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In a shock state tissue, perfusion is compromised causing hypoperfusion to organs, cellular hypoxia, and metabolic disorder resulting in cellular injury. Injury to the organs is mainly due to the duration of the hypoperfusion and the speed with which the etiology can be treated and the shock state can be reversed. When patients are hemodynamically unstable, an important and potentially life-saving intervention is the use of vasoactive therapies to restore appropriate tissue perfusion by increasing blood flow and thereby increasing oxygenation. Vasoactive agents can be categorized by their activity and are often divided into two types: vasopressors and inotropes. The term vasopressor refers to a class of drugs that cause vasoconstriction. Typically, increasing vasoconstriction leads to an increase in systemic vascular resistance (SVR), which leads to an increase in blood pressure. The term inotrope refers to a class of drugs that increase the strength of cardiac contraction. Increasing the strength of cardiac contractions will increase the stroke volume (SV). By increasing SV, the intent is to increase the cardiac output (CO) and therefore increase blood pressure.

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To review, mean arterial pressure (MAP) is the product of SVR and CO. SVR is the resistance that blood flow must overcome to reach the circulatory system; it is affected by blood viscosity, vessel length, and vessel diameter. The major determinant of SVR is the arterioles, which can manipulate blood supply by altering their diameter. Recall that keep in mind that CO is the product of SV and heart rate. SV is the quantitiy of blood that is pumped from the ventricle of the heart with each beat, which is dependent on preload (end-diastolic volume), afterload, and cardiac contractility. Vasoactive therapies are used in an attempt to manipulate these important parameters. Vasoactive drugs can also increase heart rate by increasing the sinoatrial conduction, giving them “chronotropic” properties. A “dromotropic” effect refers to an increase in atrioventricular (AV) nodal conduction.

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Prior to or concurrent with initiating vasoactive or inotropic medications, it is essential to attempt to identify the potential cause of the shock state and guide therapy based on this presumptive diagnosis.

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Vasopressors and inotropic drugs are divided into two types based on their effects: adrenergic and nonadrenergic. The adrenergic agonists function at adrenergic receptors (α1, α2, β1, β2) and dopaminergic (DA) receptors. The nonadrenergic agonists exert their effect primarily via the vasopressin-specific receptor (V1, V2) or by inhibition of phosphodiesterase 3, which potentiates the effect of cyclic adenosine monophosphate (cAMP). It is crucial to have a good understanding of the physiologic function of these medications and their corresponding receptors and to use this understanding to guide therapy. Table 16-1 provides a summary of the physiologic responses associated with each receptor.

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Table 16-1. Physiologic Actions of Receptors Stimulated by Vasopressors

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