30: Management of respiratory failure

patients with chronic respiratory insufficiency: chronic ventilatory assistance and lung transplantation.

Goals and principles underlying supportive therapy

Adequate uptake of O2 by the blood, delivery of O2 to the tissues, and elimination of CO2 all are components of normal gas exchange. In terms of O2 uptake by the blood, almost all of the O2 carried by blood is bound to hemoglobin, and only a small portion is dissolved in plasma. It is apparent from the oxyhemoglobin dissociation curve that elevating PO2 beyond the point at which hemoglobin is almost completely saturated does not significantly increase the O2 content of blood (see Chapter 1). On average, assuming that the oxyhemoglobin dissociation curve is not shifted, hemoglobin is approximately 90% saturated at a PO2 of 60 mm Hg. Increasing PO2 to this level is important for tissue oxygen delivery, but a PO2 much beyond this level does not provide that much incremental benefit. In practice, patients with respiratory failure often are maintained at a PO2 slightly higher than 60 mm Hg (or an O2 saturation slightly > 90%) to allow a “margin of safety” for fluctuations in oxygenation.

Goals of optimizing O2 transport to tissues:

1.Arterial O2 saturation greater than 90% (i.e., PO2 > 60 mm Hg)

2.Acceptable hemoglobin level (e.g., ≥7 g/dL)

3.Appropriate cardiac output

Oxygen delivery to the tissues, however, depends not only on arterial PO2 but also on hemoglobin concentration and cardiac output. In patients who are anemic, O2 content and thus O2 transport can be compromised as much by the low hemoglobin level as by hypoxemia (see Eq. 1.3). In selected circumstances, blood transfusion may be useful in raising the hemoglobin and O2 content to more desirable levels, usually in order to maintain a hemoglobin concentration ≥ 7 g/dL.

Similarly, when cardiac output is impaired, tissue O2 delivery also decreases, and measures to augment cardiac output may improve overall O2 transport and delivery. Unfortunately, the use of positive-pressure ventilation, particularly with positive end-expiratory pressure (PEEP), may have a detrimental effect on cardiac output. As a result, tissue O2 delivery may not improve (and even may worsen) despite an increase in PO2. The use of PEEP is discussed in more detail later in this chapter.

Elimination of CO2 by the lungs is important for maintaining adequate acid-base homeostasis. However, achieving an acceptable pH value, not a “normal” PCO2 of 40 mm Hg, is the primary goal in managing respiratory failure with impaired elimination of CO2. In patients with chronic hypercapnia (and metabolic compensation), abruptly restoring PCO2 to 40 mm Hg may cause significant alkalosis and thus risk precipitating either arrhythmias or seizures.

CO2 elimination is manipulated to maintain acceptable pH rather than “normal” PCO2 of 40 mm Hg.

Acute hypoxemic respiratory failure

In the patient with acute hypoxemic respiratory failure such as due to ARDS, ventilation-perfusion mismatch and shunting are responsible for the hypoxemia. Because a large fraction of the cardiac output is

being shunted through areas of unventilated lung and is therefore not oxygenated during passage through the lungs, supplemental O2 is relatively ineffective at raising PO2 to an acceptable level. In these cases, patients may require inspired O2 concentrations in the range of 60% to 100% and still may have difficulty maintaining PO2 greater than 60 mm Hg.

Such patients with ARDS typically require ventilatory assistance for support of oxygenation and relief from a high work of breathing resulting from stiff, noncompliant lungs that are filled with fluid. Although oxygenation is extremely difficult to support, CO2 retention is much less frequent in patients with ARDS, and hypoxemia rather than hypercapnia is the primary indication for mechanical ventilation.

For patients with acute hypoxemic respiratory failure, inability to achieve a PO2 of 60 mm Hg or greater on supplemental O2 readily administered by face mask or heated high-flow nasal cannula with an oxygen blender (generally delivering a fractional concentration of inspired oxygen [FiO2] of 70%-100%) is often considered a justification for intubation (i.e., placement of a flexible plastic endotracheal tube through the nose or mouth, between the vocal cords, and into the trachea). A mechanical ventilator is then connected to the endotracheal tube to provide the desired inspiratory gas under positive pressure. However, such decisions for ventilatory support are not based on just one number. Other factors taken into consideration include the nature of the underlying problem and the likelihood of a rapid response to therapy.

Mechanical ventilation is often indicated when PO2 ≥ 60 mm Hg cannot be achieved with inspired O2 concentration ≤ 70% to 100%.

