OXYGEN THERAPY AND MECHANICAL VENTILATION



Correction of the severe hypoxemia by increas­ing the fractional concentration of the inspired 02 (Fi02) is useful early in the disease. However, be­cause the hypoxemia is due to shunt this is less effective than in patients with obstructive or re­strictive lung disease in which ventilation-per-fusion inequality is the major underlying mech­anism. Figure 22—3 plots the relationship between the Fi02 and arterial Po2 (Pao2) and 02 content for different levels of shunt. Increasing the Fi02 may significantly increase 02 content and thus the 02 delivery despite the negligible increase in Pao2. While 02 content can be increased substantially, a high Fto2 by itself is toxic to the lung, and thus this strategy has distinct limitations. 02 toxicity depends on a number of factors, including Fr02,duration of treatment, and the underlying con­dition of the lung. The Fi02 likely to induce tox­icity in man is unknown, although it is probable that a continuum rather than a threshold exists. As a general rule, an Fi02 above 0.60 can be tol­erated for short periods such as 24 hours, but after 72 hours 02 toxicity may contribute to further lung damage.

When adequate oxygenation cannot be main­tained by 02 therapy alone, or if hypercapnia de­velops, mechanical ventilation is essential. The positive pressure generated by the ventilator in­creases mean airway pressure, which in turn in­creases lung volume. This results in an increase in alveolar size, spreading the fluid that is present over a greater surface area and allowing gas ex­change to take place. Mechanical ventilation also reduces the 02 demands on the body caused by increased 02 consumption by the respiratory mus­cles as patients try to cope with the increased work of breathing.

An oral or nasal endotracheal tube is necessary for mechanical ventilation. While nasal tubes often seem to be more comfortable to the patient, they usually are smaller in diameter than an oral tube and tend to cause difficulties in suctioning and to increase the work of breathing during the weaning period. In addition, a tube in the naso­pharynx may lead to the development of a pu­rulent otitis media, as it interferes with eustachian tube drainage. With proper care, low compliance cuffed tubes can be left in place for at least three to four weeks. The major complication from en­dotracheal tubes is damage to the larynx resulting from tube motion as the patient moves about, which can be minimized by adequate fixation of the tube at the mouth or nose. The decision to proceed to a tracheostomy should not be made on the basis of any arbitrary time limit. Tracheos­tomy has its own complications, e.g., tracheal stenosis, which may exceed the morbidity asso­ciated with endotracheal tubes. Thus a tracheos­tomy should be performed only if it is necessary for adequate care or if it is clear that continued mechanical ventilation will be required for a pro­longed time.
Mechanical ventilators are classified on the basis of what terminates inspiratory flow. Pres­sure-cycled ventilators terminate flow when a preset pressure is reached in the airway. Conse­quently, tidal volumes and minute ventilation vary with changes in airways resistance and lung compliance, which makes them unsuitable for use in patients with ARDS. Volume-cycled ventilators provide a preset volume to the patient over a range of airway pressures. A pressure limit is set to pre­vent the development of trauma to the lung in the event of a sudden change in pulmonary mechan­ics when airway pressure increases in an attempt to achieve the required tidal volume. Although iha Drecise volume delivered to the patient may x«rv somewhat with changes in lung mechanics and compliance of the ventilator circuit, volume-cycled ventilators allow greater control of the pa­tient’s ventilation.

Mechanical ventilators can be set to operate in a variety of modes (Fig. 22-4). Controlled venti­lation, in which both tidal volume and rate are determined by the machine, are used only when the patient is unable to initiate a spontaneous breath, e.g., drug overdose, severe neuromuscular disease, muscle relaxants, or excessive sedation. The modes most commonly used in the treatment of ARDS are intermittent mandatory ventilation (IMV) and assist-control ventilation (AC). While controversy exists as to which of these modes is more effective, no good comparison has been made, and for most patients it probably makes very little difference as long as sufficient support is provided.

The goal of increased lung volume is achieved by two strategies regardless of the ventilatory mode: (1) high tidal volume, such as 10 or even 15 ml/kg rather than the normal 6 ml/kg; (2) pos­itive end-expiratory pressure (PEEP), which prevents the airway pressure from falling back to atmospheric at end-expiration. While these strategies allow inspired gas to enter previously unventilated alveoli, there is no convincing evidence that increasing lung volume alters the primary pathological process or reverses the transudation of fluid from the blood vessels into the lung. Thus, these ventilatory techniques should be used only to the degree that they may help in achieving an adequate 02 saturation (90 per cent) at a relatively nontoxic Fi02 (0.60). How­ever, improvement in arterial oxygenation by it­self is an insufficient guide to ventilatory therapy, as the increase in airway pressure may cause a fall in cardiac output with an overall reduction in 02 delivery to the tissues. Pulmonary barotrauma, manifested as subcutaneous emphysema, pneu­momediastinum, and pneumothorax, is an addi­tional serious complication.

