Management of Respiratory Failure

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Management of Respiratory Failure



Supportive therapy aimed at maintaining adequate gas exchange is critical in the management of both acute respiratory failure and chronic respiratory insufficiency. In acute respiratory failure, survival depends on the ability to provide supportive therapy until the patient recovers from the acute illness that precipitated the need to support the respiratory system. In patients with chronic respiratory insufficiency, the goal is to maximize the patient’s function and minimize symptoms and cor pulmonale on a long-term basis. This chapter outlines the goals of supportive therapy and provides a discussion of the ways adequate gas exchange can be maintained, focusing on patients with acute respiratory failure. Because the principles for supportive management differ considerably in the two main categories of acute respiratory failure—acute respiratory distress syndrome (ARDS) and acute-on-chronic respiratory failure—these differences are emphasized in the course of the discussion. The chapter concludes with a consideration of two specific topics applicable to patients with chronic respiratory insufficiency: chronic ventilatory assistance and lung transplantation.



Goals of Supportive Therapy for Gas Exchange


Adequate uptake of O2 by the blood, delivery of O2 to the tissues, and elimination of CO2 all are parts 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. On average, assuming that the dissociation curve is not shifted, hemoglobin is approximately 90% saturated at a PO2 of 60 mm Hg. Increasing PO2 to this level is important, 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 to allow a “margin of safety” for fluctuations in PO2.



Oxygen delivery to the tissues, however, depends not only on arterial PO2 but also on hemoglobin level 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 Equation 1-3). In selected circumstances, blood transfusion may be useful in raising the hemoglobin and O2 content to more desirable levels.


Similarly, when cardiac output is impaired, tissue O2 delivery also decreases, and measures to augment cardiac output may improve overall O2 transport. Unfortunately, some of the measures used to improve arterial PO2 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. Use of positive-pressure ventilation, particularly with positive end-expiratory pressure, is most important in this regard. This technique is discussed under Maintenance of Oxygenation.


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




Maintenance of Carbon Dioxide Elimination


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 acute in certain groups of patients—individuals who have suppressed respiratory drive resulting from ingestion of certain types of drugs, for example, 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 (<7.25–7.30), ventilatory assistance with a mechanical ventilator is often necessary.* Similarly, if marked CO2 retention has impaired the patient’s mental status, ventilatory assistance is indicated. For the patient who has a good chance of rapid reversal of CO2 retention with therapy (assuming the level of CO2 retention is not life threatening), this therapy is often attempted first, with the hope of avoiding mechanical ventilation.




Measurements reflecting muscle strength and pulmonary function may be useful for the patient with acute or impending respiratory failure and can serve as an indirect guide to the patient’s ability to maintain adequate CO2 elimination. They also have been used as criteria for instituting ventilatory assistance or, conversely, for deciding when a patient aided by a mechanical ventilator might be weaned from ventilatory support. Although the decision to initiate mechanical ventilation is frequently based on clinical grounds, the objective measurements most commonly used as criteria for mechanical ventilation are (1) vital capacity (<10 mL/kg body weight) and (2) inspiratory force (<25 cm H2O negative pressure). The latter measurement, which is also called the maximal inspiratory pressure, is performed by having the patient inspire as deeply as possible through tubing connected to a pressure gauge. This technique quantifies the maximal negative pressure the patient can generate when the airway is occluded. These measurements are most useful in following patients with progressive neuromuscular weakness (e.g., myasthenia gravis) to determine when mechanical ventilation is necessary.


Although these and other specific measurements have been used to determine when a patient requires ventilatory assistance for eliminating CO2, none of the guidelines is absolute. Some of the many additional factors that enter into such decisions include the nature of the underlying disease, the tempo and direction of change of the patient’s illness, and the presence of other medical problems.



Maintenance of Oxygenation


Although hypoxemia is a feature of almost all patients with respiratory failure when breathing air (21% O2), the ease of supporting the patient and restoring adequate PO2 depends to a great degree on the type of respiratory failure. In most cases of acute-on-chronic respiratory failure, ventilation-perfusion mismatch and hypoventilation are responsible for hypoxemia. For these mechanisms of hypoxemia, administration of supplemental O2 is quite effective in improving PO2, and particularly high concentrations of inspired O2 are not necessary. Frequently O2 can be administered by face mask or nasal prongs to provide inhaled concentrations of O2 not exceeding 40%, and patients are able to achieve a PO2 greater than 60 mm Hg.


