clinical investigations in critical care Intrinsic PEEP and Unilateral Lung Hyperinflation* Pathophysiology and Clinical Significance Marin H. Kollef, M.D., F.C.C.P.; and] F. Turner, M.D. Over a 14-month period, three patients developed unilateral lung hyperin8ation during mechanical ventilation as a manifestation of intrinsic PEEP. These patients all had a history of CAO and an in8ammatory or fibrotic disease process involving the contralateral lung. Physicians caring for patients with CAO need to be familiar with this presentation of intrinsic PEEP due to the associated bam-
trauma and cardiac dysfunction which can result from it.
the static elastic recoil pressure of the N ormally respiratory system is zero at end-expiration.
chanical ventilation. The patient was ventilated with an Flo2 of 40 percent, zero PEEP, tidal volume of600 ml, in the IMV mode with a rate of 14 breaths per minute. The delivered flow rate was 45 Umin, producing a peak inspiratory pressure of32 cm H 20. Twentyfour hours after the initiation of mechanical ventilation, hyperinflation of the left lung was noted. The peak inspiratory pressure was now 40 cm H 2 0 and the intrinsic PEEP, measured after transient occlusion of the lumen of the distal port of the exhalation valve immediately before the next machine breath, was 8 cm H 20.2 The
I
Several investigators have shown the presence of a positive value for elastic recoil and alveolar pressures at end-expiration which has been termed "intrinsic" PEEp'2., Intrinsic PEEP appears to occur primarily in patients with airflow obstruction due to dynamic factors such as increased respiratory frequency, airway collapse, increased tidal volumes and inadequate expiratory times which can lead to air trapping and pulmonary hyperinfiation. I .7 We describe three patients who presented to our ICU over a 14-month period with unilateral lung hyperinflation as a manifestation of intrinsic PEEP. The pathophysiology and clinical significance of this finding are reviewed.
(Chest 1992; 102:1220-24)
=
=
CAO chronic airflow obstruction; EMD electromechanical dissociation; I:E ratio = inspiratory-expiratory ratio; IMV = intermittent mandatory ventilation
CASE REPORTS CASE
1
A 64-year-old woman with a lonlt-standing history of smoking and CAO was admitted to the MICU for impending respiratory failure. The past medical history was significant for CAO with an FEV, of 550 ml and an FVC of 1.7 L. There also was a history of pneumonia occurrinlt six years earlier. A baseline chest radiograph performed one year prior to the current admission is shown in Figure 1, demonstratinlt an opacity in the right lower lobe which has not changed during the previous five years. Upon admission to the MICU, the patient was intubated with a 7.0-mm internal diameter endotracheal tube and placed on me-
*From the Department of Medicine, Pulmonary Disease and Critical Care Division, Fitzsimons Army Medical Center, Aurora, Colo. The opinions and assertions contained herein are the private views of the authors and do not necessarily reflect the views of the Department of the Army or the Department of Defense. Manuscript received Januar\' 13; revision accepted March 26. Reprint mquests: Dr. Kolle/. Fitzsimons Anny Medical Center; Aurora, Colorado 80224
1220
FIGURE 1. Ba~eline chest radioltraph demonstrating opacity in right lower lobe. Intrinsic PEEP and Unilateral Lung Hyperinflation (Koller. Turner)
FIGLIRF. 2. Chest radio/(raph demonstratin/( left lun/( hyperinRation. patient's endotracheal tuhe was changed to a size 8.0-mm internal diameter tuhe and the tidal volume was decreased to 500 ml. Despite these interventions, the left lung hyperinRation progressed over the next 24 hours (Fi/( 2). The IMV rate was decreased to to hreaths per minute and the patient was paralyzed with vecuronium bromide (Norcuron, Organon Inc., West Orange, NJ) and sedated with midazolam hydrochloride (Versed, Roche Laboratories. Nutley, NJ). The peak inspiratory pressures increased to 48 I'm H,O and the intrinsic PEEP was 15 I'm H,O. Due to a (.'oncern over a possihle occult pneumothorax accounting for the picture of hyperinRation. a repeat chest radiograph and a lateral decubitus radiograph with the left side of the chest in the nondependent position were performed. The left chest was in the nondependent position filr 20 min prior to ohtaining the lateral decubitus film. and neither radio/(raph showed evidence of pneumothorax. Twelve hours later. the patient developed the acute onset of hypotension with a hlood pressure of 75150 mm II/(. At that time. a chest radiograph showed evidence of a new left pneumothorax and a chest tube was inserted reversing the hypotension. Gradual improvement occurred over the next five days with resolution of the left hili/( hyperinRation. The peak inspiratory pressure decreased to 34 I'm 11,0 with an intrinsic PEEP level of 8 I'm H,O. The patient was successfully weaned from mechanical ventilation and extubated. Three months filllowin/( hospital discharge. another exacerbation of the lung disease developed requiring admission to the hospital. Cardiac arrest occurred 8 h after hospital admission due to ventricular fihrillation and the patient died despite attempts at resuscitation. An autopsy was performed and showed both lungs to have bullae ranging from 0.8 to 3.0 I'm in diameter. The right lower lobe also had an old ahscess cavit\· surrounded by scarred lung tissue and pulmonary adhesions of th~ chest wall. The pathologic findin/(s in the ri/(ht lower lohe mrresponded to the ahnormalities visualized on the chest radiograph (Fig 1). Cardiovascular examination revealed severe atherosclerosis with evidence of early myocardial infarction. CASE
