CASE CONFERENCES The Clinical Physiologist Section Editor: John Kreit, M.D.
Don’t Waste Your Breath Chitra Deepak Punjabi1, Yu Kuang Lai1, Malek Numeir 2, and Ganesan Murali2 1
Department of Internal Medicine, and 2Division of Pulmonology, Einstein Medical Center, Philadelphia, Pennsylvania
Keywords: single lung ventilation; dead space ventilation; lung compliance
In Brief A patient with extensive, unilateral lung disease presented with respiratory failure and required mechanical ventilatory support. Despite an elevated minute ventilation, the patient had a severe respiratory acidosis that failed to resolve with additional increases in respiratory rate and tidal volume. An understanding of the underlying pathophysiology allowed us to find an alternate therapy that successfully corrected the patient’s hypercapnia and acidemia.
Additional history revealed that the patient had been born prematurely but had been healthy until about 8 years earlier,
when he developed cough and hemoptysis. At that time, CT showed a large left upper lobe cavity with an air-fluid level. Since that
The Clinical Challenge A 49-year-old man presented to the emergency department with progressive dyspnea. His blood pressure was160/80 mm Hg, his respiratory rate was 28 breaths per minute, his heart rate was 124 beats per minute, and his arterial hemoglobin saturation (SpO2) was 90% while wearing a “nonrebreather” oxygen mask. Crackles were heard throughout the right lung, and breath sounds were absent on the left. Digital clubbing was prominent. A chest radiograph showed absent left-sided lung markings. Computed tomography (CT) demonstrated almost complete destruction of the left lung, which was replaced by a multi-loculated cavity (Figure 1). The patient was intubated and admitted to the intensive care unit.
Figure 1. Axial and coronal computed tomography images.
(Received in original form February 11, 2014; accepted in final form April 23, 2014 ) Correspondence and requests for reprints should be addressed to Chitra Deepak Punjabi, M.D., Department of Internal Medicine, Einstein Medical Center, Klein 303, 5501 Old York Road, Philadelphia, PA 19141. E-mail: [email protected] Ann Am Thorac Soc Vol 11, No 5, pp 844–847, Jun 2014 Copyright © 2014 by the American Thoracic Society DOI: 10.1513/AnnalsATS.201402-058CC Internet address: www.atsjournals.org
844
AnnalsATS Volume 11 Number 5 | June 2014
CASE CONFERENCES Table 1. Chronologic list of interventions, ventilator settings, and arterial blood gas results
1 2 3 4 5
Single-lumen ET tube Single-lumen ET tube Double-lumen ET tube Single-lumen ET tube Bronchial blocker
VT (ml)
RR
V_ E (L/min)
pH
PCO2 (mm Hg)
450 500 385 500 350
32 34 30 30 28
14.4 17.0 11.5 15.0 9.8
7.04 7.23 7.34 6.92 7.38
124 81 56 .126 68
Definition of abbreviations: ET = endotracheal; RR = respiratory rate.
time, the patient’s sputum had grown nontuberculous Mycobacteria and Aspergillus, but despite appropriate therapy, he had developed progressive left lung cavitation and destruction. After intubation, arterial blood gas (ABG) measurements (Table 1, Row 1) showed a severe respiratory acidosis with an elevated minute ventilation. The patient remained markedly acidemic, even after additional increases in the set tidal volume and respiratory rate (Table 1, Row 2).
Questions 1. What is the cause of the patient’s hypercapnia? 2. How can his hypercapnia and respiratory acidosis be most effectively corrected?
Clinical Reasoning The PaCO2 is determined by the relationship between the rate at which CO2 enters and leaves the alveoli. Carbon dioxide diffuses into alveolar gas in proportion to the rate at : which it is produced by the tissues ðVCO2 Þ, while its excretion by the lungs : is directly related to alveolar ventilation ðVAÞ. Mathematically, this is expressed as: : : PaCO2 a VCO2 VA
We recognized that : our patient had a marked increase in VD because : he had hypercapnia despite an elevated VE. We also recognized that the left lung was the source of the excessive dead space. The marked reduction in elastic recoil (increased compliance) had diverted most of the inspired volume into the left lung. At the same time, the extensive parenchymal destruction prevented pulmonary arterial blood from contacting the inspired gas. We concluded that this marked overventilation relative to perfusion had converted most of the left lung into alveolar dead space. Normally, respiratory acidosis in a mechanically ventilated patient is easily corrected by increasing the set tidal volume and respiratory rate. This was relatively ineffective in our patient because of his asymmetric lung compliance and the : magnitude of his VD. We therefore chose “the road less traveled” and performed : interventions to directly reduce VD.