However, patients with chronic hypercapnia may be subject to further increases in PCO2 when they receive supplemental O2 (see Chapter 18). If PCO2 rises to an unacceptably high range, the patient may require intubation and assisted ventilation with a mechanical ventilator to maintain an acceptable PCO2. Fortunately, this complication is infrequent with judicious use of supplemental O2.


In the patient with hypoxemic respiratory failure such as ARDS, ventilation-perfusion mismatch and shunting are responsible for hypoxemia. When a large fraction of cardiac output is being shunted through areas of unventilated lung and 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 also require ventilatory assistance, but generally for a different reason than patients with acute-on-chronic respiratory failure. In the latter, an unacceptable degree of CO2 retention is generally the indication for intubation and mechanical ventilation. In ARDS patients, oxygenation is extremely difficult to support, CO2 retention is much less frequent, and hypoxemia rather than hypercapnia is the primary indication for mechanical ventilation.


For patients with hypoxemic respiratory failure, inability to achieve a PO2 of 60 mm Hg or greater on supplemental O2 readily administered by face mask (generally in the range of 40%–60%) is often considered reason for intubation and mechanical ventilation. 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.



In the setting of ARDS, intubation and mechanical ventilation serve several useful purposes. First, high 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 Reducing Work of Breathing), allowing the patient to receive more reliable tidal volumes than he or she 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 respiratory cycle and not just during the inspiratory phase. In common usage, positive airway pressure maintained at the end of expiration in a mechanically ventilated patient is termed positive end-expiratory pressure (PEEP).



Why is positive pressure throughout the respiratory cycle beneficial for ARDS patients? Because they often have a great deal of microatelectasis resulting from fluid occupying alveolar spaces, low tidal volumes, and probably both decreased production and inactivation of surfactant. The resting end-expiratory volume of the lung (i.e., functional residual capacity [FRC]) is quite low in these patients but can be increased substantially by administration of PEEP. At the higher FRC, many small airways and alveoli that formerly were collapsed and received no ventilation are opened and capable of gas exchange. Therefore, blood supplying these regions no longer courses through unventilated alveoli and now can be oxygenated. 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.



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 then can be lowered, and the patient is less likely to experience O2 toxicity from extremely high concentrations of O2.



Reducing Work of Breathing


One pathophysiologic feature shared by most patients with respiratory failure is an imbalance in the work of breathing relative to the ability of the respiratory muscles to perform that work. In the case of acute-on-chronic respiratory failure in the patient with chronic obstructive lung disease, the flattened and mechanically disadvantaged diaphragm must cope with an increase in airway resistance. In neuromuscular disease in either the purely acute or the acute-on-chronic setting, respiratory muscle strength may be insufficient to handle even a relatively normal work of breathing. In the patient with ARDS, the noncompliant (i.e., stiff) lungs require an inordinately high work of breathing even though respiratory muscle strength may be intact.


Consequently, ventilatory assistance in the patient with respiratory failure is important not only for temporary support of gas exchange but also for mechanical support of inspiration, allowing the respiratory muscles to rest. Dyspnea is often alleviated when such support is provided and the patient no longer must expend so much energy on the act of breathing. Fatigued respiratory muscles are allowed to recover, and the relatively large amount of blood flow required by overworking respiratory muscles can be shifted to perfusion of other organ systems.




Mechanical Ventilation


Mechanical ventilators are critical to effective management of respiratory failure. By supporting gas exchange and assisting with the work of ventilation for as long a period as necessary, mechanical ventilators can keep a patient alive while the acute process precipitating respiratory failure is treated or allowed to resolve spontaneously. This section briefly describes the operation of mechanical ventilators, the available modes of ventilation, and the complications that can ensue from their use.


Ventilators currently used for management of acute respiratory failure are positive-pressure devices: they deliver gas under positive pressure during inspiration. Most commonly, the ventilator is used in a volume-cycled fashion, meaning each inspiration is terminated (and passive expiration allowed to occur) after a specified volume has been delivered by the machine. In contrast, in pressure-limited ventilation

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Jun 12, 2016 | Posted by in RESPIRATORY | Comments Off on Management of Respiratory Failure

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