{"id":5293,"date":"2011-07-14T20:25:11","date_gmt":"2011-07-14T20:25:11","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5293.htm\/"},"modified":"2015-07-27T13:47:16","modified_gmt":"2015-07-27T17:47:16","slug":"respiratory-monitoring","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/resuscitation\/monitoring\/respiratory-monitoring.htm\/","title":{"rendered":"Respiratory Monitoring"},"content":{"rendered":"

<\/span>Pulse Oximetry (Pulse Ox)
\n<\/span><\/span><\/h2>\n

Review Article<\/a><\/p>\n

Room air sat>97% rules out hypoxemia and PaCO2 >50 (JEM 20:4)<\/p>\n

While there is a good correlation between SpO2 and SaO2 saturations in healthy patients, it may not hold true in the critically ill.<\/p>\n

While a pulse ox>90% is believed to correlate with the same SaO2, prior studies have actually put the number closer to 92-96%.\u00a0 Changes in SpO2 tend to overestimate changes in SaO2.\u00a0 Acidosis and anemia cause only small variations in correlation. (Crit Care Aug 2003 7:4)<\/p>\n

 <\/p>\n

Calibrated only down to 70%, below that, who knows?<\/p>\n

There is a lag in display of hypoxia (Ref 3 from Surg Crit Care)<\/p>\n

Perform a bupivicaine digital block to get a pulse ox reading on a clamped down patient (Crit Care Secrets)<\/p>\n

 <\/p>\n

How do skin pigmentation, nail polish, and acrylic nails affect pulse oximetry?
\nThe following studies show that:<\/p>\n

1. Pulse oximetry recordings are not significantly influenced by dark skin pigmentation in relatively stable but critically ill adults.<\/p>\n

2. Nail polish is rarely associated with clinically significant deviations in pulse oximeter readings, although polish removal might be helpful in some situations.<\/p>\n

3. Acrylic finger nails may impair the measurement of oxygen saturation, depending on the pulse oximeter used, and may cause significant inaccuracy. Hence, removal of artificial acrylic finger nails may assure an accurate and precise measurement with pulse oximetry.<\/p>\n

30. ACCURACY OF PULSE OXIMETRY IN PIGMENTED PATIENTS Bothma, P.A., et al, S Afr Med J 86(5):594, May 1996<\/p>\n

BACKGROUND: Prior studies of the influence of skin pigmentation on the accuracy of pulse oximetry have yielded conflicting results. METHODS: This prospective South African study compared the readings of three pulse oximeters (Simed S100e [Simed Co.], Nihon Koden [Nihon Koden Corp.], and Ohmeda 3740 [Ohmeda]) with arterial oxygen saturation by cooximetry in 100 consecutive darkly pigmented critically ill adults. Finger probes were employed with all three pulse oximeters, and an ear probe was also used with the Ohmeda model. RESULTS: Arterial oxygen saturations were between 88-99% (median, 96%), with pulse oximeter readings between 86-100%. The limits of agreement between the two techniques were 3.4-4.5% with the Ohmeda finger probe, 3.8-5.8% with the Ohmeda ear probe, 4.1-5.8% with the Nihon Koden, and 2.6-5.0% with the Simed, all of which were considered to be clinically acceptable. The 95% confidence intervals were small. The precision (standard deviation of the differences) ranged between 1.9 and 2.4%, and bias (mean of the differences) ranged between -1.0 and 1.2%. When the arterial oxygen saturation was below 92%, there was a trend towards lower values with pulse oximetry. Pulse oximetry results tended to be higher than arterial oxygen saturation with the finger probes, and lower with the Ohmeda ear probe. These differences were small and not considered clinically significant. CONCLUSIONS: Pulse oximetry recordings were not significantly influenced by dark skin pigmentation in these relatively stable but critically ill adults. 25 references 1\/97 – #35<\/p>\n

31. EFFECT OF NAIL POLISH ON OXYGEN SATURATION DETERMINED BY PULSE OXIMETRY IN CRITICALLY ILL PATIENTS Hinkelbein, J., et al, Resuscitation 72:82, January 2007<\/p>\n

BACKGROUND: The belief that use of nail polish can be associated with misleading results during pulse oximetry monitoring has not been extensively investigated. METHODS: These German authors examined the effects of nine nail polish colors on pulse oximetry readings in 50 adult Caucasian ICU patients undergoing mechanical ventilation. A different color of polish, ranging over the entire color spectrum from black to clear, was applied on each of nine fingernails and one fingernail without nail polish served as a control. Pulse oximetry readings were obtained using a SIEMENS pulse oximeter monitor SC1281 and a NELLCOR DS-100A Durasensor finger sensor probe. Pulse oximetry readings were compared with arterial blood gas results. RESULTS: There was a close correlation between the mean arterial and control pulse oximetry readings (difference +0.2%). The mean difference between the readings was greatest in the setting of black nail polish (difference 1.6%, 95% confidence interval [CI] -4.1% to +10.6%), purple polish (difference 1.2%, 95% CI -3.1% to +12.5%) and dark blue polish (1.1%, 95% CI -5.7% to +9.1%), and was less than 1% with all other polish colors. For all colors, the mean difference between arterial and pulse oximetry readings was within the oximeter manufacturer’s reported deviation of plus\/minus 2% in the oxygen saturation range of 70-100%. In general, pulse oximetry tended to underestimate arterial oxygenation results. CONCLUSIONS: Nail polish was rarely associated with clinically significant eviations in pulse oximeter readings, although polish removal might be helpful in some situations. 34 references 6\/07 – #34<\/p>\n

