Pleural Pressure: It’s Not Just for Chest Tubes Anymore Updates...When pneumothorax disrupts...

2
Respiratory physiology is all about pressure and gravity. Clinicians can manipulate these variables by using mechanical ventilation, changing the patient’s position and adjusting chest drain suction. It’s important to know how to enhance beneficial pressure changes and differentials and to minimize their harm- ful effects. Pressure Terms Transpulmonary pressure or transmural pressure is the differ- ence between alveolar and pleural pressure* – essentially the difference between pressures inside and outside the lung. Normally, it’s about 7cmH 2 O, but mechanical ventilation increas- es it by delivering volume under pressure. 1 Transpulmonary pressures significantly differ in regions of the lung depending on which is gravity dependent. 2 Adherence between the pleurae results in an absolute nega- tive pressure; this is what keeps the lungs expanding with the chest wall. In this discussion of respiratory mechanics when referring to the pressure outside the alveoli in relation to the atmospheric or mouth pressure, we’ll use the term intrathoracic pressure to minimize confusion with the always-negative pleural pressure. Volume Effect on Pressure Pleural pressure differentials depend on lung volume. In a study of pleural pressure changes, 3 at low lung volume during end exhalation, pleural pressure change was about -28 cmH 2 O. At 1200mL, it’s only -7, and at total lung capacity, it’s down to -2. Patients with air trapping have more air in their lungs all the time, so this explains their difficulty generating intrathoracic pressure changes needed to cough effectively. 3 Pleural pres- sure is the key to the challenges faced by patients as air trapping worsens. Research on morbidly obese patients showed airway open- ing pressure is greater than 1.3 cmH 2 O, which means intrathoracic pressure is positive at rest. The chest wall contains more volume and the lung is smaller, impairing lung mechanics and increasing work of breathing. 4 Balancing Recoil Forces Normally, the lung wants to collapse and the chest wall wants to expand. It’s the coupling of the pleurae that keep the lung and chest wall moving together. These opposing forces, called recoil, make the absolute pleural pressure negative and account for about 75% of all pleural pressure changes. 1,5,6 The resting volume of the lung is the balance between the elastic recoil pulling the lung in and the chest wall out. Resting volume is high in COPD, leaving less room for fresh air; it’s low in fibrosis (increased lung recoil), making it harder to expand the lungs. 1,5 When pneumothorax disrupts pleural adhesion, recoil takes over, worsening lung collapse and expanding the pleural space. 1 This recoil factor is why the size of the pneumothorax does not always correlate with the size of the hole in the pleura. A study of lung transplant patients 7 showed that negative pleural pressure significantly increased peak airway pressures and reduced compliance compared with neutral pleural pres- sures. Negative pleural pressure counteracted the lung’s normal recoil, causing alveolar hyperinflation. The combination of neg- ative pleural pressure with positive pressure ventilation in patients whose new lungs are undersized in relation to the size of the thoracic cavity can contribute to graft failure. To minimize this transpulmonary pressure gradient, these surgeons avoid chest drain suction on at-risk patients. 7 A number of research studies have examined how COPD affects work of breathing. 3 Increased resistance and decreased compliance require respiratory muscles to generate more nega- tive pleural pressure to overcome recoil and inflate the lung. 3 This is hard work. Persons exercising heavily or those with lung disease can use more than 30% of their energy to breathe. Normal respiratory energy expenditure is 2% at rest. 1 Weak, malnourished patients with hypoxia can wear out and go into respiratory failure simply from the work it takes to breathe. Typically, 70% of total work of breathing overcomes elastic recoil and 30% overrides the friction of air flowing through the airways. 1 Volutrauma and Barotrauma Volutrauma and barotrauma are caused by high transpul- monary pressures during mechanical ventilation. 2 This can be high alveolar pressure from the ventilator, low pleural pressure or a combination of the two. Gravity effects cause regional vari- ations in pressure and volume; these are determined by patient positioning: supine, prone, or with the head of the bed elevat- ed. 2,4,5,8 *Studies that look at pleural pressure measured esophageal pressure to avoid opening the pleural space 2,4,6,8 Pleural Pressure: It’s Not Just for Chest Tubes Anymore Clinical Update is edited by Patricia Carroll, MS, RN-BC, CEN, RRT, and supported by an educational grant from Atrium Medical Corporation. Spring 2013 Continued on page 2 Pressures Inspiration (mmHg) Exhalation (mmHg) Pleural Progressively decreases (755) Progressively increases (758) Alveolar Below atmospheric (757) Above atmospheric (763) Mouth 760 (zero reference point) 760 (zero reference point) Transpulmonary 2 5 Flow In Out Table 1. Pressures During Spontaneous Breathing

