Chapter 1

Approach to Acute Respiratory Failure

Arguably, more than any other device, mechanical ventilators symbolize intensive care and intensive care units (ICUs). Ventilators provide the most basic form of life support to critically ill or injured patients. The nearly ubiquitous presence of mechanical ventilators in ICUs reflects how commonly patients in the ICU have acute respiratory failure. In caring for these patients, ICU clinicians must decide when to start, change, or stop assisted ventilation. Knowing the mechanism that caused a patient’s acute respiratory failure helps in making these decisions and in determining what needs to improve so that the patient can breathe spontaneously again.

Despite having many causes, acute respiratory failure results from only a few basic pathophysiologic mechanisms. Thus, a mechanism-based approach to evaluation and management can be applied to a wide spectrum of patients with acute respiratory failure of different causes. Knowing the mechanism of respiratory failure involved in specific clinical disorders allows the ICU clinician to direct treatment effectively and efficiently.

Definitions

Acute respiratory failure is the final common pathway for diverse clinical disorders. Acute refers to an onset usually measured in terms of hours or days (i.e., less than 7 days) . Respiratory failure indicates a severe impairment of pulmonary gas exchange; it is categorized into two types. Hypercapnic respiratory failure occurs when a patient’s Paco₂ rises to greater than normal—that is, greater than 45 mm Hg. Hypoxemic respiratory failure occurs when a patient’s Pao₂ falls so low that it is life-threatening or has serious adverse physiologic effects. For example, in cases of acute hypoxemic respiratory failure, Pao₂ is often less than 55 mm Hg despite the administration of high, potentially toxic concentrations of oxygen. A Pao₂ of 55 mm Hg corresponds to a modestly reduced arterial hemoglobin saturation of about 88%. This is near the top of the steep part of the oxygen-hemoglobin (O₂-Hgb) dissociation curve, and further decrements result in steep, linear falls in arterial O₂ content (see Figures A1 and A2 in Appendix A for O₂-Hgb dissociation curves).

Four Components of the Respiratory System

The respiratory system can be regarded as having four functional and structural components: (1) the central nervous system (CNS) component (chemoreceptors, the controller [respiratory center in the medulla], and CNS efferents); (2) the chest bellows component (composed of the peripheral nervous system, respiratory muscles, and the chest wall and soft tissues surrounding the lung); (3) the airway component; and (4) the alveolar component. Together they form the effector arm of the respiratory system’s feedback and control loop (Figure 1.1).

Figure 1.1 The feedback loop of the respiratory system. Its effector components consist of the central nervous system (CNS) drive to ventilate, neural connections to the respiratory muscles, the muscles themselves, conducting airways, and alveoli. The controlled variables (system output) consist of minute ventilation (), alveolar ventilation (), Paco₂, and Pao₂. Changes in Pao₂ and Paco₂ are detected by peripheral and central chemoreceptors (detector), which then send information to the CNS respiratory center (controller). The controller maintains homeostasis by increasing or decreasing activity of the effector components in response to abnormalities in Pao₂ or Paco₂. (From Lanken PN: Respiratory failure. In Carlson RW, Geheb MA [eds]: Principles and Practice of Medical Intensive Care. Philadelphia: WB Saunders, 1993, pp 754-763.)

When all four components function correctly, their sequential actions result in normal pulmonary gas exchange:

1. The CNS controller initiates respiratory drive by generating neural output. The rate and intensity of its output are determined by the feedback provided by peripheral chemoreceptors (monitoring Pao₂ and Paco₂) and central chemoreceptors (monitoring Paco₂ or its effects) and by input from other neural sources.

2. The neural impulses from the CNS controller traverse the spinal cord and the phrenic and other motor neurons and reach the diaphragm and other respiratory muscles.

3. In response, these muscles expand the chest cavity, displace adjacent abdominal contents, and produce negative (subatmospheric) pleural pressure within the thorax.

4. This negative pressure is transmitted to the alveoli, creating a gradient between the alveoli and atmospheric pressure at the mouth. In response, air flows through the conducting airways to the alveoli, leading to lung inflation.