The Clinical Solution Under bronchoscopic guidance, a doublelumen endotracheal tube was inserted,
and the lumen to the left lung was occluded (Figures 2A and 2B). This was accompanied by a dramatic improvement in pH and P CO2 at a lower minute ventilation (Table 1, Row 3). Unfortunately, the double-lumen tube became dislodged and the patient again developed a severe respiratory acidosis after reintubation with a single-lumen endotracheal tube (Table 1, Row 4). Ultimately, a bronchial blocker (Figure 2C) was used to occlude the left main bronchus. A much lower minute ventilation was then needed to correct the patient’s pH (Table 1, Row 5).
The Science behind the Solution Minute Ventilation, Alveolar Ventilation, and Dead Space Ventilation :
The minute ventilation ðVEÞ is the total volume of gas that moves in and out of the lungs each minute. It is the product of tidal volume (VT) and respiratory rate (RR). :
VE ¼ VT 3 RR :
ðEq:1Þ
In a healthy adult, VE is approximately 6 L/minute. A significant portion of each tidal breath never reaches the alveoli. This is the gas that fills the anatomic dead space, which consists of the upper airway and the conducting airways of the lungs. Since this gas is never in contact with pulmonary capillary blood, it cannot participate in gas exchange. Another portion of the tidal breath reaches alveoli that either receive no blood flow or are relatively under-perfused. These high
Since alveolar ventilation is the difference between minute ventilation (VE) and dead : space ventilation ðVDÞ, this can be modified to: : : : PaCO2 a VCO2 VE2VD :
This equation tells us that if VCO2 is constant, hypercapnia must be : caused by either: (1) a :primary fall in VE, or (2) an increase in VD that is : not accompanied by an identical rise in VE.
Figure 2. A double-lumen endotracheal (ET) tube allows each lung to be (A) isolated or (B) ventilated separately. (C) A bronchial blocker is placed through a single-lumen ET tube and can isolate a lobe or an entire lung. Reproduced by permission from Prasanna Tilakaratna, M.B.B.S., http://www.howequipmentworks.com/physics/airway/ett/endotracheal_tubes.html.
Case Conferences: The Clinical Physiologist
845
CASE CONFERENCES :
:
ventilation–perfusion (V=Q) regions are referred to as the alveolar dead space, and the sum of the anatomic and alveolar dead space is known as the physiologic dead space. The portion of the tidal volume that fills the physiologic dead space is called the dead space volume (VD ). The alveolar volume (VA) is the gas that actually reaches appropriately perfused alveoli and is the difference between tidal volume and dead space volume. VA ¼ VT 2 VD
ðEq:2Þ
The volume of gas that enters and leaves the physiologic dead space each minute is called : the dead space ventilation ðVDÞ. :
VD ¼ VD 3 RR :
ðEq:3Þ
The alveolar ventilation ðVAÞ is that portion of the minute ventilation that actually supplies O2 to, and removes CO2 from, the alveolar capillary blood. :
VA ¼ VA 3 RR :
:
:
VA ¼ VE 2 VD
ðEq:4Þ ðEq:5Þ
The Ratio of Dead Space Volume to Tidal Volume
The dead space to tidal volume ratio (VD/VT) quantifies the fraction of each tidal breath that does not participate in gas exchange. At rest, VD/VT is normally 0.25– 0.30. That is, 25–30% of each breath fills : A is usually the physiologic dead space and V : about 70–75% of VE. The ratio of dead space to tidal volume rises, and the efficiency and effectiveness of ventilation falls, as VT decreases and as physiologic dead space increases. The Bohr-Enghoff equation allows VD/VT to be calculated by measuring the partial pressure of CO2 in the arterial blood (PaCO2) and in a large volume of mixed, exhaled gas (PECO2). VD=VT ¼ ðPaCO2 2 Pe CO2 Þ=PaCO2 ðEq:6 Þ Alternatively, VD/VT can be calculated using volume capnography or estimated by plotting simultaneous measurements of : PaCO2 and VE on a nomogram (Figure 3). Ventilation and PaCO2
The partial pressure of carbon dioxide in the alveolar gas (PACO2) is determined by the rates at which CO2 enters and leaves the 846
Figure 3. Nomogram showing the relationship between minute ventilation, arterial PCO2, and the ratio of physiologic dead space to tidal volume. Reproduction by permission from Selecky and colleagues, Am Rev Respir Dis 1978;117:181–184.
