Room air sat>97% rules out hypoxemia and PaCO2 >50 (JEM 20:4)
While there is a good correlation between SpO2 and SaO2 saturations in healthy patients, it may not hold true in the critically ill.
While a pulse ox>90% is believed to correlate with the same SaO2, prior studies have actually put the number closer to 92-96%. Changes in SpO2 tend to overestimate changes in SaO2. Acidosis and anemia cause only small variations in correlation. (Crit Care Aug 2003 7:4)
Calibrated only down to 70%, below that, who knows?
There is a lag in display of hypoxia (Ref 3 from Surg Crit Care)
Perform a bupivicaine digital block to get a pulse ox reading on a
clamped down patient (Crit Care Secrets)
3-5 less than PCO2, accurate if phase three is flat, not sloping
14G catheter through one nare of nasal cannula
Reflects mishaps with the ET tube but also a measure of lung perfusion and degree of dead space ventilation. Also measures degree of airway resistance.
Current terminology is summarized as follows.
A time capnogram can be divided into inspiratory (phase 0) and expiratory
segments. The expiratory segment, similar to a single breath nitrogen curve or
single breath CO2 curve, is divided into phases I, II and III, and occasionally,
phase IV, which represents the terminal rise in CO2 concentration. The angle
between phase II and phase III is the alpha angle. The nearly 90 degree angle
between phase III and the descending limb is the beta angle.
One modality that has practical application in the ED is the measurement of end-tidal carbon dioxide (etCO2). During shock (or any low-flow state), etCO2 frequently is low. This reflects the impaired venous return of metabolic by-products caused directly by the global decrease in perfusion. As resuscitation proceeds, previously hypoxic regions regain adequate perfusion, resulting in a return of CO2 to the central circulation. Hence, etCO2 increases. By following continuous etCO2 measurements, the EP can make educated inferences regarding the overall success of resuscitation. With the appropriate equipment, etCO2 can be measured and monitored from an endotracheal tube, face mask, or nasal cannula.
The phase III should be sloped because the first area of lung to offload CO2 is one with decreased airway resistance so V/Q is high therefore low PACO2. At end of exhalation it is mostly airways with high resistance which means Low V/Q which means higher PACO2.
End Tidal CO2 Capnometer
6 breaths
38cc deadspace in adult version
Color Change=>2% concentration of CO2 goes purple, 0.5-2% will turn tan
Will last 15 months outside of package and at least 10 minutes of active use.
Decreased EtCO2 may represent decreased cardiac output
Causes of relative decrease in ETCO2
Anatomic Dead Space
Open Vent Circuit
Panting Respirations
Physiologic Dead Space
Obstructive Lung Disease
Low Cardiac Output
Pulmonary Embolism
Excessive Lung Inflation
ETCO2 can rarely be higher than PaCO2
Excessive CO2 production with low inspired volume and high cardiac output
or High inspired O2 from CO2 displaced from Hb
For tube confirmation, ETCO2 is 100% sensitive when monitored by waveform, even during cardiac arrest
Late values (20 minutes from onset of ACLS) of <10 = no survival (NEJM 1997;337:301)
I have had occasion to use the new volumetric capnography. It measures
deadspace with each breath. If you make a change and it decreases perfusion
and/or increases deadspace, then VD/VT will change. So if you have a patient
that you raise the mean airway pressure, the balance of the cardio and the
pulmonary aspects should be reflected in the VD/VT.
Once had an interesting case a few years back.. On rounds in ICU. Intubated
COPDer, paralyzed and wheezing up a storm and on the usual onslaught of
bronchodilators. Auto-peep was 10 and the response was to match the auto peep
with set peep. I argued against this, they told me to fix it and catch up with
them. I reduced the RR from 10 to 14, shortened Ti, removed set peep, etc. The
next ABG came back with better pH and PaCO2 despite a reduction in minute
ventilation. But the PaO2 (on FiO2 .40) had jumped up to 140 torr. AND the VD/VT
had gotten much worse—about .6 to .7!. I turned the FIO2 down to .21, then
slowly increased to the very minimum---the SpO2 went to 86% on FiO2 .21 as I
slowly raised FiO2. The VD/VT then came back about .30 or so. Apparently the
changes which allowed a higher PaO2 then released regional hypoxic pulmonary
vasoconstriction. And again, the patient was paralyzed, so nothing to do with
the ventilatory drive.
