AIRWAY, BREATHING, CIRCULATION
| SPONTANEOUS BREATHING ON MECHANICAL VENTILATION —Jonathan L. Marinaro, MD, Assistant Professor,
Department of Surgery, Division of Trauma/Critical Care, and Department of Emergency Medicine, University of New
Mexico School of Medicine, Albuquerque
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| “Problematic triad” of ventilation: atelectasis, sedation, and nonspontaneous breathing
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| Atelectasis: decreases lung compliance, impairs oxygenation, and increases pulmonary vascular resistance, resulting in
right ventricular dysfunction and possible microvascular leakage; end result may be adult respiratory distress syndrome
(ARDS)
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 | Causes: impaired surfactant production—surfactant allows alveoli to stay open at minimal pressure; gas
resorption—forcing patient to breathe 80% or 100% oxygen washes out nitrogen and collapses alveoli, leading to
higher peak pressures and requiring higher ventilator settings; compression—material packed into abdomen to stop
bleeding also compresses posterior pulmonary aspect and distorts normal diaphragmatic architecture, decreasing patient’s
ability to open posterior lung segments
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| Sedation: prolongs time on ventilator (every day on ventilator associated with 1%-3% increase in risk for ventilator-associated
pneumonia); increases use of imaging and diagnostic procedures; makes monitoring neurologic status more difficult;
problems of sedation may produce problems with ventilation
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| Spontaneous breathing: benefits include increased cardiac index, promotion of venous return to heart, and greater
blood flow to intestinal mucosa (promotes early feeding); associated with less use of vasopressors among patients with
ARDS; no evidence that it increases oxygen consumption; improves glomerular filtration rate
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| Importance of biologic variability: one study compared 325 variable ventilations to uniform mechanical ventilations, and
found variability associated with higher Po2 , lower PCO 2 , less dead space, and improved compliance; in another study,
patients allowed respiratory variability during trials of spontaneous breathing had better chance for successful extubation
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| Models of spontaneous breathing: continuous positive airway pressure (CPAP)—restores functional residual capacity
(FRC); airway pressure release ventilation (APRV)—“just CPAP with occasional releases”; BiVent mode—
similar to APRV (different manufacturer); bilevel positive airway pressure—earlier version of BiVent or APRV
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| Mechanics of best spontaneous breathing systems: prevent atelectasis by forcing patients to breathe in, rather than passively
receiving air
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| APRV: incorporates occasional releases that allow CO2 to escape, unlike CPAP, which requires CO2 to be blown out;
people normally breathe using negative pressure ventilation; posterior portion of lungs holds more air than anterior
portion; posterior diaphragm stronger, generates more force than anterior portion, and distributes ventilation to dependent
lung areas; 3 L in each lung dedicated to FRC; spontaneous breathing involves pulling air into dependent areas of
lung that are collapsed in most other modes; redistribution of ventilation to those areas leads to alveolar recruitment;
CO2 escapes body through “an open alveolus with blood running by it”; opening more alveoli means letting more CO2
out and more oxygen in
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| Causes of hypoxia: shunts, anatomy, hypoventilation, diffusion problems, and ventilation-perfusion (VQ) mismatch
(most common); usual treatment raising positive end-expiratory pressure (PEEP); patients do better when mean airway
pressure maintained; when patients hypoxic, alter PEEP, not tidal volume; speaker suggests keeping PEEP at 28 cm
H2 O and releasing to obtain tidal volume, instead of mechanically blowing air in, which may traumatize lungs; APRV
and BiVent also allow spontaneous breathing throughout cycle (no need for paralysis)
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| Managementof ARDS: keeping patient prone recruits alveoli that might otherwise collapse, preventing atelectasis and VQ
mismatch; administer inhaled nitrous oxide to keep alveoli open; encourage patient to use atelectatic segments and pull
breath in “from the moment they’re on the ventilator”; use open-lung ventilation early in patient’s course to promote
spontaneous breathing; with APRV, occasional release to expire CO2 keeps mean and peak airway pressures low
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| Advantages of APRV: 70% reduction in need for paralytic agents, 30% to 40% reduction in need for sedation; patients
can cough while on APRV ventilator; may prevent ARDS altogether, as well as pneumonia; less sedation means lower
risk for delirium; place patient on CPAP as soon as possible; low tidal-volume ventilation plus atelectasis causes
