Preface to the Second Edition Simplify, simplify! Henry David ThoreauFor writers of technical books, there can be no better piece ofadvice. Around the time of writing the first edition – about adecade ago – there were very few monographs on this sub-ject: today, there are possibly no less than 20. Based on critical inputs, this edition stands thoroughlyrevamped. New chapters on ventilator waveforms, airwayhumidification, and aerosol therapy in the ICU now find aplace. Novel software-based modes of ventilation have beenincluded. Ventilator-associated pneumonia has been sepa-rated into a new chapter. Many new diagrams and algorithmshave been added. As in the previous edition, considerable energy has beenspent in presenting the material in a reader-friendly, conver-sational style. And as before, the book remains firmly rootedin physiology. My thanks are due to Madhu Reddy, Director of UniversitiesPress – formerly a professional associate and now a friend, P.Sudhir, my tireless Pulmonary Function Lab technician whofound the time to type the bits and pieces of this manuscriptin between patients, A. Sobha for superbly organizing mytime, Grant Weston and Cate Rogers at Springer, London,Balasaraswathi Jayakumar at Spi, India for her tremendoussupport, and to Dr. C. Eshwar Prasad, who, for his words ofadvice, I should have thanked years ago. vii
viii Preface to the Second Edition Above all, I thank my wife and daughters, forunderstanding.Hyderabad, India Ashfaq Hasan
Preface to the First EditionIn spite of technological advancements, it is generally agreedupon that mechanical ventilation is as yet not an exact science:therefore, it must still be something of an art. The sciencebehind the art of ventilation, however, has undergone a revolu-tion of sorts, with major conceptual shifts having occurred inthe last couple of decades. The care of patients with multiple life-threatening problemsis nothing short of a monumental challenge and only an enviedfew are equal to it. Burgeoning information has deluged thegeneralist and placed increasing reliance on the specialist, some-times with loss of focus in a clinical situation. Predictably, thishas led to the evolution of a team approach, but, for the novicein critical care, beginning the journey at the confluence of thevarious streams of medicine makes for a tempestuous voyage.Compounding the problem is the fact that monographs on spe-cialized areas such as mechanical ventilation are often hard tocome by. The beginner has often to sail, as it were, “an unchartedsea,” going mostly by what he hears and sees around him. It is the intent of this book to familiarize not only physicians,but also nurses and respiratory technologists with the conceptsthat underlie mechanical ventilation. A conscious attempt hasbeen made to stay in touch with medical physiology through-out this book, in order to specifically address the hows andwhys of mechanical ventilation. At the same time, this bookincorporates currently accepted strategies for the mechanicalventilation of patients with specific disorders; this should be ofsome value to specialists practicing in their respective ICUs.The graphs presented in this book are representative and arenot drawn to scale. ix
x Preface to the First Edition This book began where the writing of another was sus-pended. What was intended to be a short chapter in a hand-book of respiratory diseases outgrew its confines and expandedto the proportions of a book. No enterprise, however modest, can be successful withoutthe support of friends and well wishers, who in this case are toonumerous to mention individually. I thank my wife for herunflinching support and patience and my daughters for show-ing maturity and understanding beyond their years; in manyrespects, I have taken a long time to write this book. I alsoacknowledge Mr. Samuel Alfred for his excellent secretarialassistance and my colleagues, residents, and respiratory thera-pists for striving tirelessly, selflessly, and sometimes thanklesslyto mitigate the suffering of others. Ashfaq Hasan, 2003
2 Chapter 1. Historical Aspects of Mechanical Ventilationthe regular movement of the thorax that prevented asphyxia,but the maintenance of phasic airflow into the lungs. What waspossibly the first successful instance of human resuscitation bymouth-to-mouth breathing was described in 1744 by JohnFothergill in England. The use of bellows to resuscitate victims of near-drowningwas described by the Royal Humane Society in the eigh-teenth century.20 The society, also known as the “Society forthe Rescue of Drowned Persons” was constituted in 1767, butthe development of fatal pneumothoraces produced by vigor-ous attempts at resuscitation led to subsequent abandonmentof such techniques. John Hunter’s innovative double-bellowssystem (one bellow for blowing in fresh air, and another fordrawing out the contaminated air) was adapted by the Societyin 1782, and introduced a new concept into ventilatory care. In 1880, the endotracheal route was used, possibly for thefirst time, for cannulation of the trachea, and emerged as arealistic alternative to tracheotomy.14 Appreciation of the factthat life could be sustained by supporting the function of thelungs (and indeed the circulation) by external means led tothe development of machines devised for this purpose. In1838, Scottish physician John Dalziez described the first tankventilator. In 1864 a body-tank ventilator was developed byAlfred Jones of Kentucky.9 The patient was seated inside anair-tight box which enclosed his body, neck downwards.Negative pressure generated within the apparatus producedinspiration, and expiration was aided by the cyclical genera-tion of positive pressure at the end of each inspiratory breath.Jones took out a patent on his device which claimed that itcould cure not only paralysis, neuralgia, asthma and bronchi-tis, but also rheumatism, dyspepsia, seminal weakness anddeafness. Woillez’s hand-cranked “spirophore” (1876) andEgon Braun’s small wooden tank for the resuscitation ofasphyxiated children followed. The former, the doctor oper-ated by cranking a handle; the latter needed the treatingphysician to vigorously suck and blow into a tube attached tothe box that enclosed the patient. In respect of WilhelmShwake’s pneumatic chamber, the patient himself could lenda hand by pulling and pushing against the bellows.