FIGI'RE 3. Hyperinflation of the left lung with a poorly shown deep lateral mstophrenic an/(Ie des(.'endin/( helow the edgt' of the radiograph. myocardial infarction hvo years earlier and diahetes mellitus requiring insulin eomplieated by diahetic nephropathy. H·tinopalhy and gastropathy. The patient also had a 75-pack-year history of smoking associated with a clinical diagnosis of CAO manili.·stt·d hv chronic t1lugh and dyspnea with exertion. lie was treah·d hy ~ private physician for his presumed CAO with alhuterol administered hy metered-dose inhaler. which produt'ed improven,ent in his symptoms. On the fifth postoperative day. the patient had an episode of emesis with aspiration requiring intubation and suctioning of /(astric t1mtents from the trachea. He was transferred to the MICU for mechanical ventilation. Thirty-six hours after intuhation, the patient developed left lung hyperinflation (Fig 3) with what appeared to he a deep lateral costophrenic an/(Ie descending helow the ed/(e of the radiograph suggestive of a deep sulcus sign' A lateral dt'cuhitus chest radiograph with the left lung in the nondependent position
2
A 65-year-old man was admitted to the hospital for emergency above-the-knee amputation of the right leg due to severe peripht'ral vascular disease. The past medical history was significant for a
FIGLIRE 4. Resolution of the left lung hyperinflation. CHEST I 102 I 4 I OCTOBER. 1992
1221
tube. As the patient's sedation was decreased, he began to have episodes of agitation assodated \\;th increases in his breathing frequency up to 4S breaths per minute associated with peak inspiratory pressures of 60 Clll 11,0. lie developed tachycardia and hypotension with a bl.)(KI pressure of 70/40 mm Hg. The level of intrinsic PEEP measured at this time was 25 cm H,O. A chest radiograph demonstrated (Filt 6) right (unit hyperinflation with herniation of the lunlt across the midline. The patient was subsequently sedated, which decreased his breathinlt frequency to 10 to 14 breaths per minute and he was reintubated with a size 8.o-mm internal diameter endotracheal tube. The patient's vital signs returned to baseline followinlt sedation and slowing of his respiratory rate, and subsequent chest radiographs showed improvement in the right lunlt hyperinflation. The peak inspiratory pressnres decreased to 38 cm 11,0 with a level of intrinsk PEEP of 15 cm H,o. Tbe patient remained intubated for two weeks nntil he was weaned from mechanical ventilation and extubated. During that time, he had two additional episodes of pulmonary distress associated with hyperventilation, tachycardia and riltht Inng hyperinAation, which responded to sedation in both circumstances. DISCUSSION
FIGURE 5. Opacification of the left lunlt with cystic chanltes due to bronchiectasis. failed to demonstrate evidence of pneumothorax. Ventilator settinlts at this time were an Flo, of 40 perl-ent, zero PEEP, tidal volume of 800 ml, in the IMV mode with a rate of 13 breaths per minnte and 7 cm H,O of pressure support. The patient's respiratory rate at this time was in the ranlte 01'20 to 34 breaths per minute. The delivered flow rate was 45 Umin, producinlt a peak inspiratory pressure of 37 em H,o. The level of intrinsic PEEP was measured from tht· ventilator pressure Itaulte after transient occlusion of the lumen of the distal port of the exhalation valve immediately prior to the next machine-Itenerated IMV breath and found to be 10 l'm H,o. The tidal volume was decreased to 700 ml and the patient was sedated with midazolam hydrochloride. Twenty-four hours later, the patient's frequency of breathinlt had decreased to 14 to 17 breaths per minute and the peak inspiratory pressure was 29 cm H,O, with the intrinsic PEEP being 8 cm H,O. A repeat chest radiograph showed resolution of the left lung hyperinflatiou (Filt 4). The patient subsequently developed evidence of multiple organ system failure and the adult respiratory distress syndrome, requirinlt the administration of external PEEP. He continued to receive intravenous sedation and died eiltht days later without further evidence oflunlt hyperinflation. An autopsy was not performed. CASE
3
A 64-year-old man with a history of severe CAO was admitted to the MICU with an episode of respiratory failure. The past medical history was remarkable for an episode of left-sided pn"unumia complicated by empyema requirinlt surgical drainalte 44 years earlier and a 75-pack-year history of smoking. Baseline pulmonary function studies showed an FEV, 01'390 ml and a FVe 01'2.01 L. A chest radiograph after intuhation with a size 7.5-mm internal diameter endotracheal tube was unchanged from haseline (Fig 5). Initial ventilator seltinlts were an Flo, of 40 percent, zero PEEP, tidal volume of 550 ml, in the IMV mode with a rate of 10 breaths per minute. The delivered minute ventilation was 711 Umin, producing a peak inspiratory pressure of 30 cm H,O. Forty-eiltht hours later, the patient self-extubated hillls..rf and was reintuhated with a size 7.o-mm internal diameter endotradleal
1222
A review of the medical literature (MEDLINE) suggests that intrinsic PEEP presenting with unilaterallung hyperinflation is an uncommon event. Eveloff and colleagues" described an individual with unilateral lung hyperinflation associated with herniation of a large bulla to the contralateral hemithorax producing hemodynamic compromise. This well-documented case and our three patients share several common features which appear to be important for the development of unilateral lung hyperinflation as a presentation of intrinsic PEEP. Our three cases and the patient of Eveloff et al9 each had a history of CAO. Obstructive disease of the airways appears to be the most common predisposing
Flel'HE 6. lIyperinAation of the right lung with herniation of the hllllt across the midline at the midthoracic level. The right lateral costophrenic ,mlt1e is not visualized. Intrinsic PEEP and Unilateral lung Hyperinflation (Koller. Turner)
