Cardiocirculatory effects of acutely increased intracranial pressure and subsequent brain death

Abstract

Hemodynamic instability and functional impairment of the donor heart are currently reported problems in organ transplantation. Actual shortage of potential donor hearts continues to raise controversial discussion about adequate donor management with regard to graft quality. In an experimental open chest model, physiopathologic effects of acutely induced, irreversible intracranial hypertension (AIIHT) were investigated in situ with respect to hemodynamics, cardiac pump and muscle function, and hormonal parameters. Acutely induced irreversible intracranial hypertension was induced by rapid inflation of a subdural balloon catheter in 10 anesthetized dogs, four animals serving as controls. The observation period in both groups was 300 min. Cardiocirculatory stability was maintained by continuous crystalloid volume substitution without the use of inotropic or pressor agents. After AIIHT, three characteristic hemodynamic response phases have been observed: 1) The "acute hyperdynamic phase" lasting up to 15 min with marked increases of heart rate (HR), left ventricular pressure (LVP), cardiac output (CO) and myocardial contractility indices, 2) At the end of the "early restabilization phase", (60 min), these parameters returned close to control levels, except HR (+50%) and systemic vascular resistance (SVR) (-40%), 3) During the "late restabilization phase", filling pressures, LVP and CO remained within control limits at low SVR, contractility indices showed a decreasing tendency. All assessed plasmatic hormones (Catecholamines, triiodothyronine (T3), thyroxine (T4), adrenocorticotropic hormone (ACTH), cortisol and anti-diuretic hormone (ADH) showed a continuous fall to levels significantly below control over the phases of restabilization. Acutely induced irreversible intracranial hypertension leads to multifactorial hemodynamic and hormonal changes. At low SVR, cardiac pump function was preserved exclusively by continuous volume substitution, while myocardial contractility indicated a slight decrease. From this observed hemodynamic and functional state within the donor organism, no reliable prediction on graft functional capacity can be made.