AJR 2000; 174:1339-1340
© American Roentgen Ray Society
Cardiovascular Instability Caused by Inadvertent Positive End-Expiratory Pressure in a Patient with Panlobular Emphysema Receiving Mechanical Ventilation
Radiographic—Physiologic Correlation
Anastasia V. Deliganis1,
Kenneth P. Steinberg2 and
Eric J. Stern1
1
Department of Radiology, Harborview Medical Center, Box 359728, University of
Washington, Seattle, WA 98104.
2
Department of Medicine, Harborview Medical Center, University of Washington,
Seattle, WA 98104.
Received May 27, 1999;
accepted after revision September 30, 1999.
Address correspondence to E. J. Stern.
Introduction
Chronic obstructive pulmonary disease encompasses several lung diseases
with shared features of decreased lung elastic recoil and increased airway
resistance. These abnormalities in pulmonary physiology lead to lung
hyperinflation and air-trapping. Mechanical ventilation in patients with
chronic obstructive pulmonary disease can result in the unintentional
development of positive end-expiratory pressure in the ductal airways and
alveoli [1]. This phenomenon
has been given many names including "inherent PEEP (positive
end-expiratory pressure)," "inadvertent PEEP,"
"intrinsic PEEP," "occult PEEP," and
"auto-PEEP" [2]. In
the patient receiving mechanical ventilation, inadvertent positive
end-expiratory pressure is generally the result of a ventilator delivering a
breath before the patient has completely exhaled the previous breath, leading
to further lung hyperinflation and excess intrathoracic pressure.
Panlobular pulmonary emphysema with a basilar dominance may be caused by
1-anti-protease deficiency and, less commonly, by the IV
injection of crushed methylphenidate hydrochloride tablets (Ritalin;
Ciba-Geigy, Summit, NJ); the latter condition is termed "Ritalin
lung" [3]. We report a
patient receiving mechanical ventilation who had panlobular emphysema caused
by Ritalin lung. This patient experienced severe cardiovascular instability
coincident with changes in ventilator settings and corresponding to new chest
abnormalities shown on radiography that were consistent with inadvertent
positive end-expiratory pressure.
Case Report
A 42-year-old woman with a history of cigarette smoking and IV injection of
Ritalin and the clinical features of diffuse pulmonary emphysema presented
with acute bronchitis, leading to respiratory failure and subsequent
intubation. Initial chest radiography (Fig.
1A) showed basilar-predominant pulmonary emphysema and linear
atelectasis without evidence of pneumonia or pneumothorax.
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Fig. 1A. —42-year-old woman with chronic obstructive pulmonary disease.
Initial chest radiograph, obtained after intubation, shows basilar-predominant
pulmonary emphysema and multiple areas of linear atelectasis consistent with
"Ritalin [Ciba-Geigy, Summit, NJ] lung."
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On admission, she was afebrile and slightly tachycardic, with a heart rate
of 110 beats per minute and a blood pressure of 150 over 90 mm Hg. She was
treated with bronchodilators, methylprednisolone, and antibiotics. Her
ventilator settings were pressure-support mode with a pressure support of 10
cm H2O, inspired oxygen concentration of 0.3, and positive
end-expiratory pressure of 5 cm H2O. Her respiratory rate ranged
from 14 to 22 breaths per minute with an average tidal volume of 350 ml. Her
total minute ventilation, therefore, ranged from 5 to 8 1. The auto positive
end-expiratory pressure was 6 cm H2O, only 1 cm H2O
higher than the set positive end-expiratory pressure. She could not be weaned
from ventilatory support because of weakness and malnutrition. After a week of
stable clinical course, she began to have periods of apnea caused by excessive
sedation and was treated by changing her ventilatory support to intermittent
mandatory ventilation with a rate of 12 breaths per minute and a tidal volume
of 450 ml. Her pressure support was continued, and her total respiratory rate
ranged from 12 to 20 breaths per minute, resulting in a minute ventilation of
approximately 9 1. The positive end-expiratory pressure setting remained at 5
cm H2O, but her auto positive end-expiratory pressure was now 15 cm
H2O. The resulting peak and static inspiratory pressures were 44
and 26 cm H2O, respectively. Her blood-oxygen saturation never
deteriorated.
