A 59-year-old woman with carcinoma underwent a left hemicolectomy. She had a history of chronic obstructive pulmonary disease (COPD) secondary to long-standing tobacco use and type 2 diabetes mellitus. Surgery was complicated by aspiration after extubation and reintubation. Arterial blood gas (ABG) values are pH 7.35, carbon dioxide tension (PaCO 2 ) 37 mm Hg, and oxygen tension (PaO 2 ) 54 mm Hg on controlled mechanical ventilation (CMV) with a rate of 12 breaths per minute, tidal volume of 650 mL, fraction of inspired oxygen (FiO 2 ) of 0.5, and positive end expiratory pressure (PEEP) of 5 cm H 2 O. Peak inspiratory pressures are 26 cm H 2 O. After several days in the intensive care unit (ICU), the patient’s respiratory status improved.
Describe the two main types of acute respiratory failure.
The two main types of acute respiratory failure are as follows:
Occasionally both types may coexist.
Hypoxemic acute respiratory failure is discussed in detail in Question 5. Hypercapnic acute respiratory failure occurs when a patient develops acute respiratory acidosis, usually with a PaCO 2 >50 mmHg. It is caused by either ineffective minute ventilation or, much less commonly, excessive carbon dioxide (CO 2 ) production (e.g., malignant hyperthermia, thyroid storm). Ineffective minute ventilation has three main clinical causes, as follows:
Decreased respiratory rate (e.g., secondary to opioids, brainstem lesions)
Decreased tidal volume (e.g., residual neuromuscular blockade, myasthenia gravis, splinting)
Increased physiologic dead space (e.g., COPD, later stages of acute respiratory distress syndrome [ARDS], shock)
Hypercapnia can also result in hypoxemia, as is discussed in Question 5.
What are the indications for tracheal intubation in a patient with dyspnea?
Clinical indications include patient fatigue, accessory muscle use, paradoxical breathing pattern, and inability to protect the airway. PaO 2 ≤60 mm Hg (i.e., oxygen saturation <90%), FiO 2 ≥0.5, and increasing PaCO 2 (e.g., 10 mm Hg above baseline or ≥50 mm Hg) are ABG abnormalities that alone, and especially in combination with any of the clinical indications, support the need to intubate and initiate mechanical ventilation.
When should noninvasive ventilation be considered, and how is it prescribed?
Noninvasive ventilation may be effective in place of tracheal intubation when respiratory distress is expected to be short-lived (e.g., ideally <24 hours), and the patient can cooperate with the requisite mask fitting and protect the airway. Mild to moderate pulmonary edema responding to medical therapy, COPD exacerbation, and perhaps splinting are reasonable postoperative conditions for consideration of noninvasive ventilatory support. Generally, noninvasive ventilation is set with inspiratory pressure support (PS) and continuous positive airway pressure (CPAP), which together are termed BPAP (bilevel positive airway pressure). A common initial setting is 10 cm H 2 O/5 cm H 2 O (PS/CPAP) adjusted by appearance, respiratory rate, oxygen saturation by pulse oximetry (SpO 2 ), and measured PaCO 2 . The success rate for avoidance of eventual tracheal intubation is highly dependent on respiratory care team effort and patient selection. Extreme care must be taken to avoid the unobserved need to progress to tracheal intubation.
What are the four primary causes of hypoxemia, how are they distinguished, and which is most likely in this patient?
The four primary causes of hypoxemia are hypoventilation (i.e., hypercapnia), shunt, ventilation/perfusion ( ) mismatch, and diffusion impairment. Low FiO 2 and low barometric pressure can cause hypoxemia but do not warrant consideration in this context.
Hypoventilation is a reduction in gas flow to the alveoli. This reduction occurs whenever there is ineffective minute ventilation (see Question 2). The hallmark feature is an increased PaCO 2 . Two basic equations relate to this condition.
The first equation demonstrates the relationship between PaCO 2 and alveolar ventilation:
PaCO 2 = V˙ CO 2 V A × K
where CO 2 is the CO 2 produced, V A is the alveolar ventilation, and K is a constant equal to 0.863. This equation demonstrates that if the alveolar ventilation is halved, PaCO 2 doubles, and vice versa.
The second equation is the alveolar gas equation:
P A O 2 = FiO 2 ( P atm – P H 2 O ) – PaCO 2 RQ