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TACTICAL MEDICINE TACMED España

TACTICAL MEDICINE TACMED España
by EMS SOLUTIONS INTERNATIONAL

Facebook Dr. Ramon Reyes, MD

domingo, 27 de agosto de 2017

Capnography to Maximize Patient Care by .JEMS Journal of Emergency Medicine

Capnography EtCO2 Picture by American Heart Association


Capnography Provides Bigger Physiological Picture to Maximize Patient Care

 
Caring for patients in the prehospital setting lends itself to a finite number of resources, necessitating that the devices available on EMS units offer the most utility while occupying the smallest space.
Capnography, or in-line end-tidal carbon dioxide (EtCO2) monitoring, offers more physiological information than any other noninvasive device carried in the field. In different clinical scenarios, EtCOmeasurement can provide valuable information about total body cellular metabolism, the body’s basal metabolic rate, central venous return, pulmonary blood flow, cardiac output, minute ventilation and myriad pulmonary diseases.
EtCO2 is also used to successfully guide resuscitations and ensure that lifesaving maneuvers are done correctly. This article will review the use of EtCO2 monitoring and interpretation by EMS providers. It will also illustrate how, along with vital signs, EtCO2 monitoring can complete the physiologic profile of patients in the field.
THE BASICS OF CO2
CO2 is the byproduct of aerobic metabolism that diffuses from body tissues to the lungs via erythrocytes carried in venous blood, where it can then be released by exhalation, dependent on ventilation patterns.1

Figure 1: Normal capnography wave
Capnometry is a measurement of the partial pressure of EtCO2, which, under normal ventilation and perfusion states, approximates the alveolar partial pressure of CO2.2

Waveform capnography is a graphical representation of the concentration of CO2 exhaled, used as an indirect indicator of the actual concentration, or partial pressure, of CO2 in arterial blood.
Figure 1 illustrates a normal capnography waveform:3
  • A–B demonstrates the exhalation of the dead space;
  • B–C represents lower airway exhalation;
  • C–D represents alveolar exhalation, as measured from the lips or nares; and
  • D–E represents inhalation.3
CO2 rises rapidly from B to C in a normal ventilatory pattern, with the end of exhalation represented at point D. This point correlates with the EtCO2 reading. Normal EtCO2 values range from 35–45 mmHg. Values < 35 mmHg generally can be considered diagnostic of hyperventilation or hypocarbia. Values > 45 mmHg indicate hypoventilation or hypercarbia.

Figure 2: EtCO2 patterns
VENTILATION PATTERNS IN NON-INTUBATED PATIENTS
Hyperventilation is frequently observed in patients, often in response to a sudden stressor, mediated by a catecholamine release. Hyperventilation is also seen in asthmatics, patients with a pulmonary embolism, or drug ingestions, including stimulants like cocaine or amphetamines. It causes a decreased EtCO reading (< 40 mmHg). As the EtCO2 approaches 25 mmHg, patients may complain of numbness and tingling in the hands, and may become disoriented.
Hypoventilation causes an increase in the measured EtCO2. Common causes include depressed mental status due to head trauma, intoxication by sedatives, alcohol, narcotics or the postictal period.
Patients in bronchospasm, such as asthmatics or those with chronic obstructive pulmonary disease (COPD), may have a "shark fin" appearance on the EtCO2 waveform. With this pathology, patients have prolonged exhalation—hence the gradual sloping of the tracing. In chronically retaining COPD patients, elevated EtCO2 levels may be observed at baseline, sometimes over 60 mmHg. (See Figure 2.)
ENDOTRACHEAL INTUBATION & MECHANICAL VENTILATION
Waveform capnography is the gold standard for confirmation of prehospital intubation.
The most common use of prehospital capnography is to confirm endotracheal tube (ETT) placement. In an already critical patient, correct placement of the ETT is an essential step in management. In one study, 15% of intubations were unrecognized as being esophageal when auscultation was the only confirmation method.4
Color-changing capnometry devices are still in use in many systems and are applied immediately after placement of the ETT to confirm placement, along with auscultation. However, waveform capnography is 100% sensitive and specific in assuring correct ETT placement after the administration of seven breaths.5

