Hypoxia, Intraoperatively

Description

Intraoperative hypoxia is defined as arterial oxygen tension (PaO₂) <60 mm Hg, which correlates to a blood oxygen saturation (SpO₂) <90%.

Epidemiology

Incidence

Transient intraoperative hypoxia has been shown to occur in 7% of patients who receive an anesthetic for surgery.

Prevalence

Hypoxia can occur during all stages of the anesthetic, particularly during induction and emergence.
It occurs most frequently in patients with American Society of Anesthesiology (ASA) physical status classification III and IV.

Morbidity

Hypoxic brain injury, myocardial ischemia, stroke, renal injury

Etiology/Risk Factors

Decreased fraction of inspired oxygen (FiO₂) results from a failure to provide adequate inspired O_2. It can result from
- Pipeline O₂ supply failure, empty tank, hypoxic gas mixture
- Higher altitude
Inadequate alveolar ventilation or alveolar hypoventilation. The alveolar gas equation is as follows: F_A = [(P_barometric – P_H20)(FiO₂)] –(PaCO₂/0.8); increases in carbon dioxide in the alveoli will decrease the FAO₂ and, hence, PaO₂.
- CNS depression. Respiratory depression from drugs, structural, or ischemic lesions
- Circuit or machine disconnection
- Obstruction. Upper airway, mucous plug, endotracheal tube (ETT) kink, herniated ETT cuff
- Inadequate ventilator settings/parameters
Venous admixture. Under normal conditions, there is a fixed physiologic shunt (~5%) from pleurohilar veins, bronchial veins, and Thebesian circulation.
V/Q mismatch
- Dead space: Pulmonary embolism, profound hypotension, cardiac arrest
- Shunt: Bronchospasm, asthma, pneumonia, endobronchial intubation, pulmonary edema, aspiration, inhibition of hypoxic pulmonary vasoconstriction (HPV), pneumothorax, pleural effusion, hemothorax, acute lung injury (ALI), acute respiratory distress syndrome (ARDS)
Right-to-left anatomic shunts
- Atrial septal defects
- Ventricular septal defects
Diffusion defects. Diffusion capacity depends on the thickness of the alveolar wall, the area available for gas exchange, and the partial pressure difference of gas between the two sides.
- Thickened wall. Pulmonary fibrosis (chronic) or pulmonary edema (acute)
- Decreased equilibration time secondary to tachycardia
Excessive metabolic O₂ demand such as hyperthermia, hyperthyroidism, shivering, and malignant hyperthermia (result in a decreased mixed venous oxygen saturation).
Impaired tissue oxygen delivery/perfusion
- Myocardial infarction
- Congestive heart failure
- Shock
- Arrhythmias
- Cardiac tamponade
- Sepsis
- Arteriovenous malformation

Physiology/Pathophysiology

Aerobic metabolism. Each molecule of glucose can generate 36 ATP under normal cellular metabolism and oxidative phosphorylation.
- C₆H₁₂O₆ + 6O₂ 6CO₂ + 6H₂O + Energy
- The energy created is stored in the third phosphate bond on adenosine triphosphate (ATP). ATP is utilized for muscle contraction, ion pumps, cellular secretion, and protein synthesis: Energy + ADP + Phosphate ATP
- ATP cannot be stored and must be continually formed requiring a constant supply of substrates and O₂.
Anaerobic metabolism. When O₂ is not available, anaerobic metabolism occurs in order to manufacture ATP; however, it is inefficient (one glucose molecule yields 2 ATP) and produces lactic acid. Progressive lactic acidosis impairs enzymatic function and ion concentration gradients.
Hypoxia is sensed in the carotid bodies (at the bifurcation of the common carotid arteries) and the aortic bodies (surrounding the aortic arch). These peripheral sensors interact with central respiratory centers via the glossopharyngeal nerves to produce reflex increases in alveolar ventilation. Hypoxia receptor activity does not appreciably increase until the PaO₂ decreases below 50 mm Hg, at which point the SpO₂ is 80%.
Compensatory mechanisms. When there is an imbalance of O₂ supply to demand, the body mobilizes its compensatory mechanisms to ensure adequate availability (e.g., increased O₂ extraction and cardiac output).
Signs of hypoxia. Early signs are the result of sympathetic system activation and include tachycardia, hypertension, and an increased cardiac output. Late signs include myocardial dysrhythmias, bradycardia, hypotension, and cardiac arrest.

Prevantative Measures

Deliver adequate supplemental FiO₂
Carefully monitor for signs of hypoventilation

Verify all low SpO₂ measurements.
- Ensure that the SpO₂ rate correlates with the EKG tracing
- Verify accurate waveform
- Move pulse oximetry probe to different fingers, or an earlobe, nostril, or nasal ala.
Check in-line FiO₂ measurements.
Assess for adequate ventilation
- If the patients is not intubated, listen for stridor, snoring, lack of air movement.
- If intubated, hand ventilate to assess pulmonary compliance and expand collapsed lung segments.
  - Increased compliance: Consider cuff leak or deflation, supraglottic cuff, circuit leak
  - Decreased compliance: Consider bronchospasm, pneumothorax, mainstem intubation, pulmonary edema; biting, secretions, or kinking of the ETT
- Auscultate the lungs to assess for
  - Bilateral breath sounds; rules out mainstem intubation, pneumothorax.
  - Wheezing; rules out bronchospasm, aspiration, pulmonary embolism
  - Crackles or rales; rules out pulmonary edema
- Check end-tidal CO₂ (EtCO₂) to verify intubation and evaluate capnograph pattern for abnormalities such as obstruction.
Portable chest x-ray should be obtained to ascertain atelectasis, infiltrates, or pneumothorax.
Measure the arterial blood gas to evaluate the PaO₂. The SpO₂ is a non-invasive monitor that may not accurately reflect the PaO₂ in the setting of: Hypothermia, poor circulation, electrocautery, motion, ambient lighting, carbon monoxide poisoning, methylene blue administration, and cyanide poisoning. Additionally, PaO₂ values can be utilized to calculate the Alveolar to arterial gradient/ratio.