In the setting of ARDS, intubation and mechanical ventilation serve several useful purposes. First, higher concentrations of O2 can be administered much more reliably through a tube inserted into the trachea than through a mask placed over the face. Second, administration of positive pressure by a ventilator relieves the patient of the high work of breathing (see section “Reducing Work of Breathing”), allowing patients to receive more reliable tidal volumes than they would spontaneously take, particularly because the poorly compliant lungs of ARDS promote shallow breathing and low tidal volumes. Finally, when a tube is in place in the trachea, positive pressure can be maintained in the airway throughout the entire respiratory cycle rather than in just roughly one-half of it. In common usage, positive airway pressure maintained at the end of expiration in a mechanically ventilated patient is termed PEEP, which is described in more detail later in this chapter.

Beneficial effects of ventilatory assistance in acute respiratory distress syndrome (ARDS):

1.More reliable administration of high concentrations of inspired O2

2.Delivery of more reliable tidal volumes than those achieved spontaneously by the patient

3.Use of positive end-expiratory pressure (PEEP)

Why is positive pressure throughout the respiratory cycle beneficial for ARDS patients? In ARDS, fluid occupying alveolar spaces, low tidal volumes, and probably both decreased production and inactivation of surfactant result in microatelectasis and in decreased or absent ventilation to involved areas of the lung. The resting end-expiratory volume (i.e., functional residual capacity [FRC]) is decreased, and continued perfusion of nonventilated alveoli results in an elevation of the fraction of blood that is shunted through the lungs without being oxygenated. With administration of PEEP, FRC is

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increased, and many small airways and alveoli that formerly were collapsed and received no ventilation are now opened and available for gas exchange. Measurement of the “shunt fraction” shows that PEEP is quite effective at decreasing the amount of blood that otherwise would not be oxygenated during passage through the lungs.

PEEP is effective in ARDS by increasing functional residual capacity (FRC), preventing closure of small airways and alveoli, and decreasing the shunt fraction.

When the shunt fraction is decreased by PEEP, supplemental O2 is much more effective at elevating the patient’s PO2 to an acceptable level. The concentration of inspired O2 thus can be lowered, and the patient is less likely to experience O2 toxicity from sustained exposure to very high concentrations of O2.

Hypercapnic respiratory failure

CO2 retention is an important aspect of respiratory failure in several types of patients. Most frequently, these patients have some degree of chronic CO2 retention, and their acute problem is appropriately termed acute-on-chronic respiratory failure. Patients with chronic obstructive lung disease, chest wall disease, and neuromuscular disease are all subject to the development of hypercapnia. Hypercapnia may be purely acute in certain other groups of patients—individuals who have suppressed respiratory drive resulting from ingestion of certain drugs, especially narcotics, or occasional patients with severe asthma and status asthmaticus.

If the degree of CO2 retention is sufficiently great to cause a marked decrease in the patient’s pH (<7.25 to 7.30) or a change in mental status, ventilatory assistance with a mechanical ventilator is often necessary. Traditionally, ventilator support has been initiated following endotracheal intubation. Although this type of invasive mechanical ventilation through an endotracheal tube may be required for patients with more extreme hypercapnia or with changes in mental status, most patients with hypercapnia from an acute exacerbation of chronic obstructive lung disease, neuromuscular disease, chest wall disease, or heart failure now are managed initially using noninvasive positive-pressure ventilation (NIPPV). With NIPPV, the mechanical ventilator delivers positive pressure via a tight-fitting face mask rather than an endotracheal tube, and the need for intubating the trachea and sedating the patient can often be averted.

Mechanical ventilation for patients with hypercapnic respiratory failure often is provided initially with noninvasive positive-pressure ventilation.

Most cases of hypercapnic respiratory failure are also associated with some degree of hypoxemia, due to hypoventilation as well as ventilation-perfusion mismatch that accompanies the underlying disease. For these mechanisms of hypoxemia, administration of supplemental O2 is quite effective in improving PO2, and high concentrations of inspired O2 are usually not necessary. As previously noted in Chapter 18, patients with chronic hypercapnia may be subject to further increases in PCO2 when they receive supplemental O2. If PCO2 rises significantly after administration of supplemental O2 in a patient not already receiving ventilatory assistance, NIPPV should be started. Fortunately, this complication of significant hypercapnia is infrequent with judicious use of supplemental O2.

Reducing work of breathing

One pathophysiologic feature shared by most patients with respiratory failure is an imbalance in the work