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Contribution of asynergic contraction to halothane-induced myocardial depression
Insights
Myocardial asynergy, or dyscoordinate contraction, minimally impacts halothane-induced cardiac dysfunction. Measurements of cardiac performance like dP/dtmax remain valid during halothane anesthesia when accounting for loading conditions.
Area of Science:
- Cardiology
- Anesthesiology
- Physiology
Background:
- Halothane is an anesthetic known to impair cardiac function.
- Myocardial asynergy (dyscoordinate contraction) is a potential mechanism for this impairment.
Purpose of the Study:
- To investigate if myocardial asynergy contributes to halothane-induced cardiac dysfunction.
- To assess the validity of cardiac performance measurements during halothane anesthesia.
Main Methods:
- Coronary cineangiograms were performed in seven dogs under varying halothane concentrations (1, 2, and 3 MAC).
- Ventricular dimensions were analyzed by plotting relative motions of arterial bifurcations.
- Myocardial asynergy was quantified using anisotropy (AI) and asynchrony (AS), leading to a myocardial performance index (MPI).
Main Results:
- Mean shortening (S-) and myocardial performance index (MPI) decreased with increasing halothane concentration.
- Anisotropy (AI) showed a trend toward increase, while asynchrony (AS) remained unchanged.
- Myocardial asynergy was found to contribute minimally to halothane-induced cardiac impairment.
Conclusions:
- Myocardial asynergy is not a significant factor in halothane-induced cardiac dysfunction.
- Cardiac performance measurements, such as dP/dtmax, are likely valid during halothane anesthesia if loading conditions are considered.
Abstract:
We investigated the possibility that myocardial asynergy (dyscoordinate contraction) is a contributing mechanism to the impairment of cardiac function produced by halothane. Coronary cineangiograms were performed in seven dogs, awake and at 1, 2, and 3 MAC halothane. The relative motions between four arterial bifurcations (six segments) were plotted as an indication of changing ventricular dimensions. To quantitate ventricular asynergy, we calculated anisotropy (AI) and asynchrony (AS), the coefficient of variation of mean shortening (S-) and of mean time to half shortening (T-50), respectively, of the six segments. From these a myocardial performance index (MPI) was derived: MPI = S-/AI + T-50 + AS. In general, S- and MPI decreased with increasing halothane concentration. Anisotropy showed a trend, although usually insignificant, toward increasing, while AS did not change. These observations have two implications. First, asynergy of contraction contributes little, if anything, to halothane-induced impairment of myocardial performance. Second, changes in measurements of intact cardiac performance, such as dP/dtmax, may be reasonably valid during halothane, provided loading conditions are taken into account.