ARDS; perfect ventilation mode lacks repetitive opening and closing; APRV keeps alveoli open 90% of every minute,
and “recruited lungs require less pressure”; patients also removed from ventilation faster with APRV; augments collateral
ventilation and restores FRC, helping to maintain normal pressure-volume relationship; can be titrated to patient’s
lung compliance; in speaker’s shock–trauma unit, with 50,000 patient-hours on APRV since 2001, ARDS mortality
went from 45% to 31%
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| PARADOXES OF RESUSCITATION —Philip D. Lumb, MB, Professor and Chair, Department of Anesthesiology, Keck
School of Medicine of the University of Southern California, Los Angeles
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| Paradoxes of resuscitation: cardiovascular (advanced cardiopulmonary life support [ACLS]); trauma and hemodynamic
protocols (hypotension and delayed resuscitation; surviving sepsis guidelines); cerebral (hyperventilation, hyperthermia,
and barbiturates now out of favor, yet once were mainstays of cerebral resuscitation); end organ function
(norepinephrine now regaining favor)
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| ACLS protocols: respiratory and compresson rates have changed dramatically; patients in cardiac arrest used to receive
bicarbonate (now considered harmful); guidelines for automated external defibrillator use have changed in recent years;
pharmacology has also changed
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| Hemodynamics: hypodynamic hypotensive initial resuscitation commonly applied; may start seeing more hypotension
associated with successful resuscitation; future direction of inotropic support unclear
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| Cerebral resuscitation: future recommendations may include measuring intracranial pressure for better management of
cerebral circulation; alternatively, external devices may be sufficient for monitoring cerebral oxygenation
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| Hypothermic trauma patients: blood gas temperature often corrected to guide cerebral resuscitation when patients resuscitated
at <36o C; should perhaps reconsider
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| End organ resuscitation and preservation: renal function may be function of volume resuscitation; low-dose
dopamine (2.5 µg) may be good diuretic, but does not protect kidneys; however, low-dose steroids indicated in acute respiratory
failure; norepinephrine may have role
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| Surviving sepsis protocols: basic tenets include central venous oxygen saturation, tight glucose control, early antibiotics,
aggressive fluid resuscitation, and early hemodynamic and respiratory support; concept of volume trauma as important as
barotrauma; end-expiratory pressure as alveolar “splint”; intra-alveolar nitrogen most important alveolar splint (high fraction
of inspired oxygen [FiO2 ] associated with decreased alveolar stability); balance end-expiratory pressure against FRC
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| Initial resuscitation: maintain intravascular volume and “relatively modest” mean arterial pressure and urine output;
keep central venous oxygen saturation >70%; if not possible, administer blood and begin inotropic support; diagnose sepsis
(take cultures) and start antibiotics early; “culture everything”
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| Remaining controversies: use of vasopressors, inotropic therapy, steroids, and blood products; transfusion strategies
(restrictive approach associated with better survival than more liberal strategy); if neuromuscular blockade necessary, use
train-of-four monitoring; with mechanical ventilation, target tidal volume should be <6 mL/kg (larger tidal volumes more
comfortable for patient, but discomfort of small tidal volumes mitigated by correct FRC); keep patient prone; glucose
control difficult but important
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| PEDIATRIC TRAUMA RESUSCITATION: WHAT YOU NEED TO KNOW —Stephen W. Bickler, MD, Associate
Clinical Professor of Surgery and Pediatrics, University of California, San Diego, School of Medicine
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| Trauma as public health issue: since 1980, injuries leading cause of death in children; ≈10 million children (1 in 6)
seek emergency care annually; ≈75,000 of these injured permanently, and ≈10,000 die; injuries cause 50% of mortality in
children 1 to 14 yr of age
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| General principles of pediatric resuscitation: similar to advanced trauma life support (ATLS) principles established
for adults (airway, breathing, circulation, disability, and exposure); however, children have unique anatomic and physiologic
characteristics that result in distinct patterns of injury; example—consequences of closed-head injuries include apnea,
hypoventilation, and hypoxia; these symptoms 5 times more common than hypovolemia among pediatric patients; in
general, pediatric trauma management protocols emphasize aggressive management of airway and breathing
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| Anatomic and physiologic differences in children
