Effects of graded doses of epinephrine on both noninvasive and invasive measures of myocardial perfusion and blood flow during cardiopulmonary resuscitation

P. B. Chase, Karl B Kern, Arthur B Sanders, Charles W Otto, G. A. Ewy

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58 Citations (Scopus)

Abstract

Objectives: Epinephrine administered during cardiopulmonary resuscitation (CPR) is known to increase aortic diastolic and myocardial perfusion pressures, while enhancing myocardial blood flow. Optimal dosing of epinephrine during CPR is less certain. Interest in high-dose epinephrine use under such circumstances is increasing. The effect of different doses of epinephrine on simultaneously measured perfusion pressures, myocardial blood flow, cardiac output, and end-tidal CO2 (PCO2) (used as an indirect measure of cardiac output during CPR) is unknown. Design: Prospective, sequential evaluation of no epinephrine, standard dose epinephrine, and high-dose epinephrine. Setting: An experimental resuscitation laboratory. Subjects: Twelve domestic swine. Interventions: Myocardial perfusion pressure, myocardial blood flow, cardiac output, and end-tidal PCO2 were studied after various doses of epinephrine were administered during prolonged CPR. After 3 mins of untreated ventricular fibrillation, each animal received 5 mins of CPR without epinephrine, 5 mins of CPR after standard dose epinephrine (0.02 mg/kg), and 5 mins of CPR after high-dose epinephrine (0.2 mg/kg). Cardiac output and regional myocardial blood flow values were measured with nonradioactive, colored microspheres. Measurements and Main Results: Myocardial perfusion pressure (aortic diastolic minus right atrial diastolic) was significantly (p < .05) increased over baseline with high-dose epinephrine (35 ± 8 vs. 14 ± 4 mm Hg), but not with standard dose epinephrine (20 ± 5 vs. 14 ± 4 mm Hg). Epinephrine's effect on myocardial blood flow was similar, increasing after the high dose (71 ± 21 vs. 20 ± 5 mL/min/100 g; p > .05), but not with the standard dose (23 ± 6 vs. 20 ± 5 mL/min/100 g). Cardiac output decreased significantly (p < .05) after high- dose epinephrine (7 ± 1 vs. 13 ± 1 mL/min/kg). Mean end-tidal PCO2 levels were lower after high-dose epinephrine (15 ± 2 vs. 20 ± 2 mm Hg; p < .05) but not after standard dose epinephrine (19 ± 2 vs. 20 ± 2 mm Hg). Conclusions: Standard dose epinephrine had minimal effect on myocardial perfusion pressure, myocardial blood flow, cardiac output, or end-tidal PCO2. High-dose epinephrine enhanced myocardial perfusion pressure and myocardial blood flow despite significantly decreasing cardiac output.

Original languageEnglish (US)
Pages (from-to)413-419
Number of pages7
JournalCritical Care Medicine
Volume21
Issue number3
StatePublished - 1993

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Cardiopulmonary Resuscitation
Epinephrine
Perfusion
Cardiac Output
Blood Pressure
Regional Blood Flow
Ventricular Fibrillation
Microspheres
Resuscitation

Keywords

  • cardiac arrest
  • cardiac output
  • cardiopulmonary resuscitation
  • catecholamines
  • circulation
  • critical illness
  • epinephrine
  • expired end-tidal carbon dioxide
  • heart
  • heart attack

