End tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism

D. Mark Courtney, John A. Watts, Jeffrey A. Kline

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO2 (etCO2) and tested two hypotheses: (1) that etCO2 can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO2 during resuscitation to a greater extent than arrhythmic cardiac arrest. Methods: Anesthetized, mechanically ventilated rats (N=10 per group), were subjected to either graded PE (latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. Results: At a MAP of 40 mmHg, etCO2 was significantly decreased in the PE group (18.3±1.9 torr) compared with both the hemorrhage (24.3±1.3) and the control group (35.0±1.3 torr; ANOVA P<0.001). The decreased etCO2 occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO2 was significantly decreased in the PE group (6.5±0.9) versus both hemorrhage (16.5±1.1) and TTX (34.2±2.4 torr). Conclusions: Massive PE with shock decreases the etCO2 and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO2 readings during CPR.

Original languageEnglish (US)
Pages (from-to)83-91
Number of pages9
JournalResuscitation
Volume53
Issue number1
DOIs
StatePublished - Apr 25 2002
Externally publishedYes

Fingerprint

Heart Arrest
Pulmonary Embolism
Hypotension
Arterial Pressure
Hemorrhagic Shock
Tetrodotoxin
Hemorrhage
Microspheres
Induced Heart Arrest
Control Groups
Latex
Cardiopulmonary Resuscitation
Punctures
Resuscitation
Intravenous Injections
Ventilation
Anesthetics
Reading
Shock
Analysis of Variance

Keywords

  • Animal model
  • Capnometry
  • Cardiopulmonary resuscitation
  • End tidal carbon dioxide
  • Heart arrest
  • Pulmonary embolism
  • Shock
  • Thromboembolism

ASJC Scopus subject areas

  • Emergency Medicine
  • Emergency
  • Cardiology and Cardiovascular Medicine

Cite this

End tidal CO2 is reduced during hypotension and cardiac arrest in a rat model of massive pulmonary embolism. / Courtney, D. Mark; Watts, John A.; Kline, Jeffrey A.

In: Resuscitation, Vol. 53, No. 1, 25.04.2002, p. 83-91.

Research output: Contribution to journalArticle

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N2 - Background: We investigated the effect of massive pulmonary embolism (MPE) on end tidal CO2 (etCO2) and tested two hypotheses: (1) that etCO2 can distinguish massive PE from hemorrhagic shock and (2) that PE with cardiac arrest reduces etCO2 during resuscitation to a greater extent than arrhythmic cardiac arrest. Methods: Anesthetized, mechanically ventilated rats (N=10 per group), were subjected to either graded PE (latex microspheres), or graded hemorrhagic shock to produce a final mean arterial blood pressure, (MAP) of 40 mmHg; a third group was subjected to surgical/anesthetic control conditions. Cardiac arrest was induced by the following methods: intravenous injection of a large bolus of microspheres in the PE group, aortic puncture in the hemorrhage group, and intravenous tetrodotoxin (TTX) to produce arrhythmic cardiac arrest in the control group. Results: At a MAP of 40 mmHg, etCO2 was significantly decreased in the PE group (18.3±1.9 torr) compared with both the hemorrhage (24.3±1.3) and the control group (35.0±1.3 torr; ANOVA P<0.001). The decreased etCO2 occurred coincident with an increase in alveolar dead space fraction in the PE group. In the first minute of ventilation after cardiac arrest, the etCO2 was significantly decreased in the PE group (6.5±0.9) versus both hemorrhage (16.5±1.1) and TTX (34.2±2.4 torr). Conclusions: Massive PE with shock decreases the etCO2 and increases the dead space fraction to a greater extent than hemorrhagic shock at the same MAP. Cardiac arrest from PE is associated with extremely low etCO2 readings during CPR.

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KW - Capnometry

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KW - Heart arrest

KW - Pulmonary embolism

KW - Shock

KW - Thromboembolism

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