32. ARTIFICIAL ACRYLIC FINGERNAILS MAY ALTER PULSE OXIMETRY MEASUREMENT Hinkelbein J, Koehler H, Genzwuerker HV, Fiedler F. Resuscitation. 2007 Jul;74(1):75-82. Epub 2007 Mar 13.<\/p>\n

INTRODUCTION: Pulse oximetry is the most common technique to monitor oxygen saturation (SpO(2)) during intensive care therapy. However, intermittent co-oximetry is still the “gold standard” (SaO(2)). Besides acrylic nails, numerous other factors have been reported to interfere with pulse oximetry. Data of measurements with artificial finger nails are not sufficiently published. MATERIALS AND METHODS: A prospective clinical-experimental trial in mechanically ventilated and critically ill patients of an ICU was performed. Patients were randomly assigned to either group S (S: Siemens pulse oximeter) or group P (P: Philips pulse oximeter) prior to the measurements. SpO(2) was determined in each patient three times alternately in standard ((N)SpO(2)) and sideways position at the natural nail ((N90)SpO(2)). For the reference measurements oxygen saturation was measured by means of a haemoximeter (co-oximetry). Thereafter, SpO(2) was obtained at the acrylic finger nail in the same way ((A)SpO(2) and (A90)SpO(2)). Bias was calculated as DeltaS=(N)SpO(2)-SaO(2) and DeltaS=(A)SpO(2)-SaO(2). Accuracy (mean difference) and precision (standard deviation) were used to determine the measurement discrepancy. P<0.05 was considered significant. RESULTS: Accuracy and precision without acrylic nails applied were comparable to SaO(2) in both groups (n.s.). With acrylic nails applied a bias of DeltaS=-1.1+\/-3.14% for group S (P=0.00522) and a bias of DeltaS=+0.8+\/-3.04% for group P was calculated (n.s.). CONCLUSION: Acrylic finger nails may impair the measurement of oxygen saturation depending on the pulse oximeter used and may cause significant inaccuracy. Hence, removal of artificial acrylic finger nails may be helpful to assure an accurate and precise measurement with pulse oximetry.<\/p>\n

How do abnormal hemoglobins or infusion of hydroxocobalamin affect oximetry?
\nHydroxocobalamin is widely used in Europe as an alternative to other cyanide antidotes for the treatment of patients with cyanide poisoning associated with smoke inhalation. Increasing hydroxocobalamin concentrations are associated with a progressive increase in the oximetric reading for carboxyhemoglobin and methemoglobin, and a corresponding decrease in the oxygen saturation reading.<\/p>\n

Unlike standard oximetry, the Rainbow-SET Rad-57 Pulse CO-Oximeter (Masimo) is an eight-wavelength pulse oximeter that is capable of measuring more than two species of human hemoglobin. At the carboxyhemoglobin and methemoglobin levels achieved in healthy volunteers, the Rad-57 device appeared to be reliable. These results cannot be extrapolated to the setting of critical illness or more severe dyshemoglobinemia (or respiratory co- morbidity).<\/p>\n

33. POTENTIAL INTERFERENCE BY HYDROXOCOBALAMIN ON COOXIMETRY HEMOGLOBIN MEASUREMENTS DURING CYANIDE AND SMOKE INHALATION TREATMENTS Lee, J., et al, Ann Emerg Med 49(6):802, June 2007<\/p>\n

BACKGROUND: Hydroxocobalamin is widely used in Europe as an alternative to other cyanide antidotes for the treatment of patients with cyanide poisoning associated with smoke inhalation. It might be postulated, however, that the intense light absorption produced by hydroxocobalamin can interfere with light source-based co-oximetric blood gas measurements. METHODS: The authors, from the University of California, Irvine, examined the effect of hydroxocobalamin infusion (average dose, 625mg infused over 100 minutes) on oximetry readings in rabbits. RESULTS: Increasing hydroxocobalamin concentrations were associated with a progressive increase in the oximetric reading for carboxyhemoglobin and methemoglobin, and a corresponding decrease in the oxygen saturation reading. Similar patterns were observed in an in vitro study of whole blood samples with different hydroxocobalamin concentrations. Increasing hydroxocobalamin levels were associated with a change of up to (- )7.9% in the oxygen saturation value and (+)14.7% in the carboxyhemoglobin value. CONCLUSIONS: The authors advise caution in the interpretation of hemoglobin fractions measured with co-oximetry when hydroxocobalamin is used for the treatment of cyanide poisoning and smoke inhalation. The effects of this spectral overlap might be particularly relevant in patients receiving continuous hydroxocobalamin infusion and when blood sampling is performed immediately after bolus injection or “upstream” from the hydroxocobalamin infusion site. 10 references 10\/07 – #34<\/p>\n

