ARDS/CARDIOPULMONARY RESUSCITATION
From Survey of Current Issues in Surgical Anesthesia, sponsored by the Cleveland Clinic Foundation, Division of
Anesthesiology, Critical Care Medicine, and Comprehensive Pain Management, November 28 to December 2, 2007,
Naples, FL
Educational Objectives
| The goal of this program is to improve anesthetic management of acute respiratory distress syndrome (ARDS) and review
new evidence for cardiopulmonary resuscitation (CPR). After hearing and assimilating this program, the clinician will be
better able to:
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 | 1. Describe diagnostic criteria for ARDS.
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| 2. Clarify the concept of protective ventilation strategy.
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| 3. Recognize the usefulness of other strategies in the management of ARDS, including positioning, recruitment maneuvers,
higher vs lower positive end-expiratory pressure, restrictive vs liberal fluid management, use of a pulmonary artery
catheter, and steroids for late-stage fibroproliferative disease.
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| 4. Discuss the history of CPR and the process of developing consensus guidelines.
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| 5. Review new evidence about the performance of CPR and advanced cardiac life support.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning
committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of interest.
Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a
proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose.
Acknowledgements
Drs. Popovich and Tetzlaff spoke in Naples, FL, at Survey of Current Issues in Surgical Anesthesia, held November 28
to December 2, 2007, and sponsored by the Cleveland Clinic Foundation, Division of Anesthesiology, Critical Care
Medicine, and Comprehensive Pain Management. The Audio-Digest Foundation thanks the speakers and the sponsors
for their cooperation in the production of this program.
| MANAGEMENT OF ACUTE RESPIRATORY DISTRESS SYNDROME: AN UPDATE —Marc J. Popovich, MD, Professional
Staff Physician, Department of General Anesthesiology, and Director, Surgical Critical Care, Cleveland Clinic,
Cleveland, OH
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| History: 2007 marks 40th anniversary of first description of acute respiratory distress syndrome (ARDS) in Lancet
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| Presentation: acute onset; predisposing condition; gas exchange abnormality (PaO2 /FiO2 <200 mm Hg; less severe form
known as acute lung injury [PaO2 /FiO2 <300 mm Hg]); bilateral infiltrates seen on chest radiography; no evidence of
left-sided heart failure
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| Pathophysiology: normal alveolus consists of type I and type II cells and basement membrane; epithelial lining protects
crossover from endothelial lining and capillaries; narrow space allows for easy gas exchange; type II cells produce surfactant
to keep alveoli open with only small pressure change; in ARDS, predisposing condition leads to development of inflammatory
mediators and cells, breakdown of type I cell lining, loss of surfactant effect, and increased permeability
between epithelial layer and endothelial layer; gas exchange more difficult
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| Background: form of noncardiogenic pulmonary edema; results from acute damage to alveoli, leading to hypoxemia;
mortality rate 30% to 50%; direct—toxin to alveolar-epithelial membrane; examples include aspiration, drowning, and
toxic inhalation; indirect—generalized inflammation (standard in surgical intensive care unit [SICU] and surgical patients);
includes pancreatitis, burns, sepsis, trauma, and massive transfusion
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| Investigations: during first 30 yr, some clinicians thought that, eg, exogenous surfactant might be beneficial; studies
showed no benefit; others studied nitric oxide (no benefit), ketoconazole (no benefit), extracorporeal membrane oxygenation
(ECMO; no benefit), and liquid ventilation (fluorocarbons placed directly into endotracheal tube to improve ventilation; inconclusive)
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| First review point: ARDS heterogenous disease; Gattinoni study in 1980s used computed tomography (CT) to investigate
patients with ARDS; CT shows areas of disease surrounded by areas of normal lung
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| Path of least resistance: during mechanical ventilation, gas exchange occurs via path of least resistance, causing overdistention
of normal alveoli and leading to worsening alveolar injury; shear forces increase in diseased areas; repeated
opening and closing of diseased alveoli worsens alveolar injury
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| Second review point: ventilation strategy can improve outcomes in patients with ARDS
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| Animal studies: ventilation with large tidal volumes (TV) and large filling pressures (or large inflation pressures) leads
to development of pulmonary edema
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| Cleveland Clinic SICU experience: in 1993, introduction of pressure-limited ventilation (to limit TV) in late-stage