Historical Aspects of Mechanical Ventilation 3 In 1929, Philip Drinker, Louis Shaw, and Charles McKhannat the Department of Ventilation, Illumination, and Physiology,of the Harvard Medical School introduced what they termed“an apparatus for the prolonged administration of artificialrespiration.”9 This team which included an engineer (Drinker),a physiologist (Shaw), and a physician (McKhann) saw thedevelopment of what was dubbed “the iron lung.” Drinker’sventilator relied on the application of negative pressure toexpand the chest, in a manner similar to Alfred Jones’ venti-lator. The subject (at first a paralyzed cat, and then usually apatient of poliomyelitis) was laid within an air-tight irontank. A padded collar around the patient’s neck provided aseal, and the pressure within the tank was rhythmically low-ered by pumps or bellows. Access to the patient for nursingwas understandably limited, though ports were provided forauscultation and monitoring.* Emerson, in 1931 in a variationupon this theme incorporated an apparatus with which it waspossible to additionally deliver positive pressure breaths atthe mouth; this made nursing easier. The patient could nowbe supported on positive pressure breaths alone, while thetank was opened periodically for nursing and examination. Toward the end of the nineteenth century, a ventilatorfunctioning on a similar principle as the iron tank was inde-pendently developed by Ignaz von Hauke of Austria, RudolfEisenmenger of Vienna, and Alexander Graham Bell of theUSA. Named so because of its similarity to the fifteenth cen-tury body armor, the “Cuirass” consisted of a breast plate anda back plate secured together to form an air-tight seal. Again,negative pressure generated by means of bellows (and duringsubsequent years, by a motor from a vacuum cleaner) pro-vided the negative pressure to repetitively expand the tho-racic cage and so move air in and out of the lungs. TheCuirass, by leaving the patient’s arms unencumbered, and by* A rich American financier’s son who developed poliomyelitis during avisit to China was transported back home in a Drinker-tank by a dozencaregivers which included seven Chinese nurses. He used the iron lungfor more than two decades during which he married and fathered threechildren.
4 Chapter 1. Historical Aspects of Mechanical Ventilationcausing less circulatory embarrassment, offered certainadvantages over the tank respirator; in fact, Eisenmenger’sCuirass was as much used for circulatory assistance duringresuscitation as it was for artificial ventilation. Despite itsadvantages, the Cuirass proved to be somewhat less efficientthan the tank respirator in providing mechanical assistance tobreathing. During the earliest years of the twentieth century, advancesin the field of thoracic surgery saw the design of a surgicalchamber by Ferdinand Sauerbruch in 1904. This chamberfunctioned much on the same lines as the tank respiratorexcept that the chamber included not only the patient’s torso,but the surgeon himself.4 Brauer reversed Sauerbruch’s prin-ciple of ventilation by enclosing only the patient’s head withina much smaller chamber which provided a positive pressure.In 1911, Drager designed his “Pulmotor,” a resuscitation unitwhich provided positive pressure inflation to the patient bymeans of a mask held upon the face. A tilted head positionalong with cricoid pressure (to prevent gastric insufflation ofair) aided ventilation. The unit was powered by a compressedgas cylinder, and used by the fire and police departments forthe resuscitation of victims.18 Negative pressure ventilators were extensively used dur-ing the polio epidemic that ravaged Los Angeles in 1948 andScandinavia in 1952. During the Scandinavian epidemic,nearly three thousand polio-affected patients were treated inthe Community Diseases Hospital of Copenhagen over aperiod of less than 6 months.16 The catastrophic mortalityduring the early days of the epidemic saw the use of thecuffed tracheostomy tube for the first time, in patients out-side operating theaters. The polio epidemics in USA andDenmark saw the development and refinement of many ofthe principles of positive pressure ventilation. In 1950, responding to a need for better ventilators, RayBennet and colleagues developed an accessory attachmentwith which it became possible to intermittently administerpositive pressure breaths in synchrony with the negativepressure breaths, delivered by a tank ventilator.3 The supple-mentation of negative pressure ventilation with intermittent
Historical Aspects of Mechanical Ventilation 5positive pressure breaths did result in a substantial reductionin mortality.9,12,13 Bennet’s valve had originally been designedto enable pilots to breathe comfortably at high altitudes. Theend of the Second World War saw the adaptation of theBennet valve to regulate the flow of gases within mechanicalventilators.17 Likewise, Forrest Bird’s aviation experiencesled to the design of the Bird Mark seven ventilator. Around this time, interest predictably focused on thephysiological effects of mechanical ventilation. Courmandand then Maloney and Whittenberger made important obser-vations on the hemodynamic effects of mechanical ventila-tion.15,17 By the mid 1950s, the concept of controlled mechanicalventilation had emerged. Engstrom’s paper, published in1963, expostulated upon the clinical effects of prolonged con-trolled ventilation.7 In this landmark report, Engstrom stressedon the “complete substitution of the spontaneous ventilationof the patient by taking over both the ventilatory work andthe control of the adequacy of ventilation” and so broughtinto definition, the concept of CMV. Engstrom developedventilator models in which the minute volume requirementsof the patient could be set. Setting the respiratory rate withina given minute ventilation determined the backup tidal vol-umes, and the overall effect was remarkably similar to theIMV mode in vogue today. Improvements in the design of the Bennet ventilators sawthe emergence of the familiar Puritan-Bennet machines. Thepopularity of the Bennet and Bird ventilators in USA (bothof which were pressure cycled) soon came to be rivaled bythe development of volume-cycled piston-driven ventilators.These volume preset Emerson ventilators better guaranteedtidal volumes, and became recognized as potential anesthesiamachines, as well as respiratory devices for long-term ventila-tory support. Toward the end of the 1960s, with increasing challengesbeing presented during the treatment of critically ill patientson artificial ventilation, there arose a need for specializedareas for superior supportive care. During this period, a newdisease entity came to be recognized, the Adult RespiratoryDistress Syndrome, or the acute respiratory distress syndrome