34. MEASUREMENT OF CARBOXYHEMOGLOBIN AND METHEMOGLOBIN BY PULSE OXIMETRY: A HUMAN VOLUNTEER STUDY Barker, S.J., et al, Anesthesiology 105(5):892, November 2006<\/p>\n

BACKGROUND: Standard pulse oximeters estimate arterial hemoglobin saturation via measurement of tissue light transmission at two wavelengths. Several studies have reported serious errors in estimation of oxygen saturation in the presence of a dyshemoglobinemia. The Rainbow-SET Rad-57 Pulse CO-Oximeter (Masimo) is an eight-wavelength pulse oximeter that is capable of measuring more than two species of human hemoglobin. METHODS: The authors, from the University of Arizona and partially funded by Masimo, examined the performance of the Rad-57 device in ten healthy volunteers exposed to carbon monoxide to produce a carboxyhemoglobin level of 15%, and ten volunteers given an IV infusion of sodium nitrite to induce methemoglobinemia at a level between 5-12%. Pulse oximetry results obtained with the Rad-57 were compared with measurements performed in arterial blood. RESULTS: At a carboxyhemoglobin level of 0-15%, the uncertainty (a measure of test imprecision) of carboxyhemoglobin measurement with the Rad-57 was +\/- 2%. At a methemoglobin level of 0-12%, the uncertainty with the Rad-57 was +\/- 0.5%. For comparison purposes, the uncertainty of most standard pulse oximeters for measurement of oxygen saturation at values of 70-100% is +\/- 2%. CONCLUSIONS: At the carboxyhemoglobin and methemoglobin levels achieved in these healthy volunteers, the Rad-57 device appeared to be reliable. The authors acknowledge that these results cannot be extrapolated to the setting of critical illness of more severe dyshemoglobinemia (or respiratory co- morbidity). 17 references 3\/07 – #34<\/p>\n

Is room-air pulse oximetry sensitive for hypercapnia?
\nIn this case-control study, the frequency of hypercapnia was inversely related to the oxygen saturation on room air pulse oximetry. At an oxygen saturation cut-off of 96%, room air pulse oximetry appears to be a sensitive screening test for moderate hypercapnia.<\/p>\n

35. THE SENSITIVITY OF ROOM-AIR PULSE OXIMETRY IN THE DETECTION OF HYPERCAPNIA Witting, M.D., et al, Am J Emerg Med 23:497, July 2005<\/p>\n

BACKGROUND: The suggestion that pulse oximetry does not reliably identify hypercapnia has been based on studies conducted in patients receiving supplemental oxygen. One small study reported that, at a cut-off of 96%, room-air pulse oximetry detected all twelve patients with moderate hypercapnia. METHODS: In this case-control study, from the University of Maryland, the charts of 92 patients with hypercapnia and 257 patients without hypercapnia were reviewed to assess the diagnostic utility of an oxygen saturation of 96% or lower on room-air pulse oximetry for the detection of moderate hypercapnia (PaCO2 above 50mm Hg). All of the patients had pulse oximetry performed on room air followed within eight hours by measurement of arterial blood gases (this interval was less than two hours in 43% of patients and 5-8 hours in 12%). RESULTS: The frequency of hypercapnia was inversely related to the oxygen saturation on room air pulse oximetry. At an oxygen saturation cut-off of 96%, the sensitivity and specificity of room air pulse oximetry for the identification of moderate hypercapnia were 96% and 39%, respectively, the positive likelihood ratio (LR) was 1.6, and the negative LR was 0.1. There were four falsely-negative cases. CONCLUSIONS: The authors acknowledge the limitations of their study design but suggest that, at an oxygen saturation cut-off of 96%, room air pulse oximetry appears to be a sensitive screening test for moderate hypercapnia. 14 references 12\/05 – #36<\/p>\n

How long does it take for the equilibration of oxygen saturation using pulse oximetry?
\nFor patients placed on supplemental oxygen, the mean interval between initiation of O2 and equilibration was 2.8 minutes. The mean times to equilibration in patients with and without COPD or asthma were 3.5 and 2.5 minutes, respectively.<\/p>\n

36. TIME TO EQUILIBRATION OF OXYGEN SATURATION USING PULSE OXIMETRY Gruber, P., et al, Acad Emerg Med 2(9):810, September 1995<\/p>\n

