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Effects of therapeutic hypothermia on left ventricular function assessed by ultrasound imaging
Andreas Espinoza1, Viesturs Kerans, Anders Opdahl
1The Intervention Center, Rikshospitalet, Oslo University Hospital, Oslo, Norway; University of Oslo, Oslo, Norway.
Background:
Therapeutic hypothermia is used after cardiac arrest. The aim of this study was to investigate the effects of therapeutic hypothermia on left ventricular (LV) function assessed by ultrasonic imaging.
Methods:
In 10 pigs, LV volumes, ejection fractions, and longitudinal strain were measured using two-dimensional echocardiography. Midwall fractional shortening and end-systolic wall stress were calculated. Wall thickness was continuously measured using an epicardial ultrasonic transducer placed on the LV anterior wall. Wall thickening velocity (S') and pressure-wall thickness loops were used to assess systolic function. Diastolic function was assessed by echocardiographic transmitral flow and mitral annular velocity (e') measurements, calculation of the LV relaxation constant, and determination of LV stiffness and restoring forces using the end-diastolic pressure-wall thickness relation during volume unloading. Early wall thinning velocity (e'wt) and early diastolic wall thinning were calculated. Measurements were done at 38°C and 33°C, at spontaneous heart rate and at atrial pacing at 100 beats/min.
Results:
End-diastolic volume, stroke volume, midwall fractional shortening, and longitudinal strain remained unchanged during hypothermia, but end-systolic wall stress, S', and pressure-wall thickness loop area decreased. A shift from early to late diastolic LV filling occurred during hypothermia, with concurrent decreases in e', e'wt, and early wall thinning fraction. Relaxation was prolonged, LV stiffness was increased, and restoring force was decreased during hypothermia. Hypothermia induced a decrease in relative diastolic duration at spontaneous heart rate, which was further reduced during pacing. During paced heart rate at 33°C, stroke volume, ejection fraction, and strain were reduced.
Conclusions:
Hypothermia induced systolic and diastolic dysfunction, with reduced tolerance to increased heart rate. These findings may have implications for patient management during hypothermia.
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