6 Chapter 1. Historical Aspects of Mechanical Ventilation(ARDS) as it is known today. Physicians were confrontedwith rising demands for the supportive care of patients withthis condition. The Respiratory Intensive Care Unit emergedas an important area for the treatment of critically ill patientsrequiring intensive monitoring. The use of positive end-expiratory pressure (PEEP) for the management of ARDSpatients came into vogue, principally through Ashbaugh andPetty’s revival of Poulton and Barach’s concepts of the 1930s.A number of investigators staked claim to the developmentof the concept of PEEP, but controversy did not preclude itsuseful application.19,21 In 1971, Gregory et al applied continuous positive pressureto the care of neonates with the neonatal respiratory distresssyndrome (NRDS) and showed that pediatric mechanicalventilation was possible. Several departures from the originaltheme of positive pressure ventilation followed, including thedevelopment of heroic measures for artificial support.1,5,8 Today’s ventilators have evolved from simple mechanicaldevices into highly complex microprocessor controlled systemswhich make for smoother patient-ventilator interaction. Suchsophistication has, however, shifted the appreciation of theventilator’s operational intricacies into the sphere of a new andnow indispensable specialist – the biomedical engineer. Of late, resurgence in the popularity of noninvasive posi-tive pressure breathing and the advent of high frequencypositive pressure ventilation have further invigorated thearea of mechanical ventilation; it also remains to be seenwhether the promise of certain as yet unconventional modesof ventilation will be borne out in the near future.References 1. Anderson HL, Steimle C, Shapiro M, et al Extracorporeal life support for adult cardiorespoiratory failure. Surgery. 1993; 114:161 2. Ashbaugh DG, Bigelow DB, Petty TL, et al Acute respiratory distress in adults. Lancet. 1967;2:319–323
References 7 3. Bennet VR, Bower AE, Dillon JB, Axelrod B. Investigation on care and treatment of poliomyelitis patients. Ann West Med Surg. 1950;4:561–582 4. Comroe JH. Retrospectorscope: Insights into Medical Discovery. Menlo park, CA: Von Gehr; 1977 5. Downs JB, Stock MC. Airway pressure release ventilation: a new concept in ventilatory support. Crit Care Med. 1987;15:459 6. Drinker P, Shaw LA. An apparatus for the prolonged adminis- tration of artificial respiration. 1. A design for adults and chil- dren. J Clin Invest. 1929;7:229–247 7. Engstrom CG. The clinical application of prolonged con- trolled ventilation. Acta Anasthesiol Scand [Suppl]. 1963;13: 1–52 8. Fort PF, Farmer C, Westerman J, et al High-frequency oscillatory ventilation for adult respiratory distress syndrome. Crit Care Med. 1997;25:937 9. Grenvik A, Eross B, Powner D. Historical survey of mechanical ventilation. Int Anesthesiol Clin. 1980;18:1–91 0. Heironimus TW. Mechanical Artificial Ventilation, Springfield, III, Charles C. Thomas; 19711 1. Hooke M. Of preserving animals alive by blowing through their lungs with bellows. Philo Trans R Soc. 1667;2:539–5401 2. Ibsen B. The anesthetist’s view point on treatment of respiratory complications in polio during epidemic in Copenhagen. Proc R Soc Med. 1954;47:72–741 3. Laurie G. Ventilator users, home care and independent living: An historical perspective. In: Kutscher AH, Gilgoff I (eds). The Ventilator: Psychosocial and Medical aspects. New York Foundation of Thanatology, 2001; p147–151.1 4. Macewen W. Clinical observations on the introduction of tra- cheal tubes by the mouth instead of performing tracheotomy or laryngotomy. Br Med J. 1880;2(122–124):163–1651 5. Maloney JV, Whittenberger JL. Clinical implications of pressures used in the body respiration. Am J Med Sci. 1951;221: 425–4301 6. Meyers RA. Mechanical support of respiration. Surg Clin North Am. 1974;54:11151 7. Motley HL, Cournand A, Werko L, et al Studies of intermittent positive pressure breathing as a means of administering artificial respiration in a man. JAMA. 1948;137:370–3871 8. Mushin WI, et al Automatic Ventilation of the Lungs. 2nd ed. Oxford, England: Blackwell Scientific; 1979
8 Chapter 1. Historical Aspects of Mechanical Ventilation1 9. Petty TL, Nett LM, Ashbaugh DG. Improvement in oxygenation in the adult respiratory distress syndrome by positive end expi- ratory pressure (PEEP). Respir Care. 1971;16:173–1762 0. Randel-Baker L. History of thoracic anesthesia. In: Mushin WW, ed. Thoracic anesthesia. Philadelphia: FA Davis; 1963:598–6612 1. Springer PR, Stevens PM. The influence of PEEP on survival of patients in respiratory failure. Am J Med. 1979;66:196–2002 2. Standiford TJ, Morganroth ML. High-frequency ventilation. Chest. 1989;96:13802 3. Stock MC, Downs JB, Frolicher DA. Airway pressure release ventilation. Crit Care Med. 1987;15:4622 4. Vesalius A. De humani corporis fabrica, Lib VII, cap. XIX De vivorum sectione nonulla, Basle, Operinus, 1543;658
10 Chapter 2. The Indications for Mechanical Ventilation Indications for intubation Indications for ventilation Need to secure airway Hypoxia: acute hypoxemic Depressed sensorium respiratory failure Depressed airway reflexes Hypoventilation Upper airway instability after Unacceptably high work of trauma breathing Decreased airway patency Hemodynamic compromise Need for sedation in the Cardiorespiratory arrest setting of poor airway Refractory shock control Raised intracranial pressure Imaging (CT, MRT) and Flail chest transportation of an unstable patientFigure 2.1. Indications for intubation ventilation.of hypoxemia with relatively low inspired O2 concentrations,thereby diminishing the risk of oxygen toxicity.2.2 HypoventilationA major indication for mechanical ventilation is when thealveolar ventilation falls short of the patient’s requirements.Conditions that depress the respiratory center produce adecline in alveolar ventilation with a rise in arterial CO2 ten-sion. A rising PaCO2 can also result from the hypoventilationthat results when fatiguing respiratory muscles are unable tosustain ventilation, as in a patient who is expending consider-able effort in moving air into stiffened or obstructed lungs.Under such circumstances, mechanical ventilation may beused to support gas exchange until the patient’s respiratorydrive has been restored, or tired respiratory muscles rejuve-nated, and the inciting pathology significantly resolved(Fig. 2.2).