factor for the development of intrinsic PEE~2.3.6 Two of the three patients in this report had lung function studies supporting the diagnosis ofairflow obstruction. The remaining patient had no pulmonary function studies performed prior to his death (case 2), but his clinical history suggested the presence of airflow obstruction. Other forms of lung disease such as the adult respiratory distress syndrome also have been associated with the development of intrinsic PEE~ 10 These four individuals also had evidence ofa fibrotic or inflammatory disease process involving the contralateral nonhyperinflated lung. Significant right-sided pleural adhesions were demonstrated in our first case at autopsy along with the pulmonary scarring from the prior pneumonia. In our third case and the patient described by Eveloff et al,9 severe bronchiectasis and pneumonia were present respectively in the nonhyperinflated lungs. Our second patient had an episode of gastric aspiration and subsequently developed the adult respiratory distress syndrome. Adult respiratory distress syndrome is known to be nonuniform in its lung involvement ll and often is precipitated by gastric aspiration. It is possible that the aspiration syndrome and associated lung injury primarily involved the right lung in this individual, accounting for the asymmetric presentation of the lung hyperinflation. The importance of asymmetric pulmonary disease processes was recently illustrated by Carlon et al 12 who described a patient with unilateral lung consolidation requiring independent lung ventilation due to the development of life-threatening ventilation-perfusion inequality from the effects of externally applied PEE~ These authors hypothesized that the more compliant lung was more susceptible to the effects of applied PEE~ causing a shunting of blood flow to the consolidated lung, thus accounting for the ventilationperfusion inequalit~12 A similar phenomenon may occur when intrinsic PEEP develops in the setting of asymmetric lung disease, causing it to be unequally distributed. 9 Additionally, the more compliant lung appears to be more susceptible to the dynamic factors predisposing to the development of hyperinflation and intrinsic PEE~ Another common feature among these patients was that they all required intubation and mechanical ventilation. The influence of endotracheal tube size, minute ventilation and ventilatory patterns on the
production of intrinsic PEEP previously have been described}3.14 Modification of conventional ventilator parameters may be required in patients at risk for unilateral lung hyperinflation to minimize the dynamic factors leading to the development of intrinsic PEE~ Smaller tidal volumes may be necessary based on an estimate of the overall amount of lung tissue which is uninvolved by the asymmetrical fibrotic or inflammatory disease process.
The clinical sequelae of intrinsic PEEP are well described and include barotrauma, cardiac compromise producing hypotension with organ hypoperfusion and increasing the work of breathing. 2 •5.7 One of our patients (case 3) and the patient described by Eveloff et al9 developed evidence of hemodynamic compromise as a result of unilateral lung hyperinflation. In both patients, the alterations in blood pressure corrected after resolution of the unilateral lung hyperinflation and lowering of the intrinsic PEEP level. Barotrauma was suspected in our first two patients (cases 1 and 2) due to the radiographic presentation of unilateral lung hyperinflation. Pneumothorax was excluded in the second case but subsequently occurred in our first case and was associated with hemodynamic compromise. Intrinsic PEEP would be expected to also increase the work of breathing in these patients by adding the level of intrinsic PEEP to the pressure required to produce actual air movement when breathing spontaneously or to triggering of the ventilator for mechanical breaths. In each of these four cases, recognition of the presence of intrinsic PEEP led to interventions which decreased its level. In our three patients, sedation appeared to play an important role in decreasing the level of intrinsic PEE~ This presumably occurred due to the decrease in minute ventilation associated with sedation. Additionally, other measures aimed at minimizing minute ventilation, such as decreases in respiratory rate and tidal volume, would be expected to allow more time for expiration and less development of intrinsic PEE~ When high minute ventilation is present, use of a larger endotracheal tube also may decrease the level of intrinsic PEEp14 as can adjustment in inspiratory flow rates to allow for longer expiratory times. Eveloff et al9 demonstrated that removal of an on-line suction apparatus also produced a decrease in the level of intrinsic PEEP and unilateral lung hyperinflation. Growing familiarity with the dynamic factors which produce intrinsic PEEP and our ability to detect its presence2 has led to the recognition of other atypical presentations of intrinsic PEE~ Dries et a}15 have described a patient who developed profound hypotension after closing the chest following coronary artery bypass surgery. Upon reopening the chest, the patienfs blood pressure returned to initial levels. Tidal volume and respiratory rate were adjusted to prolong the I:E ratio allowing for successful chest closure. Recently, intrinsic PEEP also has become recognized as an etiology of EMD.16.17 In one of these reports, recognition of intrinsic PEEP as the etiology of the EMD allowed changes to be made in the patient's dynamic respiratory parameters which prolonged the expiratory time and allowed for resolution of the E MD .17 These hemodynamic effects ofintrinsic PEEP CHEST I 102 I 4 I OCTOBER, 1992
1223
appear to be precipitated in an identical manner to those caused by extrinsically applied PEE~ which produces hypotension by decreasing cardiac output due to increases in mediastinal pressure 18 and increases in right ventricular afterload. 19-21 In summary, clinicians caring for patients with airflow obstruction and a coexisting asymmetric inflammatory or fibrotic lung process need to be aware that unilateral lung hyperinBation may be the presenting manifestation of intrinsic PEE~ Recognition of this atypical presentation and its successful management may avoid complications such as barotrauma and hypotension associated with the presence of intrinsic PEE~ ACKNOWLEDGMENTS: The authors would like to acknowledge the MICU nursing staff and the Department of Medicine house staff for their assistance in the care of these patients.
