Cairo: Pilbeam's Mechanical Ventilation, 6th Edition

Chapter 17: Effects of Positive-Pressure Ventilation on the Pulmonary System

WorkBook Answer Key

Key Terms Crossword Puzzle

Chapter Review Questions
1. Volutrauma is lung injury caused by excessive volume in the lungs. Biotrauma is caused by the release of inflammatory mediators that cause problems in other organs of the body. Atelectrauma is the term used for shear stress injury and loss of surfactant in the lungs.
2. Ventilator-induced lung injury (VILI) is a form of lung injury that occurs at the alveolar level and resembles ARDS. Ventilator-associated lung injury (VALI) includes injury caused by extra-alveolar gas, patient-ventilator dyssynchrony, air trapping, and ventilator-associated pneumonia.
3. (any of the following) High peak airway pressures with low end-expiratory pressures, presence of bullae, high levels of PEEP with high tidal volumes, aspiration of gastric acid, necrotizing pneumonias, and ALI/ARDS.
4. Subcutaneous emphysema
5. A pneumothorax
6. Treatment for a pneumothorax involves placing a 14-gauge needle (or smaller) into the anterior second to third intercostal space on the affected side in the midclavicular line over the top of the rib with the patient in the upright position.
7. The patient should be manually ventilated with a resuscitation bag using 100% supplemental oxygen; an in-line manometer should be used to monitor pressure so that it can be kept as low as possible.
8. (a) Absent breath sounds on the affected side; (b) mediastinal, and possibly tracheal, deviation away from the affected side; (c) tympanic percussion note over the affected side; and (d) neck vein distention.
9. The chest radiograph would show one diaphragm more depressed than the other and possibly a deep sulcus sign with air appearing adjacent to the depressed diaphragm.
10. Pneumoperitoneum
11. 30-35 cm H2O
12. (a) The lungs are very stiff and the pleural pressure is near normal; (b) the lungs are normal, but there is a right main stem intubation with a large tidal volume; and (c) the lungs and chest wall are normal, but the pressure around the chest is high (as with an obese patient).
13. Volutrauma, or damage from overdistention, occurs because of regional differences in lung compliance. The more compliant lung areas fill more easily and expand to accommodate large volumes, whereas noncompliant areas do not. The overdistention causes acute alveolar injury and the formation of pulmonary edema both by increased permeability and by filtration mechanisms.
14. (a) Shear stress—Shear stress occurs when an alveolus that is normally expanded is adjacent to one that is collapsed (atelectasis) and unstable, (b) alteration and washout of surfactant—In the alveolus, surfactant forms a molecular layer between the air and the liquid alveolar surface. During alveolar collapse, as the surface area of the alveolus decreases, the surfactant molecules can form together until some actually pop out or get squeezed out at low lung volumes. These “used” lipids do not rapidly spread as the alveolus reopens, (c) microvascular injury—Recall that during a positive-pressure breath, alveolar capillaries flatten out, but corner micro-alveolar vessels open wider. The interstitial areas adjacent to the corner vessels develop negative pressure relative to the inside of the vessels. This negative-pressure gradient tends to pull fluid and blood products out of the vessels and into the space. Thus, the alveoli and perivascular areas become edematous.
15. Shear stress causes intense strain and rupture of lung tissue, which may lead to an inflammatory response and edema formation. Shear stress occurs when an alveolus that is normally expanded is adjacent to one that is collapsed (atelectasis) and unstable. As airway pressure increases during inspiration, the normal alveolus inflates, but the collapsed unit does not. In the interstitial space between the two, force is exerted as these two units move or slide against each other. There is a potential zone of risk at the interface of open and closed lung units. This is similar to what occurs when a paper clip is repeatedly twisted; eventually the paper clip breaks. In the lung, the stress pulls normal tissues apart, resulting in physical damage to the alveolar cells, particularly epithelial and endothelial cells (pulmonary microvasculature). The term shear stress has been applied to this type of situation. The amount of stress across the entire lung can be estimated by using transpulmonary pressure.
16. The term atelectrauma is used to describe the injuries to the lungs that occur because of repeated opening and closing of lung units at lower lung volumes. Managing a patient with ARDS using low tidal volumes and inadequate levels of PEEP.
17. (a) Cytokines and tumor necrosis factor (TNF) and (b) others include platelet-activating factor, thromboxane-B2, interleukin-1B.
18. Chemical mediators produced in the lung can leak into the pulmonary blood vessels. The circulation then carries these substances to other areas of the body and sets up an inflammatory reaction in other organs, such as the kidneys, gut, and liver. The release of mediators may, therefore, lead to multiple organ failure.
19. Multiple organ dysfunction syndrome can be avoided during mechanical ventilation by using lung-protective strategies, such as low tidal volumes and therapeutic PEEP.
20. Ventilation and perfusion are best matched in the dependent lung areas near the back.
