Improved myocardial oxygen utilization following propranolol infusion in adolescents with postburn hypermetabolism

Paul K. Minifee, Robert E. Barrow, Sally Abston, Manubhai Desai, David Herndon

Research output: Contribution to journalArticle

53 Citations (Scopus)

Abstract

The purpose of this study was to determine if propranolol (0.5 mg/kg and 1 mg/kg), administered intravenously (IV) at the height of the postburn hypermetabolic response, would decrease myocardial oxygen requirements, without adversely affecting overall oxygen delivery or total body oxygen consumption. To test this hypothesis, six nonseptic patients age 17±3 years with burns over 82%±11% total body surface area were given propranolol with continuous hemodynamic monitoring. Propranolol was administered to these patients 20±15 days postburn. Two clinically derived indices of myocardial oxygen consumption, pressure-work index (PWI) and rate-pressure product (RPP), were used to estimate the energy expenditure of the working heart. Both PWI and RPP were significantly decreased from baseline after 0.5 mg/kg propranolol, 31% for PWI (P<.001) and 30% for RPP (P<.01). Similarly, a decrease from baseline was seen after 1.0 mg/kg propranolol, 32% for PWI (P<.001) and 35% for RPP (P<.01). Cardiac index (L/min/m2) demonstrated no significant change [7.4±1.1 (prepropranol), 6.5±1.3 (after 0.5 mg/kg propranolol), and 6.8±1.0 (after 1.0 mg/kg propranolol)] and exceeded the upper limits of normal (hyperdynamic state) throughout the study. Oxygen delivery index (962±209 mL/min/m2) and oxygen consumption indices [(254±78 mL/min/m2 by Fick method and 236±78 mL/min/m2 by inspired and expired gases)] were elevated at baseline and unaffected by propranolol. The decrease in PWI and RPP was achieved mainly by propranolol's effect to lower both heart rate and BP. Prepropranolol values for heart rate were 157±17 beats/min, and this was decreased by 23% (P<.01) and by 26% (P<.01) after the 0.5-mg/kg and 1-mg/kg doses of propranolol, respectively. The mean arterial pressure (MAP), 93±6 mm Hg, was decreased 5.3% to 88±9 mm Hg after 0.5 mg/kg propranolol, and after 1.0 mg/kg propranolol, the MAP was decreased 16.1% to 78±5 mm Hg (P<.05). In these severely burned patients, propranolol decreased heart rate and myocardial oxygen requirements without adversely affecting overall oxygen delivery or total body oxygen consumption.

Original languageEnglish (US)
Pages (from-to)806-811
Number of pages6
JournalJournal of Pediatric Surgery
Volume24
Issue number8
DOIs
StatePublished - 1989
Externally publishedYes

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Propranolol
Oxygen
Pressure
Oxygen Consumption
Heart Rate
Arterial Pressure
Gases
Body Surface Area
Burns
Energy Metabolism
Hemodynamics

Keywords

  • Burns
  • propranolol infusion

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Surgery

Cite this

Improved myocardial oxygen utilization following propranolol infusion in adolescents with postburn hypermetabolism. / Minifee, Paul K.; Barrow, Robert E.; Abston, Sally; Desai, Manubhai; Herndon, David.

In: Journal of Pediatric Surgery, Vol. 24, No. 8, 1989, p. 806-811.

