title: Myocardial microcirculatory dysfunction after prolonged ventricular fibrillation and resuscitation.
abstract: OBJECTIVE
  The etiology of postresuscitation myocardial stunning is unknown but is thought to be related to either ischemia occurring during cardiac arrest and resuscitation efforts and/or reperfusion injury after restoration of circulation. A potential common pathway for postischemia/reperfusion end-organ dysfunction is microvascular injury. We hypothesized that myocardial microcirculatory function is markedly abnormal in the postresuscitation period.
  
  
  METHODS
  In vivo study of myocardial microvascular function.
  
  
  METHODS
  University animal laboratory.
  
  
  METHODS
  Five swine (25 +/- 2 kg).
  
  
  METHODS
  Measurements before and after cardiac arrest and resuscitation.
  
  
  RESULTS
  Baseline data were not different among the five subjects. Left ventricular ejection fraction was significantly lower at all postresuscitation time periods (p < .05), reaching a nadir of 19% at 1 hr postresuscitation. Cardiac output declined following fibrillation and resuscitation and was significantly lower than baseline at 1 and 4 hrs postresuscitation (p < .05). Prearrest coronary flow reserve, a ratio of normal to maximal intracoronary flow velocity, was 3.4 ("normal" ratio is 2:4), but was below normal (<2) throughout the 4-hr post resuscitation period (p < .05).
  
  
  CONCLUSIONS
  This in vivo study showed that normal myocardial microcirculatory function is quickly lost after prolonged ventricular fibrillation and resuscitation. As early as 30 min postresuscitation the myocardial microcirculatory function is less than 50% of its prearrest baseline level. This dysfunction persists for at least 4 hrs. During the postresuscitation period, both left ventricular ejection fraction and cardiac output decline from their prearrest levels. No cause and effect relationship was proven, but a parallel decline in left ventricular function and coronary flow reserve is evident.
authors.affiliation: Department of Medicine, University of Arizona Sarver Heart Center, University of Arizona, Tucson, AZ, USA. kernk@email.arizona.edu
authors.forename: Karl B
authors.initials: KB
authors.lastname: Kern
authors.forename: Mathias
authors.initials: M
authors.lastname: Zuercher
authors.forename: David
authors.initials: D
authors.lastname: Cragun
authors.forename: Suntharo
authors.initials: S
authors.lastname: Ly
authors.forename: Joseph
authors.initials: J
authors.lastname: Quash
authors.forename: Sanjay
authors.initials: S
authors.lastname: Bhartia
authors.forename: Ronald W
authors.initials: RW
authors.lastname: Hilwig
authors.forename: Robert A
authors.initials: RA
authors.lastname: Berg
authors.forename: Gordon A
authors.initials: GA
authors.lastname: Ewy
mesh_terms: D000818:Animals; D002302:Cardiac Output; D016887:Cardiopulmonary Resuscitation; D003331:Coronary Vessels / Q000503:physiopathology*; D004837:Epinephrine / Q000008:administration & dosage; D006323:Heart Arrest / Q000150:complications; D008833:Microcirculation / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000503:physiopathology*; D012121:Respiration, Artificial; D013318:Stroke Volume; D013552:Swine; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology*
chemical_list: D014662:Vasoconstrictor Agents; D004837:Epinephrine