alveoli. Carbon dioxide diffuses into the alveolar gas at a rate proportional to its partial pressure in mixed venous blood (P vCO2), which, in turn, depends on the rate at: which CO2 is produced by the tissues ðVCO2 Þ. That is, :
PACO2 a VCO2
ðEq:7 Þ
The removal or excretion of CO2 from the alveoli is directly proportional to alveolar ventilation.: Thus, PACO2 is inversely related to VA. : PACO2 a 1 VA ðEq:8Þ Combining Equations 7 and 8 yields: : : PACO2 a VCO2 VA ðEq:9Þ If we assume that alveolar and arterial PCO 2 are equal, this equation can be modified to: : : ðEq:10Þ PaCO2 a VCO2 VA This is one of the most important equations in : pulmonary physiology. It tells us that if VCO2 is : constant, PaCO2 :varies inversely with VA. For example, if VA decreases by 50%, CO2 excretion is also halved and insights are PaCO2 will double. Additional : : : provided by substituting ðVE2VDÞ for VA
(see Equation 5) and by performing some algebraic manipulations. : : : ðEq:11Þ PaCO2 a VCO2 VE2VD : : PaCO2 a VCO2 VE½12ðVD=VTÞ ðEq:12Þ
These equations tell us that CO2 excretion and PaCO2 are critically dependent on the volume of the physiologic dead space. As : : VD and VD/VT rise, VE must also increase if PaCO2 is to remain constant. Ventilation and Asymmetric Lung Disease
Compliance (C) is defined as the change in volume (DV) produced by a change in pressure (DP). C ¼ DV=DP
ðEq:13Þ
During mechanical ventilation, DP is the difference between end-expiratory and endinspiratory alveolar pressure and DV is the delivered tidal volume. If Equation 13 is rearranged, DV ¼ C 3 DP;
ðEq:14Þ
it becomes evident that for a given change in alveolar pressure, tidal volume varies directly with compliance.
AnnalsATS Volume 11 Number 5 | June 2014
CASE CONFERENCES to the compliance of each lung. For example, as illustrated in Figure 4, if one lung has twice the compliance of the other, it will receive twice as much volume. Putting It All Together
Figure 4. The relationship between lung compliance and lung volume during a mechanical breath. At a given airway pressure, the lung with higher compliance receives more of the delivered tidal volume.
Our patient had severe, unilateral lung disease. The reduction in elastic recoil (increased compliance) caused the left lung to be overventilated, while parenchymal destruction caused it to be underperfused. This high ratio of ventilation to perfusion generated a huge volume of alveolar dead space, which : markedly increased V D /VT and VD and could have been corrected: only by an equally large increase in VE. We instead chose to directly eliminate the excess dead space by stopping ventilation to the left lung. Following stabilization, the next step in our patient’s care would have been a left pneumonectomy. However, the patient had previously made it clear that he did not want surgery or prolonged mechanical ventilation. With this in mind, his family decided to withdraw life-sustaining therapy. n
It follows that in patients with unilateral or asymmetric parenchymal
Author disclosures are available with the text of this article at www.atsjournals.org.
lung disease, the inspired tidal volume will be distributed in proportion
Recommended Reading Martin L. Pulmonary physiology in clinical practice. St. Louis: C.V. Mosby Co., 1987. Selecky PA, Wasserman K, Klein M, Ziment I. A graphic approach to assessing interrelationships among minute ventilation, arterial carbon dioxide tension, and ratio of physiologic dead space to tidal volume in patients on respirators. Am Rev Respir Dis 1978;117: 181–184.
Case Conferences: The Clinical Physiologist
Carlon GC, Ray C Jr, Klein R, Goldiner PL, Miodownik S. Criteria for selective positive end-expiratory pressure and independent synchronized ventilation of each lung. Chest 1978;74:501–507. Manthous CA, Goulding P. The effect of volume infusion on dead space in mechanically ventilated patients with severe asthma. Chest 1997;112: 843–846. Kallet RH, Alonso JA, Pittet JF, Matthay MA. Prognostic value of the pulmonary dead-space fraction during the first 6 days of acute respiratory distress syndrome. Respir Care 2004;49:1008–1014.