21. The diaphragm is most displaced in the nondependent regions of the lung; therefore, gas flows easily to this area, whereas blood flow to this area is decreased. Alveolar collapse is most likely to occur in the dependent areas of the lung, where perfusion is greatest.
22. The preservation of spontaneous breathing can reduce the ventilation/perfusion changes associated with mechanical ventilation. Therefore, ventilator modes that preserve spontaneous breathing may be beneficial (e.g., pressure support ventilation [PSV]).
23. Positive-pressure ventilation increases the size of the conductive airways, which in turn increases the amount of dead space ventilation. Additionally, if normal alveoli are overexpanded during PPV and compression of pulmonary vessels results, alveolar dead space also increases.
24. The increased volume during a positive-pressure breath and PEEP squeezes the blood out of nondependent zones, sending more blood into dependent areas, where ventilation is now lower, or into disease-affected areas of the lung, where lung volumes are not substantially increased. This can lead to increased shunting and decreased PaO2.
25. Increased airway and alveolar pressures can lead to thinning and compression of pulmonary capillaries, decreased perfusion, and increased pulmonary vascular resistance (PVR).
26. Hypoventilation causes an increase in plasma hydrogen ion levels, which can contribute to high plasma potassium levels (hyperkalemia). Hyperkalemia can affect cardiac function and can lead to cardiac dysrhythmias.
27. Permissive hypercapnia may be appropriate in patients with ARDS, because maintaining a normal CO2 range without causing VILI is difficult in these patients.
28. (a) Hypoxemia, (b) pain and anxiety syndromes, (c) circulatory failure, and (d) airway inflammation.
29. Respiratory acidosis (hypoventilation, hypercapnia)
30. (a) Respiratory alkalosis can cause hypokalemia (low potassium levels), which can lead to cardiac arrhythmias; other problems include tetany and reduced cerebral perfusion, which may contribute to increased cerebral hypoxia. (b) Respiratory alkalosis also reduces the patient’s drive to breathe, making weaning difficult.
31. Hyperventilation causes respiratory alkalosis, which leads to the diffusion of CO2 out of the cerebral spinal fluid (CSF) because of the low blood CO2 levels. Accordingly, the H+ concentration in the CSF decreases, and respirations are not stimulated.
32. Intravenous administration of bicarbonate is indicated for life-threatening hyperkalemia either caused by or associated with metabolic acidosis.
33. Metabolic alkalosis can be caused by (a) gastrointestinal suctioning or vomiting, (b) diuretic administration, (c) bicarbonate administration, and (d) administration of lactate, acetate, or citrate.
34. Auto-PEEP can occur without dynamic hyperinflation when the expiratory muscles are actively contracting during exhalation. This raises alveolar pressures at end-exhalation without increasing the volume at end-exhalation (auto-PEEP without lung distention).
35. High minute ventilation (high respiratory rates, increased tidal volume), short expiratory times, mechanical devices that increase expiratory resistance, and low inspiratory flow rates.
36. Chronic obstructive airway disease; high minute ventilation (more than 10-20 L/min) in ventilated patients; age greater than 60 years; increased airway resistance (e.g., small ET size, bronchospasm, increased secretions, mucosal edema); increased lung compliance (longer time constants); high respiratory frequency; high inhalation/exhalation ratios, that is, short TE (e.g., 1:1 and 2:1); low inspiratory flow; increased VT, particularly with airflow obstruction.
37. Insert unnumbered (Fig. 17) with labels as answer
38. End-expiratory pause
39. 3-4 time constants
40. Dynamic hyperinflation is the failure of lung volume to return to passive FRC during exhalation by the time the next inspiration begins.
41. Auto-PEEP slows the beginning of gas flow during inspiration, because flow delivery does not start until mouth pressure exceeds alveolar pressure, which is now higher than the ambient pressure at the end of exhalation. Auto-PEEP also makes it more difficult for spontaneously breathing patients to trigger a ventilator breath, even when sensitivity settings are appropriate.
42. CSTAT = VT ÷ [Pplateau – (PEEP + auto-PEEP)]
= 525 mL ÷ [30 cm H2O – (12 cm H2O + 5 cm H2O)]
= 525 ÷ (30 – 17)
= 525 ÷ 13 = 40.4 mL/cm H2O
43. (a) Shorten inspiratory time and allow for a longer expiratory time by increasing the inspiratory flow rate; (b) use smaller tidal volumes and low respiratory rates to increase the expiratory time; (c) use low-resistance exhalation valves; and (d) use large endotracheal tubes to reduce air trapping.
44. (a) IMV, (b) pressure support, (c) CPAP, and (d) APRV.
45. Oxygen becomes a potential hazard when concentrations greater than 60% are administered for longer than 48 hours in an adult and if the FIO2 provides a PaO2 greater than 80 mm Hg in a newborn or premature infant.
46. 0.6. (a) Vital capacity will decrease; (b) compliance will decrease; (c) diffusing capacity will decrease; and (d) alveolar to arterial PO2 difference.
47. A target PaO2 of 60 mm Hg and an SpO2 of 90% are acceptable lower limits.
48. Absorption atelectasis
49. Normal inspiratory WOB is about 0.5 joules/L, or 0.05 kgm/L.
50. 1.5 joule/L (or 15 joule/L/min)
51. A high spontaneous respiratory rate and use of accessory muscles.
