THORACIC IMPEDANCE AND PULMONARY ATRIAL-NATRIURETIC-PEPTIDE DURING HEAD-UP TILT INDUCED HYPOVOLEMIC SHOCK IN HUMANS

Head up and down tilts were used for manipulating the central blood vo lume in eight volunteers. During head-up tilt: thoracic electrical imp edance (TI) increased from 36.7 (33.9-52.1) ohm (mean and range) to 41 .9 (36.9-59.2) ohm, heart rate from 60 (49-72) to 80 (65-90) beats min (-1) (P < 0.05) and decreased again to 57 (48-67) beats min(-1) accomp anying a fall in mean arterial pressure from 86 (76-97) to 54 (41-79) mmHg and in cardiac output from 9.2 (5.9-12. 1) to 6.9 (3.4-8.8) 1 min (-1) (n = 7, P < 0.07). Central venous pressure did not change signifi cantly, Pulmonary arterial mean, 6 (3-12) mmHg, and wedge pressures, 4 (1-9)mmHg, decreased to 4 (1-11) and 1 (0-7)mmHg, respectively, and m ixed, 78 (77-79%), and central venous oxygen saturations, 72 (71-73)%, fell to 62 (46-75) and 54 (44-58)%, respectively (P < 0.05). Atrial n atriuretic peptide (ANP) was determined from blood of the superior ven a cava and pulmonary and brachial arteries. Pulmonary artery ANP, 18.4 (7.5-30.7) pmol 1(-1), was higher than in vena cava, 13.3 (5.2-20.9) pmol 1(-1) (P < 0.05). At the time of presyncope, pulmonary artery ANP decreased from 20.8 (37.4-10.1) to 13.7 (19.7-5.7) pmol 1(-1), in ven a cava from 13.8 (23.1-7.1) to 10.2 (17.9-6.7) pmol 1(-1) and in the b rachial artery from 16.9 (34.1-5.2) to 11.3 (18.5-5.1) pmol 1(-1) (P < 0.05). Head-down tilt did not affect the recorded variables significan tly. Thoracic electrical impedance, pulmonary artery pressure and veno us oxygen saturations were sensitive indices of the central blood volu me as reflected in the release of atrial natriuretic peptide from the right side of the heart.