Short-term cardiac adaptation to severe haemodilution: an echocardiographic study in normal and hypertensive subjects.

In order to avoid transfusion risks and optimize blood bank resources, in recent years many blood sparing techniques have been proposed, including severe haemodilution. The aim of this study is to assess the pattern of normal haemodynamic and cardiac adaptation to severe haemodilution in patients undergoing major orthopaedic surgery and refusing blood transfusions for religious reasons (the patients were Jehovah's Witnesses). Two-dimensionally guided M-mode echocardiograms were performed at baseline and 4 days after major orthopaedic surgery in 26 Jehovah's Witnesses (age 61±11 years), with normal regional and global baseline left ventricular function and no valvular disease. Left ventricular (LV) volumes were estimated by using the Teichholz formula. From the latter, we calculated ejection fraction and stroke volume, cardiac output (stroke volume× heart rate), and total peripheral resistance estimated as mean arterial pressure by cuff sphygmomanometer × 80/cardiac output. On the basis of LV mass (ASE-cube corrected by Devereux), two groups were identified: non-hypertrophic (LV mass index <110 g. m−2 in women and <130g. m−2 in males) and hypertrophic. In the 19 patients without LV hypertrophy, haemoglobin decreased from 13.5±1.6 (mean ± standard deviation) g. dl−1 (at baseline) to 8.7 ± 1.3 post-operation (P<0.01), and peripheral vascular resistances fell from 2131 ± 450 to 1278±310 (dyne. s. cm−5) (P<0.01). There was an increase in heart rate (from 68±9 to 87±9 beats. min−1, P<0.01) and cardiac output (from 3.8 ±0.7 to 6.7 ±1.41 min−1, P<0.01), with a rise in ejection fraction (from 62 ± 5 to 66 ± 6%, P<0.01) and a decrease in relative wall thickness (from 0.42 ± 0.03 to 0.35 ± 0.04, P<0.01). In the seven hypertensive hypertrophic patients, haemoglobin went from 12.4 ± 1 (at baseline) to 8.4 ± 1.5 post-operation (P<0.01) and peripheral vascular resistances fell from 2551 ± 845 to 1363 ± 413 (P<0.01). There was an increase in heart rate (+38%) and cardiac output (+46%) comparable to that found in non-hypertrophic patients, but with no significant variation in LV relative wall thickness (from 0.50 ± 0.08 to 0.48 ± 0.05, P=ns) and no increase in ejection fraction (from 62 ±8 to 62.3 ±9%, P=ns). There was an inverse correlation between haemoglobin levels and LV cardiac output in both the normal ( r = - 0.74; P<0.01) and the hypertrophic ( r = -0.63, P<0.05) group. In conclusion, severe haemodilution induces a high output state with a fall in peripheral vascular resistance. This haemodynamic adaptation is accompanied by an eccentric remodelling in normal, but not in hypertrophic, hearts. In normal patients, but much less so in the hypertrophic ones, LV geometry is a dynamic variable which can be profoundly modified by a few days of severe haemodilution and can thus significantly contribute to the overall adaptation to altered haemodynamics.