Figure 3: EtCO2 waveform assessment
A study examining the ability of paramedics and paramedic students to recognize and address ETT dislodgment in simulation found the detection of dislodgement by providers using capnography was two minutes, compared to four minutes by providers without access to capnography.6
During patient transport, the ETT is at risk for dislodgement for a number of reasons including road conditions, lack of adequate tube securement or patient movement, making continuous waveform capnography an invaluable resource in ensuring the safety and ventilatory status monitoring of the patient.7
SHOCK, SEPSIS & LOW-FLOW STATES
Capnography is now considered a key diagnostic tool to detect shock and poor perfusion states. In shock, the relative hypoperfusion of oxygen causes cells and tissues to rely on anaerobic respiration, leading to an increase in lactate and metabolic acidosis. To compensate, the respiratory rate increases, causing more CO2 to be exhaled, or "blown off." Therefore, it’s expected that patients in shock would have abnormally low EtCO2 readings.
When examining the association between increased lactate levels, organ dysfunction and damage, and EtCO2 measurements, EtCO2readings are inversely correlated with lactate levels and organ failure criteria.8 (For more on the use of capnography to reliably detect septic shock, see "Utilizing Capnography in Sepsis: End-tidal CO2 may be used in place of lactate to screen for severe sepsis," by Christopher Hunter, MD, PhD, in the March 2014 issue.)
Another study examining EtCO2 levels and serum lactate in trauma patients showed a similar strong inverse correlation between low EtCO2 levels and elevated lactate levels that prompted acute surgical intervention.9 EtCO2 measurements < 25 mmHg in the setting of two or more systemic inflammatory response syndrome criteria correlated with lactate levels > 4 mmol/L and increased mortality.10 Another study of 103 patients presenting with hypotension found the mean EtCO2 value for all patients, regardless of etiology, was 29.07 mmHg.11
USE IN CARDIAC ARREST
Cardiac arrest leads to a drastic fall in EtCO2 levels due to lack of cardiac output and perfusion providing a means for CO2 to reach the lungs for expiration. (See Figure 3.) Literature demonstrates that not only can a provider gauge the quality of CPR, as demonstrated by rising EtCO2 values, and determine return of spontaneous circulation (ROSC) by a significant increase in EtCO2 levels, but they can also predict cases where ROSC is unlikely to be achieved.12
EtCO2 differences in asphyxia-related cardiac arrests versus cardiac-related cardiac arrests (v fib or pulseless v tach) showed a difference in value of EtCO2 between the groups both initially and after one minute.
Arrests due to asphyxia, whether due to foreign body obstruction, aspiration, hanging, drowning, acute asthma attack or airway tumor, initially had higher EtCO2 than patients who suffered an arrest due to cardiac causes, therefore not producing an initial prognostic value for ROSC. However, EtCO2 readings after one minute were more prognostic of outcome.13
During CPR, EtCO2 tracings have been shown to decrease with rescuer fatigue and increase when a new rescuer begins compressions, demonstrating the necessity for providers to watch the capnography and evaluate quality of CPR in real time. Although an initial EtCO2 reading of < 10 mmHg is poor prognostically, some patients have developed ROSC.14 However, no patient survived with an EtCO2 of < 10 mmHg after 20 minutes of CPR, making this a valuable practice guideline.15 Regaining ROSC was associated with an average 13.5 mmHG increase in EtCO2 readings.16
PUTTING IT ALL TOGETHER
EtCO2 monitoring is an extremely valuable tool for EMS providers that’s rapidly becoming a standard piece of equipment on all EMS response vehicles. Patterns of activity or trends can lead to findings such as:
