Effect of ventilation on resuscitation in an animal model of cardiac arrest

A. H. Idris, L. B. Becker, R. S. Fuerst, V. Wenzel, W. J. Rush, R. J. Melker, D. J. Orban

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

Background: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. Methods and Results: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of >80 mm Hg for >5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P<.05) lower mean arterial PO2 (38±17 mm Hg compared with 216±104 mm Hg) and higher PCO2 (62±16 mm Hg compared with 35±8 mm Hg), lower mixed venous PO2 (15±7 mm Hg compared with 32±7 mm Hg), and higher PCO2 (74±13 mm Hg compared with 60±7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P<.002). Conclusions: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

Original languageEnglish (US)
Pages (from-to)3063-3069
Number of pages7
JournalCirculation
Volume90
Issue number6
StatePublished - 1994

Fingerprint

Heart Arrest
Resuscitation
Ventilation
Animal Models
Thorax
Ventricular Fibrillation
Arterial Pressure
Perfusion
Gases
Out-of-Hospital Cardiac Arrest
Acidosis
Epinephrine
Swine
Public Health
Blood Pressure
Pressure

Keywords

  • carbon dioxide
  • cardiopulmonary resuscitation
  • hypoxia
  • respiratory acidosis
  • ventilation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Idris, A. H., Becker, L. B., Fuerst, R. S., Wenzel, V., Rush, W. J., Melker, R. J., & Orban, D. J. (1994). Effect of ventilation on resuscitation in an animal model of cardiac arrest. Circulation, 90(6), 3063-3069.

Effect of ventilation on resuscitation in an animal model of cardiac arrest. / Idris, A. H.; Becker, L. B.; Fuerst, R. S.; Wenzel, V.; Rush, W. J.; Melker, R. J.; Orban, D. J.

In: Circulation, Vol. 90, No. 6, 1994, p. 3063-3069.

Research output: Contribution to journalArticle

Idris, AH, Becker, LB, Fuerst, RS, Wenzel, V, Rush, WJ, Melker, RJ & Orban, DJ 1994, 'Effect of ventilation on resuscitation in an animal model of cardiac arrest', Circulation, vol. 90, no. 6, pp. 3063-3069.
Idris AH, Becker LB, Fuerst RS, Wenzel V, Rush WJ, Melker RJ et al. Effect of ventilation on resuscitation in an animal model of cardiac arrest. Circulation. 1994;90(6):3063-3069.
Idris, A. H. ; Becker, L. B. ; Fuerst, R. S. ; Wenzel, V. ; Rush, W. J. ; Melker, R. J. ; Orban, D. J. / Effect of ventilation on resuscitation in an animal model of cardiac arrest. In: Circulation. 1994 ; Vol. 90, No. 6. pp. 3063-3069.
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abstract = "Background: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. Methods and Results: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of >80 mm Hg for >5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P<.05) lower mean arterial PO2 (38±17 mm Hg compared with 216±104 mm Hg) and higher PCO2 (62±16 mm Hg compared with 35±8 mm Hg), lower mixed venous PO2 (15±7 mm Hg compared with 32±7 mm Hg), and higher PCO2 (74±13 mm Hg compared with 60±7 mm Hg). Nine of 12 (75{\%}) of the ventilated animals, and only 1 of 12 (8{\%}) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P<.002). Conclusions: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.",
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T1 - Effect of ventilation on resuscitation in an animal model of cardiac arrest

AU - Idris, A. H.

AU - Becker, L. B.

AU - Fuerst, R. S.

AU - Wenzel, V.

AU - Rush, W. J.

AU - Melker, R. J.

AU - Orban, D. J.

PY - 1994

Y1 - 1994

N2 - Background: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. Methods and Results: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of >80 mm Hg for >5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P<.05) lower mean arterial PO2 (38±17 mm Hg compared with 216±104 mm Hg) and higher PCO2 (62±16 mm Hg compared with 35±8 mm Hg), lower mixed venous PO2 (15±7 mm Hg compared with 32±7 mm Hg), and higher PCO2 (74±13 mm Hg compared with 60±7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P<.002). Conclusions: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

AB - Background: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. Methods and Results: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of >80 mm Hg for >5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P<.05) lower mean arterial PO2 (38±17 mm Hg compared with 216±104 mm Hg) and higher PCO2 (62±16 mm Hg compared with 35±8 mm Hg), lower mixed venous PO2 (15±7 mm Hg compared with 32±7 mm Hg), and higher PCO2 (74±13 mm Hg compared with 60±7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P<.002). Conclusions: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

KW - carbon dioxide

KW - cardiopulmonary resuscitation

KW - hypoxia

KW - respiratory acidosis

KW - ventilation

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