847
Don’t Waste Your Breath Chitra Deepak Punjabi1, Yu Kuang Lai1, Malek Numeir 2, and Ganesan Murali2 1
Department of Internal Medicine, and 2Division of Pulmonology, Einstein Medical Center, Philadelphia, Pennsylvania
Keywords: single lung ventilation; dead space ventilation; lung compliance
In Brief A patient with extensive, unilateral lung disease presented with respiratory failure and required mechanical ventilatory support. Despite an elevated minute ventilation, the patient had a severe respiratory acidosis that failed to resolve with additional increases in respiratory rate and tidal volume. An understanding of the underlying pathophysiology allowed us to find an alternate therapy that successfully corrected the patient’s hypercapnia and acidemia.
Additional history revealed that the patient had been born prematurely but had been healthy until about 8 years earlier,
when he developed cough and hemoptysis. At that time, CT showed a large left upper lobe cavity with an air-fluid level. Since that
The Clinical Challenge A 49-year-old man presented to the emergency department with progressive dyspnea. His blood pressure was160/80 mm Hg, his respiratory rate was 28 breaths per minute, his heart rate was 124 beats per minute, and his arterial hemoglobin saturation (SpO2) was 90% while wearing a “nonrebreather” oxygen mask. Crackles were heard throughout the right lung, and breath sounds were absent on the left. Digital clubbing was prominent. A chest radiograph showed absent left-sided lung markings. Computed tomography (CT) demonstrated almost complete destruction of the left lung, which was replaced by a multi-loculated cavity (Figure 1). The patient was intubated and admitted to the intensive care unit.
Figure 1. Axial and coronal computed tomography images.
(Received in original form February 11, 2014; accepted in final form April 23, 2014 ) Correspondence and requests for reprints should be addressed to Chitra Deepak Punjabi, M.D., Department of Internal Medicine, Einstein Medical Center, Klein 303, 5501 Old York Road, Philadelphia, PA 19141. E-mail: [email protected] Ann Am Thorac Soc Vol 11, No 5, pp 844–847, Jun 2014 Copyright © 2014 by the American Thoracic Society DOI: 10.1513/AnnalsATS.201402-058CC Internet address: www.atsjournals.org
844
AnnalsATS Volume 11 Number 5 | June 2014
CASE CONFERENCES Table 1. Chronologic list of interventions, ventilator settings, and arterial blood gas results
1 2 3 4 5
Single-lumen ET tube Single-lumen ET tube Double-lumen ET tube Single-lumen ET tube Bronchial blocker
VT (ml)
RR
V_ E (L/min)
pH
PCO2 (mm Hg)
450 500 385 500 350
32 34 30 30 28
14.4 17.0 11.5 15.0 9.8
7.04 7.23 7.34 6.92 7.38
124 81 56 .126 68
Definition of abbreviations: ET = endotracheal; RR = respiratory rate.
time, the patient’s sputum had grown nontuberculous Mycobacteria and Aspergillus, but despite appropriate therapy, he had developed progressive left lung cavitation and destruction. After intubation, arterial blood gas (ABG) measurements (Table 1, Row 1) showed a severe respiratory acidosis with an elevated minute ventilation. The patient remained markedly acidemic, even after additional increases in the set tidal volume and respiratory rate (Table 1, Row 2).
Questions 1. What is the cause of the patient’s hypercapnia? 2. How can his hypercapnia and respiratory acidosis be most effectively corrected?
Clinical Reasoning The PaCO2 is determined by the relationship between the rate at which CO2 enters and leaves the alveoli. Carbon dioxide diffuses into alveolar gas in proportion to the rate at : which it is produced by the tissues ðVCO2 Þ, while its excretion by the lungs : is directly related to alveolar ventilation ðVAÞ. Mathematically, this is expressed as: : : PaCO2 a VCO2 VA
We recognized that : our patient had a marked increase in VD because : he had hypercapnia despite an elevated VE. We also recognized that the left lung was the source of the excessive dead space. The marked reduction in elastic recoil (increased compliance) had diverted most of the inspired volume into the left lung. At the same time, the extensive parenchymal destruction prevented pulmonary arterial blood from contacting the inspired gas. We concluded that this marked overventilation relative to perfusion had converted most of the left lung into alveolar dead space. Normally, respiratory acidosis in a mechanically ventilated patient is easily corrected by increasing the set tidal volume and respiratory rate. This was relatively ineffective in our patient because of his asymmetric lung compliance and the : magnitude of his VD. We therefore chose “the road less traveled” and performed : interventions to directly reduce VD.
