Impending or established respiratory failure is a common reason for admission of patients to the intensive care unit (ICU). The application of an artificial airway and mechanical ventilation support does not mean the patient has acute respiratory failure (ARF), as many patients in the ICU require airway support but only for short times. Acute respiratory failure is defined as a sudden deterioration of the ability to maintain alveolar–blood gas exchange. When confronted with a patient in ARF, the first priority is to identify and treat redeemable causes. Examples include a pneumothorax requiring a chest tube, acute pulmonary edema requiring diuresis, or an acute asthma exacerbation that may respond to bronchodilator therapy. In the absence of a readily reversible cause, most patients with ARF require mechanical ventilation, compelling a more involved ventilatory stay. Maintaining adequate arterial oxygenation while protecting the functional lung is the goal of highest priority in both traditional and more recent approaches to pulmonary management. The second goal is to determine and treat the underlying pathophysiologic condition whenever possible. The purpose of this article is to discuss the evaluation of gas exchange failures, pulmonary mechanics, and the properties of obstructive airway disease as they relate to ARF. More detailed and specific discussions of these and other particular states are included in other chapters.

The primary goal of the pulmonary system is to promote an appropriate and reasonable gas exchange at the alveolar–capillary surface, generally evaluated at the bedside via pulse oximetry, measurement of arterial blood gases, and end-tidal CO₂ monitoring. Pulmonary function may be simply classified into ventilation and oxygenation, with ventilation and oxygenation further quantified by the ability of the respiratory system to eliminate CO₂ and form oxyhemoglobin. Although multiple factors (such as percent of atmospheric pressure that is oxygenated: F_io₂) affect this gas exchange, the most basic properties involve alveolar recruitment and recoil, a narrow distance between each alveoli, and its dedicated capillaries and effective blood flow past the alveoli (Fig. 1). With this understanding of the basic physiology, it becomes clear that the measures of gas exchange are of the utmost importance in evaluating lung function.

Fig. 1 Normal alveolar to capillary relationships.

As stated previously, ARF is the inability to maintain alveolar–blood gas exchange, resulting in a failure to remove CO₂ (due to hypoventilation) and/or failure to promote appropriate and proportionate O₂ uptake at the alveolar–capillary interface. One can evaluate the amount of O₂ added into the blood from the pulmonary circulation and the amount of CO₂ being removed from the blood in the pulmonary circulation by evaluating (via arterial blood gases) the amount of dissolved (P: pressure of) arterial O₂ as well as dissolved (P: pressure of) arterial and exhaled CO₂ (end-tidal CO₂).

Respiratory distress is the hallmark of ARF but hypoxemia may first present as an alteration in mental status or significant tachycardia. Hypercarbia may present in the same way. Typically the cutoff values for ARF are Pao₂ below 60 mm Hg and Paco₂ above 50 mm Hg while breathing room air (contextual atmospheric pressure).

Oxygenation failure is typically labeled type I (hypoxemic), whereas type II (hypercapnic) is ventilation failure. A wide variety of disease states manifest respiratory failure of types II and I simultaneously (Table 1), creating a single or mixed respiratory failure. Although ARF is typically a mixed disorder, it may be helpful to consider these problems separately.

Table 1 Differentiation of respiratory failure

The goal of respiratory monitoring in any setting is to allow the clinician to ascertain the status of the patient’s ventilation and oxygenation. The primary responsibility of the clinician is to identify and treat life-threatening conditions.

One of the simplest methods of evaluating patients and diagnosing or discussing their failure relates to the understanding of basic gas exchange.

There are four primary problems that promote interference with the normal oxygenation of the arterial blood: hypoventilation, intrapulmonary shunt, diffusion impairment (altered diffusion distance), and ventilation perfusion mismatch (V̇/Q̇).

Hypoventilation

Although hypoxemia is not the most significant symptom of hypoventilation, it is a diagnostic factor. When minute ventilation (V_E) falls, Paco₂ will increase. In fact, so related is this property that if alveolar ventilation is halved, the Paco₂ will double. For hypoventilation to be the cause of hypoxemia, the arterial Paco₂ must be elevated (Fig. 2).

