TREATMENT OPTIONS FOR HEART-FAILURE IN CA RDIAC-SURGERY

Citation
Hr. Zerkowski et al., TREATMENT OPTIONS FOR HEART-FAILURE IN CA RDIAC-SURGERY, Zeitschrift fur Kardiologie, 83, 1994, pp. 55-61
Citations number
38
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
03005860
Volume
83
Year of publication
1994
Supplement
2
Pages
55 - 61
Database
ISI
SICI code
0300-5860(1994)83:<55:TOFHIC>2.0.ZU;2-T
Abstract
Perioperative deterioration of the circulatory performance of patients undergoing heart surgery ranges from transitory impairment in cardiac output by deterioration of the compensation range of the oxygen trans port system to manifest circulatory failure without previous myocardia l damage and the acute decompensation of pre-existing chronic heart fa ilure. On the basis of the current state of knowledge in this field, a concept for rational staged treatment should be based on the differen t myocardial beta-adrenoceptor conditions related to the type and stag e of the individual underlying heart disease and on adrenoceptor subty pe specific properties of positive inotropic drugs. 1. The therapy of perioperative ''circulatory'' insufficiency after extra-corporal circu lation consists of the use of drugs to adapt the performance of the ox ygen transport system to increased overall oxygen demand. Simultaneous volume loading (by CVP) and positive inotropic support with dobutamin e are the best means of treating this (normally transitory) dysregulat ion. 2. In the case of manifest severe circulatory insufficiency (low cardiac output syndrome), sepsis or acute heart failure (e.g., followi ng acute myocardial infarction), the use of a pulmonary artery cathete r for determining perioperative cardiac output and resistance is essen tial. In such cases, positive inotropic therapy is based on catecholam ines of medium (dobutamine) to high (adrenaline) efficacy, because it can be assumed that the beta-adrenoceptor pattern will remain normal w ith regular functioning and regulation of the (remaining) myocardium u p to the onset of acute heart failure. To reduce the work load on the heart and to maintain adequate perfusion pressures, the peripheral vas cular resistance is adjusted to 800 - 1200 dyn.s.cm(-5) using vasocons trictors (phenylephrine, noradrenaline, depending on frequency) or dil ators (nifedipine, nitroglycerine, possibly ACE inhibitors). 3. Severe chronic heart failure with perioperative decompensation is accompanie d by p-adrenoreceptor down-regulation of varying degress of severity a nd a capacity for postreceptor stimulation which is, from a clinical s tandpoint, largely unaffected. Except in the severest cases of cardiom yopathy, there is little impact on cAMP/PDE-III interaction. In this s ituation, we use PDE-III inhibitors as the sole therapy. 4. If the hem odynamic improvement obtained is insufficient, the PDE-III inhibitors is supplemented by low doses of catecholamines (adrenaline). This almo st always produces sufficient improvement in circulatory performance. In the overwhelming majority of cases, the situation can be brought un der control by using this staged therapy program adapted to the cardia c and circulatory condition to be expected in each case (after problem s requiring surgery have been rigorously excluded). If this therapy is unsuccessful, steps such as the use of mechanical support devices or a transplant should be discussed.