Can titrate recruitement by the Pa-etCO2 gradient
study of ETCO2 for procedural sedation shows that it precedes desat (Acad Emerg Med 2006;13:500)
article on CO2 relation between end tidal and PaCO2 Inbox
Can J Anaesth 1996;43(8):862
capnography for procedural sedation (Ann Emerg Med 2007;50:172)
Capnographic airway assessment for procedural sedation and analgesia.
| Diagnosis | Waveform | Features | Intervention | ||
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| Normal |
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| Hypopneic Hypoventilation with periodic breathing |
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| Physiological variability |
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| Bronchospasm |
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| Partial airway obstruction |
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| Partial laryngospasm |
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| Apnea |
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| Complete airway obstruction |
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| Complete laryngospasm |
| Positive pressure ventilation | |||
Varying waveform amplitude and width.
Definition of Respiratory Depression
Respiratory depression causes a reduction in alveolar ventilation by a decrease in respiratory rate or tidal volume caused by a decrease in respiratory drive. The result is an increase in PaCO2.37 By definition, hypoventilation is arterial hypercarbia (“a state in which there is a reduced amount of air entering the pulmonary alveoli [decreased alveolar ventilation], resulting in increased carbon dioxide tension”).38 One cannot diagnose hypoventilation, and hence respiratory depression, without some measure of alveolar or arterial CO2.
Normal, Hyperventilation, and Hypoventilation Patterns
Changes in etco2 and expiratory time affect the shape of the capnogram.[2], [5], [14] and [39] The amplitude of the capnogram is determined by etco2, and the width is determined by the expiratory time. Hyperventilation (increased respiratory rate, decreased etco2) results in a low amplitude and narrow capnogram, whereas classic hypoventilation (decreased respiratory rate, increased etco2) results in a high amplitude and wide capnogram (Table 1).[2], [4], [14] and [39]
Physiological Variability
Unlike other types of vital sign monitoring during procedural sedation and analgesia (pulse rate, blood pressure, SpO2), there can be considerable breath-to-breath variability in the shape and size of the capnogram in normal, nonsedated subjects (Table 1).[2], [15] and [37] This physiologic variability results from normal variations in ventilatory pattern that occur during talking (long and short breaths, slow and fast/rapid breathing) and anxiety states (especially preprocedural anxiety) and in young children. Ventilatory pattern stabilizes and physiologic variability decreases as the depth of sedation increases.40
Drug-Induced Ventilatory Patterns
There are 7 primary drug-induced ventilatory patterns that can occur with procedural sedation and analgesia: periodic breathing, apnea, upper airway obstruction, laryngospasm, bronchospasm, hypoventilation, and respiratory failure.
Periodic Breathing
Periodic breathing is characterized by normal breathing punctuated with apneic pauses, occurring most commonly during deep sedation (Table 1).[2], [15], [37] and [39] This pattern may be self-resolving or devolve into complete central apnea.[2], [15], [37] and [40]
Apnea
Apnea can be almost instantaneously detected by capnography. Loss of the capnogram, the earliest indicator of cessation of ventilation, in conjunction with no chest wall movement and no breath sounds on auscultation, confirms the diagnosis of central apnea (Table 1).[2], [4] and [40]
Capnography may be more sensitive than clinical assessment of ventilation in detection of apnea.[12], [29], [34], [35] and [36] In a recent study, 10 of 39 (26%) patients experienced 20-second periods of apnea during procedural sedation and analgesia.29 All 10 episodes of apnea were detected by capnography but not by the anesthesia providers.
Upper Airway Obstruction
Partial upper airway obstruction can be diagnosed clinically by the presence of stridor or noisy respirations. The diagnosis of complete upper airway obstruction or obstructive apnea is based on loss of the capnogram in conjunction with 3 clinical findings: chest wall movement, no breath sounds on auscultation, and the absence of stridor or upper airway sounds.[2] and [14] The absence of the capnogram in association with the presence or absence of chest wall movement distinguishes apnea from upper airway obstruction and laryngospasm. Response to airway alignment maneuvers can further distinguish upper airway obstruction from laryngospasm (Table 1).40
Capnography also provides a nonimpedance respiratory rate directly from the airway (by oral-nasal cannula),4 which is more accurate than impedance-based respiratory monitoring, especially in patients with complete upper airway obstruction or laryngospasm, in which impedance-based monitoring will interpret chest wall movement without ventilation as a valid breath. Although turbulence associated with partial laryngospasm affects expiratory flow, it does not affect the amplitude of the capnogram unless it results in hypoventilation or is associated with another abnormal finding such as bronchospasm.
