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Consider the reasons for hypoventilation after anesthesia. It may represent residual anesthesia, but not always

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 Details: Avoiding Common Pediatric Errors, Copyright © 2008 Williams & Wilkins.

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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

 » Next page: Do not prescribe oral contraceptivepills (OCPs) to females with undiagnosed vaginal bleeding (Avoiding Common Pediatric Errors)

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