He has experienced
mild dyspnea on exertion for a few years, but more recently he has noted worsening
shortness of breath with minimal exercise and the onset of dyspnea at rest. He has difficulty
reclining, and, as a result, he spends the night sitting up in a chair trying to sleep. He reports
a cough with production of yellowish-brown sputum every morning throughout the year. He
denies chest pain, fever, chills, or lower extremity edema. He has smoked about two packs
of cigarettes per day since age 15 years. A few months ago, the patient went to an urgent
care clinic for evaluation of his symptoms, and he received a prescription for some inhalers,
the names of which he does not remember. He was also told to find a primary care physician
for further evaluation. On physical examination, his blood pressure is 135/85 mm Hg, heart
rate 96 bpm, respiratory rate 28 breaths per minute, and temperature 97.6°C. He is sitting in
a chair, leaning forward, with his arms braced on his knees. He appears uncomfortable with
labored respirations and cyanotic lips. He is using accessory muscles of respiration, and
chest examination reveals wheezes and rhonchi bilaterally, but no crackles are noted. The
anteroposterior diameter of the chest wall appears increased, and he has inward movement
of the lower rib cage with inspiration. Cardiovascular examination reveals distant heart
sounds but with a regular rate and rhythm, and his jugular venous pressure is normal. His
extremities show no cyanosis, edema, or clubbing.

3. Summary:
A 58-year-old smoker has noted worsening shortness of breath
with minimal exercise and the onset of dyspnea at rest and
difficulty reclining. He reports a productive cough with yellowish-
brown sputum every morning throughout the year.
He is sitting in a characteristic “tripod” position to facilitate use of
accessory muscles of respiration. He appears to have airway
obstruction with respiratory distress, with lower chest retractions,
and bilateral wheezes and rhonchi. His perioral cyanosis suggests
hypoxemia. The anteroposterior diameter of the chest wall appears
increased, suggesting hyperinflation. Cardiovascular examination
reveals distant heart sounds but no signs of significant cardiac
disease.

4. What is the most likely diagnosis?
What is the next best diagnostic test?
What is the best initial treatment?

5. • Most likely diagnosis: Chronic obstructive
pulmonary disease (COPD) with
acute exacerbation
• Next diagnostic step: Arterial blood gas to
assess oxygenation and acid-base
status
• Best initial treatment: Oxygen by nasal
cannula, followed closely by bronchodilators,
and steroids for inflammatory component

6. Mechanical ventilation in
patients with AECOPD

7. Noninvasive positive pressure
ventilation in acute respiratory failure in
adults

8. Exacerbations of COPD are characterized by a marked worsening of
respiratory mechanics secondary to increased airway resistance,
expiratory collapse of small airways limiting expiratory flow,
development of auto-PEEP and hyperinflation, and increased work
of breathing. The development of auto-PEEP has important
consequences including increased work of breathing (inspiratory
threshold loading), decreased respiratory muscle efficiency (flattened
diaphragms), and hemodynamic compromise. Patients are unable to
achieve sufficient Vts despite strong respiratory efforts and have
markedly elevated oxygen cost of breathing. In these patients, the
physiologic rationale for NIV is very strong.
NIV improves ventilatory efficiency, decreases respiratory rate,
decreases the work of breathing, and increases alveolar ventilation by
increasing Vt. This approach often improves the patient's level of
consciousness. Many studies have found that the use of NIV can
prevent the need for intubation and reduce mortality, often in very
severe cases.

9. If the patient requires intubation and mechanical ventilation because
of a decreased level of consciousness, severe respiratory acidosis
despite NIV, or because the initial presentation is too severe for an
NIV attempt ,don’t delay it.
the goals of MV can be considered within the context of 2 distinct
periods. In the first, often short, period, the aim is to minimize
dynamic hyperinflation while obtaining reasonably acceptable values
of pH and oxygenation but not normal PaCO2. To achieve these goals,
the patient usually undergoes ventilation in a controlled pressure or
volume mode. The strategy largely consists of minimizing minute
ventilation and increasing inspiratory flow to prolong the duration of
expiration and permit lung deflation in the presence of a high
respiratory system time constant.