REFERENCES 1 Tobin MJ, Lodato RF. PEE~ auto-PEE~ and waterfalls. Chest 1989; 96:449-51 2 Pepe PE, Marini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction. Am Rev Respir Dis 1982; 126:166-70 3 Rossi A, Gottfried 5B, Zocchi L, Higgs BD, Lennox S, Calverly PMA, et a1. Measurement of static compliance of total respiratory system in patients with acute respiratory failure during mechanical ventilation: the effect of "intrinsic PEEE'· Am Rev Respir Dis 1985; 131:672-77 4 Marini JJ. Should PEEP be used in airflow obstruction? Am Rev Respir Dis 1989; 140:1-3 5 Derenne J~ Fleury B, Pariente R. Acute respiratory failure of chronic obstructive pulmonary disease. Am Rev Respir Dis
1988; 138: 1006-33
6 Kimball WR, Leith DE, Robins AG. Dynamic hyperinflation and ventilator dependence in chronic obstructive pulmonary disease. Am Rev Respir Dis 1982; 126:991-95 7 Brown DC, Pierson DJ. Auto-PEEP is common in mechanically ventilated patients: a study of incidence, severity, and detection.
1224
Respir Care 1986; 31: 1069-74 8 Gordon R. The deep sulcus sign. Radiology 1980; 136:25-27 9 EveloffSE, Rounds S, Braman SSe Unilateral lung hyperinflation and herniation as a manifestation of intrinsic PEE~ Chest 1990; 98:228-29 10 Marini JJ. Minimizing breathing effort during mechanical ventilation. In: Zapol WM, Lemaire F. eds. Adult respiratory distress syndrome. New York, NY: l\1arcel Dekker, Inc, 1991: 163-98 11 Gattinoni L, Mascheroni D, Torresin A, Marcolin R, Fumagelli R, Vesconi S, et al. Morphological response to positive endexpiratory pressure in acute respiratory failure: computerized tomo~raphy study. Intensive Care l\1ed ]986; 12: 137-42 12 Carlon GC, Kahn R, Howland \VS, Baron R, Ramaker J. Acute life-threatening ventilation-perfusion inequality: an indication for independent lung ventilation. Crit Care Med 1978; 6:380-83 13 Tuxen D~ Lane S. The effect of ventilatory pattern on hyperinflation, aim'ay pressures, and circulation in mechanical ventilation of patients with severe air-flov.' ohstnlt'tion. Am Rev Respir Dis 1987; 136:872-79 14 Scott LR, Benson MS, Bishop ~1J. Relationship of endotracheal tube size to auto-PEEP at high minute ventilation. Respir Care 1986; 31:1080-82 15 Dries DJ, Mathru M, Salem R, RaoT, MontoyaA. Hemodynamic compromise associated with air trapping following coronary artery bypass surgery. Chest 1990; 97: 1002-03 16 Rogers PL, Schlichtig R, Miro A, Pinsky M. Auto-PEEP during CPR: an ··occult.. cause of electromechanical dissociation? Chest 1991; 99:492-93 17 Kollef MH. Lung hyperinflation caused hy inappropriate ventilation resulting in electromechanical dissociation: a ease report. Heart Lung 1992; 21:74-77 18 Marini JJ, Culver BH, Butler J. Mechanical effect of lung distension with positive pressure on cardiac function. Am Rev Respir Dis 1981; 124:382-86 19 Butler J, Paley H\\Z Lung volume and pulmonary circulation. Med Thorac 1962; 19:261-67 20 Butler J. The heart is not always in good hands. Chest 1990; 97:453-60 21 Whittenher~er JL, McGregor M. Berglund E. Borst HG. Influence of state of inflation of the lung on pulmonary vascular resistance. J Appl Physiol 1960; 15:878-82
Intrinsic PEEP and Unilateral Lung Hyperinflation (Kollet, Turner)
trauma and cardiac dysfunction which can result from it.