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

@article{b7d9c15bbc9c41e9b9cdf1c676ab8b95,
title = "Effects of graded doses of epinephrine on both noninvasive and invasive measures of myocardial perfusion and blood flow during cardiopulmonary resuscitation",
abstract = "Objectives: Epinephrine administered during cardiopulmonary resuscitation (CPR) is known to increase aortic diastolic and myocardial perfusion pressures, while enhancing myocardial blood flow. Optimal dosing of epinephrine during CPR is less certain. Interest in high-dose epinephrine use under such circumstances is increasing. The effect of different doses of epinephrine on simultaneously measured perfusion pressures, myocardial blood flow, cardiac output, and end-tidal CO2 (PCO2) (used as an indirect measure of cardiac output during CPR) is unknown. Design: Prospective, sequential evaluation of no epinephrine, standard dose epinephrine, and high-dose epinephrine. Setting: An experimental resuscitation laboratory. Subjects: Twelve domestic swine. Interventions: Myocardial perfusion pressure, myocardial blood flow, cardiac output, and end-tidal PCO2 were studied after various doses of epinephrine were administered during prolonged CPR. After 3 mins of untreated ventricular fibrillation, each animal received 5 mins of CPR without epinephrine, 5 mins of CPR after standard dose epinephrine (0.02 mg/kg), and 5 mins of CPR after high-dose epinephrine (0.2 mg/kg). Cardiac output and regional myocardial blood flow values were measured with nonradioactive, colored microspheres. Measurements and Main Results: Myocardial perfusion pressure (aortic diastolic minus right atrial diastolic) was significantly (p < .05) increased over baseline with high-dose epinephrine (35 ± 8 vs. 14 ± 4 mm Hg), but not with standard dose epinephrine (20 ± 5 vs. 14 ± 4 mm Hg). Epinephrine's effect on myocardial blood flow was similar, increasing after the high dose (71 ± 21 vs. 20 ± 5 mL/min/100 g; p > .05), but not with the standard dose (23 ± 6 vs. 20 ± 5 mL/min/100 g). Cardiac output decreased significantly (p < .05) after high- dose epinephrine (7 ± 1 vs. 13 ± 1 mL/min/kg). Mean end-tidal PCO2 levels were lower after high-dose epinephrine (15 ± 2 vs. 20 ± 2 mm Hg; p < .05) but not after standard dose epinephrine (19 ± 2 vs. 20 ± 2 mm Hg). Conclusions: Standard dose epinephrine had minimal effect on myocardial perfusion pressure, myocardial blood flow, cardiac output, or end-tidal PCO2. High-dose epinephrine enhanced myocardial perfusion pressure and myocardial blood flow despite significantly decreasing cardiac output.",
keywords = "cardiac arrest, cardiac output, cardiopulmonary resuscitation, catecholamines, circulation, critical illness, epinephrine, expired end-tidal carbon dioxide, heart, heart attack",
author = "Chase, {P. B.} and Kern, {Karl B} and Sanders, {Arthur B} and Otto, {Charles W} and Ewy, {G. A.}",
year = "1993",
language = "English (US)",
volume = "21",
pages = "413--419",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams and Wilkins",
number = "3",

}

TY - JOUR

T1 - Effects of graded doses of epinephrine on both noninvasive and invasive measures of myocardial perfusion and blood flow during cardiopulmonary resuscitation

AU - Chase, P. B.

AU - Kern, Karl B

AU - Sanders, Arthur B

AU - Otto, Charles W

AU - Ewy, G. A.

