Classification and Pathophysiologic Aspects of Respiratory Failure

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Classification and Pathophysiologic Aspects of Respiratory Failure

Many types of respiratory disease are capable of impairing 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 interstitial lung disease, 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 an intercurrent illness or from transient worsening of their underlying disease. On the other hand, respiratory failure, generally acute or subacute in onset, 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 complicated by major respiratory problems.

This chapter presents an overview of the problem of respiratory failure and discusses the different pathophysiologic types and consequences of respiratory insufficiency. Chapter 28 addresses a specific form of acute respiratory failure known as acute respiratory distress syndrome (ARDS), which does not require the presence of preexisting lung disease. Chapter 29 considers some principles of management of respiratory failure, as well as specific modalities of current therapy.

Definition of Respiratory Failure

Respiratory failure probably is best defined as 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 even 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 < 60 mm Hg or PCO₂ > 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 what 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

In practice, it is most convenient to classify acute respiratory failure into two major categories on the basis of the pattern of gas exchange abnormalities. In the first category, hypoxemia is the major problem. The patient’s PCO₂ is normal or even 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 a generalized increase in fluid within the alveolar spaces, often as a result of leakage of fluid from pulmonary capillaries. 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.* Because of the importance of this syndrome as a major form of acute respiratory failure, Chapter 28 focuses entirely on the problem of ARDS.

Categories of acute respiratory failure are:

1. Hypoxemic (with normal or low PCO₂)

2. Hypercapnic/hypoxemic

Examples of hypoxemic respiratory failure are:

1. Severe pneumonia

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 fact, many cases of hypercapnic respiratory failure have marked ventilation-perfusion mismatch as well, which further accentuates the hypoxemia. With these concepts in mind, it is clear the hypercapnic form of respiratory failure generally involves not just hypercapnia; it may be 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 Pathogenesis of Gas Exchange Abnormalities. 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 is present, compounding the potential for respiratory insufficiency.

Causes of hypercapnic/hypoxemic respiratory failure are:

1. Depression of central nervous system ventilatory control

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