[Pharmacotherapy of severe heart failure with inodilators--new approaches].
Severe congestive heart failure and cardiogenic shock don't resemble a homogeneous clinical picture, but a syndrome that is based on very different etiologies. What all the etiologies have in common is the inadequate peripheral O2-supply to essential organs with or without signs of severe pulmonary congestion up to pulmonary edema. For prognosis and therapy is a fast diagnostical clarification of the causes crucial. The therapeutical procedure for the various etiologies may be diametrically opposed. For the therapy is it also dicisive to distinguish between acute myocardial failure, e.g. acute myocardial infarction, and the development of myocardial failure from a longer existing consistent congestive heart failure (cardiomyopathy). Whenever possible, next to symptomatically therapy of cardiogenic shock the basic conditions of the disease should be cured (e.g., PTCA, lysis with acute myocardial infarction, lysis in acute pulmonary embolism). In myogenic cardiogenic shock the use of positive-inotropic substances with and without simultaneous vasodilatory effects, if necessary in combination with other vasodilators, may be life-saving. Up until now there still doesn't exist an alternative to the catecholamines in the acute phase, initially they should be used as a first-line-therapy to stabilize the hemodynamics. The insertion of a Swan-Ganz-catheter for invasive therapy-monitoring, especially for the regulation of the therapy is a "condition sine qua non" for every patient with unstable hemodynamics. Because of the prompt beta-receptor-down-regulation during shock, caused by endogenous catecholamines, successful therapy with exogenous catecholamines is limited (adrenaline, dopamine, dobutamine), on account of the acceleration and intensification of the beta-receptor-down-regulation process. Possible beta-receptor independent alternatives are beta 2-agonists (dopexamine), PDE-III-inhibitors (amrinone, milrinone, enoximone) as well as H2-receptor agonists (impromidine, arpromidine) and finally the calcium-sensitisers (pimobendane). First results give rise to optimism to effectively reduce the mortality of congestive heart failure. The combination of these new pharmacological possibilities with interventional transcutaneous applicable assist-systems (aortic counterpulsationpump IABP, hemopump, transcutaneous heart-lung-machine) as well as the transitory application of an artificial heart (Novacor) can possibly increase the success of these therapeutic strategies. So far there are no convincing results shown in the world literature.
Baumann
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I. Medizinische Klinik Kardiologie-Angiologie-Pneumologie, Universitätsklinikum Charité Humboldt-Universität Berlin.
Hader
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O
D000318:Adrenergic beta-Agonists / Q000009:adverse effects / Q000627:therapeutic use; D002316:Cardiotonic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D002395:Catecholamines / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology; D006439:Hemodynamics / Q000187:drug effects; D017442:Histamine Agonists / Q000627:therapeutic use; D006801:Humans; D010726:Phosphodiesterase Inhibitors / Q000009:adverse effects / Q000627:therapeutic use; D012770:Shock, Cardiogenic / Q000188:drug therapy / Q000209:etiology; D014665:Vasodilator Agents / Q000009:adverse effects / Q000627:therapeutic use*
D000318:Adrenergic beta-Agonists; D002316:Cardiotonic Agents; D002395:Catecholamines; D017442:Histamine Agonists; D010726:Phosphodiesterase Inhibitors; D014665:Vasodilator Agents