2.3 Increased Work of Breathing 11 Hypoventilation results from decreased bulk flow in and out of the lungs Inspiration results in the bulk flow of air into the lungs, up to the level of the smallest bronchioles. Further progress of the gas molecules is by the mechanism of facilitated diffusion peripherally Disorders in which bulk flow to the lungs is compromised include Neuro-muscular disorders Proximal airway CNS depression (extra- Spinal cord or e.g., pulmonary e.g., peripheral nerve disorders Aminoglycosides airway) Sedative agents Disorders obstruction e.g., Paralysing agents affecting the Cerebrovascular e.g., accidents Spinal trauma Steroid myopathy thoracic cage Tracheal Central sleep Amyotrophic Myasthenia e.g., obstruction by apnea lateral sclerosis gravis Kyphoscoliosis stenosis, tumor Metabolic Polio Muscular Flail chest etc alkalosis dystrophies Multiple sclerosis Ankylosing Epiglottitis Myxedema Dyselectrolyte spondylosis Guillian Barre Obstructive sleep mias Hyperoxia syndrome apnea (Hyperoxic Poor nutrition Botulism hypoventilation) Respiratory muscle fatigueFigure 2.2. Causes of Hypoventilation.2.3 Increased Work of BreathingAnother major category where assisted ventilation is used isin those situations in which excessive work of breathingresults in hemodynamic compromise. Here, even though gasexchange may not be actually impaired, the increased workof breathing because of either high airway resistance or poorlung compliance may impose a substantial burden on, forexample, a compromised myocardium. When oxygen delivery to the tissues is compromised onaccount of impaired myocardial function, mechanical ventila-tion by resting the respiratory muscles can reduce the workof breathing. This reduces the oxygen consumption of therespiratory muscles and results in better perfusion of themyocardium itself.
12 Chapter 2. The Indications for Mechanical Ventilation2.4 Other IndicationsIn addition to these major indications, mechanical ventilationmay be of value in certain specific conditions. The vasoconstric-tion produced by deliberate hyperventilation can reduce thevolume of the cerebral vascular compartment, helping to reduceraised intracranial pressures. In flail chest, mechanical ventila-tion can be used to provide internal stabilization of the thoraxwhen multiple rib fractures compromise the integrity of thechest wall; in such cases, mechanical ventilation using positiveend-expiratory pressure (PEEP) normalizes thoracic and lungmechanics, so that adequate gas exchange becomes possible. Where postoperative pain or neuromuscular disease limitslung expansion, mechanical ventilation can be employed topreserve a reasonable functional residual capacity within thelungs and prevent atelectasis. These issues have been specifi-cally addressed in Chap. 9.2.5 Criteria for Intubation and VentilationWhile the prevailing criteria for defining the need for intuba-tion and ventilation of a patient in respiratory failure havemet general acceptance, these are largely intuitive and basedupon the subjective assessment of a patient’s condition(Fig. 2.3 and Table 2.1). See also Chap. 12 . Objective criteria that are in current use are a forced expi-ratory volume in the first second (FEV1) of less than 10 mL/kgbody weight and a forced vital capacity (FVC) of less than15 mL/kg body weight, both of which indicate a poor ventila-tory capability. Similarly, a respiratory rate higher than 35 breaths/minwould mean an unacceptably high work of breathing and asubstantial degree of respiratory distress, and is recognized asone of the criteria for intubation and ventilation. A PaCO2 inexcess of 55 mmHg (especially if rising, and in the presenceof acidemia) would likewise imply the onset of respiratorymuscle fatigue. Except in habitual CO2 retainers, a PaCO2 of
2.5 Criteria for Intubation and Ventilation 13 B. In such a case a normal PaCO2 means that the CO2 has begun to rise back towards normal as a result of respiratory muscle fatigue A. Hyperventilation results in PaCO2 wash out, producing respiratory alkalosisFigure 2.3. PaCO2 in status asthmaticus.55 mmHg and over would normally reflect severe respiratorymuscle dysfunction. Documented PaCO2 from an earlier stage of the patient’spresent illness may have considerable bearing on the inter-pretation of subsequent PaCO2 levels (Fig. 2.3). For example,in an asthmatic patient in acute severe exacerbation,b ronchospasm-induced hyperventilation can be expected to“wash out” the CO2 from the blood, producing respiratoryalkalosis. If in such a patient, the blood gas analysis were toshow a normal PaCO2 level, this would imply that thehypoventilation produced by respiratory muscle fatigue hasallowed the PaCO2 to rise back to normal. It is important torealize here, that although the PaCO2 is now in the normalrange, it is actually on its way up, and if this is not appreci-ated, neither the PaCO2 nor the patient will stay normal forvery long. A supranormal PaCO2 in status asthmaticusshould certainly be a cause of alarm and reinforce the needfor mechanical ventilatory support. A PaO2 of less than 55–60 mmHg on 0.5 FIO2 or a widenedA-a DO2 gradient (of 450 mmHg and beyond on 100% O2)
14Table 2.1. Criteria for ventilation.Criteria value Normal range Critical level CommentRespiratory muscle performanceMaximum −50 to −100 cm More positive Useful in neuromuscular patients. Can be measured by a Bourdon inspiratory H2O than manometer interfaced to the patient by a mask, mouthpiece, or ET pressure (MIP) −20 cm adaptor. Ideally, MIP measurements should be made after maximal H2O exhalationMaximum +100 cm H2O Less than expiratory 40 cm pressure (MEP) H2OVital capacity (VC) 65–75 mL/kg 15 mL/kg Measured at the bedside with a pneumotachometer or a hand-held spirometerTidal volume (V1) 5–8 mL/kg 5 mL/kg Measured at the bedside with a pneumotachometer or a hand-held spirometerRespiratory 12–20 breaths/ 35 breaths/ A high respiratory frequency indicates increased work of breathing, and frequency (f) min min may be indicative of impending respiratory muscle exhaustionForced expired 50–60 mL/kg 10 mL/kg Important in evaluating the degree of airway obstruction in COPD/ volume at 1 s asthma. May be difficult or exhausting for the severely obstructed (FEV1) patientPeak expiratory 350–600 L/min 100 L/min Important in evaluating the degree of airway obstruction in COPD/ flow asthma. May be difficult or exhausting for the severely obstructed patient Chapter 2. The Indications for Mechanical VentilationVentilationpH 7.35–7.45 7.25 A falling pH from respiratory acidosis is a late feature of respiratory muscle fatigue