ARDS; in 1995, development of “ARDS protocol,” ie, systematic use of pressure-limited ventilation and low TV
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| National Heart, Lung, and Blood Institute ARDS Clinical Trials Network (ARDSNet): National Institutes
of Health (NIH)-funded multicenter study in 2000; randomized ventilation into one group that received TV ≤6 mL/
kg and inspiratory pressure <30 cm H2 O; control group received 12 mL/kg TV, with inspiratory pressure <50 cm H2 O;
trial stopped early; interim analysis showed statistically significant improvement in mortality (actual mortality reduction,
9%; relative mortality reduced 22%); number of ventilator-free days significantly lower in study group; concluded that
low-pressure, low-volume ventilation appears to improve outcomes in ARDS; avoids “volutrauma”; avoids ventilator-induced
lung injury; protective ventilation strategy; controversy involving how patients were randomized and total methodology
(subjecting control group to high volumes and pressures); nonetheless, most feel this style of ventilation
appropriate for any patient
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| Other considerations: permissive hypercapnia—when ventilating patient with low TV and low pressures, minute ventilation
lower than desired; therefore, PaCO 2 may be higher than desired; able to accept higher PaCO 2 despite amount of
ventilation delivered; also accept lower pH; considered accepted strategy, although no systematic data to support or refute
use; inverse-ratio ventilation—inspiratory/expiratory (I:E) ratio >1; mean alveolar pressure optimized without increasing
peak pressure; mean pressure directly proportional to oxygenation; accepted strategy in management of ARDS, but
no systematic data to support or refute
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| Prone positioning: multicenter randomized European trial of ARDS patients by Gattinoni; study group placed in prone position
for ≥6 hr/day for 10 days (vs supine [control] group, which was managed conventionally); found no statistically significant
improvement in outcomes, regardless of positioning used; therefore, use of prone position inconclusive; practical use in
surgical patient (with drains and tubes) “quite labor intensive”
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| Appropriate amount of positive end-expiratory pressure (PEEP): second published ARDSNet trial—
attempted to answer this question; multicenter; 548 patients randomized to receive higher or lower levels of PEEP; complex
randomization strategy (9 cm H2 O to 14 cm H2 O); study stopped early after second interim analysis demonstrated futility; no
significant differences in mortality, ventilator-free days, ICU-free days, or organ failure-free days using higher or lower
amounts of PEEP over 60 days
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| Recruitment maneuvers: sustained inflations; maintain high level of end-inspiratory pressure; apply PEEP to keep newly
recruited alveoli open; results from small studies inconclusive; ARDSNet group published study using higher PEEP
arm of previous study; subjected patients to recruitment maneuvers (35 cm H2 O continuous positive airway pressure
[CPAP] for 30 sec); short-term effects variable; beneficial effects brief; practical points—no standardized approach to
use; use earlier in disease process seems to lead to longer improvements; no effect on clinical course, outcome, or ventilator-free
days; whether to use considered inconclusive
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| Use of Swan-Ganz catheter: multiple studies over last 10 yr suggest pulmonary artery (PA) catheter not valuable; first report
from Fluid and Catheter Treatment Trial (FACTT) in 2006; randomized 1000 patients with ARDS; 50% had pneumonia;
66% in medical ICU; Acute Physiology and Chronic Health Evaluation (APACHE) III score of ≈94; randomized to receive
either PA or central venous pressure (CVP) catheter; protocol goals included reversal of hypotension, oliguria, and
ineffective circulation; findings showed no statistical differences in mortality, ventilator-free days, ICU days, organ failures,
or need for dialysis or vasopressors, whether PA or CVP catheter used in management of ARDS
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| Conservative vs liberal fluid management: second part of FACTT; additional randomization strategy of conservative vs
liberal fluids based on filling pressures determined by either CVP or PA catheter; protocol goals also included reversal
of hypotension, oliguria, or ineffective circulation; treatment strategy used fluids, diuretics, inotropic agents, or vasopressors
per protocol; findings showed no difference in mortality at 60 days; in liberal group, difference in 7-day cumulative
fluid balance ≈7 L, and in restrictive group, -136 mL; no difference in mortality or ventilator-free days; in
conservative group, decrease in both ventilator days and ICU days, but no increase in amount of shock or dialysis
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| Steroids and ARDS: Meduri study—randomized double-blind placebo-controlled trial; enrolled patients with ARDS >7
days who received course of methylprednisolone, tapered over 32 days; goals included decreases in lung injury scores,