10. In the second period, the major goal is to wean the patient from the
ventilator while decreasing the work of breathing. In this period, the patient
is allowed to generate spontaneous breathing efforts, often using PSV.
Appropriately set external PEEP (just sufficient to overcome auto-PEEP) may
help reduce the added elastic load at the start the inspiration. Care must be
taken to avoid excessive levels of pressure support (and Vts), which are
associated with lengthening of the inspiratory time and ineffective efforts
that are strongly associated with poor outcomes. When the patient
undergoes PSV, the level of pressure should be set to decrease the work of
breathing but also to limit Vt; high Vts lead to dynamic hyperinflation and
ineffective effort, and dyssynchronies are observed very frequently in these
patients. Tidal volumes of approximately 6 mL/kg PBW may be necessary to
minimize ineffective efforts.

11. • Potential indicators of success in noninvasive positive
pressure ventilation
1.Younger age
2.Lower acuity of illness (APACHE score)
3.Able to cooperate, better neurologic score
4.Less air leaking, intact dentition
5.Moderate hypercarbia (PaCO 2 >45 mmHG, <92 mmHG)
6.Moderate acidemia (pH <7.35, >7.10)
7.Improvements in gas exchange and heart respiratory rates within first
two hours

12. • Contraindications to noninvasive positive
pressure ventilation
1.Cardiac or respiratory arrest
2.Nonrespiratory organ failure
3.Severe encephalopathy (eg, GCS <10)
4.Severe upper gastrointestinal bleeding
5.Hemodynamic instability or unstable cardiac arrhythmia
6.Facial or neurological surgery, trauma, or deformity
7.Upper airway obstruction
8.Inability to cooperate/protect airway
9.Inability to clear secretions
10.High risk for aspiration

13. High quality evidence (randomized trials, meta-analyses)
indicates that NPPV improves important clinical outcomes
in patients having an acute exacerbation of COPD
complicated by hypercapnic acidosis. As an example,
consider a meta-analysis (14 randomized trials, 758 patients)
that compared standard therapy alone to NPPV plus
standard therapy in patients having a COPD exacerbation
complicated by hypercapnia (PaCO 2 >45 mmHg) . NPPV
decreased mortality (11 versus 21 percent), intubation rate
(16 versus 33 percent), and treatment failure (20 versus 42
percent). Hospital length of stay and complications related
to treatment were also reduced by NPPV.
Patients with severe exacerbations of COPD respond better
to NPPV than patients with mild COPD exacerbations .
This is illustrated by the following studies:

14. * A trial randomly assigned 52 patients with mild COPD
exacerbations (defined as dyspnea with a pH >7.3) to receive
standard therapy alone or NPPV plus standard therapy .
There were no differences in the rate of intubation or the
length of hospital stay. In addition, the NPPV was tolerated
by fewer than half of the patients.
* A meta-analysis (15 randomized trials) found that NPPV
improved clinical outcomes only in those randomized trials
that enrolled patients with severe COPD exacerbations
(defined as a baseline pH <7.3 or a control group mortality
>10 percent) and not in those trials that enrolled patients
with milder COPD exacerbations .

15. It is unclear whether NPPV has any beneficial effects
on long-term clinical outcomes.
In a randomized trial that compared NPPV to invasive
mechanical ventilation in 49 patients with severe
COPD exacerbations, patients receiving NPPV
required fewer hospital readmissions over the
subsequent year, but survival rates were similar .
Finally, NPPV has physiologic benefits. Respiratory
mechanics measured after the initiation of NPPV
demonstrate a decreased respiratory rate, an increased
tidal volume, and an increased minute ventilation . In
addition, the arterial oxygen tension (PaO 2 ) tends to
increase as the PaCO 2 decreases.