52. Work = [PIP – (0.5 × Pplateau)] ÷ (100 × VT [in L])
= [45 – (0.5 × 3(3))] ÷ [(100 × 0.47(5))]
= 28.5 ÷ 47.5
= 0.6 joule/L
53. (a) Use the largest possible endotracheal tube; (b) ensure the machine sensitivity is set appropriately; (c) ensure that there is no asynchrony; and (d) reduce the patient’s airway resistance.
54. (a) Use of accessory muscles, (b) tachypnea, (c) retractions, and (d) chest-abdominal paradox.
55. Trigger asynchrony occurs when the ventilator sensitivity setting is not appropriate for the patient. This problem may be alleviated by adjusting the trigger setting appropriately or by switching to flow triggering, which in older ventilators has a faster response time.
56. The presence of auto-PEEP can also make triggering the ventilator more difficult for the patient and result in missed patient triggers. With auto-PEEP, the patient’s effort may not be transmitted to the sensing mechanism; consequently the ventilator would not provide inspiratory gas flow. Because auto-PEEP is a dynamic condition, it can be present in one breath and absent the next. In fact, in patients normally not suspected of having auto-PEEP, it is probably one of the major contributors to trigger asynchrony, resulting in patient discomfort and an increase in the oxygen cost of breathing.
57. 80 L/min
58. Pressure-targeted breaths, such as with PCV and PSV, because the ventilator rapidly provides a high flow to achieve and maintain the set pressure. As long as the set pressure is adequate, the flow to the patient will be adequate.
59. Adjust rise time or slope.
60. Cycle dyssynchrony occurs when the patient begins to exhale before the completion of a ventilator breath (inspiration). This may occur when the inspiratory time is set too long by a control itself or as a result of a combination of rate, flow, and volume settings.
61. During full ventilatory support, either the flow rate can be increased to shorten TI or the set TI may be reduced. During spontaneous breaths, the flow cycle percentage can be changed.
62. VC-IMV
63. PEEP asynchrony occurs either when PEEP is set too low and atelectasis forms or when it is too high and overdistention occurs.
64. A ventilator does not detect all of the patient’s spontaneous efforts because of missed triggers. In a minute ventilation-based unit, the ventilator detects a decrease in rate and automatically increases the volume delivery up to 150%. Also, the ventilator may not detect all of a patient’s spontaneous efforts if a patient is on VS or PRVC and the patient’s inspiratory demand increases because of a decrease in compliance or oxygenation. The ventilator detects the high volume and interprets it as an improvement in compliance or resistance and reduces pressure.
65. (any of the following) Disconnection from the power source; failure of the power source; failure of the ventilator to function because of equipment manufacturing problems or improper maintenance; failure of alarms to work because of mechanical failure or failure of personnel to turn them on or use them properly; failure of heating or humidifying devices; failure of the pressure relief valve to open; disconnection of the patient Y-connector; leaks in the system, resulting in inadequate pressure or tidal volume delivery; failure of the expiratory valve to function, causing a large system leak or a closed system with no exit for exhaled air; inappropriate assembly of the patient circuit.
66. (any of the following) Disconnection from the power source; failure of the power source; failure of the ventilator to function because of equipment manufacturing problems or improper maintenance; failure of alarms due to mechanical failure or failure of personnel to turn them on or use them properly; failure of heating or humidifying devices; failure of the pressure relief valve to open; disconnection of the patient Y-connector; leaks in the system, resulting in inadequate pressure or tidal volume delivery; and failure of the expiratory valve to function, causing a large system leak or causing a closed system with no exit for exhaled air; inappropriate assembly of the patient circuit.
67. Hypothermia, hypoventilation, and alveolar gas trapping caused by mucous plugging of airways, possible increased resistive WOB caused by mucous plugging of airways, possible increased resistive WOB through the humidifier.
Critical Thinking Questions
1. The patient-triggered breath displays inadequate ventilator flow, which causes the pressure-time curve to take on a concave shape.
2. Increasing the ventilator flow setting should alleviate this problem.
3. This scalar shows cycle dyssynchrony. The patient is actively trying to exhale before the end of the breath, as noted by the rise in pressure toward end-inspiration.
4. The problem can be corrected by increasing the flow cycle percentage, which will end inspiration at a higher flow rate and shorten the inspiratory time.
5. Patient 1 is more likely to develop auto-PEEP from dynamic hyperinflation, because the patient has a high airway resistance. If the time constant is calculated, it comes to 1.25 second (50 mL/cm H2O = 0.05 L/cm H2O). This means that it will take 3.75-5 seconds to empty 98% of the alveoli. If the set rate is 12 breaths/min, the total cycle time is only 5 seconds. Therefore, the alveoli will not empty completely on each breath. Patient 2 has a single time constant of 0.15 second. Therefore, this patient will be able to empty 98% of the alveoli with a rate of 12 breaths/min.
Case Studies
Case Study 1

