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Clinical Aspects Bhavani Shankar Kodali MD |
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(11)
Hypermetabolic states
Dangerous
hypermetabolic conditions such as malignant hyperthermia, thyrotoxic crisis, and
severe sepsis, can be detected by C02 monitoring. Increased metabolic rates
cause greater C02 production, which can cause PETCO2 to increase. An increasing
PETCO2 may, therefore, be an early warning sign of an impending hypermetabolic
crisis.1
(12)
Cardiopulmonary resuscitation
End-tidal
C02 monitoring during closed chest compression is one of the most exciting
recent developments in CPR. It holds the promise of making available information
about the effectiveness of resuscitative efforts, that, heretofore, have been
unavailable. It is non-invasive, easy to apply to the intubated patient and the
theory of its use during CPR is relatively simple. During closed chest
compression the blood flow to the lungs is low so that relatively few alveoli
are perfused. Since tidal volumes delivered with a resuscitation bag tend to be
large, many alveoli are ventilated that are not perfused and consequently, the
PETCO2 is low. If the blood flow to the lungs improves, more alveoli are
perfused and PETCO2 will increase. Under these circumstances the C02
presentation to the lungs is the major limiting determinant of PETCO2 and it has
been found that PETCO2 correlates well with measured cardiac output during
resuscitation.2-8 Therefore PETCO2 can be used to judge the effectiveness of
resuscitative attempts and thus lead to changes in technique that could improve
the outcome.9 Further, the PETCO2 may have a prognostic significance. It has been
observed that non-survivors had lower PETCO2 than survivors and no patient with
PETCO2 <10 mmHg could be successfully resuscitated.10,11
Cardiac arrest, successful resuscitation This is a trend capnogram showing progressive decreases in cardiac output culminating in cardiac arrest. Successful resuscitation resulted in increases in cardiac output thereby leading to progressive increases in end-tidal carbon dioxide.
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(13)
High frequency jet ventilation (HFJV)
Assessment
of the adequacy of HFJV is usually done by a series of arterial blood gas
measurements. Monitoring PETCO2 can be used successfully to determine
PaC02
levels during HFJV. This is done by delivering a single breath of large tidal
volume and measuring PETCO2 during brief interruption of HFJV. If
PaC02 can be
measured simultaneously by arterial puncture, then (a-ET)PCO2 can be determined
and subsequent monitoring of HFJV can be done by measuring PETCO2 in
periodically given single large breaths.12
(14) (a-ET)PC02 and PEEP
Positive
end expiratory pressure (PEEP) can be applied to improve oxygenation, when
hypoxemia is caused by acute alveolar oedema, or in early adult respiratory
distress syndrome (ARDS). Certain levels of PEEP (the inflection pressure on
pressure volume compliance curve) must be reached in any particular patient
before improvement in oxygenation is achieved. When oxygenation is at its best
(optimum PEEP) the (a-ET)PCO2 is least. As the level of PEEP is increased beyond
this the (a-ET)PC02 increases again and oxygenation worsens. Therefore it has
been suggested that (a-ET)PC02 can be used as a sensitive indicator in order to
titrate PEEP in patients with early ARDS or with alveolar oedema.13
Most of the capnographs measure and display
inspiratory and end-expiratory oxygen, nitrous oxide and anesthetic agent
concentrations or partial pressures in addition to CO2 measurements.
Furthermore, capnographs using RAMAN or Mass Spectrography measure and
display nitrogen concentration. These additional attributes bring the benefits of
monitoring oxygen, nitrous oxide, nitrogen (detection of air embolism) and
anesthetic agents concentration (vaporizer function, inadvertent administration
of anesthetic vapor, information of uptake and elimination of anesthetic agents,
monitoring low flow anesthesia and information on depth of anesthesia).
References:
1. Baudendistel L, Goudsouzian N, Cote C, Strafford M. End-tidal CO2 monitoring: its use in the diagnosis and management of malignant hyperpyrexia. Anaesthesia 1984;39:1000-3.
2. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med 1988;318:607-11.
3. Jin X, Weil MH, Tang W, Povoas H, Pernat A, Xie Jm Bisera J. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med 2000;28(7):2415-9.
4. Isseries SA, Breen PH. Can changes in end-tidal PCO2 measure changes in cardiac output? Anesth Analg 1991;73(6):808-14.
5. Idris AH, Staples ED, 'Brien DJ, Melker RJ, Rush WJ, Del Duca KD, Falk JL. End-tidal carbon dioxide during extremely low cardiac output. Ann Emerg Med 1994;23(3):568-72.
6. Lewis LM, Stothert J, Standevan J, Chandel B, Kurtz M, Fortney J. Correlation of end-tidal CO2 to cerebral perfusion during CPR. Ann Emerg Med 1992;21(9):1131-4.
7. Varno AJ, Morrina J, Civetta JM. Clinical utility of calorimetric end-tidal CO2 detector in cardiopulmonary resuscitation and emergency intubation. J Clin Monit 1991;7(4):289-93.
8.Steedman DJ, Robertson CE. Measurement of end-tidal carbon dioxide concentration during cardiopulmonary resuscitation. Arch Emerg Med 1990;7(3);129-34.
9. Orliaguet GA, Carli PA, Rozenberg A, Janniere D, Sauval P, Delpech P. End-tidal carbon dioxide during out-of-hospital cardiac arrest resuscitation: Comparison of active compression-decompression and standard CPR. Ann Emerg Med 1993;25(1):48-51.
10. Sanders AB, Karen KB, Otto CW, Milander MM, Ewy GA. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival JAMA 1989;262:1347-51.
11. 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):301-6.
12. Mason CJ. Single breath end-tidal PCO2 measurements during high frequency jet ventilation in critical care patients. Anaesthesia 1986;41:1251-4.
13. Blanch L, Fernandez R, Benito S Mancebo J, Net A. Effects of PEEP on the arterial minus end-tidal carbon dioxide gradient. Chest 1987;92:451-4.