BACKGROUND: Although it is generally believed that equilibration of the oxygen saturation after changing the inspired oxygen concentration (FiO2) requires 20-30 minutes, the actual time required for equilibration in patients with active medical problems has not been clearly defined. METHODS: This prospective study, from Long Island Jewish Medical Center in New Hyde Park, NY, examined the actual time required for equilibration of O2 saturation after changing the FiO2 in 51 adults requiring supplemental oxygen (2-4L\/min by nasal cannula) in the ED due to acute cardiac and\/or pulmonary conditions. Equilibration times were calculated on the basis of O2 saturation measurements made at one-minute intervals for 30 minutes after a change was made in FiO2. RESULTS: For patients placed on supplemental oxygen (43 measurements), the mean room air oxygen saturation was 89.8%, the mean equilibration point was 95.3%, and the mean interval between initiation of O2 and equilibration was 2.8 minutes (95% confidence interval, 2.3-3.3 minutes). The mean times to equilibration in patients with and without COPD or asthma were 3.5 and 2.5 minutes, respectively (p=0.01). Upon discontinuation of supplemental oxygen (18 measurements), the mean initial oxygen saturation was 96.6%, the mean equilibration point was 91.7%, and the mean interval to equilibration was 3.1 minutes (95% CI, 2.3-4.4 minutes), or 4.6 minutes in patients with COPD or asthma compared with 2.7 minutes in patients without these conditions. One patient in each group demonstrated continuous variability in O2 saturation throughout the study. CONCLUSIONS: Times to equilibration after making a change in inspired O2 concentration appear to be substantially shorter than traditionally believed. Equilibration times in patients with COPD or asthma may be longer than in other patients. 15 references 12\/95 – #38<\/p>\n

Should patients who are hyperventilating be given a paper bag to breathe into?
\nNo. The author, from the University of California in San Francisco, reports three cases in which collapse occurred in patients with myocardial ischemia or hypoxemia who were erroneously believed to be hyperventilating and were instructed to breathe into a paper bag. In a subsequent volunteer study, paper bag rebreathing was associated with a substantial decrease in inspired oxygen.<\/p>\n

37. HYPOXIC HAZARDS OF TRADITIONAL PAPER BAG REBREATHING IN HYPERVENTILATING PATIENTS Callaham, M., Ann Emerg Med 18(6):622, June 1989<\/p>\n

Patients who are hyperventilating are often managed with paper bag rebreathing. The author, from the University of California in San Francisco, reports three cases in which collapse occurred in patients with myocardial ischemia or hypoxemia who were erroneously believed to be hyperventilating and were instructed to breathe into a paper bag. In two of the cases, this treatment was initiated by paramedics or by a dispatcher, and in the remaining case treatment was initiated by a nurse. Two of the three patients sustained irreversible cardiopulmonary arrests. In a subsequent study, 20 healthy adults hyperventilated to an end-tidal CO2 of 20mm Hg, and were then instructed to hyperventilate into a paper bag containing sensors for the purpose of monitoring gas concentrations. Varying inspired concentrations of CO2 (FiCO2) were achieved with three minutes of bag rebreathing. The FiCO2 did not reach 40mm Hg for 30% of the subjects, and did not reach 35mm Hg for 22%, suggesting that bag rebreathing appears to be an unreliable method of achieving an elevated FiCO2. The inspired concentration of oxygen (FiO2) progressively declined over three minutes of bag rebreathing, to a mean maximal decrease in O2 of 26mm Hg. The decrease in O2 was 34mm Hg in four subjects, and 42mm Hg in one subject. The author suggests that paper bag rebreathing may be associated with a substantial decrease in inspired oxygen that may pose a threat to hypoxic patients. It is further suggested that this technique not be employed unless myocardial ischemia can be ruled out and direct measurement of the patient’s oxygenation has been performed. The author cautions against the recommendation and use of this technique by prehospital personnel. 37 references 11\/89 – #34<\/p>\n

KEY POINTS AND RECOMMENDATIONS
\n1. Peripheral venous blood gases may be a reliable substitute for arterial blood gases in the initial assessment of patients with suspected DKA.<\/p>\n

2. Arterial blood gas analysis does not reflect the acid-base status of systemic tissue during CPR. Respiratory alkalosis in arterial blood reflects a decrease in pulmonary blood flow. Acidosis in mixed venous blood reflects accumulation of CO2 proximal to the alveolar capillary bed. This mixed venous acidosis may more accurately represent systemic acid-base status.<\/p>\n

3. Pulse oximetry recordings are not significantly influenced by dark skin pigmentation in stable but critically ill adults.<\/p>\n

4. Nail polish is rarely associated with clinically significant deviations in pulse oximeter readings, although polish removal might be helpful in some situations.<\/p>\n

5. Acrylic finger nails may impair the measurement of oxygen saturation depending on the pulse oximeter used and may cause significant inaccuracy. Hence, removal of artificial acrylic finger nails may assure an accurate and precise measurement.<\/p>\n

6. The Rainbow-SET Rad-57 Pulse CO-Oximeter (Masimo) is an eight-wavelength pulse oximeter capable of measuring carboxyhemoglobin and methemoglobin levels.<\/p>\n

7. If someone tries to put a paper bag over your head, don\u2019t let them.<\/p>\n

Stephen Colucciello MD
\nAssociate Chair, Department of Emergency Medicine
\nCarolinas Medical Center<\/h6>\n