Fig. 2 Hypoventilated lung: alveoli to capillary relationships.

Clinical suspicion + high Paco₂ and low Pao_2. Responds to increase in V_E and/or high-flow oxygen.

Diffusion Distance

O₂ and CO₂ must cross the barrier created by the alveolar epithelium, the interstitial space and the capillary endothelium. That space between is typically fluid and product free, allowing gas to move rapidly across it. Diffusion is affected when an increase in anatomic distance and/or product (fluid, proteins, neutrophils) alters the ability of gas exchange between alveoli and capillary bed. Extravascular fluid is created when there is high pulmonary vascular pressure due to heart failure, loss of capillary barriers or high hydrostatic pressures, interferes with diffusion.

The gas in both directions must pass through the interstitial space that separates the alveoli and the capillary. Normally, equilibrium is achieved, that is, the PAo₂ will roughly equal the Pao₂. Whenever the interstitial space is widened, due to fluid or proteinaceous substance, oxygen exchange will decrease substantially. Paco₂ is generally unaffected in these disorders and the patient’s Pao₂ is generally corrected by administering higher F_io₂ to the patient (Fig. 3).

Fig. 3 Widened diffusion distance: alveoli to capillary relationships.

Clinical suspicion + low Pao₂ and normal Paco_2. Responds to high flow oxygen and F_io_2.

Intrapulmonary Shunt

Right to left: Q_S/Q_T blood flow shunted/total blood flow

Proportionately low O₂ in the arterial blood or higher than expected CO₂ occurs when gas (alveoli) and blood (pulmonary capillaries) do not maximally exchange. Blood is allowed to pass from the right heart (mixed venous) to the left heart without being oxygenated. Whenever there is congenital dysfunction, profound consolidation, or dysfunctional alveoli that limit gas exchange, a shunt may occur. In addition, underventilated or unventilated alveoli also participate in the increase of shunt fraction. Shunt calculates the amount of blood passing from the right side of the heart through the pulmonary circulation and on to the left heart and then into the general circulation without receiving adequate oxygenation. This process commonly occurs when alveoli are not recruited on inspiration due to atelectasis, significant loss of the membrane integrity and surfactant, or the alveoli are flooded with fluid related to high pulmonary pressures and extravascular edema (Fig. 4).

Fig. 4 Derecruited alveoli shunt: alveoli to capillary relationships.

A mathematical formula, based on both a mixed venous and systemic arterial blood gas, provides a calculation of intrapulmonary shunting. Normal physiologic shunt is 3% to 4% and may increase to 15% to 20% with acute respiratory distress syndrome (ARDS). The routine measurements of arterial blood gases (ABGs), chest radiograph, A-a gradient (A − a)D0₂, and Pao₂/F_io₂ (P/F) ratio and the presence of refractory hypoxemia are more routinely used to support the assumption of shunt. Primary causes of intrapulmonary shunt are atelectasis and ARDS.

The greater the contribution from alveoli with mismatch (increasing shunt), the greater difference in or widening of the A-a gradient (A − a)D0₂ occurs. When the F_io₂ is above 0.21, the A-a gradient (A − a)D0₂ becomes less accurate in the measurement of proportional gas exchange, although the difference should always be less than 150 mm Hg.

Clinical suspicion + low Pao₂ and normal Paco_2. Does not respond to high flow oxygen and F_io_2.

Alveolar Dead Space Ventilation

Alveolar dead space ventilation occurs when there are primary problems with pulmonary perfusion. Alveoli may be functional, compliant, and elastic, but in this condition the perfusion is proportionately lower than the ventilation. This is measured or evaluated as a high V̇/Q̇ mismatch, that is, ventilation is proportionately greater than perfusion. This is frequently seen with low cardiac output states, or pulmonary embolus (Fig. 5).

Fig. 5 Dead space: alveolar to capillary relationships.

Clinical suspicion + low Pao₂ and normal to high Paco_2. Does not respond to high flow oxygen and F_io_2. The ETco₂ gradient is wide as Paco₂ is greater than ETco₂.

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