teaser - darkhorse

[ArchivalUser]

A 60-year-old male with chronic obstructive pulmonary disease is brought to the emergency department
with altered consciousness. His family reports a 2-day history of increasing shortness of breath that
requires nebulized albuterol every 2 h. In addition, the patient has had increasing sputum production
with a change in the sputum color from white to green. On presentation, the patient was breathing eight
times per minute and was unarousable. Initial arterial blood gas revealed a pH of 6.98, a PaCO2 of 110
mmHg, and a PaO2 of 100 mmHg while the patient was on a nonrebreather mask. The patient is
emergently intubated and brought to the intensive care unit. The initial ventilatory settings are as
follows:
Mode Assist control
Rate 12 breaths/min
Tidal volume 500 mL
PEEP 0 cmH2O
FIO2 0.5
Initially, the patient does well with improvement in arterial blood gases (ABG) to pH 7.20, a PaCO2 of 82
mmHg, and a PaO2 of 215 mmHg. You are called emergently to the patient's bedside 2 h later to deal
with hypotension. The patient currently is breathing 14 times per minute, but his oxygen saturation has
decreased from 100% to 84%. Blood pressure is 66/42. Heart rate is 130 beats/min with sinus
tachycardia. Temperature is 38.2°C (100.8°F). The patient is sedated, and his respirations do not appear
labored. Breath sounds are markedly decreased on the right side with tracheal deviation to the left. The
patient has thready peripheral pulses and is cool to touch. You notice that the patient's peak inspiratory
pressure has risen from 40 cmH2O to more than 75 cmH2O. What is the most important next step in
stabilizing this patient?


A. Disconnect the patient from the ventilator to relieve intrinsic positive end-expiratory pressure (PEEP).
B. Perform deep suctioning to relieve mucus plugging.
C. Initiate fluid resuscitation and vasopressor support for sepsis syndrome.
D. Insert a large-bore needle into the right pleural space to relieve a pneumothorax.
E. Administer a paralytic agent because the patient's decompensation can be attributed to dyssynchrony
with mechanical ventilation.

[ArchivalUser]

D.?

[ArchivalUser]

d.

[ArchivalUser]

dd

[ArchivalUser]

since the patient is not on positive peep and also he has pulmonary infection w/ thick sputum production, tension pneumothorax is unlikely and mucus plug has to be considered first.sometimes mucus plug acts like a unilateral check valve so causes hyperinflation of the ipsilateral lung
i think B is the correct answer

[ArchivalUser]

A--------

[ArchivalUser]

The answer is D.

Patients with chronic obstructive pulmonary disease (COPD) are at increased risk of several complications
associated with mechanical ventilation, and physicians must be alert for the development of those
complications. This patient has evidence of spontaneous tension pneumothorax related to the rupture of
a preexisting bulla in the presence of positive-pressure ventilation. Clinically, the manifestations are
decreased blood pressure, tachycardia, and decreased breath sounds on the affected hemithorax with a
shift of the trachea to the contralateral side. Additionally, increased inspiratory pressures are noted on
the mechanical ventilator. Immediate decompression of the pneumothorax followed by tube
thoracostomy is indicated to prevent electromechanical dissociation as the patient is demonstrating
evidence of shock with hypotension and peripheral hypoperfusion.
Other complications of mechanical ventilation in COPD include the development of intrinsic positive
end-expiratory pressure and mucus plugging. Intrinsic PEEP develops when insufficient time for
exhalation is given and is particularly important in patients with obstructive lung disease. If intrinsic PEEP
accumulates, a high intrathoracic pressure may develop, causing hypotension from decreased venous
return. Disconnecting the patient from the ventilator temporarily allows full exhalation and relieves the
positive pressure and hypotension. Many options are available to prevent intrinsic PEEP from recurring,
including slowing the respiratory rate, decreasing the tidal volume, and maximizing the
inspiratory/expiratory ratio by changing the ventilator mechanics. Mucus plugging can also cause
sudden-onset hypoxemia, decreased breath sounds, and elevated ventilatory pressures, as seen in this
patient. Hypotension, however, is rarely seen. Furthermore, mucus plugging should cause deviation of
the trachea toward the side of the lung, with the decreased breath sounds resulting from volume loss.
Ventilatory dyssynchrony is a common problem that causes hypoxemia but is not apparent clinically here
as the patient is not described as appearing agitated or tachypneic. Sepsis syndrome should be
considered if the patient develops refractory hypotension after alleviation of the pneumothorax and
adequate fluid resuscitation.