1. Normally mean airway pressure is slightly negative (below atmospheric) during inspiration (Figure 41-1, A).

2. Because positive pressure ablates the normal mechanisms for gas movement, intrapulmonary pressures are usually supraatmospheric (see Figure 41-1, B).

3. The extent that intrapulmonary pressure is increased depends on

1. Transmission of intrapulmonary pressure to the intrathoracic space depends on pulmonary and thoracic compliance. The stiffer the lung, generally the lower the amount of pressure transmitted from the intrapulmonary to the intrathoracic space. In contrast, the stiffer the thorax, the greater the amount of pressure transmitted to the intrathoracic space.

2. In most patients requiring mechanical ventilation, the mean intrathoracic pressure changes from negative to positive.

1. Because intrathoracic pressures become positive with the application of mechanical ventilation, the thoracic pump mechanism assisting venous return is eliminated.

2. As a result the pressure gradient favoring venous flow to the right side of the heart is decreased and right ventricular filling is impaired.

3. Positive pressure, especially positive end-expiratory pressure (PEEP), also increases pulmonary vascular resistance, which decreases right ventricular filling and cardiac output.

4. Positive pressure also increases right ventricular afterload and can result in right ventricular hypertrophy with a shift in the ventricular septum and compromised left ventricular function.

5. However, in patients with left ventricular dysfunction positive pressure may decrease left ventricular afterload, increasing cardiac output and left ventricular function.

6. Frequently the decreased transmural pressure across the vena cava is large enough to require fluid therapy to maintain appropriate right ventricular filling as mechanical ventilation is initially applied.

7. Most patients are hypoxemic, acidotic, and hypercapnic before the institution of mechanical ventilation, which causes an increased sympathetic tone. The normalization of acid-base balance, the relief of hypoxemia, and the decrease in work of breathing (WOB) with mechanical ventilation result in a marked decrease in sympathetic tone. This may result in

1. Because venous return and sympathetic tone are decreased, there is some decrease in cardiac output.

2. With appropriate fluid therapy and pharmacologic support, adequate cardiac output can be maintained.

1. Because venous return is decreased, blood pools in the periphery and in the cranium.

2. The increased volume of blood in the cranium increases ICP.

1. Decreased cardiac output results in decreased renal blood flow, which alters renal filtration pressures and decreases urine formation.

2. Decreased venous return and decreased right atrial pressures are interpreted as a decrease in overall blood volume. As a result, antidiuretic hormone levels and natriuretic peptide levels are increased and urine formation is decreased (see Chapters 13 and 14).

1. Because the ventilator provides at least part of the force necessary to ventilate, the patient’s WOB decreases.

2. The amount of work performed by the ventilator and the amount performed by the patient vary, depending on the approach used to ventilate and the actual setting of ventilating parameters.

1. Positive pressure causes a mechanical dilation of the conducting airways.

2. The transmural pressure gradients affecting the airways are always greater than during normal spontaneous ventilation.

3. However, intubation usually results in an increase in resistance to flow in the upper airway and puts the patient at risk for contamination of the lower respiratory tract.

1. Because positive pressure distends conducting airways and inhibits venous return, the portion of the Vt that is deadspace increases.

2. There also is an alteration in the normal distribution of ventilation. A greater percentage of ventilation goes to the apices and less to the bases than in spontaneous ventilation.

3. Normal deadspace/Vt ratios are 0.20 to 0.40; however, mechanical ventilation will cause these ratios to increase to 0.40 to 0.60 in the normal individual.

4. The level of ventilation required by a patient depends on the Paco₂, alveolar ventilation, and tissue CO₂ production.

< ?xml:namespace prefix = "mml" />Paco2∝V˙co2/V˙A (1)

(1)

    or

Paco2=(V˙co2×0.863) (V˙E×[1–VDVT]) (2)

(2)

    where co₂ CO₂ is CO₂ production, _A is alveolar ventilation, _E is minute ventilation, Vd is deadspace volume, and Vt is tidal volume.

1. With positive pressure ventilation, gas distribution and pulmonary perfusion are altered.

2. Ventilation to the most gravity-dependent aspects of the lung is decreased, whereas blood flow to these areas is increased.

3. Normal intrapulmonary shunts are approximately 2.0% to 5.0%; however, mechanical ventilation may increase the shunt fraction to approximately 10% in the normal individual.

4. Allowing some level of spontaneous ventilation (triggering the breath) minimizes the ventilation/perfusion mismatch.

1. The stress produced by positive pressure ventilation may lead to increased gastric secretion and gastric bleeding, resulting in the development of stress ulcers.

