28: Classification and pathophysiologic aspects of respiratory failure
OUTLINE
Definition of Respiratory Failure, 330
Classification of Acute Respiratory Failure, 331
Hypoxemic Type, 331
Hypercapnic/Hypoxemic Type, 331
Presentation of Gas Exchange Failure, 332
Pathogenesis of Gas Exchange Abnormalities, 332
Hypoxemic Respiratory Failure, 332
Hypercapnic/Hypoxemic Respiratory Failure, 333
Clinical and Therapeutic Aspects of Hypercapnic/Hypoxemic Respiratory Failure, 334
Many types of respiratory disease may impair the normal function of the lung as a gas-exchanging organ. In some cases, the degree of impairment is mild, and the patient suffers relatively few consequences. In other cases, dysfunction is marked, and the patient experiences disabling or life-threatening clinical sequelae. When the respiratory system can no longer function to keep gas exchange at an acceptable level, the patient is said to be in respiratory failure, irrespective of the underlying cause.
The tempo for development of respiratory failure varies, depending on the nature of the underlying problem. Many of the diseases discussed so far, such as chronic obstructive pulmonary disease (COPD) and diffuse parenchymal (interstitial) lung diseases, are characterized by a chronic clinical course accompanied by relatively slow deterioration of pulmonary function and gas exchange. However, because of limited pulmonary reserve, patients with preexisting pulmonary disease are also susceptible to episodes of acute respiratory failure, either from a superimposed intercurrent illness or from transient worsening of their underlying disease. On the other hand, acute or subacute respiratory failure also can develop in individuals without preexisting lung disease. The initiating problem in these patients is often a primary respiratory illness or a disorder of another organ system accompanied by major respiratory complications.
This chapter presents an overview of the problem of respiratory failure and discusses the different pathophysiologic types and consequences of respiratory insufficiency. Chapter 29 addresses a specific
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form of acute respiratory failure known as acute respiratory distress syndrome (ARDS), which does not require the presence of preexisting lung disease. Chapter 30 considers some principles of management of respiratory failure, as well as specific modalities of current therapy.
Definition of respiratory failure
Respiratory failure is best defined as the inability of the respiratory system to maintain adequate gas exchange. Exactly where to draw the line for “adequate gas exchange” is somewhat arbitrary, but in a previously normal individual, arterial PO2 less than 60 mm Hg or PCO2 greater than 50 mm Hg generally is considered evidence for acute respiratory failure. In the individual with preexisting lung disease, the situation is more complicated because the patient chronically has impaired gas exchange and abnormal blood gas values.
For patients with normal baseline arterial blood gas measurements, criteria for respiratory failure are PO2 less than 60 mm Hg or PCO2 more than 50 mm Hg.
For example, it would not be unusual for a patient with significant COPD to perform daily activities with PO2 approximately 60 mm Hg and PCO2 50 to 55 mm Hg. By the blood gas criteria just mentioned, this patient is always in respiratory failure, but the condition obviously is chronic, not acute. A look at the patient’s pH value shows that the kidneys have compensated for the CO2 retention, and the pH is not far from the normal value of 7.40.
At which point is the condition called acute respiratory failure? Certainly if an acute respiratory illness such as an acute pneumonia develops, the patient’s gas exchange becomes even worse. PO2 falls further, and PCO2 may rise even higher. In this case, acute respiratory failure is defined as a significant change from the patient’s baseline gas exchange status. If the patient’s usual arterial blood gases are known, the task is easier. If the blood gases are not known, the pH value can provide a clue about whether the patient’s CO2 retention is acute or chronic. When a patient is seen initially with PCO2 70 mm Hg, the implications are quite different if the accompanying pH value is 7.15 as opposed to 7.36.