<\/span>ETCO2<\/span><\/h3>\n

3-5 less than PCO2, accurate if phase three is flat, not sloping<\/p>\n

PaCO2 = to or > ETCO2 unless there is exogenous administration. (Barash Anesthesia Textbook P.802)<\/p>\n

14G catheter through one nare of nasal cannula<\/p>\n

\"\"<\/a>\"\"<\/a>\"\"<\/a><\/p>\n

 <\/p>\n

Reflects mishaps with the ET tube but also a measure of lung perfusion and degree of dead space ventilation.\u00a0 Also measures degree of airway resistance.<\/p>\n

 <\/p>\n

\"\"\"\"<\/p>\n

 <\/p>\n

 <\/p>\n

\"\"<\/p>\n

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.<\/p>\n

 <\/p>\n

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.<\/p>\n

 <\/p>\n

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.\u00a0 At end of exhalation it is mostly airways with high resistance which means Low V\/Q which means higher PACO2.<\/p>\n

 <\/p>\n

End Tidal CO2 Capnometer<\/p>\n

6 breaths<\/p>\n

38cc deadspace in adult version<\/p>\n

Color Change=>2% concentration of CO2 goes purple, 0.5-2% will turn tan<\/p>\n

Will last 15 months outside of package and at least 10 minutes of active use.<\/p>\n

 <\/p>\n

Decreased EtCO2 may represent decreased cardiac output<\/p>\n

Causes of relative decrease in ETCO2<\/p>\n

Anatomic Dead Space<\/p>\n

Open Vent Circuit<\/p>\n

Panting Respirations<\/p>\n

Physiologic Dead Space<\/p>\n

Obstructive Lung Disease<\/p>\n

Low Cardiac Output<\/p>\n

Pulmonary Embolism<\/p>\n

Excessive Lung Inflation<\/p>\n

 <\/p>\n

ETCO2 can rarely be higher than PaCO2<\/p>\n

Excessive CO2 production with low inspired volume and high cardiac output<\/p>\n

or High inspired O2 from CO2 displaced from Hb<\/p>\n

 <\/p>\n

For tube confirmation, ETCO2 is 100% sensitive when monitored by waveform, even during cardiac arrest<\/p>\n

 <\/p>\n

Late values (20 minutes from onset of ACLS) of <10 = no survival (NEJM 1997;337:301)<\/p>\n

 <\/p>\n

 <\/p>\n

Partial Pressure of End-tidal Carbon Dioxide Predict Successful<\/p>\n

Cardiopulmonary Resuscitation — A Prospective Observational Study<\/p>\n

Miran Kolar; Miljenko Kri\u009emari\u0107; Petra Klemen; \u008atefek Grmec<\/p>\n

 <\/p>\n

Crit Care. 2008;12(5) \u00a92008 Kolar et al.; licensee BioMed Central Ltd.<\/p>\n

Posted 10\/28\/2008<\/p>\n

Abstract and Introduction<\/p>\n

Abstract<\/p>\n

Introduction:<\/p>\n

 <\/p>\n

Prognosis in patients suffering out-of-hospital cardiac arrest is poor. Higher survival rates have been<\/p>\n

observed only in patients with ventricular fibrillation who were fortunate enough to have basic and advanced life support<\/p>\n

initiated soon after cardiac arrest. An ability to predict cardiac arrest outcomes would be useful for resuscitation.<\/p>\n

Changes in expired end-tidal carbon dioxide levels during cardiopulmonary resuscitation (CPR) may be a useful,<\/p>\n

noninvasive predictor of successful resuscitation and survival from cardiac arrest, and could help in determining when to<\/p>\n

cease CPR efforts.<\/p>\n

Methods:<\/p>\n

This is a prospective, observational study of 737 cases of out-of-hospital cardiac arrest. The patients were<\/p>\n

intubated and measurements of end-tidal carbon dioxide taken. Data according to the Utstein criteria, demographic<\/p>\n

information, medical data, and partial pressure of end-tidal carbon dioxide (Pet<\/p>\n

CO2) values were collected for each<\/p>\n

patient in cardiac arrest by the emergency physician. We hypothesized that an end-tidal carbon dioxide level of 1.9 kPa<\/p>\n

(14.3 mmHg) or more after 20 minutes of standard advanced cardiac life support would predict restoration of<\/p>\n

spontaneous circulation (ROSC).<\/p>\n

Results:<\/p>\n

PetCO2 after 20 minutes of advanced life support averaged 0.92 \u00b1 0.29 kPa (6.9 \u00b1 2.2 mmHg) in patients who<\/p>\n

did not have ROSC and 4.36 \u00b1 1.11 kPa (32.8 \u00b1 9.1 mmHg) in those who did (<\/p>\n

P <\/em>< 0.001). End-tidal carbon dioxide<\/p>\n

values of 1.9 kPa (14.3 mmHg) or less discriminated between the 402 patients with ROSC and 335 patients without.<\/p>\n

