Acute Respiratory Failure and Intensive Measures
Keywords
• Oxygenation • Ventilation • Failure • Dynamics • Air trapping
Introduction
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.
KEY POINTS
Physiology
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: Fio2) 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.
Evaluating and Diagnosing Gas Exchange Failures
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
Type I Failure Acute Hypoxemic | Type II Failure Acute Hypercapnic |
Pao2 <60 mm Hg | Paco2 >50 mm Hg |
Patient at rest | Patient at rest |
Breathing room air (Fio2 = 0.21 or 21% of the atmospheric pressure) | Breathing room air (Fio2 = 0.21 or 21% of the atmospheric pressure) |
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.
Causes of Hypoxemia
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 (VE) 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).
Clinical suspicion + high Paco2 and low Pao2. Responds to increase in VE 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 Fio2 to the patient (Fig. 3).
Clinical suspicion + low Pao2 and normal Paco2. Responds to high flow oxygen and Fio2.
Intrapulmonary Shunt
Right to left: QS/QT 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).
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/Fio2 (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 Fio2 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 Paco2. Does not respond to high flow oxygen and Fio2.
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).
Clinical suspicion + low Pao2 and normal to high Paco2. Does not respond to high flow oxygen and Fio2. The ETco2 gradient is wide as Paco2 is greater than ETco2.
Ventilation To Perfusion: V̇/Q̇ Mismatch
This general term refers to the relationship of gas distribution (V̇) to the amount of blood (Q̇), which passes the total alveolar surface in 1 minute. Normal alveolar ventilation occurs at a rate of 4 L/min, and normal pulmonary vascular blood flow occurs at a rate of 5 L/min. The normal V̇/Q̇ ratio is therefore 4 L/min divided by 5 L/min, or a ratio of 0.8, almost in a 1:1 ratio. Any disease process that interferes with either side of the equation upsets the physiologic balance, causing a V̇/Q̇ mismatch. This mechanism is the most common, frequently seen in the face of COPD as well as vascular disorders. Factors that may affect the V̇/Q̇ ratio include hypoventilation, COPD, oversedation, and both hyperdynamic and reduced cardiac output states. Conditions in which blood flow is inadequate for achieving gas exchange are known as increased dead space ventilation.

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