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| Size and shape: smaller size means more force per unit body surface area (BSA) and more tissue damage; children sustain
more multiple organ injuries than adults; liver and spleen not as well protected by rib cage; more shallow pelvis
makes bladder more vulnerable; head proportionately larger, making pediatric head injuries especially problematic
(mortality from severe isolated head injuries 20%; incidence of associated long-term disability 30%; if head injury associated
with other severe injuries, mortality rises to 70%)
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| BSA: large relative to body mass; high risk for heat loss and rapid development of hypothermia, especially if room cool,
with cold intravenous (IV) fluids or inhaled gases; children also have minimal subcutaneous tissue, exacerbating risk
for hypothermia, which contributes to acidosis and increases risk for coagulopathy; temperature regulation matures at
≈10 yr of age
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| Skeleton: bones incompletely calcified (more pliable), with multiple growth centers; torus and greenstick fractures more
common in children than adults, yet massive internal injuries possible with no fractures; presence of rib or long-bone
fracture implies patient sustained major force
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| Vital signs: related to age; resting heart and respiratory rates decline with age; systolic blood pressure (BP) increases
(double child’s age and add 70 for rough estimate); keep chart with appropriate values in resuscitation area
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| Broselow Pediatric Emergency Tape: permits rapid estimation of weight, drug dosages, and equipment sizes for children,
based on patient’s length
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| Shock: children—have limited ability to increase stroke volume and cardiac output by increasing heart rate; try to maintain
BP by increasing heart rate; peripheral circulation—labile and may be affected by hypothermia (makes it difficult
to assess perfusion status); in general, ability to reroute blood to vital areas better in children than adults, but at
expense of splanchnic blood flow, leaving child at risk for ileus and gastric distention; nasogastric tube decreases distention,
improves breathing, and facilitates abdominal examination; blood loss—may be severe (>20%) before BP
changes become apparent (may see tachycardia or other signs, eg, cool extremities or weakening pulses); as blood loss
approaches 30% to 35% (see table on page 3), heart rate increases, BP plummets, heart rate drops, patient becomes
bradycardic, and irreversible shock develops; take-home message—heart rate and BP alone do not always warn of severe
blood loss and possible disaster ahead
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| Psychologic status: children may become uncooperative in unfamiliar surroundings or during stressful events; behavior
may regress in very young patients; severe multisystem trauma may profoundly affect personality; in one study, 60%
of major trauma patients had major personality change 1 yr later (50% had cognitive and physical handicaps)
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| Critical skills for resuscitating pediatric trauma patients: establishing airway first priority; inability to establish
or maintain airway major cause of cardiac arrest in children; bradycardia hypoxic or respiratory until proven otherwise;
bradycardia associated with hypoxia quickly reversible
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| Anatomic differences in pediatric airway: posterior pharynx buckles easily and may obstruct airway; larynx funnel-
shaped, allowing secretions to accumulate; larynx also more cephalad and anterior in neck, compared to adults; short
trachea facilitates intubation of right mainstem bronchus
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| Airway management: in awake pediatric patients, oral airways may cause gagging, vomiting, and aspiration; secure airway by
orotracheal intubation; do not perform cricothyroidotomy in children <5 yr of age (insufficient space in younger children);
always protect against spinal cord injury; positioning—may resolve airway problems; may open airway by placing head
in “sniffing” position and slightly elevating body
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| IV access: preferred site percutaneous-peripheral, followed by intraosseous, percutaneous placement into femoral vein,
venous cutdown at saphenous vein, and percutaneous placement into external jugular vein; get as much help as possible;
if percutaneous placement difficult, establish intraosseous line as quickly as possible; subclavian access not
recommended due to high risk for pneumothorax if patient hypotensive or hypovolemic
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| Intraosseous cannulation: provides access to noncollapsible marrow venous plexus; rapid, safe, and reliable; can be
placed within 30 to 60 sec; can use to administer drugs, IV fluids, and blood products; place peripheral IV after patient
resuscitated; most common site fingerbreadth below patella, directly into tibia