Criteria value Normal range Critical level CommentPaCO2 35–45 mmHg 55 mmHg, A rising PaCO2 from respiratory acidosis is a late feature of respiratory and rising muscle fatigueVD/VT 0.3–0.4 0.6 Dead-space ventilation can be easily calculated at the bedside using capnometry and blood gas analysis (see Chap. 3)Oxygenation (low values indicate the need for oxygen therapy or PEEP/CPAP; mechanical ventilation may be required if hypoxemia is nonresponsive to the above support, or is very severe)PaO2 80–100 mmHg 60 mmHg A PaO2 of 60 mmHg represents the approximate point where the slope (on FIO2 of the oxy-hemoglobin dissociation curve abruptly changes. As the 0.5) PaO2 drops further below 60 mmHg, the SpO2 can be expected to fall sharplyAlveolar-to- 3–30 mmHg 450 mmHg The A-a DO2 is the difference between the alveolar O2 tension (PAO2) arterial oxygen (on high and the arterial oxygen tension (PaO2), and is a measure of the ease difference concen with which the administered oxygen diffuses into the pulmonary trations of capillary blood O2)Arterial/alveolar 0.75 0.15 The PaO2/PAO2 ratio is the proportion of oxygen in the alveolus that PO2 eventually gains entry into the pulmonary capillary blood. The PaO2 is easily read out from the ABG, but the PAO2 cannot be directly measured and needs to be calculated from the alveolar gas equation (see section 7.1) 2.5 Criteria for Intubation and VentilationPaO2/FIO2 475 200 The PaO2/FIO2 ratio obviates the need to calculate PAO2 (which can be something of an effort for those who are mathematically challenged!) 15
16 Chapter 2. The Indications for Mechanical Ventilationmeans that the gas exchange mechanisms in the lung arederanged to a degree that cannot be supported by externaloxygen devices alone, and that intubation and ventilation isrequired for effective support. It is important to emphasize that the criteria for intubationand ventilation are meant to serve as a guide to the physicianwho must view them in the context of the clinical situation.Conversely, the patient does not necessarily have to satisfyevery criterion for intubation and ventilation in order to be acandidate for invasive ventilatory management. Importantly,improvement or worsening in the trends within these num-bers provide the key to judgment in a borderline situation. Itmust also be pointed out that with the advent of noninvasivepositive pressure ventilation as a potential tool for the treat-ment of early respiratory failure, some of the criteria for theinstitution of mechanical ventilatory support may need to berevisited. These issues have been discussed in Chap. 13.References 1. Brochard L. Profuse diaphoresis as an important sign for the differential diagnosis of acute respiratory distress. Intensive Care Med. 1992;18:445 2. Comroe JH, Botelho S. The unreliability of cyanosis in the rec- ognition of arterial anoxemia. Am J Med Sci. 1947;214:1–6 3. Gibson GJ, Pride NB, Davis JN, et al Pulmonary mechanics in patients with respiratory muscle weakness. Am Rev Respir Dis. 1977;115:389–395 4. Gilston A. Facial signs of respiratory distress after cardiac sur- gery: a plea for the clinical approach to mechanical ventilation. Anaesthesia. 1976;31:385–397 5. Hess DR, Branson RD. In: Hess DR, MacIntyre NR, Mishoe SC, et al, eds. Respiratory care: principles and practices. Philadelphia: WB Saunders; 2003 6. Kacmarek RM, Cheever P, Foley K, et al Deterination of vital capacity in mechanically ventilated patients: a comparison of techniques. Respir Care. 1990;35(11):129
References 17 7. Lundsgaard C, Van Slyke DD. Cyanosis. Medicine. 1923;2:1–76 8. Manthous CA, Hall JB, Kushner R, et al The effect of mechani- cal ventilation on oxygen consumption in critically ill patients. Am J Respir Crit Care Med. 1995;151:210–214 9. Medd WE, French EB, McA Wyllie V. Cyanosis as a guide to arterial oxygen desaturation. Thorax. 1959;14:247–25010. Mithoefer JC, Bossman OG, Thibeault DW, Mead GD. The clini- cal estimation of alveolar ventilation. Am Rev Respir Dis. 1968;98:868–87111. Perrigault PF, Pouzeratte YH, Jaber S, et al Changes in occlusion pressure (P0.1) and breathing pattern during pressure support ventilation. Thorax. 1999;54:119–12312. Semmes BJ, Tobin MJ, Snyder JV, Grenvik A. Subjective and objective measurement of tidal volume in critically ill patients. Chest. 1985;87:577–57913. Slutsky AS. Mechanical ventilation. American College of Chest Physicians’ Consensus Conference. Chest. 1993;104:183314. Strohl KP, O’Cain CF, Slutsky AS. Alae nasi activation and nasal resistance in healthy subjects. J Appl Physiol. 1982;52:1432–143715. Tobin MJ, Guenther SM, Perez W, et al Konno-Mead analysis of ridcage- abdominal motion during successful and unsuccessful trials of weaning from mechanical ventilation. Am Rev Respir Dis. 1987;135:1320–132816. Tobin MJ, Jenouri GA, Watson H, Sackner MA. Noninvasive measurement of pleural pressure by surface inductive plethys- mography. J Appl Physiol. 1983;55:267–27517. Tobin MJ, Mador MJ, Guenther SM, et al Variability of resting respiratory drive and timing in healthy subjects. J Appl Physiol. 1988;65:309–31718. Tobin MJ. Respiratory muscles in disease. Clin Chest Med. 1988;9:263–28619. Tobin MJ. Noninvasive monitoring of ventilation. In: Tobin MJ, ed. Principles and Practice of Intensive Care Monitoring. New York: NcGraw-Hill; 1998:465–49520. Tobin MJ, Perez W, Guenther SM, et al Does rib cage-abdominal paradox signify respiratory muscle fatigue? J Appl Physiol. 1987;63:851–860