The Clinical Solution Under bronchoscopic guidance, a doublelumen endotracheal tube was inserted,
and the lumen to the left lung was occluded (Figures 2A and 2B). This was accompanied by a dramatic improvement in pH and P CO2 at a lower minute ventilation (Table 1, Row 3). Unfortunately, the double-lumen tube became dislodged and the patient again developed a severe respiratory acidosis after reintubation with a single-lumen endotracheal tube (Table 1, Row 4). Ultimately, a bronchial blocker (Figure 2C) was used to occlude the left main bronchus. A much lower minute ventilation was then needed to correct the patient’s pH (Table 1, Row 5).
The Science behind the Solution Minute Ventilation, Alveolar Ventilation, and Dead Space Ventilation :
The minute ventilation ðVEÞ is the total volume of gas that moves in and out of the lungs each minute. It is the product of tidal volume (VT) and respiratory rate (RR). :
VE ¼ VT 3 RR :
ðEq:1Þ
In a healthy adult, VE is approximately 6 L/minute. A significant portion of each tidal breath never reaches the alveoli. This is the gas that fills the anatomic dead space, which consists of the upper airway and the conducting airways of the lungs. Since this gas is never in contact with pulmonary capillary blood, it cannot participate in gas exchange. Another portion of the tidal breath reaches alveoli that either receive no blood flow or are relatively under-perfused. These high
Since alveolar ventilation is the difference between minute ventilation (VE) and dead : space ventilation ðVDÞ, this can be modified to: : : : PaCO2 a VCO2 VE2VD :
This equation tells us that if VCO2 is constant, hypercapnia must be : caused by either: (1) a :primary fall in VE, or (2) an increase in VD that is : not accompanied by an identical rise in VE.
Figure 2. A double-lumen endotracheal (ET) tube allows each lung to be (A) isolated or (B) ventilated separately. (C) A bronchial blocker is placed through a single-lumen ET tube and can isolate a lobe or an entire lung. Reproduced by permission from Prasanna Tilakaratna, M.B.B.S., http://www.howequipmentworks.com/physics/airway/ett/endotracheal_tubes.html.
Case Conferences: The Clinical Physiologist
845
CASE CONFERENCES :
:
ventilation–perfusion (V=Q) regions are referred to as the alveolar dead space, and the sum of the anatomic and alveolar dead space is known as the physiologic dead space. The portion of the tidal volume that fills the physiologic dead space is called the dead space volume (VD ). The alveolar volume (VA) is the gas that actually reaches appropriately perfused alveoli and is the difference between tidal volume and dead space volume. VA ¼ VT 2 VD
ðEq:2Þ
The volume of gas that enters and leaves the physiologic dead space each minute is called : the dead space ventilation ðVDÞ. :
VD ¼ VD 3 RR :
ðEq:3Þ
The alveolar ventilation ðVAÞ is that portion of the minute ventilation that actually supplies O2 to, and removes CO2 from, the alveolar capillary blood. :
VA ¼ VA 3 RR :
:
:
VA ¼ VE 2 VD
ðEq:4Þ ðEq:5Þ
The Ratio of Dead Space Volume to Tidal Volume
The dead space to tidal volume ratio (VD/VT) quantifies the fraction of each tidal breath that does not participate in gas exchange. At rest, VD/VT is normally 0.25– 0.30. That is, 25–30% of each breath fills : A is usually the physiologic dead space and V : about 70–75% of VE. The ratio of dead space to tidal volume rises, and the efficiency and effectiveness of ventilation falls, as VT decreases and as physiologic dead space increases. The Bohr-Enghoff equation allows VD/VT to be calculated by measuring the partial pressure of CO2 in the arterial blood (PaCO2) and in a large volume of mixed, exhaled gas (PECO2). VD=VT ¼ ðPaCO2 2 Pe CO2 Þ=PaCO2 ðEq:6 Þ Alternatively, VD/VT can be calculated using volume capnography or estimated by plotting simultaneous measurements of : PaCO2 and VE on a nomogram (Figure 3). Ventilation and PaCO2
The partial pressure of carbon dioxide in the alveolar gas (PACO2) is determined by the rates at which CO2 enters and leaves the 846
Figure 3. Nomogram showing the relationship between minute ventilation, arterial PCO2, and the ratio of physiologic dead space to tidal volume. Reproduction by permission from Selecky and colleagues, Am Rev Respir Dis 1978;117:181–184.