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| When to administer IV fluids: decide early if need exists; check for subtle signs of shock, and anticipate problems
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| Goal of fluid resuscitation: to rapidly replace circulating volume; child’s blood volume ≈80 mL/kg; if shock suspected,
administer 20 mL/kg warm normal saline; 3 boluses may be needed (60 mL/kg); 3:1 rule—administer blood for every
3 boluses of saline
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| Indications for transfusion: suspect continuing hemorrhage if hemodynamic abnormalities do not improve after first
bolus; administer type-specific or O-negative warmed, packed red blood cells
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| Assessing adequate resuscitation: requires ongoing observation; signs of progress include slower heart rate, increased
pulse pressure and systolic BP, strong peripheral pulses, warm extremities, and rapid capillary refill; improved sensorium;
and correction of base deficit (<-5 mEq/L predicts severe injury and poor outcome); failure to clear base
deficit after resuscitation “extremely poor prognostic indicator”
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| Importance of injury prevention: 60% to 70% of trauma-related childhood deaths occur outside hospital; well-designed
programs can reduce injury rates 50% to 75%
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Suggested Reading
Atkinson C, Bowman A: Pediatric airway differences. J Trauma Nurs 10:118, 2003; Dart BW 4th et al: Preliminary
experience with airway pressure release ventilation in a trauma/surgical intensive care unit. J Trauma 59:71, 2005; De
Miguel-Yanes JM et al: Failure to implement evidence-based clinical guidelines for sepsis in the ED. Am J Emerg Med
24:553, 2006; Dellinger RP et al: Surviving Sepsis Campaign guidelines for management of severe sepsis and septic
shock. Crit Care Med 32:858, 2004; Dellinger RP, Vincent JL: The Surviving Sepsis Campaign sepsis change bundles
and clinical practice. Crit Care 9:653, 2005; Habashi N, Andrews P: Ventilator strategies for posttraumatic acute respiratory
distress syndrome: airway pressure release ventilation and the role of spontaneous breathing in critically ill patients.
Curr Opin Crit Care 10:549, 2004; Hering R et al: Effects of spontaneous breathing during airway pressure release ventilation
on respiratory work and muscle blood flow in experimental lung injury. Chest 128:2991, 2005; Hering R et al: Effects
of spontaneous breathing during airway pressure release ventilation on renal perfusion and function in patients with acute
lung injury. Intensive Care Med 28:1426, 2002; McCunn M, Habashi NM: Airway pressure release ventilation in the
acute respiratory distress syndrome following traumatic injury. Int Anesthesiol Clin 40:89, 2002; Mendelson KG, Fallat
ME: Pediatric injuries: prevention to resolution. Surg Clin North Am 87:207, 2007; Neumann P, Hedenstierna G:
Ventilatory support by continuous positive airway pressure breathing improves gas exchange as compared with partial ventilatory
support with airway pressure release ventilation. Anesth Analg 92:950, 2001; Petsinger DE et al: What is the role of
airway pressure release ventilation in the management of acute lung injury? Respir Care Clin N Am 12:483, 2006; Shapiro
NI et al: A blueprint for a sepsis protocol. Acad Emerg Med 12:352, 2005; Smith R et al: The utilization of intraosseous
infusion in the resuscitation of paediatric major trauma patients. Injury 36:1034, 2005; Vella AE et al: Predictors of fluid
resuscitation in pediatric trauma patients. J Emerg Med 31:151, 2006.
Educational Objectives
| The goal of this program is to improve trauma care for adult and pediatric patients. After hearing and assimilating this program,
the clinician will be better able to:
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| 1. Identify the “problematic triad” of ventilation.
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| 2. Describe the benefits of spontaneous breathing with adjunctive continuous positive airway pressure or airway pressure
release ventilation, compared to mechanical ventilation.
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| 3. List recent changes in advanced cardiopulmonary life support (ACLS) protocols.
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| 4. Compare the basic principles of adult and pediatric trauma resuscitation.
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| 5. Discuss the main priorities of pediatric trauma care.
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Faculty Disclosure
In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty members 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 reported nothing to disclose.
Acknowledgements
Dr. Marinaro spoke at Current Concepts in General Surgery and Trauma Update, held September 6-8, 2006, in Albuquerque,
NM, and sponsored by the University of New Mexico Health Sciences Center Department of Surgery and Office
of Continuing Medical Education. Dr. Lumb was recorded at 13th Annual USC Trauma/Critical Care Symposium, held
May 22-23, 2006, in Pasadena, CA, and sponsored by the Division of Trauma/Critical Care and the Office of Continuing
Medical Education at the Keck School of Medicine of the Univers |