the static elastic recoil pressure of the N ormally respiratory system is zero at end-expiration.
chanical ventilation. The patient was ventilated with an Flo2 of 40 percent, zero PEEP, tidal volume of600 ml, in the IMV mode with a rate of 14 breaths per minute. The delivered flow rate was 45 Umin, producing a peak inspiratory pressure of32 cm H 20. Twentyfour hours after the initiation of mechanical ventilation, hyperinflation of the left lung was noted. The peak inspiratory pressure was now 40 cm H 2 0 and the intrinsic PEEP, measured after transient occlusion of the lumen of the distal port of the exhalation valve immediately before the next machine breath, was 8 cm H 20.2 The
I
Several investigators have shown the presence of a positive value for elastic recoil and alveolar pressures at end-expiration which has been termed "intrinsic" PEEp'2., Intrinsic PEEP appears to occur primarily in patients with airflow obstruction due to dynamic factors such as increased respiratory frequency, airway collapse, increased tidal volumes and inadequate expiratory times which can lead to air trapping and pulmonary hyperinfiation. I .7 We describe three patients who presented to our ICU over a 14-month period with unilateral lung hyperinflation as a manifestation of intrinsic PEEP. The pathophysiology and clinical significance of this finding are reviewed.
(Chest 1992; 102:1220-24)
=
=
CAO chronic airflow obstruction; EMD electromechanical dissociation; I:E ratio = inspiratory-expiratory ratio; IMV = intermittent mandatory ventilation
CASE REPORTS CASE
1
A 64-year-old woman with a lonlt-standing history of smoking and CAO was admitted to the MICU for impending respiratory failure. The past medical history was significant for CAO with an FEV, of 550 ml and an FVC of 1.7 L. There also was a history of pneumonia occurrinlt six years earlier. A baseline chest radiograph performed one year prior to the current admission is shown in Figure 1, demonstratinlt an opacity in the right lower lobe which has not changed during the previous five years. Upon admission to the MICU, the patient was intubated with a 7.0-mm internal diameter endotracheal tube and placed on me-
*From the Department of Medicine, Pulmonary Disease and Critical Care Division, Fitzsimons Army Medical Center, Aurora, Colo. The opinions and assertions contained herein are the private views of the authors and do not necessarily reflect the views of the Department of the Army or the Department of Defense. Manuscript received Januar\' 13; revision accepted March 26. Reprint mquests: Dr. Kolle/. Fitzsimons Anny Medical Center; Aurora, Colorado 80224
1220
FIGURE 1. Ba~eline chest radioltraph demonstrating opacity in right lower lobe. Intrinsic PEEP and Unilateral Lung Hyperinflation (Koller. Turner)
FIGLIRF. 2. Chest radio/(raph demonstratin/( left lun/( hyperinRation. patient's endotracheal tuhe was changed to a size 8.0-mm internal diameter tuhe and the tidal volume was decreased to 500 ml. Despite these interventions, the left lung hyperinRation progressed over the next 24 hours (Fi/( 2). The IMV rate was decreased to to hreaths per minute and the patient was paralyzed with vecuronium bromide (Norcuron, Organon Inc., West Orange, NJ) and sedated with midazolam hydrochloride (Versed, Roche Laboratories. Nutley, NJ). The peak inspiratory pressures increased to 48 I'm H,O and the intrinsic PEEP was 15 I'm H,O. Due to a (.'oncern over a possihle occult pneumothorax accounting for the picture of hyperinRation. a repeat chest radiograph and a lateral decubitus radiograph with the left side of the chest in the nondependent position were performed. The left chest was in the nondependent position filr 20 min prior to ohtaining the lateral decubitus film. and neither radio/(raph showed evidence of pneumothorax. Twelve hours later. the patient developed the acute onset of hypotension with a hlood pressure of 75150 mm II/(. At that time. a chest radiograph showed evidence of a new left pneumothorax and a chest tube was inserted reversing the hypotension. Gradual improvement occurred over the next five days with resolution of the left hili/( hyperinRation. The peak inspiratory pressure decreased to 34 I'm 11,0 with an intrinsic PEEP level of 8 I'm H,O. The patient was successfully weaned from mechanical ventilation and extubated. Three months filllowin/( hospital discharge. another exacerbation of the lung disease developed requiring admission to the hospital. Cardiac arrest occurred 8 h after hospital admission due to ventricular fihrillation and the patient died despite attempts at resuscitation. An autopsy was performed and showed both lungs to have bullae ranging from 0.8 to 3.0 I'm in diameter. The right lower lobe also had an old ahscess cavit\· surrounded by scarred lung tissue and pulmonary adhesions of th~ chest wall. The pathologic findin/(s in the ri/(ht lower lohe mrresponded to the ahnormalities visualized on the chest radiograph (Fig 1). Cardiovascular examination revealed severe atherosclerosis with evidence of early myocardial infarction. CASE
FIGI'RE 3. Hyperinflation of the left lung with a poorly shown deep lateral mstophrenic an/(Ie des(.'endin/( helow the edgt' of the radiograph. myocardial infarction hvo years earlier and diahetes mellitus requiring insulin eomplieated by diahetic nephropathy. H·tinopalhy and gastropathy. The patient also had a 75-pack-year history of smoking associated with a clinical diagnosis of CAO manili.·stt·d hv chronic t1lugh and dyspnea with exertion. lie was treah·d hy ~ private physician for his presumed CAO with alhuterol administered hy metered-dose inhaler. which produt'ed improven,ent in his symptoms. On the fifth postoperative day. the patient had an episode of emesis with aspiration requiring intubation and suctioning of /(astric t1mtents from the trachea. He was transferred to the MICU for mechanical ventilation. Thirty-six hours after intuhation, the patient developed left lung hyperinflation (Fig 3) with what appeared to he a deep lateral costophrenic an/(Ie descending helow the ed/(e of the radiograph suggestive of a deep sulcus sign' A lateral dt'cuhitus chest radiograph with the left lung in the nondependent position