Transcript of Pleural Pressure: It’s Not Just for Chest Tubes Anymore Updates...When pneumothorax disrupts...

Page 1: Pleural Pressure: It’s Not Just for Chest Tubes Anymore Updates...When pneumothorax disrupts pleural adhesion, recoil takes over, worsening lung collapse and expanding the pleural

Respiratory physiology is all about pressure and gravity.Clinicians can manipulate these variables by using mechanicalventilation, changing the patient’s position and adjusting chestdrain suction. It’s important to know how to enhance beneficialpressure changes and differentials and to minimize their harm-ful effects.

Pressure TermsTranspulmonary pressure or transmural pressure is the differ-

ence between alveolar and pleural pressure* – essentially thedifference between pressures inside and outside the lung.Normally, it’s about 7cmH2O, but mechanical ventilation increas-es it by delivering volume under pressure.1 Transpulmonarypressures significantly differ in regions of the lung depending onwhich is gravity dependent.2

Adherence between the pleurae results in an absolute nega-tive pressure; this is what keeps the lungs expanding with thechest wall. In this discussion of respiratory mechanics whenreferring to the pressure outside the alveoli in relation to theatmospheric or mouth pressure, we’ll use the term intrathoracicpressure to minimize confusion with the always-negative pleuralpressure.

Volume Effect on PressurePleural pressure differentials depend on lung volume. In a

study of pleural pressure changes,3 at low lung volume duringend exhalation, pleural pressure change was about -28 cmH2O.At 1200mL, it’s only -7, and at total lung capacity, it’s down to -2. Patients with air trapping have more air in their lungs all thetime, so this explains their difficulty generating intrathoracicpressure changes needed to cough effectively.3 Pleural pres-sure is the key to the challenges faced by patients as air trappingworsens.

Research on morbidly obese patients showed airway open-ing pressure is greater than 1.3 cmH2O, which meansintrathoracic pressure is positive at rest. The chest wall contains

more volume and the lung is smaller, impairing lung mechanicsand increasing work of breathing.4

Balancing Recoil ForcesNormally, the lung wants to collapse and the chest wall wants

to expand. It’s the coupling of the pleurae that keep the lung andchest wall moving together. These opposing forces, calledrecoil, make the absolute pleural pressure negative and accountfor about 75% of all pleural pressure changes.1,5,6 The restingvolume of the lung is the balance between the elastic recoilpulling the lung in and the chest wall out. Resting volume is highin COPD, leaving less room for fresh air; it’s low in fibrosis(increased lung recoil), making it harder to expand the lungs.1,5When pneumothorax disrupts pleural adhesion, recoil takesover, worsening lung collapse and expanding the pleuralspace.1 This recoil factor is why the size of the pneumothoraxdoes not always correlate with the size of the hole in the pleura.