20 Chapter 3. Physiological Considerations Poiseuille’s law states that the resistance (Raw) to the flowof fluids through a long and narrow tube is proportional tothe length of the tube (l) and the viscosity of the fluid (h). Significantly, resistance is inversely proportional to thefourth power of the radius (r). This means that small changes inthe radius can have inordinate effects on airway resistance.6, 13 Poiseuille’s law applies to the continuous flow of fluids atlow flow rates (laminar flow) in long straight tubes. The endotracheal tube, however, is neither long norstraight. The length of an endotracheal tube is typically24–26 cm. This length may not suffice for the conditions forlaminar flow to develop, as demanded by Poiseuille’s classicequation. Bends in the endotracheal tube interfere with lami-nar flow and produce turbulence, as do the almost ubiquitoussecretions that are adherent to its luminal surface.84 Moreover,the flow within the endotracheal tube is not constant: a highflow rate engenders further turbulence. Turbulent rather than laminar flow is therefore the rule inthe endotracheal tube, and this adds to the airflow resis-tance.46 Increased resistance to the airflow translates intoincreased work of breathing. Contributing to the work ofbreathing, as an independent factor, is the bend in the tubeitself.73 The endotracheal tube is especially liable to becomesharply angulated when the nasotracheal route is preferred.Any kinking of the tube or biting upon it by the patient isliable to compromise the tubal diameter and has a majorimpact on airflow resistance. Despite the fact that Poiseuille’s equation may not be rel-evant in its totality in clinical situations, the effect of variationin endotracheal tube radius can have a tremendous effect onairway resistance.50 Interestingly, the replacement of the relatively straight endotracheal tube with the shorter but more angulated tracheos-tomy tube (of an identical internal diameter) appears to conferno additional advantage with respect to airflow resistance: inexperimental animals, the work of breathing in either situationremains the same.72 Owing to its shorter length, the tracheos-tomy tube can be expected to offer less resistance to airflow,compared to the endotracheal tube. In fact, the dditionala
3.2 Positive Pressure Breathing 21turbulence in airflow produced by the crook in the tracheos-tomy tube negates the advantage of its shorter length. Box 3.1 Poiseuille’s Law According to Poiseuille’s law, the resistance to air flow varies as a function of tube diameter. Poiseuille’s law is summarized by the equation Raw = 8 hl/pr4 where Raw is the resistance to flow of fluids (in this case, air) within long and narrow tubes (airways), h is the viscosity of the fluid (air) flowing within the tubes (airways), r is the radius of the tubes (airways). In the clinical context, the length of the airways and the viscosity of the air cannot vary. The only variable is the radius of the tubes, which, of course, is proportional to the airway diameter. If, hypothetically speaking, airway radius were to be halved, the airflow resistance calculated as per Poiseuille’s formula would go up 16-fold because airway radius is raised to the power of 4. What this means is that even a slight nar- rowing in the diameter of either the patient’s intrinsic airways or in the endotracheal tube is likely to amplify airway resis- tance greatly.3.2 Positive Pressure BreathingIn the spontaneously breathing individual, inspiration is active.The descent of the diaphragm during inspiration increases thevertical size of the thorax; contraction of the scalenii increasesthe anteroposterior thoracic diameter (by elevating the ribs bya pump-handle movement), and contraction of the parasternalgroup of muscles increases the transverse thoracic diameter (bya bucket-handle movement). The overall result is an increasedintrathoracic volume, and a fall in intrathoracic pressure (ITP)secondary to it. From its usual end-expiratory level of –5 cmH2O, the intrapleural pressure falls to −10 cm H2O at the heightof inspiration. As a result, the alveolar pressure becomes nega-tive relative to atmospheric pressure, and air flows into the
22 Chapter 3. Physiological Considerationsbronchial tree, and through it, to the alveoli. Exhalation is pas-sive and returns the intrathoracic volume to FRC at the end oftidal expiration. During positive pressure breathing (PPB), inspirationoccurs when the central airway pressure is raised above atmo-spheric pressure, impelling the air into the respiratory tract. Asin the spontaneously breathing subject, expiration is passive. The commonly encountered intrathoracic pressures dur-ing breathing have been defined in Fig. 3.1. Four types of pressure gradients are encountered withinthe lung70 (see Fig. 3.2). The transpulmonary pressure (PTA),also known as the lung distending pressure, is the pressuredifference between the alveolar pressure (PALV) and intrapleu-ral pressure (see also Chap 8). Lung inflation occurs when thePTA increases. During spontaneous breathing and negativepressure ventilation, it is the drop in intrathoracic pressurethat causes the PTA to increase; on the other hand, the increasein PTA during PPB occurs as a result of an increase in PALV (seeFig. 3.2). PTA is unchanged when forced inspiratory or expira-tory efforts are made against the closed glottis, and so there isno bulk airflow, respectively, in or out of the lungs. The pressure required for overcoming resistance andelastance during lung inflation can now be worked out(Figs. 3.3 and 3.4). The major difference between physiological breathing andpositive pressure ventilation lies in the intrathoracic pres-sures during inspiration. In the spontaneously breathing sub-ject, the intrathoracic pressure during inspiration is negativeto the atmospheric pressure. In the mechanically ventilatedpatient on positive pressure ventilation, intrathoracic pres-sure is positive – this has far reaching implications on therespiratory and circulatory systems (Fig. 3.5). In the normal lung, in an erect individual, there exists avertical gradient in the pleural pressure. Intrapleural pressureis more negative at the lung apices than at the bases, primar-ily because of the effect of the weight of the lung. Intrapleuralpressure falls by approximately 0.25 cm of H2O for each cen-timeter of lung height. This gradient is also influenced by thehilar attachments of the lung, the shape of the thorax (which