16. Protocol for initiation of noninvasive positive
pressure ventilation
1. Appropriately monitored location, oximetry, respiratory
impedance, vital signs as clinically indicated
2. Patient in bed or chair at >30 angle
3. Select and fit interface
4. Select ventilator
5. Apply headgear; avoid excessive strap tension (one or
two fingers under strap)
6. Connect interface to ventilator tubing and turn on
ventilator
7. Start with low pressure in spontaneously triggered
mode with backup rate; pressure limited: 8 to 12 cm H2O
inspiratory pressure; 3 to 5 cm H2O expiratory pressure

17. 8. Gradually increase inspiratory pressure (10 to 20 cm H2O)
as tolerated to achieve alleviation of dyspnea, decreased
respiratory rate, increased tidal volume (if being monitored),
and good patient-ventilator synchrony
9. Provide O2 supplementation as need to keep O2 sat >90
percent
10. Check for air leaks, readjust straps as needed
11. Add humidifier as indicated
12. Consider mild sedation (eg, intravenously administered
lorazepam 0.5 mg) in agitated patients
13. Encouragement, reassurance, and frequent checks and
adjustments as needed
14. Monitor occasional blood gases (within 1 to 2 hours) and
then as needed

18. Invasive positive pressure ventilation
in acute respiratory failure in adults

19. • patients with acute respiratory failure due to COPD exacerbation to
be ventilated with ACV or IMV/PSV, rather than IMV alone or PSV
alone, until the underlying process that precipitated the acute
respiratory failure has improved and the patient is ready to begin
weaning. This is based upon our clinical experience during which
we have found that the goals of mechanical ventilation are most
easily achieved using these modes.
• Optimal ventilator settings can minimize the work of breathing, but
not eliminate it. Conversely, inappropriate settings can create work
that is greater than that required for spontaneous breathing.
• We recommend titrating the fraction of inspired oxygen (FiO2) to
achieve an arterial oxygen tension (PaO2) ≥60 mmHg. The arterial
oxyhemoglobin saturation (SaO2) should be correlated with the
PaO2 in order to determine the appropriate target SaO2 if pulse
oximetry is used in lieu of arterial blood gases. As an example, an
SpO2 of 92 percent predicts satisfactory oxygenation in white
patients, but may be associated with hypoxemia in black patients.
A higher target SpO2 will prevent hypoxemia in black patients, but
some patients may develop oxygen toxicity. It is prudent to
correlate the SpO2 and PaO2 before determining the target SpO2.

20. • In patients receiving intermittent mandatory ventilation
(IMV) and patients who have increased inspiratory effort
while triggering pressure support ventilation (PSV), we
suggest flow triggering, rather than pressure triggering. In all
other patients, we do not have a preference for pressure or
flow triggering.
• Reasonable initial settings include a trigger sensitivity of -2
cm H2O when using pressure triggering or 2 L/min when
using flow triggering. Regardless of the trigger method
chosen, we use an initial flow rate of 1 L/second (ie, 60
L/min) in most patients.
• In patients who have intrinsic positive end-expiratory
pressure (ie, intrinsic PEEP or auto-PEEP), we suggest adding
applied PEEP (ie, extrinsic PEEP). An appropriate amount of
applied PEEP is ≤80 percent of the measured auto-PEEP.

21. • In patients receiving volume-targeted modes of mechanical
ventilation (eg, ACV, IMV, IMV/PSV), tidal volumes of 5 to 7
mL/kg may decrease the risk of ventilator-induced lung
injury, hyperinflation, and barotrauma.
• In patients receiving ACV, we use an initial ventilator rate
that is approximately four breaths per minute less than the
respiratory rate. In patients receiving IMV or IMV/PSV, we
base the initial ventilator rate upon our estimate of the
required minute ventilation.
• In patients receiving PSV, the pressure support level should
be increased until the patient's respiratory rate is below 30
breaths per min because this respiratory rate suggests that
the inspiratory effort has been reduced to a reasonable
level.