A study of lung transplant patients7 showed that negativepleural pressure significantly increased peak airway pressuresand reduced compliance compared with neutral pleural pres-sures. Negative pleural pressure counteracted the lung’s normalrecoil, causing alveolar hyperinflation. The combination of neg-ative pleural pressure with positive pressure ventilation inpatients whose new lungs are undersized in relation to the sizeof the thoracic cavity can contribute to graft failure. To minimizethis transpulmonary pressure gradient, these surgeons avoidchest drain suction on at-risk patients.7

A number of research studies have examined how COPDaffects work of breathing.3 Increased resistance and decreasedcompliance require respiratory muscles to generate more nega-tive pleural pressure to overcome recoil and inflate the lung.3This is hard work. Persons exercising heavily or those with lungdisease can use more than 30% of their energy to breathe.Normal respiratory energy expenditure is 2% at rest.1 Weak,malnourished patients with hypoxia can wear out and go intorespiratory failure simply from the work it takes to breathe.Typically, 70% of total work of breathing overcomes elastic recoiland 30% overrides the friction of air flowing through the airways.1

Volutrauma and BarotraumaVolutrauma and barotrauma are caused by high transpul-

monary pressures during mechanical ventilation.2 This can behigh alveolar pressure from the ventilator, low pleural pressureor a combination of the two. Gravity effects cause regional vari-ations in pressure and volume; these are determined by patientpositioning: supine, prone, or with the head of the bed elevat-ed.2,4,5,8

*Studies that look at pleural pressure measured esophageal pressure to avoid opening thepleural space2,4,6,8

Pleural Pressure: It’s Not Just for Chest Tubes Anymore

Clinical Update is edited by Patricia Carroll, MS, RN-BC, CEN, RRT, andsupported by an educational grant from Atrium Medical Corporation.

Spring 2013

Continued on page 2

Pressures Inspiration (mmHg) Exhalation (mmHg)

Pleural Progressively decreases(755)

Progressively increases(758)

Alveolar Below atmospheric (757) Above atmospheric (763)

Mouth 760 (zero reference point) 760 (zero reference point)

Transpulmonary 2 5

Flow In Out

Table 1. Pressures During Spontaneous Breathing

Page 2: Pleural Pressure: It’s Not Just for Chest Tubes Anymore Updates...When pneumothorax disrupts pleural adhesion, recoil takes over, worsening lung collapse and expanding the pleural

In the LiteratureThe Cycle of Comorbidities

The current issue of Orthopaedic Nursing features an article thatdescribes a model to explain potential risks associated with delay-ing joint replacement surgery. The authors describe intersectingcycles: inactivity, chronic pain, and sleep disturbance and note thatit is not enough to identify risks of delay, but to also analyze howthese factors interplay with each other. While their focus is on jointreplacement, the model has value to examine comorbidities asso-ciated with inactivity resulting from a variety of conditions. Source: Camillo P, et al: The cycle of comorbidities. Orthopaedic Nursing2013;32(1):6-13. PubMed Citation

Early ICU Mobility Makes Dollars and SenseResearchers at Johns Hopkins and the University of Kentucky

report on their financial model for analyzing early mobility and phys-ical rehabilitation of critically ill patients in the current Critical CareMedicine. Variables include length-of-stay, per-day costs, programimplementation cost, and annual number of ICU admissions. Themodel was designed and implemented in an Excel spreadsheet, soit can be replicated without extensive data management support. Source: Lord RK et al: ICU early physical rehabilitation programs: financial mod-eling of cost savings. Critical Care Medicine 2013;41:717-724. PubMed Citation

End of Life Education ConsortiumThis consortium, initially funded by the Robert WoodJohnson Foundation, is a national education programdesigned to improve palliative nursing care. There aretrain-the-trainer and provider courses in the core cur-riculum, pediatrics, critical care, veterans care, and forAPRNs with prescriptive authority. In addition, the sitehas a number of online and publication resources.

http://www.aacn.nche.edu/elnec

Create Your Own InfographicsInfographics are the hot new way to share data. Whatstarted as a little box on the front page of USA Todayhas now grown to complex, beautiful, and easilyunderstood images. To create your own, you can visitthese sites (their blogs also have great tips for datavisualization and creating infographic resumes)

http://infogr.am/http://blog.visual.ly/http://www.piktochart.com

Spring 2013

Volutrauma is damage from too much volume in each ventila-tor breath. In gravity-dependent areas, alveoli remain closed, andin the uppermost regions, alveoli overfill and even rupture.5Overdistension causes an inflammatory response and injury atthe cellular level (now called biotrauma), contributing to ARDS.The low tidal volume strategy of 4 to 8 mL/kg IBW has producedsignificantly higher survival from ARDS worldwide, but no evi-dence that this is the best strategy for all patients requiringmechanical ventilation.