When a 20-minute end-tidal carbon dioxide value of 1.9 kPa (14.3 mmHg) or less was used as a screening test to<\/p>\n

predict ROSC, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100%.<\/p>\n

Conclusions:<\/p>\n

End-tidal carbon dioxide levels of more than 1.9 kPa (14.3 mmHg) after 20 minutes may be used to<\/p>\n

predict ROSC with accuracy. End-tidal carbon dioxide levels should be monitored during CPR and considered a useful<\/p>\n

prognostic value for determining the outcome of resuscitative efforts and when to cease CPR in the field.<\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

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\u0097about .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.<\/p>\n

Can titrate recruitement by the Pa-etCO2 gradient<\/p>\n

 <\/p>\n

study of ETCO2 for procedural sedation shows that it precedes desat (Acad Emerg Med 2006;13:500)<\/p>\n

 <\/p>\n

article on CO2 relation between end tidal and PaCO2 Inbox Can J Anaesth 1996;43(8):862<\/p>\n

 <\/p>\n

capnography for procedural sedation (Ann Emerg Med 2007;50:172)<\/strong><\/p>\n

Capnographic airway assessment for procedural sedation and analgesia.<\/p>\n

DiagnosisWaveformFeatures\u00a0Intervention Normal<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

normal<\/p>\n

normal<\/p>\n

normal<\/p>\n

normal<\/p>\n

No intervention required<\/p>\n

Continue sedation<\/p>\n

Hyperventilation<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

normal<\/p>\n

\u2193<\/p>\n

decreased amplitude and width<\/p>\n

\u2191<\/p>\n

Bradypneic<\/strong><\/p>\n

Hypoventilation<\/strong><\/p>\n

(Type 1)<\/strong><\/p>\n

\"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

normal<\/p>\n

\u2191<\/p>\n

increased amplitude and width<\/p>\n

\u2193\u2193\u2193<\/p>\n

Reassess patient<\/p>\n

Continue sedation<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

\u2193<\/p>\n

\u2191<\/p>\n

increased amplitude and width<\/p>\n

\u2193\u2193\u2193<\/p>\n

Reassess patient<\/p>\n

Assess for airway obstruction<\/p>\n

Supplemental oxygen<\/p>\n

Cease drug administration or reduce dosing<\/p>\n

Hypopneic<\/strong><\/p>\n

Hypoventilation<\/strong><\/p>\n

(Type 2)<\/strong><\/p>\n

\"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

normal<\/p>\n

\u2193<\/p>\n

decreased amplitude<\/p>\n

\u2193<\/p>\n

Reassess patient<\/p>\n

Continue sedation<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

\u2193<\/p>\n

\u2193<\/p>\n

decreased amplitude<\/p>\n

\u2193<\/p>\n

Reassess patient<\/p>\n

Assess for airway obstruction<\/p>\n

Supplemental oxygen<\/p>\n

Cease drug administration or reduce dosing<\/p>\n

Hypopneic Hypoventilation with periodic breathing<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