Classification of acute respiratory failure
Hypoxemic type
In practice, it is most convenient to classify acute respiratory failure into two major categories based on the pattern of gas exchange abnormalities. In the first category, hypoxemia is the major problem, with the patient’s PCO2 normal or low. This condition is the hypoxemic variety of acute respiratory failure. For example, localized diseases of the pulmonary parenchyma (e.g., pneumonia) can result in this type of respiratory failure if the disease is sufficiently severe. However, an even broader group of etiologic factors causes hypoxemic respiratory failure by means of increased permeability of pulmonary capillaries, leading to leakage of fluid from the pulmonary capillaries into alveolar spaces and a generalized increase in fluid within alveoli. The latter problem is frequently called ARDS and can be the consequence of a wide variety of disorders that cause an increase in pulmonary capillary permeability.1 Because of the importance of this syndrome as a major form of acute respiratory failure, Chapter 29 focuses entirely on the problem of ARDS. Another relatively common cause of hypoxemic respiratory failure is hydrostatic pulmonary edema due to heart failure or renal failure.
Categories of acute respiratory failure:
1.Hypoxemic (with normal or low PCO2)
2.Hypercapnic/hypoxemic
Examples of hypoxemic respiratory failure:
1.Severe pneumonia
2.ARDS
3.Hydrostatic pulmonary edema from decompensated heart failure or renal failure
Hypercapnic/hypoxemic type
In the second category, hypercapnia is present. For the respiratory failure to be considered acute, the pH must show absent or incomplete metabolic compensation for the respiratory acidosis. From the discussion of alveolar gas composition and the alveolar gas equation in Chapter 1, it is apparent that hypercapnia is associated with decreased arterial PO2 because of altered alveolar PO2. Therefore, even if ventilation and perfusion are relatively well matched and the fraction of blood shunted across the pulmonary vasculature is not increased, arterial PO2 falls in the presence of hypoventilation and consequent hypercapnia. In practice, many cases of hypercapnic respiratory failure also have marked ventilation-perfusion mismatch, which further accentuates the hypoxemia. With these concepts in mind, it is clear that the hypercapnic form of respiratory failure typically involves both hypercapnia and hypoxemia, and thus is more appropriately considered the hypercapnic/hypoxemic form of respiratory failure.
A number of types of respiratory disease are potentially associated with this second form of respiratory failure. How the various disorders result in hypercapnic/hypoxemic respiratory failure is explained in the “Pathogenesis of Gas Exchange Abnormalities” section of this chapter. These disorders primarily include: (1) depression of the neurologic system responsible for respiratory control; (2) disease of the respiratory bellows, either the chest wall or the neuromuscular apparatus responsible for thoracic expansion; and (3) COPD. More than one of these three problems commonly ares present, compounding the potential for respiratory insufficiency.
Causes of hypercapnic/hypoxemic respiratory failure:
1.Depression of central nervous system ventilatory control
2.Disease of the respiratory bellows
3.COPD
In the hypercapnic/hypoxemic form of respiratory failure, patients often have preexisting disease causing either chronic respiratory insufficiency or limitations in respiratory reserve, making them much more susceptible to decompensation with an acute superimposed problem. This form of respiratory failure is called acute-on-chronic respiratory failure, reflecting prior problems or limitations with respiratory reserve. This expression is used most commonly to describe the patient with COPD in whom acute respiratory failure develops at the time of an infection or another acute respiratory insult.
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Presentation of gas exchange failure
When acute respiratory failure develops, the patient’s symptom complex generally includes the manifestations of hypoxemia, hypercapnia, or both, accompanied by the specific symptoms related to the precipitating disorder. Dyspnea is present in the majority of cases and is the symptom that often suggests to the physician the possibility of respiratory failure.
Clinical presentation with respiratory failure may consist of:
1.Dyspnea
2.Impaired mental status
3.Headache
4.Tachycardia
5.Papilledema (with ↑ PCO2)
6.Variable findings on lung examination
7.Cyanosis (with severe hypoxemia)
Changes in mental status are frequent results of either hypoxemia or hypercapnia. Patients may become disoriented, confused, and unable to conduct their normal level of activity. With profound hypercapnia, patients may become stuporous and eventually lapse into a coma. Headache is a common finding in patients with hypercapnia; dilation of cerebral blood vessels as a consequence of increased PCO2 is probably an important factor in its pathogenesis.
