Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR: a comparison with mechanical ventilation

Ahamed H. Idris, Michael J. Banner, Volker Wenzel, Ronnie S. Fuerst, Lance B. Becker, Richard J. Melker

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

Objective: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. Design: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. Interventions: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. Results: During the first minute of chest compression, mean (± S.D.) minute ventilation was 11.2 ± 5.91 l/min in the mechanically ventilated group and 4.5 ± 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 ± 1.4 1/min and 1.7 ± 1.6 1/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 ± 0.13 compared with 7.30 ± 0.07 units) and Pco2 was higher (62 ± 19 compared with 35 ± 9 mmHg). Mixed venous Pco2 was also higher (76 ± 15 compared with 61 ± 8 mmHg). Conclusion: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

Original languageEnglish (US)
Pages (from-to)143-150
Number of pages8
JournalResuscitation
Volume28
Issue number2
DOIs
StatePublished - 1994

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Cardiopulmonary Resuscitation
Artificial Respiration
Ventilation
Thorax
Gases
Tidal Volume
Ventricular Fibrillation
Pulmonary Gas Exchange
Acidosis
Heart Arrest
Swine
Perfusion
Pressure

Keywords

  • Acid-base equilibrium
  • Cardiopulmonary resuscitation
  • Hypercarbia
  • Hypoxia
  • Ventilation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Nursing(all)

Cite this

Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR : a comparison with mechanical ventilation. / Idris, Ahamed H.; Banner, Michael J.; Wenzel, Volker; Fuerst, Ronnie S.; Becker, Lance B.; Melker, Richard J.

In: Resuscitation, Vol. 28, No. 2, 1994, p. 143-150.

Research output: Contribution to journalArticle

Idris, Ahamed H. ; Banner, Michael J. ; Wenzel, Volker ; Fuerst, Ronnie S. ; Becker, Lance B. ; Melker, Richard J. / Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR : a comparison with mechanical ventilation. In: Resuscitation. 1994 ; Vol. 28, No. 2. pp. 143-150.
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abstract = "Objective: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. Design: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. Interventions: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. Results: During the first minute of chest compression, mean (± S.D.) minute ventilation was 11.2 ± 5.91 l/min in the mechanically ventilated group and 4.5 ± 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 ± 1.4 1/min and 1.7 ± 1.6 1/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 ± 0.13 compared with 7.30 ± 0.07 units) and Pco2 was higher (62 ± 19 compared with 35 ± 9 mmHg). Mixed venous Pco2 was also higher (76 ± 15 compared with 61 ± 8 mmHg). Conclusion: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.",
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AU - Idris, Ahamed H.

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AU - Fuerst, Ronnie S.

AU - Becker, Lance B.

AU - Melker, Richard J.

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N2 - Objective: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. Design: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. Interventions: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. Results: During the first minute of chest compression, mean (± S.D.) minute ventilation was 11.2 ± 5.91 l/min in the mechanically ventilated group and 4.5 ± 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 ± 1.4 1/min and 1.7 ± 1.6 1/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 ± 0.13 compared with 7.30 ± 0.07 units) and Pco2 was higher (62 ± 19 compared with 35 ± 9 mmHg). Mixed venous Pco2 was also higher (76 ± 15 compared with 61 ± 8 mmHg). Conclusion: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

AB - Objective: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. Design: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. Interventions: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. Results: During the first minute of chest compression, mean (± S.D.) minute ventilation was 11.2 ± 5.91 l/min in the mechanically ventilated group and 4.5 ± 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 ± 1.4 1/min and 1.7 ± 1.6 1/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 ± 0.13 compared with 7.30 ± 0.07 units) and Pco2 was higher (62 ± 19 compared with 35 ± 9 mmHg). Mixed venous Pco2 was also higher (76 ± 15 compared with 61 ± 8 mmHg). Conclusion: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

KW - Acid-base equilibrium

KW - Cardiopulmonary resuscitation

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KW - Hypoxia

KW - Ventilation

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