Laryngospasm
Partial laryngospasm is detected by the presence of noisy breathing and normal oxygenation that is not relieved by airway alignment maneuvers in a previously normal subject receiving procedural sedation and analgesia agents (Table 1). The diagnosis of complete laryngospasm is based on loss of the CO2 waveform in conjunction with 4 clinical findings: chest wall movement, no breath sounds on auscultation, absence of stridor or upper airway sounds, and no response to airway alignment maneuvers (no capnogram despite airway alignment maneuvers).[40] and [41]
Bronchospasm
The characteristic capnogram (curved ascending phase and upsloping alveolar plateau) observed with lower airway obstruction indicates the presence of acute bronchospasm or obstructive lung disease (Table 1).23
Respiratory Failure
An etco2 greater than 70 mm Hg in patients without chronic hypoventilation indicates respiratory failure.[36], [39] and [42]
Drug-Induced Hypoventilation
There are 2 types of hypoventilation that occur during procedural sedation and analgesia (Table 1, Table 2 and Table 3). Bradypneic hypoventilation (type 1) is characterized by an increased etco2 and an increased PaCO2. Respiratory rate is depressed proportionally greater than tidal volume, resulting in bradypnea, an increase in expiratory time, and an increase in etco2, graphically represented by a high amplitude and wide capnogram (Table 1, Table 2 and Table 3, Figure 2).[2], [14], [37], [40] and [42] Bradypneic hypoventilation is commonly observed with opioids. Bradypneic hypoventilation (decreased respiratory rate, high amplitude, and wide capnogram) can readily be distinguished from hyperventilation (increased respiratory rate, low amplitude, and narrow capnogram; Table 1, Table 2 and Table 3; Figure 2).[2], [14] and [15]
Characteristics of bradypneic (type 1) and hypopneic (type 2) hypoventilation.
Hypoventilation Type Respiratory Rate VT Airway Dead Space VD/VT etco2 PaCO2 Bradypneic (type 1) ↓↓↓ ↓ Constant/no change Minimal change ↑ ↑ Hypopneic (type 2) ↓ ↓↓↓ Constant/no change ↑↑↑ ↓, Or no change ↑ VD, Dead space volume; VT, tidal volume.
Table 3.Drug-induced hypoventilation patterns.
Type Physiology Subtype Features Normal No appreciable change in respiratory pattern
No change in respiratory rate or VT
Normal etco2 and normal SpO2
Mild respiratory depression Minimal change in respiratory pattern
Minimal decrease in respiratory rate and minimal decrease in VT
Normal etco2
Normal SpO2
Bradypneic hypoventilation (type 1)
Hypoventilation with minimal tidal volume change
Drugs that affect RR
VT
a
Decreased minute ventilation
High etco2
Normal SpO2
b
Decreased minute ventilation
High etco2
Decreased SpO2
Hypopneic hypoventilation (type 2)
Hypoventilation with low tidal volume breathing
Drugs that affect VT
a
Decreased minute ventilation
Low etco2 and normal SpO2
b
Decreased minute ventilation
Low etco2 and decreased SpO2
Can devolve to:
Intermittent apneic pauses interspersed with normal ventilation (periodic breathing)
Central apnea
RR, Respiratory rate; VT, tidal volume.
Hypopneic hypoventilation (type 2) is characterized by a normal or decreased
etco2 and an increased PaCO2, reflecting the relationship between tidal volume
and airway dead space, in which airway dead space is constant (eg, 150 mL in the
normal adult lung) and tidal volume is decreasing (Table 1, Table 2 and Table 3;
Figure 2). Here, tidal volume is depressed proportionally greater than
respiratory rate, resulting in low tidal volume breathing that leads to an
increase in airway dead-space fraction (dead-space volume/tidal volume). As
tidal volume decreases, airway dead space fraction increases. The gradient
between PaCO2 and etco2 increases with the increase in dead-space fraction.26
Even though PaCO2 is increasing, etco2 may remain normal or be decreasing, which
is graphically represented by a low-amplitude capnogram and occurs most commonly
with sedative-hypnotic drugs (Table 1, Table 2 and Table 3; Figure 2).
