The appropriate use of inotropes in shock

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Shock is best defined as a syndrome of failure of the heart to pump blood into the aorta in sufficient quantity or under sufficient pressure to maintain the pressure-flow relationship for adequate tissue perfusion. The various therapeutic options available are best selected to insure the most efficient correction of identifiable pathophysiology. One such approach utilizes the principles of cardiac function outlined by Ernest Starling at the turn of the century.t Using the concept in Figure 1, the clinician attempts to identify the dynamic state of the myocardium hypothesizing the existence of a hyperdynamic contractile heart as might exist with sepsis or a hypodynamic state as seen in cardiogenic shock. Beyond this must be estimated the preload or end-diastolic volume further influencing ventricular output. Preload serves as an indication of adequacy of intravascular volume, yet varies dependent on the contractile state of the myocardium. Thus, in Figure 1 a number of points is designated on the Starling curves depicting states of altered preload and/or contractility. Once assessment of the patient in shock leads to an approximation of this existing pathophysiology selection of therapy follows. Figure 2 outlines the various therapeutic options available dependent on the identified abnormalities. Rapid assessment of response to the chosen therapy must be made to either insure the correctness of the initial selection or to indicate the need for alternative treatment. lnotropic therapy to increase myocardial contractility is commonly selected. Many considerations are involved in the timing for inotropic stimulation, the correct selection of agent, the desirability for concurrent pharmacology (i.e., afterload reduction) and the proper limits/'or increase in cardiac output. The goal of increased ventricular output first requires optimal levels of preload, lnotropic stimulation in the presence of intravascular hypovolaemia often fails to achieve increased stroke volume but rather results in undesirable effects of increased afterload, tachycardia and dysrhythmias. Achieving pulmonary artery wedge pressures in excess of 10-12 mmHg and preferably between 15 and 18 mmHg should precede institution of pharmacological inotropic stimulation. The relationship of afterload as indicated by calculation of vascular resistance should also be understood. Afterload reduction with arterial dilator therapy may be preferable to i notropic drugs when systemic arterial pressure is adequate, as such therapy may reduce myocardial wall tension and myocarVENTRtCULAR OUTPUT A = Hypovolemia B = Hypocontraclilo C = Hypervoh:mla Hypordynamlc