Physical findings associated with abnormal gas exchange are relatively few. Patients may be tachypneic, tachycardic, and restless, findings that are relatively nonspecific. Examination of the optic fundi may reveal papilledema (swelling and elevation of the optic disk) resulting from hypercapnia, cerebral vasodilation, and increased intracranial pressure. Findings in the lung are related to the specific form of disease present—for example, wheezing and/or rhonchi in COPD, or crackles due to fluid in the small airways and alveolar spaces. When hypoxemia is severe, patients may become cyanotic, which is apparent as a dusky or bluish hue to the nail beds and mucous membranes. Of note, a critical amount of deoxygenated hemoglobin is required for cyanosis to manifest, and anemic patients may not become cyanotic despite profound hypoxemia.
Pathogenesis of gas exchange abnormalities
The basic principles of abnormal gas exchange were discussed in Chapter 1. The focus here is on applying these principles to patients with respiratory failure. A discussion of hypoxemic respiratory failure is followed by a discussion of hypercapnic/hypoxemic failure.
Hypoxemic respiratory failure
In patients with hypoxemic respiratory failure, two major pathophysiologic factors contribute to lowering of arterial PO2: ventilation-perfusion mismatch and shunting. In patients with significant ventilationperfusion mismatch, regions with a low ventilation-to-perfusion ratio return relatively desaturated blood to the systemic circulation. What sorts of problems cause a decrease in ventilation relative to perfusion in a particular region of the lung? If an alveolus or a group of alveoli is partially filled with fluid, only a limited amount of ventilation reaches that particular area, whereas perfusion to the region may remain
relatively preserved. Similarly, if an airway supplying a region of lung is diseased, either by pathology affecting the airway wall or by secretions occupying the lumen, then ventilation is limited.
When these problems become extreme, ventilation to a region of perfused lung may be totally absent so that a true shunt—perfusion without ventilation—exists. For example, alveoli may be completely filled with fluid, or an airway may be completely obstructed, preventing any ventilation to the involved area. Although the response of the pulmonary vasculature is to constrict and thereby limit perfusion to an underventilated or unventilated portion of the lung, this protective mechanism often cannot fully compensate for the loss of ventilation, and hypoxemia results. Of note, inflammation in the lung, as occurs in the presence of pneumonia, tends to decrease the effectiveness of hypoxic vasoconstriction and further worsen ventilation-perfusion matching. Alveolar filling with fluid and collapse of small airways and alveoli seem to be the main pathogenetic features leading to ventilation-perfusion mismatch and shunting in ARDS (see Chapter 29). An earlier consideration of the ability of supplemental O2 to raise PO2 in conditions of ventilation-perfusion mismatch versus shunt indicated that O2 cannot improve PO2 substantially for truly shunted blood (see Chapter 1). Therefore, when the shunt fraction of cardiac output is quite high, oxygenation may be helped much less than expected by administration of high concentrations of supplemental O2.
Despite the marked derangement of oxygenation in ARDS, CO2 elimination typically remains adequate because, at least early in the course of the syndrome, patients are able to maintain alveolar ventilation at an acceptable level. Even when regions of the lung have a high ventilation-perfusion ratio and thus effectively act as dead space, patients are generally able to compensate by increasing their overall minute ventilation.
Hypercapnic/hypoxemic respiratory failure
In the hypercapnic form of respiratory failure, patients are unable to maintain a level of alveolar ventilation sufficient to eliminate CO2 and keep arterial PCO2 within the normal range. Because ventilation is determined by a sequence of events ranging from generation of impulses by the respiratory controller to movement of air through the airways, there are multiple stages at which problems can adversely affect alveolar ventilation. This sequence is shown in Fig. 28.1, which also lists some of the disorders that can interfere at each level. Recall that only alveolar ventilation participates in gas exchange. Thus, if the proportion of each breath going to dead space (i.e., ratio of volume of dead space to tidal volume [VD/VT]) increases substantially, alveolar ventilation may fall to a level sufficient to cause elevated PCO2, even if total minute ventilation is preserved.
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