1. The most outstanding problem noted on the ventilator flow sheet is the failure of the arterial PCO2 to fall with incremental increases in the delivered minute ventilation.
2. The increasing PCO2 in this patient cannot be caused by an increase in CO2 production, because the patient is unresponsive. This increase in CO2 could only be caused by a progressive increase in dead space. The increased dead space is caused by auto-PEEP.
3. Barotrauma (subcutaneous emphysema, pneumothorax, and pneumomediastinum); atelectrauma (shear stress, surfactant alteration, and biotrauma); multiple organ dysfunction syndrome; increased work of breathing; and ineffective triggering of the ventilator, leading to respiratory muscle fatigue.
4. The respiratory rate is set too high, which does not allow enough time for exhalation. This is causing the auto-PEEP in this situation. At 1400 hours, with a respiratory rate of 40 breaths/min, the CSTAT is 8.4 mL/cm H2O; this is due to overinflation of the lungs.

Case Study 2

1. The patient was being hyperventilated while on the original VC-CMV setting. This is evident because the patient’s baseline ABG results show chronic hypercapnia. The patient was hyperventilated for 36 hours, which restored the pH to normal in the plasma and the CSF. The patient is unable to maintain the high levels of alveolar ventilation that the VC-CMV mode had maintained.
2. The respiratory therapist could increase the set rate in the VC-SIMV mode to eliminate the immediate patient fatigue problem; the rate then can be adjusted to allow the PaCO2 to rise to its baseline level. Pressure support should be used to eliminate the airway resistance caused by the endotracheal tube.
3. The spike at the end of the pressure-time scalar is the patient’s active exhalation. This usually appears when the flow cycle is set too low, causing cycle asynchrony.
4. The problem can be alleviated by increasing the percent flow cycle. This will cause inspiration to end sooner, giving the patient more expiratory time.

Case Study 3

1. Stridor is the high-pitched sound heard, often with an unaided ear, when air passes through a partially obstructed upper airway.
2. Laryngeal edema and glottis injury (swelling) are possible complications following extubation.
3. VS assessment is necessary. Along with lung sounds, auscultation over the trachea should be done to assess the stridor.
4. Nebulized cool mist or 2.25% racemic epinephrine may be needed. IV steroids may also help alleviate the swelling. The patient should be closely monitored in case the need for reintubation occurs.
NBRC-Style Questions
1. C
2. C
3. D
4. D
5. A
6. A
7. B
8. C
9. A
10. B