2
A 65-year-old man was admitted to the hospital for emergency above-the-knee amputation of the right leg due to severe peripht'ral vascular disease. The past medical history was significant for a
FIGLIRE 4. Resolution of the left lung hyperinflation. CHEST I 102 I 4 I OCTOBER. 1992
1221
tube. As the patient's sedation was decreased, he began to have episodes of agitation assodated \\;th increases in his breathing frequency up to 4S breaths per minute associated with peak inspiratory pressures of 60 Clll 11,0. lie developed tachycardia and hypotension with a bl.)(KI pressure of 70/40 mm Hg. The level of intrinsic PEEP measured at this time was 25 cm H,O. A chest radiograph demonstrated (Filt 6) right (unit hyperinflation with herniation of the lunlt across the midline. The patient was subsequently sedated, which decreased his breathinlt frequency to 10 to 14 breaths per minute and he was reintubated with a size 8.o-mm internal diameter endotracheal tube. The patient's vital signs returned to baseline followinlt sedation and slowing of his respiratory rate, and subsequent chest radiographs showed improvement in the right lunlt hyperinflation. The peak inspiratory pressnres decreased to 38 cm 11,0 with a level of intrinsk PEEP of 15 cm H,o. Tbe patient remained intubated for two weeks nntil he was weaned from mechanical ventilation and extubated. During that time, he had two additional episodes of pulmonary distress associated with hyperventilation, tachycardia and riltht Inng hyperinAation, which responded to sedation in both circumstances. DISCUSSION
FIGURE 5. Opacification of the left lunlt with cystic chanltes due to bronchiectasis. failed to demonstrate evidence of pneumothorax. Ventilator settinlts at this time were an Flo, of 40 perl-ent, zero PEEP, tidal volume of 800 ml, in the IMV mode with a rate of 13 breaths per minnte and 7 cm H,O of pressure support. The patient's respiratory rate at this time was in the ranlte 01'20 to 34 breaths per minute. The delivered flow rate was 45 Umin, producinlt a peak inspiratory pressure of 37 em H,o. The level of intrinsic PEEP was measured from tht· ventilator pressure Itaulte after transient occlusion of the lumen of the distal port of the exhalation valve immediately prior to the next machine-Itenerated IMV breath and found to be 10 l'm H,o. The tidal volume was decreased to 700 ml and the patient was sedated with midazolam hydrochloride. Twenty-four hours later, the patient's frequency of breathinlt had decreased to 14 to 17 breaths per minute and the peak inspiratory pressure was 29 cm H,O, with the intrinsic PEEP being 8 cm H,O. A repeat chest radiograph showed resolution of the left lung hyperinflatiou (Filt 4). The patient subsequently developed evidence of multiple organ system failure and the adult respiratory distress syndrome, requirinlt the administration of external PEEP. He continued to receive intravenous sedation and died eiltht days later without further evidence oflunlt hyperinflation. An autopsy was not performed. CASE
3
A 64-year-old man with a history of severe CAO was admitted to the MICU with an episode of respiratory failure. The past medical history was remarkable for an episode of left-sided pn"unumia complicated by empyema requirinlt surgical drainalte 44 years earlier and a 75-pack-year history of smoking. Baseline pulmonary function studies showed an FEV, 01'390 ml and a FVe 01'2.01 L. A chest radiograph after intuhation with a size 7.5-mm internal diameter endotracheal tube was unchanged from haseline (Fig 5). Initial ventilator seltinlts were an Flo, of 40 percent, zero PEEP, tidal volume of 550 ml, in the IMV mode with a rate of 10 breaths per minute. The delivered minute ventilation was 711 Umin, producing a peak inspiratory pressure of 30 cm H,O. Forty-eiltht hours later, the patient self-extubated hillls..rf and was reintuhated with a size 7.o-mm internal diameter endotradleal
1222
A review of the medical literature (MEDLINE) suggests that intrinsic PEEP presenting with unilaterallung hyperinflation is an uncommon event. Eveloff and colleagues" described an individual with unilateral lung hyperinflation associated with herniation of a large bulla to the contralateral hemithorax producing hemodynamic compromise. This well-documented case and our three patients share several common features which appear to be important for the development of unilateral lung hyperinflation as a presentation of intrinsic PEEP. Our three cases and the patient of Eveloff et al9 each had a history of CAO. Obstructive disease of the airways appears to be the most common predisposing
Flel'HE 6. lIyperinAation of the right lung with herniation of the hllllt across the midline at the midthoracic level. The right lateral costophrenic ,mlt1e is not visualized. Intrinsic PEEP and Unilateral lung Hyperinflation (Koller. Turner)