5. Finally, alveolar O₂ passively diffuses across the alveolar-capillary membrane so that red blood cells become fully equilibrated with alveolar Po₂ as they pass through alveolar capillaries. The same process, but in the reverse direction, occurs for CO₂.

Respiratory Pump and Control of Paco₂

Under normal conditions, the feedback and control loop (see Figure 1.1) maintain the system’s set point for Paco₂ at 40 mm Hg. Pathologic conditions, however, can move this set point up or down. Under such circumstances, the CNS controller tries to achieve the “proper” level of Paco₂ at this new set point by changing minute ventilation.

Because the actions of the respiratory system’s first three components (CNS, chest bellows, and airway) determine a patient’s minute ventilation, they have been called the respiratory pump. Minute ventilation can be increased or decreased by the respiratory pump by changing tidal volume, respiratory rate, or both (Box 1.1, Equation 1). Because this pump controls Paco₂ levels, failure of one or more of its components can result in hypercapnic respiratory failure.

BOX 1.1 Basic Physiologic Equations

Equation 1:

where is the expired minute ventilation, V_T is the tidal volume, and RR is the respiratory rate

Equation 2:

where K is a constant (863 mm Hg), co₂ is CO₂ production per minute, and _A is alveolar ventilation

Equation 3:

where V_A is the part of the tidal volume that contributes to alveolar ventilation, and V_D is the dead space (i.e., that part of the tidal volume not contributing to gas exchange)

Equation 4:

where _A is alveolar ventilation (_A =VA × RR), and _D is dead space ventilation (_D = V_D × RR)

Equation 5:

where RR = /V_T by rearranging Equation 1, and V_D/V_T is the dead space to tidal volume ratio

Equation 6:

where _D in Equation 4 is replaced by (V_D/V_T) as derived in Equation 5

Equation 7: /(1 – V_D/V_T)

which is derived by solving Equation 6 for

Equation 8: × (1 – V_D/V_T)

which is derived by solving Equation 6 for _A

Equation 9: Paco₂ = K × co₂/[(1 – V_D/V_T) × ]

after right-hand side of Equation 8 is substituted for _A in Equation 2

Equation 10: Paco₂ × = K × co₂/(1 – V_D/V_T)

which is derived from Equation 9 by rearrangement of the term

Equation 11: = K × co₂/[Paco₂ × (1 – V_D/V_T)]

which solves Equation 10 for

Equation 12 (Alveolar Gas Equation): Pao₂ = Pio₂ – Paco₂/R

where Pao₂ is mean ideal alveolar Po₂, Pio₂ is the inspired Po₂, Paco₂ is the alveolar Pco₂ estimated as equal to Paco₂, and R is the respiratory ratio, usually assumed to be 0.8 (except when Fio₂ = 1.0, R = 1); R is the non–steady-state equivalent of the steady-state respiratory quotient, RQ, which is defined as

Although the respiratory pump changes minute ventilation (abbreviated as , because one measures expired minute ventilation), how those changes affect Paco₂ depend on associated changes in alveolar ventilation, (Table 1.1, Equation 2). Unlike , which is measurable by a spirometer, is a theoretic quantity that cannot be measured directly but can be illustrated if the lung is viewed as a two-compartment model. In this model, the lung has an alveolar space (for gas exchange) and a dead space (for convective gas flow) (Box 1.1, Equation 3). The latter includes anatomic dead space (the trachea and other conducting airways) and alveolar dead space (alveoli with ventilation/perfusion ratios [] >1.0). In this model, minute ventilation, , is the sum of alveolar ventilation, , and dead space ventilation, (Box 1.1, Equation 4) or, alternatively, can be expressed as a function of alveolar ventilation and ratio of dead space to tidal volume () (Box 1.1, Equation 7).

If V_D/V_T and (Table 1.1, Equation 10) remain constant, Paco₂ has a hyperbolic relationship with (as the right-hand side of Equation 10 would be a constant). Figure 1.2 illustrates this relationship and how changes in affect Paco₂ at different values of V_D/V_T.