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CHAPTER 49: Management of the Ventilated Patient 433

assessment of respiratory system mechanics, and focuses attention on the systemic oxygen consumption. These nonpulmonary causes of hypox-
patient and not the machine. emia are particularly common in patients with severe shunt lung disease
and may herald life-threatening crises (eg, pneumothorax).
High-Pressure Alarm: Aside from alarm or gauge malfunction, increased
airway pressure indicates obstruction of the airway, obstruction to gas Hypercapnia: A rising Pa CO 2 often elicits a change in the ventilator orders
flow through the ventilator circuit, patient effort against the ventilator, (increased frequency or tidal volume). However, a pathophysiologic
or a change in the mechanics of the respiratory system. If manual bag approach is useful here too. From the equation for Pa CO 2 :
ventilation is difficult, a suction catheter should be passed immediately
through the endotracheal tube. If the catheter cannot be advanced 25 cm Pa CO 2 = (V CO 2 × k)/[V × f × (1 − V /V )]
T
D
T
or more, obstruction of the airway is likely. If repositioning of the head is carbon dioxide production; k is a constant; and V is
D
Where V CO 2
does not relieve kinking, and if the patient is not biting the airway, the dead space, it can be seen that in addition to a fall in minute ventila-
reintubation is necessary. If the patient is biting an endotracheal tube, tion, rising CO production (eg, fever, shivering, agitation) or increasing
2
a bite block should be placed, or if this cannot be done, a short-acting dead space (eg, hypovolemia, pulmonary embolism, PEEP) may account
neuromuscular blocking drug should be administered. for new hypercapnia. Responding to hypercapnia by simply raising the
If the airway is patent yet manual ventilation is difficult and the and
patient is struggling, a sedative should be given. If the patient is now easy minute ventilation is dangerous because causes of increased V CO 2
dead space may be important to diagnose in their own right. In addi-
to ventilate (implicating vigorous respiratory muscle activity), the cause tion, augmenting minute ventilation has the potential to (paradoxically)
of the patient’s distress should be sought. Possibilities include hypox- decrease alveolar ventilation if the increase in V or f worsens dead space
emia, hypercapnia, shock, or a new central nervous system process. T
If ventilation remains difficult after deep sedation or muscle paralysis (such as when autoPEEP is present). Indeed, in this setting, the Pa CO 2
may rise when minute ventilation is increased and fall when minute
of a patient with a patent endotracheal tube, a new lower airway, pleural, ventilation is reduced. These issues are further discussed in Chap. 55.
lung, or chest wall process should be sought. Auscultation and bedside
ultrasound often identify pneumothorax, collapse, or consolidation. ■ LIBERATION OF THE PATIENT FROM MECHANICAL VENTILATION
Early portable chest radiography confirms these diagnoses or identifies We refer to the discontinuation of mechanical ventilation not as wean-
an alternative cause of the crisis. Placing the patient back on the ventila- ing (which implies the withdrawal of a nurturing life-support system)
tor and measuring peak and plateau pressures as well as autoPEEP will but rather as liberation (connoting freedom from a confining, noxious,
further delineate the problem, as described above.
and dangerous circumstance). Since liberation from the ventilator is
57
Low-Pressure Alarm: Low-pressure alarms signal machine malfunction, fully discussed in Chap. 60, we make here only a few points relevant to
a leak, or inspiratory effort by the patient (usually obvious). Large persis- all ventilated patients. Patients recover the ability to breathe spontane-
tent leaks can occur within the ventilator itself, in the inspiratory limb, ously because central drive is regained, neuromuscular competence is
at the connection to the Y-adaptor and endotracheal tube, around the restored, or respiratory system load is reduced. Once these are achieved,
endotracheal tube cuff, or through a bronchopleural fistula. If normal the ventilator is no longer needed. Gradual adjustments of IMV rates or
resistance to ventilation is noted during manual ventilation, the prob- pressure-support levels that are too slow for the patient’s needs simply
lem lies with the ventilator or tubing. If hand-bagging reveals minimal serve to prolong the duration of mechanical ventilation, as shown in
resistance, an endotracheal tube cuff leak is likely. This can be confirmed large trials of weaning strategies. 23,24 On the other hand, if drive, strength,
by listening over the neck or by placing a hand over the mouth. A large and load are not repaired, no amount of ventilator technology will allow
bronchopleural fistula can be identified by inspection of the chest tube the patient to breathe on his or her own. Most often, when physi-
and pleural drainage system. cians believe they are “weaning” the patient, they are simply allowing
time for their other therapies to treat the respiratory failure; ventilator
Worsened Oxygenation: When a patient develops hypoxemia, sufficient changes are prescribed coincidentally but are irrelevant. Accordingly,
oxygen should be given immediately to return the saturation to 88%. effective liberation of each patient begins at intubation and stabiliza-
However, this must be followed by a search for the cause of deteriora- tion on the ventilator, with the measurement of respiratory mechanics
tion. Of course, progression of the primary cause of respiratory failure to assist in evaluating the reversible features of the patient’s abnormally
(ARDS, pneumonia, lung hemorrhage) will impair gas exchange, but increased load; as soon as is clinically relevant, the respiratory muscle
this should not be assumed to be the case. Also possible is a new lesion strength is evaluated for reversible causes of weakness; and frequent
(eg, nosocomial pneumonia, pneumothorax), which may be identified attempts are made to identify the earliest point at which the patient has
by physical examination, ultrasound, or chest radiograph. However, a regained the capacity to breathe.
systematic approach is useful to identify the myriad (including nonpul-
monary) causes of hypoxemia.
From a pathophysiologic perspective, new hypoxemia implies a
(including ventilator malfunction), hypoventilation, ven- KEY REFERENCES
reduced Fi O 2
tilation-perfusion mismatching, shunt, or a fall in the mixed venous • Coussa ML, Guérin C, Eissa NT, et al. Partitioning of work of
oxygen saturation. Hypoventilation is usually obvious, being signaled breathing in mechanically ventilated COPD patients. J Appl
by hypercapnia, and does not cause oxygen-refractory hypoxemia. Physiol. 1993;75:1711-1719.
Ventilation-perfusion mismatch typically causes mild hypoxemia that
is easily corrected with supplemental oxygen. Bronchospasm, airway • Demoule A, Jung B, Prodanovic H, et al. Diaphragm dysfunction
secretions, and airway plugging are common contributors in intubated on admission to the intensive care unit: prevalence, risk factors,
patients. The combination of worsened ventilation-perfusion match- and prognostic impact—a prospective study. Am J Respir Crit Care
ing and an increase in dead space should prompt consideration of Med. 2013;188:213-219.
pulmonary embolism. Most often, when new hypoxemia develops in a • Futier E, Constantin J-M, Paugam-Burtz C, et al. A trial of intra-
mechanically ventilated patient, shunt or a fall in mixed venous oxygen- operative low-tidal-volume ventilation in abdominal surgery.
ation can be found. A new shunt (eg, pulmonary edema, pneumonia, or N Engl J Med. 2013;369:428-437.
atelectasis) typically can be found on the chest radiograph, while mixed • Girard TD, Kress JP, Fuchs BD, et al. Efficacy and safety of a
venous desaturation is detected by analyzing a venous blood sample or paired sedation and ventilator weaning protocol for mechani-
performing venous oximetry. The causes of venous desaturation include cally ventilated patients in intensive care (Awakening and
reduced cardiac output or hemoglobin concentration or increased

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