It is essential for emergency physicians to understand the physiology of
hypopneic hypoventilation because it occurs frequently with sedative/hypnotics
and with deep sedation and can otherwise go unrecognized or misinterpreted as
hyperventilation. This is presumably the mechanism for the low etco2 reported by
Burton et al12 and Miner et al,[9], [10] and [11] which occurred in about 50% of
cases of respiratory depression.
Hypopneic hypoventilation follows a variable course and may remain stable, with
low tidal volume breathing resolving over time as central nervous system drug
levels decrease and redistribution to the periphery occurs, progress to periodic
breathing with intermittent apneic pauses (which may resolve spontaneously or
progress to central apnea), or progress directly to central apnea.[37] and [40]
Bradypneic hypoventilation follows a more predictable course, with etco2
increasing progressively until respiratory failure and apnea occur. Although
there is no absolute threshold at which apnea occurs, patients without chronic
hypoventilation and with etco2 greater than 80 mm Hg are at significant
risk.[37] and [39]
Abnormal respiratory patterns during a single sedation event can vary in their
type and severity (Table 1, Table 2 and Table 3).[1] and [40] Further, the onset
of hypoventilation during procedural sedation and analgesia can be sudden,
rapid, or gradual depending on the rapidity of central nervous system
penetration and the time course of drug distribution.[40] and [43]
Several factors contribute to the development of hypoxia, apnea, and upper
airway obstruction during ED procedural sedation and analgesia, especially
during deep sedation: supine position, decreased tidal volume, and direct
depression of respiratory drive. When a patient is placed in the supine position
during procedural sedation and analgesia, the abdominal viscera cause cephalad
displacement of the diaphragm, decreasing functional residual capacity by 0.5 to
1 L.44 Further reductions in functional residual capacity may result from
atelectasis as a result of low tidal volume breathing in hypopneic
hypoventilation.[45] and [46] This cumulative reduction in functional residual
capacity can initiate a cascade of events that result in decreased lung
compliance and airway caliber, leading to upper airway obstruction, which in
turn increases airway resistance and results in a decrease in oxygenation and
ultimately results in hypoxemia.[37] and [47]
Low tidal volume breathing increases dead-space ventilation when normal
compensatory mechanisms are inhibited by drug effects. Here, minute ventilation,
which normally increases to compensate for an increase in dead space, does not
change or may decrease.37 Further, as minute ventilation decreases, there is a
decrease in arterial oxygenation.48 As minute ventilation decreases further,
oxygenation is further impaired.48 However, etco2 may initially be high
(bradypneic hypoventilation) or low (hypopneic hypoventilation) without
significant changes in oxygenation, particularly if the patient is breathing
supplemental oxygen. We can now begin to understand why a drug-induced increase
or decrease in etco2 does not necessarily lead to oxygen desaturation and may
not require intervention.
Reasons for gradient between PaCO2 and ETCO2
dead space increases the gradient
shunt will send CO2 to arterial side that will never reach alveoli
ig 3 This diagram demonstrates how opiates can induce apnoea at the same PaCO2 as before opioid administration (dotted line) and also demonstrates that significant reductions in the HCVR only cause small changes in steady-state PaCO2. Curve A represents the normal ventilatory response to CO2 in an awake individual, demonstrating that ventilation is maintained at very low PaCO2 levels and that apnoea does not occur. Line B represents a 50% depression of the HCVR caused by opioid administration. A notable difference between curve A and line B is that in B apnoea can occur. Note also that in this case PaCO2 must rise to steady-state values (i.e. along the x-axis) for breathing to recommence (line B’). Curve C represents the CO2 excretion hyperbola and demonstrates how changes in ventilation affect PaCO2. Point X represents the awake state and point Y represents opioid-depressed breathing. Despite a 50% depression of the HCVR, the CO2 changes only relatively modestly, illustrating the limited utility of single measurements of CO2 in assessing respiratory depression. Figure reproduced with permission from Gross.52