factor for the development of intrinsic PEE~2.3.6 Two of the three patients in this report had lung function studies supporting the diagnosis ofairflow obstruction. The remaining patient had no pulmonary function studies performed prior to his death (case 2), but his clinical history suggested the presence of airflow obstruction. Other forms of lung disease such as the adult respiratory distress syndrome also have been associated with the development of intrinsic PEE~ 10 These four individuals also had evidence ofa fibrotic or inflammatory disease process involving the contralateral nonhyperinflated lung. Significant right-sided pleural adhesions were demonstrated in our first case at autopsy along with the pulmonary scarring from the prior pneumonia. In our third case and the patient described by Eveloff et al,9 severe bronchiectasis and pneumonia were present respectively in the nonhyperinflated lungs. Our second patient had an episode of gastric aspiration and subsequently developed the adult respiratory distress syndrome. Adult respiratory distress syndrome is known to be nonuniform in its lung involvement ll and often is precipitated by gastric aspiration. It is possible that the aspiration syndrome and associated lung injury primarily involved the right lung in this individual, accounting for the asymmetric presentation of the lung hyperinflation. The importance of asymmetric pulmonary disease processes was recently illustrated by Carlon et al 12 who described a patient with unilateral lung consolidation requiring independent lung ventilation due to the development of life-threatening ventilation-perfusion inequality from the effects of externally applied PEE~ These authors hypothesized that the more compliant lung was more susceptible to the effects of applied PEE~ causing a shunting of blood flow to the consolidated lung, thus accounting for the ventilationperfusion inequalit~12 A similar phenomenon may occur when intrinsic PEEP develops in the setting of asymmetric lung disease, causing it to be unequally distributed. 9 Additionally, the more compliant lung appears to be more susceptible to the dynamic factors predisposing to the development of hyperinflation and intrinsic PEE~ Another common feature among these patients was that they all required intubation and mechanical ventilation. The influence of endotracheal tube size, minute ventilation and ventilatory patterns on the
production of intrinsic PEEP previously have been described}3.14 Modification of conventional ventilator parameters may be required in patients at risk for unilateral lung hyperinflation to minimize the dynamic factors leading to the development of intrinsic PEE~ Smaller tidal volumes may be necessary based on an estimate of the overall amount of lung tissue which is uninvolved by the asymmetrical fibrotic or inflammatory disease process.
The clinical sequelae of intrinsic PEEP are well described and include barotrauma, cardiac compromise producing hypotension with organ hypoperfusion and increasing the work of breathing. 2 •5.7 One of our patients (case 3) and the patient described by Eveloff et al9 developed evidence of hemodynamic compromise as a result of unilateral lung hyperinflation. In both patients, the alterations in blood pressure corrected after resolution of the unilateral lung hyperinflation and lowering of the intrinsic PEEP level. Barotrauma was suspected in our first two patients (cases 1 and 2) due to the radiographic presentation of unilateral lung hyperinflation. Pneumothorax was excluded in the second case but subsequently occurred in our first case and was associated with hemodynamic compromise. Intrinsic PEEP would be expected to also increase the work of breathing in these patients by adding the level of intrinsic PEEP to the pressure required to produce actual air movement when breathing spontaneously or to triggering of the ventilator for mechanical breaths. In each of these four cases, recognition of the presence of intrinsic PEEP led to interventions which decreased its level. In our three patients, sedation appeared to play an important role in decreasing the level of intrinsic PEE~ This presumably occurred due to the decrease in minute ventilation associated with sedation. Additionally, other measures aimed at minimizing minute ventilation, such as decreases in respiratory rate and tidal volume, would be expected to allow more time for expiration and less development of intrinsic PEE~ When high minute ventilation is present, use of a larger endotracheal tube also may decrease the level of intrinsic PEEp14 as can adjustment in inspiratory flow rates to allow for longer expiratory times. Eveloff et al9 demonstrated that removal of an on-line suction apparatus also produced a decrease in the level of intrinsic PEEP and unilateral lung hyperinflation. Growing familiarity with the dynamic factors which produce intrinsic PEEP and our ability to detect its presence2 has led to the recognition of other atypical presentations of intrinsic PEE~ Dries et a}15 have described a patient who developed profound hypotension after closing the chest following coronary artery bypass surgery. Upon reopening the chest, the patienfs blood pressure returned to initial levels. Tidal volume and respiratory rate were adjusted to prolong the I:E ratio allowing for successful chest closure. Recently, intrinsic PEEP also has become recognized as an etiology of EMD.16.17 In one of these reports, recognition of intrinsic PEEP as the etiology of the EMD allowed changes to be made in the patient's dynamic respiratory parameters which prolonged the expiratory time and allowed for resolution of the E MD .17 These hemodynamic effects ofintrinsic PEEP CHEST I 102 I 4 I OCTOBER, 1992
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appear to be precipitated in an identical manner to those caused by extrinsically applied PEE~ which produces hypotension by decreasing cardiac output due to increases in mediastinal pressure 18 and increases in right ventricular afterload. 19-21 In summary, clinicians caring for patients with airflow obstruction and a coexisting asymmetric inflammatory or fibrotic lung process need to be aware that unilateral lung hyperinBation may be the presenting manifestation of intrinsic PEE~ Recognition of this atypical presentation and its successful management may avoid complications such as barotrauma and hypotension associated with the presence of intrinsic PEE~ ACKNOWLEDGMENTS: The authors would like to acknowledge the MICU nursing staff and the Department of Medicine house staff for their assistance in the care of these patients.
