The American Dental Association and several dental specialty organizations have published guidelines that detail requirements for monitoring patients during various levels of sedation and, in some cases, general anesthesia. In general, all these are consistent with those guidelines suggested by the American Society of Anesthesiologists for sedation and analgesia by nonanesthesiologists. It is well accepted that the principal negative impact of sedation and anesthesia is the compromise of respiratory function. While monitoring per se is a technical issue, an appreciation of its purpose and the interpretation of the information provided require an understanding of respiratory anatomy and physiology. The focus of this continuing education article is to address the physiological aspects of respiration and to understand the appropriate use of monitors, including the interpretation of the information they provide.Abstract
Oxygen-Hemoglobin Dissociation Curve. There is a nonlinear relationship between the percentage of total hemoglobin saturated with oxygen (SaO2) and PaO2, as demonstrated by the oxygen-hemoglobin dissociation curve illustrated in Figure 1. Hemoglobin saturations of 95% and higher sustain PaO2 at or above 80 mm Hg, preventing hypoxemia. At 90% saturation, the curve becomes steep, and within a relatively narrow period, the percent hemoglobin saturation and PaO2 decline dramatically. The relationship between SaO2 and PaO2, although in different units, approximates a value of 30 during this rapid decline. Intracellular oxygen tension or that of mixed venous blood is normally 40 mm Hg, so that hemoglobin saturation below 70% would indicate that normal cellular function is compromised.
Approximate Lung Volumes and Capacities.
Hemoglobin Desaturation Following Apnea. All patients were preoxygenated prior to apnea following neuromuscular blockade. Normal adults remain well oxygenated for 8–9 minutes despite absence of ventilation. Obese patients and children have reduced functional residual capacity, so despite preoxygenation, commence significant desaturation within 3–4 minutes. In all cases, desaturation would have occurred far more rapidly had the functional residual capacity not been concentrated with oxygen by preoxygenation (adapted from Benumof JL 7 ).
Amplified Precordial Stethoscope. Continuous auscultation of breath sounds can be accomplished using a stethoscope head and amplifier (A) connected to either conventional ear plugs (B) or a Blue Tooth listening device (C).
Capnographic Waveform. A capnographic waveform reflects carbon dioxide content of gas during a ventilatory cycle. In Figure 5 expiration occurs along points A to D as follows: A–B, exhalation of dead space; B–C, exhalation of lower airway; and C–D, exhalation of alveoli. Inspiration occurs from points D to E. End-tidal CO2 is recorded at point D.
Supplemental Oxygen and Respiratory Monitoring. Capnography (ETCO2) is the purest measure of hypoventilation. The lower tracing in this graph shows a simultaneous elevation in ETCO2 as hypoventilation commences. The top 2 tracings show pulse oximeter readings for patients supplemented with oxygen and those breathing room air. Note the top tracing shows no warning of hypoventilation, but the tracing for patients breathing room air declines in concert with the capnographic reading (adapted from Fu ES et al 8 ).
Contributor Notes
Address correspondence to Daniel E Becker, DDS, 444 West 3rd Street, Dayton, OH 45402, e-mail: dan.becker@sinclair.edu
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