Other<\/p>\n

normal or \u2193<\/p>\n

\u2193<\/p>\n

decreased amplitude<\/p>\n

\u2193<\/p>\n

apneic pauses<\/p>\n

Physiological variability<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

normal<\/p>\n

normal<\/p>\n

varying\"low<\/a><\/p>\n

normal<\/p>\n

No intervention required<\/p>\n

Continue sedation<\/p>\n

Bronchospasm<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

Other<\/p>\n

normal or \u2193<\/p>\n

normal, \u2191, or \u2193\u0086<\/a><\/p>\n

curved<\/p>\n

normal, \u2191, or \u2193\u0086<\/a><\/p>\n

wheezing<\/p>\n

Reassess patient<\/p>\n

Bronchodilator therapy<\/p>\n

Cease drug administration<\/p>\n

Partial airway obstruction<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

Other<\/p>\n

normal or \u2193<\/p>\n

normal<\/p>\n

normal<\/p>\n

variable<\/p>\n

noisy breathing<\/p>\n

and\/or inspiratory stridor<\/p>\n

Full airway patency restored with airway alignment<\/p>\n

Noisy breathing and stridor resolve<\/p>\n

Reassess patient<\/p>\n

Establish IV access<\/p>\n

Supplemental O2 (as needed)<\/p>\n

Cease drug administration<\/p>\n

Partial laryngospasm<\/strong><\/p>\n

Airway not fullypatent with airway alignment<\/p>\n

Noisy breathing and stridor persist<\/p>\n

Apnea<\/strong> \"Image\"<\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

Other<\/p>\n

normal or \u2193\u0087<\/a><\/p>\n

zero<\/p>\n

absent<\/p>\n

zero<\/p>\n

no chest wallmovement orbreath sounds<\/p>\n

Reassess patient<\/p>\n

Stimulation<\/p>\n

Bag mask ventilation<\/p>\n

Reversal agents (where appropriate)<\/p>\n

Cease drug administration<\/p>\n

Complete airway obstruction<\/strong><\/p>\n

SpO2<\/p>\n

ETCO2<\/p>\n

Waveform<\/p>\n

RR<\/p>\n

Other<\/p>\n

normal or \u2193\u0087<\/a><\/p>\n

zero<\/p>\n

absent<\/p>\n

zero<\/p>\n

chest wall<\/p>\n

movement and<\/p>\n

breath sounds<\/p>\n

present<\/p>\n

Airway patency restored with airway alignment<\/p>\n

Waveform present<\/p>\n

Complete laryngospasm<\/strong><\/p>\n

Airway not patent with airway alignment<\/p>\n

No waveform<\/p>\n

Positive pressure ventilation \"low\u00a0Varying waveform amplitude and width.\u0086\u00a0Depending on duration and severity of bronchospasm.\u0087\u00a0Depending on duration of episode.<\/p>\n

 <\/p>\n

Definition of Respiratory Depression<\/p>\n

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<\/a> By definition, hypoventilation is arterial hypercarbia (\u0093a state in which there is a reduced amount of air entering the pulmonary alveoli [decreased alveolar ventilation], resulting in increased carbon dioxide tension\u0094).38<\/a> One cannot diagnose hypoventilation, and hence respiratory depression, without some measure of alveolar or arterial CO2.<\/p>\n

Normal Ventilatory Patterns<\/p>\n

Normal, Hyperventilation, and Hypoventilation Patterns<\/p>\n

Changes in etco2 and expiratory time affect the shape of the capnogram.[2]<\/a>, [5]<\/a>, [14]<\/a> and [39]<\/a> 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<\/a>).[2]<\/a>, [4]<\/a>, [14]<\/a> and [39]<\/a><\/p>\n

Physiological Variability<\/p>\n

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<\/a>).[2]<\/a>, [15]<\/a> and [37]<\/a> 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<\/a><\/p>\n

Drug-Induced Ventilatory Patterns<\/p>\n

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.<\/p>\n

Periodic Breathing<\/p>\n

Periodic breathing is characterized by normal breathing punctuated with apneic pauses, occurring most commonly during deep sedation (Table 1<\/a>).[2]<\/a>, [15]<\/a>, [37]<\/a> and [39]<\/a> This pattern may be self-resolving or devolve into complete central apnea.[2]<\/a>, [15]<\/a>, [37]<\/a> and [40]<\/a><\/p>\n

Apnea<\/p>\n

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<\/a>).[2]<\/a>, [4]<\/a> and [40]<\/a><\/p>\n

Capnography may be more sensitive than clinical assessment of ventilation in detection of apnea.[12]<\/a>, [29]<\/a>, [34]<\/a>, [35]<\/a> and [36]<\/a> In a recent study, 10 of 39 (26%) patients experienced 20-second periods of apnea during procedural sedation and analgesia.29<\/a> All 10 episodes of apnea were detected by capnography but not by the anesthesia providers.<\/p>\n

Upper Airway Obstruction<\/p>\n

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]<\/a> and [14]<\/a> 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<\/a>).40<\/a><\/p>\n

Capnography also provides a nonimpedance respiratory rate directly from the airway (by oral-nasal cannula),4<\/a> 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.<\/p>\n

Laryngospasm<\/p>\n

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<\/a>). 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]<\/a> and [41]<\/a><\/p>\n

Bronchospasm<\/p>\n

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<\/a>).23<\/a><\/p>\n

Respiratory Failure<\/p>\n

An etco2 greater than 70 mm Hg in patients without chronic hypoventilation indicates respiratory failure.[36]<\/a>, [39]<\/a> and [42]<\/a><\/p>\n

Drug-Induced Hypoventilation<\/p>\n

There are 2 types of hypoventilation that occur during procedural sedation and analgesia (Table 1<\/a>, Table 2<\/a> and Table 3<\/a>). 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<\/a>, Table 2<\/a> and Table 3<\/a>, Figure 2<\/a>).[2]<\/a>, [14]<\/a>, [37]<\/a>, [40]<\/a> and [42]<\/a> 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<\/a>, Table 2<\/a> and Table 3<\/a>; Figure 2<\/a>).[2]<\/a>, [14]<\/a> and [15]<\/a><\/p>\n

Table 2.<\/p>\n

Characteristics of bradypneic (type 1) and hypopneic (type 2) hypoventilation.<\/p>\n

Hypoventilation TypeRespiratory RateVTAirway Dead SpaceVD\/VTetco2PaCO2 Bradypneic (type 1)\u2193\u2193\u2193\u2193Constant\/no changeMinimal change\u2191\u2191 Hypopneic (type 2)\u2193\u2193\u2193\u2193Constant\/no change\u2191\u2191\u2191\u2193, Or no change\u2191<\/p>\n

VD<\/em>, Dead space volume; VT<\/em>, tidal volume.<\/p><\/blockquote>\n

Table 3.<\/p>\n

Drug-induced hypoventilation patterns.<\/p>\n

TypePhysiologySubtypeFeatures NormalNo appreciable change in respiratory pattern<\/p>\n

