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Acute volume infusion improves left ventricular diastolic function during heat stress
Author(s) -
Brothers R. Matthew,
Wilson Thad,
Dalsgaard Morten,
BundgaardNielsen Morten,
Pecini Redi,
Secher Niels,
Crandall Craig
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1053.5
Subject(s) - cardiology , diastolic function , medicine , ventricular function , volume (thermodynamics) , diastole , heat stress , blood pressure , physics , thermodynamics , atmospheric sciences
Reduced left ventricular (LV) filling pressure impairs diastolic function in normothermic individuals. However, during heat stress LV filling pressure is similarly reduced but diastolic function is preserved, suggesting that heat stress improves diastolic function but this is masked by reductions in LV filling pressure. If this is correct, then normalizing LV filling pressure during heat stress should improve diastolic function. This study tested the hypothesis that restoration of LV filling pressure to normothermic values by acute volume loading during heat stress would improve diastolic function relative to control heat stress conditions. Early diastolic mitral inflow and early diastolic mitral annular tissue velocities were assessed via echocardiography in nine subjects after an increase in pulmonary artery blood temperature of 1.3±0.2 °C (HS) and after volume infusion sufficient to restore central venous pressure to the normothermic value (HS + Inf). Early diastolic mitral inflow velocity (HS: 78±13 cm·sec −1 , HS +Inf: 94±17 cm·sec −1 ; P= 0.01) and early diastolic mitral annular tissue velocity (HS: 14.4±2.5 cm·sec −1 , HS +Inf: 16.1±3.1 cm·sec −1 ; P= 0.04) were increased following restoration of LV filling pressure, as indexed by central venous pressure, back to the normothermic value. These data indicate that heat stress improves LV diastolic function. Supported by NIH Grant NIH‐HL61388 & HL84072