3.2 Positive Pressure Breathing 23 Airway Opening Pressure (Pawo) • This is the pressure applied at the airway Syn: opening (mouth or the patient tube) Airway pressure (Paw), • In the absence of positive pressure breathing Mouth pressure (PM), (through endotracheal tube, tracheostomy Upper airway pressure, tube or noninvasively by mask), the Paw is proximal airway pressure, equal to atmospheric pressure mask pressure • The pressure at the body surface • Again this pressure is equal to atmospheric Body surface pressure pressure unless the patient’s body is (Pbs) subjected to negative pressure (as within a negative pressure ventilator see chapter 14) or a positive pressure (hyperbaric chamber) • The pressure within the pleural space • During spontaneous breathing this is Intrapleural normally, minus 5cm H2O at end-exhalation, pressure (Ppl) and minus 10 cm H2O at end-inspiration. • The surrogate measurement for Ppl is esophageal pressure (Pes) which can be measured using an esophageal balloon Alveolar pressure • During spontaneous breathing, alveolar (PA or PALV) pressure is negative to the atmosphericSyn: pressure during inspiration (minus 1 cm H2O), and positive to atmosphericIntrapulmonary pressure, pressure during exhalation (1 cm H2O)Lung pressureFigure 3.1. Intrathoracic pressures.is more tapered toward the top) and the abdominal contents(which push upward upon the lung bases). As the negativity of intrapleural pressure is greater in theupper regions of the lung, the alveoli in the upper lung zoneswill be larger and more patent than those in the lower zones.During a normal inspiration, the alveoli in the lower lung
24 Chapter 3. Physiological Considerations Trans-airway pressure (PTA)The difference between • It is the pressure responsible for driving thethe airway opening bulk flow through the airways.pressure (Pawo) and the • Produced by the resistance to airflow withinalveolar pressure (PALV): the conducting airways. PTA = Pawo − PALV Transpulmonary pressure (PTP)Syn • The pressure required to distened the lung • When PTP increases, the lung distendsTransalveolar pressure • PTP can be made to increase by either (PA), Alveolar distending increasing the Palv (by positive pressure pressure: The difference ventilation) or by decreasing the PPL between the alveolar (by negative pressure ventilation). pressure (PALV) and the See also fig. 3.4 intrapleural pressure (PPL): PTP = PALV − PPL Trans-Thoracic Pressure (P w or p TT)The difference betweenthe alveolar pressure • It is the pressure required to distend the(PALV) and the body lungs along with the thoracic cage.surface pressure (Pbs): PTT = PALV − PbsTransrespiratory-system • It is the pressure required to expand the pressure lungs (pressure required to overcomeThe difference between elastance), and also to produce airflowthe airway opening (pressure required to overcome resistance).pressure (pressure at the • P therefore has two components: TRmouth or patient tube) and Transairway pressure (P ) which performs TAthe pressure at the body the resistive work, and transthoracic pressuresurface): (PTT) which performs the elastic work. PTR = Pawo − PbsFigure 3.2. Pressure gradients within the thorax.zones (which are of relatively smaller end-expiratory volume)are capable of greater expansion, and so comparatively moreinspired air goes to the dependent zones. The lower lung
3.2 Positive Pressure Breathing 25 Transrespiratory system Transairway Transthoracic pressure pressure (PTA) pressure (PTT) The pressure at the Airway opening Alveolar pressure airway opening (mouth pressure minus minus body surface or patient tube) minus the alveolar pressure the pressure at the pressure body surface)Figure 3.3. Distending pressures of the respiratory system. Spontaneous Valsalva Muller breathing or manoeuvre manoeuvre Positive negative (forced (forced pressure pressure expiration inspiration breathing: breathing: against the against the inspiration inspiration closed glottis) closed glottis) Both ITP and Both ITP and Decrease in ITP PALV increase by PALV decrease Increase in PALV relative to PALV the same by the same relative to ITP amount amount PTA increases PTA does not PTA does not PTA increases change change Lung does not Lung does not Lung inflation deflate despite inflate despite Lung inflation occurs an increase in an decrease in occurs the ITP the ITPFigure 3.4. Intrathoracic pressures during spontaneous and positivepressure breaths.regions due to gravitational effects are also better perfused,and since they are better ventilated as well, there is more com-plete matching of ventilation and perfusion in these areas. When the patient is ventilated with positive pressure breaths,the normal intrapleural pressure gradient is reduced. Also, asthe alveolar units in the nondependent regions of the lung aremore compliant than those in the dependent areas, they are
26 Chapter 3. Physiological Considerations Intrapleural pressure is more negative at the apices of the lung As a result of this, air units in the upper zones are relatively large at end expiration Air units in the dependent parts of the lung are relatively small at end expiration: they are therefore capable of greater expansion when inflated Insipratory tidal volumes are therefore mostly dispersed to the dependent lung units (In other words, dependent lung units are better ventilated) Due to the effects of gravity the dependent portions lung are relatively well perfused There is better matching of ventiation and perfusion in the dependent lung unitsFigure 3.5. Matching of ventilation and perfusion during spontane-ous breathing.