Abruptly after the ventilator change, she became hypotensive (blood
pressure of 60 over 40 mm Hg), tachycardic, and then unconscious. For the next
several hours, she had severe autonomic instability with systolic blood
pressures ranging from 60 to 155 mm Hg and pulse from 90 to 160 beats per
minute. A portable chest radiograph (Fig.
1B) showed a decrease in cardiac size and severe air-trapping at
the lung bases, more severe in the left lung, without evidence of a
pneumothorax. She required IV fluid boluses and low-dose dopamine for blood
pressure support during the episodes of hypotension. Her urine output remained
good and a pulmonary artery catheter was never inserted. The ventilator was
returned to its previous settings (pressure-support mode alone), resulting in
a lower tidal volume of 325 ml and a lower minute ventilation of 6 1. Her
autonomic instability resolved. Twenty-four hours after stabilization, another
portable chest radiograph showed a decrease in basilar air-trapping and a
return of cardiac size to baseline (Fig.
1C). Three weeks later, she was weaned from the ventilator and
discharged to a skilled nursing facility for further pulmonary
rehabilitation.
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Fig. 1B. —42-year-old woman with chronic obstructive pulmonary disease. Chest
radiograph, obtained after change in mechanical ventilation with subsequent
labile vital signs, shows extensive and increased air-trapping at lung bases,
particularly on left lung, with new eversion of left hemidiaphragm. Heart size
is markedly decreased from that seen in A.
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Fig. 1C. —42-year-old woman with chronic obstructive pulmonary disease. Chest
radiograph, obtained after correction of mechanical ventilation and subsequent
stabilization in vital signs, shows lung bases, diaphragm, and heart have
returned to baseline appearance.
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Discussion
Patients receiving mechanical ventilation who have chronic obstructive
pulmonary disease are at particular risk for developing inadvertent positive
end-expiratory pressure caused by air-trapping; such patients need a prolonged
exhalation time. The clinical implications of inadvertent positive
end-expiratory pressure vary dramatically from no detectable effect
[2] to transient lung
hyperinflation [4,
5] and even to profound
hemodynamic compromise at higher ventilatory settings
[6].
The association of chronic obstructive pulmonary disease with
cardiovascular compromise because of excessive positive end-expiratory
pressure has been recognized and studied in both the clinical setting and in
experimental animal models. In a case report by Rogers et al.
[6], a patient with severe
chronic obstructive pulmonary disease who was receiving mechanical ventilation
during cardiopulmonary resuscitation developed pulseless electric activity.
Fifteen minutes after resuscitative efforts were halted, the patient showed
spontaneous respirations, a systolic blood pressure of 60 mm Hg, and sinus
tachycardia, presumably resulting from restored venous inflow after prolonged
exhalation.
In a dog model described by Marini et al.
[7], selective hyperinflation
of the lower lobes (particularly the right lower lobe) or any distention of
lung tissue adjacent to the right heart was associated with decreased stroke
volume. The decrease in stroke volume was more closely related to increased
right atrial pressure, rather than left atrial pressure, implying that
impaired venous return was the dominant cause of reduced cardiac output. This
mechanism is the likely cause for hypotension in patients with inadvertent
positive end-expiratory pressure. In our patient, cardiac output was never
directly measured, but a reduction in stroke volume and cardiac output was
presumed from her hypotension, tachycardia, and decline in mental status. No
other cause for the hypotension, such as sepsis or hemorrhage, was identified.
Myocardial infarction was ruled out by ECG and serial cardiac enzymes.
Our patient showed the radiographic manifestations of inadvertent positive
end-expiratory pressure causing cardiovascular instability. Although excessive
sedation may cause hypotension, we believe that was an unlikely cause in our
patient because of the temporal relationship between the ventilator changes
and the associated abnormalities shown on radiography. Patients with
predominately basilar pulmonary emphysema are at particular risk of
cardiovascular compromise with physiology analogous to that of a tension
pneumothorax and cardiac tamponade. Inadvertent positive end-expiratory
pressure may cause significant hyperinflation of the lung adjacent to the
heart and elevated intrathoracic pressures, thereby reducing venous return and
cardiac output, potentially leading to cardiac tamponade physiology.
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