ventilator days, length of stay, and mortality; controversial (only 24 patients; 2-to-1 randomization protocol; medical
patients only); led speaker’s institution to consider use in patients with ARDS >7 days (ie, infections not new and being
treated); saw decrease in required ventilation, but no effect on outcome; ARDSNet group steroid trial (2006)—enrolled
180 patients with ARDS >7 days; primary end point mortality at 60 days; secondary end point ventilator-free days and
organ failure-free days; administered methylprednisolone, 250 mg on first day, then tapered over 23 to 25 days; found
patients randomized <14 days after onset had no difference in outcome, but those randomized >14 days after onset had
worse outcome in steroid group; in addition, steroid group had increase in ventilator-free and shock-free days, improvement
in oxygenation, and increase in neuromuscular weakness; conclusion that steroids should not be used routinely
and not started after 14 days; Meduri study (2007)—placebo-controlled trial in which steroid infusion (1 mg/kg
per day) administered to 91 patients (2-to-1 randomization strategy); started infusion in “early, severe ARDS” (low
dose; tapered up to 28 days); reduction in ventilator time, ICU length of stay, and hospital length of stay seen in patients
who received methylprednisolone infusion
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| NEW EVIDENCE FOR CARDIOPULMONARY RESUSCITATION (CPR)—John E. Tetzlaff, MD, Professor of Anesthesiology,
Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, and Vice Chair for Education,
Division of Anesthesiology, Critical Care Medicine, and Comprehensive Pain Management, Cleveland Clinic,
Cleveland, OH
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| History: before 1960, success limited to respiratory arrest; reports of open-chest cardiac compression in battlefield setting;
first report of electrical defibrillation in 1956; mouth-to-mouth ventilation in adults first reported in 1958; forceful
depression of sternum reported to result in peripheral pulse in 1960
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| Cardiopulmonary resuscitation: Safer and Kouwenhoven recognized synergy of ventilation and perfusion; early demonstrations
during cardiac arrest in operating room; 1966 consensus guidelines for CPR sponsored by National Academy of
Science; training in resuscitation advocated for all practitioners of emergency cardiac care (ECC)
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| Consensus guideline process: initial founders of CPR and ECC were anesthesiologists; domain transferred to American
Heart Association; by 2000, evidence that advanced cardiac life support (ACLS) cards and basic life support (BLS)
cards issued in every state and 40 foreign countries; consensus group of physicians from many countries formed; participated
in 2-yr process of evidence-based medicine; meeting in year 2000 published international guidelines for CPR and
ECC; commitment made to ongoing and continued use of evidence to determine good techniques for resuscitation
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| International consensus: agreements made on effective ECC, chain of survival, efficacy of early defibrillation, public
access CPR, and public access to defibrillation (eg, automated external defibrillator [AED])
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| Current issues with resuscitation: despite world-wide training, consensus guidelines, evidence-based medicine, biphasic
defibrillators, and pharmacologic advances, success rates (in- and out-of-hospital) little changed; guidelines published in
2000 advocated biphasic current for defibrillation, amiodarone, Combitube, laryngeal mask airway (LMA), and pulse oximetry;
5 yr later, with new technology, skill set present, and money and time spent, “things [are] not getting any better”
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| Abella: in-hospital cardiac arrest; trained observers (eg, registered nurses, residents; not involved in patient care) collected
data; observers trained to grade resuscitation on scale of 1 to 4; criteria included, eg, placing hands on sternum
correctly, depression of sternum one-half to one-third diameter of thorax, depression of sternum directly down or at angle,
full relaxation between compressions; >50% of cases had ≥1 min of time during 10-min period in which compressions
judged either fair or poor; in at least one-third of cases, 50% of compressions judged fair or poor
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| Abella: second trial using same methodology (in-hospital cardiac arrest; used some of same trained observers as in previous
study) found inadequate compression rate (heart rate [HR] parameter, 80-120 bpm); at least one-third had 1 min of
HR outside parameter
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| Aufderheide: excessive ventilation creates hypocarbia and vasoconstriction; causes sustained peak intrathoracic pressure;
interferes with preload and prevents left ventricular (LV) filling; inadequate cardiac filling reduces cardiac output
achieved with chest compression
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| Kern: looked at chest compression alone, compared to chest compression with ventilation; found early in resuscitation,
