Estimation of myocardial ischemic injury during ventricular fibrillation with total circulatory arrest using high-energy phosphates and lactate as metabolic markers

https://doi.org/10.1016/S0196-0644(05)80927-8Get rights and content

Study objective:

To define the time course of myocardial ischemic injury using high-energy phosphate (HEP) depletion and the cessation of lactate production as metabolic markers.

Setting:

Data were collected in a laboratory animal model.

Type of participants:

Ten immature mixed breed swine weighing 23.2 ± 3.5 kg.

Design:

After thoracotomy transmural myocardial biopsies were taken in vivo during normal sinus rhythm and at designated times during ventricular fibrillation with total circulatory arrest (VF-TCA).

Measurements and main results:

Frozen tissue samples were analyzed for adenine nucleotides, by high-performance liquid chromatography, and lactate by enzymatic assay. At five minutes of VF-TCA, myocardial adenosine triphosphate averaged 50% of control. At 15 minutes of VF-TCA, 89% of animals had myocardial adenosine triphosphate levels above 20% of control and adenylate charge ratio above 0.60. With more than 30 minutes of VF-TCA, all animals had adenosine triphosphate levels below 10% of control and adenylate charge ratio below 0.30. In addition, myocardial lactate levels plateaued after 30-minutes of VF-TCA, indicating the cessation of lactate production.

Conclusion:

These results suggest that the myocardium can tolerate VF-TCA for as long as 15 minutes without irreversible injury; however, postischemic myocardial dysfunction may occur after as little as five minutes of VF-TCA. With more than 30 minutes of VF-TCA, myocardial injury is likely to be irreversible.

References (53)

  • HammerDF et al.

    Extraction and measurement of myocardial nucleotides, nucleosides, and purine bases by high-performance liquid chromatography

    Analy Biochem

    (1988)
  • LowryOH et al.

    Protein measurement with the folin phenol reagent

    J Biol Chem

    (1951)
  • TherouxP et al.

    Coronary arterial reperfusion: III. Early and late effects on regional myocardial function and dimensions in conscious dogs

    Am J Cardiol

    (1976)
  • HessML et al.

    Mechanical and biochemical effects of transient myocardial ischemia

    J Surg Res

    (1979)
  • PreussKC et al.

    Time course of recovery of “stunned myocardium” following variable periods of ischemia in conscious and anesthetized dogs

    Am Heart J

    (1987)
  • EllisSG et al.

    Response of reperfusion-salvaged, stunned myocardium to inotropic stimulation

    Am Heart J

    (1984)
  • BolliR et al.

    Beta-adrenergic stimulation reverses postischemic myocardial dysfunction without producing subsequent functional deterioration

    Am J Cardiol

    (1985)
  • BeckerLC et al.

    Reversal of dysfunctioning postischemic stunned myocardium by epinephrine and post extrasystolic potentiation

    J Am Coll Cardiol

    (1986)
  • ColesJG et al.

    Age-related differences in the response to myocardial ischemic stress

    J Thorac Cardiovasc Surg

    (1987)
  • HoekstraJ et al.

    The effectiveness of bystander CPR in an animal model

    Ann Emerg Med

    (1989)
  • RadovskyA et al.

    Morphology of myocardial necrosis after 15 and 17 minutes of ventricular fibrillation cardiac arrest and cardiopulmonary bypass in dogs

    Ann Emerg Med

    (1989)
  • EisenbergM et al.

    Paramedic programs and out-of-hospital cardiac arrest: I. Factors associated with successful resuscitation

    Am J Public Health

    (1979)
  • BrownCG et al.

    The effect of direct mechanical ventricular assistance on myocardial hemodynamics during ventricular fibrillation

    Crit Care Med

    (1989)
  • ReichH et al.

    Reversibility limits for heart and brain of ventricular fibrillation cardiac arrest in dogs

    Crit Care Med

    (1988)
  • JenningsRB et al.

    Relation between high energy phosphate and lethal injury in myocardial ischemia in the dog

    Am I Pathol

    (1978)
  • JenningsRB et al.

    Effect of reperfusion late in the phase of reversible ischemic injury: Changes in cell volume, electrolytes, metabolytes, and ultrastructure

    Circ Res

    (1985)
  • Cited by (48)

    • Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model

      2020, American Journal of Emergency Medicine
      Citation Excerpt :

      It can only use glycogen, indicating indirectly that effective CPR can provide limited perfusion to the heart. In the VF phase, the heart's energy will gradually decrease until the cardiomyocytes are completely dead if no CPR is applied, and the depletion of myocardial energy during VF could be reflected from ECG signals [30,31]. In the present study, the AMSA value during the untreated VF phase was decreased in a time dependent manner, and it increased as CPR was applied.

    • The association of chronic health status and survival following ventricular fibrillation cardiac arrest: Investigation of a primary myocardial mechanism

      2019, Resuscitation
      Citation Excerpt :

      Specifically, we used the AMSA quantitative waveform measure derived from the ECG captured just prior to the initial shock. Previous research suggests that waveform measures such as AMSA might serve as a surrogate for coronary perfusion pressure and myocardial energy during resuscitation.7,8 Indeed we observed a strong and independent relationship between increasing AMSA and a greater likelihood of survival.

    • Early Effects of Prolonged Cardiac Arrest and Ischemic Postconditioning during Cardiopulmonary Resuscitation on Cardiac and Brain Mitochondrial Function in Pigs

      2017, Resuscitation
      Citation Excerpt :

      The increase in cardiac mitochondrial RCI with IPC-CPR occurred in tandem with an increase in the rate of ATP synthesis. Maintenance of cardiac bioenergetics enhances the probability of successful resuscitation [16–18]. Tighter coupling of oxidative phosphorylation with IPC-CPR may be critically important for efficient oxygen utilization during the hypoxic conditions of CA and hypoperfusion with CPR, and may thus minimize myocardial damage and preserve LVEF as previously observed [5,6].

    • The ventricular fibrillation waveform approach to direct postshock chest compressions in a swine model of VF arrest

      2015, Journal of Emergency Medicine
      Citation Excerpt :

      AMSA has also been demonstrated to reflect higher energy phosphate (adenosine triphosphate) reserves, and therefore may reflect a myocardium that is more likely to defibrillate successfully to a perfusing rhythm (27). Additionally, VF is a high-energy consumption state, and strategies that can shorten the duration of VF may improve outcome (27–29). This association between AMSA and myocardial milieu and achievement of ROSC motivated our hypothesis that postshock chest compression duration, based upon the real-time measurement of AMSA, would achieve ROSC sooner.

    View all citing articles on Scopus

    Presented at the Society for Academic Emergency Medicine Annual Meeting in San Diego, May 1989.

    Supported in part by grants from the Stanley J Sarnoff Foundation for Cardiovascular Science and the Eli Lilly Corporation/Emergency Medicine Foundation.

    View full text