The mechanism by which high intrathoracic pressure interferes with cardiac output is com­plex, with a reduction in venous return to the heart playing a major role. With small increases in intrathoracic pressure (5 to 10 cm of PEEP) im­pairment of cardiac output may be minimal as long as cardiac filling pressures are adequate. With higher levels of PEEP, cardiac output is in­variably reduced unless filling pressures are in­creased above normal. This reduction in cardiac output results in a decrease in 02 delivery to the tissues despite a concomitant increase in Pao2. The increase in filling pressure required to main­tain cardiac output in the face of large increases in PEEP is likely to increase the accumulation of extravascular lung water. To monitor these im­portant variables, especially in patients with a questionable cardiovascular status or those in whom high levels of PEEP are required, a flow-directed pulmonary artery catheter is often useful. The catheter is inserted at the bedside, preferably through an internal jugular vein, and is carried by the flow of blood through the right heart until its balloon occludes a pulmonary artery. In this po­sition both pulmonary artery and occlusion pres­sure (an index of left arterial pressure) can be monitored as well as cardiac output measured by thermodilution. In addition to evaluating the ad­equacy of cardiac filling pressure, the catheter is often required to distinguish between ARDS and congestive heart failure, a distinction that is dif­ficult by physical examination alone in many sick patients. The insertion and maintenance of the pulmonary artery catheter must be accomplished with great care to limit the risk of complications, including pneumothorax, myocardial or vascular perforation, bleeding, air embolism, arrhythmias, valve trauma or endocarditis, sepsis, and pul­monary infarction.

Care must be taken in interpreting readings ob­tained from the pulmonary artery catheters in pa­tients on mechanical ventilation, since a variable amount of the positive pressure applied to the lungs is transmitted to the heart. This leads to an apparent rise in vascular pressures during inspiration. The amount of the pressure transmitted de­pends on a number of complex factors, including the compliance of the lungs and the cardiovas­cular system and the intravascular volume. The vascular pressures should be read at the same point in the breathing cycle, preferably at end-expiration. This requires reading the pressures from a continuous recording, since digital dis­plays record mean pressures throughout the res­piratory cycle.

Since hypoxemia in ARDS is due to shunting of systemic venous blood through the lung, any alteration in mixed venous Po2 (Pv02) proportion­ally alters the Pao2 resulting from a given amount of shunt. Increase in the 02 consumption, de­crease in cardiac output, and fall in the hemoglo­bin concentration may all necessitate increased 02 extraction by the tissues and thus decrease Pv02. Unless this is kept in mind, it is possible that a fall in Pao2 due to one of these factors may be misinterpreted as a worsening of ARDS and corrective therapy aimed in the wrong direction.

Assessing the adequacy of 02 and ventilatory therapy in these complex conditions is a major challenge. Clearly, Pao2 is an inadequate index, since it reflects only one facet of 02 delivery (02 Del), which is defined as:02 Del = cardiac output x arterial 02 content Thus, 02 Del also includes a convection term, car­diac output, and a capacitance term, 02 content, which, in addition to Pao2, includes 02 saturation and hemoglobin concentration. All components must be adequate to ensure sufficient peripheral delivery of 02. In addition to 02 Del, tissue ox­ygenation depends on the distribution of blood flow within various tissues, about which little is known.

Is there a useful parameter to monitor which will reflect the adequacy of 02 Del? The Py02 has been suggested, but this represents the weighted mean from all the tissues and thus is markedly influenced by the distribution of blood flow. For example, in septic shock, because blood flow is redistributed to tissues with a low 02 extraction, the Pv02 may actually rise pari passu with the de­velopment of systemic acidosis. In this instance, Pv02 misrepresents the true status of 02 delivery. Lactic acidosis is a sure sign of inadequate tissue 02 Del, but since lactic acid is rapidly cleared by a well-perfused and functioning liver while its washout is delayed from poorly perfused tissues, the appearance of lactic acidosis is a late indicator of 02 deficiency. The best current indicators are the performance of the end-organs (heart, kidney, and liver).