Showing papers by "Torben Pedersen published in 1983"
Journal Article•
TL;DR: Changes in the DPTI/SPTI ratio showed that the improvement in left ventricular performance was at the expense of myocardial oxygen balance, which caused a greater incidence ofMyocardial underperfusion, particularly in patients with cardiac failure.
Abstract: The effects of hemodialysis on cardiac performance and myocardial oxygen balance were evaluated by impedance cardiography in 16 patients with end-stage renal failure treated with regular hemodialysis. Cardiac symptoms and/or failure were present in 8 patients (group A) whereas 8 patients (group B) had no signs of heart dysfunction. The hemodialysis were carried out without ultrafiltration so that the body weight was the same before and after dialysis. The two groups did not differ significantly with regard to either biochemical values or hemodynamic parameters before dialysis. During dialysis mean cardiac output (CO) increased significantly 7.1 +/- 2.8 l/min to 9.1 +/- 3.6 l/min (P less than 0.01), mainly in patients group A, and was maximum after 90 min. The myocardial oxygen balance estimated from the supply/demand ratio (DPTI/SPTI) was significantly reduced after 20 min from 1.14 +/- 0.16 to 0.99 +/- 0.12 (P less than 0.01). After 60 min DPTI/SPTI decreased to its lowest value due to an excess of myocardial oxygen demand (SPTI) over myocardial oxygen supply (DPTI), signifying a transitory underperfusion of the subendocardium which occurred mainly in patients with cardiac failure (group A). Mean arterial blood pressure remained unchanged whereas mean heart rate increased significantly after 90 min and remained raised throughout the rest of dialysis (78.8 +/- 10.4 bpm to 87.1 +/- 12.6 bpm [P less than 0.01]). Total peripheral resistance (TPR) was decreased significantly after 5 min (P less than 0.01), but subsequent falls were not significant. Changes in the DPTI/SPTI ratio showed that the improvement in left ventricular performance was at the expense of myocardial oxygen balance, which caused a greater incidence of myocardial underperfusion, particularly in patients with cardiac failure.
9 citations
TL;DR: It is concluded that prenalterol has positive inotropic and chronotropic effects in patients with chronic renal failure, that the improvement in left ventricular performance is at the expense of a decreased transmural myocardial perfusion, and that metoprolol is a specific antidote.
Abstract: The acute haemodynamic effects of the beta-adrenoreceptor agonist, prenalterol, were studied in six patients with chronic end-stage renal failure. Prenalterol 0.8 mg, 1.6 mg, and 3.2 mg was administered i.v. as a bolus, and after the last dose the selective adrenergic beta-1-receptor antagonist metoprolol was administered i.v. in doses of 5 and 10 mg. The haemodynamic effects of the drugs were investigated using impedance cardiography and radionuclide angiocardiography. The main haemodynamic effects were a dose-related chronotropic effect, demonstrated by an increase in heart rate (26%; <0.05), and an inotropic effect, shown by an increase in stroke volume index (20%;p<0.05) and left ventricular ejection time (12%;p<0.05); the cardiac index was increased by 47% (p<0.05). Transmural myocardial perfusion (DPTI/SPTI ratio) was decreased by 22% (p<0.05) after prenalterol. It is concluded that prenalterol has positive inotropic and chronotropic effects in patients with chronic renal failure, that the improvement in left ventricular performance is at the expense of a decreased transmural myocardial perfusion, and that metoprolol is a specific antidote.
4 citations