REFERENCES 1 Tobin MJ, Lodato RF. PEE~ auto-PEE~ and waterfalls. Chest 1989; 96:449-51 2 Pepe PE, Marini JJ. Occult positive end-expiratory pressure in mechanically ventilated patients with airflow obstruction. Am Rev Respir Dis 1982; 126:166-70 3 Rossi A, Gottfried 5B, Zocchi L, Higgs BD, Lennox S, Calverly PMA, et a1. Measurement of static compliance of total respiratory system in patients with acute respiratory failure during mechanical ventilation: the effect of "intrinsic PEEE'· Am Rev Respir Dis 1985; 131:672-77 4 Marini JJ. Should PEEP be used in airflow obstruction? Am Rev Respir Dis 1989; 140:1-3 5 Derenne J~ Fleury B, Pariente R. Acute respiratory failure of chronic obstructive pulmonary disease. Am Rev Respir Dis
1988; 138: 1006-33
6 Kimball WR, Leith DE, Robins AG. Dynamic hyperinflation and ventilator dependence in chronic obstructive pulmonary disease. Am Rev Respir Dis 1982; 126:991-95 7 Brown DC, Pierson DJ. Auto-PEEP is common in mechanically ventilated patients: a study of incidence, severity, and detection.
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Respir Care 1986; 31: 1069-74 8 Gordon R. The deep sulcus sign. Radiology 1980; 136:25-27 9 EveloffSE, Rounds S, Braman SSe Unilateral lung hyperinflation and herniation as a manifestation of intrinsic PEE~ Chest 1990; 98:228-29 10 Marini JJ. Minimizing breathing effort during mechanical ventilation. In: Zapol WM, Lemaire F. eds. Adult respiratory distress syndrome. New York, NY: l\1arcel Dekker, Inc, 1991: 163-98 11 Gattinoni L, Mascheroni D, Torresin A, Marcolin R, Fumagelli R, Vesconi S, et al. Morphological response to positive endexpiratory pressure in acute respiratory failure: computerized tomo~raphy study. Intensive Care l\1ed ]986; 12: 137-42 12 Carlon GC, Kahn R, Howland \VS, Baron R, Ramaker J. Acute life-threatening ventilation-perfusion inequality: an indication for independent lung ventilation. Crit Care Med 1978; 6:380-83 13 Tuxen D~ Lane S. The effect of ventilatory pattern on hyperinflation, aim'ay pressures, and circulation in mechanical ventilation of patients with severe air-flov.' ohstnlt'tion. Am Rev Respir Dis 1987; 136:872-79 14 Scott LR, Benson MS, Bishop ~1J. Relationship of endotracheal tube size to auto-PEEP at high minute ventilation. Respir Care 1986; 31:1080-82 15 Dries DJ, Mathru M, Salem R, RaoT, MontoyaA. Hemodynamic compromise associated with air trapping following coronary artery bypass surgery. Chest 1990; 97: 1002-03 16 Rogers PL, Schlichtig R, Miro A, Pinsky M. Auto-PEEP during CPR: an ··occult.. cause of electromechanical dissociation? Chest 1991; 99:492-93 17 Kollef MH. Lung hyperinflation caused hy inappropriate ventilation resulting in electromechanical dissociation: a ease report. Heart Lung 1992; 21:74-77 18 Marini JJ, Culver BH, Butler J. Mechanical effect of lung distension with positive pressure on cardiac function. Am Rev Respir Dis 1981; 124:382-86 19 Butler J, Paley H\\Z Lung volume and pulmonary circulation. Med Thorac 1962; 19:261-67 20 Butler J. The heart is not always in good hands. Chest 1990; 97:453-60 21 Whittenher~er JL, McGregor M. Berglund E. Borst HG. Influence of state of inflation of the lung on pulmonary vascular resistance. J Appl Physiol 1960; 15:878-82
Intrinsic PEEP and Unilateral Lung Hyperinflation (Kollet, Turner)