alveoli. Carbon dioxide diffuses into the alveolar gas at a rate proportional to its partial pressure in mixed venous blood (P vCO2), which, in turn, depends on the rate at: which CO2 is produced by the tissues ðVCO2 Þ. That is, :
PACO2 a VCO2
ðEq:7 Þ
The removal or excretion of CO2 from the alveoli is directly proportional to alveolar ventilation.: Thus, PACO2 is inversely related to VA. : PACO2 a 1 VA ðEq:8Þ Combining Equations 7 and 8 yields: : : PACO2 a VCO2 VA ðEq:9Þ If we assume that alveolar and arterial PCO 2 are equal, this equation can be modified to: : : ðEq:10Þ PaCO2 a VCO2 VA This is one of the most important equations in : pulmonary physiology. It tells us that if VCO2 is : constant, PaCO2 :varies inversely with VA. For example, if VA decreases by 50%, CO2 excretion is also halved and insights are PaCO2 will double. Additional : : : provided by substituting ðVE2VDÞ for VA
(see Equation 5) and by performing some algebraic manipulations. : : : ðEq:11Þ PaCO2 a VCO2 VE2VD : : PaCO2 a VCO2 VE½12ðVD=VTÞ ðEq:12Þ
These equations tell us that CO2 excretion and PaCO2 are critically dependent on the volume of the physiologic dead space. As : : VD and VD/VT rise, VE must also increase if PaCO2 is to remain constant. Ventilation and Asymmetric Lung Disease
Compliance (C) is defined as the change in volume (DV) produced by a change in pressure (DP). C ¼ DV=DP
ðEq:13Þ
During mechanical ventilation, DP is the difference between end-expiratory and endinspiratory alveolar pressure and DV is the delivered tidal volume. If Equation 13 is rearranged, DV ¼ C 3 DP;
ðEq:14Þ
it becomes evident that for a given change in alveolar pressure, tidal volume varies directly with compliance.
AnnalsATS Volume 11 Number 5 | June 2014
CASE CONFERENCES to the compliance of each lung. For example, as illustrated in Figure 4, if one lung has twice the compliance of the other, it will receive twice as much volume. Putting It All Together
Figure 4. The relationship between lung compliance and lung volume during a mechanical breath. At a given airway pressure, the lung with higher compliance receives more of the delivered tidal volume.
Our patient had severe, unilateral lung disease. The reduction in elastic recoil (increased compliance) caused the left lung to be overventilated, while parenchymal destruction caused it to be underperfused. This high ratio of ventilation to perfusion generated a huge volume of alveolar dead space, which : markedly increased V D /VT and VD and could have been corrected: only by an equally large increase in VE. We instead chose to directly eliminate the excess dead space by stopping ventilation to the left lung. Following stabilization, the next step in our patient’s care would have been a left pneumonectomy. However, the patient had previously made it clear that he did not want surgery or prolonged mechanical ventilation. With this in mind, his family decided to withdraw life-sustaining therapy. n
It follows that in patients with unilateral or asymmetric parenchymal
Author disclosures are available with the text of this article at www.atsjournals.org.
lung disease, the inspired tidal volume will be distributed in proportion
Recommended Reading Martin L. Pulmonary physiology in clinical practice. St. Louis: C.V. Mosby Co., 1987. Selecky PA, Wasserman K, Klein M, Ziment I. A graphic approach to assessing interrelationships among minute ventilation, arterial carbon dioxide tension, and ratio of physiologic dead space to tidal volume in patients on respirators. Am Rev Respir Dis 1978;117: 181–184.
Case Conferences: The Clinical Physiologist
Carlon GC, Ray C Jr, Klein R, Goldiner PL, Miodownik S. Criteria for selective positive end-expiratory pressure and independent synchronized ventilation of each lung. Chest 1978;74:501–507. Manthous CA, Goulding P. The effect of volume infusion on dead space in mechanically ventilated patients with severe asthma. Chest 1997;112: 843–846. Kallet RH, Alonso JA, Pittet JF, Matthay MA. Prognostic value of the pulmonary dead-space fraction during the first 6 days of acute respiratory distress syndrome. Respir Care 2004;49:1008–1014.
847
