Tuesday, February 6, 2018

Respiratory monitoring: physiological and technical considerations

Resident’s Name: Brian Darling                                                                     Date: 2/7/18

Article Title: Respiratory monitoring: physiological and technical considerations
Author(s): Becker DE, Casabianca AB
Journal: Anesthesia Progress
Date: 2009; 56(1): 14-20
Major Topic: Respiratory monitoring for sedation
Type of Article: Topic overview
Main Purpose:  This article describes basics about respiratory monitoring for sedation in dentistry.
Key Points: Airway monitoring is crucial to safe pediatric sedation. Ventilation and oxygenation are distinct entities that should be monitored during sedation.
4 Categories of events comprise respiration:
1.     Ventilation
2.     Gas exchange
3.     Gas transport
4.     Control of ventilation
Ventilation and oxygenation are distinct physiological processes.
Ventilation: movement of gas between the environment and pulmonary alveoli
·      Must be monitored periodically in moderate sedation and continuously in deep sedation/GA
·      Ventilation may be normal while oxygenation may be inadequate due to lack of oxygen in inhaled air or compromised perfusion to pulmonary alveoli
·      Respiratory control center is in medulla and is hypercapnic driven
o   Opioids depress central chemosensitive area
·      Peripheral chemoreceptors at aortic and carotid bodies are hyperoxemic driven
o   Benzodiazepines influence these more than central chemoreceptors
·      Respiratory depression: reduced activity of respiratory center in stimulating ventilation
·      Normal PaCO2 is 40mmHg (PaCO2 is true measure of ventilation)
·      Deflation and inflation of reservoir bag is a useful way to monitor ventilation
·      CO2 is best way to measure ventilation
·      Normal end-tidal CO2 is 35-38 mmHg
·      Capnography: monitors that display continuous waveform reflecting inspiration and expiration
·      Little reason for decreased oxygenation in moderate sedation other than for reasons of hypoventilation like from respiratory depression or airway obstruction
·      Precordial auscultation is exceptional for continuous monitoring of breath sounds and air exchange
Oxygenation: actual oxygen content of arterial blood
·      Determined by adequate ventilation and perfusion of pulmonary capillaries
·      Must be monitored continuously in moderate, deep sedation, and GA
Pulse Oximetry
·      LED measures absorption of light wavelengths to determine arterial hemoglobin oxygen saturation
·      660nm (red) is absorbed by oxygenated hemoglobin and 940nm (infrared) is absorbed by deoxygenated hemoglobin
·      Readings depend on pulsatile blood flow because measurements are taken at the point of maximum intensity of the waveform
·      Indirectly measures arterial oxygen tension (gas pressure dissolved in plasma, oxygen not bound to hemoglobin) by measuring percent of hemoglobin oxygen saturation
o   Measures hemoglobin saturation and NOT PaO2
·      Reading alterations can be caused by:
o   Anything that alters blood flow – low blood flow from hypotension, hypothermia, vasoconstriction
o   Dark or metallic nail polish
o   Acrylic finger nails
o   Motion
·      SpO2 of 95% correlates with PaO2 of 80mmHg, which is the lower limit of normal oxygenation
·      SpO2 of 90% correlates with PaO2 of 60mmHg, which is hypoxemic. Most alarms are set to go off at 90%. Important point on oxygen-hemoglobin dissociation curve where saturation drops significantly after this
·      30-40 second delay in readings
Cyanosis usually not detectable until hemoglobin saturations are well below 80% (PaO2 <50mmHg)
Tidal Volume: volume of gas inspired and expired during a normal ventilator cycle. 500mL average in adults and 6-8mL/kg of ideal body weight.
Functional Residual Capacity: volume of gas remaining in the lungs at the end of tidal respiration
·      Reflects “oxygen reserve”
·      Children have decreased FRC and 2x increased oxygen consumption
·      Oxygen supplementation aims to increase amount of oxygen in FRC to allow more time to intervene if hypoventilation or apnea occurs
o   Children must receive supplemental oxygenation for sedation
Moderate sedation doses of opioids and benzodiazepines cause only mild respiratory depression. Relaxed state of patient is much more likely to cause anatomical airway obstruction from soft tissues.
·      Upper airway muscle tone becomes more relaxed
·      Tongue may fall backward
·      Relaxed pharyngeal musculature
·      Recumbent position makes obstruction more likely
Airway patency is most essential caveat in safe sedation to assure adequate ventilation.

Must continuously monitor ventilation if using supplemental oxygenation because the extra oxygen can mask hypoventilation if you are just monitoring with pulse oximeter.

Signs of airway obstruction (chest normally expands upward and outward)
·      Nasal flaring
·      Discordant chest wall movement
·      Retraction at suprasternal area (tracheal tug) with respiratory effort
·      Chest wall rocks – chest wall contracts inward and abdomen pushes outward
·      Increase in sonorous sounds 
Head tilt-chin lift-jaw thrust is best way to treat airway obstruction
Precordial stethoscope monitors airway patency and ventilation and is good for continuous monitoring of breath sounds and air exchange.


Remarks:
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Assessment of Article:  Level of Evidence/Comments: III

1 comment:

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