2. Agents that maintain gastric acidity may be useful to prevent ventilator-associated pneumonia (VAP).

3. Gastric distention does develop in some patients as a result of aerophagia (swallowing of air), requiring the use of a nasogastric tube.

1. Many patients mechanically ventilated develop ventilator-associated pneumonia (VAP).

2. VAP is not a result of the ventilator circuit if appropriate precautions are taken (see Chapter 3).

3. VAP is a result of aspiration of contaminated oral and gastric secretions.

4. The incidence of VAP can be reduced by

1. Appropriate nutritional support is difficult during mechanical ventilation.

2. Respiratory muscle wasting and an increased risk of pneumonia and pulmonary edema develop if patients are underfed.

3. Ventilatory requirements are increased because of increased CO₂ production if patients are overfed.

1. Mechanical ventilation disturbs normal sleep patterns.

2. Sleep deprivation may produce delirium, patient-ventilatory dys-synchrony, and sedation-induced ventilator dependency.

1. Insomnia

2. Anxiety

3. Frustration

4. Depression

5. Apprehension

6. Fear

1. Oxygen toxicity

2. Barotrauma

3. Volutrauma

4. Atelectrauma

5. Biotrauma

1. High inhaled oxygen concentrations result in the formation of oxygen free radicals (e.g., superoxide, hydrogen peroxide, and hydroxyl ion).

2. These free radicals cause ultrastructional changes in the lung similar to acute lung injury (ALI).

3. In animal models inhalation of 100% oxygen causes death in 48 to 72 hours.

4. Healthy volunteers breathing 100% oxygen develop inflammatory airway changes in 24 hours.

5. However, concern regarding oxygen toxicity should never prevent the use of a high F_IO₂ in a patient who is hypoxemic.

6. An F_IO₂ of 1.0 should always be used

7. But F_IO₂ should always be lowered as soon as possible to the lowest level maintaining the Pao₂ >60 mm Hg.

8. Concerns about oxygen toxicity should not override concerns about tissue hypoxia.

9. Ideally the F_IO₂ should be maintained ≤0.6 to minimize concerns regarding toxicity.

10. There is some evidence that the presence of severe lung injury provides protection from oxygen toxicity.

1. Barotrauma is the most acute and immediately severe form of ventilator-induced lung injury.

2. Barotrauma is literally air within a body space or compartment.

3. It is a result of disruption of the alveolar capillary membrane that allows air to dissect along fascial planes and accumulate within the pleural space or some other compartment (Figure 41-2).

4. The higher the peak alveolar (plateau) pressure and the greater the lung disease, the greater the likelihood of barotrauma.

5. Subcutaneous emphysema is air within the tissue.

6. The development of barotrauma can be minimized by limiting the peak alveolar pressure.

1. Volutrauma is lung parenchymal damage similar in presentation to acute respiratory distress syndrome (ARDS).

2. Volutrauma is a result of localized overdistention of the lung.

3. It is manifested by an increase in the permeability of the alveolar capillary membrane, the development of pulmonary edema, the accumulation of neutrophils and protein, the disruption of surfactant production, the development of hyaline membranes, and a decrease in compliance of the lung.

4. Overdistending volume is best determined by assessing transpulmonary pressure (alveolar-pleural pressure).

5. Ideally to prevent volutrauma P_plat should be maintained <25 cm H₂O in all patients.

6. If the P_plat is <25 cm H₂O, Vts of 6 to 10 ml/kg ideal body weight (IBW) can be used.

7. IBW is determined by the following formulas.

Male=50+2.3[height(inches)–60] (3)

(3)

Female=45.5+2.3[height(inches)–60] (4)

(4)

8. If the P_plat is 25 to 30 cm H₂O Vts should be maintained between 5 and 8 ml/kg IBW.

9. If the P_plat is ≥30 cm H₂O, Vt should be ≤6 ml/kg IBW.

1. Ventilator-induced lung injury is caused by the recruitment and derecruitment of unstable lung units during each ventilator cycle.

2. Disruption of the alveolar capillary membrane is caused by the stress and strain exerted on the alveolar wall by lung recruitment.

3. The application of 30 cm H₂O to an open lung unit can result in the development of approximately 140 cm H₂O stress on the wall of the collapsed alveoli adjacent to it.

4. This repeated stress with each breath causes injury.

5. To avoid this form of lung injury adequate PEEP must be applied to avoid the end-expiratory collapse of unstable lung (see Chapter 40) (Figure 41-4).

6. As a general rule the following levels of PEEP should be applied to mechanically ventilated patients.

1. The activation of inflammatory mediators in the lung by the use of an overdistending Vt and repetitive opening and closing of unstable lung units.