PY - 1993

Y1 - 1993

N2 - Objectives: Epinephrine administered during cardiopulmonary resuscitation (CPR) is known to increase aortic diastolic and myocardial perfusion pressures, while enhancing myocardial blood flow. Optimal dosing of epinephrine during CPR is less certain. Interest in high-dose epinephrine use under such circumstances is increasing. The effect of different doses of epinephrine on simultaneously measured perfusion pressures, myocardial blood flow, cardiac output, and end-tidal CO2 (PCO2) (used as an indirect measure of cardiac output during CPR) is unknown. Design: Prospective, sequential evaluation of no epinephrine, standard dose epinephrine, and high-dose epinephrine. Setting: An experimental resuscitation laboratory. Subjects: Twelve domestic swine. Interventions: Myocardial perfusion pressure, myocardial blood flow, cardiac output, and end-tidal PCO2 were studied after various doses of epinephrine were administered during prolonged CPR. After 3 mins of untreated ventricular fibrillation, each animal received 5 mins of CPR without epinephrine, 5 mins of CPR after standard dose epinephrine (0.02 mg/kg), and 5 mins of CPR after high-dose epinephrine (0.2 mg/kg). Cardiac output and regional myocardial blood flow values were measured with nonradioactive, colored microspheres. Measurements and Main Results: Myocardial perfusion pressure (aortic diastolic minus right atrial diastolic) was significantly (p < .05) increased over baseline with high-dose epinephrine (35 ± 8 vs. 14 ± 4 mm Hg), but not with standard dose epinephrine (20 ± 5 vs. 14 ± 4 mm Hg). Epinephrine's effect on myocardial blood flow was similar, increasing after the high dose (71 ± 21 vs. 20 ± 5 mL/min/100 g; p > .05), but not with the standard dose (23 ± 6 vs. 20 ± 5 mL/min/100 g). Cardiac output decreased significantly (p < .05) after high- dose epinephrine (7 ± 1 vs. 13 ± 1 mL/min/kg). Mean end-tidal PCO2 levels were lower after high-dose epinephrine (15 ± 2 vs. 20 ± 2 mm Hg; p < .05) but not after standard dose epinephrine (19 ± 2 vs. 20 ± 2 mm Hg). Conclusions: Standard dose epinephrine had minimal effect on myocardial perfusion pressure, myocardial blood flow, cardiac output, or end-tidal PCO2. High-dose epinephrine enhanced myocardial perfusion pressure and myocardial blood flow despite significantly decreasing cardiac output.

AB - Objectives: Epinephrine administered during cardiopulmonary resuscitation (CPR) is known to increase aortic diastolic and myocardial perfusion pressures, while enhancing myocardial blood flow. Optimal dosing of epinephrine during CPR is less certain. Interest in high-dose epinephrine use under such circumstances is increasing. The effect of different doses of epinephrine on simultaneously measured perfusion pressures, myocardial blood flow, cardiac output, and end-tidal CO2 (PCO2) (used as an indirect measure of cardiac output during CPR) is unknown. Design: Prospective, sequential evaluation of no epinephrine, standard dose epinephrine, and high-dose epinephrine. Setting: An experimental resuscitation laboratory. Subjects: Twelve domestic swine. Interventions: Myocardial perfusion pressure, myocardial blood flow, cardiac output, and end-tidal PCO2 were studied after various doses of epinephrine were administered during prolonged CPR. After 3 mins of untreated ventricular fibrillation, each animal received 5 mins of CPR without epinephrine, 5 mins of CPR after standard dose epinephrine (0.02 mg/kg), and 5 mins of CPR after high-dose epinephrine (0.2 mg/kg). Cardiac output and regional myocardial blood flow values were measured with nonradioactive, colored microspheres. Measurements and Main Results: Myocardial perfusion pressure (aortic diastolic minus right atrial diastolic) was significantly (p < .05) increased over baseline with high-dose epinephrine (35 ± 8 vs. 14 ± 4 mm Hg), but not with standard dose epinephrine (20 ± 5 vs. 14 ± 4 mm Hg). Epinephrine's effect on myocardial blood flow was similar, increasing after the high dose (71 ± 21 vs. 20 ± 5 mL/min/100 g; p > .05), but not with the standard dose (23 ± 6 vs. 20 ± 5 mL/min/100 g). Cardiac output decreased significantly (p < .05) after high- dose epinephrine (7 ± 1 vs. 13 ± 1 mL/min/kg). Mean end-tidal PCO2 levels were lower after high-dose epinephrine (15 ± 2 vs. 20 ± 2 mm Hg; p < .05) but not after standard dose epinephrine (19 ± 2 vs. 20 ± 2 mm Hg). Conclusions: Standard dose epinephrine had minimal effect on myocardial perfusion pressure, myocardial blood flow, cardiac output, or end-tidal PCO2. High-dose epinephrine enhanced myocardial perfusion pressure and myocardial blood flow despite significantly decreasing cardiac output.

KW - cardiac arrest

KW - cardiac output

KW - cardiopulmonary resuscitation

KW - catecholamines

KW - circulation

KW - critical illness

KW - epinephrine

KW - expired end-tidal carbon dioxide

KW - heart

KW - heart attack

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M3 - Article

VL - 21

SP - 413

EP - 419

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

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