title: Evolution of the stone heart after prolonged cardiac arrest.
abstract: OBJECTIVE
  We hypothesized that progressive impairment in diastolic function during cardiopulmonary resuscitation (CPR) precedes evolution of the "stone heart" after failure of CPR. We therefore measured sequential changes in left ventricular (LV) volumes and free-wall thickness of the heart during CPR in an experimental model.
  
  
  METHODS
  Prospective, observational animal study.
  
  
  METHODS
  Medical research laboratory in an university-affiliated research and educational institute.
  
  
  METHODS
  Domestic pigs.
  
  
  METHODS
  Ventricular fibrillation (VF) was induced in 40 anesthetized male domestic pigs weighing between 38 kg and 43 kg. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Failing to reverse VF in each instance, precordial compression at a rate of 80/min was begun coincident with mechanical ventilation. Coronary perfusion pressures (CPPs) were computed from the differences in time-coincident diastolic aortic and right atrial pressures. Left ventricular (LV) systolic and diastolic ventricular volumes and thickness of the LV free wall were estimated with transesophageal echocardiography. The stroke volumes (SVs) were computed from the differences in decompression diastolic and compression systolic volumes. Free-wall thickness was measured on the hearts at autopsy.
  
  
  RESULTS
  Significantly greater CPPs were generated with the 4 min of untreated cardiac arrest. Progressive reductions in LV diastolic and SV and increases in LV free-wall thickness were documented with increasing duration of untreated VF. A stone heart was confirmed at autopsy in each animal that failed resuscitative efforts. Correlations with indicator dilution method and physical measurements at autopsy corresponded closely with the echocardiographic measurements.
  
  
  CONCLUSIONS
  Progressive impairment in diastolic function terminates in a stone heart after prolonged intervals of cardiac arrest.
authors.affiliation: Institute of Critical Care Medicine, Palm Springs, CA, USA.
authors.forename: Kada
authors.initials: K
authors.lastname: Klouche
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Heitor P
authors.initials: HP
authors.lastname: Povoas
authors.forename: Takashi
authors.initials: T
authors.lastname: Kamohara
authors.forename: Joe
authors.initials: J
authors.lastname: Bisera
mesh_terms: D000818:Animals; D002306:Cardiac Volume / Q000502:physiology*; D016887:Cardiopulmonary Resuscitation; D003971:Diastole / Q000502:physiology*; D004452:Echocardiography; D006323:Heart Arrest / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D017682:Myocardial Stunning / Q000503:physiopathology*; D011180:Postmortem Changes; D013318:Stroke Volume / Q000502:physiology*; D013552:Swine; D013815:Thermodilution; D014693:Ventricular Fibrillation / Q000503:physiopathology; D016277:Ventricular Function, Left / Q000502:physiology*