A shock state is characterized by 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 oxygen delivery. 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. Refer to Chapter 61, Classification of Shock, for further information.
To review, mean arterial pressure (MAP) is the product of systemic vascular resistance (SVR) and cardiac output (CO). SVR is affected by blood viscosity, vessel length, and vessel diameter. The major determinant of SVR is the arterioles, which manipulate blood supply by dilating or contracting. CO is the product of stroke volume (SV) and heart rate (HR). SV is dependent on preload (end-diastolic volume), afterload, and cardiac contractility. Vasoactive therapies are used in an attempt to manipulate these important parameters and these relationships can be visualized using Formula 1. As demonstrated there, an increase in SVR, SV or HR will result an increase in MAP.
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 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. By increasing SV, the intent is to increase the cardiac output (CO) and therefore increase blood pressure. Ultimately, the goal of either increasing SVR or increasing CO is to increase oxygen delivery to hypoperfused organs. Vasoactive drugs can also increase HR by increasing the sinoatrial conduction, giving them “chronotropic” properties. A “dromotropic” effect refers to an increase in atrioventricular (AV) nodal conduction.
Vasopressors and inotropic drugs can also be divided into two types based on their effects: adrenergic and non-adrenergic. The adrenergic agonists function at adrenergic receptors (α1, α2, β1, β2) and dopaminergic (DA) receptors. The non-adrenergic 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 19-1 provides a summary ...