2. This can cause inflammatory injury to the lung.

3. There also are good animal data to indicate that cells and other substances can be translocated from the lung to systemic circulation by inappropriate ventilatory patterns, resulting in lung injury.

4. The translocated inflammatory mediators can cause injury to other organs.

5. Clinical studies clearly show that systemic inflammatory mediator levels are decreased by a ventilatory pattern that is lung protective.

6. Many believe that multisystem organ failure can be caused by the use of inappropriate ventilatory patterns.

1. This term refers to a ventilatory pattern that prevents the lung from the development of ventilator-induced lung injury.

2. The key aspects of this pattern are

1. This is a clinical impression based on serial laboratory data and clinical findings indicating that the patient is progressing toward ventilatory failure.

2. Clinical problems frequently resulting in impending acute ventilatory failure may be categorized as

3. Clinical evaluation of the patient in impending acute ventilatory failure

1. An inability to oxygenate without failure to ventilate is an unlikely indication for mechanical ventilation.

2. In most settings oxygenation problems can be managed with oxygen therapy, continuous positive pressure ventilation via mask, and cardiovascular stabilization.

3. However, there are some patients in whom the increased WOB caused by a failure to oxygenate leads to ventilatory failure and the need for intubation and mechanical ventilation.

1. In this setting care must be taken to ensure that the ventilator provides a sufficient Vt and adequate peak flow rate is delivered in an appropriate time to meet the patient’s ventilatory demand.

2. During volume ventilation when patients are sedated and ventilation changes from assisted to controlled, peak airway pressure generally increases because the patient no longer is providing muscular effort assisting in gas delivery.

3. During pressure ventilation Vt decreases when the transition is made from assisted to controlled ventilation for the same reason.

1. Trigger sensitivity

2. Initial flow rate

3. Flow pattern

4. Ti

5. Vt

1. Figure 41-5 illustrates the effect of an inadequate peak inspiratory flow rate on patient effort.

2. The ideal relationship between patient effort and ventilator response to a volume-targeted breath is depicted in Figure 41-5, A. The airway pressure versus time curve during assisted ventilation should be the same as that during controlled ventilation except for the pressure decrease to trigger the ventilator.

3. The greater the difference between these two curves, the greater the WOB performed by the patient.

4. In Figure 41-5, B, the dotted line is the airway pressure curve during assisted ventilation, and the hatched area between the solid and dotted lines represents the work done by the patient. The greater the area, the greater the patient work.

5. Any time the airway pressure curve is concave or not matching the idealized curve, the patient is performing much of the WOB.

6. By increasing the peak inspiratory flow, patient work can be minimized.

a. Figure 41-6 illustrates the impact of increasing peak flow and decreasing Ti on the airway pressure curve and patient WOB.

b. As you go from left to right in Figure 41-6, patient effort decreases because peak flow increases.

c. In most adults receiving assisted volume-targeted ventilation, peak flows ≥80 L/min are needed to meet patient demand.

1. Essentially two waveforms are available during volume-targeted ventilation.

2. With square wave flow, gas flow is constant throughout inspiration.

3. With decelerating flow, gas flow peaks at the onset of inspiration and decreases as inspiration continues.

4. During assisted ventilation a decelerating flow pattern generally is most useful because it allows a high initial peak flow to meet patient demand but decelerates over time, ensuring that Ti will be long enough to match patient demand.

5. With a decelerating flow pattern compared with a square wave flow pattern

6. During controlled ventilation either a square or decelerating flow pattern can be used.

1. In most patients a Ti of ≤1.0 second is most appropriate.

2. Some markedly stressed patients desire a Ti as short as 0.6 second.

3. Patients with chronic restrictive lung disease may desire a Ti of 0.5 second.

4. Regardless of the use of pressure or volume ventilation, Ti during patient-triggered ventilation should always match the patient’s desired Ti.

1. The average resting Vt of all mammals is approximately 6.0 ml/kg IBW.

2. As a result patients requiring ventilatory support if not stressed should also require an actual delivered Vt of approximately 6.0 ml/kg IBW.

3. However, the Vt desired by many patients is greater because of an increased ventilatory demand.

4. As discussed in Section II, Ventilator-Induced Lung Injury, the greater the Vt, the greater the potential for end-inspiratory overdistention. As a result Vt should be related to P_plat.

1. As discussed in Chapter 39, pressure ventilation is better able to meet the ventilatory demands of the stressed patient than volume ventilation.

2. Because flow delivery in pressure ventilation increases as demand increases, adequate flow is provided unless the pressure level is too low.

3. With pressure ventilation adjustments of the following may be needed to ensure synchrony.

4. Pressure level may be either too high or too low.