Consider the reasons for hypoventilation after anesthesia. It may represent residual anesthesia, but not always
Consider the reasons for hypoventilation after anesthesia. It may represent residual anesthesia, but not always: Excerpt from Avoiding Common Pediatric Errors
Author:
Renée Roberts, MD
What to Do - Gather Appropriate Data
Mild hypoxemia, airway obstruction, hypercapnia, atelectasis, and bronchospasm are so common during emergence from anesthesia that anesthesiologists and postanesthetic nurses routinely provide good prophylactic therapy in the modern surgical setting. These problems are often considered a
natural consequence of giving drugs that depress central respiratory drive,
temporarily decrease lung volume, impair protective airway reflexes, depress
secretion mobilization, and eliminate sighing (auto-positive end-expiratory
pressure[auto-PEEP],preventingatelectasis).Adversepulmonaryoutcomes
are often attributed to anesthesia care, but a significant component of perioperative risk derives from the surgical site, postoperative pain, and effects
of pharmacologic pain management. These risks must be recognized by the
perioperative staff so that more serious perioperative pulmonary complications, such as bronchitis, pneumonia, pulmonary edema, aspiration, and
respiratory failure, do not evolve.
Problems with oxygenation, ventilation, and airway maintenance are
cardinalsignsofperioperativepulmonarycomplicationsandcanbediscussed
withinthecontextofhypoxia.Hypoxiaisdefinedasdecreasedoxygentension
with concomitant decreased oxygen supply in the blood delivered to the
tissues.Thecommonpostoperativecausesofhypoxiafallintotwocategories:
anemic hypoxia and hypoxemic hypoxia. Anemic hypoxia results from a
reduction in hemoglobin concentration, either from diseases such as sickle
cell disease, or from unreplaced surgical losses. Anemic hypoxia can also be
due to the conditions that shift the oxyhemoglobin dissociation curve (acid
basebalance,temperature)andorchangethebindingcapacityofhemoglobin
suchasHbFfoundininfants.Postoperativehypoxemichypoxiaresultswhen
oxygen exchange in the lungs is problematic and can be divided into two
categories: ventilation/perfusion mismatch and hypoventilation.
When the ratio of ventilation (V) and perfusion (Q) of the lungs is not
normal, the resulting hypoxemia is from V/Q mismatch. Acute changes in
V and Q take place as a function of changes in chest wall configuration,
surgical positioning, intraoperative ventilation modes, and anesthetic effects
on pulmonary blood flow. Acute anesthetic effects are largely reversed at the
endofsurgery;however,certainsurgerieshavepostoperativeimplicationsfor
lungfunction.Forinstance,afterupperabdominalandthoracicsurgery,lung
capacities are reduced by approximately 40% for the first few days following
surgery, and measurable decrement in respiratory mechanics persists for up
to 2 weeks. Other causes of V/Q mismatch include partial airway obstruction
(postextubation stridor, laryngospasm or bronchospasm); inadequate tidal
volumesandcough(fromrecurarizationorresidualsedation);andatelectasis
(from sustained reduction of peak air flows and total lung volume during and
after anesthesia).
Moderate V/Q mismatch may evolve to severe mismatch otherwise
known as shunt (there is no oxygen exchange (V) with the circulating blood
(Q). Pneumonia, bronchitis, and pulmonary edema are examples of shunt.
Pulmonary aspiration and the ensuing pneumonia is widely viewed as the
most common serious complication of anesthesia that can be avoided by
adherence to fasting and preventative measures. An increased risk for aspiration includes emergency surgery, obesity, reflux, neuromuscular disease, a
full stomach, and sedation. Another preoperative risk factor for a PPC that
can lead to shunt is sleep apnea (from congenital syndromes, craniofacial
abnormalities, obesity, cardiac dysfunction). If not managed carefully, dramatic hypoxic episodes in the postoperative period can cause cardiovascular
decompensation, postobstructive pulmonary edema, or pulmonary aspiration syndrome. And finally, negative pressure pulmonary edema caused by
inspiration against closed vocal cords after extubation should also be in the
differential for hypoxemic hypoxia from shunt.
The other etiology of hypoxemic hypoxiais hypoventilation:inadequate
minute ventilation (respiratory rate × tidal volume) to remove the carbon
dioxide produced. Whenever alveolar ventilation is inadequate, carbon dioxide increases in the blood and alveolus and there is little remaining for other
gases(including oxygen); whenhypoventilation occursin a patientbreathing
room air, hypoxia inevitably occurs. Causes of postoperative hypoventilation
in spontaneously ventilating patients are airway obstruction, acute depression of the brainstem respiratory center by drugs (opiates, barbiturates, inhaled agents), pain (after thoracotomy, chest trauma, high upper abdominal
incision), pneumothorax, neuromuscular blocking drugs, abnormalities of
spinal conductingpathways (C3–5) asin high cervical surgery, phrenicnerve
injury via cold injury (cardiopulmonary bypass) or ablation. Postoperative
hypoventilation may also result from respiratory muscle weakness from unrecognized dystrophy, malnutrition, prolonged mechanical ventilation, and
problemswiththerespiratorydrivefromthemedullarycenterduetosurgery
for trauma, neoplasm, or hemorrhage.
The neurologic symptoms of hypoxemia (anxiety, confusion, restlessness, somnolence, and coma) may be masked in the postanesthetized patient. Because anesthetics attenuate, many of the normal cardiorespiratory
responses to hypoxia, other subtle warning signs, such as tachycardia and
tachypnea, are blunted. Furthermore, oxygen consumption in the newborn
is two to three times that of older children and adults and the newborn
responds to hypercarbia and hypoxia paradoxically with apnea rather than
hyperventilation. This paradoxic response is even more prominent in premature infants.
Anesthesia and postanesthetic care unit nursing staff routinely manage partial airway obstruction, hypoventilation, and hypoxemia associated
with the residual effects of muscle relaxants, sedatives, narcotics, and anestheticagents.Itisimperativethatpostoperativepatientshavetheirsaturation
monitored with pulse oximetry and their ventilation carefully monitored. If
hypoxemia persists or worsens despite supplemental oxygen, bronchodilators, airway management, techniques to expand atelectatic lungs, or reversal
of sedative/narcotic and relaxant drugs, the patient should undergo new
clinical assessment directed toward the most likely problems and supportive maneuvers such as continuous positive airway pressure or ventilation.
Evolving respiratory distress should be worked up with studies to rule out
pulmonary edema, pneumothorax, pulmonary embolism, or obstruction of
upper or lower airway. In the case of hypoxemia after thoracic and upper
abdominal surgery, postoperative care should recognize the need for multimodal pain control without excessive narcotic, sedative, mobilize patient
and secretions, preserve lung volume, and ambulate (if appropriate) as soon
as possible.
Suggested Readings
Watson CB. Respiratory complications associated with anesthesia. Anesthesiol Clin North Am.
2002;20(3):513–537.
Wilson WC, Shapiro B. Perioperative hypoxia. The clinical spectrum and current oxygen
monitoring methodology. Anesthesiol Clin North Am. 2001;19(4):1271–1282.
Book Source Details
- Book Title: Avoiding Common Pediatric Errors
- Author(s): Anthony D Slonim MD, DrPH; Lisa Marcucci MD
- Year of Publication: 2008
- Copyright Details: Avoiding Common Pediatric Errors, Copyright © 2008 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Avoiding Common Pediatric Errors
Authors: Anthony D Slonim MD, DrPH; Lisa Marcucci MD
Publisher: Lippincott Williams & Wilkins
Copyright: 2008
ISBN: 0-7817-7489-6
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