chest compression alone superior (need for oxygen not as critical as need for circulation); inappropriate ventilation interferes
with circulation
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| Wik: challenges “shock first” protocol in unwitnessed onset of nonperfusing rhythm; out-of-hospital cardiac arrest setting;
delaying first shock to give chest compressions for 3 min improves success rate (most effective way of maintaining
heart tissue pH in cardiac arrest)
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| Kern: coronary perfusion directly relates to number of minutes of chest compression; improved coronary circulation (and
presumably cerebral circulation) when interruption of chest compression avoided; interruptions disproportionately decrease
coronary perfusion
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| Hightower: study involved trained observers not involved in clinical care; quality of chest compressions decayed over
time; provider became ineffective at giving chest compressions at 5 min; important to find 2 providers who alternate on
sequence to perform compressions
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| van Alem: challenges sequence of 3 consecutive shocks; success rate (90%-95%) highest on first attempt; when tissue pH
drops, ability to shock disappears
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| New consensus about conduct of resuscitation: maximize chest compression time, especially in first 10 min;
avoid hyperventilation (low TV); chest compression before defibrillation if cardiac arrest not witnessed or if unsure;
one shock per CPR cycle (and at optimum shock rate); focus on role of team leader
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| Team leader: anesthesia provider has natural tendency to not only be team leader, but also interventionist (especially
in hospital setting); however, team leader should not “be doing the primary performance”; 2 people should be assigned
to chest compressions (change every 3 min); continuous search for cause of cardiac arrest (10 min time limit); ensure
chest compressions performed effectively; prevent hyperventilation; make determination about when to stop; avoid
starting resuscitation when inappropriate (eg, with do-not-resuscitate order)
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| Conclusions: resuscitation depends on technique and technology; basic resuscitation skills must be emphasized;
maximum time for chest compression essential; avoid hyperventilation; ensure someone (preferably anesthesia provider)
in charge
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Suggested Reading
Abella BS et al: Chest compression rates during cardiopulmonary resuscitation are suboptimal: a prospective study during
in-hospital cardiac arrest. Circulation 111:428, 2005; Abella BS et al: Quality of cardiopulmonary resuscitation during
in-hospital cardiac arrest. JAMA 293:305, 2005; Aufderheide TP et al: Hyperventilation-induced hypotension
during cardiopulmonary resuscitation. Circulation 109:1960, 2004; Brower RG et al: National Heart, Lung, and Blood
Institute ARDS Clinical Trials Network. Higher versus lower positive end-expiratory pressures in patients with the acute
respiratory distress syndrome. N Engl J Med 351:327, 2004; Gattinoni L et al: Adult respiratory distress syndrome profiles
by computed tomography. J Thorac Imaging 1:25, 1986; Gattinoni L et al: Prone-Supine Study Group. Effect of
prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 345:568, 2001; Hightower D et
al: Decay in quality of closed-chest compressions over time. Ann Emerg Med 26:300, 1995; Kern KB et al: Importance
of continuous chest compressions during cardiopulmonary resuscitation: improved outcome during a simulated single lay-
rescuer scenario. Circulation 105:645, 2002; Meduri GU et al: Effect of prolonged methylprednisolone therapy in unresolving
acute respiratory distress syndrome: a randomized controlled trial. JAMA 280:159, 1998; Steinberg KP et al:
National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network. Efficacy
and safety of corticosteroids for persistent acute respiratory distress syndrome. N Engl J Med 354:1671, 2006; van Alem
AP et al: A prospective, randomised and blinded comparison of first shock success of monophasic and biphasic waveforms
in out-of-hospital cardiac arrest. Resuscitation 58:17, 2003; Ventilation with lower tidal volumes as compared with
traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress
Syndrome Network. N Engl J Med 342:1301, 2000; Ware LB et al: The acute respiratory distress syndrome. N Engl J
Med 342:1334, 2000; Wheeler AP et al: National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome
(ARDS) Clinical Trials Network. Pulmonary-artery versus central venous catheter to guide treatment of acute lung
injury. N Engl J Med 354:2213, 2006; Wiedemann HP et al: National Heart, Lung, and Blood Institute Acute Respiratory
Distress Syndrome (ARDS) Clinical Trials Network. Comparison of two fluid-management strategies in acute lung injury.
N Engl J Med 354:2564, 2006; Wiedemann HP: A perspective on the fluids and catheters treatment trial (FACTT).
Fluid restriction is superior in acute lung injury and ARDS. Cleve Clin J Med 75:42, 2008; Wik L et al: Delaying
defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized
trial. JAMA 289:1389, 2003.
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