3.2 Positive Pressure Breathing 27preferentially ventilated with positive pressure breaths. Theincreased ventilation to these relatively poorly perfused areasresults in wasted ventilation. In other words, alveolar dead-space increases. With those modes of ventilation, that do not require activeparticipation from the patient’s inspiratory muscles, lack of dia-phragmatic contractility encourages regional closure of alveoliat the lung bases; though ventilation in these areas is compro-mised, perfusion is still intact, and shunting of blood occurscausing a further derangement in blood gases (Fig. 3.6). Ventilation of dependent lung units is decreasedPositive pressure breathing enlarges theend-expiratory volume of dependent lung During full mechanicalunits (which are better perfused than the ventilatory support, non-dependent units). there is lack of Since these air units undergo less diaphragmatic activity volume change from end-expiration to end-inspiration, they are therefore no longer preferentially ventilated.Ventilation of non-dependent air units is increased Alveolar units in the Non-dependent air units are generally dependent units of themore compliant than dependent air units. lung undergo closureTidal volumes are therefore preferentially directed into these units Increase in dead-spaceIn comparsion to spontaneous breathing, Increase in shunt fraction mechanical ventilation better ventilates the non-dependent air units. Since the Since perfusion to these nondependent units are relatively less ill-ventilated areas is intact, perfused (due to gravitational effects), the V/Q ratio decreases V/Q ratio increases (i.e., dead (i.e., shunt fraction increases) space increases)Figure 3.6. Matching of ventilation and perfusion during positivepressure breathing.
28 Chapter 3. Physiological Considerations Nevertheless, despite the potential regional derangementsin pulmonary physiology that occur as a consequence of PPB,the overall benefits of mechanical ventilation brought aboutby the restoration and maintenance of alveolar patency andby the elevation of mean alveolar pressures usually overrideits potential drawbacks. Box 3.2 Pressure Required for Overcoming Resistance and Elastance PTR = PTA + PTT , Since PTA = Pawo – PALV and PTT = PALV – Pbs , Substituting, PTR = Pawo – PALV + PALV – Pbs Since Pbs is atmospheric pressure, its value is regarded as 0. The equation now becomes: PTR = Pawo – PALV + PALV – 0 PTA = Pawo Pawo is read off the ventilator panel3.3 Lung ComplianceCompliant = yielding (The Oxford Dictionary). The compliance of the lung is a measure of its distensibility.If a large change in volume is achieved by applying a rela-tively small amount of airway pressure, the lung is easily dis-tensible and is said to be highly compliant. A stiff and poorlycompliant lung resists expansion and only a small change involume occurs with a relatively large change in pressure. When lung compliance is plotted on a graph, with volumeon the y-axis and pressure on the x-axis, the pressure–volumecurve that is obtained is relatively flat and horizontal in itsupper and lower portions, and steep and vertical in between.
3.3 Lung Compliance 29In health, the lung operates on the middle steep part of thepressure–volume curve. At very low and very high lung vol-umes, the lung operates on the lower and upper flat portionsof the curve, respectively, where the pressure required tobring about a given change in volume is considerable. Here,consequently, respiratory mechanics are inefficient and thework of breathing is high. The total compliance of the respiratory system is the resultof summation of the effects of lung compliance and thoracicwall compliance. Compliance has two components, static and dynamic.3.3.1 Static ComplianceThe term compliance when used alone and in an unqualifiedmanner (i.e., without a prefix) usually refers to static compli-ance. Static compliance is the true measure of distensibility ofthe respiratory system (lung + chest wall). The change in volume between the beginning and end of atidal breath (DV) is the tidal volume itself (Vt). The change inthe pressure required (DP) to accomplish this change in volumeis the plateau pressure when the lung is at rest. If there is anyapplied PEEP or auto-PEEP, this value must be subtractedfrom the plateau pressure to give the true DP (otherwise, therewill be a spurious decrease in measured compliance). With rare exception, the chest wall compliance remains sta-ble within fairly narrow limits, and this is true in most clinicalsituations. It is rather the compliance of the lung parenchymawhich varies, and underlines any change in the compliance ofthe respiratory system as a whole. Another factor that influences the measured complianceof the respiratory system in the ventilated patient is the elas-tic pressure exerted by the ventilator tubing on the air in theventilator circuit. This too, like thoracic wall compliance,remains fairly constant in a given patient. In a mechanically ventilated patient with an essentiallynormal chest wall and lungs, the static compliance of therespiratory system is usually in the range of 70–100 mL/cm