  • A drastic decrease in EtCO2 may demonstrate sudden hyperventilation, ETT occlusion or dislodgement, or a massive pulmonary embolism.
  • A gradual decrease in EtCO2 can be caused by hyperventilation or decreased CO2 production.
  • Patients who are tachypnic with a gradually rising EtCO2 tracing or a rising baseline, indicating CO2 rebreathing, may be tiring out and progressing to respiratory failure, requiring ventilatory support and/or intubation.
  • If the EtCO2 is gradually dropping during CPR, a rescuer may be tired and providing less adequate compressions, and therefore needs to change roles.
  • A sudden increase in EtCO2 is seen when ROSC is achieved or when sodium bicarbonate is administered.
  • A gradual increase in EtCO2 may be caused by hypoventilation, perhaps caused by sedatives or analgesics administered, or an increase in CO2 production.
  • In patients with acute pulmonary edema or congestive heart failure (CHF) receiving continuous positive airway pressure, EtCO2 can be an indicator of the success of treatment, as a previously tachypnic patient has an EtCO2 tracing slowly returning to normal.
  • A gradual increase in EtCO2 in a patient with a suspected intracranial hemorrhage may help the provider recognize a worsening clinical picture and the need for intubation.
CONCLUSION
Vital signs, clinical impression and EtCO2 monitoring can work together to give a more complete picture of the patient. Routine use of EtCO2 monitoring in the prehospital setting will allow providers to give better, more timely and more effective care.
REFERENCES
1. Kupnik D, Skok P. Capnometry in the prehospital setting: Are we using its potential? Emerg Med J. 2007;24(9):614–617.
2. Sanders AB. Capnometry in emergency medicine. Ann Emerg Med. 1989;18(12):1287–1290.
3. Farish SE, Garcia PS. Capnography primer for oral and maxillofacial surgery: Review and technical considerations. J Anesthe Clinic Res. 2013;4(3):295.
4. Anderson KH, Hald A. Assessing the position of tracheal tube. The reliability of different methods. Anaesthesia. 1989;44(12):984–985.
5. Grmec S, Mally S. Prehospital determination of tracheal tube placement in severe head injury. Emerg Med J. 2004;21(4):518–520.
6. Langhan ML, Ching K, Northrup V, et al. A randomized controlled trial of capnography in the correction of simulated endotracheal tube dislodgement. Acad Emerg Med. 2011;18(6):590–596.
7. Bhende MS, LaCovey DC. End-tidal carbon dioxide in the prehospital setting. Prehosp Emerg Care. 2001;5(2):208–213.
8. McGillicuddy D, Tang A, Cataldo L, et al. Evaluation of end-tidal carbon dioxide role in predicting elevated SOFA scores and lactic acidosis. Intern Emerg Med. 2009;4(1):41–44.
9. Caputo N, Fraser R, Paliga A, et al. Nasal cannula end-tidal CO2 correlates with serum lactate levels and odds of operative intervention in penetrating trauma patients; A prospective cohort study. J Trauma Acute Care Surg. 2012;73(5):1202–1207.
10. Hunter CL, Silvestri S, Dean M, et al. End-tidal carbon dioxide is associated with lactate levels and mortality in emergency department patients with suspected sepsis. Am J Emerg Med. 2013;31(1):64–71.
11. Kheng CP, Rahman NH. The use of end-tidal carbon dioxide monitoring in patients with hypotension in the emergency department. Int J Emerg Med. 2012;5(1):31.
12. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med. 1988;318(10):607–611.
13. Grmec S, Lah K, Tusek-Bunc K. Difference in end-tidal CO2 between asphyxia cardiac arrest and ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest in the prehospital setting. Crit Care. 2003;7(6):R139–R144.
14. Callaham M, Barton C. Prediction of outcome of cardiopulmonary resuscitation from end-tidal carbon dioxide concentration. Crit Care Med. 1990;18(4):358–362.
15. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med. 1997;337(5):301–306.
16. Grmec S, Krizmaric M, Mally S, et al. Utstein style analysis of out-of-hospital cardiac arrest—Bystander CPR and end expired carbon dioxide. Resuscitation. 2007;72(3):404–414.