Myocardial depression after cardiac surgery is a well-described phenomenon. Possible causes for the depressed myocardial performance include the underlying cardiac disease, residual effects of cold potassium cardioplegia, inadequate myocardial protection during aortic cross-clamping, or direct reperfusion injury to the myocardium. Depressed myocardial function may be present for many hours following separation from cardiopulmonary bypass. To help maintain vital organ perfusion during the perioperative period, various inotropic drugs are used, including B-adrenergic agonists and phosphodiesterase inhibitors. Intra-aortic balloon counterpulsation offers increased coronary artery perfusion and additional mechanical assistance to the left ventricle to improve vital organ perfusion, and may also be used in the immediate postoperative period. flovent inhaler
The adrenergic input to the myocardium is primarily B-adrenoceptor mediated, with two distinct subtypes of beta adrenoceptors (B1 and B2) present in all chambers of the human heart The heart relies predominantly on B-adrenergic inotropic mechanisms to increase contractility and cardiac output in response to acute or chronic stress The net result of /З-adrenoceptor stimulation is an increase in intracellular cyclic AMP (cAMP) during systole which ultimately increases intracellular calcium for interaction with actin and myosin filaments. The increased cAMP concentration also favors more rapid reductions in intracellular calcium during diastole, thus allowing for more effective diastolic relaxation and ventricular filling. Although different B-agonists may bind to the same B-adrenoceptor, the result of this stimulation may be dramatically different, as some agonists have a more potent ability to increase cAMP than others. Moreover, many of the available B-adrenergic agonists bind to other receptor types, including dopaminergic (DA-1) receptors (dopamine, dopexamine) or ai-receptors (dopamine, epinephrine, norepinephrine). Not only do B-agonists vary in their ability to increase cAMP (and therefore intracellular calcium), but stimulation of a single B-adrenoceptor leads to the production of up to 10 times more cAMP molecules than does stimulation of a single B1-adrenoceptor Under normal conditions, the ratio of B1 to B2 receptors in the right and left ventricular tissue is 4:1.