Barotrauma is a high level of positive pressure within the lungthat causes air to escape from alveolar spaces resulting in air leaksyndromes, pneumothorax, pulmonary interstitial emphysema,and free air in the thoracic cavity. It is most common with mechan-ical ventilation, but can also occur with diving (during ascent),blast injury, submarine escape training, and air bag deployment.Alveolar overstretching with high pressures will disrupt tissueinjured after thoracotomy or trauma much more than normal lungtissue. The stretching and shearing from the difference betweenpleural and alveolar pressures progress along this margin ofinjury.8 One study of pneumothorax determined the swings inpleural pressure during the respiratory cycle had greater effect onoxygenation than peak pressures. Smaller pressure swings wereassociated with smaller pneumothorax and had less effect onoxygenation.9

Under normal conditions, about 1.25% of a pneumothorax isabsorbed every 24 hours. It would take 16 days to absorb a 20%pneumothorax. Gas absorption depends on the gradient betweenthe PO2 in the pneumothorax and the capillaries. If the FIO2 isnear 100%, absorption will occur four to six times faster.

Pleural Pressure is KeyThe bottom line is that pleural pressure is the key to everything

that happens in breathing. When negative, it pulls the lungs openduring inspiration and when intrathoracic pressure is positive, it

compresses the alveoli to create a strong cough that will clear thelungs of secretions and maintain an open airway. That’s why pro-longed air leaks, pleural effusions and other complications relatingto the pleural space can be devastating to patient recovery.Sources1. Goodman BE: Pulmonary and renal pressure-flow relationships: what should betaught? Advances in Physiology Education 2001;25(2):15-28. PubMed Citation2. Sarge T, D Talmor: Targeting transpulmonary pressure to prevent ventilator inducedlung injury. Minerva Anestesiol 2009;75(5):293-299. PubMed Citation3. De Troyer A, TA Wilson: Effect of acute inflation on the mechanics of the inspiratorymuscles. Journal of Applied Physiology 2009;107(1):315-323. PubMed Citation4. Behazin N, SB Jones, RI Cohen, SH Loring: Respiratory restriction and elevated pleu-ral and esophageal pressures in morbid obesity. Journal of Applied Physiology2010;108(1):212-218. PubMed Citation5. DiCarlo SE: Teaching alveolar ventilation with simple, inexpensive models. Advancesin Physiology Education 2008;32(3):185-191. PubMed Citation6. McCarren B, JA Alison, RD Herbert: Manual vibration increases expiratory flow ratevia increased intrapleural pressure in healthy adults: an experimental study. AustralianJournal of Physiotherapy 2006;52(4):267-271. PubMed Citation7. Kozower BD, BF Meyers, AM Ciccone, TJ Guthrie, GA Patterson: Potential for detri-mental hyperinflation after lung transplantation with application of negative pleuralpressure to undersized lung grafts. J Thorac Cardiovasc Surg 2003;125(2):430-432.PubMed Citation8. Dries DJ, AB Adams, JJ Marini: Time course of physiologic variables in response toventilator-induced lung injury. Respiratory Care 2007;52(1):31-37. PubMed Citation9. Subotic D, D Mandaric, M Gajic, M Vukcevic: Uncertainties in the current understand-ing of gas exchange in spontaneous pneumothorax: effective lung ventilation may persistin a smaller-sized pneumothorax. Medical Hypotheses 2005;64(6):1144-1149. PubMedCitation

Continued from page 1