Research output: Contribution to journalArticle

Minifee, Paul K. ; Barrow, Robert E. ; Abston, Sally ; Desai, Manubhai ; Herndon, David. / Improved myocardial oxygen utilization following propranolol infusion in adolescents with postburn hypermetabolism. In: Journal of Pediatric Surgery. 1989 ; Vol. 24, No. 8. pp. 806-811.
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abstract = "The purpose of this study was to determine if propranolol (0.5 mg/kg and 1 mg/kg), administered intravenously (IV) at the height of the postburn hypermetabolic response, would decrease myocardial oxygen requirements, without adversely affecting overall oxygen delivery or total body oxygen consumption. To test this hypothesis, six nonseptic patients age 17±3 years with burns over 82{\%}±11{\%} total body surface area were given propranolol with continuous hemodynamic monitoring. Propranolol was administered to these patients 20±15 days postburn. Two clinically derived indices of myocardial oxygen consumption, pressure-work index (PWI) and rate-pressure product (RPP), were used to estimate the energy expenditure of the working heart. Both PWI and RPP were significantly decreased from baseline after 0.5 mg/kg propranolol, 31{\%} for PWI (P<.001) and 30{\%} for RPP (P<.01). Similarly, a decrease from baseline was seen after 1.0 mg/kg propranolol, 32{\%} for PWI (P<.001) and 35{\%} for RPP (P<.01). Cardiac index (L/min/m2) demonstrated no significant change [7.4±1.1 (prepropranol), 6.5±1.3 (after 0.5 mg/kg propranolol), and 6.8±1.0 (after 1.0 mg/kg propranolol)] and exceeded the upper limits of normal (hyperdynamic state) throughout the study. Oxygen delivery index (962±209 mL/min/m2) and oxygen consumption indices [(254±78 mL/min/m2 by Fick method and 236±78 mL/min/m2 by inspired and expired gases)] were elevated at baseline and unaffected by propranolol. The decrease in PWI and RPP was achieved mainly by propranolol's effect to lower both heart rate and BP. Prepropranolol values for heart rate were 157±17 beats/min, and this was decreased by 23{\%} (P<.01) and by 26{\%} (P<.01) after the 0.5-mg/kg and 1-mg/kg doses of propranolol, respectively. The mean arterial pressure (MAP), 93±6 mm Hg, was decreased 5.3{\%} to 88±9 mm Hg after 0.5 mg/kg propranolol, and after 1.0 mg/kg propranolol, the MAP was decreased 16.1{\%} to 78±5 mm Hg (P<.05). In these severely burned patients, propranolol decreased heart rate and myocardial oxygen requirements without adversely affecting overall oxygen delivery or total body oxygen consumption.",
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N2 - The purpose of this study was to determine if propranolol (0.5 mg/kg and 1 mg/kg), administered intravenously (IV) at the height of the postburn hypermetabolic response, would decrease myocardial oxygen requirements, without adversely affecting overall oxygen delivery or total body oxygen consumption. To test this hypothesis, six nonseptic patients age 17±3 years with burns over 82%±11% total body surface area were given propranolol with continuous hemodynamic monitoring. Propranolol was administered to these patients 20±15 days postburn. Two clinically derived indices of myocardial oxygen consumption, pressure-work index (PWI) and rate-pressure product (RPP), were used to estimate the energy expenditure of the working heart. Both PWI and RPP were significantly decreased from baseline after 0.5 mg/kg propranolol, 31% for PWI (P<.001) and 30% for RPP (P<.01). Similarly, a decrease from baseline was seen after 1.0 mg/kg propranolol, 32% for PWI (P<.001) and 35% for RPP (P<.01). Cardiac index (L/min/m2) demonstrated no significant change [7.4±1.1 (prepropranol), 6.5±1.3 (after 0.5 mg/kg propranolol), and 6.8±1.0 (after 1.0 mg/kg propranolol)] and exceeded the upper limits of normal (hyperdynamic state) throughout the study. Oxygen delivery index (962±209 mL/min/m2) and oxygen consumption indices [(254±78 mL/min/m2 by Fick method and 236±78 mL/min/m2 by inspired and expired gases)] were elevated at baseline and unaffected by propranolol. The decrease in PWI and RPP was achieved mainly by propranolol's effect to lower both heart rate and BP. Prepropranolol values for heart rate were 157±17 beats/min, and this was decreased by 23% (P<.01) and by 26% (P<.01) after the 0.5-mg/kg and 1-mg/kg doses of propranolol, respectively. The mean arterial pressure (MAP), 93±6 mm Hg, was decreased 5.3% to 88±9 mm Hg after 0.5 mg/kg propranolol, and after 1.0 mg/kg propranolol, the MAP was decreased 16.1% to 78±5 mm Hg (P<.05). In these severely burned patients, propranolol decreased heart rate and myocardial oxygen requirements without adversely affecting overall oxygen delivery or total body oxygen consumption.

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