No change in respiratory rate or VT<\/p>\n

Normal etco2 and normal SpO2<\/p>\n

Mild respiratory depressionMinimal change in respiratory pattern<\/p>\n

Minimal decrease in respiratory rate and minimal decrease in VT<\/p>\n

Normal etco2<\/p>\n

Normal SpO2<\/p>\n

Bradypneic hypoventilation (type 1)<\/p>\n

Hypoventilation with minimal tidal volume change<\/p>\n

Drugs that affect RR \"much VT<\/p>\n

a<\/p>\n

Decreased minute ventilation<\/p>\n

High etco2<\/p>\n

Normal SpO2<\/p>\n

b<\/p>\n

Decreased minute ventilation<\/p>\n

High etco2<\/p>\n

Decreased SpO2<\/p>\n

Hypopneic hypoventilation (type 2)<\/p>\n

Hypoventilation with low tidal volume breathing<\/p>\n

Drugs that affect VT\"much RR<\/p>\n

a<\/p>\n

Decreased minute ventilation<\/p>\n

Low etco2 and normal SpO2<\/p>\n

b<\/p>\n

Decreased minute ventilation<\/p>\n

Low etco2 and decreased SpO2<\/p>\n

Can devolve to:<\/p>\n

Intermittent apneic pauses interspersed with normal ventilation (periodic breathing)<\/p>\n

Central apnea<\/p>\n

RR<\/em>, Respiratory rate; VT<\/em>, tidal volume.<\/p><\/blockquote>\n

\"\"<\/a><\/p>\n

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.<\/p>\n

 <\/p>\n

Reasons for gradient between PaCO2 and ETCO2<\/p>\n

dead space increases the gradient<\/p>\n

shunt will send CO2 to arterial side that will never reach alveoli<\/p>\n

 <\/p>\n

\"\"<\/a><\/p>\n

ig\u00a03 This diagram demonstrates how opiates can induce apnoea at the same P<\/em>aCO2 as before opioid administration (dotted line) and also demonstrates that significant reductions in the HCVR only cause small changes in steady-state P<\/em>aCO2. Curve A represents the normal ventilatory response to CO2 in an awake individual, demonstrating that ventilation is maintained at very low P<\/em>aCO2 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 P<\/em>aCO2 must rise to steady-state values (i.e. along the x<\/em>-axis) for breathing to recommence (line B\u0092). Curve C represents the CO2 excretion hyperbola and demonstrates how changes in ventilation affect P<\/em>aCO2. 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<\/p>\n

 <\/p>\n

\"\"<\/a>()<\/p>\n

 <\/p>\n

 <\/p>\n

In sick patients with head injury, little concordance between ETCO2 and PaCO2 (J Trauma 2009;67(3):526) and Can J Anesth (2001;48:396)<\/p>\n

 <\/p>\n

deadspace using ETCO2=Vd\/Vt=0.32 + 0.0106 (PaCO2 – ETCO2) + 0.003 (RR) + 0.0015 (Age) Crit Care Med 2010 38:288<\/p>\n

 <\/p>\n

Newest study in the annals shows ETCO2 should definitely be used (Ann Emerg Med 2010;55:258)<\/p>\n

 <\/p>\n

Meta-analysis (J Clin Anesth 2011;23:189) resp depression 17.6 times more likely to be detected<\/p>\n

<\/span>Trauma Patients<\/span><\/h2>\n

no acceptable correlation in TBI patients (J Trauma 2009;Volume 66(1),\u00a0January 2009,\u00a0pp 26-31)<\/p>\n

 <\/p>\n

<\/span>Sublingual Capnometry<\/a><\/span><\/h3>\n

 <\/p>\n

 <\/p>\n

 <\/p>\n

|\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 \u00a0\u00a0 |\u00a0\u00a0 Podcast<\/p>\n","protected":false},"excerpt":{"rendered":"

Array<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"_genesis_hide_title":false,"_genesis_hide_breadcrumbs":false,"_genesis_hide_singular_image":false,"_genesis_hide_footer_widgets":false,"_genesis_custom_body_class":"","_genesis_custom_post_class":"","_genesis_layout":"","footnotes":""},"categories":[40],"tags":[],"yoast_head":"\nRespiratory Monitoring - Crashing Patient<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/crashingpatient.com\/resuscitation\/monitoring\/respiratory-monitoring.htm\/\" \/>\n<meta name=\"twitter:label1\" content=\"Written by\" \/>\n\t<meta name=\"twitter:data1\" content=\"CrashMaster\" \/>\n\t<meta name=\"twitter:label2\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data2\" content=\"30 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\/\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\/\/crashingpatient.com\/resuscitation\/monitoring\/respiratory-monitoring.htm\/\",\"url\":\"https:\/\/crashingpatient.com\/resuscitation\/monitoring\/respiratory-monitoring.htm\/\",\"name\":\"Respiratory Monitoring - 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