Differential Diagnosis

Evaluating the Alveolar to arterial (A-a) gradient may help determine the cause. Alternatively the a/A ratio can be utilized when increased FiO₂ is being implemented.
Oxygen administration may help differentiate between hypoventilation and V/Q mismatch. In patients with:
- Low FiO₂, hypoventilation, and V/Q mismatching, increasing the FiO₂ will increase the oxygen saturation.
- Large shunts (>25% of total cardiac output), the blood flow that returns from unventilated alveoli or right-to-left anatomic shunts will be unchanged; it is not exposed to the increased oxygen fraction.

Increase delivered FiO₂ to 100% while evaluating reversible causes
Atelectasis is the most common cause; recruitment maneuvers can be very effective:
- Increase tidal volumes (Vt) to 10–12 mL/kg
- Add positive end-expiratory pressure (PEEP)
- Recruitment maneuvers
- Alternatively, some patients with hypoxia have ALI or ARDS and management is based on a lung protective ventilation strategy (LPVS) that minimize additional ventilator-associated lung injury using lower Vt.
Secretions: Suction the ETT, consider bronchoscopy
Biting: Place a bite block, deepen anesthetic, administer neuromuscular blocking drugs.
Bronchospasm: Administer aerosolized bronchodilators, deepen the anesthetic with volatile agents or propofol
Hypoventilation: Adjust minute ventilation. In patients that are not intubated, alleviate possible upper airway obstruction (chin life, jaw thrust, oronasopharyngeal airway insertion, suction oropharynx, apply positive pressure ventilation with a mask, or consider LMA/ETT insertion).
Pneumothorax: Needle decompression if hemodynamically unstable; if time permits, a chest tube should be inserted
Diffusion problems: If pulmonary edema, increase the surface area for diffusion by increasing the transalveolar pressure (administration of continuous positive airway pressure [CPAP] if not intubated, PEEP if intubated).
Machine issue: If suspected, immediately convert to an Ambu bag while searching for the cause (disconnect, internal issue); do not let the patient deteriorate while searching for the cause
Maintain adequate cardiac output and hemoglobin levels
If hypoxia does not resolve with appropriate interventions, terminate surgery as soon as possible

Closed Claims Data

In the 1986 Closed Claims review, adverse outcomes associated with respiratory events constitute the single largest class of injury (522 of 1,541 cases; 34%). Death or brain damage occurred in 85% of cases. Most outcomes (72%) were considered preventable with better monitoring. Inadequate ventilation (196; 38%) was one of the three mechanisms of injury and accounted for 75% of the adverse respiratory events.
In the 2000 review, which looked at the period of time after widespread introduction of pulse oximetry and EtCO₂ monitoring, the adverse outcomes associated with respiratory events decreased significantly.

Blum JM , Fetterman DM , Park PK , et al. A description of intraoperative ventilator management and ventilation strategies in hypoxic patients. Anesth Anal. 2010;110(6):1616–1622.
Hare G , Kavanagh B. Hypoxemia during surgery: Learning from history, science, and current practice. Can J Anesth/J Can Anesth. 2010;57:877–881.

Pedersen T , Moller AM , Hoyannisyan K. Pulse oximetry for perioperative monitoring. Cochrane Database Syst Rev. 2009;4:CD002013.
Ehrenfeld JM , Funk LM , Van Schalkwyk J , et al. The incidence of hypoxemia during surgery: Evidence from two institutions. Can J Anesth. 2010;57.

See Also (Topic, Algorithm, Electronic Media Element)

Hypoxia, Postoperatively
Carotid Body
Dead Space
Anaerobic Metabolism
Alveolar-Arterial Gradient and Ratio
Pneumothorax

ICD9

799.02 Hypoxemia
998.9 Unspecified complication of procedure, not elsewhere classified

ICD10

R09.02 Hypoxemia
T81.89XA Oth complications of procedures, NEC, init

Always assume a low SpO₂ is accurate until proven otherwise.
Atelectasis is the most common cause of intraoperative hypoxia. Recruitment maneuvers may need to be done regularly in intubated patients with decreased functional residual capacity (FRC) such as obesity, pregnancy, laparoscopic procedures, and Trendelenburg position. Similarly, recruitment maneuvers might be necessary in those with increased closing capacity such as the elderly.
Hypoxia should always be at the top of a differential diagnosis for abnormal cardiovascular vital signs such as hypertension, tachycardia, and arrhythmia, as well as nausea and altered mental status.

Suzanne Strom , MD

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Basics ⬇

Incidence

Prevalence

Morbidity

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

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